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_ DISEASES OF DOMESTICATED BIRDS |

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THE MACMILLAN COMPANY
NEW YORK - BOSTON - CHICAGO - DALLAS
ATLANTA * SAN FRANCISCO

MACMILLAN & CO., LimrTED
LONDON + BOMBAY - CALCUTTA
MELBOURNE

THE MACMILLAN CO. OF CANADA, Lrp.
TORONTO

Y DISEASES
OF DOMESTICATED BIRDS

BY
ARCHIBALD ROBINSON WARD, B.S. A., D.V.M.

Director, Research Department, The Jensen-S.lsbery
Laboratories, Kansas City, Missouri

AND

BERNARD A. GALLAGHER, D.V.M.

Bacteriologist, Bureau of Anima! Industry, United States
Department of Agriculture, Washington, D. C.

WITH INTRODUCTION BY
VERANUS ALVA MOORE, B.S., M.D., V.M.D.

Professor of Comparative Pathology, Bacterivlogy and Meat Inspection,
New York State Veterinary College at Cornell University,
and Director of the College

IQew Pork
THE MACMILLAN COMPANY
1920

All rights reserved

.

; CopyricutT, 1920, hi

al By THE MACMILLAN COMPANY

| i ; e Set up and electrotyped. Published, January, 1920

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PREFACE

The writing of this book has been prompted by a conviction held
by the authors, regarding the magnitude of the losses experienced
by poultry producers as a result of preventable infectious diseases
and parasitic infestations. /

It is believed that the importance of these losses warrants the
effort expended in presenting the essential facts concerning poultry
diseases to meet the needs of veterinary practitioners, veterinary stu-
dents and poultrymen.

The title of the book indicates a slight broadening of scope beyond
the field of a work on diseases of poultry. Material included deals
with the ostrich, cage birds and wild birds in semi-domestication in
zoological gardens. Chapters dealing with anatomy of birds, and
killing of poultry have been included.

The peculiarities of diseases of birds are indicated by the emphasis
laid on certain features of the subject matter. In general, skill in
diagnosing diseases of birds by observing symptoms is of less impor-
tance than ability to recognize the identity of disease at autopsy.
Symptoms are slightly characteristic, but autopsy material is freely
available. Consequently more facts concerning details of gross
lesions are given than those relating to symptoms. In many cases,
particularly in the septicemias, symptoms and lesions are not dis-
tinctive, and fine distinctions of etiology must be made by a bacteri-
ologist. On this account considerable material useful to a bacteri-
ologist alone has been included.

Available sources of information are indicated in the references
appended to each chapter and by specific references to authors in the
text. Special acknowledgment is made for assistance obtained from
Neumann’s “ Parasites et Maladies Parasitaires des Oiseaux Do-
mestiques ” in the preparation of the chapters on parasites. Much
material concerning the less common parasites has been drawn from
this book and Neumann’s zoological nomenclature has been largely
followed. c

A. RR. W.
by A. G.

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INTRODUCTION

The statement is accepted that diseases are the greatest hindrance
to the development of animal and poultry husbandry. Measures
for the prevention, successful treatment or control of these maladies
must come from those who understand their nature. It is grati-
fying, therefore, that veterinarians, and others interested in the
subject, are to have access to a volume dealing with the diseases
of poultry, prepared by men of long experience in the study of the
phenomena of disease. Likewise, poultry raisers will appreciate
a treatise setting forth the known facts concerning the maladies
which sooner or later may affect their flocks. A book of this kind
will be of indispensable value in eliminating many of the miscon-
ceptions regarding the diseases of poultry and in pointing out the
things that are known and the precautions that must be observed in
maintaining healthy flocks.

The extent of the poultry industry in the United States is little
appreciated by veterinarians. There is no other species in the
animal kingdom that contributes to the material support of so large
a number of people as the domesticated fowl. In addition turkeys,
geese, ducks and pigeons are significant factors in food production
while the ostrich and other birds play an important part in orna-
mentation. In the Hartz Mountains, the raising of canary birds for
the amusement and entertainment of people is an important in-
dustry.

The barnyard fowl plays a large part in the food supply of the
country. The extent of the poultry business can be approximated
from the fact that in 1910 there were 5,578,525 farms in the United
States that reported a total of 280,350,000 fowls with a value of
$140,205,000. With the prices at the present time, their value
would be treble that of 1910. In 1915, the United States exported
20,784,000 dozen eggs but it imported over 3,000,000 dozen and
over 8,000,000 pounds of egg yolks and frozen eggs. These figures
indicate the large number of people who are financially interested
in the poultry business.

The raising of turkeys and other species is also significant. In
1910 there were in the United States 3,688,000 turkeys with a value

vil

vlil INTRODUCTION

of $6,605,000; 2,906,000 ducks valued at $1,567,000; 4,431,000
geese valued at $3,194,000; 1,765,000 guinea fowls valued at
$613,000; 2,730,000 pigeons with a value of $762,000; 6,458 pea
fowls estimated at $18,000; and 5,361 ostriches valued at $1,-
696,000. In 1915, this country imported ostrich and other feathers
to the value of $2,500,000. Besides, there is a large business in
song and other birds maintained as pets.

In certain localities, the raising of one or more species of poultry
constitutes the essential occupation of many of the people. The pro-
ductivity of domestic fowls is greater than that of any other species
of animals in proportion to their value. The price of the annual
products from a flock of ducks, hens or turkeys may be many times
larger than the cost of the original flock.

There is no other form of animal life that suffers more from the
ravages of disease than fowls. The losses from the general maladies
are heavy and those from the infectious ones are sometimes appal-
ling. Various estimates have been made of the annual losses occa-
sioned by these causes. They vary from 10 to 30 per cent. Hens
in particular suffer from a wide range of diseases and parasitisms.
Some of these are veritable plagues and at times are the cause of
serious losses. In 1903, while studying poultry diseases in a lo-
cality where eggs and chickens were the chief articles of commerce,
it was not unusual to learn of individual losses ranging from a few
hundred to several thousand dollars due to roup or diphtheria.
Other large flocks were decimated by tuberculosis. While it is easy
to understand that heavy losses may occur in localities where fowls
are kept in large numbers, it should be recognized that they are
proportionately heavy in smaller flocks.. In such circumstances, the
death of a few hens is often the cause of much privation if not actual
suffering among their owners who are dependent upon the products
of their fowls for the necessities of life.

The general diseases of poultry present many points of interest,
although they have received relatively little attention. The general
pathology of the feathered tribes is not well understood. Little
seems to be known of their tissue reactions to injury. Their resist-
ance to ordinary wound infections differs strikingly from that of
mammals. Pasteur suggested that this might be due to their higher
body temperature. On the other hand, the infectious diseases and
parasitisms have been more carefully studied. The findings of
many valuable researches are recorded on the nature of the more
serious ones. Certain of them, such.as bacillary white diarrhea and

INTRODUCTION iy

the parasitisms, have been elucidated sufficiently to enable veterin-
arians or poultry owners to prevent them. Others that cause heavy
losses, such as roup or diphtheria and tuberculosis, can be controlled.
When this is done, millions of dollars worth of poultry that is now
lost will be saved. This can be done as soon as the technical knowl-
edge, now available, is utilized to its full extent.

It is believed that veterinarians can render a valuable service to
this heretofore professionally neglected, yet important industry, es-
pecially in localities conspicuous for the raising of poultry. Be-
cause of the relatively small value of the individual, and the large
numbers to be dealt with, methods for preventing disease must be
applied to the flock. With the exception of the more Valuable
birds, individual treatment may not be practicable, but the princi-
ples of sanitation and the preventive measures are as helpful here
as elsewhere in the raising of animals. Veterinarians should re-
alize that the treatment, prevention or control of diseases in poultry,
as well as in quadrupeds, is primarily an economic question and that
a score of dollars saved by preventing or treating diseases in fowls
is Just as essential as the saving of a like amount in sheep or calves.
This book, dealing with the diseases and the parasites of poultry,
will be of much aid to veterinarians who wish to render full service

to their communities.
V. A. Moors.

TABLE OF CONTENTS

CHAPTER I PAGE
aes CMAN LSE REESE e a ld SYRIA MOT ON) Te cat Page LE glo JM
CHAPTER II
ELV GIENE AND eS OANTDATION: Geo isk sce Gs Wwe oS si os « «+ @ 8 20

CHAPTER III

APOPLECTIFORM SEPTICEMIA AND SLEEPING DISEASE... ... . 28
CHAPTER IV

TR unity ) COPS TS TD AN Ae RNs Mg LI RT gees
CHAPTER Vi

Howl CYPHOM-AND SIMILAR UNEROTIONS . “U0 a 1 .« « « « %&, « 50
CHAPTER Wi

ENCE AR yO NEIERG TFARRUGIAQI MRE 5) Nel use Oe Se eww ee ES

CHAPTER VII
MOEN IRE Meee Me PR te ce we Va etre he ca ad ine oe

CHAPTER VIII

A ARMANUREROEINOSIS a ci of cl eAca a fe %s ek er we ke ww 88
CHAPTER IX

AtTANn IPED aeRIACAND IIRD POX). 06 <6 ee ew we et ne | 96
OHAPTER: X

ASEARRIMIORI TANI OAVUIG) 5) te Gs a ust ee we Ue we we Cw
CHAPTER XI

InFEcTIOUS ENTERO-HEPATITIS OF TURKEYS. . ....-.. . 120

CHAPTER XII
Sasewevene 4) gl OO RS ae ee rae 6 if

CHAPTER XIII
SprROCHETOSIS AND RARE INFECTIOUS DISEASES. . . . . . ~ ~ 185
xi

Xil

CONTENTS

CHAPTER XIV

LEUKEMIA AND Pseupo. LEUKEMIA .

GENERAL DISEASES

INTERNAL PARASITES .

EXTERNAL PARASITES .

CHAPTER. X¢V

CHAPTER XVI

CHAPTER XVII

CHAPTER XVIII
INFECTIOUS DISEASES AND PARASITES OF THE OSTRICH .

CHAPTER XIX

Inrectious DISEASES OF GEESE AND Ducks .

CHAPTER XX

InrectTious DISEASES oF CaANnarRy Birps .

Tumors In Fow.ts

ToxICOLOGY

SurcicaL DISEASES

CAPONIZING

Kinuing Pouutry

CHAPTER XXI

CHAPTER XXII

CHAPTER XXIII

CHAPTER XXIV

CHAPTER XXV

PAGE -

« 146

. 226

. 242

. 252

DISEASES OF DOMESTICATED BIRDS

CHAPTER I
ANATOMY OF BIRDS

The structure of birds differs in many respects from that of
mammals and deserves a special description. The aim of the authors
is to bring to the attention of the veterinarian the more important
differences which are observed in the structure of domesticated birds
as compared with that of domesticated mammals. The subject will
be considered under the following sub-divisions. 1. Skeleton, 2.
Musculature, 3. Circulatory system, 4. Nervous system, 5. Ali-
mentary system, 6. Respiratory system, 7. Urinary system, 8.
Generative system, and 9. The skin and its appendages.

SKELETON

Skull. The bones of the skull become united shortly after hatch-
ing and lose their individual identity except in the case of the as-
cending processes of the premaxillary and nasal bones which are
not rigidly joined to the frontal bone but through their cartilaginous
attachment permit the elevation of the superior mandible. The in-
ferior processes of the premaxillary bone, the supermaxillaries and
the palatine bones which form the roof of the palate do not meet
in the median line, with the result that the palate presents an
elongated opening or cleft.

Vertebral column. The cervical vertebree vary in number in
the different species. Statements of anatomists differ concerning the
number, because of difficulties experienced in defining cervical and
thoracic vertebre. The atlas or first cervical vertebra is ring-like in
form and articulates with the occipital bone of the skull by means of
a deep concavity into which the condyle of the occipital bone is re-
ceived. This articular arrangement and that of the other cervical
vertebrx gives the head and neck great mobility. The articular sur-
face is concave from side to side and convex in a dorso-ventral direc-
tion on the anterior extremity of each vertebra, presenting a saddle
shaped appearance. The posterior-extremity is the reverse, that is,
concave dorso-ventrally and convex from side to side.

il

2 DISEASES OF DOMESTICATED BIRDS

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-~Metacarpus

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Pygostyle

Sternum.”

Patella

~~ Metatarsus

Fic. 1. The skeleton of the fowl. (Bradley)

The thoracic vertebree are nearly always fused together by the con-
solidation of their spinous and transverse processes. The first may
be free and the last may be fused with the lumbar vertebre.

The lumbar and sacral regions of the vertebral column show no
special line of demarcation. The fourteen vertebre are consoli-
dated into one bony mass which carries ridges on its ventral surface
representing the transverse processes of the original independent
vertebree.

The coceygeal vertebree are seven in number. The last is the
largest, is flattened on both sides and curves in a dorsal direction

ANATOMY OF BIRDS 3

at the end. It is known as the pygostyle. The coccygeal vertebrae
are movable upon each other.

Ribs. These bones articulate dorsally with the thoracic vertebre,
and ventrally with the sternum by means of the inferior ribs, except
in the case of the first two which do not reach the sternum. The
last rib is often united to the one adjoining and does not connect with
the sternum. Some of the ribs have flat uncinate processes which
extend from the posterior border and lie over the external face of the
following rib near its middle.

The sternum is highly developed in birds and forms the floor
of the thoracic cavity and to some extent, of the abdominal cavity.
It is concave on its dorsal or internal face and convex on its ventral
or external face. In fowls and pigeons a deep ridge extends along
the median line of the ventral face. This is known as the brisket or
keel. It serves to increase the area of attachment for the powerful
breast muscles. The sternum of the duck and goose does not present
as large a keel as that of the fowl and pigeon, but owing to the greater
breadth of the sternum and more solid construction the area for
muscular attachment is as great. In the fowl two long slender
lateral processes are formed on each side as a result of deep notches
which extend anteriorly into the body of the sternum. The lateral
external process is shorter than the lateral internal process and covers
the last two ribs with a broadened terminal bony plate. The lateral
borders of the body of the sternum support articular facets for the
reception of the inferior ribs. The anterior border presents an
eminence, the episternal process to which the furculum (wishbone)
is attached by a ligament. The articular surfaces for the coracoids
are located on each side of the episternal process on the anterior
border.

The internal surface of the sternum exhibits several openings
through which air is passed to the interior of the bony structure.

Bones of the wing. These comprise the scapula, coracoid, and
clavicle in the shoulder region; the humerus in the arm; the radius
and ulna in the forearm; two carpal bones, the radio-carpal bone and
ulno-carpal bone; one carpo-metacarpal bone, and three digits the
second of which has two phalanges.

The scapula is long, narrow, thin and curved like a sabre. It
extends caudad over the ribs to near the pelvis. Anteriorly it is
united with the coracoid with which it forms an articular cavity for
the reception of the head of the humerus. The coracoid also
articulates with the sternum by its ventral extremity. It is rod

+ DISEASES OF DOMESTICATED BIRDS

shaped and extends in a posterior direction obliquely ventrad from
scapular to sternum. The coracoid at its ventral extremity presents
an opening for the passage of air to the internal air space. ‘The
clavicle is attached to the coracoid at its superior end. It extends
ventrad and cdudad and curves in to the median line at the point
of the sternum where the two clavicles unite in a flattened plate and
become attached to the episternal process by a igament. The united
clavicles form a V or U shaped bone termed the fork or furculum.
This bone represents an elastic spring and serves to prevent the
wings from approaching each other during contraction of the de-
pressor muscles.

The humerus is long in palmipeds and the gallinz, and short in
the pigeon. It is stout, slightly curved and presents a pneumatic
foramen near its articular head.

The ulna is much larger than the radius and is separated from it
except at the extremities, where the two are united by hgamentous
bands. The olecranon process of the ulna is only slightly developed.

The two carpal bones represent fusions in embryonie life, of the
four bones of the proximal row. The distal carpal row of three
bones fuse with the metacarpal bones.

Bones of the leg. ‘These are the pelvic or hip bone; the femur
or thigh bone; the patella, tibio-tarsus and fibula in the lower leg
region ; a tarso-metatarsal bone, and four digits.

The pelvic bone is made up of three bones as in mammals, the
ilium, ischium and pubis. It differs from the mammalian bone in
that the pelvie girdle is not complete on the ventral floor, the two
pubic bones failing to meet in the center to form the pubic sym-
physis. This arrangement facilitates the passing of the egg through
the cavity. The ilium is the largest segment and extends along the
vertebral column in the lumbar and sacral regions. It is consoli-
dated with the last two thoracic vertebre and the lumbar and sacral
vertebrie, this extensive fusion giving the pelvis a rigidity which
compensates for the lack of a pubic union. The ischium partly
forms the side of the pelvic cavity. The pubis is mainly attached
to the ischium along the lower border and bends inward to form the
incomplete floor of the pelvic cavity. The ilium, ischium and pubis
are united at the acetabulum or articular cavity for the reception
of the head of the femur.

The femur articulates at its distal extremity with the patella, tibia
and fibula. The latter bone is united to the tibia, but does not ex-
tend to its distal articulation. The tibia is comparatively long.

ANATOMY OF BIRDS 4)

Tt has two articular surfaces on its distal extremity which articulate
with the tarso-metatarsal bone. The tarsus is absent in birds. In
males the tarso-metatarsus exhibits a slightly curved conical projec-
tion near the distal third for the support of the spur.

Four digits articulate with the distal extremity of the tarso-meta-
tarsus. Three are directed radially cephalad. The internal digit
has three phalanges; the middle, four and the external, five. The
fourth digit is directed caudad and has two phalanges succeeding
a rudimentary first metatarsal bone attached to the metatarsus by
fibro-cartilaginous tissue. The distal bone of each digit is covered
by a horny claw.

MUSCULAR SYSTEM

In general the muscles of birds correspond to those of mammals,
with such modifications as are most suited to the mechanism of avian
structure. The tendency, especially in turkeys and fowls, is to-
ward extensive ossification of the muscle tendons. ‘This is partic-
ularly noticeable in the tendons of the legs but may also be observed
in the wing and neck in some cases. The fowl and turkey also
present a marked contrast in the appearance of the muscles of the
breast and wings as compared with those of the legs. The breast
and wing muscles are white, due to the relatively small amount of
sarcoplasm in the muscle fibers. The red muscles are rich'in sarco-
plasm. White muscles are more powerful but have less endurance
than red ones. Free flying birds have red pectoral or breast muscles.

The pectoral muscles are two in number, the superficial or great
and the deep or small pectoral. The former depresses the wing
and the latter elevates it. These muscles are very massive. The
great pectoral muscle is attached to the clavicle, to the sternal crest
near its border, to the posterior lateral process of the sternum and to
the last ribs. It is inserted into the lateral tuberosity near the head
of the humerus. It is this muscle that propels the bird in flight.

The small pectoral muscle originates from the portion of the
ventral face of the sternum not occupied by the great pectoral and
also from the clavicle and membrane between the latter and the
sternum. Its tendon is inserted into the humerus opposite that of
the great pectoral muscle after passing through the foramen trios
seum which acts as a pulley. This foramen is formed by the union
of the scapula, coracoid and furculum.

The diaphragm does not exhibit the muscular development of that

6 DISEASES OF DOMESTICATED BIRDS

of mammals. It is principally membranous with fine muscular
bundles attached to the ribs. Two thin, delicate membranes com-
pose the diaphragm and divide it into two planes, a pulmonary and
a thoracic-abdominal plane. The former is spread over the in-
ferior face of the lungs and is attached to the ribs on its border. It
assists in respiration. The thoracic-abdominal plane has its origin
on the dorsal spine in common with the pulmonary plane. It is
convex anteriorly and extends to the sternum, dividing the body
cavity into a thoracic and an abdominal cavity. It also assists in
respiration and is particularly concerned with the abdominal air
sacs.

The pectineus muscle assists in the mechanical flexion of the toes
in the act of perching on the roost. It originates on a tuberosity
of the hip bone in front of the acetabulum and is continued by a
long thin tendon to a short distance distad from the head of the
tibia where it joins the flexor perforatus of the three anterior digits.

CIRCULATORY SYSTEM

The heart of birds is cone shaped, short and wide in the ostrich,
elongated and possessing a more acute apex in the common fowl. It
is placed in the anterior extremity of the thoracic cavity. Three
veins, two anterior venz cavee and one posterior vena cava, terminate
in the sinus of the right auricle. A peculiarity of the heart of
birds is the absence of a tricuspid valve at the right auriculo-ven-
tricular opening. Instead, a strong muscular fold which becomes
closely applied to the ventricular septum during systole prevents re-
gurgitation of blood into the auricular cavity. Two pulmonary veins
empty into the left auricle. The left auriculo-ventricular opening
is provided with a bi-cuspid or mitral valve. The pulmonary artery
and aorta each has a semilunar valve.

Arteries. The aorta gives off two innominate arteries, right and
left. brachio-cephalic, on leaving the heart and then passes over the
right bronchus to become the descending or dorsal aorta. It con-
tinues along the spine, giving off numerous branches, to the coccygeal
region where it separates into three terminal arteries.

The two carotids leave the innominate arteries and curve toward
the ventral median line of the neck where they ascend in close prox-
imity to each other to near the head. At the angle of the jaw each
carotid divides into the external and internal carotid arteries. The
arteries, especially those of the head and viscera, are distinguished

ANATOMY OF BIRDS 7

by their frequent anastomoses. This is also true of the veins of
birds.

Veins. The blood is returned to the heart by three trunks, the
two anterior venz cave and the posterior vena cava. The right
jugular exceeds the left in size. The two communicate with each
other by means of a cross branch at the base of the cranium.

Lymphatics. The lymphatics of birds do not form two strata,
a superficial and a deep seated, as in mammals. The latter only is
observed. Lymphatic glands are few. The most conspicuous are
located at the base of the neck and in the anterior thoracic cavity.
They are replaced by plexuses of lymphatic vessels surrounding the
principal blood vessels. From the aortic plexus arise two thoracic
ducts which pass cephalad on the ventral surface of the lungs and
terminate respectively in the jugular vein of the same side.

NORMAL AVIAN BLOOD

In birds as in mammals the blood is composed of a straw colored
fluid or plasma in which float several types of blood corpuscles. One
important difference between avian and mammalian blood, excepting
the camel, is the presence of nuclei in the red corpuscles of the
former. The formed elements or corpuscles are divided into two
main divisions, the red cells or erythrocytes and the white cells
or leucocytes. These elements vary greatly in number in different
birds, and even in the same bird at different ages. Each cubic
millimeter of an adult fowl’s blood contains approximately 3,250,000
red cells and 26,000 white cells, giving a percentage relation of 125
to 1. In certain pathologic conditions this relation is markedly
changed, the red cells rapidly decreasing and the white cells increas-
ing in numbers.

Red blood corpuscles or erythrocytes are straw colored, nucle-
ated, oval, flattened dises, about 12 microns in length and 7.3 mi-
erons in width. The nuclei take a deep blue stain with methylene
blue, or Giemsa. The surrounding protoplasm takes a light yellow
with methylene blue and a pink color with Giemsa’s stain.

White blood corpuscles or leucocytes are nucleated, colorless
cells, rounded or irregular in form. They exhibit ameboid
movement in the blood stream, some being more actively motile than
others. The variations in their size, character of the nuclei, pres-
ence of granules and character of the inclosed granules differentiate
these cells into five varieties. These varieties with their percentage
ratio are as follows:

8 DISEASES OF DOMESTICATED BIRDS

Small mononuclear leucocytes (lymphocytes) ........ 40

Large mononuclear leucocytes ......ciscescacsacnces 18
Polymorphonuclear leucocytes ........-cceeeesceeees 35
Hosinophilest-\7 a tioscnce omvcteetina t catetvemneeete i teetalons 4
Mast cellos tcc coeper ae ot loreton ere ene certo cies okay ear cnere 3

Lymphocytes. In these blood cells the nucleus is rounded or
oval and almost completely fills the cell. It stains a deep blue with
Giemsa. The narrow band of cell body stains a lighter blue and is
not readily differentiated from the nucleus by sikh staining.
The lymphocytes are from 5 to 7 microns in diameter.

Large mononuclears have a round or oval nucleus surrounded
by a well defined border of cell protoplasm. The nucleus takes a
deep blue stain, the cell body a pale blue. The cell diameter is
10 to 15 microns.

Polymorphonuclears have the appearance of having several nu-
clei held together by threads or nuclear bands. They contain con-
siderable protoplasm inclosing rod shaped or rounded granules. The
nucleus stains blue, the protoplasm, a lighter color and the granules
violet or brownish red with Giemsa’s stain. Diameter, 10 to 15
microns.

Kosinophiles have an irregular nucleus. The cell protoplasm
is filled with rounded granules Dien stain a bright red with Giemsa’s
stain. The nucleus takes a blue stain and the cell body a pale blue.
Diameter, 12 microns.

Mast cells have a lobulated nucleus which stains a deep blue.
The cell protoplasm takes a pale stain. The granules are small and
rounded and stain a dull violet with Giemsa and a deep blue with
methylene blue. Diameter, 8 to 10 microns.

Other blood cells of less importance which may be observed are
as follows:

Blood platelets are small colorless dises with granular centers.
They are 3 to 4 microns in diameter and are usually found in small
heaps of 6 to 8 cells.

Shadow cells contain a rounded or broad oval nucleus which
takes a deep blue stain. The cell body is colorless and not well de-
fined or irregular in outline. These apparently represent red blood
corpuscles undergoing degeneration. The stroma of the corpuscle
loses its pigment, becomes colorless and gradually disappears leaving
the nucleus partially or wholly separated. They are especially nu-
merous in pathologic blood.

Microblasts and macroblasts are found in the blood of young

ANATOMY OF BIRDS 5

fowls. These represent red corpuscles which are smaller and larger
respectively than the average red corpuscle.

Myelogenous leucocytes appear frequently in young fowls.
They are like mast cells except that their protoplasm is vacuolated.

NERVOUS SYSTEM

The nervous system of birds, with few exceptions, corresponds
with that of mammals. However, there are several modifications
which are of considerable interest. The cerebral hemispheres of
the brain are well developed but have a smooth surface in contrast
to the convoluted surface observed in the cerebrum of mammals.
The cerebellum is conspicuous by the smallness of its lateral lobes.
The optic lobes are placed in a lateral inferior position at the
sides of the cerebellum. The large size of the optic chiasma and
nerves indicates the paramount importance of the visual apparatus.
The diameter of an optic nerve is equal to that of the spinal cord in
its dorsal region. The olfactory lobes are relatively small. The
hippocampi are absent in the cerebrum of birds. An important fea-
ture of the nervous system of birds is the absence of nervous tracts
leading to the spinal cord from the cerebrum. The cerebrum does
however exert an influence over the rest of the nervous system
through its nervous tracts connecting it with the other divisions of
the brain. The anatomical evidence of the absence of nervous tracts
between the cerebral hemispheres and the spinal cord is supported
by the absence of any marked defects of movement succeeding the
removal of the cerebrum. The fowl so treated, on recovery from the
operation, is not sensitive to light or sound. It fails to pick up
erains and must be fed. Movement is not interfered with as the
bird constantly walks about aimlessly. Its avoidance of obstacles
shows that it is guided by some obscure means. Ability to perch
and to maintain its balance is not lost. The weight of the brain of
a medium sized fowl is ten grams.

The spinal cord of birds extends into the coccygeal vertebrae. It
is cylindrical throughout its length except in the sacral and cervico-
dorsal regions where two expansions are noted. The dorsal columns
of the cord diverge from each other in the sacrum to form the cavity
known as the sinus rhomboidalis which represents a ventricular
dilatation of the spinal canal. The brachial plexus is formed by the
last cervical and first two dorsal spinal nerves in ducks and geese and

10 DISEASES OF DOMESTICATED BIRDS

by the last three cervical and first thoracic spinal nerves in fowls,
turkeys and pigeons. It furnishes branches to the pectoral region
and wing. The pelvic region and legs are supplied by the lumbo-
sacral plexus which is formed by two lumbar and four sacral spinal
nerves. The spinal nerves vary in number according to the number
of vertebre present in each species. They arise from the spinal cord
by two roots. The anterior or ventral root is motory, the posterior
or dorsal, sensory in function. The ganglia on the latter are propor-
tionately large.

ALIMENTARY SYSTEM

The alimentary system of birds differs to a considerable degree
from that of other animals. There is no provision for mastication
of food in the mouth owing to the absence of teeth. The food is
taken up by the beak and is immediately passed by the tongue into
the pharynx. From there it enters the esophagus and is carried to
the crop where it is stored, partially softened, and slowly passed
on to the proventriculus or glandular stomach. The gall bladder
is absent in the pigeon and ostrich and occasionally in the guinea
fowl.

Mouth. The mouth is triangular in shape in such birds as the
chicken, turkey, pigeon and canary. In the duck, goose and ostrich
the mouth is comparatively long, with parallel borders and rounded
anterior extremity. The roof of the mouth or hard palate is di-
vided in the median line from near its anterior extremity to the
pharynx, thus allowing free communication with the nasal passages.
The soft palate observed in mammals is absent. The pharynx is
relatively voluminous and permits the passage of large grains, or
food masses. On its floor is the entrance to the larynx. The esoph-
agus lacks the well developed muscular wall of mammals but rela-
tively has a much greater diameter.

Crop. Gallinaceous birds possess a crop or ingluvies which rep-
resents a dilatation of the esophagus near its entrance to the thoracic
cavity. Its wall, like that of the esophagus, consists of an outer
membrane, a longitudinal muscular layer, a circular muscular layer,
and an inner mucous membrane. Passage of its contents to the first
stomach is aided by a wide circular muscle in the subcutaneous tissue
surrounding the crop. Palmipeds, such as ducks and geese, are not
provided with a distinct crop. Instead, the cervical portion of the
esophagus may beccme greatly distended in such a manner as to form
a long fusiform reservoir.

Fic. 2. Diagrammatic representation of
the principal internal organs of the
fowl. 1, tongue; 2, pharynx; 3, up-
per portion of esophagus; 4, crop; 5,
lower portion of esophagus; 6, proven-
triculus; 7, gizzard; 8, origin of duo-
denum; 9, first branch of duodenum; 7
10, second branch of duodenum; 11,
origin of floating portion of small in- 2g
testine; 12, small intestine; 12’, ter-
minal portion of small intestine; 13,
free ends of ceca; 14, origin of ceca;
15, rectum; 16, cloaca; 17, vent; 18,
mesentery; 19, left lobe of liver; 20,
right lobe of liver; 21, gall bladder; 7%
22, spleen; 23, pancreas; 24, lung;
(Heart not shown but located approxi-
mately here) ; 25, ovary; 26, oviduct;
27, kidney; 28, ureter; 29, upper
larynx; 30, trachea; 31,
lower larynx or syrinx;
32, bronchus; 33, cleft
palate; 34, common ori- #
fice of eustachian tubes.
(Redrawn from Chauveau,
with slight additions}

25.

ll

12 DISEASES OF DOMESTICATED BIRDS

In pigeons the crop is divided into two lateral pouches. In both
male and female, marked changes take place in the mucous mem
brane shortly before the young are hatched. The membrane becomes
thickened, epithelial cells are rapidly proliferated, undergo fatty
degeneration and lead to the formation of a milky fluid which aceu-
mulates in the depressions between the ridges of the mucosa. This
fluid is used to feed the young during the first days of life.

A certain amount of fluid is secreted by the alveolar glands of the
esophagus which together with the water consumed serves to soften
grains to some extent and also to produce a slight fermentation of the
crop contents. The crop has no secretory glands other than mucous
glands. It is connected with the proventriculus or first stomach by
a continuation of the esophagus which passes into the thoracic cavity
and along the ventral face of the left lung.

Proventriculus. The proventriculus is small and fusiform in
shape. Its walls are thick and contain numerous secretory glands
which pour out gastrie juice. The food is not held in the proven-
triculus to be digested but after becoming saturated with the gastric
secretion is forced into the gizzard where it is triturated by the
powerful muscles of this organ with the aid of pebbles picked up
by the bird.

Gizzard. The gizzard or ventriculus bulbosus is a dense, mus
cular organ, flattened on two surfaces, with rounded border. In-
ternally it is lined by a thick, tough, corrugated membrane which
incloses a cavity of considerable volume, in which may be found
food in various stages of disintegration and numerous pebbles, or
bits of stone. Secretion of gastric juice also takes place in the
gizzard according to Jobert. However, this organ acts principally
in a mechanical way to grind the food and serves as a substitute
for teeth. It is more highly developed in grain eating birds than
in those subsisting principally on fish or animal food. In strictly
carnivorous birds such as eagles, or hawks, the dense muscular wall
is absent, or is limited to a portion of the organ, the remainder
consisting of a membranous cul-de-sac. When reduced to a semi-
fluid mass the food is released into the duodenum or first portion
of the intestine, which joins the gizzard at a point near the entrance
of the proventriculus.

Intestines. On leaving the gizzard the duodenum extends pos-
teriorly, bends on itself and returns to near its origin. Between
its two parallel branches rests the pancreas which gives off its
secretion into the lumen of the duodenum near its termination.

ANATOMY OF BIRDS 13

The pancreatic juice acts on the starchy material while the secre-
tion of the proventriculus acts on the proteins in the food. Suce-
ceeding the duodenum are, according to some writers, the other two
divisions of the small intestine, the jejunum and ileum. These form
several convolutions and are continued by the rectum to the cloaca.

At the point of juncture of the small intestine and rectum, in
certain species of birds, are found two elongated diverticula lead-
ing from the intestine. These are the ceca or blind pouches. In
grown fowls and turkeys they are from 4 to 7 inches in length and
may be distended to a diameter of 14 to 34 of an inch. Especial
importance is attached to them because of the fact that they are the
seat of marked lesions in coccidiosis of chickens, and of turkeys, and
in infectious entero-hepatitis of turkeys. In some species of wild
birds, the ceca may reach a length of 10 inches while in others they
are absent or merely rudimentary. Their function is apparently the
retention of food material which has not been absorbed in passage
through the small intestine.

The cloaca serves as a common cavity for the entrance of the
intestine, ureters, oviduct in the female, and vasa deferentiz in
the male. It is divided into three parts. The rectum enters the
first part, the ureters and genital canals open on the lateral faces of
the second and the bursa of Fabricus, a blind sae or glandular cavity,
opens on the dorsal wall of the third or outer division. The bursa of
Fabricus may disappear in adults. The one oviduct in the female
opens on the left side of the second division. The material from the
intestine and ureters is held in the cloaca to form the character-
istic droppings and is then passed out through the anus or vent.

Mucosa of the alimentary canal. The alimentary canal is
lined internally by a mucous membrane which is thick, and com-
posed of many layers of cells in the mouth, pharynx, esophagus
and crop. The mucosa is thin, and composed of one layer of
columnar epithelial cells in the proventriculus, gizzard and intestine.
In the gizzard the membrane is covered by a horny surface layer.
In the submucous tissue of the mouth and pharynx are found
several pairs of glands. ‘These, however, are not considered as
true salivary glands but produce a mucous secretion. The esoph-
agus exhibits numerous alveolar secretory glands in the submucous
tissue. The glandular stomach is conspicuous for the layer of
tubular secretory glands which are set perpendicularly to the mu-
cous membrane and which pour their secretion of gastric juice into
the interior of the stomach. Over the mucous membrane of the

14 DISEASES OF DOMESTICATED BIRDS

gizzard is a tough horn-like covering formed by the hardening of
the products secreted by the underlying simple glands.

The mucous membrane of the intestine presents innumerable
cylindrical elevations known as villi. It is through these that the
digested food is assimilated and carried by means of the chyle-
vessels or lacteals to the portal vein and thence to the liver. Nu-
merous goblet cells for the secretion of mucin are present in the
villi.

Liver. This organ is dark brown in color and composed of a
right and left lobe, the former being the larger. The right lobe
has a gall bladder on its ventral surface, while the bile from the
left lobe is poured directly into the duodenum through a separate
bile duct, the hepatic or choledic duct, which empties a short dis- ~
tance behind the two pancreatic ducts. The cystic duct opens caudad
of the hepatic duct and drains the gall bladder.

Pancreas. This organ is long, narrow and lobulated. In color
it is pale red. It is highly developed in birds and occupies the
space between the two branches of the duodenum. Two or some-
times three ducts carry its secretion into the ascending arm of the
duodenum near its extremity and just anterior to the hepatic duct.

RESPIRATORY SYSTEM

The organs of respiration in birds differ markedly from those of
mammals. They resemble more nearly the reptilian type of
formation. ;

Air passages. The nostrils are represented by two narrow
openings at the base of the upper mandible of the beak. The nasal
chambers are short and narrow and are separated by a septum which
is partly bony and partly cartilaginous. The turbinated bones of
mammals are represented by three cartilaginous structures. The
nasal cavities open into the mouth by a common, elongated slit in
the median line of the hard palate. Cavities known as the sub-
orbital or infraorbital sinuses occupy a position on either side of
the head. They communicate with the nasal cavity by narrow
passages which extend from a comparatively low level in the sinus,
upward into the nasal cavity. The arrangement prevents natural
drainage of the sinuses.

Birds possess an upper and a lower larynx. The former cor-
responds to the larynx of mammals but serves only as an opening
for the passage of air. An epiglottis is absent but its function is

ANATOMY OF BIRDS 15

assumed by two lateral lips which close the laryngeal opening dur-
ing the passage of food through the pharynx. ‘The inferior larynx,
or syrinx, is the voice organ. It is located in the anterior thorax
at the division of the trachea into two bronchi. The end of the
trachea, in fowls, is compressed from side to side and. forms the
wall of the syrinx. In certain birds the syrinx is complicated in
structure and may be formed of a number of tracheal rings ex-
panded to form large bony cavities. Sound is produced by the
vibration of membranes within the walls of the lower larynx.

The trachea is long in birds and its cartilaginous rings are com-
plete. In the bronchi the cartilaginous rings are incomplete, a
portion of the wall being formed by a membrane. The bronchi
enter the lungs at the anterior extremities, become membranous and
give off branches to these organs and to the air cells of the thorax
and abdomen.

The lungs are pale or bright red in color and of a spongy tex-
ture. They are closely applied to the dorsal surface of the thorax
and present several deep indentations into which the ribs fit. The
ventral surface is smooth and is covered by a fold of the diaphragm.
Only a small portion of the thoracic cavity is occupied by the lungs.

Air sacs. These are membranous receptacles into which the air is
carried by terminal branches of the bronchi. Through these branches
the cells are in direct communication with the lungs. They also,
with certain exceptions, communicate with canals or spaces in the
various bones, to which they supply air. The membranous wall
is composed of two delicate layers, an external serous and an in-
ternal mucous layer. The latter is a continuation of the mucosa of
the bronchi, the former is regarded as a reflection of the peritoneum
and pleura. Nine air sacs are found in the thoracic and abdominal
cavities. The single anterior thoracic air sac surrounds the inferior
larynx, bronchi and large blood vessels of the region. It receives
air from the anterior part of the lungs by two openings and com-
municates with deep seated air cells of the neck and with the cla-
vicle, coracoid, scapula and sternum. ‘Two lateral thoracic sacs
receive air from the internal edge of each lung opposite the base
of the heart. They transmit air currents to the air cells of the
axillary region, vertebre, ribs and humerus. The diaphragmatic
air cells are four in number, two anterior and two posterior. They
are inclosed between the two diaphragmatic folds. Air is received
from the lungs but is not communicated to bony structures from
these. Two abdominal air sacs each receive a long voluminous bron-

16 DISEASES OF DOMESTICATED BIRDS

chial branch which leaves the respective lung on its posterior in-
ferior surface. ‘These sacs extend from the lungs to the cloaca and —
are the largest in the body. They supply the bones of the pelvic
region and femur in those species. in which these bones are aeri-
ferous. The femur of the pigeon and the humerus of the ostrich
have no air spaces but retain their marrow.

URINARY SYSTEM

The urinary tract is composed of two kidneys each drained by a
ureter lying along its ventral face and proceeding caudad to empty
into the cloaca posterior to the terminus of the rectum. The kid-
neys are elongated, reddish brown bodies divided into three prin-
cipal lobes. They are closely applied to cavities in the pelvis on
each side of the spinal column. ‘These organs are not divided into
macroscopically visible cortical and medullary zones as in mammals
but have a homogeneous structure. In texture they are quite soft
and rupture easily when pressed by the finger. The ureter does
not originate in a renal pelvis but is formed by the union of several
uriniferous tubules along the ventral face of the kidney. Its course
may be traced by the white color of the urates which it carries, a
material corresponding to the urine of mammals.

GENERATIVE SYSTEM

The male generative organs consist of two testicles each provided
with a vas deferens or excretory duct. The testicles are oval shaped
organs situated in the sub-lumbar region at the anterior extremities
of the kidneys. They vary greatly in size at different seasons, but
show a remarkable development during the breeding season. The
two vasa deferentie pass along the kidneys by the side of the
ureters, exhibiting transverse convolutions along their course.
Each opens on a small papilla situated in the uro-genital division
of the cloaca. The base of each papilla is surrounded by a plexus
of blood vessels which serve the purpose of an erectile tissue during
coitus. In the drake and gander a long single penis is developed.

The female generative organs consist of a single ovary and an
oviduct situated on the left side of the abdominal cavity. The
right ovary and oviduct usually fail to develop. Occasionally a rudi-
mentary right oviduct is present. In one actively laying hen Gal-
lagher observed a right oviduct which was nearly as long as the

ANATOMY OF BIRDS Me

left oviduct and equally voluminous. Its anterior extremity ex-
hibited an infundibular membrane in contact with the ovary. Pos-
teriorly it opened into the cloaca opposite the left oviduct. The
appearance of its mucous membrane suggested that it was capable of
functionating.

The ovary is placed in the left sub-lumbar region, opposed on its
superior surface to the ribs. In fowls it contains from twelve to
fifteen hundred germ cells in various stages of development from
microscopic granules to fully formed yolks in functionating ovaries.
The oviduct terminates in the urogenital division of the cloaca just
anterior to the left ureter. It is divided into five regions, each of
which has a specific function. The first region, the infundibulum,
is a delicate membrane of a funnel-like form which receives the
ovum. Succeeding this is the part secreting albumen followed by
the isthmus which secretes the shell membrane. The uterus or
fourth region forms the shell. The last region, the vagina, is short
and is provided with a sphincter muscle at its entrance to the cloaca.

SKIN AND ITS APPENDAGES

The skin of birds is without sweat glands. There are some small
glands in the exterior passage of the ear, which secrete an unctious
fluid. There is also a protruding glandular organ located above the
coccyx between the tail feathers and known as the uropygium or
rump gland, an organ peculiar to birds. It is round or oval in
form and is divided into two halves by a medial septum. The exit
passage is through a teat-like cone which projects above the level
of the skin. Two external orifices are observed in the gland of the
duck. In hens the gland is about the size of a pea, in geese about
as large as a hazel nut and in the swan about an inch and one half
in length. Its function is to secrete an oily fluid for water-proofing
and dressing the feathers. The secretion is taken up by the beak
and spread over the plumage.

The feathers are complicated modifications of epidermic struc-
ture. Each feather is composed of a quill, a shaft and a vane.
The quill is embedded in a feather follicle of the skin and extends
outwardly to the point where the barbs of the vane arise. It has
an opening at its base for the reception of the dermal papilla and
another opening at its point of junction with the vane. The shaft
continues the quill to the extremity of the feather. The vane con-
sists of two rows of barbs which arise on opposite sides of the shaft.

18 DISEASES OF DOMESTICATED BIRDS

These barbs each carry two rows of barbules which interlock with
those of adjoining barbs. The feather is elevated by a small muscle
located in the skin at the root of the quill.

The comb and wattles of fowls and the caruncle of turkeys are
developed from the skin.

INCUBATING PERIODS

The length of time necessary for hatching eggs by natural incu-
bation shows some variation. The normal period for the common
hen is 21 days but this period may be shortened to 19 or 20 days
by warm weather and unusually constant brooding by the hen. On
the other hand, if the eggs have been abandoned and allowed to cool
for a time, hatching may be delayed for several days. These varia-
tions doubtless occur in the case of other birds. The incubation
periods of various birds, subject to variations as explained are as
follows.

TaBLeE I.— IncuBATING PERIODS

HAITI praceconceshs codon talna situate a neta 21 days

Me iee arti sees ce ot ala B cpr ooeyn earls caminiete 25 days
Mele Mr sealer chs @ ae elo aa a Para ane 28 days
AORN 8 ways oie 1 cicXar ca) Sua at wick Daeg Menictee ae 28 days
Guimeastow ll ei6i batch eee Lenka cote pepe aye
CoORe me ceo weeks Midae beer 30 days
Wimkewe Payers tel a 2 Oe eve st ie ayesha oases 28 days
IROOM ee ones Bee eciagieieoie o pons en heer 18 days

PULSE, TEMPERATURE AND RESPIRATION

Loer has made an extensive series of observations on the tempera-
ture, frequency of pulse and respiration in domestic birds. His re-
sults are summarized as follows.

Frequency of heart beat as determined by digital palpation after
opening the thoracic cavity was 128 to 140 per minute in the hen
and 141 to 149 per minute in the pigeon. The heart beat of the
duck as determined by auscultation varied from 150 to 180 per
minute.

me ee ee

ee ——————

—_—— -

ANATOMY OF BIRDS 19

TasLeE JI.— Respiration FREQUENCY AND NorMAL TEMPERATURES OF

Birps
Respiration Centigrade Fahrenheit
Species frequency degrees degrees

Min. | Max.| Min. | Max. | Min. Max.
Mabe. tis 93 | 40.5 49.0 | 104.9 107.6
‘hs: ie 12 16 40.0 41.5 104.0 106.7
Pheasant ....% = -= 41.0 44.0 105.8 111.2
RST), © bs os acre 16 36 41.0 43.0 105.8 109.4
(LTE i See aie ee 16 28 41.0 43.0 105.8 109.4
RH alte e ed s,s 12 20 40.0 41.0 104.0 105.8

REFERENCES

1. Boyce and Warrington. Observations on the anatomy, physiology and
degenerations of the nervous system of the bird. Tr. Roy. Soc., Vol. 191,
1899.

2. Bradley. The structure of the fowl. London: A. & C. Black, Ltd.,
1915.

3. Burnett. Clinical pathology of the blood of domesticated animals.
New York: The Macmillan Company, 1918.

4. Chauveau. Comparative anatomy of the domesticated animals. New
York: D. Appleton and Company, 1905.

5. Ellenberger. Handbuch der vergleichenden mikroskopischen Anat-
omie der Haustiere. Erster Band. Berlin: Paul Parey, 1906.

6. Ellenberger u. Baum. Handbuch der vergleichenden Anatomie der
Haustiere. Berlin: August Hirschwald, 1900.

7. Kaupp. The anatomy of the domestic fowl. Philadelphia: W. B.
Saunders Co.

8. Loer. Vergleichend physiologische Untersuchungen iiber die normal
Rektal temperature, Atem und Pulzfrequenz der Vogel. Inaug. Diss.
Bern, 1909.

9. Owen. Comparative anatomy and physiology of vertebrates. Birds
and mammals, Vol. II. London: Longmans Green & Co., 1866.

10. Steen. Blutuntersuchungen bei gesunden Hiihnern. Jnaug. Diss.
Leipzig, 1913.

CHAPTER II

HYGIENE AND SANITATION

SECURING HEALTHY STOCK

In establishing a flock of poultry it is highly important that pre-
cautions be taken to prevent the introduction of disease with the
original stock. It is a common desire among beginners, to con-
sider purchasing adult birds, in order to secure speedy returns. It
should be borne in mind that the number of instances in which
healthy young pullets may be purchased is comparatively rare. Too
often hens are sold because they are old and past the best laying
period, or because the flock has become unprofitable because of some
disease. Fowl cholera, avian tuberculosis and diphtheria are com-
monly introduced by the purchase of adult stock.

Starting a flock from hatching eggs or day old chickens is the
least dangerous method of introducing stock but there remains the
danger of introducing white diarrhea.

RELATION OF SOIL TO HEALTH

Well drained soil is desirable in that the presence of moisture
and mud is minimized. <A wet soil favors parasites. Least desir-
able for poultry yards is sticky clay or adobe. In wet weather the
latter soil collects on the toes of chickens in the form of balls so
large as to impede walking. Chickens kept on such soil require
individual treatment to free the toes, and in doing this they are
lable to be injured.

The continued use of a given area of soil for poultry, results
in its becoming excessively infested with the eggs of various para-
sites and consequently a source of danger to the birds kept thereon.
Therefore, it is highly desirable that chickens be not kept on the
same soil year after year.

The problem of securing fresh areas for chickens is solved in
various ways. Where the chicken house is a permanent, immov-
able structure, yards may be fenced off on either side and used in
alternate years. When birds are kept under the colony system, the

structures necessary for the fowls are built on skids. A team may
20

HYGIENE AND SANITATION 21

be hitched to the building to move it as desired. A very desirable
method of securing fresh soil is to move chicken houses in harmony
with a crop rotation system. In this manner a given area is cropped
for three or four years after chickens have occupied it, before the
land is used for birds again. When quarters are so cramped that
no change can be made in the chicken yards, deep plowing is of
some advantage in turning up fresh earth and covering contaminated
soil. Small areas may be sprinkled with lime, or be thoroughly
soaked to some depth by the hberal application of a disinfectant.

LOCATION AND CONSTRUCTION OF POULTRY HOUSES

Dampness is very injurious to fowls, and consequently the build-
ings should be located with reference to securing good drainage after
rains. Where choice is possible, sandy soil should be chosen on
account of its permeability to water. Provision should be made to
secure free ventilation without drafts of air. No especial effort
need be made to secure warmth in a poultry house in the daytime
even in a severe climate. The building should be so located as to
permit the unobstructed illumination of the interior by sunlight.

The frequency with which poultry houses must be cleaned and
sprayed with parasiticides should be borne in mind when they are
being constructed. Any structural detail which interferes with the
free access to any part of a house by a man, should be avoided for
it will interfere with routine cleaning. The habit displayed by
mites, of collecting in cracks, should be recognized in providing
buildings with a minimum of such places where vermin may col-
lect. Nest boxes, perches and similar fittings should not be per-
manently attached to the building, but should be readily removable
for cleaning and spraying. ,

Certain details of construction will at least constitute impedi-
ments to the dissemination of parasites and infective material from
bird to bird. Thus, stretching chicken wire under the roosts will
largely prevent birds from coming in contact with droppings in the
roosting quarters.

In houses designed for laying hens in a cold climate, each bird
should be provided with from three to four square feet. Exercise,
which is absolutely essential to health, will be provided by mixing
some of the feed with clean litter on the floor.

22 DISEASES OF DOMESTICATED BIRDS

CLEANING AND DISINFECTING BUILDINGS

Previous to applying a disinfectant to a building it is essential
that all dirt and filth be removed by sweeping, scraping or washing.
This is necessary in order to expose the woodwork to the unob-
structed action of the disinfectant.

A considerable range of choice of disinfectants is possible. Selec-
tion of a disinfectant will be made on the basis of relative cheap-
ness, availability and suitability to the requirements imposed by the
article to be disinfected.

Compound solution of cresol. This substance also known as
liquor cresolis compositus, consists of a mixture of equal parts of
eresol with a linseed oil-potash soap. It mixes well with soft water,
but is less satisfactory in this respect when hard water is used. This
disinfectant may be obtained at any drug store and on account of
cheaper price is to be preferred to carbolic acid. It is employed
for general disinfection in the proportion of four ounces to a gal-
lon of water.

Formaldehyde gas. Formaldehyde is ordinarily obtainable in
a forty per cent solution in water, a product which is known as
formalin. Formaldehyde is a strong non-poisonous disinfectant, is
not hindered in its action by albuminous material and in general
is not harmful to metals. The gas is a good surface disinfectant
and may be employed in disinfecting incubators and such rooms
as may be easily made air tight. Ordinary poultry houses are not
constructed tightly enough to warrant the trouble of sealing all cracks.
Under conditions warranting its use, the room in which the gas is
to be used is carefully examined and all cracks are sealed with strips
of paper applied with paste.

The gas is liberated from the watery solution by mixing formalin
with needle crystals of potassium permanganate. For each 1,000
cubic feet of air space there should be used 20 ounces of formalin
and 16% ounces of potassium permanganate. The permanganate is
placed in a shallow pan with flaring sides and the proper amount of
formalin is poured in the pan. Provision should be made to protect
the floor as the ingredients of the mixture may splash during the
violent reaction that ensues. Splashing will be minimized by using
a bucket, but in this case considerable formaldehyde gas may con-
dense on the walls of the vessel. After mixing the chemicals, the
operator should leave the room promptly to avoid inhaling the irri-
tating fumes. The room should be kept sealed for eight hours.

HYGIENE AND SANITATION 23

This method of fumigation is not applicable when the temperature
falls below 65° F. for the gas condenses under such conditions.

Disinfection may be accomplished by spraying objects with a
mixture of 5 parts of formalin to 95 parts of water.

Carbolic acid or phenol. Pure carbolic acid exists at ordinary
temperatures as needle-like crystals. This substance is frequently
used in the form of liquefied carbolic acid which consists of 9 parts
of the crystals mixed with 1 part of water. Carbolic acid is ordi-
narily employed as a disinfectant in a five per cent solution of the
crystals. As the crystals dissolve slowly, solution is hastened by the
use of hot water. The fluid may be applied liberally to surfaces as
a spray, or fabrics and implements may be immersed in the fluid for
an hour. Carbolie acid is somewhat expensive, and on this account
some other cheaper agent may be employed. The substance in ques-
tion should not be confused with “crude carbolic acid” which is
quite different in composition.

Crude carbolic acid. Commercial crude earbolic acid is a by-
product of the distillation of coal tar. It contains certain insoluble
oils and a mixture of cresols and similar substances which possess
disinfectant value. When the content of these is known, an effective
disinfectant may be made by including these substances in two per
cent solution. The disinfectant in question should not be confused
with true carbolic acid (phenol).

Chloride of lime. Chloride of lime or chlorinated lime consists
of slaked lime which has been exposed to the action of chlorine.
It is a white powder which deteriorates in strength rapidly after
opening the hermetically sealed container in which it is supplied.
This disinfectant is particularly useful where the action of a de-
odorant is desired besides a disinfectant. It is commonly employed
diluted with water in the proportion of six ounces to a gallon of
water. The presence of organic matter interferes with the effective-
ness of this agent.

Various coal-tar creosote disinfectants. Mixtures of various
coal-tar products, principally creosote oil, with soap in the form of
emulsions are on the market under a large variety of trade names.
The disinfecting value of these products varies greatly, but when
the carbolic acid coefficient is stated, one of these products may be
used with assurance as to its efficiency. The expression carbolic acid
coefficient, refers to the relative germicidal value of a product as
compared with ecarbolic acid.

Bichloride of mercury or corrosive sublimate. This agent is

24 DISEASES OF DOMESTICATED BIRDS

usually employed in the strength of 1 part to 1000 parts of water.
It is available in the form of tablets mixed with ammonium chloride
to facilitate solution in water. <A tablet may be added to a certain
specified amount of water to make a disinfectant of a definite
strength. Bichloride of mercury has the disadvantage of attacking
metals and its activity is seriously impaired by contact with albu-
minoid substances. Its poisonous nature is some disadvantage.

Whitewash. Whitewash is made by adding about one pint of
water to each two pounds of freshly burned lime. The vessel con-
taining the mixture is covered and allowed to stand for about an hour
while slaking occurs. Water is then added to the mixture until it
is thinned to such a consistency that it may be readily applied.

Weather proof whitewash may be made as follows: Slake one
bushel of quicklime in twelve gallons of hot water. Dissolve two
pounds of common salt and one pound of zine sulphate in two gal-
lons of boiling water. Pour this mixture into the slaked lime and
add two gallons of skim milk, mixing thoroughly.

Whitewash has feeble disinfectant powers, but is useful in im-
proving the illumination of interiors. To a certain extent it covers
up infective material and fills up the smaller cracks which might
harbor parasites.

The value of scattering air slaked lime about poultry houses is
questioned in view of the irritation of the eyes and air passages
induced by the dust.

Application of disinfectants. The frequency with which poul-
try houses are disinfected warrants investment in some form of
pump. For the smaller establishments, a pump built to be used
in a pail may suffice. In larger poultry farms a pressure spray
pump mounted in a barrel on wheels forms a very convenient outfit.

CLEANLINESS OF FOOD AND DRINKING WATER

Feeding troughs may be provided with a cover of slats in the
form of a peaked roof. Birds will be compelled to reach through
the slats to eat mash, and cannot walk in the feed. Sanitary water
fountains entirely prevent birds from walking in the drinking water.
Further protection of the drinking water by the use of potassium
permanganate is very generally practiced. A saturated solution of
this substance is prepared in a large bottle or jar and is kept con-
veniently near the drinking fountain. When water is drawn for the
birds, enough of the stock solution is added to impart a deep wine
color to the water.

HYGIENE AND SANITATION 20

POST-MORTEM EXAMINATION

The first step in making an autopsy on a bird is to examine
carefully the exterior of the carcass for lesions of the diseases
which exhibit external manifestations. The skin may show the
presence of lice, mites or epithelial tumors. The head may be the
seat of bird pox nodules, favus, or swelling due to roup. The skin
of the head may present a pale appearance as in infectious leu-
kemia, fowl typhoid, coccidiosis and tuberculosis or a congested or
darkened appearance as in cholera, enteritis, pneumonia and in-
fectious entero-hepatitis. Exudates of diphtheria may be observed
in the mouth. Swellings of the joints of the wing or legs may in-
dicate tuberculosis or gout. Evidence of diarrhea should be looked
for on the feathers surrounding the vent. The general condition
of nourishment of the bird is determined by palpation, especially in
the breast region.

In preparation for the examination of the internal organs it is
best to pluck the feathers from the under surface of the body from
the base of the neck to the vent and well up on each side of the body
beneath the wings. The carcass is then stretched back downward
over a table or board and held in position by cords attached to each
leg and to the neck near the head. The other ends of the three
cords are tied at the sides and one end of the table or board. An-
other method of holding the carcass in position is to nail each
foot and the neck to the board. Those who have occasion to make
frequent autopsies find it convenient to lay the bird out on a shal-
low, rectangular, flat bottomed tin pan fitted with eyelets on the
sides and ends for the reception of cords tied to the feet and neck
of the carcass. The pan serves to retain fluids, intestinal contents,
ete., which may escape during the autopsy, and also is easily cleaned
and disinfected.

The internal organs are exposed by making an incision through
the skin and body wall on either side of the breast near the base
of the wing and continuing it along the side to the vent and then
forward to a point opposite the beginning of the incision. The
ribs may be cut through with a knife at the cartilaginous articula-
tion between the superior and inferior ribs or they may be severed
by means of a pair of scissors or bone forceps. The breast bone
and abdominal wall can be removed by cutting through the bones
of the shoulder girdle at the entrance to the chest with bone forceps.

26 DISEASES OF DOMESTICATED BIRDS

Peritoneal and other attachments are cleared away with the knife
as the inferior body wall is being removed. |

Before removing any of the organs a general survey of the parts
may reveal one of the following conditions: The presence of fluid
in the abdominal cavity, which would be suggestive of peritonitis
or enteritis; the presence of blood clots in either cavity indicating
internal hemorrhage; yolk concretions or other egg material free in
the abdominal cavity of females; tubercular masses on the intestine,
liver or spleen; tumors in the various organs; or moldy growths
in the air sacs, indicating aspergillosis.

The liver is then examined. It may be congested or show small
necrotic spots in cholera and several bacillary septicemias or be
pale and enlarged in infectious leukemia and fowl typhoid. In
tuberculosis fat-lke nodules with yellowish centers would be found.
In entero-hepatitis the areas of necrosis would be yellowish or
greenish. Various sorts of tumors may be present on the surface of
the liver.

The alimentary tract requires a careful examination since many
of the diseases are manifested by lesions at some point along its
course. Frequently the congested areas of the mucosa may be de-
tected through the serous membrane before the intestine is opened.
It is advisable, however, to lay the whole tract open from the crop
to the vent. The crop and proventriculus may show congested or
inflamed areas as a result of the ingestion of strong irritants or
poisons. The gizzard is relatively free of disease but may contain
parasitic worms in its wall. The duodenum is often the seat of
intense inflammation especially in the septicemic diseases such as
cholera and fowl plague. Coccidia also cause congestion of the
duodenal mucosa. In infectious entero-hepatitis and coccidiosis the
ceca are usually distended with necrotic material and the cecal
walls are ulcerated or desquamated. In enteritis the inflammation
may involve a considerable portion of the intestinal mucosa and may
be observed in any part of the small intestine or in the ceca or
rectum. The cloaca is to be inspected for evidence of vent gleet.
Intestinal worms may be present in any portion of the intestinal
tract. Unless present in comparatively large numbers they should
not receive special consideration. Round worms may be found
gathered into large masses which tend to obstruct the passage of the
contents of the intestine. When numerous they may also produce
a catarrhal condition of the intestinal mucosa. Some tapeworms

HYGIENE AND SANITATION 27

when numerous cause nodular formations on the intestinal wall
which resemble the lesions of intestinal tuberculosis.

An enlarged, congested spleen may be associated with the acute
bacterial septicemias. An enlarged, firm, mottled appearing spleen
would suggest infectious leukemia. In the latter disease the kid-
neys are also enlarged and of firmer consistency. Tubercular nod-
ules may be present.

A gangrenous or cystic ovary or an ovary exhibiting hard, angular,
shrunken ova, in the case of the fowl, is practically diagnostic of
B. pullorum infection. Occasionally gangrene of the ovary may be
due to some other microorganism. In such cases peritonitis is apt
to be present.

The oviduct should be opened and examined for inflammatory
changes, constrictions, tumors or the condition known as egg bound.

Normally the lungs are found deflated and closely applied to the
breast wall. In acute congestion and pneumonia the lungs are
distended and stand out in a firm position surrounding the heart.
The pneumonie lung is solidified and will sink in water. Nodular
growths in the lungs may represent tuberculosis or aspergillosis.
The former is much less frequently found involving the lungs of
birds than the abdominal organs. Aspergillar nodules are usually
accompanied by moldy growths on the mucosa of the bronchioles
or air sacs.

In young chickens the trachea and larger bronchi are slit open
to discover the presence of the red worm, Syngamus trachealis, or
of aspergillar growths.

Pericarditis, thickened pericardial fluid or hemorrhagic points
on the heart indicate a septicemia such as cholera or fowl typhoid.
The pericardium and also the liver may be covered by a fine white
deposit consisting of urate of soda crystals in visceral gout, or as
a result of disturbances of metabolism due to a diseased condition.

REFERENCES

1. Kaupp. Poultry diseases and their treatment. Chicago: American
Journal of Veterinary Medicine, 1919.

2. Pearl, Surface and Curtis. Diseases of poultry. New York: The
Macmillan Company, 1918.

3. Salmon. Diseases of poultry. Washington: George E. Howard &
Co.

4. Salmon. Important poultry diseases. Revised by Gallagher and
Foster. U.S. Dep. Agr., Farmers’ Bull. 957, 1918.

CHAPTER Tit

APOPLECTIFORM SEPTICEMIA AND SLEEPING DISEASE
APOPLECTIFORM SEPTICEMIA

Characterization. The disease is a highly fatal septicemic in-
fection of chickens caused by a streptococcus. _

History. The disease was first described by Norgaard and
Mohler in the United States and later was observed by Magnussen
in Sweden.

Etiology. The causative organism is a streptococcus, the in-
dividual elements being .6 to .8 microns in diameter. There is
great diversity in the length of chains. In tissues they are short
and in cultures, long.

The organism is Gram positive, non-motile, and no capsule for-
mation has been observed. It is an aerobe and a facultative an-
aerobe. Growth occurs on common solid and liquid media most
abundantly at 37° C., and less rapidly at room temperature.

In alkaline bouillon growth occurs within 24 hours at 37° C.
Long chains develop which form skeins or balls of flocculent ap-
pearance which are deposited on the sides and bottom of the tube.
After three days the growth settles to the bottom in the form of a
white non-viscid deposit. This upon agitation breaks up into nu-
merous small particles.

After a sparse seeding on agar, growth is visible after 24 hours
in the form of small shiny, grayish colonies about 1.5 mm. in
diameter. By transmitted light these appear to have a brown
center surrounded by an irregular pale bluish border. The max-
imum size is attained on the third day. In agar stab cultures, mi-
nute spherical grayish white colonies with fimbriated borders, appear
along the line of puncture. They do not coalesce, and very slight
growth is observed on the surface.

The surface colonies on agar plates are very similar to those
developing on a sparsely seeded slant culture. The colonies in
the depths of the medium are seen as minute pearly points of

granular appearance. With the aid of a hand lens the outline ap-
28

APOPLECTIFORM SEPTICEMIA AND SLEEPING DISEASE 29

pears ciliated. Similar but more profuse growth oceurs on glycer-
ine agar, and serum-gelatin-agar.

In stab cultures on gelatin, growth is not observed until the
fourth or fifth day. It consists of a finely granular line of minute
spherical colonies, grayish white in color. The colonies have a
fimbriated border and do not exceed a pinhead in size. The growth
is not abundant nor characteristic and does not spread on the sur-
face. No liquefaction occurs. Colonies on gelatin plates resemble
those on agar, but are slightly more opalescent.

Growth on blood serum appears within 24 hours in the form of
small whitish colonies .6 to .8 mm. in diameter. Sometimes the
color has a yellowish tmt. The colonies do not coalesce. The water
of condensation becomes turbid by reason of the presence of small
gray clusters of the streptococci.

Growth in milk occurs without causing visible change. In old
cultures there is observed a solidification of the lower stratum, vis-
ible when the tube is turned upside down.

In litmus milk, the blue color is changed to a pale madder pink,
indicating acid formation. No growth occurs on potato. No indol
is formed.

Bouillon containing one per cent of glucose, lactose and saccha-
rose, in fermentation tubes, forms a favorable medium. Growth
is more profuse than in plain bouillon and extends into the closed
arm. Gas is not produced in these sugars, but acid formation oc-
curs. Similar results are obtained with galactose, maltose and the
alcohols mannite, dulcite and sorbite.

No hemolytic effect occurs in Conradi-Drigalski plate cultures.
Acid formation occurs on litmus-lactose-agar plates.

Morbid anatomy. The skin displays hemorrhagic discolora-
tion on the breast and neck, due to diffuse hemorrhages in the sub-
cutaneous and muscular tissues. The abdominal cavity contains
an abundance of sero-sanguinous exudate. Similar exudate some-
times is present in the pericardial sac. The veins of the mesentery
are engorged. The liver is greatly enlarged, paler in color than
normal and the entire surface is covered with a semi-organized
plastic exudate. The spleen may be similarly swollen. The gall
bladder is distended with bile, while the kidneys are hyperemic
and swollen. The intestines, especially the duodenum, are observed
from the peritoneal surface to be congested in patches. On opening
the intestines, the mucosa corresponding to the discolored areas
is considerably swollen. The contents of the intestine consist of

30 DISEASES OF DOMESTICATED BIRDS

blood stained feces and mucus. The lungs show circumscribed areas
of congestion. On opening the cranium a profuse subdural exudate
is observed. The meninges are injected and the ventricles contain
an abnormal amount of discolored serum.

Symptoms. Information regarding symptoms is limited to ob-
servations made on the behavior of inoculated cases only. A short
time after inoculation, birds display evidence of depression. There
is staggering gait with effort to balance with the aid of the wings.
If the birds are not disturbed they will lie in one place until death
occurs in coma. Sometimes diarrhea occurs immediately before
death.

Pathogenesis. Fowls are susceptible to intravenous or subcu-
taneous inoculation and by the feeding of cultures. The mortality
is heavy among fowls when the disease is spreading under natural
conditions. Pigeons, rabbits and mice are susceptible. Intravenous
inoculation of the duck may cause loss of coordination and death
with endocarditis. Sparrows are more resistant than pigeons and
chickens but succumb to large intramuscular and intraperitoneal
doses. In the dog, intravenous inoculation causes rise of tempera-
ture and lameness apparently due to a transitory arthritis. Ab-
scesses may occur in the dog, a point of interest in that suppuration
has not been observed in other animals. Guinea pigs, swine and
sheep prove refractory. Cats may succumb to intraperitoneal in-
oculation. Horses exhibit a disturbance of health following intra-
venous inoculation.

Immunization. It is possible to immunize a fowl by intra-
venous inoculation of killed culture so that the bird will tolerate
an otherwise fatal dose of virulent culture. Successive injections
of virulent culture cause the blood serum to take on protective prop-
erties. Norgaard and Mohler have found this serum administered
intravenously in a .5 cc. dose, protective against a .1 ¢.c. intra-
venous inoculation of culture.

SLEEPING DISEASE

Synonym. Schlafkrankheit, Schlafsucht, (German) ; maladie du
somneil, (French).

Characterization. The disease is a septicemic infection of
fowls characterized by symptoms of sleepiness and caused by an
encapsulated streptococcus.

History. The disease was first described by Dammann and

APOPLECTIFORM SEPTICEMIA AND SLEEPING DISEASE 31

Manegold in Germany and later by Greve in the same country.

Symptoms. The symptom most frequently occurring is a more
or less marked desire to sleep. The hen sits for hours at a time
with closed eyes and ruffled feathers, with the head bent backward
in the feathers of the neck. At intervals the bird awakens and opens
the beak wide as if panting. The conjunctiva, usually of one eye
only, becomes reddened and markedly swollen. Secretion from the
conjunctival sac dries on the edges of the lids. Except when the dis-
ease has a very short duration, the comb and wattles gradually
become pale. Commonly diarrhea exists for several days and the
bird dies in a highly emaciated condition. Birds may die suddenly
after showing symptoms for only a day or less.

Morbid anatomy. The carcass exhibits the appearances com-
mon in hemorrhagic septicemia, such as distention of the subcu-
taneous veins with dark red blood, infiltration of portions of the
musculature with bloody, watery fluid. There is bloody, shiny,
viscid fluid in the abdominal cavity and the peritoneum is swollen
and diffusely reddened. The mucosa of the proventriculus and of
the intestine is swollen while that of the latter is diffusely red-
dened. ‘The liver is enlarged, brownish yellow in color and is fri-
able in texture. It is studded irregularly with dark red hem-
orrhages. The spleen is enlarged and the capsule is distended while
the pulp is fragile in texture. The kidneys are swollen and dirty
yellow in color. The lungs are congested and permeated with nu-
merous small, dark red hemorrhages and may be edematous. Fi-
brinous exudate may occur on the costal surfaces of the lungs.
Punctiform hemorrhages may occur under the epicardium. The
heart is distended with coagulated blood. The pericardium is often
distended with pale serous fluid and a tough, fibrous layer of ex-
udate frequently forms on the pericardium. Smears from the heart
blood stained with ecarbol fuchsin are seen to contain chains of
streptococci. The capsules are also seen distinctly enveloping single
cocci as well as diplococci.

Etiology. ‘The streptococcus causing the disease is designated
Streptococcus capsulatus gallinarum. It differs in the length of the
chains and in the size of the elements according to the sort of animal
in which it appears as a natural disease or into which it is inocu-
lated. These differences occur also in artificial cultivation. In
animal blood and in fluid media, chains of up to 30 elements are ob-
served and in sugar bouillon as many as 100 elements may occur.
The size of the single elements varies between .3 and .5 micron.

32 DISEASES OF DOMESTICATED BIRDS

The individuals in the chains occur as diplococci. No motility is
present.

The streptococci are stained by all of the common anilin dyes
and are Gram positive. With Kiihn’s carbol methylene blue the
capsules appear greenish in color. With a modification of Klett’s
anthrax capsule stain the cocci appear dark blue while the capsules
are pale red or pink, with dark red undulating contours. ‘The cap-
sules are seen distinctly only in material from the animal body.
The streptococci grown on the various culture media show them
very poorly or not at all.

The organism grows aerobically and anaerobically and its optimum
growth temperature is that of the body. It thrives best on solid
blood serum, and grows well in milk. It can also be grown on meat
extract bouillon, gelatin, agar, agar gelatin and grows least well on po-
tato. In order to cause rich growth an addition of 4 to 6 per cent
of glycerin or one per cent of sugar is necessary.

Acid is formed in saccharose bouillon and indol in limited amount.
Gelatin is not liquefied.

It is very sensitive to drying and also to heat. In bouillon cul-
tures which have been warmed to 80° C., for five minutes it is killed.
At 100° C. it is killed in 44 minute. One per cent solution of
earbolic acid kills in 2 minutes, while a similar solution of liquor
eresoli saponatus, lysol, and creolin renders it inactive in three
minutes.

Pathogenesis. The disease is transmitted to hens by inocula-
tion of blood or pieces of organs as well as by inoculation with cul-
ture. Infection with the latter succeeds through subcutaneous in-
oculation or when finely dissipated bouillon culture is inhaled. In
carcasses of birds dead after subcutaneous inoculation, evidence of
coagulation necrosis is seen frequently, accompanied by infiltration
of the surrounding tissues with bloody or purulent fluid.

The time of appearance of symptoms in hens after artificial in
fection varies greatly. Sometimes sickness is noted after six days,
with death occurring after seven days more. Again, it is possible
for 30 to 70 days to elapse between the time of inoculation and death.
The disease is transmissible by subcutaneous inoculation to pigeons,
rabbits, white mice, gray mice, and lambs. The course of the disease
is more acute in pigeons than in hens, but the lesions are similar.
Dogs, ducks and guinea pigs do not succumb to artificial infec-
tion.

Differential diagnosis. The observation of capsules surround-

APOPLECTIFORM SEPTICEMIA AND SLEEPING DISEASE 33

ing the streptococci in smears from tissues will differentiate the af-

fection from apoplectiform septicemia, a very similar infection.
Prevention. Measures similar to those recommended in the

discussion of fowl cholera are indicated.
Treatment. No medicinal treatment is available.

REFERENCES

1. Dammann u. Manegold. Die Schlafkrankheit der Hiihner. Deutsche

tierarztl. Wchnschr., Bd. 13, 1905, S. 577.
2. Greve. Beitrag zur Kenntniss der Streptokokken-Krankheit (Schlaf-

krankheit) der Hiihner. Deutsche tierdrztl. Wchnschr., Bd. 16, 1908, S.

213.
3. Magnussen. Ueber Eine fiir Europa neue Hiihnerseuche. Centralbl.
f. Bakteriol. (Etc.), Orig., 1, Abt., Bd. 56, 1910, S. 411.

4. Norgaard and Mohler. Apoplectiform septicemia in chickens. U. 8.

Dep. Agr. Bureau Animal Indust. Bull. 36, 1902.

CHAPTER IV

FOWL CHOLERA

Synonyms. Chicken cholera, pasteurellosis avium, cholera gal-
linarum, hemorrhagic septicemia of fowls; Hiihnercholera, (Ger-
man) ; choléra des poules, (French).

Characterization. Fowl cholera is an acute contagious septi-
cemic disease affecting domesticated birds, which is accompanied by
febrile temperature and causes heavy mortality. The popular desig-
nation “ cholera” is frequently used to indicate any highly destruc-
tive disease of poultry.

Etiology. The causative organism is a member of the septi-
cemia hemorrhagica group and has been designated by various names,
among them, Bacillus avisepticus, B. bipolaris septicus, B. avicida,
B. cholere gallinarum, and Pasteurella avium. A strain isolated
by Ward possessed the following characteristics:

“ Morphology. The individual cells are short, non-motile rods, with
rounded ends. They usually occur singly, but a few are seen in pairs.
Spherical forms are numerous in actively growing cultures. The size
varies from .4 to .6 micron broad and from 1 to 2 microns long. A bipolar
arrangement of the protoplasm is demonstrated when ecarbol fuchsin and
alkaline methylene blue stains are used. The bipolar staining is notice-
able frequently in smear preparations from tissues. The presence of a
capsule is suggested by an unstained area surrounding each organism when
a background of stain is deposited upon the cover glass. The same appear-
ance is noticeable in smear preparations from tissues. The organism re-
tains the stain but faintly when treated after Gram’s method.

“ Biologic Characters. The organism is aerobie and facultative anaero-
bic. It grows readily at 37.5° C., and with much less rapidity at room
temperature.

“Agar. The colonies on one per cent agar, after forty-eight hours incu-
bation at 37.5° C., appear as round, smooth, thin, shiny disks, with entire
border and measuring about 2 mm. in diameter. Under a two-thirds ob-
jective they appear coarsely granular and show concentric circular markings.
They appear smoky brown in color by directly transmitted light, and gray
by reflected light. Colonies beneath the surface are usually lenticular in
shape, and the granular appearance is more marked under a two-thirds
objective than in the surface colonies. After twenty-four hours the growth
on the agar slant culture is flat, smooth, shining, translucent, grayish
white by reflected light, and smoky brown by transmitted light, with un-

34

FOWL CHOLERA Bi)

dulate border. The condensation water becomes decidedly turbid. After
the first week of growth the liquid clears somewhat with the deposition of
a viscous sediment. No pellicle has been observed on the condensation
water.

“Glycerine Agar. .Growth upon this medium presents no features dis-
tinguishable from that upon agar slant.

“Gelatin. Surface colonies, after about two weeks’ growth at room tem-
perature, are round, vitreous masses, with entire border and smooth shiny
surface. <A large proportion of the colonies are raised, forming a conical
mass not exceeding 1 mm. in diameter. Such colonies appear highly re-
fractive by directly transmitted light. Under a two-thirds objective the
colonies have a finely granular appearance and show concentric circular
markings. Sub-surface colonies are lenticular in shape and granular.

“ After three days’ growth under similar conditions the growth in gelatin
stab cultures is noticeable as a mass of closely aggregated colonies near
the surface. After about two weeks the surface growth appears as a round,
thin gray mass, with contoured surface and undulate border. At the same
time the growth along the whole length of the path of the inoculating
needle appears as a mass of closely aggregated distinct colonies.

“Potato. Implantations on this medium have not resulted in visible
growth.

“Alkaline Bouillon. After forty-eight hours at 37.5° C. the fluid becomes
slightly clouded and does not clear up on standing, even after four months.
In cultures two or three days old no sediment is deposited, but in older
cultures a viscous sediment accumulates. The reaction is alkaline to
litmus and markedly so in old cultures. No pellicle is formed, but occa-
sionally a circular bluish band of growth adheres to the tube at the level
of the surface of the fluid.

“ Sugar-free Boutllon. Growth is similar to that in alkaline bouillon.

“Acid Bouillon. The growth is similar in appearance to that in alkaline,
except that the turbidity is less marked and no accumulations have been
noticed at either surface or bottom of liquid. Reaction becomes alkaline
in old cultures.

“ Milk. No change occurs in this medium during the length of time that
it is ordinarily kept under observation.

“Fermentation Tubes. (1) One per cent glucose bouillon: The liquid
throughout the tube becomes uniformly slightly clouded in twenty-four
hours at 37.5°C., and remains so. The reaction becomes acid in two days.
No gas is formed. A slight amount of viscous sediment collects.

““(2) One per cent lactose bouillon: The character of growth is similar
to that in glucose. The reaction remains alkaline.

“(3) One per cent saccharose bouillon: The growth is similar to that of
the two preceding. The reaction becomes acid in two days, but eventually
becomes alkaline in cultures several weeks old.

“ Dog Blood Serum. After twenty-four hours at 37.5° C. the path of the
needle is occupied by a smooth, shiny, raised growth of a color determined
by that of the serum. The condensation water is markedly turbid. Six
days later the growth, as well as the surface of a pellicle on the condensa-
tion water, has a coppery lustre.

36 DISEASES OF DOMESTICATED BIRDS

“ Lofier’s Blood Serum. After twenty-four hours’ growth at 37.5° ©,
the path of the needle is marked by a white, raised growth, with shiny, con-
toured or smooth surface and undulate border. The condensation liquid
becomes decidedly turbid. After several days the surface of the growth
becomes dull. The liquid is then observed to contain a viscous sediment
and to have patches of pellicle floating upon the surface.

“Indol. A positive reaction is obtained in sugar-free bouillon cultures.

“Animal Inoculation. Subcutaneous or intravenous injection of fowls
with 1 c.c. of a 24-hour bouillon culture resulted in death in about fifteen
hours. Doses as small as 0.05 ¢.c. killed in about three days. A young
rabbit inoculated with 0.5 ¢c. in an ear vein was found dead fourteen
hours later. A guinea pig inoculated with 1 e¢.c. subeutem was found
dead in fourteen hours. Another receiving 0.5 ¢@.c. subeutem survived
thirty-six hours. A pigeon swallowing 1 ¢.c. died in twenty-one hours, and
another receiving 0.12 ¢.c. subeutem was found dead fourteen hours later.”

Pathogenicity. Besides common fowls, geese, ducks, turkeys,
pheasants, pigeons and a large number of wild birds are susceptible
to infection. | Hemorrhagic septicemia in geese is discussed in Chap-
ter XIX.

The virulence of the fowl cholera organism varies greatly. Had-
ley has shown that the minimum lethal dose for fowls may lie at
any point between 10 ¢e.c. and 0.000,000,000,000,001 cc. of a 48
hour bouillon culture. Hadley states that infection results from
the inoculation into the breast muscle of less than fifty organisms
and probably by the inoculation of no more than four. To test the
infectiveness of the carcasses of fowls dead of the disease in a natural
outbreak, Ward fed such materia! to ten healthy cockerels. On the
first day following the exposure by feeding, three birds were dead;
on the second day, three; on the third, fourth, fifth and sixth days,
one bird each died. The incubation period may vary from eighteen
hours to as many days.

The blood and all discharges of a sick bird are infective. Eggs
have been demonstrated to contain the virus.

Infection may be induced in very small doses in a large variety
of ways such as ingestion, subcutaneous, intravenous or intramus-
cular injection, introduction of culture into the conjunctival sac, or
into the scarified skin.

Repeated passage of the virus through birds or through guinea
pigs results in an increase of virulence of a strain. On the other
hand diminution of virulence occurs under conditions not well un-
derstood. Doubtless there are also variations of virulence with re-
spect to the species attacked during various outbreaks.

FOWL CHOLERA a7

In the case of infection by ingestion the organisms are believed
to penetrate the uninjured mucosa of the intestines and gain access
to the lymph and thence to the blood. Death is undoubtedly caused
by toxins. There is however, lack of unanimity of opinion as to
whether the toxic effect is due to intracellular or to extracellular
toxins.

Prognosis. Prognosis is serious, for 90 to 95 per cent of acute
cases succumb.

Symptoms. In the peracute form, the bird either drops dead
suddenly or more often dies on the roost at night.

In the acute form the first noticeable symptom in the fowl is
the yellow color of the droppings. The yellow material consists
of urates and is usually found on the feathers near the vent. Di-
arrhea follows later. The discharge varies considerably in color
and consistency. It may be a greenish mass of pasty consistency, a
brownish red mucus or a viscous transparent fluid. The yellow
color of the urates is the most constant character.

Evidence of sickness is afforded by the unnatural attitude of the
feathers and by disinclination of the bird to move about. During
the later stages, no food is taken, but very sick fowls may drink
copiously. Drowsiness is marked in the later stages. Frequently
a mucous discharge drips from the mouth. The temperature varies
from 109° -to 112° F.

Death usually occurs within three days from exposure to infec-
tion but has been observed to occur within eighteen hours after in-
gestion of material from the carcass of another bird dead of the
disease. During an acute outbreak, sickness is seldom noticed more
than twenty-four hours before death.

The chronic form of the disease generally appears at the end of
an outbreak. The birds are dull, depressed and show persistent or
intermittent diarrhea. The mucose are pale and emaciation is
marked. Arthritis may develop in one or more joints, and leads to
ankylosis.

Morbid anatomy. A reddening of the skin of the breast and
abdomen is frequently observed. The comb often is dark red in
color, but may be pale. There is a general congestion of the blood
vessels of the visceral organs. The heart, in almost every case, is
studded with punctiform hemorrhages. Less frequently are observed
a fibrinous or a gelatinous exudate in the pericardium. One of the
lesions occurring most frequently consists of hemorrhages in the first
and second duodenal flexures. They may be so deep seated as to be

38 DISEASES OF DOMESTICATED BIRDS

visible from the peritoneal surface. Under such conditions the con-
tents of the duodenum consist of a pasty mass permeated with blood
clots. The contents of the intestines sometimes consist of a cream-
colored pasty mass, or may be green or brownish-red in color. In
many cases the liver is permeated with whitish punctiform areas of
necrosis. The oral, nasal, and pharyngeal cavities frequently con-
tain a viscid mucous fluid.

The lungs may show congestion and catarrhal or hemorrhagic
pneumonia. More rarely caseous foci are present. Sero-fibrinous
exudate may occur in the air sacs.

Hemorrhages are usually
restricted to the heart and
duodenum, and occur else-
where in the _ intestines
rarely. Still less frequent-
ly are they observed to be
abundant throughout the
skeletal muscles.

Microscopie examination
of stained smears from
heart blood and organs will
reveal numerous bipolar
staining rods.

Differential diagnosis.
Avian plague can be dif-
ferentiated by the fact that
no organisms are present 1n

Fic. 3. Blood smear from blood of a pigeon the blood as demonstrated
infected with fowl cholern. a, red blood - ye . - 7
cells; b, fowl cholera bacteria. (Klee) PY Cultures or by the mi

croscopic examination of
smears. Further, inoculation of pigeons and rabbits with ma-
terial from a case of plague will not produce infection in these ani-
mals.

Fowl cholera has features in common with fowl typhoid. How-
ever, diarrhea is not usual in the latter and at autopsy the intes-
tines are found to be pale, and the contents are normal in con-
sistency. In fowl typhoid the heart is pale and dotted with grayish
points due to cell infiltration. A bacteriological examination is
necessary for differentiating the various cholera-like septicemias.
This is not necessary in practice for no information is available to

FOWL CHOLERA 39

warrant handling such outbreaks by methods other than those used
to combat cholera unless biologic products are used.

Treatment. The treatment of individual sick birds is not rec-
ommended, and their immediate slaughter is advised.

Immunization. Pasteur in his memorable studies on immuni-
zation against disease first worked with the fowl cholera organism
in an attempt to produce an immunity against the disease caused
by this organism. He utilized in his experiments cultures of the
fowl cholera bacterium which he believed had become attenuated
by exposure to air for a period of several months. His favorable
results laid the foundation for the further study of the control
of disease by the utilization of the specific causative organism as
an agency of prevention. Kitt, Cogny, Vages and others working
along the lines pursued by Pasteur have failed to substantiate his
findings. However, it is quite possible that Pasteur worked with a
strain of the fowl cholera organism which had immunizing value.
Such an inference may be drawn through the researches of Hadley
who demonstrated that a particular strain of the fowl cholera or-
ganism designated strain 52, although practically avirulent, had the
power, when injected in the live state, of conferring immunity to
rabbits against the subsequent injection of a highly virulent strain.
These findings were, to a considerable degree, confirmed by Gal-
lagher who also found that fowls acquired a marked resistance to
comparatively large amounts of a virulent culture following the
injection of immunizing strain 52. At the same time the latter’s
experiments with killed cultures of several strains of the fowl
cholera organism, including strain 52, as immunizing agents gave
negative results. In each case fowls injected with bouillon cul-
tures of organisms killed by heating at 60° C. for 1 hour, by car-
bolizing to .5 per cent or by mixing with ether in equal parts,
failed to show resistance to a subsequent injection of .000,000,001
e.c. of a virulent strain.

Mack failed to produce immunity by the use of killed organisms
against artificial infection but claims successful results in a num-
ber of natural outbreaks. The use of an avirulent living organism
with immunizing properties offers the most promising method of
prevention. One cc. of a 24 to 48 hour bouillon culture grown
at 37° C. is injected subcutaneously. The point most convenient
for injection is the unfeathered area of the breast beneath the
wing.

It is possible to produce an antiserum by injecting a horse re-

40 DISEASES OF DOMESTICATED BIRDS

peatedly with cultures of the fowl cholera organism. The passive
immunity induced by its injection into fowls is short, and its use-
fulness is limited to flocks already infected or in grave danger of
becoming so.

Immunization with an aggressin has been accomplished in an
experimental way by Weil. He produces a pleural exudate in a
rabbit by injecting with fowl cholera bacilli. This exudate is ear-
bolized and heated for three hours at 44° C. A dose of 5 ce. is said
to immunize against subsequent injection of a lethal dose.

Prevention. Sanitation with reference to known methods of
dissemination should be the basis of combating the disease. The
chief sources of infection within an infected flock are dead birds
eaten by members of the flock, and contamination of food and water
by droppings. On large poultry farms, measures to secure isola-
tion of the center of infection should be enforced promptly. This
may involve temporary fencing, or moving the buildings, if portable.

Daily inspection of the roosting houses at daybreak should be
made to remove dead birds and to secure sick ones before they have
opportunity to go afield. Constant watch during the day will reveal
droopy birds which should be killed.

Feeding troughs may be so arranged that the birds can only put
in the head and do not have opportunity to contaminate the feed
with their feet. The drinking water may be rendered safe by
adding to it mercuric chloride in the proportion of one part to six
thousand parts of water. Earthenware containers should be used.

Disinfection of houses and adjacent areas should be carried out
daily. Since the floor of the roosting house is highly contaminated
by droppings, it should be disinfected if possible, before the birds
leave the roost. At any rate, the birds should be excluded from the
roosting house until it is possible to disinfect.

Poultrymen, familiar with the ravages of cholera, have been
known to ship sick and exposed birds to market, as the simplest
way to avoid financial loss. Apart from the obvious effect in re-
moving a center of infection, it has another effect in further spread-
ing infection. Birds dying during the trip to the shipping point
are thrown by the roadside, where they are liable to be partially
eaten by any fowls encountering them. The disease may be intro-
duced into a flock in a large number of ways such as introducing
birds in the incubation period of the disease, the carrying in of
infection on the shoes, by water, by animals, by pigeons or wild

FOWL CHOLERA 41

birds. All these possibilities, except perhaps the last two, suggest
appropriate defensive measures.

EDEMA OF THE WATTLES OF FOWLS

Characterization. Edema of the wattles is an infectious dis-
ease involving the wattles and which usually runs a chronic course.

History. The disease has been described by Seddon who ob-
served it among fowls in the suburbs of Melbourne, Australia.

Etiology. From all acute cases it is possible to isolate a short
rod indistinguishable from the one causing fowl cholera. In view
of this fact and since fowl cholera is very common in the region
in question it is likely that the wattle lesion merely represents a
localized chronic form of disease caused by the fowl cholera bac-
terium.

Pathogenicity. Scarification of the wattle of fowls and rubbing
in of culture in one case resulted in general illness, conjunctivitis,
edema of wattle, diarrhea and formation of necrotic material. The
bird when killed showed little change beyond the head lesion which
was found to contain the organism that was inoculated. Another
fowl inoculated in the same way showed edema and necrosis at the
point of inoculation. The bird subsequently displayed immunity
to infection through scarification or by subcutaneous injection of
virulent culture. A hen receiving one fourth c.c. of culture intra-
muscularly died in 24 hours and showed septicemic lesions at au-
topsy.

The disease occurred spontaneously among White Leghorns pos-
sessing large wattles. These brushed on the ground during feeding,
which offered an opportunity for injury and infection. Wounds re-
ceived during fighting offer another opportunity for entrance of
virus.

The pigeon is killed by intramuscular inoculation of culture.
Rabbits suecumb to the infection with lesions of hemorrhagic sep-
ticemia.

Symptoms. There is sudden enlargement of the wattles due to
more or less distention with fluid. In the beginning stage the wat-
tles are hot, dark red in color and upon incision a clear fluid exudes.
The birds manifest symptoms of general illness, loss of appetite, ete.
Sometimes there is conjunctivitis. Subsequently there is gradual
absorption of fluid accompanied by thickening of the wattle by
fibrous tissue. Nodules sometimes form in the tissues beneath the

42 DISEASES OF DOMESTICATED BIRDS

mandible or under the scars of wounds acquired during fighting.
The morbid process leads to disfigurement of the wattles by swell-
ings and by their assuming a crinkly form. In a small percentage
of cases of the disease fatal septicemia occurs.

Morbid anatomy. The more highly thickened areas in the wat-
tles consist of masses of caseous material. In some cases the ne-
crotie mass is surrounded by fibrous tissue, yellowish brown in
color and hard, almost horny in texture.

Treatment. Cropping the wattles offers the most satisfactory
means for dealing with the infection. The operation is described
on page 298.

Prophylaxis. Preventive measures must be essentially those
employed against fowl cholera.

CHOLERA-LIKE SEPTICEMIAS

The literature contains descriptions of a considerable number
of acute infections occurring among fowls, turkeys, geese, ducks,
swans and other birds. In a number of instances the diseases have
been shown not to be fowl cholera by bacteriological evidence that
is convincing today. In other instances the features differentiat-
ing the disease from fowl cholera do not appear convincing at the
present time. The reports cover a considerable period of time
during which many changes have occurred in methods of identify-
ing cultures. Thus the old bacteriological descriptions are inade-
quate for making an accurate classification of these infections.

There is little practical need for a close examination of the
etiology of these septicemias. The general methods of prophylaxis
are identical with those necessary in combating fowl cholera.

DISEASES IDENTICAL WITH FOWL CHOLERA

There are examples of diseases substantially identical with fowl
cholera which have been described under different names or without
assignment of name. Lisi described a fatal septicemia occurring
in fowls which caused the death of all the birds in the flocks in-
vaded. Nocard and Leclainche agree with Ligniéres that the dis-
ease was fowl cholera. Rabieaux observed a disease which he des-
ignates as a hemorrhagic septicemia of the duck and fowl. Lig-
niéres as well as Hutyra and Marek agree that Rabieaux does not
show that the disease described by him is different from fowl cholera.

FOWL CHOLERA 43

EPIZOOTIC DYSENTERY OF FOWLS AND TURKEYS

Lucet describes a septicemic disease of fowls and turkeys. He
differentiates the disease from fowl cholera by the insusceptibility
of the rabbit to subcutaneous inoculation and other peculiarities even
less convincing.

Etiology. The organism causing the infection is a short, slightly
motile rod which does not stain by the Gram method. It does not
grow on potato and gelatin is not liquefied.

Pathogenicity. The disease is inoculable from fowl to fowl,
from the fowl to the turkey, from turkey to turkey and reciprocally.
It is also transmissible between the two species by ingestion. The
pigeon is insusceptible to subcutaneous inoculation. The guinea
pig is not affected by subcutaneous or intraperitoneal injection. The
rabbit is insusceptible to injections in the same way, but succumbs
to intravenous inoculation.

Symptoms and lesions. There is nothing distinctive in the
symptoms displayed while the lesions are those of fowl cholera.

EPIZOOTIC PNEUMO-PERICARDITIS IN THE TURKEY

Characterization. The disease is an infection of the turkey
characterized by lesions of the lung and pericardium.

History. M’Fadyean first described the infection in England,
while Jowett encountered it near Cape Town.

Etiology. The organism causing the disease is a small ovoid rod
closely resembling that causing fowl cholera. M’Fadyean notes that
it possesses motility, while Jowett is silent on the point. It is Gram
negative and is readily stained by the ordinary dyes. No lique-
faction is produced in gelatin, no gas is formed in agar shake cul-
tures, no acid formation nor coagulation occurs in milk and no vis-
ible growth is observed on potato. Growth occurs equally well under
aerobic or anaerobic conditions. No unusual or striking character-
istics are presented by the growth on agar slant or bouillon cultures.

Pathogenicity. In the natural outbreak observed by Jowett,
turkeys only succumbed, while fowls, geese and pigeons in close
contact with them escaped infection. Subcutaneous inoculation of
the turkey with cultures caused symptoms of dullness, stiffness and
mouth breathing followed by death in a few days. Guinea pigs
and rabbits succumb to inoculation. owls are only slightly sus-
ceptible while pigeons succumb to intraperitoneal inoculation.

+4 DISEASES OF DOMESTICATED BIRDS

White rats die after intraperitoneal inoculation, but subcutaneous
inoculation may fail.

Morbid anatomy. Severe pericarditis is one of the most no-
ticeable characteristics observed at autopsy. The pericardium may
show extensive adhesions to the heart wall, and the latter may be
covered with a layer of yellow colored fibrinous exudate. The peri-
cardial sac may contain sero-fibrinous exudate. The lungs show
pneumonic changes and are frequently completely hepatized. Be-
yond possible fatty changes in the liver and paleness and swelling
of the kidneys, changes in other organs are not marked.

Microscopic examination of blood smears from heart blood, peri-
cardial exudate, lung and various organs, reveals the presence of a
bipolar rod.

Relation of disease to fowl cholera. M’Fadyean believes that
the effects produced on various animals by the organism described
by him, warrant the differentiation of the disease from fowl cholera.
He notes that pericarditis and pneumonia occur in fowl cholera, but
not with such constancy as they occur in the disease described by
him.

AN EPIZOOTIC AMONG FOWLS

Mazza reported upon a disease that caused heavy mortality in
various parts of upper Italy.

Etiology. Cultures from various organs almost always yield
growth of a motile rod, while culture media seeded from exudate,
blood and brain are more often sterile. Mazza concludes that the
organism differs from that of fowl cholera in several particulars.
It is larger than B. avisepticus,. does not usually exhibit bipolar
staining, is motile, is not very pathogenic for rabbits and is rarely
observed in the blood.

Pathogenicity. Hens and pigeons succumb to the infection
without exception. Guinea pigs are completely insusceptible while
rabbits are very slightly susceptible.

Symptoms. In general the hens die suddenly during the night
without having previously shown distinct symptoms of disease. In
other cases, symptoms like those occurring in fowl cholera are ob-
served.

Morbid anatomy. In external appearance the fowls usually
show no signs of emaciation. The only abnormal conditions en-
countered are darkening of the comb and large red areas on the skin
of the abdomen and of the breast. The subcutaneous cellular tissue

FOWL CHOLERA 45

appears scanty and occasionally hemorrhages are observed in this
locality. Quite constant lesions are encountered in the chest and in-
volve one or both lungs. There is a serous exudate in the chest
cavity sometimes with other signs of inflammation. More rarely
there is observed serous bloody fluid in the pericardium and red-
dening of the mucosa of the duodenum. In the cranial cavity there
is rarely observed a reddening of the pia mater and of the brain
substance.

HEMORRHAGIC SEPTICEMIA OF THE RING DOVE

Leclainche reports the occurrence of a septicemic disease of ring
doves from which he isolated an organism regarded as belonging
to the hemorrhagic septicemia group.

Etiology. ‘The causative organism is an ovoid rod identical in
shape with that causing fowl cholera, but somewhat larger. The
organism shows bipolar staining and is Gram negative. Growth
occurs on potato and gelatin is not liquefied.

Pathogenicity. The infection is transmissible to the ring dove
by inoculation and by ingestion. The domestic pigeon is much more
resistant. The fowl is absolutely refractory while the rabbit and
guinea pig are susceptible.

Symptoms. The symptoms are those usually presented by birds
affected with a septicemia.

Morbid anatomy. Lesions consist chiefly of hemorrhagic in-
flammation of the small intestine.

CHOLERA OF COSCOROBA SWANS

Tretrop observed a septicemia among swans in the zoological gar-
den of Antwerp to which he has given the above designation. The
species involved was Coscoroba candida. About fifty birds were in
the flock, of which the majority died. A large number of other
species of swans and other waterfowl were in contact with the dis-
eased ones but escaped infection.

Etiology. There is found constantly in the organs of the dis-
eased birds, a microorganism designated Bacillus coscoroba. It is
an ovoid motile rod 1.5 to 2.5 microns long and 1 to 1.4 microns
broad. Bipolar staining is observed and the organism is Gram
negative. The organism grows equally well in bouillon, milk, gel-

46 DISEASES OF DOMESTICATED BIRDS

atin and not on potato. Milk is coagulated and indol formed. Gel-
atin is not liquefied.

Pathogenicity. The mouse is very susceptible to inoculation but
the white mouse will not contract the infection by ingestion. Birds
of the order passeres succumb rapidly to intramuscular injection
of culture. The duck and fowl are insusceptible. Numerous spe-
cies of swans, geese and ducks in contact with the diseased birds,
escaped infection.

Symptoms. The birds remain in a squatting position, and show
the usual manifestations of sickness exhibited by those affected with
a septicemia.

Morbid anatomy. The subjects are generally in good condi-
tion. The muscles offer nothing special and the heart appears nor-
mal. Commonly, active congestion is observed in the lungs. Some-
times one or two caseous foci are present, which are easily enucle-
ated. ‘The liver is enlarged, dark in color and frequently shows
small whitish spots. The spleen is sometimes slightly engorged,
sometimes slightly increased in size. The intestine always shows
diarrhea with contents yellowish or yellowish green in color. The
intestines do not show marked injection of the blood vessels. No-
dules the size of a small pea are frequently found in the abdominal
cavity in the vicinity of the vertebral column.

HEMORRHAGIC SEPTICEMIA OF THE SWAN

Fiorentini observed a septicemic infection among swans in the
zoological gardens of Milan.

Morbid anatomy. In young birds that have died quickly there
is an edematous infiltration of the lungs with ecchymoses on the
serous membranes. There is also a slight hyperemia of the intes-
tinal mucosa, dark blood clots in the heart cavity and cloudy degen-
eration of the liver cells. In older birds that have died after several
days sickness there are more severe lesions. The lungs show fibrous
pneumonia in the stage of gray hepatization. The upper lobes of
the liver show a grayish yellow exudate composed mostly of lym-
phoid elements, besides marked thickening of Glisson’s capsule.
The hepatic tissue shows a marked infiltration with red blood cells
in the spaces between the liver cells. In numerous places in the
liver there are yellowish zones caused by the fatty degeneration of the
cellular elements. In the intestine there is slight hyperemia but
no exudate nor swelling. On the serous membranes there are numer-

FOWL CHOLERA 47

ous confluent ecchymoses, especially along the course of the coronary
arteries.

Etiology. The blood of dead swans yields cultures of a short rod
with rounded ends and which shows bipolar staining. ‘The shape
of the organism is very similar to that of the fowl cholera bacterium,
but it is somewhat larger. The organism has some characteristics
in common with that of fowl cholera. Both stain alike by the Gram
method and do not give an indol reaction. However, they differ
in other characteristics as the swan organism is motile. It also
forms rods as long as 4 microns. Growth in bouillon, agar and gel-
atin furnishes no distinguishing characteristic. Copious brown col-
ored growth occurs on potato accompanied by a bad odor.

Pathogenicity. The organism is virulent for the swan and a
goose (Anser aegyptiacus) while various aquatic and other birds
escaped infection.

Rabbits, guinea pigs, ducks, geese, hens and pigeons succumb to
intramuscular inoculation of culture.

INFECTIOUS ENTERITIS OF PHEASANTS

Fiorontini observed an epizootic among pheasants in the public
gardens of Milan which occurred a short time after an epizootic
of the same nature among swans. The disease was slightly con-
tagious for after many months the greater part of the birds escaped
infection.

Etiology. The organism causing the disease resembles that of
fowl cholera. It measures .7 micron in diameter and 1 to 2 mi-
erons in length. In cultures the organism forms chains which are
sometimes very long. Growth in bouillon is rapid at 22° to 24° C.
Indol is produced. On gelatin in 48 hours, a gray layer of growth
develops. On potato the color varies according to the development
of the growth. After 48 hours, the color is pale yellow, which
changes to brown while the borders are rose brown. ‘The culture
has the appearance of honey.

Pathogenicity. Pheasants alone are attacked and a preference
for males is exhibited. The infection is transmitted by inoculation
of cultures subcutaneously or intravenously in small amounts. In-
gestion of culture induces disease identical with that occurring natu-
rally. Hens are not affected by receiving 2 to 3 ¢.c. of virulent
culture and such inoculation does not assure immunity to fowl
' cholera. Rabbits and guinea pigs are immune.

48 DISEASES OF DOMESTICATED BIRDS

Symptoms. The birds display depression and the gait is uncer-
tain. The appetite is poor. Late in the disease an abundant di-
arrhea occurs, with the passage of grayish yellow or greenish colored
material. The state of coma and somnolence seen in fowl cholera
does not occur. The attack lasts five to eight days.

Morbid anatomy. Lesions occur throughout the intestine. The
mucosa is congested, is reddish brown in color and is covered with
a viscid layer or by a croupous exudate. LEcchymoses are not found
on the serous membranes. The liver is friable and the spleen is
swollen but not hemorrhagic.

REFERENCES

1. Fiorentint. Enterite infettiva dei fagiani. Atti della Societa
italiana di scenze naturali, 1896, p. 89.

2. Fiorentini. Himorrhagische Septikamie der Schwane. Centralbl. f.
Bakteriol. (Htc.), 1. Abt. Orig., Bd. 19, 1896, S. 932.

3. Gallagher. Fowl cholera and other hemorrhagic septicemia immuni-
zation experiments. J. Am. Vet. M. Ass., Vol. 50, (ns. Vol. 3), 1917,
p. 708.

4, Hadley. Fowl cholera and methods of combating it. Rhode Island
Agr. Exp. Sta. Bull. 144, 1910.

5. Hadley. A biological study of eleven pathogenic organisms from
cholera like diseases in poultry. Rhode Island Agr. Exp. Sta. Bull. 146,
1910.

6. Higgins. Notes upon an epidemic of fowl cholera and upon the com-
parative production of acid by allied bacteria. Jour. Exper. Med., Vol. 3,
1898, p. 651.

7. Jowett. Epizootic pneumo-pericarditis in the turkey. J. Comp.
Path. and Therap., Vol. 21, 1908, p. 324.

8. Kitt. Die Serumimpfung gegen Gefliigelcholera. Monatshefte f.
prakt. Tierh., Bd. 16, 1904, S. 1.

9. Leclainche. Sur une nouvelle septicémie hemorrhagique. La maladie
des palombes. Ann. de Tl Inst. Pasteur, T. 8, 1894, p. 490.

10. Lucet. Dysenterie épizootique des poules et des dindes. Ann. de I’
Inst. Pasteur, T. 5, 1891, p. 312.

11. Mazza. Bakteriologische Untersuchungen iiber eine neuerdings auf
getretene Hiihnerepizootie. Centralbl. f. Bakteriol. (Etc), 1. Abt. Orig.,
Bd. 26, 1899, S. 181.

12. Mack and Records. The use of bacterins in the control of fowl
cholera. Univ. Agr. Exp. Sta. Bull. 85, 1916.

13. M’Fadyean. Epizootic pneumo-pericarditis in the turkey. J. Comp.
Path. and Therap., Vol. 6, 1893, p. 334.

14. Nocard and Leclainche. Les maladies microbiennes des animauz.
Paris: Masson et Cie. 1903.

15. Pasteur. De l attenuation du virus du choléra des poules. Compt.
Rend. Acad. Sci. Paris, T. 91, 1880, p. 673.

FOWL CHOLERA 49

16. Pasteur. Sur les maladies virulentes, et en particular sur la maladie
appelée vulgairement choléra des poules. Compt. Rend. Acad. Sci. Paris,
T. 90, 1880, p. 239.

17. Rabieaux. Sur une septicémie hémorrhagique du canard et de la
poule. J. de méd. vét. et de zootech., T. 51, 1900, p. 129.

18. Seddon. Oedema of the wattles of fowls due to an organism of the
pasteurella group. Vet. J., Vol. 21, 1914, p. 24.

19. Seddon. <A diseases of the wattles of the fowl. J. Agr. Victoria,
Vol. 12, 1914, p. 426.

20. Tretrop. La maladie des cygnes coscoroba. Ann. del Inst. Pasteur,
T. 14, 1900, p. 224.

21. Ward. Fowl cholera. Univ. of Cal. Agr. Exp, Sta. Bull. 156, 1904.

CHAPTER V

FOWL TYPHOID AND SIMILAR INFECTIONS
FOWL TYPHOID

Synonym. Hiihner typhus (German).

Characterization. Fowl typhoid is a specific infectious disease
of fowls, having the general characteristics of a septicemia and is
caused by Bacterium sanguinarium (Bacillus gallinarum).

History. The disease seems to have been first described by Klein
in England in 1889 under the name of infectious enteritis of fowls.
The organism was designated by him, Bacillus gallinarum. Had-
ley states that a culture of this organism has been preserved since
its isolation by Klein, and that a study recently made by him re-
veals the organism to be identical with Bacterium sanguinarium.
The disease and its causative agent were described by Moore in
1895. Other outbreaks in the United States have been described by
Dawson, Curtice and by Taylor.

Pfeiler and Rehse observed the same disease in 1912, gave it the
name “‘ Hiihner typhus,” and described the organism under the name
Bacterium typhi gallinarum alcalifaciens. A second outbreak oc-
curring in 1915 has been described by Pfeiler and Roepke.

Etiology. The characteristics of the organism are described by
Moore as follows:

“Morphology. Bacterium sanguinarium varies somewhat in size ac-
cording to the medium in which it has developed. In tissues of fowls or
rabbits it is from 1.2 to 1.8 microns long and from 1 to 1.3 microns broad.
The ends are tapering or rounded in cultures; in the short forms it could
easily be mistaken for a micrococcus. In tissue it frequently appears in
small clumps, but usually in pairs united end to end. Spores or vacuoles
have not been discovered. Involution forms are common. In cultures on
agar it is more slender than in tissues. When examined in a hanging
drop preparation, especially at the edge, it frequently shows a marked
polar arrangement of the cellular protoplasm. In these preparations there
is observed a marked dancing motion of the organism. In old bouillon
cultures short chains composed of these organisms united end to end are
sometimes observed.

“ Staining. It stains with the aniline dyes ordinarily used, but retains
the coloring matter very feebly, or not at all, when treated after the Gram
method.

50

FOWL TYPHOID AND SIMILAR INFECTIONS 51

“Cultivation. This organism is readily cultivated on the ordinary
media. It is obtained in pure cultures from the heart blood or liver of a
fowl just dead from the disease.

“Agar. On this medium, at 37° C., the growth is moderately vigorous.
It has a grayish glistening appearance. Isolated colonies are from 1 to
2mm. in diameter, convex, and with sharply defined borders. Agar plates
emit a peculiar penetrating odor, which differs decidedly from the pungent
odor given off by Bacterium suisepticum. The growth on this medium
resembles very closely that of B. suipestifer.

“Gelatin. In this medium the growth is less vigorous. In stick cul-
tures it is more abundant along the line of inoculation than on the surface.
Isolated colonies are about 0.25 mm. in diameter, appearing to the un-
aided eye as homogeneous bodies, but slightly granular under low mag-
nification. On the surface of the gelatin the colonies are granular and
slightly spreading. They are not characterized by any distinctive mark-
ings. There is no liquefaction or softening of the medium.

“Potato. On the surface of potatoes a delicate grayish yellow growth
appears after forty-eight hours when kept at a temperature of 35° C.
Frequently there is no development, owing, presumably, to the acids in the
potato.

“ Bowillon. In alkaline peptone bouillon at 36° C. the growth imparts
a uniform cloudiness to the liquid within twenty-four hours. If the
bouillon contains much sugar the reaction becomes acid, otherwise it re-
mains alkaline. A grayish friable sediment forms in the bottom of the
tube. After several days’ standing the growth settles, leaving a clear
supernatant fluid. In a simple peptone solution containing one-half of 1
per cent sodium chloride the growth is less vigorous than in the one con-
taining the meat juice. In meat extract bouillon the growth is likewise
feeble. In acid peptone bouillon there is a very faint cloudiness imparted
to the liquid.

“ Alkaline bouillon containing 1 per cent dextrose in the fermentation
tube becomes cloudy within twenty-four hours after inoculating and
strongly acid in reaction. Similar tubes of bouillon containing saccharose
and lactose become clouded throughout but they remain alkaline in reac-
tion. The degree of alkalinity increases with age. Gas is not produced
during the growth in bouillon containing these sugars.

“ Life conditions and properties. This organism develops at a temnera-
ture from 20 to 41° C. It does not grow well in acid media. It produces
indol.

“ Resistance. It is destroyed at 50° C. in fifteen minutes. A 1 per
cent solution of carbolic acid was fatal to it in 5 minutes. It resists
drying when in films on cover-glasses for from 7 to 15 days.

“ Pathogenesis. This organism is fatal to fowls, pigeons, rabbits, guinea
pigs, and mice. Other animals have not been tested. Excepting in in-
travenous injections, comparatively large quantities of a pure culture
were required to produce fatal results. Fowls inoculated in the wing vein
with 0.3 ec.c. of a fresh bouillon culture died in from three to thirteen
days; usually on the fifth or sixth day. The temperature begins to rise
on the second day after inoculation. It reaches 109 to 111° F. a few days

52 DISEASES OF DOMESTICATED BIRDS

before death occurs. In cases where the fowls live from five to six days
they appear perfectly well for at least three days, when the feathers begin
to have a slightly ruffled appearance. Pigeons inoculated with 0.2 cc. of
a bouillon culture die in from four to five days. In rabbits the lesions re-
semble very closely those produced by attenuated hog cholera bacteria
(B. suipestifer). Guinea pigs inoculated in the abdominal cavity with
from 0.2 to 0.3 «ce. of a bouillon culture die in from five to eight days.”

Differences from B. pullorum. The two causative organisms
differ materially in their action on sugar media. B. pullorum pro-
duces gas in dextrose, mannite and levulose, while B. sanguinarium
does not produce gas in any of the sugars in common use. Milk is
rendered acid by B. pullorwm and alkaline by B. sanguinariwm with
or without saponification in the latter instance. B. pullorum is neg-
ative to the methyl red test when grown in 1 per cent maltose bouil-
lon, while B. sanguinarium gives a positive reaction.

Symptoms. These are quite similar to those of other acute
septicemic diseases. Drowsiness and indifference to surroundings
are marked. ‘There is loss of appetite and general weakness. The
head may be drawn in close to the body or may hang limp. The
mucose of the head are pale. Diarrhea is present in the majority
of cases. The droppings are yellowish and may be tinged with
green. The comb and wattles are usually paler than normal but
may be darkened with venous congestion. The blood is pale red
in color and presents a marked decrease in red cells and great in-
crease of white cells. The period of incubation is four to six days
and the duration of symptoms in fatal cases from four to twelve
days. A temperature elevation of three to five degrees is noted.

Morbid anatomy. There is a general anemic appearance of the
serous membranes. The mucous membrane of the intestine is usu-
ally pale. At times it may show slight areas of congestion, or hem-
orrhagic points. The most marked changes observed on post mortem
examination are in the liver, spleen, kidneys and blood. The liver
is greatly enlarged and generally dotted with grayish necrotic spots.
It may, at times, be congested throughout or show spots or bands of
congestion. It has a tendency to become friable. Microscopic ex-
amination of sections of the organ reveals an engorgement of the
blood vessels and a breaking down of the parenchymatous tissue.
The hepatic cells present different stages of degeneration from cloudy
swelling to complete necrosis. The necrotic areas vary in size from
that of a few cells to macroscopic lesions. The spleen is sometimes

FOWL TYPHOID AND SIMILAR INFECTIONS 53

enlarged, dark colored and pulpy. It may show necrotic points.
The kidneys are somewhat enlarged, may be lighter in color and
slightly injected with blood.

The vascular system shows the most constant changes. The heart
appears normal or else pale with grayish spots of necrosis. The
blood is lighter in color and does not clot readily. Microscopie ex-
amination reveals a great disproportion between the number of red
and white cells present. The red cells decrease in numbers to a
marked degree as the disease advances while the white cells become
greatly increased in numbers. This increase is confined principally
to the polymorphonuclear leucocytes. The following table from
Moore will illustrate the proportionate relationship between the red
and white cells during the course of the disease.

TaBLe IJI.— Biroop CHANGES IN Fowt FEp CuLtTuRE Marcy 26.

Neyo ee
Temper- | red corpus- ae
Date a corpuscles Remarks.
ature ° F cles per
per
c.mm.
ce. mm.
Mar. 26 106.2 3,535,000 18,940 Well.
Mar. 28 110.0 2,430,000 70,000 Fowl eats very little.
Apr. 2 110.6 1,684,210 80,000 Blood very pale; fowl
weak; refuses food.
Apr. 3 106.0 1,745,000 245,000 Very weak; many red
corpuscles attacked by
leucocytes.
Apr. 4 eeu oe ee AE Found dead.

In stained preparations of the blood numerous red corpuscles are
observed undergoing degeneration. This is manifested by the fail-
ure of the cellular protoplasm surrounding the nucleus to stain reg-
ularly or at all, and also by vacuolization of the protoplasm of the
cell.

Bacterium sanguinarium may be recovered in pure culture on arti-
ficial culture media from the blood, liver, spleen and kidneys of
fowls recently dead of the disease.

Differential diagnosis. Fowl typhoid is distinguished from
fowl cholera by the absence of severe congestion of the mucous mem-
brane of the intestine especially the duodenum, by the absence of
hemorrhagic spots on the heart, by the failure to find bipolar stain-
ing bacteria in the blood, and by the finding and isolation of B.

o4 DISEASES OF DOMESTICATED BIRDS

sanguinarium. Also, the duration of symptoms is apt to be much
shorter in the case of cholera.

Fowl typhoid is differentiated from fowl pest by the absence of
severe intestinal congestion, failure to find petechiz in the mucosa
of the proventriculus and by the fact that fowl pest is caused by
a filterable virus and no organisms can be detected in the blood
stream, or isolated on artificial culture media.

Infectious leukemia has somewhat similar lesions and also shows
a greatly changed condition of the blood. However, in this disease
the loss of red cells and increase of white cells is much more marked
than in fowl typhoid. Also, it is the mononuclear cells, instead
of the polymorphonuclears, which show the principal increase in
numbers in infectious leukemia. Unlike fowl typhoid, infectious
leukemia is caused by a filterable virus and no microorganism can
be grown, from the blood or organs on artificial culture media.

Fowl typhoid and acute Bacterium pullorum infection of grown
fowls have symptoms and lesions which are somewhat similar. The
causative organisms also closely resemble each other both morpho-
logically and in their cultural characteristics. In B. pullorum in-
fection, however, the ovary is congested and nearly always presents
several hard irregular ova. It is the principal seat of predilection
for the pullorum bacterium.

PSITTACOSIS OF PARROTS

Synonyms. Septic fever of the parrot, parrot septicemia, (Eng-
lish) ; septicemie des perruches, mycose des perroquets, (French) ;
Psittacosis, (German).

Characterization. The disease is a contagious septicemia in-
volving parrots and parrakeets and causing fever, weakness, stupor
and diarrhea.

Transmission to man. The disease has received considerable
attention because suspicion has been aroused that the infection may
be transmitted to man. A number of outbreaks of infectious pneu-
monia in man have been observed to occur simultaneously with the
bird disease.

Leichtenstern sums up the question of the transmission of the dis-
ease to man as follows:

“4. Epidemiological, clinical and especially bacteriological evidence is
not disclosed to prove that the infection of house epidemics of pneumonia
suspected of being psittacosis, did originate from sick parrots.

“9 Tt is proven that bacterial diseases, especially enteritis, occur fre-

FOWL TYPHOID AND SIMILAR INFECTIONS sy)

quently in parrots, particularly those freshly imported, and inflict sporadic
and also excessive mortality.

“3. No one will doubt that the streptococci, staphylococci, pneumococci,
eoli and proteus varieties occurring in these fatal parrot diseases may
under certain circumstances also become dangerous for man.

“4, The disease of man designated psittacosis is in clinical and ana-
tomical features an atypical pneumonia coupled with typhoid symptoms
and the disease has the same character in all epidemics.

“5. The same house epidemics of pneumonia occur not rarely, without
the intervention of parrots and one may from this draw the conclusion
that all the former psittacosis epidemics were nothing more than atypical
pneumonia in which the sick parrot, accidentally present in the house,
played no etiological réle.

“6. The above conclusions under 5 are contradicted in some measure by
the no small number of former so-called psittacosis house epidemics.
Especially contradictory to these conclusions is the Paris epidemic of 1892
in which the transmission of the disease from the sick parrots to man
must be considered on the basis of epidemiological facts as, at the least,
apparently wholly indicated.”

Etiology. An organism belonging to the hog cholera group has
been isolated from cases of the disease in parrots, by Nocard and
by Palamidessa. It is an actively motile, Gram negative rod which
grows equally well under aerobic or anaerobic conditions. The
growth in bouillon and on agar presents no characteristic features.
Growth on gelatin at first consists of a shiny, transparent, iridescent
streak which develops into a porcelain-white growth. No liquefac-
tion of gelatin occurs, and milk is not coagulated. Growth on potato
resembles that of B. coli. The organism may be isolated from the
blood, bone marrow, spleen and other organs of infected birds. It
has been isolated from the intestinal contents of parrakeets which
were in apparent good health.

Pathogenesis. The causative organism is pathogenic for the
parrot, parrakeet, pigeon, fowl, mouse, rabbit and guinea pig. All
discharges of an infected bird are infective and in view of the close
contact between birds there is every opportunity for transmission
of infection. The disease occurs most frequently among birds dur-
ing shipment from the tropics and shortly after landing. Contribu-
tory factors to its occurrence seem to be the unusual restraint, erowd-
ing, filthy cage conditions, climatic conditions and general hard-
ships suffered during shipment.

Symptoms. The disease is manifested by shivering, inappe-
tence, diarrhea with frothy greenish droppings which are sometimes
blocdy. The bird exhibits great thirst, drowsiness and disinclination

56 DISEASES OF DOMESTICATED BIRDS

to move. The wings droop, the eyes are closed, the feathers are
ruffled and the head is turned on the shoulder. When attempt is
made to move, great weakness is evident. The bird usually avoids
the perch. Convulsions precede death by a short period. In more
chronic cases there is a discharge from the nostrils and eyelids,
coughing, snuffling and difficult, panting respiration. Emaciation
is evidenced by prominent breast bone and loss of weight. Vomiting
is occasionally observed.

The disease is usually fatal and hope of recovery may be enter-
tained only in cases which survive for eight or nine days and which
display some appetite. Most die in from three to five days after
sickness is noted.

The incubation period in natural exposure varies from three days
to several weeks.

Morbid anatomy. The organs of the abdominal cavity show
intense congestion and ecchymoses are present in the peritoneum.
Small grayish spots may be observed in the liver, spleen and kid-
neys. The spleen is usually enlarged and soft in texture. The
intestines show general congestion, or catarrh and often contain
ulcers on the mucosa. The muscles often present a striated and
‘spotted appearance. The heart muscle is often dark or hemor-
rhagic. Eechymoses may be present in the endocardium and peri-
eardium. The lungs may present various conditions such as total
consolidation, yellowish pneumonic patches, areas of atelectasis or
of congestion. The air sacs may contain fibrinous or fluid exudate.

Treatment. The patient should be kept in a room having a
temperature of from 90° to 100° F. continuously. Gray advises
that aspirin or cyllin may be given in the drinking water. In cases
showing improvement, the aspirin may be replaced by aromatic sul-
phurie acid and quinine sulphate. Food may consist of bread and
milk, banana, sponge cake soaked in sherry, ete.

Prevention. The most effective prevention would consist of
improvement of methods of isolation of individuals and of general
conditions on shipboard. Prophylaxis on shore involves perfect
segregation of birds and the application of disinfection.

DISEASE OF PIGEONS CAUSED BY A BACILLUS OF THE
HOG CHOLERA GROUP

Moore observed an infection in pigeons in New Jersey caused by
an organism closely related to Bacillus suipestifer.

FOWL TYPHOID AND SIMILAR INFECTIONS 7

Symptoms. The disease is characterized by emaciation and a
peculiar turning of the head from one side to the other. Occasion-
ally there are paroxysms of aimless flying about. The disease is
popularly designated ‘“ megrims.”

Etiology. The organism belongs to the hog cholera group of
bacteria but differs in several particulars from the specific organism
isolated from affected hogs. The organism from the pigeon is ap-
preciably larger. In bouillon a delicate pellicle develops on the
surface of the fluid, and in old cultures, a deposit is formed on the
sides of the tube. A marked indol reaction occurs. The pigeon
culture is less rapidly fatal for experimental animals than B. swi-
pestifer.

Morbid anatomy. Autopsy of a bird that had shown the pe-
culiar head movement for several days revealed no lesions in the
thoracic or abdominal cavities. There was a friable exudate about
1 mm. in thickness, in the subarachnoid space over the cerebellum
and the posterior lobes of the cerebrum. It was grayish yellow in
color and easily removed. The subjacent brain tissue was reddened
but otherwise the brain was normal in appearance. The organism
in question was recovered in pure culture from the brain lesion but
not from the heart blood. Another pigeon found dead, showed great
emaciation but few other changes beyond pale, fatty heart muscle.
The same organism was recovered in pure culture from the liver and

blood.

AN INFECTION IN PIGEONS CAUSED BY BACILLUS PARATYPHOSUS B.

Zingle observed an infection in pigeons apparently caused by B.
paratyphosus B.

Morbid anatomy. ‘The external appearance of the carcass, be-
yond marked emaciation, presents nothing suspicious. The oral
cavity in all cases is free from lesions. Upon skinning, the breast
muscle is seen to be colored yellow in some places and permeated
with bright yellow knots like oat grains. The liver frequently has
a yellowish gray color, and on closer observation it is seen to be cov-
ered over the whole surface with countless hyperemic areas, which
are sharply defined from the surroundings. In more cases the liver
is permeated with yellow, round, compact knots varying in size from
that of a grain of wheat to that of a bean, which give the surface a
roughened appearance. The spleen is generally small without par-
ticular macroscopic changes. The intestine appears somewhat hem-

58 DISEASES OF DOMESTICATED BIRDS

orrhagic. The most marked lesions are shown by the kidneys.
These are extraordinarily large, and the borders of the several
lobules have completely disappeared. The color of the kidneys is
mostly gray-yellow. They appear to be sprinkled through with
numerous speck-like foci and they are very fragile in consistency.
The lungs appear free from lesions in many cases. Frequently,
however, the lungs contain numerous opaque, gray-white foci the size
of a hemp seed which are uniformly distributed. Lesions are not ob-
served in the trachea, but the mucous membrane of the crop in iso-
lated cases contains yellow crumbly, button-like areas of exudate.

Etiology. In the bacteriological examination of blood, muscu-
lature and organs a bacillus was found which agreed with paraty-
phoid B in cultural, morphological and serological characters. The
culture agglutinated in a dilution of 1: 15,000 completely and par-
tially at 1: 25,000 with B. paratyphosus B serum of a titre of
1: 30,000.

All the strains showed the same characteristics as B. paratyphosus
B in litmus milk, glucose, Endo agar, malachite green agar, gelatin,
Barsiekow solution 1 and 2, neutral red agar, orzein agar as well
as milk, potato and bouillon.

Pathogenicity. White mice succumbed to subcutaneous injec-
tion in two days. It was especially noticeable that the organism
cecurred in great numbers, and was never observed mixed with
other organisms.

Pathological histology. In microscopic sections of the kidneys
there are found inflammatory foci somewhat larger than a millet
seed with round eell infiltration of the interstitial area. Also
parenchymatous degeneration of the epithelium of the convoluted
tubules in that the nuclei of the same in part are poorly stained and
the protoplasm appears to be granular. The lumina of the tubules
are filled with masses of desquamated epithelial tissue. When
stained with Sudan they show fatty degeneration of medium degree
in the epithelium of the labyrinths.

The investigation of the liver shows that the organ is permeated
with numerous abscesses.

The knots in the musculature present themselves microscopically
as abscesses varying in size from that of an oat grain to that of a
pepper seed, with distinct lymphocyte walls which mingle with the
neighboring muscle fibers. In the center of the abscesses there is
much fibrin and also pus cells.

FOWL TYPHOID AND SIMILAR INFECTIONS 59

In the lungs there are numerous abscesses analogous in structure
to those in the muscle.

Relation to bird pox. Because of a suspicion that bird pox
virus was present, inoculation experiments were undertaken. By
rubbing of pus from liver, kidneys, lungs, ete., as well as blood and
musculature, skin, muscle nodules, and crop exudate, into scarified
breast skin of pigeons, there appeared after 2 to 3 days, yellowish
swellings which looked exactly like pox. After a week they reached
the maximum size of a pea. During this time the breast muscle fell
away very markedly. These swellings began to shrink and dry up,
while as a rule no fresh swellings appeared. Some of the pigeons
died within 2 to 4 weeks after inoculation. By that time the pox-
like swellings on the breast skin were totally dried up or had fallen
off. The musculature was atrophied, flecked with yellow and in
some cases contained numerous knots shaped like an oat grain with
section findings like those in the original pigeons.

Other pigeons lived. After some time the pox scabs fell off, the
breast muscle filled out, so that the bird appeared clinically healthy.

These results were obtained easily through inoculation of gener-
ation after generation, also with dried out material, and the B. para-
typhosus B could be recovered each time.

The question arose as to whether these organisms were the pri-
mary cause of this pigeon disease or whether like hog cholera, the
paratyphoid bacillus played a part of a leader. There was the pos-
sibility of a mixed infection with bird pox, and on this account ex-
periments were started with contamination free filtrates of cultures
and organs.

Also inoculation experiments were undertaken with cultures that
had been grown for many generations in fluid and solid media.

While the filtrate experiments gave no positive result, inoculations
with pigeon paratyphosus culture always gave pox-like appearances
in two days.

AVIAN SALMONELLOSIS

Ligniéres and Zabala describe an infection in fowls caused by an
organism which they regard as showing all the specific characters of
the hog cholera bacillus. The authors note that their organism is
non-motile, while the hog cholera organism of Salmon and Smith is
motile. However, they conclude that this difference is not sufficient
to differentiate the organisms. Consequently they propose the name
avian salmonellosis for the disease observed.

60 DISEASES OF DOMESTICATED BIRDS

Etiology. The organism isolated is a non-motile rod which is
Gram negative. Whether a precipitation of casein occurs in milk
or not, the medium becomes liquid again in 5 to 8 days. The color
is grayish and the reaction is strongly alkaline. Indol is not pro-
duced and gelatin is not liquefied. Growth occurs on potato. There
is nothing distinctive about growth on other media.

Pathogenicity. It is possible to inoculate healthy hens and rab-
bits with several drops of infected blood without killing them. Sub-
cutaneous inoculation with culture does not always kill hens but
intravenous injection of 1 to 2 c.c. of culture has a fatal result. The
pigeon is easily killed by intravenous and subcutaneous inoculation.
Ducks and geese are resistant to the infection. The rabbit inocu-
lated intravenously with 1 ¢.c. of culture is killed, while subeutaneous
inoculation merely causes tumefaction at the point of inoculation.

Symptoms. No symptoms characteristic of the infection in
question are displayed.

Morbid anatomy. The comb is black, and sometimes dark
ecchymoses are observed on the skin. There is a clear fluid in the
pericardium. The liver and the kidneys are congested. The spleen
is enlarged and much more so than in fowl cholera. The mucosa
of the digestive tract is reddened in places, but hemorrhages are
rarely found.

PATHOGENICITY OF B..ENTERITIDIS AND B. PARATYPHOSUS B
TO BIRDS

Reinholdt has found that introduction of either B. enteritidis or
B. paratyphosus B into hens, pigeons, geese and ducks, sometimes
causes a transitory disease and sometimes a fatal disease. This is
true of a wide variety of methods of inoculation such as intravenous,
intraperitoneal, subcutaneous and intramuscular injection, as well as
administration by the stomach. Pigeons are most susceptible to in-
fection, followed in order by geese and hens. Administration of the
organisms per os under normal conditions of feeding is of least
influence. A very large number of organisms is necessary to induce
infection. The organisms are always recovered when the bird dies,
but this is not always true when a bird is slaughtered while healthy.
Ageglutinins are detected six days after infection.

FOWL TYPHOID AND SIMILAR INFECTIONS 61

SEPTICEMIAS CAUSED BY COLON BACILLI

Fowls. Outbreaks of septicemic infections in fowls caused by
B. coli have been reported by Ligniéres, Martel, Claussen, Zeiss and
Schlegel.

The symptoms are practically indistinguishable from those of
fowl cholera. The birds show somnolence, depression, diarrhea and
inappetence. In the late stages, the comb may be dark colored as
in cholera.

At autopsy, there is inflammation of the intestines with hemor-
rhages in places. There may be a small amount of serous exudate
in the abdominal cavity. The spleen is softened and hypertrophied.
There is pericarditis manifested either by the presence of hemor-
rhages, solid exudate or fluid exudate. Microscopic examination of
stained smears from the blood and organs shows numerous bipolar
staining rods. However, the organisms average twice as large as
those of fowl cholera.

In inoculation experiments made by Ligniéres, hens resisted sub-
cutaneous and intramuscular injection of 1 to 2 cc. of culture. On
the other hand the pigeon succumbed to a dose of 1 cc. The same
dose injected subcutaneously into the rabbit and guinea pig caused
only a local abscess, while intrapleural or intraperitoneal injection
killed.

Martel killed hens by intramuscular injection of small amounts
of culture. Failure resulted from attempts to cause infection by
intravenous injection or by ingestion of cultures, excrement and
virulent products. The guinea pig, rabbit, white rat and white
mouse were found to be susceptible to injections.

Claussen isolated a strain that was uniformly fatal to canary
birds, white mice and guinea pigs. Pigeons, hens and ducks became
sick only exceptionally. The infection led to the death of only 50
per cent of the inoculated birds, while the remainder recovered
after three to six days. The incubation period was on an average,
twelve hours long. Rabbits were very refractory to inoculation.

Claussen concludes that colon organisms occurring in the intes-
tines of healthy hens possess the ability of becoming virulent under
certain conditions and cause a cholera-like infection. These spe-
cial conditions are believed to be furnished by the harmful influ-
ence exerted by shipment for long distances with resulting hunger,
thirst, cold and lack of ventilation.

Zeiss reports a case in which two hens in a healthy flock sud-

62 DISEASES OF DOMESTICATED BIRDS

denly displayed lack of appetite with depression and died soon.
Autopsy revealed extraordinary softness of the spleen and liver to-—
gether with limited subcutaneous hemorrhages. Preparations from
the blood revealed bipolar rods. The organism isolated from the
eases showed the morphology and biologie characteristics of B. coli.

The organism was pathogenic for canaries. On the other hand,
guinea pigs could not be infected by either subcutaneous nor intra-
venous injection with 2 ¢c.c. doses of 24 hour bouillon culture.

Pigeons. Sanfelice observed an outbreak of a disease among
pigeons caused by B. coli. Most of the birds appeared at autopsy
as follows: On opening the abdominal cavity a sero-fibrinous exu-
date is noted on the whole surface of the intestines. The abdominal
fluid is increased in amount. The spleen is swollen. There are
adhesions of the intestines, the heart and the liver. The exudate
appears in the form of a pseudomembrane in that when grasped
with tweezers, it pulls off completely. In some pigeons besides the
peritonitis described, there is inflammation of the mucosa of the
oviduct, which is covered with a purulent exudate. Often eggs are
found in the oviduct, which could not be laid on account of the
inflammation. An organism identified as B. coli was observed in
smears and was recovered in culture from the organs. Pigeons
inoculated subcutaneously with one to one and one half ¢.c. of cul-
ture, developed an abscess at the point of inoculation but did not
die. Larger doses injected into the abdominal cavity caused death.

Pheasants. Klein described an organism isolated from young
pheasants dead of an infectious disease. The organism was motile,
somewhat shorter than B. coli and did not coagulate milk. He
concludes that the organism, though belonging to the same family as
B. coli, was a different species.

GROUSE DISEASE

Under the name of grouse disease, Klein has described a pneu-
monia caused by a member of the B. coli group. Subsequent inves-
tigation by a committee of inquiry on grouse disease revealed the
fact that the condition of the lungs described by Klein represents
post-mortem changes. The supposed etiological agent is regarded
by the committee as a post-mortem invader. It was noted that
Klein had opportunity to study only birds that had been dead sev-
eral days. The cause of mortality among grouse was watched by
the committee very closely for six years and in no instance was

FOWL TYPHOID AND SIMILAR INFECTIONS 63

there observed an epizootic like that described by Klein. A large
number of agencies are responsible for the death of grouse, and
probably the most important is infestation with T'richostrongylus
pergracilis as pointed out first by Cobbold.

QUAIL DISEASE

Synonym. Colibacillosis tetraonidarum.

Characterization. Quail disease is an infectious disease which
according to Morse is caused by a member of the colon group and
characterized by congestion of the lungs, focal necrosis of the liver
and ulceration of the intestine. It has been recognized only among
birds in captivity.

Species affected. The disease has been observed in the bob-
white (Colinus virginianus), the California quail (Lophortyx cali-
fornicus vallicola), the Gambel quail (Lophortyx gambelv), the
mountain quail (Oreortyx pictus), the scaled quail (Callupepla
squamata) and the sharp-tailed grouse (Pediocaetes phasianellus
campestris ).

History. The disease for many years has been observed among
quail shipped for stocking areas of land and appears during trans-
portation, or immediately after. It seems evident that the unusual
conditions and hardships endured during the shipment constitute
an important factor predisposing to the occurrence of the infection.
Many outbreaks occur among quail which have been recently cap-
tured in Mexico. Morse has written an article summing up the
available information regarding the characteristics of the disease.

Etiology. Morse reports finding a bacillus of the B. colt group
present in diseased birds, with striking constancy. Cultures are
readily isolated from the liver and intestines. It cannot always be
cultivated from the heart blood of birds dead of the disease, nor
always from the lungs.

Pathogenesis. The organism is not pathogenic for chickens,
pigeons nor rabbits but kills mice and guinea pigs with characteristic
-lesions. Experiments with quail are hindered by the difficulty in
obtaining birds that have not been exposed to infection.

Symptoms. The symptoms first become manifest by dullness,
inappetence and ruffling of the feathers. Death may occur within
two or three days after the appearance of symptoms. In chronic
cases emaciation becomes extreme.

Morbid anatomy. As a rule, the carcass is in good condition.

64 DISEASES OF DOMESTICATED BIRDS

There is slight congestion of the lungs, and of the liver. The sur-
face of the latter organ presents a few areas of necrosis. Some-
times the liver contains no necrotic spots and is merely congested,
but in some cases the necrosis involves a large area. The intestinal
wall contains numerous small yellowish areas of necrosis which may
be seen through the peritoneal surface. These may be exceedingly
minute, or reach the size of a pinhead. In some cases the necrotic
process appears in the form of ulcers, some of which may perforate
the intestinal wall. In other cases the intestinal lesions may con-
sist of mere reddened areas.

Prophylaxis. It is likely that the removal of birds from the
natural wild environment, interference with natural food supply,
crowding in cages and shipment are the fundamental factors pre-
disposing birds to infection. These undesirable conditions of un-
natural crowding are difficult to correct.

The cleaning and disinfection of shipping cages should be carried
out very thoroughly. So far as possible, birds should be isolated
in small lots during shipment. All possible precautions to prevent
the contamination of feed and water should be carried out. .

Treatment. The nature of the disease and subjects are such as
to prevent successful treatment.

ASTHENIA IN FOWLS

(GOING LIGHT)

Characterization. The affection is characterized by extreme
emaciation associated with reddening of the walls of the duodenum.

History. Dawson described the disease as occurring in the vi-
cinity of Washington, D. C.

Etiology. The organism isolated from the duodenum of af-
fected birds is designated Bacterium asthentew and is regarded as
a variety of the colon species.

Pathogenicity. Dawson was unable to induce disease in chick-
ens by feeding organs or cultures, or by inoculating them intra-
abdominally, subcutaneously and intravenously. Nevertheless he
was inclined to believe that the organism in question was the cause
of the disease.

Dawson considers that the presence of the organism in the part
of the alimentary canal where the digestive process is most active

FOWL TYPHOID AND SIMILAR INFECTIONS 65

interferes with nutrition. Pigeons, mice and rats proved equally
refractory. A guinea pig inoculated subcutaneously with duodenal
contents succumbed to the infection. Rabbits inoculated subeutane-
ously with culture and fed the same, proved refractory. Intra-
abdominal inoculation of half a cubic centimeter of culture proved
fatal to a rabbit.

Symptoms. Extreme emaciation is the most noticeable symp-
tom. The appetite is voracious. There is no evidence of diarrhea
and no increase of temperature. The comb and wattles are slightly
more pale than normal.

Morbid anatomy. Autopsy of affected fowls reveals extreme
emaciation of the muscular system and viscera with almost complete
absence of fat. There is reddening of the walls of the duodenum
and the contents are mucoid in appearance.

Treatment. Dawson recommends purgation to remove the or-
ganisms in the duodenum. For this purpose he administers castor
oil in a dose of two teaspoonfuls or calomel in one fourth grain doses
repeated frequently. He suggests that purgation be followed by a
stimulating tonic recommended by Mégnin as follows: Powdered
fennel, anise, coriander seed, cinchona, each 30 grains; powdered
gentian and ginger, of each 1 dram; powdered sulphate of iron,
15 grains. Mix. Add from 2 to 4 grains of this mixture for each
fowl to the food twice a day.

REFERENCES

1. Claussen. Ueber Kolibakterienseptikimie bei Hiihnern als Trans-
portkrankheit. Ztschr. f. Infektionskr. d. Haustiere, Bd. 3, 1907, S. 69.

2. Committee of inquiry on grouse disease. The grouse in health and
disease. London: Smith, Elder & Co., 1911.

3. Curtice. Fowl typhoid. Rhode Island Agr. Exp. Sta. Bull. 87, 1902.

4. Dupuy. De la psittacose au point de vue epidemiologique. Prog.
Med., 1897, p. 225.

5. Hadley. Infections caused by bacterium pullorum. Rhode Island
Agr. Exp. Sta. Bull. 172.

6. Klein. Ueber eine akute infektidse Krankheit des schottischen Moor-
huhnes (Lagopus scoticus). Centralbl. f. Bakteriol., Bd. 6, 1889, S. 36.

7. Klein. Ein weiterer Beitrag zur Kenntniss des Bacillus der Grouse-
disease, Centralbl. f. Bakteriol., Bd. 6, 1889, S. 593.

8. Klein. Ueber eine epidemische Krankheit der Hiihner, verursacht
dureh einen Bacillus-Bacillus Gallinarum. Centralbl. f. Bakteriol., Bd. 5,
1889, S. 689.

9. Leichtenstern. Ueber infektidse Lungenentzundungen und_= den

66 DISEASES OF DOMESTICATED BIRDS

heutigen Stand der Psittacosis-Frage-— Werden durch spezifish erkrankte
Papageien bosartige Lungenentzundungen beim Menschen hervorgerufen ?
Centralbl. allgem. Gesundheitspfl., Bd. 18, 1899, S. 241. Abs. in Centralbl.
f. Bakteriol. (EKtc.), 1. Abt., Orig., Bd. 26, 1899, S. 651.

10. Ligniéres. Septicémie a coli-bacille chez la poule Compt. rend.
Soc. de biol., T. 46, 1894, p. 135.

11. Ligniéres and Zabala. Sur une nouvelle maladie des poules. Bull.
Soc. Cent. de Méd. Vét., T. 59, 1905, p. 453.

12. Martel. Maladie a coli-bacille de la poule et de la dinde. Compt.
rend. Soc. de boil., T. 49, 1897, p. 500.

13. Moore. On a pathogenic bacillus of the hog-cholera group associ-
ated with a fatal disease in pigeons. U. 8S. Dep. Agr. Bur. Animal In-
dust. Bull. 8, 1895.

14. Moore. A study of a bacillus obtained from three outbreaks of
fowl cholera. U. S. Dep. Agr. Bureau Animal Indust. Bull. 8, 1895.

15. Moore. Infectious leukemia in fowls—A_ bacterial disease fre-
quently mistaken for fowl cholera. U. S. Dep. Agr. Bureau Animal In-
dust. 12th and 13th Ann. Rep., 1895-96.

16. Morse. Quail disease in the United States. U.S. Dep. Agr. Bureau
Animal Indust. Circ. 109, 1907.

17. Palamidessi. Di una infectione nell’ womo transmesso probabilmenti
dai pappagalli. Policlinico, 1895. Abs. in Centralbl. f. Bakteriol. (Htc.),
1. Abt., Ofig., Bd. 20, 1896, S. 316.

18. Pfeiler und Rehse. Bacillus typhi gallinarum alealifaciens und die
durch thn verursachte Hiihnerseuche. Mitteil. a. d. Kaiser Wilhelm In-
stitut f. Landwirthschaft in Bromberg, Bd. 5, 1913, S. 306; Abs. in Cen.
tralbl. f. Bakteriol. (Htc.), 1 Abt. Ref., Bd. 58, 1913, S. 575.

19. Pfeiler and Roepke. Zweite Mitteilung iiber das Auftreten des
Hiihnertyphus und die Eigenschaften seines Erregers. Centralbl. f. Bak-
teriol. (Htc.), 1 Abt. Orig:, Bd. 79, 1917, S. 125.

20. Reinholdt. Infektionsversuche mit den “ Fleischvergiftern ” (Bacil-
lus enteritidis Gartner und Bacillus paratyphosus B) beim Geflugel. Cen-
tralbl. f. Bakteriol. (Htc.), 1. Abt. Orig., Bd. 62,1912, S. 312.

21. Rettger and Koser. A comparative study of Bacterium pullorum
(Rettger) and Bacterium sanguinarium (Moore). J. Med. Research, Vol.
35, 1917, p. 448.

22. Sanfelice. Eine Seuche dei Tauben durch Bacterium coli verur-
sacht. Ztschr. f. Hyg. u. Infektionskr., Bd. 20, 1895, S. 23.

23. Smith and Ten Broeck. Ageglutination affinities of a pathogenic
bacillus from fowls (fowl typhoid). (Bacterium sanguinarium, Moore.)
J. Med. Research, Vol. 31, 1915, p. 503.

24. Smith and Ten Broeck. The pathogenic action of the fowl typhoid
bacillus with special reference to certain toxins. J. Med. Research, Vol.
31, 1915, p. 523.

25. Smith and Ten Broeck. A note on the relation between B. pul-
lorum (Rettger) and the fowl typhoid bacillus (Moore). J. Med. Re-
search, Vol. 31, 1915, p. 547.

26. Taylor. A report upon an outbreak of fowl typhoid. J. Am. Vet.
M. Aiss.,.n. s. Vol. 2, 1916, p. 35.

FOWL TYPHOID AND SIMILAR INFECTIONS 67

27. Zeiss. Koliseptikiimie bei Hithnern. Archiv f. Hyg., Bd. 82, 1914,
S. 27.

28. Zingle. Untersuchungen iiber eine Taubenseuche mit Paratyphus-B-
Bazillenbefund. Zeitschr. Infektionskr. d. Haustiere, Bd. 15, 1914, S. 269.

CHAPTER VI

BACILLARY WHITE DIARRHEA

Characterization. Bacillary white diarrhea is an acute, highly
fatal septicemic disease of young chicks caused by Bacterium pul-
lorum. The infection also exists in adult hens in a chronic, rarely
fatal form, usually confined to the ovary. The disease as it occurs
in hens bears no specific name and is merely referred to as B. pul-
lorum infection.

Etiology. Rettger and Harvey describe the characteristics of
the organism substantially as follows:

“ Morphology, staining properties, etc. The organism is a long, slender
bacillus (.8-.5 micron x 1-2.5 microns) with slightly rounded ends. It
usually occurs single, chains of more than two bacilli being rarely found.
It is non-motile, non-liquefying, non-chromogenic, aérobic and facultatively
anaérobic. In its microscopic appearances it resembles the bacillus of
typhoid fever. It is stained readily by the ordinary basic anilin dyes.
It does not stain by the Gram method; neither does it retain its color
when treated with dilute acetic and mineral acids. The organism does
not produce spores, or at least they have never been observed.

“The maximum temperature tolerated is 56 to 57° C. (moist) for an
exposure of fifteen minutes. The optimum temperature is 35 to 37° C.

“Cultural characters: Agar plates. Small white colonies make their
appearance within twenty-four hours. They increase in size slowly and
seldom attain more than one millimeter in diameter, even after three or
four days’ ineubation. Under the microscope they appear yellow and vary
in form from oval and spindle-shaped to round. The surface is usually
marked with a rosette figure or what seems to be a lobed nucleus. Occa-
sionally two or even three of these markings may be seen.

“Slant agar. Growth is quite visible in twenty-four hours, and re-
sembles that of the typhoid bacillus. It spreads little and remains deli-
cate, even after prolonged incubation. On glycerine agar the growth is
practically the same.

“ Gelatin plates. Small white colonies may be seen in forty-eight hours.
They remain small for several days, and only under exceptional conditions
do they develop into characteristic surface colonies which to a certain ex-
tent resemble the grape-leaf colony of B. typhosus.

“Gelatin stab. A delicate growth occurs in forty-eight hours along the
whole line of inoculation. It is of distinctly granular appearance and
spreads very little on the surface. The gelatin is not liquefied.

“On potato development is very slow. A narrow, almost invisible’
68

BACILLARY WHITE DIARRHEA 69

streak is produced along the line of inoculation. In litmus milk little or
no apparent change occurs within the first forty-eight hours, after which
the milk becomes slightly acidified without any signs of coagulation of
the casein.

“Gas production in sugar bouillon. Negative results were obtained
with maltose, lactose, saccharose, inulin, and dextrin bouillon. Dextrose
and mannite were attacked, however, with both acid and gas production.
In the dextrose fermentation tubes about twenty per cent of the closed
arm was filled with gas, and the mannite tubes averaged about the same.
The gas consisted of Co, and H in the ratio of 1 :3.

“Indol and nitrite production. Neither indol nor nitrite could be de-
tected in Dunham’s peptone solution at the end of one week’s growth in the
incubator.”

Toxin production. B. pullorum has been shown by Smith and
Ten Broeck to produce a toxin fatal to rabbits. Filtrates of bouillon
cultures when injected intravenously may cause death within two
hours, or marked dyspnea followed by death over night, or cause loss
of weight followed by recovery. The lesions induced, include con-
gestion of various organs such as liver, spleen, kidneys, adrenals,
lungs and mesenteric lymph glands together with hemorrhage into the
gastric mucosa.

Source of infection. Infection may occur in several ways.
The most common source is through infected eggs. It has been
demonstrated that affected chicks which survive the disease fre-
quently retain the causative organisms in the system and later, in
the event that the ovary becomes infected, pass them off in the eggs.
Many infected eggs fail to hatch, the embryos dying in the shell at
an early or late stage of development. Should one or more chicks
be hatched, harboring the disease, the others of the lot are exposed
early and nearly all become affected. The chicks are especially
susceptible during the first 48 hours of life, but are practically in-
susceptible after the third day. Another source of infection is
through brooders and incubators that have previously held infected
chicks. Day-old chicks frequently carry the disease to other points
and contaminate brooders or infect other chicks with which they
come in contact. However, the largest percentage of outbreaks is
traced directly to the presence of infected hens in the flock from
which the eggs for hatching were derived. There is a well defined
eyele through which the bacterium passes; namely, from the in-
fected ovary of the hen through the egg to the chick and back to the
ovary of the pullet which has survived the disease as a chick.

Pathogenicity. Susceptibility to infection bears a remarkable

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DISEASES OF DOMESTICATED BIRDS

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BACILLARY WHITE DIARRHEA (a!

previously affected. At the end of four days, the unattacked chicks
have generally acquired a resistance to acute infection. The re-
sistance at this age, while very apparent in broods of young chicks,
is not absolute, since fatal outbreaks in old fowls are recorded in the
literature on the disease.

Half grown guinea pigs are killed in from 24 to 48 hours when
injected subcutaneously. The chief lesion is a large edematous area
beneath the skin of the abdomen. MJabbits are killed in three to
seven days by subcutaneous injection of one to two ¢.c. of 48 hour
bouillon culture. In the case of all experimental inoculations, the
‘organism may be recovered in pure culture from all the internal
organs.

Mortality. Bacillary white diarrhea is, without doubt, the most
fatal disease of young chickens. Among those broods affected, the
death rate varies between 40 and 90 per cent. The high percentage
is more often registered than the low one.

Symptoms. The external symptoms of bacillary white diar-
rhea are similar to those of coccidial and aspergillar white diarrhea.
The presence of soft, whitish droppings and similar symptoms in
each case caused these three diseases to be grouped under the com-
mon term “ white diarrhea.” The position of each as an important
specific disease requires that they should be treated separately, espe-
cially since they are not confined to young chicks but affect grown
fowls as well.

The affected bird is drowsy, and dejected in appearance. The
feathers are ruffled, the wings droop and the chick sways back and
forth in a standing position. The appetite is diminished. The
irritation of the droppings when being voided often causes the
ehick pain as evidenced by a peculiar ery at the time. The drop-
pings may adhere to the down about the vent, blocking the opening.
This gives rise to the expression “ pasting up behind.” In acute
eases the chick soon falls to the floor and death occurs after a short
period of coma. In more chronic cases the chick remains standing
in a dull inattentive position a good portion of the time while not
under the hover or hen. It acquires the appearance of having a
short back and a large abdomen. Often one or both feet swell.
The chick stands on one leg with the toes of the elevated foot just
touching the floor. Lameness is shown in attempts to walk.

The disease may show itself within two or three days after the
chicks are hatched and spread rapidly through the brood. The
period of incubation is four to ten days. Deaths begin to occur

(2 DISEASES OF DOMESTICATED BIRDS

soon after hatching and continue to the third or fourth week.
Chicks which survive, remain stunted and unthrifty for some time.

Morbid anatomy. The lesions observed on autopsy are not
clearly distinctive for this disease which is purely septicemic in
nature. The early, rapid development of the disease, in a_ host
unprepared to combat it, prevents the formation of many distinctive
lesions. The failure of the yolk to be absorbed is the principal
abnormal condition that is apparent. However, this condition is
observed in very young chicks which have died through other causes,
such as weak constitution, faulty incubation, and brooder defects.
The liver usually shows an ochre color, with bands or streaks of
congestion. This appearance is not constant as in some cases an
apparently normal mahogany or chocolate colored liver is observed.
Tn some instances the liver has the normal appearance, and the yolk
sac has been absorbed. This is especially common in less acute
cases. The lungs may show minute necrotic areas and, as a rule,
congestion.

Diagnosis. Diagnostic features of the disease are its early
appearance, the high mortality within the first month, the occurrence
of deaths within a few days after hatching, and the absence of inter-
nal lesions other than unabsorbed yolk or striations on the surface of
the liver. Confirmatory positive evidence is obtained by examina-
tion of stained smears of the blood, liver or yolk with discovery of the
causative organism. Further evidence is yielded by feeding or in-
oculation experiments with young chicks.

Artificial cultural methods are more precise. The causative or-
ganism may be readily isolated in a pure culture from the heart
blood, liver, spleen, kidneys or unabsorbed yolk. It may be differ-
entiated from other organisms of a similar type by its cultural and
biochemic characteristics, and by its agglutinating properties against
a homologous serum.

Differential diagnosis. Bacillary white diarrhea is differenti-
ated from the other diseases commonly classed as white diarrhea by
its early occurrence, the exceptional mortality, and the absence of
the characteristic lesions of coccidiosis, or of aspergillosis. Coecidi-
osis is slower in its development and usually affects chicks at a later
period. It is manifested by hemorrhagic areas in the ceca, dilatation
of these organs, and the presence of necrotic casts in their lumina.
In the event that this disease is present, the coccidial cysts may be
readily demonstrated on microscopic examination of the cecal con-
tents.

BACILLARY WHITE DIARRHEA 73

Aspergillosis is comparatively rare in young chicks. Its charac-
teristic growth may be found in the air passages, and the mycelia,
or spores of the fungus can be observed by microscopic study of the
moldy growth.

Treatment. Attempts to cure bacillary white diarrhea are fu-
tile. Some recover, owing to natural resistance, or other reasons.
The so-called treatments recommended by some advisers are not to
be relied upon. Once the disease has become established in the sys-
tem, the causative microorganisms are distributed through the vari-
ous organs by way of the blood stream and a septicemia has developed
which is beyond the reach of any antiseptic treatment which has yet
been discovered. By careful nursing, certain individuals might be
assisted in surviving; however, this is inadvisable because of the fact
that the monetary value of the baby chick does not justify the ex-
penditure of the time devoted to its treatment. Furthermore, the
fact that those which recover are likely to serve as reservoirs for the
causative organisms and constitute the sources of future outbreaks
would speak against the policy of treatment.

Where the disease is known to exist in a flock of breeding fowls
and is anticipated in the hatch of baby chicks, precautions may be
taken to lessen its attack by advanced treatment of the chicks. \ Per-
manganate of potash may be placed in the drinking water in sufficient
quantity to give the latter a deep red color.) This corresponds to dilu-
tion of approximately 1 to 10,000. In such dilution, the antiseptic is
non-irritating to the sensitive mucous membranes of the chick and
may serve to inhibit the growth of the pullorum bacterium in contami-
nated drinking water, and in the digestive tract of the chicks. But-
termilk may be used as a food, as it combats the development of
the bacterium in the intestine, due to the lactic acid which it
carries.

Prevention. The first principle of prevention is the eradication
of carriers in the breeding stock, or the use of eggs for hatching
which come from flocks known to be free of pullorum infection.
Certain tests which are later discussed may be depended upon to
detect the presence of the disease in a large percentage, if not all,
of the infected hens of a flock. These birds may be discarded for
breeding purposes or disposed of as the owner may desire. In this
connection, it has come to our attention indirectly that in rare in-
stances normal hatches have succeeded ones in which high mortality
has occurred, the eggs in each case being derived from flocks in which
a number of infected hens have been detected but retained as breeders.

74 DISEASES OF DOMESTICATED BIRDS

The significance of this is not apparent, but opens an interesting field
for study, if the observations are accurate.

If it is desired to breed from an infected flock for the purpose of
perpetuating the particular strain of fowl, or for other reasons, pre-
caution may be taken to minimize the losses by the following pro-
cedure. Incubator trays, or shelves, of the pedigree type which are
partitioned off into compartments capable of inclosing a few chicks,
say from six to ten as the owner may decide, are to be used. The
partitions are to be sufficiently high to prevent the chicks in adjacent
compartments from coming in contact. This also means that the
partitions should be of solid structure to prevent picking back and
forth. It is only necessary to use such trays a day or two before
the hatch is expected to come off, and for three days after it 1s com-
pleted. The chicks are to be retained in their respective compart-
ments and need not be fed for 48 or even 72 hours, since they are
provided with food material during this period through the yolk
which is drawn into the abdominal cavity previous to hatching.
Should symptoms of disease develop, the chicks in the particular
compartment are to be removed and disposed of. The attendant
should then disinfect his hands before watering or caring for the
others. As the disease is contracted principally during the first 48
hours of life, and only to a slight extent during the succeeding 24,
this method of procedure will prevent a general spread to the hatch.
The temperature and air requirements may be regulated to suit the
needs of the chicks. Humidity, due to close confinement and lack
of air circulation, is to be guarded against. The trays may be re-
moved to the brooders, or similar structures may be placed in the
latter and the chicks transferred to them, with care to avoid mixing
the segregated lots. After three days, the danger of infection is re-
duced to a minimum, and all of the hatch may be allowed to run
together.

BACTERIUM PULLORUM INFECTION OF GROWN FOWLS

Occurrence. Infection of hens by the organism in question is
not marked by external changes nor is it regarded as a common
cause of death. Jones reports one outbreak due to B. pullorum in-
fection which assumed an acute character with marked symptoms and
considerable mortality. In this case the fowls were infected through
the feeding of eggs which had failed to hatch and which came from
an infected flock. About 50 birds died during the outbreak. The

BACILLARY WHITE DIARRHEA 75

present writers have encountered at autopsy a naturally infeeted
fowl which had developed fatal B. pullorum septicemia from primary
ovarian infection.

Symptoms. In the chronic form, no symptoms are apparent to
the observer. The fowls continue to lay, although from the number
of retained and undeveloped ova, it is evident that laying is retarded.
In the acute cases reported by Jones, within a period varying from
two to six weeks after exposure by feeding, the affected birds showed
a loss of appetite and energy. They appeared droopy and somnolent,
with ruffled feathers and retracted heads. The combs and wattles
were pale and more or less diarrhea was present. In the fatal cases,
death ensued in from one to several days after the onset of symptoms.

Morbid anatomy. In the acute cases autopsied by Jones the
most constant lesions were the presence of small necrotic foci in the
liver, spleen, pancreas and heart. The capsule of the liver, the peri-
cardium and the heart were in many instances covered by a fibrinous
exudate.

In the majority of chronic cases, autopsy will show the lesions to
be confined to the ovary. This organ usually presents an appear-
ance quite characteristic. The diseased ova which have partially or
wholly developed are hard, shrunken and angular. The natural yolk
color has changed to a dark brown or greenish color. On cut section
the ova are of a tough cheesy consistency, with a yellowish red, or
greenish tinge. The condition of the ova closely resembles “ gan-
grene of the ovary” of earlier writers. The morbid ova may also
appear as cysts, with darkened fluid contents. Occasionally only
small cysts are present in the ovary and it is through cultural meth-
ods alone that the presence of pullorum infection may be detected.
Small foci consisting of sac-like structures with yellowish colored
solid or fluid contents may occur in almost any portion of the ab-
dominal or pleural cavities. Involvement of the pericardial sae is
not uncommon.

The causative bacterium may be readily isolated from the angular
ova or cysts and grown on artificial culture media. In some eases
where ovarian lesions are not pronounced, it is necessary to remove
the ovary and disintegrate aseptically. The mass is placed in a
flask of bouillon, from which cultures may be plated on agar and
the organism isolated in pure culture.

Diagnosis. Several methods of diagnosing the presence of B.
pullorum in fowls are available and are more or less satisfactory.
The presence of bacillary white diarrhea in a brood of chicks which

76 DISEASES OF DOMESTICATED BIRDS

Fig. 5. Normal ovary. (Redrawn from Rettger, Kirkpatrick and Jones)

has been hatched from eggs from a particular flock of hens is proof
enough of infection in the flock, providing that there is a reasonable
certainty that contamination has not been introduced by outside
sources or from infected incubators or brooders. Detection of the
characteristic pullorum-infected ovaries, on post mortem examina-
tion, is definite proof that the disease is prevalent in the flock. Bace-

Fie. 6. Ovary infected with B. pullorum. (Redrawn from Rettger, Kirkpatrick
and Jones)

BACILLARY WHITE DIARRHEA 77

teriological examination of eggs from a suspected flock also leads to
a diagnosis. However, this method is impractical because of the
fact that an infected hen only occasionally drops an infected egg and
considerable laboratory work is necessary to establish the presence of
the disease. or the detection of individual carriers among hens
held for breeders, two other methods which give positive proof of the
presence of infection in the flock and pick out the infected individuals
with a high degree of accuracy have been developed. These are the
agelutination test applied first by Jones, and the intradermal test
developed by the authors.

Agglutination test. ‘This test is based on the fact that the blood
serum of an animal which has experienced the attack of a given
species of bacteria will in some instances cause the organisms to
agelutinate or form into clumps when a suspension of the bacteria
is mixed with the serum of the animal in proper dilution.

The wing vein is severed at the point where it passes over the
elbow joint and 3 to 5 ee. of blood collected in a sterile test-tube or
vial. The flow of blood is then stopped by momentary pressure over
the cut, or by the application of a small pledget of cotton. Usually
no effort is necessary to stop the flow of blood, as chicken blood clots
readily. Blood may be drawn more rapidly by severing the promi-
nent vein visible on the ventral surface of the wing near the shoul-
der. The collected sample is set aside and allowed to clot. It
should not be agitated while the clot is forming, as this tends to
prevent the collection of a clear serum. After the clot has formed,
the sample may be placed in a refrigerator or other cool place. In
a few hours the serum will have been pressed out by the contraction
of the fibrin and can be drawn off as a clear fluid, free of blood cor-
puscles or hemoglobin. If the test is not to be made immediately,
the serum may be preserved by the addition of carbolic acid in suf-
ficient quantity to form a .5 per cent solution. Jor this purpose,
it is convenient to use a 5 per cent solution of carbolic acid as a
standard, .1 ¢.c. being added to .9 ¢.c. of serum, or 1 drop to 9 drops.
For the test a standardized suspension of B. pullorum is prepared.
This may be heated at 60° C. for one hour, to kill the organisms, or
used in the live state. The latter has been the practice of the au-
thors. However, there appears to be no marked advantage in the
use of live antigen, and killing by heat or .5 per cent carbolization
has the advantage that the organisms are dead and hence absolutely
harmless.

In the test, the bacterial suspension is placed in the test tubes

78 DISEASES OF DOMESTICATED BIRDS

in the quantity of 1 ec. to each tube. A series of tubes is em-
ployed for each serum, depending on the number of serum dilu-
tions to be made. In practice, a serum which causes agglutination
in a dilution of .01 or even .02 is sufficient to establish a positive
diagnosis. Using 1 ec. as the standard amount of bacterial sus-
pension, sera which have been diluted by the addition of normal salt
solution to the extent of .04, .02, and .01 per cent of the original,
are distributed in their respective tubes in quantities of 1 ¢.c. each.
The tubes are labeled to show the identity of the various sera and
the dilutions. In practice, it is found convenient to dilute the serum
to 10 per cent of its original volume and add .4, .2, and .1 of a «ec.
to the 1 ¢.c. of bacterial suspension. The tubes are shaken to insure
a thorough mixture of the contents and may be set aside at a tem-
perature of 37° C. for from twenty-four to forty-eight hours, when
readings may be made. Instead, when rapid diagnosis is desired,
they may be placed in an incubator at 37° C. for 14 hour and then
centrifuged at the rate of 1500 to 1800 revolutions to the minute for
several minutes. Either course gives similar results. In positive
eases the organisms in the fluid collect in floceulent masses which
have a tendency to form a diffuse coating over the bottom of the tube,
while in the negative cases the organisms are deposited in a small
circular mass in the center of the bottom of the tube. This is par-
ticularly apparent where centrifugalization has been employed. On
shaking the tubes the clearly positive ones will show a clear fluid
containing floceulent masses while the negative ones are uniformly
clouded.

The agglutinating serum dilution which will establish a diagnosis
has not been definitely fixed. It is a well known fact that normal
blood serum is capable of agglutinating organisms to a greater or
less degree. In B. pullorum infection tests, a serum which in the
amount of .02 c.c. or less causes agglutination, undoubtedly indicates
a positive case.

Intradermal test. This test depends for its results upon the
principle underlying allergic reactions. It is very similar in char-
acter to the intradermal tuberculin test, especially as used to detect
tuberculosis in fowls.

A culture of several strains of B. pullorum from widely separated
sources is grown in bouillon at a temperature of 37.5° C. for a
period of thirty days to three months. Whether these time limits
are necessary has not been determined. The product is then steril-
ized at a temperature of 60° C. for a period of one hour and carbolic

BACILLARY WHITE DIARRHEA (2)

acid is added in sufficient quantity to form a .5 per cent solution
for preserving purposes. In the earlier experiments of the authors,
the product was passed through a Berkefeld filter and concentrated
to one-tenth of its original volume. Later it was found that the
original sterilized product concentrated to 7% its volume gave as
satisfactory results.

The material is injected into either wattle of the fowl in the
amount of approximately .2
e.c. The injection is made
with a hypodermic syringe
eraduated in tenths of a c.c.,
and a needle of fine caliber
is used to avoid causing
traumatic swellings. The
injection is made at a point
near the lower border of the
wattle. Where the flock is
apparently free of. infec- Fic. 7. Edematous swelling of wattle in-

E ere ars dicating positive reaction to the intrader-
tious disease, no disinfect- mal test for B. pullorum _ infection.
ants are employed at the (Original)

point of injection since the natural resistance of birds to ordinary
wound infection is sufficient to guard against infection. In the ab-
sence of a graduated syringe, the amount to be injected may be
gauged by injecting enough to cause a perceptible swelling at the
point of inoculation. During the first three hours after injection
the wattle shows an edematous condition which rapidly disappears in
non-reacting birds. Readings are taken at twenty-four to thirty
hours after injection. The wattle may be swollen to several times
its natural thickness and may be readily observed at a distance, or
the swelling may be so slight that palpation, or comparison with the
uninjected wattle will be necessary. Any swelling other than that
due to traumatism as a result of faulty technique, should be consid-
ered significant.

REFERENCES

1. Bushnell and Maurer. The use of milk cultures of B. bulgaricus in
the prevention and treatment of bacillary white diarrhea of young chicks.
Am. Vet. Rev., Vol. 44, 1913, p. 195.

2. Gage and Martin. Notes on the histo-pathology of the intestines in
young chicks infected with bacterium pullorum. J. Med. Research, Vol.
34, 1916, p. 149.

3. Gage and Hyland. On the diagnosis of infection with bacterium

80 DISEASES OF DOMESTICATED BIRDS

pullorum in the domestic fowl. Mass. Agr. Exp. Sta. Bull. 148, 1914.

4. Gage and Paige. Bacillary white diarrhea (Bacterium pullorum in-
fection) in young chicks in Massachusetts. Mass. Agr. Exp. Sta. Bull. 163.
TOM:

5. Jones. The value of the microscopic agglutination test in detecting
fowls that are harboring Bact. pullorum. J. Med. Research, Vol. 27,.
11913, p. 481.

6. Jones. Further studies on bacillary white diarrhea in young chickens.
Rept. N. Y. State Vet. Col. 1910-1911, p. 69.

7. Jones. An outbreak of an acute disease in adult fowls, due to Bact.
pullorum. J. Med. Research, Vol. 27, 1913, p. 471.

8. Rettger. Septicemia among young chickens. N. York M. J., Vol.
71, 1900, p. 802.

9. Rettger. Septicemia in young chickens. N. York M. J., Vol. 73,
1901, p. 267.

10. Rettger. Further studies on fatal septicemia in young chickens or .
“white diarrhea.” J. Med. Research, Vol. 21, 1909, p. 115.

11. Rettger. Ovarian infection in the domestic fowl and direct trans-
mission of the disease to the offspring. J. Hxper. M., Vol. 19, 1914, p. 552.

12. Rettger and Harvey. Fatal septicemia in young chickens, or “ white
diarrhea.” J. Med. Research, Vol. 18; 1908, p. 277.

13. Rettger, Hull and Sturges. Feeding experiments with Bacterium
pullorum. The toxicity of infected eggs. J. Haper. M., Vol. 23, 1916,
p: 475.

14. Rettger, Kirkpatrick and Card. Chickens: Milk feeding and its
influence on growth and mortality. Comparative study of the value of
sweet and sour milk. Storrs Agr. Exp. Sta. Bull. 80, 1915.

15. Rettger, Kirkpatrick and Stoneburn. Bacillary white diarrhea of
young chicks. Third report. Storrs Agr. Exp. Sta. Bull. 74, 1912.

16. Rettger, Kirkpatrick and Jones. Bacillary white diarrhea of young
chicks. Fourth report. Storrs Agr. Exp. Sta. Bull. 77, 1914.

17. Rettger, Kirkpatrick and Jones. Bacillary white diarrhea of young
chicks. Storrs Agr. Exp. Sta. Bull. 85, 1915.

18. Rettger, Kirkpatrick and Jones. Bacillary white diarrhea of young
chicks — VI. Storrs Agr. Exp. Sta. Bull. 88, 1916.

19. Rettger and Stoneburn. Bacillary white diarrhea of young chicks.
Storrs Agr. Exp. Sta. Bull. 60.

20. Scherago and Benson. Experiments on the intradermal test for
Bacterium pullorum. Cornell Vet., Vol. 9, 1919, p. 111.

21. Ward and Gallagher. An intradermal test for Bacterium pullorum
infection in fowls. U. 8. Dep. Agr. Bull. 517. ‘

CHAPTER VII

FOWL PLAGUE

Synonyms. Bird plague, fowl pest, bird pest, infectious peri-
tonitis of birds, exudative typhus of birds, Brunswick bird plague;
Peste aviarire, Peste des oiseaux (French) ; Gefliigelpest, Huhner-
seuche, Huhnerpest, Vogelpest, Geflugelseuche, Kyanolophiea gallin-
arum, Putenseuche (German); Peste aviaria, Epizoozia tifoide dell
pollame, Tifo essudativo dei gallinacei (Italian).

Characterization. Fowl plague is an acute infectious disease
of birds, caused by an ultra microscopic virus. It runs a rapid
course and causes high mortality.

Geographical distribution. The disease has been reported in
Italy, Germany, France and Belgium.

Etiology. The virus is ultra microscopic, passes through porce-
lain filters, and is believed to be a protozoan. The presence of the
virus has been demonstrated in the blood, the nervous system, nasal
and oral discharges, serous exudates and feces.

The virus is believed to be largely localized in the red blood cor-
puscles. The virulence of the red corpuscles is such that death has
been produced by a dose of .000,000,000,163,84 c.c.

Dessication is not rapidly fatal to the virus for it has been ob-
served to remain active for several weeks. It has been rendered
inactive by exposure to direct sunlight or to a temperature of 65°
to 70° C. for afew minutes. The activity of the virus is destroyed
rapidly by whitewash and the common disinfectants.

Certain granules have been observed in the brain of geese, hens
and pigeons dead of the disease. Ottolenghi believes that they are
derived from the nuclei of the cells. Certain peculiarities suggest
to him the supposition that they contain the virus of fowl plague.
Other granules in the brains of geese and hens are differentiated
from the former by the fact that the cytoplasm of the cell is involved
in their formation.

Pathogenicity. The disease has been observed in fowls, turkeys,
peafowls, guinea-fowls, geese, pheasants, pigeons, ducks, and a large
number of wild birds. Wild ducks when placed under conditions

of semi-domestication contract the infection.
8]

82 DISEASES OF DOMESTICATED BIRDS

The virus is believed to be transmitted naturally by nasal and
oral secretions, by the droppings of diseased birds or by eating
carcasses of dead birds. Wounds of the skin when contaminated
with virus readily result in infection. Mites (Dermanyssus avium)
have been tested as to their ability to transmit the disease, with nega-
tive results. Likewise ticks have given negative results.

The disease is most frequent in early spring, declines in preva-
lence in the summer and does not occur during the winter. In arti-
ficial transmission, fowls succumb to subeutaneous or intramuscular
injection or to application of the virus to the scarified skin. They
likewise become infected by ingestion.

After the subcutaneous or intramuscular injection of moderate
amounts of heart blood and pieces of spleen or kidney the size of
a pea the inoculated hens die as a rule within 36 to 48 hours, often
in 3 to 4 days, and quite rarely only after 5 to 7 days. Feeding of
larger amounts of pieces of organs causes death after about the same
length of time or a few hours longer than in the case of subeutane-
ous injection. J iltrates of nasal mucus, contents of the small in-
testine, bile, brain, blood and internal organs are infective for hens.
Many authors have failed to transmit the disease to old and young
ducks or to young pigeons. Young geese are susceptible to sub-
cutaneous and intramuscular inoculation or by the mouth, and die
as a rule after about seven days. On the other hand, old geese
are very slightly susceptible to ordinary methods of inoculation.
Subdural inoculation of these has succeeded, and caused the nervous
type of the disease.

The disease exhibits peculiarities in showing a preference at dif-
ferent times for different species of birds all in contact with one
another, such as fowls, pigeons, geese and ducks. Mammals are
immune to infection.

In young geese and in pigeons the disease assumes the nervous
type, which runs a much less rapid course. In these the virus at
first localized in the blood corpuscles seems to disappear therefrom,
and becomes established in the central nervous system. However,
the virus may reappear in the blood shortly before death.

Cominotti has observed the nervous type of the disease in wild
ducks in confinement under conditions resembling those under which
domesticated birds are kept. The virus was found always in the
central nervous system and was never demonstrated in the blood or
the internal organs even when large quantities of inoculating mate-
rial were used. Transmission of the infection from wild ducks to

FOWL PLAGUE 83

fowls was possible by subcutaneous injection of portions of cerebral
substance. It was not possible to infect domesticated ducks with
wild duck virus in doses however large, and administered by intra-
venous inoculation, ingestion, intracerebral inoculation or instilla-
tion into the conjunctive.

Symptoms. The incubation period is usually 3 to 5 days, but
exceptionally 2 days or even 7 days. It is much shorter when birds
are inoculated. -The symptoms greatly resemble those of fowl chol-
era. Death may occur while the bird is on the roost or on the nest
without its having previously exhibited symptoms.

There is an acute type of the disease in which the bird lives at
the most three or four days. In a subacute form the birds survive
7 or 8 days. Recovery practically never occurs.

In the acute type, the first noticeable symptom is inappetence.
Then the bird declines into a condition of weakness and somnolence,
hides in corners, becomes indifferent to surroundings, with half
closed eyes, drooping comb, and ruffled feathers. The temperature
rises to 110° or 112° F., but may drop to subnormal before death.
The comb commonly takes on a violet color which proceeds from the
borders, or spots form on the sides, but it soon appears black. In
some cases the comb is covered with white scales. The bird gen-
erally dies quietly in a somnolent condition, which is only occa-
sionally interrupted by spasms.

In the subacute form which occurs quite frequently in cases of
natural infection, the bird ceases to eat and drink, and goes on
the nest for protection from the light. The general appearance is
deceptive as indicative of the diseased condition. Upon investiga-
tion and when an effort is made to see the bird walk, it may not
rise to the feet, or moves the feet with difficulty, staggers, with the
head wabbling and turned backwards which attitude appears to be
involuntary. With the development of the disease, paresis occurs
and stupor becomes deeper. In some cases in this stage a viscid
secretion flows from the nostrils and mouth or the material may be
squeezed from the nostrils. A diphtheritic type has been observed,
in which fibrinous exudate occurs in the nasal, oral and pharyngeal
cavities. Conjunctivitis and lachrymation may occur.

As a rule there is no diarrhea. The feces are quite solid, often
green in color and of the usual amount. In the later stages of the
disease some birds discharge hardly any feces. At death and after,
a fluid is discharged from the cloaca and beak.

Morbid anatomy. Freese has conducted numerous autopsies

84 DISEASES OF DOMESTICATED BIRDS

of naturally infected birds and describes the lesions as follows:

Hemorrhages in the mucous membrane of the passage between the
proventriculus and gizzard are highly characteristic of the disease.
They also occur in the mucosa of the true proventriculus between
the conical elevations or very seldom they are limited only to these
elevations. It is possible for the hemorrhages to occur in both
places in the same fowl. The hemorrhages of the mucosa between
the papille or in the opening between the two stomachs may be
superficial, in the mucosa or in the tissues lying beneath. They
vary greatly in size and may be barely visible or several centimeters
in diameter. They are red or dark red in color and often are not
sharply cireumscribed. If the conical papillee are involved, either
the whole mass is reddened or only the upper border about the
mouth of the gland. The hemorrhages in the proventriculus in
many cases are very small and are often quite separated, so that
their presence might not be observed on superficial examination.
This is all the more likely unless the viscid, gray, white, cloudy
mucus is removed.

Small hemorrhages are frequently found in the fatty tissue sur-
rounding the gizzard, on the mesentery of the small intestine and
superficially under the cuticle of the gizzard. More rarely, fine
subepicardial hemorrhages are observed in the pericardium, espe-
cially in the heart fat, and in the tracheal, laryngeal and pharyngeal
mucose. They are rarely found in the pulmonary pleure.

The kidneys are swollen to an extraordinary extent. They are
either grayish brown in color and clouded or in the acute cases,
dark brown on account of the presence of an excessive amount of
blood.

In the functional ovary, there is a marked congestion of the
vessels of the yolk capsules. Occasionally hemorrhages are ob-
served under the serosa in the yolk mass.

In acute cases a certain degree of swelling of the spleen is ob-
served. As a rule, however, lesions of this organ do not occur.
The liver does not show important lesions, but some writers describe
congestion in acute cases.

Inflammation of the small intestine is at the most limited to the
first portion of its length. In some eases there is observed only a
slight catarrhal inflammation, while in other cases there is a marked
inflammation with hemorrhages. The ceca and the remaining large
intestine are very rarely inflamed. Inflammation of the intestine
occurs in about half of the cases.

FOWL PLAGUE 85

Exudate in the abdominal cavity is either serous or sero-fibrinous.
The fibrin as a rule is in suspension in the serous fluid in the form
of flakes, or is deposited loose on the peritoneum in the form of
threads or sheets.

The peritoneum is not inflamed but is smooth, shiny and trans-
parent. Exudate occurs in the abdominal cavity in about a quarter
of the cases.

Exudate occurs in the pericardium in the form of a serous or
sero-fibrinous fluid, which on opening of the pericardial sac often
coagulates into a gelatinous mass. The presence of exudate in the
pericardium occurs somewhat less often than in the abdominal
cavity.

A bluish red coloration of the comb occurs very often. There
is nothing characteristic about it as compared with a number of
other diseases.

Some authors emphasize the significance of catarrh of the upper
air passages and of the pharynx. They note the occurrence of
viscid gray white mucus in the beak, throat and nasal cavity, but it
is considered to be a normal secretion which remains in its place
of production for some time before death.

In wild ducks dying of the nervous type it has been noted that
autopsy reveals no characteristic gross changes.

Diagnosis. The presence of hemorrhages in the proventriculus,
the swelling of the kidneys and the severe injection of the blood
vessels in the yolk capsules of the ovary, occasionally associated with
the presence of hemorrhages, in birds dying of a pest-like disease,
are most significant. The autopsy findings alone will not always
suffice for making a diagnosis. In some eases as in other infectious
diseases, the lesions may be so slight as not to warrant drawing
conclusions. A diagnosis of fowl plague can be established most
certainly by successful transmission to a hen with absence of a
causative agent recognizable in tissues or in cultures from the blood
and organs.

Differential diagnosis. Phosphorus poisoning causes lesions
having the greatest similarity to those of fowl pest and also causes
a high mortality. In general the hemorrhages in the proventriculus
occurring in phosphorus poisoning extend deeper than in fowl pest,
also in the poisoning, erosions occur in the hemorrhagic mucosa.
In phosphorus poisoning there is also a marked inflammation of the
upper part of the intestine. Notwithstanding the great similarity
of the lesions the two conditions can be differentiated at autopsy by

86 DISEASES OF DOMESTICATED BIRDS

the escape of the so-called phosphorus vapor from an opening in the
gizzard or crop and by the characteristic smell.

Next in similarity is fowl cholera. This is characterized by the
occurrence of subepicardial hemorrhages, an exudate in the peri-
cardium, a marked inflammation of the intestine and by the in-
flammation frequently occurring in the lungs. In only a few cases
would these lesions be confounded with those of fowl pest.

Rabbit inoculation is valuable, for this animal is immune to
fowl pest and susceptible to fowl cholera. Spirochetosis will be
suggested by the drowsiness and paralytic symptoms and must be
differentiated by microscopic examination of blood taken during an
early stage. In spirochetosis such blood will be found to contain
spirochetes, but such an examination will be misleading, if the
sample be drawn after the crisis has occurred.

Preventive measures. Treatment is unavailing. The general
sanitary measures such as recommended for cholera, should be em-
ployed.

Attempts to immunize by vaccination with diluted red corpuscles
have failed. A shght measure of success by vaccination with virus
killed by ether, has been obtained. Birds after two vaccinations
were protected to a slight extent in that death was delayed.

The agency of poultry exhibitions in rapidly disseminating the
infection should be borne in mind. The disease apparently gained
a wide distribution in Germany as a result of a show held in Bruns-
wick in 1901.

REFERENCES

1. Belfanti and Ascoli. Spigolature nella Peste Aviaria e nell’ Afta.
Clin. Vet., Vol. 39, 1916, p. 577.

2. Centanni. Die Vogelpest; Beitrag zu dem durch Kerzen filtrirbaren
Virus. Centralbl. f. Bakteriol. (Htc.), 1 Abt. Orig., Bd. 31, 1902, S. 145.

3. Cominotti. Peste aviaria nella anitre. Clin. Vet., Vol. 39, 1916,
p. 129.

4. Dubois. Une maladie infectieuse des poules 4 microbes invisibles.
Compt. rend. Soc. de biol., Vol. 54, 1902, p. 1162.

5. Freese. Ueber MHiihnerpest mit besonderer Beriicksichtung der
pathologischen Anatomie. Deutsche tierdrztl. Wchenschr., Bd. 16, 1908,
S. 173.

6. Hertel. Ueber Gefliigel-cholera und MHiihnerpest. Arb. a. d. k.
Gsndhtsamte., Bd. 20, 1904, S. 453.

7. Joest. Beitrag zur Kenntnis der Bakterienflora des Hiihnerdarmes
nebst einigen Bermerkungen iiber eine neue Hiihnerseuche. Berl.
tierarztl. Wehnschr., 1902, S. 241.

FOWL PLAGUE 87

8. Kleine und Moellers.. Ueber Hiihnerpest bei Ginsen. Centralbl. f.
Bakteriol., Bd. 39, 1905, S. 545.

9. Kraus und Schiffmann. Studien itiber Immunisierung gegen das
Virus der Hiihnerpest. Centralbl. f. Bakteriol. (Etc.), 1. Abt. Orig., Bd.
43, 1907, S. 825.

10. Landsteiner u. Berliner. Ueber die Kultivierung des Virus der
Hiihnerpest. Centralbl. f. Bakteriol. (Etc.), 1 Abt. Orig., Bd. 67, 1912,
S. 165.

11. Leclainche. La Peste Aviaire. Revue Gén. de. Méd. Vét., T. 3,
1904, p. 49.

12. Lipsechiitz. Ueber mikroskopisch sichtbare filtierbare Virusarten.
Centralbl. f. Bakteriol., Bd. 48, S. 77.

13. Lode und Gruber. Bakteriologische Studien iiber die Aetiologie
einer epidemischen Erkrankungen der Hiihner in Tirol. Centralbl. f. Bak-
teriol. (Etc.), 1 Abt., Orig., Bd. 30, 1901, S. 593.

14. Maggiora und Valenti. Ueber eine Seuche von exudativen Typhus
bei Hiihnern. Zeit. f. Hyg., Bd. 42, 1903, S. 185.

15. Mane. JImmunizierungsversuche bei Hiihnerpest. Arb. a. d. k.
Gsndhtsamte, Bd. 21, 1904, S. 537.

16. Ostertag und Bugge. Weitere Untersuchungen iiber die Hiihner-
pest. Zeitschr. f. Infektionskr. d. Haustiere, Bd. 2, 1906, S. 1.

17. Ostertag und Wolffhiigel. Untersuchungen iiber die ‘ Hiihnerpest,”
die neue Geflugelseuche. Monatschr. f. prakt. Tierh., Bd. 14, 1903, S. 49.

18. Ottolenghi. Ueber einen besonderen Befund bei der Gefliigelpest.
Centralbl. f. Bakteriol. (Etc.), 1 Abt. Orig., Bd. 67, S. 510.

19. Russ. Beobachtungen iiber das Virus der Hiihnerpest. Arch. f.
Hyg., Bd. 59, 1906, S. 286.

CHAPTER VIII

AVIAN TUBERCULOSIS

Characterization. Avian tuberculosis constitutes an affection
closely related to the same disease in mammals, characterized by the
development of tubercles principally in the visceral organs.

Poultrymen refer to the disease as spotted liver, liver complaint,
rheumatism, or describe the birds as going lght.

Species affected. A considerable number of domesticated and
wild birds are affected. The disease has been observed in the
fowl, guinea-fowl, peafowl, turkey, duck, goose, swan, pigeon, os-
trich, parrot, canary, pheasant, sparrow, and in a large number of
species of wild birds kept in zoological gardens.

Etiology. Typical strains of the avian variety of B. tubercu-
losis possess characteristics enabling them to be differentiated from
the human and bovine varieties. Avian bacilli are more readily
isolated and cultivated in pure culture, than are the mammalian
varieties. The avian organisms are somewhat shorter and stain
more evenly than those of the mammalian variety. While the
guinea pig is most susceptible to mammalian strains, inoculation
with avian material may result in emaciation with no visible lesions,
or in relatively slight lesions of a non-progressive character. When
lesions are not visible after inoculation, it does not preclude the
possibility that tubercle bacilli may be present and demonstrable
microscopically, or culturally, or by further inoculation of the tis-
sue into other guinea pigs.

The transmissibility of avian tuberculosis to mammals and vice
versa 1s of interest in connection with the control of the disease.
As a general rule, fowls are not susceptible to the human and _bo-
vine varieties. Experimental evidence exists to show that calves
may be infected by injections of avian tubercle bacilli, and that
fowls have been artificially infected with tubercle bacilli of mam-
malian origin. The majority of experiments to test this trans-
mission have given negative results. In view of these findings,
the simultaneous occurrence of tuberculosis in cattle or man, and
in fowls exposed to infection from them, has slight value as evi-

dence of transmission. All three varieties of the disease are so
88

AVIAN TUBERCULOSIS 89

common that coincidences may occur. The literature of tuber-
culosis reveals comparatively few instances in which avian tubercle
bacilli have been found naturally in cattle or in man.

With the exception of the intertransmissibility of avian tuber-
culosis between pigs and fowls, the disease in fowls stands by itself
as an economic and hygienic problem. ‘There is considerable evi-
dence that parrots and canaries may be infected from a mammalian
source.

While pigs undoubtedly contract tuberculosis most frequently
from bovine sources, they do to a lesser extent acquire it from avian
sources. The possibility of the transmission of tuberculosis between
pigs and fowls should not be overlooked in connection with hygienic
measures against the disease in either. Outbreaks of avian tuber-
culosis in pigs in contact with infected fowls have been observed
both in Denmark and in the United States. Eastwood and Grif-
fith made cultures from a series of seventy-eight pigs exhibiting
only localized tuberculosis. The avian tubercle bacillus was found
alone in twenty-six of these pigs, or thirty-four per cent. Of the
remainder, the avian organism was found to be present along with
bovine bacilli in two cases.

Symptoms. Until the disease has developed sufficiently to cause
emaciaticn, there are no characteristic symptoms, except in the rare
eases when the skin or joints are involved. In the latter case poul-
trymen describe the condition as rheumatism. This term as applied
to a disease in birds is practically synonymous with arthritis. An-
emia and emaciation are constant in advanced cases, the latter be-
coming extremely marked. The loss of weight is very noticeable ;
the bird -becomes weak and moves about very little. This disin-
clination to move may be due either to extreme weakness or, more
rarely, to involvement of the joints. Under such conditions, the
bird spends much of the time in a crouching position. An unnatural
character of the gait is noticeable.

The eyes are bright and appetite remains markedly good in ad-
vanced cases. The skin and visible mucose are pale, and the
feathers are ruffled. The temperature is usually within the normal
range, and rarely is subnormal. Young birds affected with the dis-
ease enough to show symptoms are not encountered, doubtless due
to the time necessary for the development of serious lesions.

The separation of deaths from one another in point of time is a
characteristic feature of the disease.

Morbid anatomy. Emaciation is striking in most cases that

90 DISEASES OF DOMESTICATED BIRDS

die of the disease. The muscles of the breast may be represented by
barely a trace.

Avian tubercles do not differ greatly in gross appearance from
those of the mammalian type. The smallest ones consist of nodules
of tissue in which central caseation has not yet begun. In larger
ones varying degree of caseation is illustrated, but calcification
is not frequently observed. Avian tuberculosis differs from mam-
malian tuberculosis markedly in that the visceral organs primarily
are involved and lesions of lymph nodes are of subordinate im-
portance.

The liver is usually studded throughout with nodules which are
easily separated from the hepatic tissue. There may be several sizes
of nodules, suggesting that several corresponding invasions of bac-
teria have occurred. The smaller tubercles are white or grayish
white, while the larger, older ones are more yellow in color. The
presence of the tubercles brings about secondary degenerative
changes in the liver, as a result of which the tissue becomes pale and
friable. As a consequence, fatal hemorrhages may occur. ‘The or-
gan is enlarged in advanced cases, and in éxceptional cases may con-
stitute one-fourth of the weight of the bird.

The spleen, like the liver, is found involved in practically all
advanced cases. The relative enlargement is greater, for this organ
may attain the size of a walnut. The small amount of functional
tissue remaining is often striking.

The smallest tubercles of the intestine are located in the deeper
layers of the mucous membrane. Slghtly larger ones are in inti-
mate contact with the intestinal wall but project somewhat. Still
larger ones, as much as an inch in diameter, are pedunculated and
in most cases the interior of such tubercles communicates with the
lumen of the intestine. Lesions of the intestine also occur in the
form of numerous but isolated ulcers on the mucous membrane.

The kidneys, ovary, mesentery, and lungs are involved less often,
while cases of tuberculosis of the pancreas, gizzard, and skin are
rare in fowls. In the kidneys, the tubercles are discrete, hard, and
glassy. These organs alone may be affected. Small tubercles are
observed on the mesentery associated with tubercles on the intestine.
Involvement of the lung apparently is associated with advanced de-
velopment of the disease and then it occurs comparatively rarely.
The tubercles may be isolated or aggregated into extensive areas.
Skin lesions may consist of single spherical masses, each surround-
ing the root of a feather, or more often, consist of larger masses.

AVIAN TUBERCULOSIS 91

A form of nodular disease of the skin has been observed in which
tubercle-like organisms are found, and efforts to cultivate them give
negative results. Another point of difference is that the organisms
are. decolorized by acidulated alcohol, which does not occur in the
ease of true avian tubercle bacilli. Unquestionable tuberculous le-
sions of the skin occur in pigeons. A tuberculous lesion consisting
of a cutaneous horn is relatively common in parrots.

Bone lesions have been observed particularly on the breast bone
and ribs. Lesions occur in the knee, back, digital and shoulder
joints. The extremities of the bones enlarge with accumulation of
cheesy material, or may discharge a semi-fluid substance.

Differential diagnosis. A diagnosis of tuberculosis by physical
examination of the living bird is hardly possible in most cases, nor
is this important. Emaciation creates a strong presumption of the
existence of tuberculosis but is not conclusive, for it occurs in as-
thenia, in serious infestation with air sac mites and in other condi-
tions less well understood.

At autopsy of fowls, the possibility of the occurrence of tumors
of the liver, and nodular teniasis of the intestines should be borne
in mind. Nodular lesions not involving the liver and spleen, may
quite safely be considered as not tuberculosis. In the turkey the
more highly colored areas occurring in infectious entero hepatitis
are not likely to mislead one familiar with these lesions. Gouty
arthritis and bumblefoot in the fowl are suggestive of tuberculosis.
Nodules in the lung caused by aspergillosis may be differentiated
from tuberculosis by migroscopic examination.

Microscopic examination of smears for tubercle bacilli is available
as a means of diagnosis, especially since organisms are unusually
abundant in lesions of avian tuberculosis.

Tuberculin test. Numerous efforts have been made to apply
the subcutaneous tuberculin test to fowls, using tuberculin prepared
from both avian and mammalian cultures, but without success.

Better results have attended trials with the intradermal (intra-
cutaneous) form of the test in manner similar to that in which it
is applied to cattle. The wattle is chosen as the site of injection
and a very fine needle of No. 26 or 27 gauge is employed. The aim
is to deposit the tuberculin not in the deeper layers, but in the
stratum Malpighii. It should not be injected so superficially that
the tuberculin will be lost by rupture of the epithelium.

The tuberculin employed is prepared in the usual manner from
an avian tubercle culture, and is diluted fifty per cent for use. The

92 DISEASES OF DOMESTICATED BIRDS

dose varies from one-twentieth to one-thirtieth of a cubic centimeter.
After short experience, attention to the graduations on the syringe
will be abandoned and the dose judged by the appearance of the tis-
sues at the point of injection. The head of the fowl should be held
with considerable firmness by an assistant during the injection, in
order to obviate the. necessity for inflicting unnecessary damage to
the tissues, which would interfere with observing the results. Care
must be taken to avoid injury of the wattle by rough handling.

A positive reaction to the test consists of a swelling of the in-
jected wattle. Perhaps ten per cent of the swellings will be so
slight as to be doubtful.. Observations made by Van Es and Schalk
indicate that among the reactions considered by them as doubtful,
about one-half were found on slaughter, to contain lesions, and half
to be free from lesions. The majority of reactions will leave no
doubt as to the existence of a pronounced edematous swelling, which
may increase the thickness of the wattle to several times normal.

Of 90 birds tested by Van Es and Schalk, showing typical reac-
tions, 88 were found tuberculous at cp nehee and 2 aherce no vis-
ible ae Of 130 birds slaughtered Fad found without lesions,
120 or 91.5 per cent had failed to react to the test. About 8.5 per
cent of the non-reacting fowls were found to have lesions. Thus the
results shown indicate that the intradermal tuberculin test for fowls
is about as accurate as the same test or the subcutaneous test in
cattle.

The test surely furnishes information regarding the extent to
which infection has spread in a flock and consequently provides in-
formation regarding which birds should be eliminated. Of three
and four year old birds in an infected flock, as high as 86 per cent
may react. Of two year olds, 24 per cent and of pullets, 3 per
cent have reacted. It may further be of use in determining whether
or not tuberculosis exists in a flock from which it is contemplated
to purchase birds.

Transmission. The tendency of lesions involving the intestine
to perforate the wall and discharge into the lumen, provides the
main channel for the dissemination of tubercle bacilli. Microscopie
examination of such lesions reveals enormous numbers of the or-
ganisms. In view of the rarity of pulmonary lesions and the rela-
tive frequency with which intestinal lesions occur, the feces must be
regarded as the chief channel of elimination of infection. Tubercle
bacilli have been demonstrated to be present in the feces of infected

AVIAN TUBERCULOSIS 93

birds but are not found in the feces of a very large percentage of
such birds.

Tubercle bacilli have been demonstrated in eggs laid by tubercu-
lous hens but it has not been demonstrated that such a channel of
dissemination of the infection is an important one. It seems quite
certain that the disease is not observed in young birds as might be
expected if transmission through the egg were common.

Tubercle bacilli, when directly exposed, are sensitive to sunlight,
but the conditions about poultry establishments are such as to war-
rant belief that they may persist alive for months.

Feeding experiments leave no doubt but that the alimentary tract
is the chief portal for entrance of infective material. Exposure of
healthy birds by contact with infected birds sets up disease which
may persist for a year before important lesions develop. The eat-
ing of carcasses of birds dead of the disease undoubtedly contributes
to dissemination of infection. In some cases, exposure by feeding
infected droppings has induced disease that was fatal in six months.

While the introduction of tuberculous fowls must be regarded as
the most common means of infecting a flock, there exists the possi-
bility of its being accomplished by infected pigeons, among which
the disease is not uncommon, or by pigs.

Economic importance. Tuberculosis is capable under favor-
able conditions of causing a very heavy death rate during the course
of a year. Comparatively few accurate observations have been
made in this country, but annual losses up to nearly 50 per cent
have been reported.

Enough reports are available from the northern half of the United
States, the Pacific Coast, and Canada to indicate that the disease
is prevalent in the area mentioned.

The insidious nature of the disease contributes to the unconcern
of the owner of an infected flock. Deaths will not occur until the
flock has been extensively infected and when they occur, are so
scattered in point of time that they do not cause the same concern
on the part of the owner as would be occasioned by the same num-
ber occurring in a short time. Consequently there is lack of in-
centive to take up repressive measures.

Prevention. The problem of the control of tuberculosis in
fowls presents several features that render it much simpler than
the corresponding problem in cattle. The productive usefulness of
hens is ended at three years of age, when it is the common practice

94 DISEASES OF DOMESTICATED BIRDS

to market the birds for table use, if this indeed is not done after
two years. Thus total replacement of stock is possible in a short
period. The extensive use of incubators and brooders assures the
isolation of the young from infected old birds. Where the business
is conducted on an intensive scale on a small area, isolation of birds
of various ages is quite often practiced. Thus ideal conditions for
combating the disease already exist in certain plants, if indeed the
disease does ever make considerable progress under such conditions.
It is undoubtedly true that the disease only becomes serious when
there is unlimited opportunity for mingling of birds of various ages
as exists where poultry are kept without restraint. This is the con-
dition in the average small poultry yard, or in an extensive poultry
business where the system of using unfenced colonies is practiced.

In attempting to control the disease among unfenced birds, the
end sought is to secure isolation of young birds and maintain it
throughout life.

In every extensively infected flock there will be a certain number
of badly diseased, worthless birds, which may be recognized by
physical means, and destroyed. The intradermal test may be ap-
plied to determine the extent of the infection. The results of this
test, the age of the birds and egg yield, will aid in reaching a de-
cision as to whether all or part should be marketed at once. Many
reacting birds will be found at autopsy, to contain very minute
lesions and there should be no prejudice against killing such for
food.

Appropriate disinfection of contaminated buildings, and tempo-
rary abandonment of areas of soil too large to disinfect, will natur-
ally suggest themselves.

Van Es reports upon results of testing a flock of 249 birds, of
which 43.37 per cent were tuberculous. All reacting and undesir-
able birds were eliminated, leaving 56 non-reacting birds. These,
together with 47 birds purchased after the test, increased the next
year to 249. One bird died of tuberculosis after the first test and
had undoubtedly failed to react on account of severe lesions. A
second test made a year after the first one revealed 2.41 per cent of
reactors. These were regarded as having contracted the disease
from the one non-reactor of the first test.

Mention of hygienic measures such as good ventilation, sunlight,
and warm quarters has no place in a discussion of the control of
tuberculosis in fowls. The disease is a veritable scourge in parts
of California where such hygienic conditions are most favorable.

AVIAN TUBERCULOSIS 95

Wild birds. Deaths from tuberculosis are frequent among wild
birds kept in captivity. Out of 459 birds dying in the Berlin
Zoological Gardens during a given period, 118 or 25.7 per cent were
tuberculous. The disease was present in specimens belonging to
10 of the 15 orders of birds represented. The other five orders were
represented by few specimens, and the observers, Koch and Rabin-
owitsch, believe that all orders of birds are susceptible. A similar
examination of 500 birds from the London Zoological Garden re-
vealed tuberculosis in 30 per cent of the birds dying.

REFERENCES

1. Hastings and Halpin. Avian tuberculosis. Univ. of Wis. Agr. Eup.
Sta. Research Bull. 28, 1913.

2. Moore. The morbid anatomy and etiology of avian tuberculosis.
J. Med. Research, n. s. Vol. 6, 1904, p. 521.

3. Van Es and Schalk. Avian tuberculosis. North Dakota Agr. Exp.
Sta. Bull. 108.

4. Ward. Tuberculosis in fowls. Univ. of Cal. Agr. Exp. Sta. Bull.
161, 1904.

CHAPTER IX

AVIAN DIPHTHERIA AND BIRD POX

General discussion. The group of pathological conditions re-
ferred to by various authors under such designations as simple ca-
tarrh, colds, contagious catarrh, influenza, coryza, roup, canker,
diphtheria and bird pox present a complicated subject for discussion.

The pathological features presented by the lesions of the mucosa
of the fowl’s head in the conditions described as roup or diphtheria,
have been concisely summarized by Moore. He studied the disease
in the eastern United States and has described three stages or va-
rieties of lesions as follows

“(1) An exudate of a serous or muco-purulent character in the con-
junctiva or nasal cavities. Ordinarily this condition cannot be recognized
in the mouth. The mucosa in these cases is apparently but slightly
altered.

“ (2) The mucosa over a small or larger area is covered with a spreading
exudate of a grayish or yellow color. It is firmly attached to the mucous
membrane and when removed leaves a raw, bleeding surface. Sections
through this exudate and the subadjacent tissues show that the epithelial
layer is destroyed, and the underlying tissue infiltrated with cells. The
extent of the infiltration varies in different individuals.

“ (3) The mucosa is covered with a thick mass of exudate, varying in
color from a milky white to a lemon yellow or brown. It is easily re-
moved, leaving a more or less granular and healed surface. This sloughed
mass is frequently dried at its margins to the adjacent tissue. It emits
a strong putrid odor, due to decomposition. The drying of the margins
prevents the fowl from expelling the exudate after it becomes separated
from the underlying tissue.”

In the far West and South, the lesions described will commonly
be found accompanied by the tumor-like lesions known as chicken
pox or epithelioma contagiosum.

The earlier studies of the etiology of the diphtheritic lesions of
fowls extending over a long period have resulted in a mass of con-
clusions, in the main contradictory and confusing. Various authors
have ascribed the lesions as due to gregarina, chlamdyozoa, coccidia
and numerous species of bacteria.

The discovery that the filterable virus of chicken pox is capable

of causing diphtheritic lesions has now received abundant confirma-
96

AVIAN DIPHTHERIA AND BIRD POX 97

tion and furnishes a basis for clearing up the confusion. Among
writers who have studied both avian diphtheria and pox and who
agree on this point are Uhlenhuth and Manteufel, Schmid, Bertegh,
and Sigwart.

Whether there are other specific infectious diseases of fowls char-
acterized by diphtheritic lesions not due to pox virus, remains to be
determined by further investigation. The idea has been advanced
that diphtheritic lesions of the mucosa of the head of the fowl may
result from invasion by various bacteria.

There is ground for questioning the validity of differentiating
into separate disease entities such conditions as simple catarrh, com-
mon colds, contagious catarrh, influenza and coryza. In large in-
fected flocks, birds with catarrhal lesions alone, diphtheritic lesions
alone, and pox lesions alone will be found in close association with
others perhaps exhibiting all these lesions. Clinical evidence in
such flocks points very strongly to the conclusion that the cases
characterized by the presence of serous exudate in the nostrils are
but the early stages of avian diphtheria. Insufficient etiological ev-
idence is available to justify recognizing such conditions as specific
infectious diseases.

Characterization. Avian diphtheria is an infectious disease,
manifested by the formation of catarrhal exudate in the nasal cavity,
eyes, and sinuses associated with pseudo-membranes in the mouth
and wart-like nodules on the external surface of the head. Until
recent years, the term diphtheria or roup was applied to cases
showing the internal exudative lesions, while those with external
growths were designated bird pox, chicken pox or epithelioma con-
tagiosum. The discovery that a single causative agent can produce
both types has resulted in the two conditions being classed as simply
external and internal lesions of one disease.

Etiology. Diphtheria and bird pox are caused by a virus the
nature of which is not well known. The organism has not been cer-
tainly identified micresecopically and is so small that it will pass
through a Berkefeld filter. However, according to Marx and
Sticker, it will not pass through a porcelain filter.

Widely diverging opinions concerning the nature of the virus
have been expressed by the various writers who have studied the dis-
ease. riedberger and Froéhner assigned protozoa of the class gre-
garina as the cause. Borrel described certain ‘cell inclusions for
which Lipschiitz has suggested the name Strongyloplasma avium.
Halasi believes the etiological agent to be a chlamydozoon.

98 DISEASES OF DOMESTICATED BIRDS

Tenacity of virus. Burnet observes that finely powdered virus

in physiological salt solution placed in sealed ampoules in a water
bath at 60° C. is killed in about 8 minutes. At 56° C. the finely
powdered virus does not resist longer than half an hour. In sus-
pension in water at 37° C. it has been found inactive after 8 days;
active after 3 days; active after 30 days at 22° C.; active after 6
days at 25° C. Marx and Sticker found virus active after 3 hours
at 60° C., but the material probably was not as finely powdered as
in the experiment conducted by Burnett. The same authors found
that desiccated virus in ampoules deprived of air remained active
after an hour at 100° C. Scabs exposed to the sunlight in a Petri
dish were still virulent after two months. Reischauer observes that
- the virus resists dry heat at 80° ©. for 15 to 30 minutes and moist
heat 5 minutes at 100° C. Marx and Sticker found a suspension of
crusts virulent after 114 hours in a 1 per cent solution of carbolic
acid. In solutions of 2 and 214 per cent it lost its virulence.
Reischauer notes that the virus is killed in 5 minutes by.1 per cent
solution of potash, acetic acid or carbolic acid. Burnett kept a sus-
pension of virus in ordinary water in a refrigerator at 6° C. for 60
days and found it virulent after that length of time. Finely pow-
dered virus mixed with glycerine was found to be virulent after 120
days.
Haring and Kofoid tested the effect of various germicides upon
powdered pox virus. The virus was saturated with the germicide
and after the lapse of a certain amount of time, the virus was in-
oculated into a fowl by scarification. Five per cent carbolic acid
failed to kill in 20 minutes; 2 per cent liquor cresolis compositus
failed to kill in 20 minutes; 2 per cent potassium permanganate
failed to kill in 20 minutes; 2 per cent copper sulphate failed to kill
in 20 minutes; tincture of iodine failed to kill in 10 minutes; mer-
euric chloride in 1: 1000 solution failed to kill in 20 minutes; steam
heat at 100° C. failed to kill the virus in 5 minutes but did do so in
30 minutes; dry heat at 200° C. killed the virus in 30 minutes.
Powdered pox scabs saturated with physiologic salt solution and al-
lowed to decompose for 10 days in a warm place proved non-virulent.
Dry powdered pox scabs kept in a test tube from May, 1906, to Sep-
tember, 1911, proved virulent.

Pathogenicity. Diphtheria and pox are especially prevalent
in chickens and pigeons, and are also common in turkeys, geese,
ducks and guinea-fowl. Pheasants, quail and various wild birds are
susceptible.

AVIAN DIPHTHERIA AND BIRD POX 99

Natural infection. Natural infection occurs under conditions
which are not yet well understood. Apparently, the virus pene-
trates through a slight lesion of the skin or mucous membranes and
reaches the skin or the mucous membranes of the mouth by way of
the blood stream. Infection by ingestion probably oceurs. An in-
stance of infection by a biting fly, Stomoxysis calritrans, has been
reported.

Experimental transmission. The infection may be readily
passed from the infected to susceptible birds by rubbing infective
material into the skin or mucous membrane of the latter, especially
if the parts be slightly scarified.

In the pigeon the disease occurs on feathered portions of the body.
To secure infection it is only necessary to pull out the feathers and
rub in the virus lightly. After five or six days the skin shows a
characteristic swelling. The follicles are greatly enlarged and upon
pressure, whitish plugs are forced out.

The virus is readily transmitted from the pigeon to the fowl but
is transmitted from the fowl to the pigeon with great difficulty, if at
‘all. Passage through the fowl appears to lower the virulence of the
virus for the pigeon.

Intravencus injection of the fowl with pox virus as a rule causes
only diphtheritic lesions of the mucosa of the head, with no changes
of the skin. This is true whether the virus which was injected,
originated from the skin or the mucous membrane lesions.

Inoculation of the comb with material from mucous membrane
lesions does not always result in the occurrence of pox lesions.
Some observers interpret these negative results as proving the ab-
sence of pox virus in the diphtheritic material. Others regard the
results as mere failures of pox virus to take.

The virus is present in the circulating blood and internal organs
in acute cases, as demonstrated by inoculation experiments. In
some cases injection of liver and blood of birds affected with chronic
lesions of the mucous membranes of the head, will reproduce the
disease. When positive results occur, the incubation period is long
and the cases induced are mild. In chronic cases, the virus in the
blood appears to be weakened or lessened in amount. The virus
from either skin or mucous membrane lesions, when filtered, will
give positive results in most cases. Even if the material filtered is
of high virulence, it will only produce mild cases of mucous mem-
brane infection.

The incubation period for both diphtheritic and pox lesions varies

100 DISEASES OF DOMESTICATED BIRDS

from 3 to 12 days, depending upon the virulence of the virus and
the method of inoculation. After injection of filtered virus, the
period varies from 6 to 15 days. Isolated instances of incubation
periods to 25 days have been observed.

Mortality. The fatalities occurring in an infected flock vary
within a wide range depending upon individual circumstances.
Under favorable conditions, the disease may not spread to more than
10 per cent of exposed birds, with the death rate proportionately
low, while in other cases 80 per cent of the exposed may become in-
fected, with deaths relatively numerous, approaching in some in-
stances 50 per cent of those affected. The virulence of the virus
is variable and constitutes the main element for consideration in
each outbreak. The mortality depends, to a large extent, on climatic
conditions. Fowls are more severely affected during the fall and
winter months and it is during this period that the heaviest losses
are encountered.

Course of disease. Avian diphtheria may follow an extremely
acute course, affected birds dying without showing noticeable ex-
ternal symptoms which would attract the casual observer. In less
acute cases the disease may be resisted for several days after symp-
toms are apparent, the fowl finally succumbing apparently as a re-
sult of toxemia, or of starvation due to eye affection which inhibits
feeding. In’ the milder, and especially in the more chronic eases,
marked symptoms may persist for several weeks and finally result
in recovery, in so far as outward appearances are indicative.

Symptoms. The disease is manifested by three clinical forms:
(1) a pure mucous membrane disease, (2) a pure skin disease, and
(3) a combination of skin and mucous membrane affection. The
disease usually first manifests itself in a discharge from the nostrils
which soon becomes viscid and plugs the nasal passages. In some
individuals the first evidence of disease presents itself in the eye.
One or both eyes may show a sticky discharge that tends to gum the
eyelids and obstruct vision. The exudate continues to form in the
conjunctival sac, causing a swollen appearance of the eye and as-
suming a cheesy character. This, through pressure and the accom-
panying inflammation, may produce panophthalmia and loss of the
eye. The exudate in the nostrils also becomes cheesy in consistency
and causes a pressure on the cleft palate and distortion of the bony
structures of the adjacent parts. The affected bird early shows ex-
treme dullness and loss of vitality. The tendency is to mope around

AVIAN DIPHTHERIA AND BIRD POX 101

indifferent to its mates, surroundings, or to a person’s approach.
The head feels warm to the touch and there may be a rise of tem-
perature. Diarrhea is often present. Death may result within
two or three days in severe outbreaks or the bird may linger for a
week or more with progressively increasing debility and more
marked lesions. The head in many cases shows a pronounced swel-
ling on one or both sides below and in front of the eye due to the
accumulation of a cheesy mass within the suborbital sinus. Sneez-
ing, which has been apparent in the early stages, gives way to a
whistling or rattling in the throat. The inflammation in the nos-
trils may spread to the mouth and pharynx, or even to the larynx
and trachea, where exudates are formed which are principally of the
eroupous type. Breathing is entirely carried on through the mouth
and the continual passage of air over the tongue tends to dry the
tip with the result that its surface becomes hard and contracted.
This condition is commonly termed ‘‘ Pip” and may occur in any
affection which closes the nostrils, and compels breathing through
the mouth. Death may be caused by dyspnea from the presence of
massive accumulations in or upon the larynx, from toxins absorbed
from the primary causative agents and secondary invading organ-
isms, or from starvation, owing to inappetence, or the failure to dis-
eover food in blind cases. No doubt the combination of causes act-
ing together are responsible for the heavy mortality, amounting to
90 per cent in some instances, among young birds. Before death,
the subject becomes emaciated, sleepy, and finally unconscious for
a period of several hours.

Mild cases show less marked disturbances and may go on exhibit-
ing symptoms for several weeks, finally apparently recovering their
normal condition. Certain individuals retain the disease in a
chrcnic state and serve as carriers for future outbreaks.

Oftentimes the bird shows no external manifestations of illness.
The comb and wattles have a deep red appearance and the hen con-
tinues to lay. She dies quite suddenly and, on examination, the
only lesion apparent is the formation of a false membrane on the
border of the larynx or just inside that organ. This exudate has
occluded the air passage and caused death by suffocation. Fre-
quently the condition is discovered in time to save the fowl through
the owner’s attention being attracted by a peculiar noise which ac-
companies the effort of the bird to breathe. It will be observed to
open its mouth widely and attempt to dislodge the exudate by a spas-
modic movement of the respiratory apparatus. The resulting ef-

102 DISEASES OF DOMESTICATED BIRDS

fect may be termed a “ bird cough.” Prompt attention in such cases
nearly always saves the life of the fowl.

The disease spreads rapidly through a flock affecting a large per-
centage of the birds and causing the death of a variable percentage
according to the virulence
of the virus. Young birds
are especially susceptible,
adults less so, and a few
exhibit complete resist-
ance.

Morbid anatomy. The
external lesions have the
appearance of wart-like
growths prominently raised
from the surface of the
skin. The size may vary
to a considerable degree
according to location, or
through combination of
RSS -

Br aw several nodules. General-
\ ly they have a diameter of
1% to 4% of an inch.
These pox tumors occur
chiefly on the unfeathered
or lightly feathered por-
tions of the body, and par-
ticularly on the comb, wat-
tles, eyelids and at the
commissures of the beak.

They may also be found at
Fie. 8. Head of a Plymouth Rock cock affected

eae times on the under surface
with epithelioma contagiosum (bird pox). z F ,
(Klee) of the wings, particularly

if there has been an abrasion or bruise at this point. They may be
rarely observed around the vent. The nodules first appear as small
whitish points which rapidly increase in size, reaching their maxi-
mum size in four to six days. They form an integral part of the
epithelium, being in reality an extrusion of enlarged epithelial cells.
If the superficial scale of exudate is removed, the tumor will be seen
to consist of whitish cylindrical masses arranged perpendicularly to
the skin. The mass assumes a yellowish color which later changes
to a dark brown or black as the tuberosity degenerates and develops

—
ety)

AVIAN DIPHTHERIA AND BIRD POX 103

into a hard dry scab. After seven to nine days this scab may be
easily removed leaving a whitish area only slightly elevated above
the surface and usually pitted. The scabs retain the virus of the
disease and when rubbed on the scarified skin or mucous membrane

7
REALS
v : ~ Fine
a) 2 Bis. Linas
AOI

v
SY

Fic. 9. Head of a turkey affected with epithelioma
contagiosum (bird pox). (Klee)

of the mouth, even after a period of five years, may reproduce typical
lesions.

Haring and Kofoid describe the microscopic structure of chicken
pox tissue as follows:

“ The epithelial tumors are produced by a hyperplasia of the epithelium
due to an increase both in the size and number of cells. The zone of
growth is in the stratum of Malpighii, the principal region of prolifera-
tion being in the outer edges from which the cells increase in both direc-
tions. A proliferating epithelium forms cell nests surrounded by thick
bands of connective tissue, which contain blood vessels with thickened
walls. The rapidly proliferating peripheral cells of the Malpighian layer
are seen thickly studded with granules. The nucleus contains deeply
staining chromatin bodies which are in an active process of proliferation.
Karyokinetic figures are common in this region. More deeply in the
epithelial tumor mass the cells are greatly increased in size and have rela-
tively fewer granules. The nuclei are nale and show little evidence of
cell division. In these cells, are large cell inclusions which are very strik-
ing in appearance, and which Reischauer and others have thought to be
protozoa. There is usually but one of these bodies in each cell. They
vary in size from five to twenty microns, most of them are round, al-
though some of them are quite irregular in shape. They are evidently
fatty in structure as they stain black with osmie acid. When eosin and
methylene blue are used, they stain a faint pink, resembling somewhat the
Negri bodies found in the brain tissue of rabid animals, although they are

104 DISEASES OF DOMESTICATED BIRDS

usually much larger. They seem to have no definite internal structure,
being usually homogeneous in appearance. Deeper in the epithelial mass
the cells are very large and show evidence of degeneration, here the cyto-
plasm stains poorly and has but few granules. Burnett has called this con-
dition hydropic. In the center of the older epithelial cell masses, the cells
are so degenerated that they form a necrotic mass. The nucleus. of the
cell first degenerates. The cause of this degeneration is probably due to
the fact that the cell nests increase in size by multiplication at the peri-
phery. The outside cells consume all the nutriment at the expense of the
central ones and cause their degeneration. The central necrosis rapidly
extends, involving the greater part of the tumor mass.”

The cell inclusions characteristic of pox have been studied ex-
tensively and the interpretation of their nature and significance has
been the subject of much discussion. Some observers see in them,
stages in the life of a protozoan, while others regard them as products
of degeneration of the cell.

In the early stage of false membrane formation, the external layer
of the mucosa is principally involved. There is an exfoliation of
the cells, which become swollen and amorphous. The cell proto-
plasm early loses its identity, while the nuclei disintegrate more
slowly and appear as independent bodies showing different degrees
of degeneration. Mucous exudates which have undergone coagula-
tion, together with the epithelial cells, enclose leucocytes in various
stages of degeneration. An edematous area is formed around the
membrane, and wandering leucocytes are observed in the Malpighian
layer of the mucosa. During this stage there is a well marked line
of differentiation between the morbid area and the comparatively
unaffected base. As the pseudo membranes are extended, the under-
lying tissues are more deeply involved. The deeper epithelial cells
become infiltrated and exhibit cloudy swelling. A fibrinous exudate
accumulates which holds the cell elements in a compact tenacious
mass. In this may be observed numerous organisms, principally of
the bacterial type, which are to be considered as secondary invaders.
Protozoal organisms may also be present including flagellates, amebas,
eoccidia and other forms. Some investigators have attributed the
origin of avian diphtheria to certain of these protozoa. However, the
evidence brought out has not been sufficient to establish these organ-
isms as specific causes. The course of development of filterable
viruses in the animal system is a problem which has not been satis-
factorily solved, and until this is accomplished, it is unsafe to give
etiologic significance to organisms or cell inclusions which may be
found associated with certain morbid conditions.

AVIAN DIPHTHERIA AND BIRD POX 105

The gross lesions of the mucous membranes are not characteristic
of infection with pox virus alone. Haring and Kofoid have pro-
duced similar lesions by mechanical injury or by the injection of
pyogenic bacteria. However, in diphtheritic lesions not due to pox
virus, the cell inclusions characteristic of pox infection are not
present.

Diagnosis. In typical outbreaks, the disease is readily recog-
nized by the closely adherent pseudo membranes on the mucosa of
the mouth and pharynx, and by the characteristic nodules on the comb
and wattles. When the latter are present, the diagnosis is estab-
lished.

Treatment. This, to a certain extent, must be individual and
according to the stage of the disease. When the excretions are watery
or viscid they may be partially removed from the nostrils by pressing
on both sides with the fingers in a manner which will force the ma-
terial through the openings. The nasal channels are then flushed out
with an antiseptic solution such as permanganate of potash in 2 per
cent solution, or boracic acid in 3 per cent solution. This can be ac-
complished by means of a syringe or medicine dropper. The most
effective method, however, is to submerge the head in the antiseptic
solution for a period of 30 seconds, keeping the mouth open and the
beak elevated to permit the air to escape from the nostrils and be
replaced by the fluid. The treatment should preferably be repeated .
twice daily.

Certain features of the structure of the fowl’s head interfere with
natural drainage in diseased conditions, and likewise, interfere with
medication. The sub-orbital sinuses so often involved, have no nat-
ural drainage. The passages connecting them with the nasal cavity
lead upward, with the result that fluids cannot escape. The tur-
binated bones also impede the exit of tenacious exudate. The pres-
ence of exudate in both the turbinated bones and in the sub-orbital
sinuses prevents access of fluid to the affected mucosa.

When patches are present in the mouth, they should be carefully
removed mechanically before treating as above; or the affected areas
may be swabbed with tincture of iodine, 2 per cent carbolic acid, 70
per cent alcohol or argyrol in 20 per cent solution. Swellings of the
sides of the head are to be freely opened and the contents removed.
The eyes should be kept free of exudate and a mild antiseptic instilled
between the eyelids. For this purpose argyrol in 20 per cent solu-
tion has given the best results. Two drops are placed beneath the
eyelid twice daily. The lachrymal duct and nostrils are also bene-

106 DISEASES OF DOMESTICATED BIRDS

fited by the eye injection since the solution passes into them from the
eye. In the case of severe eye involvement it may be necessary to
feed the fowl artifically because of the difticulty encountered by the
bird in finding its food. The question of whether it is profitable to
treat all cases rests with the individual owner.

Since the pox tumors disappear in the natural course of the dis-
ease, the value of medicinal agents in hastening this end is ques-
tioned. Among the remedies that have been recommended are tinc-
ture of iodine, an ointment of glycerine, vaseline or lard containing
2 per cent of carbolic acid and 70 per cent alcohol.

Prevention. In some instances infection is brought to a flock
by new birds from infected flocks, or by exposure at shows. It is
possible that infection is carried on the clothing of persons who have
been among infected birds, or by materials on which the excretions
of diseased birds have been deposited. Free flying birds may also
serve as carriers although it is quite likely that they are rarely re-
sponsible for outbreaks. Newly purchased fowls and those which
have been exhibited at shows should be quarantined on their arrival
for a period of two weeks and carefully examined before being set
free among others. When a fowl is observed to be ill with symp-
toms of diphtheria, it should be isolated immediately. Often it is
good policy to destroy the patient because of the danger of the
attendant who is treating the bird carrying the virus to healthy
fowls. Those handling diseased fowls should disinfect their hands
before feeding or caring for others. It would also be advisable to
wear rubbers in the hospital and remove them on leaving in order
to guard against carrying infection on the shoes.

When infection has breken out in a flock particular care should
be exercised in keeping the houses as clean as possible. They should
be disinfected by spraying or washing with carbolic acid in 5 per
cent solution, compound cresol in 2 per cent solution, or formaldehyde
in 2 per cent solution. The yards may be spread with unslaked lime
or chloride of lime, or the soil should be plowed under. All birds
that die should be burned or buried deep. Those which have re-
covered, if retaining any evidence of the disease, should be destroyed,
as certain ones may serve as carriers and furnish the source of a
future outbreak. The drinking water may be medicated with per-
manganate of potash. A sufficient amount of the latter should be
employed to give the water a deep purple color.

Immunization. An attack of the disease confers an immunity
complete in from 12 days to 3 weeks but which varies in duration

AVIAN DIPHTHERIA AND BIRD POX 107

and degree according to the severity of the infection. Thus, chronic
mild infection of the mucous membrane does not always produce ab-
solute immunity. Infection of the mucous membranes alone will
induce an absolute immunity against inoculation of the skin. Vari-
ous authors have demonstrated immunity in fowls for periods vary-
ing from 2 months to 2 years. Live virus only has been shown to
confer immunity and the injection of killed virus has no immunizing
effect.

A number of workers have attempted the immunization of fowls
against diphtheria and chicken pox and treatment of the same
conditions by means of a vaccine prepared from the exudates and
pox nodules of affected fowls. The material is ground up in a suf-
ficient amount of normal salt solution to form a suspension and is
filtered through cotton to remove large particles. It is then diluted
until it appears moderately cloudy and heated at 55° C. for 1 hour.
Doses of 1 ¢.c. are injected subcutaneously on two or three occasions
with intervals of 5 to 7 days.

A product prepared by this method has been favorably reported
upon as an immunizing and curative agent by several workers. Ex-
periments by the present writers have not sustained the claims made
for the immunizing value of a vaccine prepared by this method.
Fowls which have been vaccinated and later artificially inoculated
with virulent material have developed characteristic internal and ex-
ternal lesions of diphtheria with accompanying fatalities.

Bacteriology of avian diphtheria. Many investigations of the
bacteriology of avian diphtheria were made previous to the recogni-
tion of the role of pox virus in causing diphtheritic lesions, so it
is not possible to determine whether the lesions were primarily due
to pox virus, or were due to bacteria alone. Other reports of in-
vestigations conducted more recently do not contain evidence that
pox virus was not concerned in the causation of the lesions.

Extensive investigations of the bacteriology of avian diphtheria
have been made by Harrison and Streit, Bordet and Fally and by
Hausser.

Moore first reported finding a member of the hemorrhagic septi-
cemia group in diphtheritic lesions in fowls, which observation has
been confirmed by a large number of investigators. Sigwart has
observed the spontaneous appearance of fowl cholera in birds af-
fected with diphtheritic lesions of the mucous membranes. In these
cases the primary cause of the diphtheritic lesions was considered
to be pox virus. He explains the occurrence by assuming that the

108 DISEASES OF DOMESTICATED BIRDS

pox lesions favored the increase of virulence of saprophytic hem-
orrhagic septicemia organisms commonly present in the mouth.

Jackley has worked on the bacteriology of roup, reaching the fol-
lowing conclusions :

“1. A bacterium, designated culture ‘33A,’ having all of the morpho-
logical, cultural and biochemic characters of the pasteurella group, ap-
parently deserves recognition as the etiological factor in roup.

“2. The organism has been recognized by smears in all cases of roup
examined.

“3. It has been isolated and grown upon artificial culture media and
the characteristic local lesions of the disease again reproduced.

“4. Finally, an absolute protection has been shown against the natural
disease after immunization with a pure culture bacterin of this organism.”

Beach, Lother and Halpin isolated from roup lesions an organism
probably belonging to the hemorrhagic septicemia group. Injection
of killed culture was shown to produce immunity against injection
with virulent culture. The organism was regarded as a secondary in-
vader, as 1t did not produce lesions of roup or chicken pox. It was
regarded as of importance as a secondary invader in wound infection.

The identity in name and similarity of lesions of diphtheria in
man and in birds has attracted attention to the possible relationship
between the two diseases. There is no doubt that the two diseases
are quite distinct in etiology even though rare cases of infection of
birds with Bacterium diphtherie have been reported.

SIMPLE CATARRH OR COLD

This condition is a mild inflammation of the nasal passages and
is common to all species of domesticated birds. It cannot be differ-
entiated from the early stage of avian diphtheria.

Etiology. No definite cause may be assigned to this affection.
It has been asserted that weak or improperly nourished birds are
more likely to be attacked than strong, vigorous, well nourished in-
dividuals. Exposure to unfavorable conditions in which rain or
dampness accompanied by cold draughts tend to so affect the mucous
membranes of the nostrils that the various organisms which are nor-
mally present in this region become pathogenic, has been held to be
the primary contributing cause.

Symptoms. The affected fowl is more or less dull in appearance,
according to the severity of the attack. The appetite is diminished,
breathing becomes difficult, and a watery discharge from one or both
nostrils is early in evidence. This discharge may disappear in the

AVIAN DIPHTHERIA AND BIRD POX — 109

course of two to four days, or it may take on a viscid consistency,
closing the nasal openings and necessitating breathing through the
mouth. The discharge may also escape through the mouth. This
is rendered easy by the cleft palate peculiar to birds.

Morbid anatomy. ‘The mucous membrane of the nasal passages
becomes swollen and congested and an excessive secretion of mucous
fluid is poured out.

Treatment. As the disease is of short duration, it is usually
only necessary to place the patient under more favorable conditions
to bring about recovery. In the more severe cases, the nostrils should
be washed out twice daily with boracie acid in 3 per cent solution, or
ereolin in 1 per cent solution.

REFERENCES

1. Beach. Suggestions to poultrymen concerning chicken pox. Univ.
of Calif. Coll. of Agr. Cire. No. 145, 1915.

2. Beach, Lothe and Halpin. An outbreak of roup and chicken-pox in
which the high mortality was apparently caused by a secondary invader.
J. Agr. Research, Vol. 17, 1915, p. 554.

3. Bertegh. Ueber die Beziehungen zwischen Gefliigeldiphtherie und
Gefliigelpocken. Centralbl. f. Bakteriol. (Htc.), 1. Abt., Orig., Bd. 67,
1912, S. 43.

4, Bordet and Fally. Le microbe de la diphtherie des poules. Ann. de
l’ Inst. Pasteur, T. 24, 1910, p. 563.

5. Burnet. Contribution a V’epithelioma contagieux des oiseaux. Ann.
de I’. Inst. Pasteur, T. 20, 1906, p. 742.

6. Gallagher. Epithelioma contagiosum of quail. J. Am. Vet. Med.
Ass., Vol. 3, 1916, p. 366.

7. Hadley and Beach. Controlling chicken-pox, sore-head or contagious
epithelioma by vaccination. Proc. Am. Vet. Med. Ass., 1913, p. 704.

8. Halasi. Beitrage zur Kenntniss de Geflugelpocke und der Geflugel
diphtherie. Jnaug. Diss. Koz].

9. Haring and Kofoid. Observations concerning the pathology of roup
and chicken pox. Proc. Am. Vet. Med. Ass., 1911, p.°418.

10. Harrison and Streit. Roup. Ontario Agr. College. Bulls. 125 and
1382.

11. Hausser. Bactericlogische Untersuchungen iiber Geflugeldiphtherie.
Centralbl. f. Bakteriol. (Etc.), 1 Abt. Orig., Bd. 48, 1909, S. 535.

12. Jackley. A study of the etiology of roup in birds. Kansas Agr.
Exp. Sta. Tech. Bull. 4, 1917.

13. Mack. The etiology and morbid anatomy of diphtheria in chickens.
Am. Vet. Rev., Vol. 28, 1905, p. 919.

14. Mack and Records. The control of epithelioma in chickens by vac-
cination. Nevada Agr. Exp. Sta. Bulls. 82 and 84.

15. Manteufel. Beitrige zur Kenntniss der Immunitiitserscheinungen
hoi den sogennannten Gefliigelpocken. Arb. a. d. k. Gsndhtsamte., Bd. 33,
1909-10, S. 305.

110 DISEASES OF DOMESTICATED BIRDS

16. Marx u’ Sticker. Untersuchungen iiber das Epithelioma contag-
iosum des Gefliigels. Deutsche Med. Woch., Bd. 28, 1902, S. 893.

17. Moore. A preliminary investigation of diphtheria in fowls. U. S.
Dep. Agr. Bureau Animal Indust., Bull. No. 8, 1904.

18. Miiller. Zur Aetiologie der Gefliigeldiphtherie. Centralbl. f. Bak-
teriol. (Etc.) 1 Abt. Orig., Bd. 41, 1906, S. 423.

19. Reischauer. Uber die Pocken der Vogel, ihre Beziehungen zu den
echten Pocken und ihren Erreger. Centralbl. f. Bakteriol. (Htc.), 1 Abt.
Orig., Bd. 40, S. 356.

20. Schmid. Untersuchungen iiber der Beziehungen zwischen Gefliigel-
diphtherie und Epithelioma contagiosum. Centralbl. f. Bakteriol. (Etc.),
1 Abt. Orig., Bd. 52, 1909, S. 200.

21. Sigwart. Experimentelle Beitrige zur Frage der Identitit von
Gefliigeldiphtherie und Gefliigepocken. Cenlralbl. f. Bakteriol. (Htc.), 1
Abt. Orig., Bd. 56, 1910, S. 428.

22. Sweet. A study of epithelioma contagiosum of the common fowl.
Unw. of Calif. Pubs. in Zoology, Vol. 71, 1913, p. 29.

23. Uhlenhuth und Manteufel. Neue Untersuchungen iiber die
atiologischen Beziehungen zwischen Gefiiigeldiphtherie (Diphtheria
avium) und Gefliigelpocken (Epithelioma contagiosum). Arb. a. d. k.
Gsndhtsamte, Bd. 23, 1909-10, S. 288.

24. Ward. Poultry diseases in California. Proc. Am. Vet. Med. Ass.,
1904, p. 164.

25. Ward. Observations on roup in chickens. Proc. Am. Vet. Med.
Ass., 1905, p. 198.

CHAPTER. X

ASPERGILLOSIS AND FAVUS
ASPERGILLOSIS

Synonyms. Pneumo-mycosis, brooder pneumonia.

Characterization. Aspergillosis is a disease of the pulmonary
region due to infection with fungi. It is characterized by the form-
ation of an exudate, usually of a moldy appearance, on the mucous
membrane of the air passages, principally the air sacs of the ab-
dominal cavity.

Etiology. The disease is almost invariably introduced by fungi
of the genus Aspergillus, Aspergillus fumigatus being the most con-
stant causative agent. Other members of the aspergillus group have
been identified in the morbid processes. These, however, are of
slight significance as they have not been associated with the incidence
of pulmonary mycosis to any great extent.

Aspergillus fumigatus is widely distributed in nature and is often
observed on vegetable matter of all kinds which has been exposed
to dampness. Birds scratching
among moldy grains or in moldy
litter may inhale the spores.
These find a favorable place for
propagation on the mucosze of the
bronchi, or of the air sacs.

The fungus may be readily
grown on potato, rye bread or
plain agar which is acid in reac-
tion. The most suitable temper-
ature is between 35° and 40° C.
The growth appears after 24
hours incubation as a whitish
downy layer over the surface of Fic. 10. Aspergillus —_ fumigatus.
the medium. This is composed Me sa from Mohler and Buck-
of an interwoven mass of trans- ;
parent mycelial threads which later give off branches capped by fruit

heads. ach of the latter is composed of a mass of small rounded
111

112 DISEASES OF DOMESTICATED BIRDS

bodies closely associated in the form of a ball, the outer area of which
shows radiating lines of spores. These are clear and highly refrac-_
tile. Their diameter varies from 2.5 to 3.5 microns. The color of
the growth changes with age, succeeding from white to greenish and
later, in old cultures, to a brownish color. The spores are quite re-
sistant. They are not destroyed by heating at 65° C. for a period
of seven hours and require an exposure of 12 hours to a 5 per cent
solution of carbolic acid for their destruction. In the dried state,
they are very resistant and may germinate after several months or
even several years when conditions are favorable.

Pathogenicity. Of the aspergillus group, A. fumigatus is the
most pathogenic to birds. A. nigressens, A. glaucus and A. candidus
are less pathogenic in the order named.

All species of birds are apparently susceptible to infection. Do-
mesticated ones, especially those confined in large flocks and exposed
to moldy organic matter, are most often affected. These include
chickens and pigeons. Young chicks frequently are attacked by an
acute form known as brooder pneumonia. Cage birds, particularly
those in zoological gardens, are often fatally affected. In France
thousands of pigeons are fed by men in a manner similar to the
method used by parent pigeons in feeding their young; viz., loading
the mouth with grain and fluid and passing it directly to the mouth
of the pigeon. Among these men severe cases of pulmonary aspergil-
losis occur as a result of their exposure to contaminated grain.

The disease may be transmitted artificially to animals and birds
by inoculation or by causing the organism to be inhaled. Inoeula-
tion of smal] quantities of spores into the veins or peritoneal cavity
of rabbits, guinea pigs, fowls, or pigeons causes death from septi-
cemia in from 24 hours to 1 or 2 weeks. In the older cases necrotic
areas are present in the visceral organs and the aspergillus fungus
is readily isolated from these. Lesions resulting from inhalation
infection are usually confined to the air passages. Fowls and ani-
mals exposed in rooms to dust or rye flour containing aspergillus
spores, have contracted the disease and died as a result.

Aspergillosis in the ostrich is discussed on pp. 228 and 229.

Mortality. Fatalities may be high in broods of chicks that\have
been extensively exposed to infection. Those attacked apparently
all succumb. Older birds are quite resistant. Evidence points to
the conclusion that once the disease is established in the system a
fatal termination follows.

Symptoms. Considerable variation in the external signs of as-

ASPERGILLOSIS 118

pergillosis may be expected. As a rule the morbid condition has
existed for some time before symptoms are noticed. When the le-
sions are located in the trachea or bronchi, hoarseness of breathing,
or a rattle in the throat may be the only indication of infection in the
early stages. In air sac involvement alone no respiratory symptoms
are shown. It is doubtful if external symptoms of infection of the
air channels of the bones of the wing are manifested.

As the disease progresses the bird becomes dull and less active.
There is a noticeable decrease in weight accompanied by emaciation.
The term “ going light ” is frequently applied to this condition. Di-
arrhea is not a constant symptom but is usually present in the later
stages. Temperature elevation is not constant in the more chronic
form. Difficult respiration, sleepiness, extreme weakness and marked
emaciation precede death. The appetite decreases as the disease pro-
gresses. Death results from asphyxia and toxemia.

In baby chicks the symptoms are apparent early and are similar
to those of bacillary white diarrhea and intestinal coccidiosis. In
both young and old birds the lesions observed at post mortem readily
reveal the nature of the disease.

Morbid anatomy. The lesions are principally confined to the
respiratory system. This system is complicated in birds for in addi-
tion to the lungs it includes several air sacs in the peritoneal cavity
and air channels in certain of the bones. In some instances through
penetration of the walls of blood vessels by the mycelia, new areas
of infection may be established in other organs as a result of meta-
stasis.

The mold may develop at any point on the respiratory mucous
membrane or may be spread over a large portion of its surface. Our
observations at numerous autopsies place the abdominal air sacs as
the most severely involved region. The morbid process is manifested
by the presence of a membrane of greater or less thickness depend-
ing on its location on the mucosa, or at times by nodules in the
parenchyma of the lungs. In the trachea and bronchi the false
membrane is comparatively thin while in the air sacs it may be
much thicker and give a rigid contour to these organs. Frequently
the sacs are filled with fungoid growth and cellular exudate, the
whole forming a solid mass. The bronchioles may also be plugged
with mycelia, spores and cellular exudate consisting of exfoliated
epithelial cells, leucocytes and occasionally red blood corpuscles.
The surface of the membrane may be grayish or greenish in color.
The latter color is nearly always in evidence at some point. It is in

114 DISEASES OF DOMESTICATED BIRDS

this area that numerous spores may be demonstrated on microscopic
examination.

The mycelial threads penetrate the mucosa to the submucosa or
may enter the adjacent blood vessels forming thrombi and establishing
an area of necrosis resulting in a nodular formation similar to that
of tuberculosis. In the abdominal region the organs in contact with
the air sacs are often involved through adhesions or direct passage
of the fungus into their interior.

In the main, the pathologic condition progresses by direct contact.
Organs affected through the blood stream reveal small areas of ne-
crosis in which the mycelial threads may be detected. The kidneys
are more often affected in this manner than the liver. Artificial
inoculation through hypodermic injection, intraperitoneally or in-
travenously, produces extensive lesions in these organs.

The mycelia may be demonstrated microscopically in necrotic
areas or in nodules in the earlier stages of development. Mycelia
may also be observed in the mucous membrane lesions, and espe-
cially in greenish colored areas are spores readily discovered. The
tissues surrounding the growths are found infiltrated with small
round cells, leucocytes and connective tissue cells, indicating an at-
tempt on the part of the system to build a protective wall against the
spread of the parasite. This attempt is usually abortive although
evidence of regenerative changes are apparent in some lesions.
Giant cells are also occasionally present in the tubercle forma-
tions.

Course of disease. Among older birds the disease has a tend-
ency to occur sporadically, more or less extensive intervals elapsing
between deaths from this cause in a particular flock. Where the ex-
posure is great, outbreaks of considerable importance may result.
The resistance of vigorous individuals, however, is high and epi-
zootics such as are associated with certain other diseases are rarely
encountered. In grown birds aspergillosis follows a semi-acute or
chronic course. Death may occur in from 1 to 8 weeks. In brooder
chicks resistance is less pronounced and acute outbreaks often follow
exposure to moldy food or material. The disease runs a rapid course
with fatal termination in 2 to 7 days. Birds confined to limited
areas as 1s the case in zoological gardens, show a high percentage
of fatalities from this cause.

Diagnosis. Tuberculosis, coccidiosis and aspergillosis are not
readily differentiated symptomatically in grown fowls. On autopsy
the lesions are quite distinctive. Tuberculosis principally affects the

ASPERGILLOSIS 115

liver, intestine and spleen, being less of a pulmonary disease in
birds than is the case in other animals. The tubercles are of a
fleshy type on cross section and show small yellowish points. Coc-
cidiosis is practically confined to the intestinal tract. Its lesions
are of a necrotic type involving principally the duodenum and ceca.
Aspergillosis tends to localize on the walls of the air passages and
forms a moldy growth generally exhibiting a greenish tinge, at least
in spots.

Microscopic examination of the morbid material furnishes a spe-
cific diagnosis since the causative organisms in each case are usually
numerous and very different in morphology.

The disease in young chicks called brooder pneumonia, shows
symptoms similar to those of bacillary white diarrhea and cocci-
diosis. In all three the chicks have a droopy appearance associated
with diarrhea and loss of appetite. In general it may be said that
bacillary white diarrhea is more highly fatal, with deaths occurring
shortly after hatching. Coccidiosis usually appears at a later period
and is also apt to result in heavy losses. Autopsy is necessary, how-
ever, for positive diagnosis. The lesions in the air passages are not
as extensive as in older fowls because of the acuteness of the af-
fection, but may be discerned by careful examination. Bacillary
white diarrhea is a purely septicemic disease, while coccidiosis usu-
ally shows intestinal lesions with accumulation of necrotic or blood
stained material in the ceca. Microscopic or cultural methods may
be resorted to in obscure cases.

Treatment. It is inadvisable to attempt treatment because of
the deep seated position of the parasitic fungus, its resistance to
remedial agents and the advanced stage of the attack when symptoms
are observed.

Prevention. The widespread distribution of Aspergillus fumi-
gatus renders absolute prevention difficult. Care in the selection of
grain and litter will minimize to a great degree the chances of in-
fection. Good housing arrangements which guard against dampness
will prevent the propagation of molds if present to a slight extent in
feed or litter. When the disease is discovered in a flock the source
of infection should be located. The feed may have a musty odor or
a greenish appearance in places, or straw litter may be moldy. In
the former instance cooking will destroy the fungus. Moldy litter
should be discarded.

Experiments have shown the possibility of infection being carried
to newly hatched chicks through the egg. The mycelia of the fungus

116 DISEASES OF DOMESTICATED BIRDS

are known to be capable of penetrating the egg shell and developing
in the albuminous material with consequent destruction of the em-
bryo. The aspergillus colony may be observed as a dark spot on
the internal membrane of the air chamber. Infection through this
source is no doubt rare. It may be guarded against by using clean
straw or chaff in nests for laying or sitting hens, and by dipping
eges for hatching in grain or wood alechol before incubating. Feed-
ing discarded eggs to young chicks is dangerous since these may
carry the causative organisms of several diseases.

FAVUS

Synonyms. White comb; favus de la poule (French); Weisser
Kamm (German).

Characterization. [avus is a contagious, chronic disease of the
skin characterized by the presence of white areas most commonly
localized on the head and is caused by a fungus.

Etiology. The fungus causing the disease is designated Lopho-
phyton galline. It grows readily on agar containing 1 per cent
peptone and 4 per cent of glucose or maltose at room temperature
when the medium is seeded with material from the diseased patches.
Growth first appears as a small, round, pure white, downy colony.
As it enlarges it takes the form of a button which is slightly cup
shaped. The culture ordinarily remains white if kept at a low
temperature. At 27° to 37° C. the colony takes on a delicate rose
color, becomes umbilicated, wrinkled and divided into sectors by
lines radiating from the center. At 30° C. the culture is wholly
rose colored, but more or less deep depending upon the culture.
Sometimes the color varies in the same culture tube. The diffusion
of the raspberry color in the medium is said to be an exclusive char-
acter of the species in question.

Pathogenicity. The infection is readily transmitted to a fowl
by rubbing the comb with scales from a diseased bird. The disease
is unmistakably present on the fifteenth day after inoculation and
persists for months. Similar results are obtained with cultures.
Mice, rabbits, guinea pigs and man are susceptible. Infection may
occur through direct or indirect contact.

Symptoms and morbid anatomy. The disease first appears on
the head and its appendages such as the comb, wattles and barbs.
Nearly always the initial lesion is in the vicinity of the beak, in the
form of numerous small white points. Under a magnifying glass

ASPERGILLOSIS 117

they are seen to be covered with a fine, short down which later
disappears quickly and does not return again. The white point en-
larges and forms a layer 1 or 2 mm. thick adhering to the epidermis
underneath. The color is generally white or gray. In time the
thickness of the crusts increases
as do the surface dimensions.
Finally the small patches origi-
nally isolated, coalesce. The ex-
tension is regular. A white patch
may reach the dimensions of the
comb itself. Sometimes the di-
mensions of a patch remain small
but it is not rare to observe ¢
patches 7 or 8 em. long and 3 or
4 em. broad on large combs.

The diseased area examined
closely presents for study thin
places and thick places. Those
which form small hard eminences
of a grayish white color or slight- |
ly reddened at the top, are irregu- Fic. 11. Favus, involving the head.
larly disseminated over the area (Drawn from photograph by Sabour-

‘ aud, Suis and Suffran)
of the plaque. Between these
elevations the patch is merely a thin membrane of a pearly white
color. Wherever the white area is thickened, the scratching detaches
small fragments like a white powder, of which certain pieces resem-
ble mica flakes.

When the lesion in extending, encounters the feathers, its appear-
ance changes slightly. A deposit of whitish crusts accumulates at
the base of each feather. Some feathers fall out spontaneously, and
all those which have this squamous collar at the base, have little re-
sistance against being plucked. If a feather is pulled it comes out
entire with its yellow root part, but it bears with it, like a collar, the
whitish deposit which surrounds the point where the feather emerges
from the skin.

Course of disease. The disease is benign. Instances in which
affected birds become cachectic and die, are exceedingly rare. Re-
covery may occur in three months spontaneously, or the disease may
last for years. Long duration may be considered as an example of a
succession of infections, rather than the persistence of one infec-
tion. The disease persists in subjects associating with other infected

118 DISEASES OF DOMESTICATED BIRDS

Fig. 12. Deposit of crusts on quills of feathers occurring in favus involving
feathered areas. (Drawn from photograph by Sabouraud, Suis and
Suffran )

birds, in infected quarters, while there is a tendency to recovery
when affected birds are isolated.

Treatment. Isolation of affected birds from the flock and from
other infected individuals in some eases is sufficient to cause the
disappearance of the disease. Previous to the application of any
remedy the affected areas should be softened with soap and warm
water, after which as much of the deposit as possible should be re-
moved. The comb lesions may be treated with carbolized vaseline
or green soap containing five per cent of carbolic acid. A mixture
of glycerine 6 parts and iodine 1 part has been employed on the comb
as have salicylic acid ointment (1 : 10); tincture of iodine diluted
with equal parts or more of alcohol; five per cent formalin ointment
or solution; and an ointment made of red oxide of mercury 1 part,
to 8 parts of lard. A 1-500 solution of bichloride of mercury may
be used among the feathers.

Prophylaxis. In an infected flock, the closest examination of
the exposed birds should be made, so that those slightly infected may
be isolated and treated. Otherwise they will perpetuate the infec-
tion in the flock. Care should be exercised to prevent the introduc-
tion of birds from flocks not positively known to be free from the
disease. In an infected flock, thorough cleaning and disinfection
of the quarters should be carried out.

REFERENCES

1. Balfour. Aspergillary pneumokoniosis in the lung of a turkey.
Fourth Rep. Wellcome Research Lab., 1911.

2. Beach and Halnin. iteerenions on an outbreak of favus. J. Agric.
Research, Vol 15, 1918, p. 415.

ASPERGILLOSIS 119

3. Ligniéres et Petit. Péritonite aspergillaire des dindon. Rec. de
Meéd. Vét., T. 75, 1898, p. 145.

4. Lucet De Il Aspergillus fumigatus chez animaux domestiques et
dans les oefs en incubation. Paris, 1897.

5. Matruchot et Dassonville. Recherches expérimentales sur une der-
matomycose des poules et sur son parasite. Rev. Gén. de Bot., T. XI,
1899, p. 480.

6. Mohler and Buckley. Pulmonary mycosis of birds. U.S. Dep. Agr.
Bureau Animal Indust. Circ. 58, 1904.

7. Neumann. Aspergillosis in domesticated birds. J. Comp. Path. and
Therap., Vol. 21, 1908, p. 260.

8. Sabouraud. Le trichophyton de la poule et la maladie humaine qu’il
détermine. Arch. de Méd. Expérim., Mai 1909.

9. Sabouraud, Suis et Suffran. La “créte blanche” (favus) de la poule
et son parasite. Rev. Vét., T. 34, 1909, p. 601.

CHAPTER XI

INFECTIOUS ENTERO-HEPATITIS OF TURKEYS

Synonym. Blackhead.

Characterization. Entero-hepatitis is an infectious disease of
turkeys and fowls, characterized by distention of the ceca with ne-
crotic material and the formation of yellowish or yellowish-green ne-
crotic areas in the liver.

Geographic distribution. It is widely distributed over the
United States, and has also been reported from Canada, Europe, Aus-
tralia and Africa.

Etiology. The causative organism as described by Smith belongs
to the genus ameba and has been designated by him Ameba mele-
agridis. Through the researches of Hadley, the role of an ameba in
the causation is disputed. The latter investigator asserts that a fla-
gellated protozoal organism, T'richomonas, is the causative agent and
that the organism described by Smith merely represents a transitory
stage in the hfe cycle of the flagellate. The difficulties to be met
with in establishing the etiologic factor of this disease are far greater
than is the case in bacterial affections. In routine examination of
entero-hepatitis cases by the present writers, it has been observed that
flagellate forms are frequently present in the cecal exudate of tur-
keys dead of entero-hepatitis while more often protozoal organisms
of the ameba type are seen in comparatively large numbers. Fur-
ther and more extensive investigation appears to be necessary in order
to establish firmly the specific etiology of this disease.

The organism described by Smith is round or oval in form with
a single contoured outline. The structure appears homogeneous
throughout with the exception of a small granular area eccentrically
located and representing the nucleus. This encloses a smaller
rounded body distinguished as the nucleolus. The protozoa in fixed
or hardened tissue are from 6 to 10 microns in diameter, in fresh
smears from 8 to 15 microns in diameter.

The organism attributed by Hadley as the causative agent is a
flagellate. This is most easily recognized in the motile stage. In
this form it presents an irregular outline. It may be pear shaped,

ovoid, triangular or elliptical in form. It has three anterior fla-
120

INFECTIOUS ENTERO-HEPATITIS OF TURKEYS 121

gella, a vibratory membrane and one posterior flagellum. The nu-
cleus is placed anteriorly. One or more food vacuoles may be ob-
served. The average length of this form is about 10 microns.

Pathogenicity. Young turkeys are especially susceptible, al-
though there appears to be no period of immunity to primary in-
fection during the life of the bird. The greatest losses occur during
the first two or three months of life. Practically all of the exposed
poults contract the disease at this time. Young chickens are only
slightly susceptible but may serve as carriers of the organism.

Source of infection. The disease is principally spread through
exposure to infested ground. Once the causative agent has been
brought on the premises, it is apt to continue its activity year
after year. Whether this is wholly due to the resistance of the
encysted stage of the parasite, to climatic or other external influ-
ences or whether it is perpetuated in the intestinal tract of compara-
tively resistant turkeys or chickens is open to speculation. From
the fact that mature turkeys may show symptoms of entero-hepatitis
during all seasons of the year, it is reasonable to assume that they
constantly harbor the organism in a saprophytic form and only de-
velop the disease as a result of adverse conditions or weakened con-
stitution from other causes. Curtice states that chickens though
rarely infected may serve as carriers. In any case, the disease is
contracted by the poults ranging on ground infested by the droppings
of carriers of the parasite. The parasite passes from the intestine in
the encysted or resistant stage. In this form when not exposed to
the direct rays of the sun or to considerable drying it may retain its
vitality for a long period, possibly one to two years. Earth worms
may play some part as mechanical carriers of cysts which have sur-
vived in the soil under favorable conditions. When these encysted
forms are taken into the alimentary tract by poults in feeding, they
undergo changes which renew their activity. The tough resistant
covering is discarded and forms developed from the central granular
mass or nucleus penetrate the mucosa of the intestine, especially the
ceca and may be carried by the blood stream to the liver. The para-
sites multiply rapidly in the intestine and are passed out in enormous
numbers in the droppings. By this means, other susceptible birds
in the flock are directly infected through coming in contact with the
contaminated material in feeding.

Symptoms. The symptoms of entero-hepatitis become apparent
within a period of four weeks after exposure. Young birds show
less resistance and develop manifestations earlier than grown ones.

122 DISEASES OF DOMESTICATED BIRDS

The disease runs a rapid course in the former and deaths may
follow in a few days. Older turkeys, fatally affected, usually suc-
cumb within four weeks after the onset of symptoms. The mortality
approaches 90 per cent in poults and 10 per cent or more in the
grown birds, according to the extent of exposure. Affected poults
exhibit a drowsy attitude with constantly increasing lack of vigor.
They are unable to keep up with the flock in its daily travel over
large areas. The appetite is diminished, the feathers ruffled, wings
are pendant, and a general air of debility is manifested. Diarrhea
is nearly always present and quite characteristic. The droppings
are soft and yellowish in color or may be mixed with brownish ex-
crement. During the later stages the head may present a darkened
or purple appearance due to impaired circulation of the blood.
This symptom has led to the disease being termed “ blackhead.”
However, this term is misleading since the darkened appearance
of the head is not a constant symptom and may also be observed in
other diseases which lead to a weakened heart action. In older
turkeys the symptoms are less pronounced and may be of much
longer duration. They show loss of appetite, unthrifty appearance,
lessened activity, progressive emaciation and diarrhea, with soft
yellowish droppings. The disease may persist for a period of two
weeks to two months and result fatally or the bird may regain its
normal condition. Relapses frequently occur during the following
year. The disease is more prevalent during the late summer or
fall in young poults but may occur at any season and is frequently
reported among grown turkeys during the winter and spring.
Morbid anatomy. The lesions of entero-hepatitis are confined
to the intestine and liver. In the intestinal tract the ceca are the
principal seat of infection. In many cases only one cecum exhibits
macroscopic alterations but quite frequently both ceca are equally
involved. The walls become greatly thickened and covered by a
necrotic exudate which completely fills the cavity or leaves but a
small central space. The accumulation of exudate gives rise to a
marked distention of these blind pouches plainly apparent when
the intestine is exposed at autopsy. The exudate is dull gray in
color and of a friable or cheesy consistency. The entire length of
the ceeum may be involved or only a limited area, depending on the
severity or duration of the morbid process. In the majority of
eases the liver is found infected to a greater or less degree. The
lesions are characteristic. Areas of degeneration appear on the sur-
face in circular form and of varying size. They are usually about

INFECTIOUS ENTERO-HEPATITIS OF TURKEYS 123

1% to 7% of an inch in diameter and may be isolated and few in num-
ber or numerous and closely associated, even coalescent. Their color
varies from a yellowish to a yellowish-green. These areas of ne-
crosis extend more or less deeply into the structure of the liver and
result from plugging of the smaller arterioles with the parasites and
cellular debris. They are not always of a homogeneous color, but
may appear mottled with small areas of approximately normal liver
tissue. No elevation above the liver surface is in evidence as may
be the case in tuberculosis or sarcomatosis of the liver and the tend-
ency is rather to a slight depression beneath the capsule. The liver
is often enlarged to a considerable degree and congested. |

In very acute cases the ceca show slight evidence of exudate but
are more or less inflamed while the liver is free of lesions. Other
areas of the intestine, especially the duodenum and rectum, harbor
the causative parasite and may exhibit congestion of the mucous
membrane, hemorrhagic points or even spots of necrosis. However,
the ceca and liver are the main seats of disease and more to be
relied upon for diagnostic evidence. Infrequently the morbid process
within the lumen of the cecum extends through the mucosa, sub-
mucosa, muscular layers and serous coat causing perforation and exu-
dation into the peritoneal cavity leading to peritonitis or extensive
adhesions of the cecum to the surrounding loops of intestine. This
condition is apparently due to the action of invading bacteria since
the protozoal organisms have not been demonstrated in these sec-
ondary lesions.

Microscopically the cecal exudate is found to be composed of
protozoal bodies, exfoliated mucosa cells in various stages of degen-
eration, connective tissue shreds, blood cells and an amorphous de-
tritus. The cecal wall is greatly thickened due to infiltration and
connective tissue hypertrophy. The mucosa shows extensive de-
generative changes or is absent in areas. Depending on the depth
of the ulceration, the circular or longitudinal muscular layers show
more or less infiltration with small round cells and congestion, which
may extend to the serosa. In the liver the necrotic foci show vary-
ing stages of cell degeneration and are surrounded by a congested
area. Walling off of the affected spots is not well marked or is
totally absent. Small round cells, protozoal organisms and nuclear
remnants are distinguished in the amorphous necrotic material. In
both the intestinal membrane and in the liver the protozoa oceur
either singly or in groups between the epithelial, or parenchymatous
cells where they may be enclosed in a connective tissue network.

124 DISEASES OF DOMESTICATED BIRDS

They have also been observed in the interior of giant cells (Smith),
and epithelial and endothelial cells (Hadley).

Diagnosis. Entero-hepatitis is readily differentiated from other
diseases by the definite character of its internal manifestations.
The presence of yellowish or yellowish-green spots on the surface of
the liver is specific. Turkeys are much less frequently affected
with tuberculosis, or malignant tumors than fowls and these dis-
eases may be eliminated where several birds in a flock become in-
fected at the same time, especially in the case of poults. The lesions
of tuberculosis, on cut section, present a fleshy appearance whitish in
color with yellowish points and usually extend to the spleen, intestine
and mesentery where they appear as rounded nodules. Tumor
formations vary greatly in size, are fleshy in character and are usu-
ally found on the serous membrane. They are of a chronic char-
acter and occur sporadically. In tuberculous infection, tubercle ba-
ceilli will be found in large numbers on microscopic examination of
smears from the nodules.

Treatment. Extensive experiments looking to the treatment of
entero-hepatitis have so far failed to develop a satisfactory method.
The insidious nature of the affection and the deep seated location
of its parasite in the wall of the intestine and in the liver render
it practically immune from interference by curative agents.. Eme-
tin hydrochlorid, a derivative of ipecac, by repeated hypodermic
injection has given more or less satisfactory results in the treat-
ment of amebic dysentery in man, a disease somewhat analogous
to entero-hepatitis of turkeys. However, the above disease of man
is of a chronic nature and lends itself to a more prolonged course
of treatment than is permitted in the case of the comparatively acute
disease under consideration. Also the value of young turkeys does
not justify the time and expense which would be involved even were
the treatment fairly successful. Giving ipecac in small doses might
prove beneficial. The most promising and economical treatment is
the administration of crude catechu by means of the drinking water.
This has been recommended by Fantham for coccidiosis of fowls
and has given good results in our experience. One-third teaspoon-
ful of crushed crude catechu is added to each gallon of water. It is
quite possible that the use of catechu in this manner during the first
three months would bring the exposed poults safely through the most
dangerous period. Should signs of constipation develop as a result
of this treatment, the entire flock may be given Epsom salts in the
proportion of one teaspoonful to every ten poults. The salts can

INFECTIOUS ENTERO-HEPATITIS OF TURKEYS 125

be dissolved in water and the solution mixed with a feed to be given
early in the morning. Turkeys on range would require special at-
tention for the successful operation of the above measures. Isola-
tion or disposal of birds showing symptoms of disease is of the first
importance in guarding against a further spread of the malady.
Thorough cleaning and disinfection of quarters and yards will tend
to keep the outbreaks in check. Carbolic acid in 5 per cent solution,
or compound cresol in 3 per cent solution are efficient disinfectants.

Prevention. Prevention of entero-hepatitis in infected com-
munities is more difficult than the prevention of other diseases of
domesticated birds, because of the fact that turkeys range over an
area of several miles in diameter when allowed to run at large as is
the usual custom in this country. The possibility of healthy flocks
becoming infected by feeding on ground contaminated by diseased
flocks is very apparent and renders preventive measures under such
conditions rather difficult of execution. Where turkeys are con-
fined to a limited area or do not come in contact with other flocks
which harbor the parasite, simple precautionary measures may in-
sure freedom from the disease. The main channel of entrance is
through the introduction of birds which come from infected flocks.
Particular care in selecting purchased birds should be exercised.
The fact should be established beyond doubt that they are of a
flock which has shown no symptoms of disease and have not been
associated with neighboring diseased flocks. A period of quarantine
extending over 30 days is also advisable before newly acquired tur-
keys are placed with the home flock.

Where the disease has been prevalent on premises to such an ex-
tent as to make the raising of turkeys unprofitable, it is advisable
to dispose of the entire lot and allow a period of approximately two
years to elapse before restocking. Local conditions may modify or
suggest preventive measures. Limeing or plowing the runs or home
feeding yards is indicated. The principal fact to be considered is
that the disease must first be introduced, either by infected birds
(almost invariably the turkey) or by mechanical carriers, such as
persons coming from infected farms and carrying the causative par-
asite on their shoes. Wild birds may possibly serve as carriers.
Other agencies could be mentioned by means of which the organism
of entero-hepatitis might be carried from infected farms; however,
these are of minor importance and cannot easily be guarded against.
Eggs for hatching, from infected turkeys may be dipped in 95 per
-cent alcohol to destroy any parasites which may have become at-

126 DISEASES OF DOMESTICATED BIRDS

tached to the shell. Practically the only danger in using eggs from
infected flocks is that the shells may have come in contact with drop-
pings harboring the infectious parasite.

On first indication of the presence of entero-hepatitis the affected
birds should be destroyed and their carcasses burned or deeply
buried. The quarters should be thoroughly cleaned and disinfected
with 5 per cent carbolic acid or compound cresol in 3 per cent solu-
tion. The runs or local feeding ground should be cleaned and
limed or plowed under as the chance for infection is greatest at the
points where the flock congregates most often. The confinement of
turkeys to inclosed yards has been tried with apparently favorable
results. By this method of rearing, entero-hepatitis could be more
easily controlled.

Hadley regards the prevention of Trichomonas infection in tur-
keys as presenting a somewhat different problem from that involved
in the prophylaxis of many diseases. The parasites are found nor-
mally present in the intestines of all poultry. Their pathogenic
activity in turkeys, in his opinion, depends upon factors present
in the host which are probably quite unrelated to virulence on the
part of the infecting organism. This view would suggest the exer-
cise of great care in feeding in order to preserve health even though
the flagellates are present in the intestine.

REFERENCES

1. Curtice. Notes on experiments with blackhead of turkeys. U. S.
Dep. Agr. Bureau Animal Indust. Cire. 119, 1907.

2. Curtice. The rearing and management of turkeys with special refer-
ence to the “ blackhead” disease. Rhode Island Agr. Exp. Sta. Bull. 123.

3. Curtice. Further experiments in connection with the blackhead dis-
ease of turkeys. Rhode Island Agr. Exp. Sta. Bull. 124.

4. Cushman. Nature of blackhead in turkeys. Rep. Rhode Island Agr.
Exp. Sta. 1894.

5. Hadley. Blackhead in turkeys. A study in avian coccidiosis.
Rhode Island Agr. Exp. Sta. Bull. 141.

6. Hadley. The role of the flagellated protozoa in infective processes
of the intestines and liver. Rhode Island Agr. Exp. Sta. Bull. 166.

7. Milks. A preliminary report on some diseases of chickens. Louist-
ana Agr. Exp. Sta. Bull. 108.

8. Moore. The direct transmission of infectious entero-hepatitis in
turkeys. U.S. Dep. Agr. Bureau Animal Indust. Cire. 5, 1896.

9. Smith. Infectious entero-hepatitis in turkeys. U. S. Dep. Agr.
Bureau Animal Indust. Bull. 8, 1895.

10. Smith. Further investigations into the etiology of the protozoan
disease of turkeys known as blackhead, entero-hepatitis, typhlitis, ete.
J. Med. Res., Vol. 33, 1915, p. 248.

CHAPTER XII
COCCIDIOSIS

Characterization. Coccidiosis is primarily a disease of the in-
testinal tract. In young chicks it may also affect the liver and
in geese, the causative organism may be localized in the kidneys.
It is one of the greatest scourges of fowls, pigeons and turkeys.

Etiology. The organism causing coccidiosis is designated Hi-
meria (Coccidium) aviwm and belongs to a class of protozoan para-
sites known as sporozoa. The organism is included in the animal
kingdom and reproduces by both sexual and asexual processes. The
parasite was long known as Coccidium avium but owing to the rules
of priority in zoological nomenclature, the familiar name of the
genus Coccidiwm has been replaced by Eimeria.

In the odcyst or resistant stage, the one most easily recognized on
microscopic examination of the intestinal contents, the protozoan
generally appears as an oval body containing a central granular
mass surrounded by a highly refractile zone with a double con-
toured border. The size varies from 25 microns to 35 microns in
length and from 15 microns to 20 microns in breadth.

Life history of Eimeria avium. ‘The life history has been ad-
mirably worked out by Fantham. There are two principal stages in
the life cycle, a stage of asexual multiplication, termed schizogony,
and a stage of sexual reproduction in which male and female elements
unite to form resistant bodies for life outside the animal cells. In
the asexual stage the newly formed parasites pass from one cell to
another, and it is during this cycle that the great destruction of in-
testinal mucosa occurs.

(a) The young, growing parasite. The odcyst reaches the duo-
denum of the bird through the medium of the food or water. Here
the tough cyst wall is softened and four small oval bodies or spores
are released. From each of these are given off two actively motile
vermiform bodies with one end more pointed than the other, which
vary from 7 to 10 microns in length. These are the primary infect-
ing germs or sporozoites (fig. 13 A). The sporozoite passes into an
epithelial cell lining the first portion of the intestine where it curls

on itself (fig. 13 B), takes on a spherical outline (fig. 13 C) and be-
127

Fic. 13. Diagram of life
cycle of Eimeria (cocci-
dium) avium. (Fantham)

B-H. Illustrate the asex-
ual reproduction (schizog-
ony) of H. avium. Epithe-
lial host cells diagrammat-
ically outlined.

I-L. Illustrate the pro-
duction of sexual forms
(gametogony).

N-T. Illustrate spore
formation (sporogony).

A. Sporozoite or primary
infecting germ which pene-
trates the epithelial cell of
the duodenum of the host.

B. Sporozoite curving on
itself before becoming
rounded within the host
cell.

C. Young, growing para-
site.

D. Fully grown parasite

(Trophozoite) .
E. Schizont, with numer-
ous daughter nuclei _peri-
pherally arranged. (Seen
in transverse section. )

F. Schizont, showing fur-
ther differentiation of mero-
zoites.

G. Merozoites arranged
“en barillet,” about to issue
from the host cell.

H. Free merozoites.

I?. Young macrogame-
tocyte with coarse granules.

~~ GAMETOGONy.

'

H

>
2
te]

oO
°o
4

°o
&
ny)

I¢. Young microgametocyte with fine granules.

J?. Growing female mother cell, showing chromatoid and plastinoid granules.

J¢. Microgrametocyte with nucleus divided to form a number of bent, rod-
like portions, the future microgametes.

K¢. Macrogamete which has formed a cyst wall for itself but left a thin
spot for the entry of the microgamete.
; Ko. Microgametocyte with many biflagellate microgametes about to separate
rom it.

L. Fertilization. One microgamete is shown penetrating the macrogamete,
while other male cells are near the micropyle but will be excluded.

M. Fertilization. The male pronucleus is lying above the female chromatin.
Degenerating microgametes are shown outside the odcyst.

N. Odeyst (encysted zygote) with contents filling it completely.

O. Odcyst with contents concentrated, forming a central, spherical mass.
Many such cysts seen in infected cecal droppings.

P. Odeyst with four nuclei.

Q. Odcyst with contents segmented to form four rounded sporoblasts. (As
seen in fresh preparations. )

R. Odcyst with four sporoblasts which have grown oval and are becoming
sporocysts.

8S. Odcyst with four sporocysts, in each of which two sporozoites have dif-
ferentiated.

T. Free sporocyst in which the sporozoites have assumed the most suitable
position for emergence.

128

COCCIDIOSIS 129

gins to grow in size at the expense of the host cell. This is known as
the trophozoite stage (fig. 13 D).

(b) Asexual multiplication or schizogony. When fully developed
the trophozoite has a diameter of 10 to 12 microns. In preparation
for propagation the nucleus divides into a number of daughter nuclei
which arrange themselves in a zone at the periphery. This consti-
tutes the schizont stage and represents the beginning of asexual mul-
tiplication or schizogony (fig. 13 E). Each nucleus becomes sur-
rounded with protoplasm and assumes a long narrow form with
pointed ends. The length ranges from 6 to 10 microns (fig. 13 F G).
These bodies, known as merozoites, differ from sporozoites in that
their nuclei contain a small particle of chromatin, the karyosome.
From 8 to 20 merozoites are formed from 1 schizont. On separation
from one another (fig. 13 H), the merozoites work their way into
other cells, ining the intestinal tract and may repeat the process
of development just outlined, or differentiation into sexual forms
may take place within the newly invaded cells. This process is
termed gametogony.

(c) Sexual reproduction er gametogony. Two forms of the or-
ganism are now produced, the macrogametocyte or female mother
eell (fig. 18 I J) and the microgametocyte or male mother cell (fig.
13 IJ). Both forms are oval in shape, the former being somewhat
larger and more granular than the latter. Also the former gives
rise to only one daughter cell or macrogamete (fig. 13 K) while
the latter produces a large number of minute, biflagellate, actively
motile male cells or microgametes (fig. 13 K). The macrogametes
are from 11.8 to 17.5 microns in length and 6 to 11 microns in
breadth, in sections. The microgametes are 3 to 4 microns in length,
in sections.

(d) Fertilization. Fertilization takes place through the entrance
of the microgamete or male cell into the structure of the female
cell or macrogamete at the thin spot at one end known as the mi-
cropyle (fig. 18 L). After the entrance of the male cell the macro-
gamete secretes protoplasm which plugs the opening and prevents
the entrance of other microgametes. On union of the nuclei of the
two gametes, a zygote is formed which proceeds to spore formation or
sporogony (fig. 13 M N).

(e) Sporogony. The zygote is surrounded by a tough double con-
toured membrane which is extremely resistant. This stage is known
as the egg stage, or odcyst. The contents are at first granular and
grayish in appearance (fig. 13 N). Later the granular material is

130 DISEASES OF DOMESTICATED BIRDS

gathered into a compact circular mass approximately in the center
of the odeyst (fig. 13 O). The nucleus imbedded in the central mat-
ter now undergoes division into two and these in turn divide, form-
ing four daughter nuclei (fig. 13 P). These are surrounded by cyto-
plasm and separated from each other. As a result four rounded
bodies are formed within the cyst. These are sporoblasts (fig. 13 Q).
Later the sporoblast loses its rounded form, becomes oval and is
inclosed in a cell wall (fig. 13 R). In this form it is termed a
sporocyst and from it develops a spore which contains two young
infective parasites or sporozoites. The life cycle is completed by
the rupture of the odcyst wall in the intestinal tract of the host,
which releases the spores and the primary infecting sporozoites.

From experiments made by feeding fowl chicks with coccidian
odeysts, Fantham concludes that the period for the total life cycle
of the parasite is from eight to ten days.

Pathogenicity. Apparently coccidiosis is infectious to all do-
mesticated and wild birds which are exposed to its causative organ-
ism. It has been observed in a wide variety of these birds and its
incidence has been marked by high mortality, especially in those con-
fined to limited areas. It is highly destructive to young chickens
and frequently affects baby chicks. Its greatest ravages are seen
in chickens which have passed the brooder stage and are exposed
to the infective agent in infected houses or grounds. Limited range,
as is customary in the rearing of domesticated birds, and especially
in the case of chickens closely confined in large flocks, is conducive
to heavy infection and high mortality in the event that coccidia are
present. Next to chickens, pigeons are no doubt most severely af-
fected. Outbreaks among ducks and geese occur less often as an
epizootic unless the birds are closely confined, but individual infec-
tion commonly occurs.

Birds of all ages are susceptible. Mature birds exhibit a fair de-
gree of resistance. They may harbor the coeccidia and appear nor-
mal until they become grossly infected, or become weakened through
other causes to such an extent that their power of resistance is lost.

Mortality. In chicks affected at the age of two to ten weeks,
the disease runs a rapid course and the mortality may reach 100 per
cent in closely confined flocks. In older fowls, the fatalities, while
not so great, are usually very heavy in those surrounded by unsan-
itary conditions. Mature hens have a greater power of resistance
but even among these, severe losses may be observed. The mortality
is governed by the degree of exposure.

COCCIDIOSIS 131

Course of the disease. The coccidium when once introduced into
a flock develops rapidly in the cells of the intestinal mucosa, giving
rise to a great number of sexual and asexual forms which are passed
out in the droppings and are ingested by healthy birds. Accumu-
lation of infected droppings naturally tends to increase the number
of these organisms ingested and results in gross infection. Where
fairly good sanitary conditions are maintained, the spread of the
disease is less general and the amount of infectious material con-
sumed is proportionally lessened. As a result, birds which have a
degree of normal resistance are protected against heavy infection.

Symptoms. The outward manifestations of coccidiosis depend
to a considerable degree upon the age of the birds attacked. In
young chicks, the disease develops rapidly and the mortality is high.
The affected ones display the usual appearance associated with de-
bilitating internal disorders, such as weakness, disordered feathers,
droopy wings, bunched appearance, loss of appetite, and somnolence.
The droppings are semi-fluid and usually whitish in color, but may
be of a fluid nature with brownish tinge. In very acute cases in
young chicks the droppings are deeply stained with blood. Affected
chicks of an age of three weeks or less to two months seldom survive
in a severe outbreak and those that recover are stunted and worthless.
Chicks affected fatally succumb in from one to several days after out-
ward symptoms are apparent, depending upon their age. The older
ones show a stronger resistance, but in these too, the fatalities are
extremely heavy.

In grown fowls, the disease usually assumes a more chronic type,
although acute outbreaks are not infrequent. In these acute out-
breaks, the affected birds show the droopy appearance which is more
or less characteristic of all infectious diseases of fowls, and which,
in itself, has comparatively little value as a diagnostic feature. In
semi-acute cases, the fowl develops a progressively increasing list-
lessness and loss of activity. The comb becomes pale and periods of
dejection, during which the bird stands in an isolated position, in-
crease as the disease progresses. The appetite may remain normal
and is frequently ravenous when the fowl is aroused at feeding time.
During intervals between regular feeding, there is little effort to
seratch for food with the others of the flock. The symptoms may be
apparent for from one to three weeks, death occurring quite sud-
denly or after a short period of coma. In the more chronic form,
the fowl retains a pale appearance of the comb and wattles for
several weeks, the appetite appears normal while the bird is eating,

132 DISEASES OF DOMESTICATED BIRDS

but the amount of food consumed is less than usual, owing to the
general indifference to food during prolonged intervals. Emacia-
tion is marked both in semi-acute and chronic cases, principally due
to the fact that the destruction of the lining membrane of portions
cf the intestine prevents normal assimilation of the food. Leg
weakness and paralysis are frequently observed.

Affected geese become greatly weakened and emaciated. After
walking a few steps they will fall and after a struggle roll on their
backs, a position which is frequently assumed.

Morbid anatomy. The lesions are principally confined to the
intestinal tract and are most noticeable in the ceea, in chickens and
turkeys. In young chicks in which the disease assumes an acute
course, the ceca are filled with a bloody semi-solid mass which shows
through the intact tubes and gives them a distended contour. This
mass consists of blood cells, exfoliated mucosa, fecal matter, and ex-
tremely numerous coccidial forms of which the odcysts or egg forms
are especially apparent on microscopic examination. In older fowls,
the ceca may be distended to a greater or less degree. In the ma-
jority of cases, the distention is marked and the tubes are firm to the
touch over a considerable extent of their length. Hemorrhagic areas
may show through the serous membrane, or the affected parts may ap-
pear pale and deadened. One cecum only may give evidence of mor-
bid changes, but as a rule both are equally affected. On incision,
the lumina are found packed with a solid necrotic mass of a grayish
color and cheesy consistency. ‘The mucous membrane is completely
degenerated and forms a part of the caseated mass. On microscopic
examination, the necrotic material appears as an amorphous mass
in which mucus, cells in various stages of degeneration, food material
and numerous coccidial cysts are incorporated. The mucous lining
of the duodenum is invariably the seat of pathologic changes and is
the portion of the intestine first affected. Im many instances, this
is the only part which shows lesions on post-mortem examination.
The lining membrane is deeply congested, or hemorrhagic.

Diagnosis. Coccidiosis is readily diagnosed by a microscopic
examination of the droppings of infected birds, or of the intestinal
contents at autopsy. A small amount of the material is broken up in
several drops of a 1 per cent potassium hydrate solution, normal
salt solution, or water and about two drops of the mixture are placed
on a glass slide and a cover glass applied. The coccidia usually
are very numerous in advanced cases and are easily recognized in
the odcyst or resistant stage. They have an oval appearance with

COCCIDIOSIS 133

a central, rounded, darkened area surrounded by a wide, clear,
transparent zone with double contoured border. Other stages of de-
velopment may be observed, however, the odcyst form is most easily
recognized. Symptomatically the disease may be confused with ba-
cillary white diarrhea and aspergillosis in young chicks, and with
tuberculosis, aspergillosis, and infectious leukemia in older fowls.
It is differentiated from bacillary white diarrhea by the fact that
deaths from the latter occur principally within the first three weeks
of life, while coccidiosis usually appears at a later period. As-
pergillosis cceurs more rarely and is generally restricted to a rela-
tively small number of the flock. It is easily differentiated from
coccidiosis on post-mortem examination by the localization of its
lesions in the air passages, especially in the air sacs of the abdomen.
Tuberculosis is readily distinguished by its characteristic nodular
formations in the liver and intestines, or by microscopic examina-
tion. In infectious leukemia, the liver is enlarged and usually
studded with small necrotic spots while the ceca are free of masses
of caseated material.

Treatment. Attempts at treatment have not given very satis-
factory results owing to the highly resistant powers of the organism
during certain stages of its life cycle and to the position which it
occupies in the intestinal membranes. Crude catechu, recommended
by Fantham, has, in our experience, proved more effective than other
preparations which have been recommended. The most convenient
method of administration is by means of the drinking water. The
lumps should be broken up by grinding or pounding into a coarse
powder and added to the water in the proportion of 4 teaspoonful
to each gallon of water. This solution is to be kept constantly avail-
able to the flock while the disease is prevalent. Should signs of
constipation develop, the entire flock may be given a dose of Epsom
salts in the proportion of % teaspoonful to each adult fowl. The
salts can be dissolved in water and mixed in a mash. The purgative
effect is greatest if the mash is fed in the morning when the crop
contains a minimum amount of food. It is advisable when symp-
toms of coccidiosis are first noticed to give the flock a dose of Epsom
salts before the crude catechu treatment is started. Where catechu
is not available, bichloride of mercury may be substituted. It is
given in the drinking water in the strength of 1 to 6000. Perman-
ganate of potash 1 part in 500 parts of drinking water has also
proved effective.

Prevention. Once this disease has been introduced, the most sat-

134 DISEASES OF DOMESTICATED BIRDS

isfactory method of combating it is through preventive measures
against its spread. Birds showing symptoms should be isolated im-
mediately, the houses thoroughly cleaned, and the floors, dropping
boards and roosts soaked with ecarbolic acid in 5 per cent solution,
or crude carbolic acid, or compound cresol, in 2 per cent solution.
Other disinfectants, especially the coal tar products, may be substi-
tuted, provided sufficiently strong solutions are applied. The dis-
infectant may be spread by means of a spray pump or brush, but it
is Important that the places exposed to droppings should be covered
by the fluid. During the course of an outbreak the droppings are
to be removed frequently as it is through these that the infection
is passed to healthy birds while feeding in contaminated pens. Runs
to which diseased fowls have had access are highly dangerous to the
non-infected and should be abandoned for a year at least if possible.
These may be plowed and seeded, or if their use as runs is impera-
tive the soil may be med and plowed under. Since earth worms are
eredited with serving as hosts of the coccidium, stringent measures are
necessary on badly infected premises, to accomplish complete eradi-
cation of the disease. Covering the ground with chloride of lime or
unslacked lime at intervals may prove sufficient, especially where
preventive measures have been adopted early and a minimum ex-
posure to infested droppings is indicated. owls received from out-
side sources, unless known to be unexposed, should be quarantined
for a period of three to four weeks before being placed in the flock.

REFERENCES

1. Fantham. Experimental studies in avian coccidiosis. Proc. Zool.
Soc. London, Vol. 3, 1910, p. 708.

2. Fantham. Cocceidiosis in British game birds and poultry. J. Econ.
Biol, Vol. 6, 190d, p. (5.

3. Jowett. Coccidiosis of the fowl and calf. J. Comp. Path. and
Therap., Vol. 24, 1911, p. 207.

4. Meyer and Crocker. Some experiments on medical treatment of
coccidiosis in chickens. Am. Vet. Rev., Vol. 48, 1913, p. 497.

CHAPTER XIII
SPIROCHETOSIS AND RARE INFECTIOUS DISEASES

SPIROCHETOSIS

Synonyms. Fowl fever, spirillosis of fowls, spirillose des poules,
Hiihnerspirillose.

Characterization. Spirochetosis is an acute, highly fatal, fe-
brile, septicemic disease of birds caused by spirochetes and trans-
mitted by fowl ticks.

Geographical distribution. The disease has been reported in
North and South Africa, India, Australia, Russia, Hungary, Rou-
mania, Bulgaria, Cyprus, South America and the West Indies.

The existence of the disease in the United States within the area
of distribution of the fowl tick (See Fig. 53, p. 221) has been
suspected by various writers, but so far as known its presence has not
been definitely proven. Symptoms ascribed to excessive tick infesta-
tion, such as paralysis, drooping of wings, ruffled feathers, loss of ap-
petite and even death have suggested the idea that spirochetosis may
be present.

Etiology. Spirocheta (Treponema) gallinarum (SS. march-
ouxt) causes the disease in fowls, while Spirocheta anserina has
been identified as the cause of a similar infection in geese. Some
consider S. anserina as identical with S. gallinarum.

The general shape of a fully developed spirochete is that of a nar-
row sinuous thread, in some cases reaching nearly 20 microns in
length. The cells possess active motility. Spirochetes are generally
regarded as protozoan organisms, although the belief that they are
bacteria has many adherents. The organisms may be stained in
blood films by fixing with osmie acid vapor, after which the films are
hardened in absolute aleohol and stained with Giemsa or one of the
modifications of that stain. Carbol fuchsin may be employed as a
stain.

Noguchi has cultivated S. gallinarum in a special medium de-
vised to provide suitable conditions. An infected bird is placed
under ether anesthesia and blood is drawn aseptically from the heart.

To prevent coagulation the blood is mixed with an equal amount of
135

136 DISEASES OF DOMESTICATED BIRDS

1.5 per cent solution of sodium citrate in a .9 per cent solution of
sodium chlorid. A piece of kidney of a normal rabbit or a piece of
pectoral muscle of a fowl is placed in a test tube. Ascitie fluid is
added to make the column of fluid 10 em. high or about 10 to 15 ee.
To this is added a few drops of the infected blood. The fluid is
covered with a layer of paraffin oil that has been autoclaved twice.
Ascitic fluid is not always suitable and it may be necessary to try
many lots.

The maximum growth is reached at about the fifth day, the cells
being fully developed typical spirochetes. After the fifth day de-
generation of the cells begins and proceeds slowly. The organism has
been demonstrated to remain virulent for chickens through 13 gen-
erations of culture. However, under certain cultural conditions it
may lose its virulence. The inoculation of birds with such aviru-
lent strains induces a resistance to subsequent infection with a viru-
lent strain.

Pathogenicity. Fowls, geese, ducks, guinea-fowls, turtle doves
and sparrows have been reported as susceptible. Animals com-
monly employed in laboratory work are immune, but Levaditi re-
ports that he produced a transitory spircchetosis in a rabbit lasting
three or four days.

Poultrymen, when spirochetosis occurs, are apt to attribute losses
to excessive tick infestation and to the resulting loss of blood with-
out recognizing that an infectious disease is the cause of the losses.

The prevalence of the disease will coincide with the season that
is most favorable to the multiplication of ticks, but deaths will oc-
cur at any time when susceptible stock is introduced, providing ticks
are at all active.

Bevan notes that birds in infected flocks become immune. How-
ever, the birds previously immune will succumb after the introduc-
tion of newly arrived susceptible birds starts the infection anew. It
is possible that the passage through susceptible birds increases the
virulence of the virus.

Upon introduction of infection into a flock hitherto uninfected,
spirochetosis may be exceedingly fatal and exterminate a flock in a
few days. Young birds are particularly susceptible.

The course of the experimentally produced disease varies accord-
ing to the method of the introduction of the virus, the activity of
the spirochetes and the receptivity of the bird. When the inocu-
lation is made by means of the tick, after 6 to 8 days and sometimes
more, the spirochetes are encountered in the circulation. If inocu-

SPIROCHETOSIS AND RARE INFECTIOUS DISEASES 137

lation is made with virulent blood through the skin, the period of
incubation is reduced to a period varying from 48 to 72 hours. The
period of incubation is longer when the virus is placed on the skin
superficially.

The disease is acquired easily through the mouth, especially if the
virulence of the parasite has been raised by a number of passages.

Symptoms. Very commonly the disease occurs in such an acute
form that birds apparently healthy at night are found dead under
the roost in the morning. In the less rapidly fatal form there is
dullness, ruffling of the feathers, somnolence and diarrhea. The
comb becomes pale as a result of anemia. The temperature reaches
110° or 112° F. but drops abruptly at the crisis, which coincides
with the disappearance of the spirochetes from the circulating blood.
During the course of the disease, there is a marked decrease in the
number of red corpuscles and a leucocytosis characterized by increase
in the number of polynuclear leucocytes. After the crisis, the poly-
nuclear cells diminish and the mononuclear cells increase in num-
ber. The acute type of disease may be terminated by death in from
four to five days. after the onset of symptoms. Death often occurs
during convulsions.

The chronic type may follow the acute phase or appear inde-
pendently. Death may not occur for fifteen days. Paralytic symp-
toms are noted. The wings may droop, or the head be twisted back,
or the legs may be involved. Inability to use the claws is an early
symptom of leg paralysis. There may be disturbances of gait, and
the bird may appear knock kneed or bowlegged. Emaciation and
anemia are also particularly characteristic of the chronic type.

Morbid anatomy. In birds dead of an acute attack, the spleen
is found to be enlarged to several times normal. The liver also is
greatly enlarged, shows fatty degeneration and sometimes focal ne-
crosis. The other organs do not usually show marked lesions beyond
the paleness of muscles, lungs and kidneys resulting from the ane-
mia. The intestines sometimes are congested, and show punctiform
hemorrhages. In chronic cases on the other hand, the liver and
spleen are smaller than normal.

The skin shows evidence of tick bites in the form of subcutaneous
hemorrhagic areas.

Micrescopic examination of the blood of a bird dead of the disease,
or during life after the crisis, will not reveal spirochetes.

Life cycle of spirochetes. After the spirochete in the blood
reaches a length of 16 to 19 microns it divides by a transverse divi-

138 DISEASES OF DOMESTICATED BIRDS

Pre

a ee

Fic. 14. Various stages in the flexions and transverse divisions of Treponema
(Spirocheta gallinarum). (Hindle)

b c

8

sion. This is accomplished only after a series of movements con-
sisting of doubling back on itself, coiling of the two portions, un-
coiling and eventual separation. The process is illustrated in Fig.
14, the successive stages of the process being indicated by the let-
ters a to h. Sometimes the separation occurs as illustrated in e,
but usually takes place after the position h is reached. Whether or
not transverse division takes place directly without previous flexion
has not been definitely determined. The act of uncoiling and sep-
aration as illustrated in d, f, and g of Fig. 14 very closely sim-
ulates a process of longitudinal division and has been erroneously so
interpreted by some observers. The process of transverse division
doubtless oceurs repeatedly in the blood.

Penetration of red blood cells and invasion by spirochetes has
been observed but seems to be uncommon.

At the time of the crisis of the disease, which is synchronous with
the disappearance of spircchetes from the circulating blood, some
spirochetes break up into a number of coccoid bodies in a manner
analogous to the formation of spores within a bacterial cell. It is
not certain that these coccoid bodies formed under the conditions in
question redevelop into spirochetes within the blood of the fowl.

Some of the spircchetes taken into the tick with a feeding of fowl
blood, penetrate the wall of the gut and gain access to the coelomic
fluid which occupies the body cavity of ticks. After a short time

SPIROCHETOSIS AND RARE INFECTIOUS DISEASES 139

DEVELOPMENT

FROM
COCCOID BODIES MULTIPLICATION
BY :
TRANSVERSE. DIVISION

b> | MULTIPLICATION OF

+") GOCcoiD BODIES

/ IN CELLS OF ARGAS

FORMATION OF

COCCOID BODIES

IN BLOOD
Pre aine OF

COCCOID BODIES
IN CELLS OF ARGAS

Fic. 15. The life-cycle of Treponema (Spirocheta) gallinarum illustrated dia-
grammatically. (Hindle)
the spirochetes further penetrate into various organs of the tick,
including the ovary and Malpighian tubules where they multiply
by ordinary fission. In the cells of these organs the spirochetes
break up into coccoid bodies. Other spirochetes remaining in the
lumen of the gut also form coccoid bodies. These circumstances re-
5

140 DISEASES OF DOMESTICATED BIRDS

sult in the infection of the Malpighian secretion and excrement with
coccoid bodies.

While the salivary gland has been considered with reference to the
part played by saliva in introducing infection into fowls, the obser-
vations tend to show that contamination of the tick-bite wound by
coccoid bodies in excrement and coxal fluid, is responsible.

Coecoid bodies are capable of development into the typical spiro-
chete by a process of gradual lengthening. This has been observed
in the ticks but not in the blood of a fowl.

The eggs of an infected tick contain coceoid bodies and the progeny
of such a tick is infective either by feeding on a fowl or when in-
gested by a fowl.

Ticks after feeding on infected blood are most liable to be in-
fective when kept at a temperature of 30-35° C. When ticks are
kept at 15-18° C., the spirochetes disappear from the alimentary
tract, and such ticks do not transmit the infection.

Differential diagnosis. ‘The various septicemias of fowls, more
particularly fowl cholera, might readily cause symptoms and lesions
simulating spirochetosis. Microscopic examination of stained blood
smears should furnish conclusive evidence by showing whether the
septicemia is caused by spirochetes or by bacteria. The limited
area of the United States in which ticks occur, see p. 221, should be
borne in mind.

Treatment. Dodd reports that % grain of soamin dissolved in
one ¢.c. of sterile water and injected intramuscularly, modified and
shortened the attacks with rapid and complete recovery. Uhlen-
huth gave atoxyl in an average dose of 5 centigrams at the time of
infection or two days later. It prevented infection or cured but
the blood remained infective.

Hauer concludes that salvarsan is capable of destroying spirochetes
in the body. The curative action of this substance is established
in all cases on the day of treatment and acts in a remarkable manner
even after the use of a limited amount of salvarsan. Even in cases
where the treatment was first given on the fourth day after infection,
when the bird was somnolent and when the blood was swarming with
spirochetes, one injection of the agent in not too small a dose led to
striking improvement and recovery. The immunity which salvarsan
confers upon birds protected with it, is of high degree and of long
duration.

Hauer experimented on fowls with a wide variety of doses of
the drug. The lowest lethal dose was found to be .3 gram and .15

SPIROCHETOSIS AND RARE INFECTIOUS DISEASES 141

gram was the maximum dose tolerated. The curative dose on the
second day of infection when spirochetes were observed in the blood,
varied from .02 to .003 gram per kilo of body weight. Even the
lowest dose caused the disappearance of spirochetes from the circu-
lation and the birds recovered. Birds treated on the third day of
infection received doses varying from .03 gram to .0025 gram per
kilo of body weight. The lowest dose that uniformly caused the dis-
appearance of the spirochetes was .005 gram per kilo. A dose of
.05 gram per kilo was effective when administered to birds on the
fifth day of infection. Aragaio recommends atoxyl in a dose of .03
gram, salvarsan .0035 gram and neosalvarsan in .0015 gram per
kilo of body weight.

Immunization. An attack of spirochetosis confers a certain
amount of immunity. The blood serum of such a bird possesses
strong immunizing properties and shows marked agglutinative action
in vitro.

Aragao induces immunity by injecting a vaccine prepared from
the blood of infected fowls. On the fifth day of the infection the
blood is drawn aseptically into flasks holding 300 c.c. each and de-
fibrinated by shaking with shot. Blood drawings from the various
fowls are mixed to secure a uniform distribution. The defibrinated
blood is distributed in quantities of 50 c.c. each in flasks of a ca-
pacity of 125 cc. The flasks are plugged with cotton which has
been dipped in formalin. The fluid is left thus exposed to the
vapor of formalin for eight days and is shaken occasionally during
that period. After carrying out suitable tests for sterility, it is m-
jected subcutaneously in one e.c. doses for immunizing birds be-
fore introduction into infected flocks. A similar product is pre-
pared by Aragio by mixing defibrinated blood and glycerine in equal
parts, omitting the formalin vapor treatment. It is used in two c.e.
doses and is preferred to the one prepared by using formalin. A
single injection is employed, for subsequent attacks by ticks in an
infected flock are relied upon to strengthen the immunity. In unin-
fected flocks where the vaccination is employed as a_ protection
against imported infection only, revaccination is recommended once
a year.

Marchoux and Salimbini have observed that the virulence of the
spirillum in blood is greatly diminished or lost after a period of about
48 hours. ‘They produce successful vaccination by using virulent
blood held for two to four days, or after heating at 55° C. for five
to ten minutes.

142 DISEASES OF DOMESTICATED BIRDS

Control of spirochetosis. The relation of fowl ticks to the
spread of the disease is so direct, that the destruction of ticks is of
necessity the first measure to be employed in combating the disease.
See p. 223. Fowls not infested with ticks, but lable to become
so, might be immunized with Aragao’s vaccine. Susceptible birds
before introduction into tick infected localities might be so im-
munized.

RARE INFECTIOUS DISEASES
RABIES

Several writers report the occurrence of rabies among fowls. Af-
fected birds show restlessness and great fright. The feathers are
ruffled and the bird attacks its fellows, other domestic animals and
even man.

Autopsy findings reveal no marked lesions. Injuries of the skin,
foreign bodies in the gizzard together with congestion of the kidneys
and intestines are conditions most frequently found.

The prophylactic measures indicated are isolation of birds during
outbreaks of rabies with slaughter of infected birds.

Intracranial inceulation of fowls with rabies virus causes paraly-
sis of the feet and neck, associated with uncertain gait.

FOOT AND MOUTH DISEASE

The ceeurrence of foot and mouth disease has been observed in
fowls, waterfowl and pigeons but a few times. The lesions have
been reported as occurring on the skin of the head, on the buccal
mucous membrane and about the feet.

Ehrhardt states that this disease is very rarely transmitted to
fowls from cloven hoofed animals, for birds show a very high re-
sistance to both natural and artificial infection. The disease is man-
ifested by the occurrence of vesicles on the appendages of the head,
on the mucous membrane of the mouth and throat as well as on the
feet. In waterfowl the lesions appear mostly on the webs of the
toes, and on the mucosa of the mouth and throat. In most cases the
course of the disease is favorable and the lesions heal spontaneously
in from eight to fourteen days without treatment. As a result of .
the cessation of eating, the affected birds appear weak and cease
laying. In severe cases lameness and fever are observed followed
by decline and death.

SPIROCHETOSIS AND RARE INFECTIOUS DISEASES 143

MALTA FEVER IN FOWLS

Dubois reports the occurrence of this disease in fowls. The out-
break lasted three months, with a mortality of 70 per cent.

Symptoms. Birds of all ages are affected. The disease pre-
‘sents two clinical forms: an acute or subacute form in which the
duration is 8 to 10 days at the most, and a fulminating form lasting
only a few hours.

In the acute form the affected birds appear feeble, walk with dif-
ficulty and display inappetence. After three or four hours the birds
stop moving and appear depressed. The wings drop, the birds
allow themselves to be caught easily, and sometimes show diarrhea
with green discharges. There is extreme emaciation at the last.

In the fulminating type few characteristic signs are observed.
There is only weakness and depression. Some birds die suddenly
without having shown symptoms.

Morbid anatomy. In the fulminating type the lesions consist
of ecchymoses on the lungs, a marked hypertrophy of the spleen and
a certain degree of congestion of the liver.

Inceulations made with the liver, the spleen, and heart blood of
sick birds have given negative results. Likewise, inoculation of
rabbit, guinea pig and pigeon with the pulp of the spleen and heart
blood of sick birds has always failed to affect these animals.

The writer determined the agglutinative properties against J.
melitensis possessed by the blood of the affected birds. Of 8 fowls
2—5 years old, 3 presented a positive reaction; of 9 birds 2-4 months
old, 5 gave positive reaction.

ANTHRAX

Dawson points out that chickens may contract anthrax by eating
the carcass of an animal dead of that disease. The disease runs a
rapid and fatal course within 24 hours. The affected bird shows
fever, high temperature, weakness, tremors and convulsions, together
with bloody fecal discharges. Swellings may occur on the comb, wat-
tles, sides of the head, in the mouth or on the feet.

Mollhoff concludes that birds are more or less susceptible to in-
oculation with anthrax. Exception is made in the ease of hens,
which in his experiments showed high resistance. Out of sixteen
hens exposed by subcutaneous, intramuscular and intraocular in-
jection, with doses as high as 2 cc. or by feeding, only one suc-

144 DISEASES OF DOMESTICATED BIRDS

cumbed. This bird before inoculation was observed to be highly
emaciated and anemic. Two geese receiving subcutaneous injections
of 4 c.c. resisted infection. Of 16 pigeons inoculated, 7 contracted
anthrax. Other birds such as ducks, sparrows, canaries, Jays, hawks
and crows, were very susceptible to inoculation. That writer makes
a distinction between susceptibility to anthrax by inoculation, and
susceptibility to the natural spontaneous infection. He knows of no
instance of the latter.

Mollhoff concludes that the resistance of the hen to anthrax con-
sists of action of the body fluids or lymph by virtue of strongly
bactericidal materials contained in them. The anthrax bacilli in
the subcutaneous tissues are killed in a short time by the bacteri-
cidal action of the lymph, so that no local development nor general
infection can occur.

The origin of this bactericidal material of the lymph, especially
with reference to whether or not it originated in the leucocytes,
could not be determined. Phagocytosis is not of decisive importance
in connection with the destruction of anthrax infection in the hen.
The resistance of hens against anthrax does not depend upon their
high body temperature.

Anthrax occurs in the ostrich as a common natural infection

and is discussed in Chapter XVIII.

REFERENCES

1. Aragdo. Espirochetose (treponemose) das Gallinhas. Rev. de Vet. e
Zootech. (Rio de Janeiro), Vol. 7, 1917, p. 3.

2. Bevan. Spirochetosis of fowls in Southern Rhodesia. J. Comp.
Path. and Ther., Vol. 21, 1908, p. 43.

3. Dawson. Anthrax with special reference to the production of im-
munity. U.S. Dep. Agr. Bureau Animal Indust. Bull. 13.

4. Dubois. La fiévre de Malto chez les poules. Rev. Vet., Vol. 67,
1910, p. 490.

5. Ehrhardt. Die Krankheiten des hausgefliigels. 3. aufl. Aarau: E.
Wirz. 1914.

6. Hauer. Untersuchungen iiber die Wirkung des Mittels 606 auf die
Hiihnerspirillose. Centralbl. f. Bakteriol. (Etc.), 1 Abt. Orig., Bd. 62,
1912, p. 477.

7. Hindle. On the life-cycle of spirocheta gallinarum. Parasitology,
Vol. 4, 1911, p.. 463.

8. Jowett. Fowl spirochetosis at Cape Town. Vet. Jour., Vol. 18,
1911, p. 240.

9. Mhrehoux et Salimbini. La spirillose des poules. Ann. de I’Inst.
Pasteur, T. 17, 1903, p. 570.

10. Mollhoff. Untersuchungen iiber die Empfanglichkeit des Gefliigels

SPIROCHETOSIS AND RARE INFECTIOUS DISEASES 145

fiir Milzbrand und iiber die Griinde der Resistenz des Huhner gegen diese
Krankheit. Inaug. Diss. Bern.

41. Noguchi. Cultivation of spirocheta gallinarum. J. Exper. M.,
Vol. 16, 1912, p. 620.

192. Pereira. A Espirochetose das Gallinhas. Rev. de Vet. e Zootech.,
Vol. VI, 1916, p. 327.

CHAPTER XIV
LEUKEMIA AND PSEUDO LEUKEMIA

Characterization. Leukemia in fowls is a disease of the blood,
and blood forming organs. It is marked by changes in the com-
position of the blood manifested principally by an enormous in-
crease in the number of leucocytes and an accompanying decrease in
the number of erythrocytes. Besides these changes, lymphoid en-
largement of the liver, spleen and kidneys is usually to be observed.
Pseudo leukemia is a term designating a condition in which lymph-
oid tissue is present in the various organs, without changes in the
circulating blood. The two conditions are very closely related, if in-
deed they are not different stages of the same process.

History. The disease in fowls was first recognized by Warthin
in 1907 and soon after by Ellerman and Bang. Butterfield in 1905
and Yutaka Kon in 1907 very likely observed cases of leukemia,
but did not examine the blood. Pickens presents a thorough survey
of the literature of the disease accompanied by original observations
on a series of cases. The disease has been reported in Denmark,
Germany and the United States.

Etiology. Ellerman and Bang and also Yutaka Kon found pro-
tozoa-like bodies in the organs and bone marrow of affected fowls.
The significance of these bodies has not been definitely determined.
In typical cases of leukemia encountered by the present writers, at-
tempts to isolate an organism from the blood and parenchymatous
organs have given negative results. The fact that Ellerman and
Bang succeeded in transmitting leukemia to fowls by intravenous
and intraperitoneal injection of a cell free filtrate of infected exu-
dates, points to an ultra-microscopie virus as the causative agent.

The disease is readily transmitted by non-filtered organ suspen-
sion. The virus is present in all affected organs, but the infective
properties of these organs are lost in a few days after death.

There are three principal theories as to the etiology of the dis-
ease in man which are reflected by various writers in the interpre-
tation of lesions in the fowl: 1. The lesions of leukemia are a
simple hyperplasia. 2. Leukemia is a neoplasm. (See lymphoma).

3. Leukemia is a result of the multiplication of an infective agent.
146

LEUKEMIA AND PSEUDO LEUKEMIA 147

Pathogenicity. Leukemia has not been reported as occurring in
pigeons, turkeys or guinea-fowls and experimental efforts have failed
to produce the disease in these birds. Fowls appear insusceptible to
subcutaneous inoculation but are infected in about 50 per cent of
cases through intravenous or intraperitoneal injection of a suspension
of the organs or of the blood of affected fowls. Ellerman and Bang
observed that inoculation may produce either leukemia or pseudo
leukemia.

Course. The duration of the disease is variable. The period of
incubation ranges from about 2 to 8 weeks. Death may result within
several days after the appearance of symptoms or may: be delayed
for one to three months. Recovery is only rarely observed.

Symptoms. While birds may die suddenly from an acute at-
tack, the manifestations of leukemia are usually of a chronic char-
acter. There is observed a progressive emaciation with dull, de-
pressed appearance and noticeable weakness. In some cases the
abdomen droops. The appetite generally remains good in the
chronic cases but may fail in acute cases. The comb, wattles and
skin are pale as a result of the diminution of the red blood cells and
increase of the white cells. Blood when drawn presents a pale red
color and fails to clot readily, while normal fowl blood clots very
rapidly.

Morbid anatomy. The carcass has an anemic appearance. Us-
ually the liver and spleen show the most marked changes. The kid-
neys are at times also severely involved. The liver may be slightly
enlarged, congested and sprinkled with minute whitish points, or it
may be markedly enlarged and congested. Not infrequently rupture
of the liver resulting in internal hemorrhage is observed. The en-
larged liver may appear much darkened, soft and pulpy in more
acute cases. In cases of longer duration, this organ is greatly en-
larged and pale in appearance or else mottled and sprinkled with
grayish white spots. It has a firm consistency and rigid contour.
On cut section the tissue appears bloodless. The spleen generally
shows changes in conformity with those of the liver. It may be
only slightly congested or may be greatly enlarged and congested.
As in the case of the liver, the consistency varies from soft and
pulpy to a firm, compact mass. The color is bright mahogany in
the case of severe congestion and sometimes grayish and brownish
in spots. The kidneys may be several times the normal size, con-
gested in the early stage or firm and pale at a later period. The
intestine appears pale on the serous surface but areas of congestion

148 DISEASES OF DOMESTICATED BIRDS

may be present on the mucous membrane, especially in the duo-
denum.

Microscopically, the blood is found to contain a greatly increased
proportion of leucocytes to red blood cells. The normal number of
leucocytes per cubic millimeter is approximately 30,000. This is
increased in leukemia to from 100,000 to 500,000 per cubic milli-
meter, while the normal number of red blood corpuscles, approxi-
mately 3,000,000 per cubic millimeter is reduced to nearly 1,000,000
per cubic millimeter. The normal proportion of about 1 white cell
to 100 red cells is thus changed to 1 to 2 or 1 to 8. The mononu-
clear leucocytes increase more rapidly than the polynuclear leuco-
cytes, or the smaller lymphocytes. Round nucleated red blood cells
representing normoblasts and megaloblasts are to be seen in stained
preparations. The hemoglobin content decreases from a normal
of 50-65° to 15-20°. The blood is pale red in color and clots with
difficulty. The liver, spleen and kidneys are found engorged with
leucocytes. These fill the smaller capillaries and occupy a peri-
vascular position in the parenchyma. ‘There is a hyperplasia of the
cells of the bone marrow and spleen, the latter being an important
source of the leucocytes which infiltrate the liver and kidneys. De-
generative changes are observed in the affected organs.

Diagnosis. The presence of the disease is indicated by the an-
emic condition of the fowl, the enlarged liver and spleen, and the
absence of a demonstrable microorganism in these tissues. This lat-
ter feature distinguishes it from bacterial septicemias in which the
liver and spleen may be swollen and congested. Microscopical ex-
amination of the blood is of the greatest value in differentiating from
other affections. In simple leucocytosis accompanying infectious
diseases, the proportion of white to red blood cells while at times ap-
preaching 1-25 is not as striking as in infectious leukemia. Also
the absence cf myelocytes is noted in the former disease. In leu-
kemia the white cells in the blood have approximately the following
percentage relation: Mononuclear 70 per cent, small lymphocytes
20 per cent and eosinophiles 6 per cent. The diagnosis cf pseudo
leukemia during life presents great difficulties.

Treatment. As in the case of other deep seated diseases of a
malignant type, treatment of individuals is unfortunately of question-
able value. There is no definite method of treatment known which
alters the course cf the disease so as to bring about recovery. Potas-
sium icdide in doses of 3 to 7 grams daily, and careful nursing to-
gether with the administration of tonics, such as gentian, nux vomica

LEUKEMIA AND PSEUDO LEUKEMIA 149

and iron, may be of benefit in mild forms of the disease. Arsenic
might also prove beneficial.

Prevention. In sporadic cases of leukemia, no special precau-
tions against the spread of the disease can be recommended other
than the usual precaution of isolating or destroying the sick bird.
Where several cases develop in the course of a few days, all birds
showing the slightest abnormal appearance should be immediately
separated from the flock. The droppings, litter, etc., should be re-
moved and the quarters thoroughly disinfected. The drinking water
may be medicated with permanganate of potash up to a 1—1000 so-
lution.

Pseudo leukemia. Ellerman and Bang regard this affection as
being indicated by the same lesions as the true leukemia. The en-
largement of the spleen and of the liver is often very noticeable.
The blood is not leukemic. They consider it very probable that this
disease has the same cause as true leukemia for cases of pseudo
leukemia are encountered in outbreaks of the true disease. Inocu-
lation of a hen with organs from a case of pseudo leukemia caused
alteration of organs, typical of leukemia, with a blood picture sug~
gesting the beginning stage of leukemia.

REFERENCES

1. Pickens. Leukemia and pseudo leukemia. Rept. N. Y. State Vet.
Col.'1915-1916, p. 226.

2. Ellerman u Bang. Experimentelle leukimie bei Hiihnern. (Cen.
tralbl. f. Bakteriol. (Htc.), 1 Abt. Orig., Bd. 46, 1908, S. 595.

3. Warthin. Leukemia of the common fowl. J. Inf. Dis., Vol. 4,
1907, p. 309.

CHAPTER XV
GENERAL DISEASES

GOUT

Characterization. Gout is a disease characterized by the in-
crease of uric acid content of the blood and the deposition of uric
acid salts in the joints as well as in various organs, especially on the
serous membranes. The disease apparently does not occur in birds
living free but is frequent in cage birds of zoological gardens and in
all sorts of domestic birds. Among these, hens are affected most fre-
quently, waterfowl less frequently, and pigeons least.

Etiology. Gout appears to depend for its causation, upon the
use of feeds rich in protein in the absence of which many breeders
believe that it will not occur. Furthermore, a one sided diet, close
confinement, lack of exercise and heredity appear to be predisposing
factors.

Two types of gout are recognized, a rare gouty arthritis and a
more common visceral gout.

Visceral gout. In visceral gout the serous membranes of the
chest and abdominal cavities are covered with a layer of uric acid
erystals of greater or less thickness. In the pericardium which is
affected with gout with greatest frequency, there is often a deposition
of a layer of uric acid salts 1 to 2 mm. in thickness.

Articular gout. This type preponderates in the joints of the
feet as well as in those of the wings. The joints are thickened and
inflamed, while the joint capsule shows a doughy swelling. Knotty
swellings varying in size up to that of a cherry, occur in the vicinity
and break outwards, discharging white or grayish yellow masses
which consist of uric acid salts.

Hebrant and Antoine describe a case showing unusually marked
articular lesions. The subject from which the legs were taken was
a cock two years old. The bird otherwise appeared in good health.
The feed had been corn and wheat. The subject could not walk for
it was unable to stand upon the feet.

The lesions consist of a number of tumors, some of which are as

large as a pea. They are particularly numerous on the inferior
150

GENERAL DISEASES 151

Fie. 16. Legs of cock showing lesions of articular gout. (Drawn from photo-

graph by Hebrant and Antoine)
surface of the digital region in the vicinity of the articulations.
Because of interference with circulation the tumors have a grayish
yellow color. Some of the tumors fluctuate and their appearance is
suggestive of peri-articular abscesses. On incision the tumors are
found to contain a whitish, creamy, pasty mass consisting of crystals
of uric acid. The majority of the tumors are located in the peri-
articular connective tissue and a small number communicate with the
articulation.

Gout produced experimentally. In order to determine what
influence is exerted by protein on nutrition and the occurrence
of gout, Kionka fed hens exclusively on horse meat that had been
minced, and freed completely from fat. They were allowed to drink
water as desired and soon became accustomed to the compulsory
diet. Within a period varying from three to fifteen months they
all became affected with gout appearing in three forms.

In every case at first the gait became uncertain and difficult and
the affected birds fell often while walking. In the first type of

152 DISEASES OF DOMESTICATED BIRDS

the disease the pain seemed to appear suddenly and on account of
it the bird crouched and stopped eating. This coincided with the
appearance of isolated gouty nodules. Gradually the periods of
pain became more frequent, the appetite was entirely lost and death
followed. The deposits of uric acid crystals in the joints were not
especially marked. In the second form the attacks of pain did not
appear in so typical a manner, but the nodules were larger and oc-
curred principally on the joint capsules and tendon sheaths of the
wings. The third type was visceral and the deposits were limited
principally to the serous membranes and the kidneys. The experi-
ment proves the dietetic origin of gout.

Diagnosis. The symptoms We the joint inflammation are dis-
tinct: occasional loss of appetite, swelling of the joints, disinclina-
tion to move. At other intervals, the appetite is good and the swell-
ings decrease. At last there is no eating, inability to move, ema-
ciation, rapid loss of strength and death.

Visceral gout cannot be recognized in the living bird.

Treatment. Operative treatment is of little use but may be re-
sorted to in valuable birds. ‘The joint tubercles should be opened
to evacuate the contents and an antiseptic dressing applied.

As soon as the cause of death is revealed by autopsy an appropriate
diet should be provided for the other birds kept under similar
conditions. The feeding of a rich proteid diet should be restricted,
with a fast of one day a week. Grain feed, abundant green feed
or roots should be provided.

RACHITIS

Characterization. The disease consists of disturbance of normal
bone formation of which the most prominent evidence is the deficient
deposition of calcium salts. While the course of the disease is not
well understood, it seems clear that it is caused by a general inter-
ference with nutrition. Deficiency of intake of lime is concerned.
Rachitis is a disease of young birds and seldom occurs in birds over
half a year old. It is limited almost exclusively to fowls and occurs
seldom in the turkey, waterfowl and pigeons.

Symptoms. The birds show exhaustion, difficulty in locomo-
tion, inappetence, diarrhea, paleness of the mucosee and emacia-
tion.

Morbid anatomy. Autopsy reveals intestinal catarrh and
lesions of the bones. The large bones of the extremities are bent as

GENERAL DISEASES 153

is also the breast bone which becomes S shaped. The present
writers conducted an autopsy on a young turkey in which the
skeleton was apparently wholly lacking in mineral constituents. The
larger bones could be bent with the fingers and sliced with a knife.
The bird was reported as being one of a number affected in a similar
manner.

Treatment. Normal feeding should be the first matter con-
sidered. Birds should be supplied with dry, warm quarters, with
access to grass if possible. Feed coarsely cracked grain, cracklings,
or meat meal and burned oyster shells. Calcium phosphate may be
administered in doses of .5 to 2.0 grams per bird, according to size.
Small amounts of sulphate of iron may be given by putting this ma-
terial in the drinking water in the proportion of one or two parts
per 1000 parts cf water. No treatment should be attempted on
those birds liable to become cripples. Such should be killed.

LEG WEAKNESS

Leg weakness is a term designating unsteadiness of gait, which
may be followed by total inability to stand on the legs. At first
the bird otherwise appears healthy, but soon shows the effeet of in-
ability to compete with its fellows for food. If the condition con-
stitutes paralysis, “limberneck” may also be observed. Leg
weakness also is observed in rachitis. It occurs in well fed young
growing birds under conditions not well understood. Under such
circumstances the ration should be reduced and green feed should
be supphed. At other times it occurs in closely confined birds kept
on a monotonous diet. In such cases trouble disappears when birds
have access to the soil with consequent variety of diet.

Polyneuritis of fowls, a condition induced by feeding polished
rice or similar products, is the one form of leg weakness, the etiology
of which is understood. The affection may be produced experi-
mentally in from fifteen to twenty-five days by feeding a diet limited
exclusively to polished rice, while a diet of natural unpolished rice
does not produce this result. The condition of the fowl designated
polyneuritis is generally regarded as identical with the disease of
man called beri beri, which latter is common among people living
almost exclusively on polished rice. It is evident that the rice hull
contains substances, the absence of which induces neuritis. These
have been designated vitamines.

Vitamines of this character are not restricted to rice. It has

154 DISEASES OF DOMESTICATED BIRDS

been demonstrated that they are found in a large number of natural
foodstuffs. They are very common in the seeds of plants such as |
cereals. In these, the vitamines are mainly deposited in the germ
or embryo and to a less extent in the bran. White wheat flour is
deficient in vitamines and is capable of producing polyneuritis.

The facts observed during experimentation on fowls in connection
with the study of the etiology of beri beri of man, suggest the possi-
bility that in isolated instances, leg weakness of chickens may be
induced by a similar cause.

LIMBERNECK

Limberneck is a symptom resulting from partial or complete loss
of control of the muscles of the neck. Probably various causes such
as. digestive disturbances, intestinal parasites and the eating of
spoiled meat may cause this symptom. Feeding on maggots from
decaying meat will cause limberneck.

According to Dickson, chickens when fed botulinus toxin, become
dull and inactive, refuse to eat, remain quiet in one place with the
feathers ruffled. They gradually develop weakness of the legs, wings
and neck so that they are unable to stand. The wings droop and the
beak or the side of the head rests upon the floor of the cage. Death
oceurs within 24 hours after feeding.

Treatment consists of administering castor oil. Preventive meas-
ures should include precautions against allowing birds access to de-
caying meat.

DISEASES OF THE ALIMENTARY TRACT

PrP

The condition commonly termed “ pip” does not represent a spe-
cific disease, but is usually found associated with avian diphtheria.
When the nasal passages become closed by the presence of mucous
secretion or exudate, the fowl is compelled to breathe through the
mouth. The constant passage of air over the tongue tends to dry
and harden it at the tip. The dry, horny covering contracts and
presses upon the soft tissues beneath, causing the fowl much annoy-
ance. The hardened layer may partially separate from the soft
tissues and expose a raw, inflamed surface. The practice among
some poultrymen of removing the horny tip should be discouraged
since it only increases the discomfort of the fowl by leaving a raw,
sensitive surface exposed to foreign irritants and microorganisms.

GENERAL DISEASES 155

To alleviate this condition the primary cause should be removed.
An effort should be made to keep the nostrils open by removing exu-
dates and syringing the parts with an antiseptic solution such as 3
per cent boracie acid or 2 per cent permanganate of potash. If the
disease which is responsible for “ pip” is successfully treated the
condition will disappear.

When the symptom is noticed it is advisable to rub the tongue with
some substance such as vaseline, cottonseed oil or glycerine.

THRUSH

Thrush or soor has been observed to affect the mouth and crop
of fowls, pigeons and turkeys. The
affection is characterized by the for-
mation of grayish white or yellowish
colored patches adhering to the mu-
cous membrane without inflammatory
changes in the latter. Severe involve-
ment causes death. The organism
causing the infection is designated O7d-
ium (Saccharomyces) albicans. 'Treat-
ment of oral lesions may consist of the
application of bichloride of mercury in ;
4 solution of 1:1000. The crop May a. 17. Oidiwm albicans. a, eyl-
be irrigated with boric acid solution as _ indrical mycelium; b, spore; ¢,
in ecatarrh of the crop. Authoritative ‘Pithelial cells
reports of the occurrence of the disease in fowls are rare.

9)
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CATARRH OF THE CROP

This is a mild inflammation of the lining membrane of the crop
due to excessive irritation by ingestion of material of an irritating
nature, or by the products of fermentation when food for one reason
or another, stays in the crop for an unusual length of time. It
occurs in cases of impaction and may also be associated with certain
infectious diseases. Parasites at times may cause the condition.

Symptoms. The crop is usually distended with food or gas.
The fowl appears sluggish and the appetite is diminished or lost.
Occasionally the beak is opened wide as if to catch the breath or as
if attempting to vomit. The head and neck also describe tossing
movements. Later a gray, sour, ill-smelling fluid is discharged from

156 DISEASES OF DOMESTICATED BIRDS

the beak or from the nostrils. Without treatment the strength of the
subject fails rapidly.

When the disease has existed for some time in a chronic mild form
it may assume the condition designated hanging crop. In such cases
the musculature of the crop has been overstretched, so that after
recovery from the ecatarrh, the organ does not return to its normal
position.

Treatment. This consists of the removal of the contents of the
crop as soon as symptoms are noticed. If the contents are soft the
fowl may be held head downward and the crop manipulated in such
a manner that the material will be passed back through the esophagus
to the mouth. This is relatively easy owing to the large diameter of
the esophagus of fowls. Should the crop contents be hard or dry
they may be softened by giving the bird several teaspoonfuls of water
before attempting to remove the material. When the crop is empty,
administer 1 teaspoonful of castor oil. Feed should be withheld for
about 24 hours, but buttermilk, or sour milk may be freely given
together with water. A small amount of bicarbonate of soda may
be administered and the bird should have access to charcoal in case
fermentation is noticeable. Fowls showing frequent attacks or
chronic catarrh of the crop should not be retained.

IMPACTION OF THE CROP

Feeding with dry grains such as corn, peas, oats, or with bran
may cause a distention of the crop. Various foreign bodies may
cause the same condition. The enlargement of the organ will first
attract attention. If not remedied, the condition will cause death
of fowls in a few days, and in waterfowl in a few hours, because
of pressure on the trachea. Massage may permit the removal of ma-
terial through the beak, but usually incision of the crop is indicated.

INFLAMMATION OF THE CROP IN PIGEONS

The crop of the pigeon secretes a milk-like fluid for the nourish-
ment of the young. If the parent birds lose their young while the
crop is secreting this fluid, an inflammation of the crop glands
frequently results and the organ feels hard and solid. The disease
may be quickly remedied by substituting another squab. Only one
should be substituted for often pigeons will not adopt two young
ones, but kill them and throw them out of the nest. Besides, if two

GENERAL DISEASES 157

were taken, the parents thus robbed of their young, would develop
the same trouble. If such a procedure is not possible, the sick ones
should be isolated without food. They may be allowed water slightly
acidulated with vinegar. If abscess-like lesions occur on the breast
they should be opened.

GASTRITIS

Gastritis is an inflammation of the mucous membrane of the pro-
ventriculus or first stomach. It may result from digestive disturb-
ances but is generally associated with the presence of strong irritants
such as certain mineral poisons, or with infectious diseases of a
septicemic type. Inflammation of the crop may extend to the pro-
ventriculus. In itself, it is not of great importance.

Symptoms. The diagnosis of gastritis is difficult. If no symp-
toms of disease are noticed other than a loss, of appetite and a slug-
gish appearance, simple gastritis may be suspected. When associated
with other diseases the symptoms which accompany these will be
observed.

Treatment. The affected fowl should be given 2 teaspoonfuls of
castor oil to which 10 drops of oil of turpentine have been added.
Feed lightly for a time. Buttermilk or sour milk may be freely
given. Give 30 drops of tincture of gentian twice daily.

INDIGESTION

Mégnin distinguishes four sorts of indigestion in birds. It may
result from lack of quality or appropriate volume of food or by
ingestion of foreign bodies. Thus pigeons which naturally are
granivorous will suffer if circumstances necessitate their consum-
ing herbage. Birds in zoological gardens are liable to suffer from
lack of appropriate food. Storks, herons, swans, geese and ducks
in the winter and spring failing to obtain their natural food such as
molluses, slugs, ete., attempt to cheat the appetite with plants or
aquatic mosses. These materials are to them true foreign bodies
which cause fatal indigestion. It is the same in the case of the
small insectivorous or semi-insectivorous birds. When it is at-
tempted to feed them exclusively on grains or vegetable mashes they
succumb to the diet.

Grains too large for the digestive organs of a bird act like a for-
eign body and cause fatal indigestion. Parroquets and young pheas-
ants may be killed in this way by grains of maize.

158 DISEASES OF DOMESTICATED BIRDS

Overloading the digestive organs is a second general cause of indi-
gestion. Dry grain which is inviting to certain birds like the
gallinaces is less suitable to others such as palmipeds which are ac-
customed to soaking their food in water. Thus such birds may
readily overload their stomachs with dry grain which may swell and
cause death.

Indigestion may be caused by lack of silicious gravel in the giz-
zard. This material is indispensable to granivorous birds to tritu-
rate the grain in that organ. Omnivorous birds likewise need grit.
In the absence of such material, trituration is not accomplished and
grain accumulates in the gizzard. Thus death may be caused by
indigestion occasioned by repletion, or whole grains may pass into the
intestine and cause a fatal inflammation. This may occur among a
large number of birds. The present writers have observed severe
enteritis in a wild goose occasioned by heavy snowfall and prolonged
freezing of a pond, which circumstances prevented access to grit. In
the absence of grit of suitable size, birds will attempt to swallow
articles entirely too large, with fatal results.

There is in the opinion of Mégnin, an indigestion resulting from
lack of food, or disease of hunger. Domesticated birds may acci-
dentally be deprived of food or may be prevented from eating by
stronger companions.

Indigestion in birds is rarely recognized during life and is only
encountered at autopsy. That caused by overloading may be recog-
nized and treated with a little olive oil. Prevention along the line
of providing suitable food and grit must be relied upon chiefly.

INDIGESTION IN PARROTS

The affection may result from a variety of causes such as improper
feeding and failure to provide grit which impairs the natural
function of the gizzard. The affected bird yawns, displays loss of
appetite and occasionally manifests nervous symptoms. Correction
of feeding is of first importance. Castor oil in a dose of from 5 to
10 minims may be administered. Bicarbonate of soda in 5 grain
doses may be given in the drinking water for several days. Nux
vomiea is indicated.

ENTERITIS

Enteritis is an inflammation of the mucous membrane of the in-
testine. It is perhaps the most common symptom observed in con- |
nection with poultry diseases.

GENERAL DISEASES 159

Etiology. Enteritis is associated with a large number of impor-
tant diseases. It varies in the intensity of the inflammation with
different affections. In fowl cholera, fowl plague and several other
septicemias the inflammation is very severe, while in fowl typhoid
and infectious leukemia the mucous membrane may show little or no
congestion. Enteritis is associated with such protozoal diseases as
coccidiosis and infectious entero-hepatitis, and with intestinal worm
infestation.

Mineral poisons may set up an inflammatory condition, as may
also moldy or putrid food.

In birds deprived of grit, the food passes from the gizzard with-
out being triturated and causes severe enteritis with hemorrhage into
the lumen of the intestine.

Symptoms. The most prominent symptom of enteritis is diar-
rhea. The droppings may be watery or semi-solid. The color
varies according to the particular disease which is present. It may
be white, brownish, greenish, yellowish or mixed in color. The fowl
displays a loss of appetite in the more severe forms of enteritis, be-
comes droopy, weak and somnolent. Paralysis of the legs frequently
occurs in connection with inflammations of the intestine. Unusual
thirst is often in evidence.

Treatment. As enteritis is usually associated with some more
important disease, the disease should be properly diagnosed and
treated. Simple enteritis due to minor causes may be treated by re-
moving the irritating substances from the intestinal tract by means
of a purgative such as castor oil in 2 teaspoonful doses or Epsom salts
in 44 to % teaspoonful doses. A tonic consisting of powdered gentian
1 dram, powdered ginger 1 dram and powdered sulphate of iron 15
grains may be given. Mix /4 teaspoonful in the feed twice daily.
The water for the entire flock may be made antiseptic by the addition
of *%4 oz. of earbolie acid to the gallon of water. This will tend to
prevent the spread of infection to others of the flock in the event that
the affected bird or birds are harboring an infectious disease. The
carbolic acid treatment may be discontinued after a few days in the
event that no more fowls are attacked.

SIMPLE DIARRHEA

Fowls are sometimes affected by a diarrhea which is not appar-
ently associated with one of the more important diseases. A watery
or semi-fluid discharge may result from an irritation or derangement

160 DISEASES OF DOMESTICATED BIRDS

of the intestine independent of the action of infectious organisms.
Among the causes which may produce a catarrhal condition of the
intestinal mucous membrane and result in simple diarrhea are diges-
tive disturbances of an obscure nature, sudden changes in the feed
or an unusually large supply of green feed, too much meat scrap,
especially irritating substances in the feed, moldy grains or decom-
posed flesh. Mineral or other irritants which are not taken in suf-
ficient quantity to cause poisoning or enteritis may produce a simple
diarrhea. Fermentation of the contents of the intestine may result
in diarrhea.

Treatment. The cause of simple diarrhea being direct intestinal
irritation, the obvious remedy is to remove the cause. Where only a
few birds are affected they should be given 2 teaspoonfuls of castor
oil each. The entire flock may be given Epsom salts if necessary,
in the proportion of 43 to % teaspoonful to each grown fowl. The
salts may be dissolved in water and mixed in a mash to be fed early
in the morning. If suspicion points to the feed as the cause of diar-
rhea it should be changed or fed in smaller amounts combined with
other feeds.

CONSTIPATION

This is apparently not a common ailment of fowls. It does, how-
ever, occur to some extent in fowls confined in small quarters for
long periods with insufficient exercise. Lack of green or succulent
feed also tends toward constipation. Following diarrhea there may
be a temporary or slight constipation. The condition in young chicks
suffering from white diarrhea known as “ pasting up behind ” can-
not be considered a true constipation since the droppings are merely
held back by the drying of the discharges in the down surrounding the
vent. owls allowed free range, or large runs and properly fed are
practically free of constipation.

Treatment. The condition may be relieved by administering
substances which will cause an increased secretion of fluid from the
intestinal mucosa, or increased peristalsis. Two teaspoonfuls of
castor oil or 73 to % teaspoonful of Epsom salts to each affected bird
would be indicated.

Gage and Opperman have determined the dosage of Epsom salts for
birds of various ages as follows:

GENERAL DISEASES 161

Age Dose
1 to 5 weeks 10 grains
5 to 10 weeks 15 grains
10 to 15 weeks 20 grains
15 weeks to 6 months 30 grains
1 year and over 40 to 45 grains

To facilitate figuring quickly the number of ounces required for
treating a number of birds they furnish the following information
concerning equivalent weights:

1 pound avoirdupois equals 7000 grains.

1 ounce avoirdupois equals 437.5 grains.

1 pound Troy or apothecary equals 5,760 grains.
1 ounce Troy or apothecary equals 480 grains,

The constipation may be due to obstruction by foreign bodies, to
worms in the intestines, or to matting of feathers over the cloaca. In
the latter condition, softening of the mass and removal of the obstruc-
tion is first in order. After removal of the material in the cloaca,
rectal injections of soapy water or olive oil may be made. In very
small birds a probe wet with glycerine or castor oil may be in-
serted in the rectum.

DISTENTION OF THE BURSA OF FABRICUS

Occasionally the bursa of Fabricus may become enormously dis-
tended into a cyst-like structure containing a clear, colorless fluid.
Schantyr has observed two cases in which the fluid amounted to over
700 c.c. He observes that when an exploratory puncture is made
in case of distention of the abdomen with fluid, a yellowish fluid in-
dicates ascites, while a colorless fluid indicates hydrops of the bursa
of Fabricus.

DISORDERS OF THE LIVER

Disorders of the liver such as enlargement, fatty degeneration,
jaundice and the occurrence of various sorts of diseased areas in
the organ cannot be classified as separate entities. In most cases,
liver lesions merely consist of a portion of the lesions characteristic
of the common infectious diseases. Various septicemias, tuber-
culosis, entero-hepatitis, leukemia and tumors may display more or
less characteristic lesions in the liver. Perhaps under some condi-
tions hypertrophy or enlargement of the organ may be due to heavy

162 DISEASES OF DOMESTICATED BIRDS

feeding under close confinement as occurs among fowls fed on corn
in the winter.

DISEASES OF THE RESPIRATORY TRACT
BRONCHITIS

Fowls are quite frequently affected by a catarrhal inflammation of
the mucous membrane lining the air passages of the throat and lungs.
This condition usually results from the extension of inflammation
from the mouth and nasal chambers. Often birds which have recoy-
ered from avian diphtheria are observed to be affected with bron-
chitis. This may persist for a short time or become chronic.

Symptoms. In severe cases the fowl displays a marked difficulty
in breathing. The neck is more or less straightened out to facilitate
the passage of air. The breathing is noisy and the fowl may gasp
in a manner similar to that shown by a chicken affected with gapes.
The beak may be kept open, and a mucous discharge is given off
through the mouth. The bird is observed to make efforts to dislodge
this discharge by shaking the head.

In less severe or chronic bronchitis the symptoms are not so notice-
able. There may be only slight difficulty in breathing, accompanied
by a wheezing sound. The mucous membrane of the bronchi and
trachea becomes thickened and may show patches of yellowish exu-
date especially in the two large bronchi.

Treatment. Since bronchitis is often attributed to exposure to
cold draughts and dampness these conditions should be corrected.
Affected birds should be placed in warm quarters, free from air cur-
rents. Under good hygienic surroundings the attack may pass off
in a short time. In acute cases the administration of 5 drops of
wine of ipecac is beneficial. In chronic bronchitis treatment is not
satisfactory. .

CONGESTION OF THE LUNGS

The lungs may become congested as a result of the extension of
an inflammation from the larger bronchi into the minute air tubes
and air sacs. The congestion is generally of an acute type. It may
be induced by the fowl becoming wet and severely chilled. In the
early stages of pneumonia congestion of the lungs is the most marked
symptom.

Symptoms. Simple congestion is differentiated from pneumonia
on post mortem examination by the bright red appearance of the

GENERAL DISEASES 163

lungs in the former and by the fact that pneumonic lungs are hepa-
tized and will sink when placed in water. Affected birds show a
distressed appearance and breathe with difficulty. The respirations
are short and panting. The discharge and wheezing observed in
bronchitis are absent. The normal temperature of 107° to 108° F.
is raised 2 or 3 degrees. The birds have an increased thirst. Evi-
dence of pain is produced by pressure on the ribs over the lung area.

Where both lungs are affected death may follow shortly after the
onset through pressure on the air cells resulting in a shutting off of
the air supply and suffocation. In less severe cases the congestion
may subside or the condition may develop into pneumonia.

Treatment. ‘The bird should be placed in warm quarters and
given a diet consisting largely of green food. One third to one half
teaspoonful of Epsom salts dissolved in water should be administered
once a day for two or three days. Also give 10 drops of spirits of
nitre twice daily.

PNEUMONIA

Characterization. Pneumonia of fowls is of relatively rare oc-
currence in the classic form distinctive of this disease in other ani-
mals. The disease is sporadic in character and frequently only one
bird in a large flock may be infected.

Etiology. Pure pneumonia cases which have come under the
observation of Gallagher have been due to the presence of the
pneumococcus. It has the characteristic diplococcus form on micro-
scopic examination and is similar in its cultural characteristics to
the pneumococcus of Frankel. Its infrequent sporadic invasion sug-
gests that the fowl is normally resistant, and that predisposing causes
of an obscure nature are responsible for its pathogenicity in certain
individuals.

Symptoms. The most characteristic symptoms are more rapid
breathing with physical signs of distress and general malaise.
There may be a mucous discharge from the nostrils, and the tempera-
ture is elevated. As the disease progresses, the comb assumes a
darker color at the tips, or rear, or in hanging combs at the more
dependent portions. This darkened appearance progresses with the
disease and practically the entire comb may assume a purplish color
due to lack of oxygen in the circulating blood and weakened heart
action. In fatal attacks, the strength fails rapidly and the bird
reaches a comatose condition in which it may linger for several hours
before death.

164 DISEASES OF DOMESTICATED BIRDS

Morbid anatomy. In the normal fowl, on post-mortem examina-
tion, the lungs are found deflated, fairly compact and closely applied
to the ribs. They occupy less volume relatively, than is the case in
other animals. This is, no doubt, due to the peculiar respiratory
system of birds which has, in addition to the lungs, a number of air
sacs in the pleural and abdominal cavities, and also air canals in
the larger bones. In a pneumonic condition the lungs are distended,
darkened and solidified to a greater or less degree, approaching the
condition known as red hepatization or liver consistency. They will
sink in water, while normal or simply congested lungs will float.
The pneumonic lung stands out in a firm position surrounding the
heart and may be found adhering to the pericardial sac. There are
usually no visible areas of necrosis, but the bronchioles and larger air
tubes are filled with an emphysematous mucous discharge.

Treatment. Owing to the fact that pneumonia is induced by the
presence of organisms in the lung tissues, and that these cannot be
reached by disinfectants which would not destroy the sensitive mem-
branes of the air cells, treatment has been found futile in most cases.
During the early stages, or in milder cases, stimulants such as strych-
nine in doses of %o to Y%o gr., or 50 per cent alcohol in quantities
of % dram may be given by way of the mouth. Because of the
dense breast muscles, local external applications are not indicated.
The patient should be placed in quarters where the temperature ap-
proximates 70° F. and soft mashes, or sweet or buttermilk given as
a food. Since the disease is sporadic in a flock, no special prevent-
ive measures are necessary to guard against its spread.

DISEASES OF THE OVIDUCT
INFLAMMATION OF THE OVIDUCT

The oviduct may be highly congested or inflamed as a result of the
condition known as “ egg bound,” prolapse, or the presence of ac-
cumulated egg material which has been arrested by a tumor forma-
tion in the wall of the oviduct. Organisms which gain access to
the oviduct find a favorable medium for development in such ma-
terial. They give rise to decomposition products which irritate the
mucosa of the organ and set up an inflammatory condition. Broken
egos in the oviduct or excessive effort in laying may lead to inflam-
mation. The oviduct may become affected through the spread of
inflammation from the ovary or other adjacent organ or it may be
involved with other organs in certain generalized diseases.

GENERAL DISEASES 165

Symptoms. Where the inflammation is confined to the oviduct
no general change in the appearance may be apparent except in
severe cases. A tendency of the fowl to make efforts to lay at fre-
quent intervals is often noticed. Eggs which are abnormal either
in their structure or form may be passed. These may be blood
stained. Most frequently the eggs are small and contain only al-
bumin. Shell-less eggs are also laid. In fatal cases the fowl ex-
hibits symptoms of general debility, with loss of appetite, pale comb
and leg paralysis.

Treatment. When symptoms are apparent an effort should be
made to locate the cause of the trouble. Manipulation with the
finger through the cloaca or over the abdominal wall may disclose the
presence of an obstructed egg, broken egg or egg concretion which
may be removed after the manner described for the treatment of
“eoo bound.” The fowl should be isolated, given green food, soft
mashes and 4% teaspoonful of Epsom salts.

RUPTURE OF THE OVIDUCT

In severe inflammation of the oviduct when a large mass of egg
concretion is present, or an attempt to pass an egg of large size is
made, the wall of the oviduct may be split allowing the mass or egg
to pass into the peritoneal cavity. Other eggs or egg material
may follow through the opening and accumulate in the cavity.
These later induce peritonitis, or the rupture may heal and the ovi-
duct continue its normal activities.

The condition would be suspected by the sudden suspension of
laying accompanied in many cases by a rapid increase in the size of
the abdomen. Manipulation would disclose the presence of abdomi-
nal egg concretions or accumulated eggs.

Rupture of the oviduct is of comparatively rare occurrence.
Treatment if advisable would be by surgical means.

EGG BOUND

This condition is of frequent occurrence in fowls, especially in
young pullets. It represents an inability on the part of the bird to
pass the egg in the normal manner from the oviduct, or cloaca.
This failure may be due to an inflammatory condition, stricture, or
tumor formation in the posterior portion of the oviduct, or cloaca,
or to prolapse of the oviduct. In pullets which are beginning to
lay, however, the usual cause is the undeveloped state of the egg

166 DISEASES OF DOMESTICATED BIRDS

passage which has not yet become sufficiently dilated to accommodate
egos of large size. Mature hens may become egg bound through at-
tempts to pass malformed, or double yolked eggs. It is generally
noted that the first eggs of the pullet are elongated and of smaller
diameter than those delivered after laying has become well estab-
lished. Also the first eggs frequently show streaks of blood indicating
the difficult passage through the last portion of the oviduct or through
the vent. Cross breeding which unites a breed of large egg type with
one of a smaller egg type would be conducive to the formation of a
large ege for which the egg passage might not be developed in
proportion.

Symptoms. The affected hen is observed to be restless, leaving
the others and going frequently to the nest to make attempts to lay.
The effort after a time results in an inflamed condition of the oviduct
and cloaca. The condition often results in an eversion or prolapse of
these organs. The distress of the fowl and the extruded, inflamed
parts may attract other fowls. These begin to pick at the mem-
branes and if the victim is not rescued in time a large portion of the
intestine may be torn away and dragged through the vent causing
the death of the bird. Where prolapse has not occurred the affected
fowl may continue to make an effort to lay the egg until successful
or overcome by weakness.

Diagnosis. The presence of an egg in the oviduct may be de-
termined by palpation of the posterior abdomen or exploration
through the vent.

Treatment. Several methods of treatment are practiced. The
fowl may be held vent downward over steaming water for a time
and then placed upon the nest. The steam has a tendency to relax
the parts and make easier the voiding of the egg. Lubricating the
vent and cloaca with sweet or linseed oil may also aid the fowl in
mild cases of egg bound. However, the quickest and surest method
is the removal of the egg by the following procedure. The hen is
held by an assistant with her back downward, while the operator
passes the forefinger through the vent and pushes aside the mem-
branes until the egg shell is felt. With the fingers of the other hand
pressing on the external wall of the abdomen the egg is forced toward
the vent, being guided along the inflamed membranes of the egg
passage by the inserted finger. When the shell is visible through the
vent it is punctured by means of a sharp pointed instrument such
as a knife or awl. It is broken into small pieces with a pair of
forceps or with the finger and is removed with its contents. The

GENERAL DISEASES 167

patient should be isolated and the inflammation reduced by fre-
quent injections of cold or ice water into the cloaca.

Fowls which have suffered from egg bound due to the presence of
a large egg or to tardy development of the egg passage are not perma-
nently affected. Ege bound due to pathologie alterations in the
oviduct is not open to practical treatment.

PROLAPSE OF THE OVIDUCT

Eversion of the oviduct is usually associated with difficulty in lay-
ing as in the condition known as “egg bound.” The mucosa of
the extruded cloaca and oviduct becomes highly congested. The pro-
lapsed organs are observed as a dark red or purplish mass projecting
through the vent. The affected fowl is soon noticed by the others of
the flock and if it is not rescued in time it will be attacked and de-
stroyed as a result of the protruding tissue being torn away and
devoured.

As soon as the bird is discovered it should be placed by itself and
earefully treated. The oviduct should be explored with the finger,
which should be greased or oiled, to locate an egg or other cause. If
an ego is present it may be removed as described for ‘‘ egg bound.”
The prolapsed tissue is carefully returned through the vent, after
which cold water is injected to reduce the congestion and promote
the contraction of the oviduct wall. This may be continued for
some time or repeated at frequent intervals until a cure has been
effected.

VENT GLEET

Characterization. Vent gleet or cloacitis is an inflammatory
disease of the vent and cloaca of fowls. It appears to be spread en-
tirely by coitus and may be considered an infectious venereal disease.
Its causative agent has not been determined.

Symptoms. In the early stages of the disease there is a conges-
tion of the membrane of the posterior portion of the cloaca and mar-
gin of the vent. This may extend to the lower portion of the oviduct
and rectum. The fowl exhibits signs of severe irritation, frequently
voiding small droppings. A watery discharge which later becomes
purulent and foul smelling is passed out through the vent. The skin
around the vent becomes swollen and reddened and an offensive odor
is usually present. The irritation causes the fowl to peck at the
part. Other fowls may be attracted by the discharge, and the red-
dened appearance of the affected region and may peck at the skin

168 DISEASES OF DOMESTICATED BIRDS

causing an ulceration of the surface. Frequently the diseased fowl
dies as a result of the tearing of the cloaca and rectum by its canni-
balistie mates. The presence of the disease in a flock causes a
marked falling off in the egg yield and a decrease in the fertility of
the eggs.

Treatment. Vent gleet is very resistant to treatment. It is
usually better to destroy the diseased bird than to attempt treatment.
This is especially so in the case of the first birds attacked as by this
means its spread may be prevented. Where treatment is desired the
affected birds should be isolated. The discharge may be removed
from the skin and feathers by washing with warm water. Anti-
septics such as 5 per cent carbolic acid, or 1-1000 corrosive sublimate
are to be applied to the external affected area, or a 2 per cent car-
bolic ointment may be rubbed over the part. Argyrol in 15 per cent
solution or cresol in 2 per cent solution may be injected into the
cloaca twice daily. Roosters should be removed from the flock
while the disease is present and if any are found diseased it would be
advisable to destroy them.

STRUCTURE OF THE FECUNDATED EGG OF THE FOWL

The ovum or yolk on its release from the ovary and entrance to the
oviduct appears as a yellowish ellipsoid body about one inch in diame-

Fic. 18. 1, air sac; 2, shell; 3, white yolk; 4, blastoderm; 5, yellow yolk ; 6,
dense albumin; 7, chalaziferous layer of albumin; 8, fluid albumin; 9,
chalaza; 10, shell membrane. (Original)

ter. It is somewhat flattened on one surface, which presents an
opaque whitish circular spot, the germinal dise (Fig. 18). Cell

GENERAL DISEASES 169

multiplication is already taking place in this disc, from which the
embryo develops. The yolk is composed of a central light colored
portion (Fig. 18) and an outer mass colored a deeper yellow. The
latter is formed of concentric layers showing different stages of yolk
deposit (Fig. 18). The germinal dise and yolk are surrounded by
a thin strong vitelline membrane (Fig. 18). The ovarian ovum on
entering the oviduct is passed along by peristaltic movement in a
rotary course to its completion in the uterus or shell secreting por-
tion. In the anterior portion of the oviduct the membrane chal-
azifera is applied over the vitelline membrane. It consists of a
dense layer of albumin and gives rise to the two chalazee which ex-
tend from each pole of the ovum. These strands become twisted in
opposite direction during the further passage of the ovum through
the oviduct. Over the chalaziferous membrane are several albumi-
nous layers secreted by the glands of the oviduct. When the ovum
enters the isthmus or narrow portion two egg membranes are secreted.
These become separated at the large end of the egg as air is absorbed.
The shell is acquired in the uterus.

FOREIGN BODIES IN EGGS

Eggs may contain a variety of foreign bodies such as pebbles, frag-
ments of plants, feathers, roundworms, ete. Such bodies after gain-
ing access to the cloaca penetrate the oviduct far enough to encounter
an egg and thus be included within the shell.

Otherwise normal eggs have been found to contain such parasites
as the fluke Prosthogonimus ovatus and the roundworm Ascaridia
perspicilum. The latter worm may be present surrounded by al-
bumin in an abnormal egg lacking a yolk. It is apparent that under
such circumstances the presence of the worm has stimulated the secre-
tion of the albumin. Tapeworms and segments of the same have been
found in eggs. The parasites found in eggs evidently have migrated
into the oviduct for a sufficient distance to meet a developing egg and
to become enclosed in shell. Parasites of microscopic size such as

coccidia, amebee, aspergillus fungi and bacteria have been demon-
strated in eggs.

BLOOD SPOTS IN EGGS. (LIVER SPOTS)
It frequently happens that streaks of blood, or clots of varying size
are found in eggs. This abnormality is especially noticed during the
heavy laying period. At such time the ovary is plentifully supplied

170 DISEASES OF DOMESTICATED BIRDS

with blood to promote the rapid formation of ova. As an ovarian
follicle ruptures to release an ovum some blood may escape from a
ecngested blood vessel of the follicle. The blood passes into the
oviduct aleng with the ovum where it becomes surrounded by al-
bumin and is incorporated in the egg. The size of the spot or clot
depends upon the amount of blood which has escaped. ‘These clots
are often taken for pieces of flesh and are commonly referred to as
liver or meat spots. The wholesomeness of such an egg is not 1m-
paired. There is no practicable means known for preventing the
occurrence of blood spots in eggs. However by candling the entire
product of a flock, it is possible to prevent such eggs from going on
the market.

DISCOLORED YOLKS

Newly laid eggs in some instances exhibit a darkened appearance
of the yolk which is not due to developmental changes in the ovum or
to decomposition as a result of bacterial action. The entire yolk
may appear dark in color or the discoloration may be confined to
spots or streaks on the surface or in the depths of the yolk material.
In testing for freshness by ecandling or on opening the egg, such a
discoloration may be mistaken for an evidence of addling. The con-
dition results apparently from the action of sulphur, normally pres-
ent in the yolk, on small globules of cottonseed oi] which are absorbed
into the yolk. This occurs when the fowls are being fed cottonseed
meal or material containing cottonseed oil. This oil may be present
in table scraps since it is often an ingredient of butter, oleomar-
garin or cooking oils. Cattle or hog fats or their products may
contain cotton seed oil where the animals have been fed cotton
seed meal shortly before slaughter.

Yolk is composed of albumin 17.50 per cent, oil and salts 28.75
per cent, and water 53.75 per cent. The yolk granules are ar-
ranged in thin concentric layers as they are received through the
surrounding vitelline membrane from the blood vessels in the ovarian
capsule or follicle. This arrangement would explain the disposi-
tion of the discoloration, depending on whether the fowl was re-
ceiving cottonseed oil constantly or only at intervals. The color
reaction between sulphur and cottonseed oil is utilized in the
Halphen test for the presence of the latter as an adulterant in
certain food products. In a positive test a pink color is produced
but this is changed in the yolk to a brownish or dark yellowish color.
It is not improbable that discolored yolks may result also from the

GENERAL DISEASES 171

action of the contained sulphur on certain metallic salts which the
fowl may ingest and which through metabolism may be incorporated
into a yolk.

There is no apparent reason why eggs so affected should be un-
wholesome. They may be detected by candling.

DOUBLE YOLKED EGGS

The inclusion of two yolks within one shell is due to rapid
ovulation or delay of one yolk in its progress to the isthmus or egg
membrane-secreting part of the oviduct, thus allowing the following
yolk to reach it and be surrounded by a common membrane. When
the two yolks do not meet until arrival at the isthmus, each is sur-
rounded by a separate layer of albumin. When two yolks are ovu-
lated within a short interval or meet in the anterior portion of the
oviduct they may have a common layer of albumin and common
membranes.

SOFT SHELLED EGGS

When the egg reaches the uterine portion of the oviduct under
normal conditions the double membrane secreted by the isthmus
is covered by a felty fibrous layer into which is deposited the ma-
terial which forms the caleareous shell. Absence of the hard shell
may be due to several causes. If the bird does not have feed con-
taining hme salts in sufficient quantity, or access to substances rich
in these salts it is apparent that a normal shell cannot be produced.
Providing the fowls with crushed oyster shells or mortar will remedy
this defect. Irritation of the oviduct as a result of inflammation
may cause an abortion of the egg before it is properly formed.
Sudden fright may also lead to a premature laying of the egg before
it has acquired its hard shell. Excessive attention by the male is
said to cause the laying of soft-shelled eggs. Where this is con-
sidered as the cause the removal of the cock is indicated. Except
when-eggs are desired for incubation the presence of a male bird in
the flock is not necessary since fowls lay equally well or better in his
absence. Unfertilized eggs keep better than fertilized ones, a fact
which causes many poultry men to place cock birds in the flock
during the breeding season enly.

172 DISEASES OF DOMESTICATED BIRDS

DISEASES OF THE PERITONEAL CAVITY
ABDOMINAL YOLK CONCRETIONS

The presence of masses of yolk material lying free in the peri-
toneal cavity of hens is frequently observed on post-mortem ex-
amination. The cause of this condition is not always apparent.
Injuries to the membrane of the fallopian tube, or tumor forma-
tions in the oviduct which interfere with the entrance of the yolk
or its passage through the oviduct are usually responsible. Yolks
or partly formed eggs may be returned through the oviduct and
aborted into the peritoneal cavity by reverse peristalsis induced by
inflammatory changes in the wall of the oviduct. At times the
contents of only one yolk or ovum may be present while in other
cases the concentric layers of yolk substance indicate that the process
has been going on for a considerable period of time. In the latter
instance the mass may be as large as a tennis or base ball and of
firm consistency. The layers are easily separated when newly
formed or before organization or decomposition changes have pro-
gressed. Some accumulations reveal a center of albumin, or par-
tially formed shell membrane, while others exhibit a yolk formation
throughout. Occasionally a normal yolk is found surrounded by
a small amount of albumin and inclosed in a soft or partially cal-
cified membrane. In this case there is evidence that the ovum
has passed into the oviduct and owing to an abnormal state of this
organ, reverse peristalsis has caused its return through the fallo-
pian membrane into the abdominal cavity. Quite frequently as
many as five to seven perfectly formed yolks in a good state of
preservation are found between the intestinal convolutions. These
apparently represent a recent discharge from the ovary in contrast
to the solidified yolk substance constituting the typical yolk con-
cretion.

Symptoms. ‘The presence of yolk deposits is not disclosed by
external appearances where putrefactive changes are absent. The
tendency is for the material to become partially absorbed. The un-
absorbed portion is formed into a rounded body which increases in
size according to the number of ova aborted into the cavity. In the
event that organisms find their way into the peritoneal cavity, pre-
sumably by way of the oviduct, a favorable culture medium is at
hand and decomposition changes may be inaugurated which lead to a
septic condition and result in peritonitis, or septicemia.

GENERAL DISEASES 173

Treatment. The removal of the yolk masses is easily accom-
plished by an incision through the abdominal wall once the nature
of the affection has been determined by digital exploration. As a
rule the presence of aborted egg material is not suspected during the
life of the fowl and treatment is therefore not practiced. It is also
apparent that treatment to be effective would require the correction
of the factors which lead to the misplacement of the ova. The ob-
scure nature of these renders attempts at their control impractical.

DROOPING ABDOMEN

In the heavy breeds, especially, the abdomen may show a tend-
ency to assume a pendant position, frequently coming into contact
with the ground when the bird is in a standing position. The skin
of the abdomen may be devoid of feathers, and usually shows a
reddened appearance. This is often due to a marked accumulation
of fat in the abdominal wall and visceral organs. More often it
results from a displacement of the gizzard. This organ, owing to an
elongation of the proventriculus or true stomach, is carried back-
ward and instead of resting in its normal position on the posterior
floor of the sternum, takes up a position on the much less resistant
membranous wall of the abdomen. As a result of its weight and
muscular activity in a cavity already overfilled with distended in-
testines and accumulated fat it forces the inferior abdominal wall
into a drooping or dragging position. The abnormal position of the
gizzard may be detected by palpation of the parts immediately
behind the sternum where the outline of the dense muscular organ
can easily be followed.

Treatment consists of the restriction of fat forming foods in
the diet. It is inadvisable to use birds showing this condition for
breeding purposes, since the evident tendency to lack of tone and
resistance in the parts concerned would be perpetuated to a greater
or less extent in the progeny.

ASCITES (DROPSY)

Characterization. This condition consists of an accumulation
of fluid in the peritoneal cavity or abdomen.

Etiology. No one specific causative agent is responsible. The
accumulation of fluid results from a filtration of blood serum
through the serous membranes of the intestine, or the peritoneal
covering of the abdominal cavity or paryenchymatous organs. It

174 DISEASES OF DOMESTICATED BIRDS

may be present in severe, or chronic cases of enteritis, sarcomatosis,
tuberculosis, peritonitis or other debilitating diseases affecting the
abdominal organs.

Symptoms. Except in a marked dropsical condition, no external
manifestations of ascites are readily noticeable. On palpation of
the abdominal region the presence of fluid may be detected. Its
presence has no great diagnostic importance since it is merely as-
sociated with a more serious affection which may be difficult of ac-
curate determinaticn during the life of the bird and which in the
large percentage of cases is not open to practical treatment.

Differential diagnosis. Ascites is often confused with an ex-
cessive formation of fat in the abdominal wall or with a drooping
abdomen. Palpation of the abdomen and the absence of emaciation
or other signs of disease would eliminate ascites. When the latter
is present a distinct fluctuation of liquid is felt, much the same as
in the palpation of a water bag.

Treatment. When detected, the fluid may be evacuated by pune-
ture of the abdominal wall with a hypodermic needle. Except in
cases of septic ascites this method of procedure would be of little
permanent value since the fluid would be readily absorbed in the
event that the primary cause of its presence were corrected.

PERITONITIS

Characterization. Peritonitis occurs frequently in domesticated
birds. It is manifested by an inflammatory condition of the serous
coverings of the visceral organs accompanied by a serous, or coagu-
lated exudate in the peritoneal cavity.

Etiology. Various causes may be responsible for this affection.
There are numerous specific diseases of a septicemic nature in which
the involvement of the peritoneum is of secondary consideration.
Besides these the most important direct causes of peritonitis are
infected yolk concretions or deposits, ovarian infections, extension
of inflammation of the oviduct, or rectum, as a result of rupture,
perforation of the digestive tract by foreign bodies or as a result of
ulcerative changes in the intestinal wall such as sometimes occur in
coccidiosis of fowls, or entero-hepatitis of turkeys.

Symptoms. These are nonspecific since the general attitude of
an affected bird is similar to that displayed in several other in-
fectious diseases. Diagnosis is difficult except through post-mortem
examination. The disease is usually of an acute nature, death

GENERAL DISEASES 175

resulting shortly after the appearance of symptoms. The affected
fowl shows loss of appetite, ruffled feathers, elevation of temperature,
weakness and extreme depression. Diarrhea is frequently observed
especially when the intestinal serosa is extensively involved. In
eases of peritonitis due to rupture of the rectum, the droppings are
scanty owing to the passage of a portion of the intestinal contents
into the peritoneal cavity. The presence of yolk concretions, or
fluid in the abdominal cavity may assist in a diagnosis. In either
ease the abdomen may show a pendant position. On palpation, the
fluctuation of liquid may be felt, while the presence of concretions
is determined by their dense consistency, free disposition and rounded
contour.

Morbid anatomy. The pathologic picture in peritonitis in birds
is not usually marked by extensive congestion of the serous lining of
the abdominal cavity and visceral organs. There may be localized
areas of congestion, or hemorrhagic spots on the visceral peritoneum,
especially that covering the ovary. In the majority of cases no
macroscopic evidence of congestion is apparent. The disease is more
often marked by exudates either of a serous, or semi-solid form.
Evidently the morbid condition results principally from the absorp-
tion of toxins generated by the action of microorganisms on foreign
matter which has gained entrance to the cavity. The serous exudate
is at times clear and straw colored, at other times cloudy and putrid.
The septic condition is generally associated with a cheesy exudate
which covers the viscera in small masses and is non-adherent to the
membrane. Yolk concretions, or individual aborted yolks, display
putrefactive changes. Where rupture of the oviduct or intestine has
eccurred, egg material or intestinal contents respectively will be
found and the rupture may be easily located.

Treatment. The difficulty in diagnosing peritonitis during the
life of the bird and the advanced stage reached when symptoms be-
come apparent renders attempts at treatment impractical. Should a
physical examination reveal the presence of yolk masses free in the
abdcminal cavity, or a dropsical condition of the abdomen, surgical
methods could be employed to remove the accumulations. The cavity
could then be washed with sterile water or a mild antiseptic to remove
septic exudates.

VICIOUS HABITS

Toe pecking. The conditions surrounding incubator chicks kept
together in large numbers in brooders, are very different from those

176 DISEASES OF DOMESTICATED BIRDS

afforded a brood of chicks under the care of a hen. One of the most
troublesome results is the habit of pecking toes. Anything unusual
about the foot of a chick attracts the attention of another member
of the flock which pecks at the foot. The attention of others is drawn
to the action and they repeat the pecking. As soon as blood is
drawn, the deep seated instinct of chickens to attack the injured
or the weakling, is aroused and the victim is soon killed or seriously
maimed. The habit is likewise manifested by pecking at the vent.
In this way a chicken is disembowled in a surprisingly short length
of time. Once the taste for blood is aroused, the chicks attack one
another indiscriminately and cause heavy losses.

The immediate remedy is to remove instantly all wounded birds,
which must be kept in isolation until entirely recovered. General
precautionary measures will include those designed to keep the chicks
occupied with harmless pursuits. Various kinds of food hung so as
to be somewhat inaccessible, furnish diversion. Dried meat has
been so employed.

Egg eating. The habit of eating eggs is often established by
the accidental breaking of an egg. The practice spreads rapidly by
imitation. Careful observation will reveal yolk stains on the beaks
of offenders, who should be isolated or killed.

Nests well supplied with straw will minimize the possibility of
the accidental breaking of eggs, and darkened nests will prevent a
broken egg from being seen. Craving for lime in the egg shells
may be forestalled by supplying an abundance of oyster shells and
bone.

Feather eating and feather pulling. These habits constitute
very troublesome vices not only among fowls but also in cage birds.
A bird may pull out its own feathers or those of its companions.
The sensation of having the feathers plucked apparently is not dis-
agreeable, for a bird will stand quietly while another pulls out its
feathers. Finally the birds taste blood on the emerging feather and
as a result, never allow a feather to develop. The vice is often
observed in cage birds such as parrots, among hens that are closely
confined, and occasionally among hens lacking certain elements in
the feed. Parasites of the skin are important causes of the itching
leading to feather pulling. In some instances the eruption of nor-
mal feathers during molting, occasions an itching sensation and
starts the habit. Perhaps the most common cause is a monotonous
diet of a restricted number of elements. Hens at large in warm
weather can satisfy individual food requirements from among the

GENERAL DISEASES AT?

various materials available, such as grass, insects and mineral sub-
stances.

Klee finds it very useful to supply blood in a cooked form, mixed
with bran and curd. Under these conditions the birds do not acquire
a taste for blood. Burned shells and green feed are also desirable
elements in the ration. Green feed is best surrounded by a wire
netting in such a way that the birds are compelled to reach through
the meshes to obtain the feed. In winter time cooked beets or
sprouted oats may be used.

Breaking up the habit in parrots often causes difficulty. Daily
sprinkling with water and providing variety of feed are useful.
Klee also has observed many cases benefited by smearing the feathers
with sepia, or unsweetened chocolate and by keeping the bird in the
dark. It is possible to fit a broad aluminum collar on the neck of
a parrot in such a way as to prevent the bird from reaching the
feathers.

According to Klee, lack of feathers is observed in pigeons from
time to time without being due to feather pulling. In some in-
stances the pin feathers are present in the skin but do not break
through. Persistence of the feather sheath also occurs in pigeons,
in which case the feathers develop while rolled up in a horny cover-
ing. Under normal conditions this sheath is shed early in the de-
velopment of the feather. Sometimes if the bird is kept until the
molting period the new feathers will develop normally.

In chickens and in any growing birds, interference with nutrition
such as intestinal catarrh will cause retardation of the feather de-
velopment in the molting period. Molting exerts such a drain upon
the strength of birds that only a well nourished bird is able to molt
normally. As a result, birds are more inclined to become diseased
during molting than afterwards.

REFERENCES

1. Dickson. Botulism. A cause of limberneck in chickens. J. Am.
Vet. Med. Ass., Vol. 3, 1917, p. 612.

2. Hebrant et Antoine. <A propos de la goutte ou diathése urique. Ann.
de Méd. Vét., T. 58, 1909, p. 321.

3. Klee. Die hauptsichlichsten Geflugel-Krankheiten. Leipsig. 1905.

CHAPTER XVI

INTERNAL PARASITES
PARASITES OF THE ESOPHAGUS, CROP, PROVENTRICULUS AND GIZZARD
FOWLS

Dispharagus nasutus, a filarial worm 7 to 9 mm. long, is one of
the most important parasites occurring in the portion of the ali-
mentary tract of fowls anterior to the gizzard. The worms are
found in great numbers in the mucosa of the proventriculus and of
the gizzard. The affected birds become emaciated and depressed
without losing appetite. The mucosa of the gizzard has been ob-
served to be bristling with the parasites, some in the mucosa and
others attached to the mucosa by one end and floating free in the
lumen. The proventriculus when infested may be increased to
double the usual size, becoming spherical in form. The mucosa is
greatly thickened in places where the parasites are most numerous.
Cases have been observed in which the worms were so numerous as

Fic. 19. Spiroptera pectinifera. Male. Caudal extremity. 175. Neumann)

to give the glands a villous appearance. Colucci obtained good re-
sults by the administration of capsules of .5 gram of oil of turpentine
morning and evening.

D. hamulosus has been reported from fowls in Brazil as occurring
in little fleshy excrescences on the surface of the gizzard. LD. laticeps
has been found in the fowl and certain rapacious birds. Physa-
loptera truncata has been observed in the gizzard of a fowl in Brazil.

Spiroptera pectinifera is a hair worm which infests the gizzard of

178

INTERNAL PARASITES ‘79

fowls. Individuals vary from 4 to 9.5 mm. in length and are 2
mm. broad. The worms are attached to the mucosa of the gizzard
by their anterior extremities. The mucosa is covered by a brownish
deposit 2 to 3 mm. thick, consisting of a mixture of blood and debris
of the parasites. The affected mucosa shows irregular depressions
which are granulated, reddened and hemorrhagic. The affected birds
show anemia, progressive cachexia and good appetite to the last.
One to three months may elapse between appearance of symptoms
and death, depending upon the age and vigor of the subject. This
parasite has been reported as causing heavy mortality among
chickens in France. Its presence in the guinea-fowl has been re-
ported.

Ransom has described a nematode worm Gonglyonema ingluvicola
parasitic in the crop of fowls. The presence of the females may be
detected by noting the cceurrence of small coiled ridges on the sur-
face of the mucosa, discernible with the naked eye. The males are
only discovered by the use of a hand lens. Specimens may be ob-
tained for detailed study by teasing the tissue. The females vary
from 32 to 45 mm. in length, while the males are from 17 to 19 mm.
long. The infestation does not so far as known, result in serious
disturbance of health. The same parasite has been recognized in
Europe by Ciurea.

Trichosoma annulatum is a worm 15 to 80 mm. in length which
has been reported as occurring under the epithelium of the mucosa
cf the esophagus of the fowl. Another member of this genus, 7. no-
dularis causes serious trouble in waterfowl.

Dispharagus spiralis, a worm 7 to 9 mm. long has been reported in
the same location as well as in the gizzard. Prosthogonimus pellu-
cidus, a trematode, has been found in the esophagus of fowls.

PHEASANTS

Trichosoma strumosum causes serious loss among young pheasants.
It lives in the large folds of the epithelium of the esophagus and
sometimes penetrates the mucosa. It
forms passages in which the female de-
posits eggs. This destruction of epi-
thelium occurs in the esophagus, buccal

ia ie lradl TI} digeud Fic. 20. Trichosoma strumosum.
cavity an 1e tracned. oe ; 5 sie Female. Anterior extremity.
eauses great weakness at the beginning, —(Reibisch)
followed by rapid emaciation. Death

180 DISEASES OF DOMESTICATED BIRDS

occurs four to six days after the appearance of the first symptoms.
Treatment consists of administering a 2.5 per cent solution of car-
bolic acid in the drinking water or in the mash.

WATERFOWL

Strongylus nodularis has been reported as occurring in water-
fowls, most frequently in the mucosa of the gizzard. The female
worms vary in length from 12 to 22 mm. while the males vary from
10 to16 mm. The parasites are about 5 mm. in diameter, and are
threadlike in form. They are more narrow at the ends, especially
at the head end. Freese reports a loss of 200 out of 700 geese, due
to the parasite.

Symptoms. Single individuals occur very frequently in healthy
geese without causing symptoms or noteworthy lesions. Extensive
invasion of young geese is attended with serious results. At the
beginning of sickness the young geese appear weak, sit most of the
time and move with reluctance. They make characteristic choking
movements and soon show more or less diarrhea. ‘The birds have a
very good appetite and consume their feed ravenously. In spite of
the large amount of food consumed, the birds gradually become ema-
ciated almost to skeletons. Finally they fall from weakness and
are unable to rise again. In this stage the birds stop eating and die
in a day or so. The whole course of sickness occupies three to eight
days. The younger the geese, the more they are affected. The
young, as a rule, die.

Morbid anatomy. The carcass is excessively emaciated and only
traces of the breast muscles remain. The mucosa of the small in-
testine, especially near the gizzard, is reddened, thickened and coy-
ered with a large amount of viscid mucus. The principal lesions are
found in the gizzard. Except where the epithelium normally forms
horny plates, it is covered with a thick, bark-like mass, dark brown
or dark brownish red in color. The consistency of the mass is more
or less tough and in some places, is more like mucus. In and under
this material are innumerable parasites in coils. Not infrequently
the worms are attached to the bark-like mass by their heads, with
the other ends free in the lumen. Sometimes a mucous layer, with
worms, is located in the lower third of the esophagus. Occasionally
a few worms may be found on the mucosa of the small intestine. The
statement of some authors that the parasites occur under the mucosa
is incorrect, for they occur only under the epithelium and less com-
monly directly in the epithelium.

INTERNAL PARASITES

181

Dispharagus uncinatus has been reported as occurring in the esoph-
agus and proventriculus of geese, ducks and swans. They occupy
eyst-like structures which are most frequently encountered in the wall

Fic. 21. Dispharagus

of the proventriculus.
opened the worms are found surrounded by
a bloody fluid or a yellowish caseous mass.
The wall of the proventriculus is thickened
and the mucosa is covered by a large amount
of yellowish green viscid mucus. A stage of -
the life cycle of the parasite is passed in a
certain aquatic form, Daphnia pulex. The
embryos, free in the stomach of the bird,
gain access to the water where they are
taken in by the Daphma, which creature is
in turn eaten by the waterfowl.

Prophylaxis must depend chiefly upon
killing of infected birds, and upon keeping
birds away from stagnant water, colored
brownish or yellowish by the presence of
Daphnia in large numbers.

Sclerostomum anseris infests the gullet,

When these are

uncinatus. Dorsal proventriculus and gizzard of geese. It
view of anterior ex- burrows under the mucous membrane and

tremity. Enlarged 60

times, (Schneider) causes the formation of dark brown crust-

like layers on the epithelium. In young

ducks it causes gradual emaciation and debility. The location of
the parasites discourages the use of antihelminthics.

Hystrichis tricolor is a worm which infests the proventriculus

of ducks, and causes extensive destruction of
tissue. Very large ulcers are formed which al-
most perforate the walls of the organ. Cysts
about the size of a bean, containing the parasite,
are also found. A similar parasite Hystrichis
elegans also occurs in the proventriculus of
ducks and of a large number of palmipeds. #.
cygnmt oceurs in similar location in the swan.

Tropisurus fissipinus form eysts in the sub-
mucous region of the esophagus of ducks, some-
times causing a fatal inflammation.

Fie. 22. Hystrichis
tricolor Cephalic ex-
tremity. (v. Ratz)

Trichosoma contortum occurs in ducks and geese besides other
birds. They infest the dilated portion of the gullet, which in ducks

182 DISEASES OF DOMESTICATED BIRDS

Fic. 23. Trichosoma contortum. A, caudal
extremity of female; B, eggs from the
uterus in various stages; C, caudal ex-
tremity of the male. Enlarged 300 diam-
eters. (Railliet)

and geese, performs the func-
tions of a crop. The pres-
ence of the parasites causes a
distention of the gullet and a
condition quite similar to dis-
tention of the crop in fowls.
The infested birds display ar-
rested development, emacia-
tion, difficult locomotion, epi-
leptic movements, somnolence
and lack of appetite. Death
is frequently due to asphyxia
resulting from over disten-
tion of the gullet.

At autopsy it is observed
that the galleries formed by
the worms appear as whitish
curved lines which stand out
in prominent relief against
the congested mucosa. Mi-
croscopic examination of the
tissue will reveal the presence
in the galleries of the worms
and their eggs.

Positive diagnosis is diffi-
cult during life unless micro-
scopic examination is made
of the feces or of water with
which the crop has_ been
rinsed.

Treatment may consist of administering two tablespoonfuls of a
mixture of turpentine with twice its volume of olive oil.
Filaria cygni has been observed in the intestine and ceca of a

swan which was exceedingly emaciated.

TAPEWORMS

General character. Tapeworms, also designated cestodes, con-
stitute important parasites of the intestines of birds. When present
in large numbers they occasion a disease designated teniasis. The
individual worm is composed of a head called the scolex and a

INTERNAL PARASITES 183

variable number of segments
designated proglottides. The
scolex is armed with a series of
hooks by which it becomes at-
tached to the intestinal mucosa
of the host. Each proglottid or
segment of the worm is virtually ; }
an individual and is bisexual. ™,24,, Segment, of, Pavsinea, crhino
The segments are not provided gans. Enlarged. (Ransom)

with an alimentary canal, but

absorb nourishment directly from the intestinal contents of the lost.
As the terminal segments in turn mature, they are separated from
the worm and are discharged in the droppings.

Species of cestodes. A large number of species of tapeworms
have been reported as occurring in the intestines of domesticated
and wild birds. Ransom has examined nine species in American
chickens and turkeys as follows: In chickens, Hymenolepis carioca,
Choanotaenia infundibulum, Davainea tetragona, D. echinobothrida,
D. proglottina, Amoebotaenia sphenoides; in chickens and turkeys,
D. cesticillus, Hymenolepis cantaniana; in turkeys, Metroliasthes
lucida. He notes that the tapeworms of American ducks, geese, and
pigeons have not yet been investigated. Neumann lists four more
species as having been found in fowls. These are Cotugnia diagono-
pora, Taenia fasctolaris, T. exilis and Bothriotaenia longicollis.

Tapeworms found in the various birds are listed by Neumann as
follows:

Turkey: Choanotaenia infundibulum, Metroliasthes lucida,
Davainea cantaniana, D. cesticillus, D. friedbergeri, Hymenolepis
carioca, H. musculosa, H. meleagris, Not named.

Pheasant: Choanotaenia infundibulum, Davainea echinoboth-
rida, D. cantamana, D. friedbergert, Hymenolepis phasianina.

Pigeon: Choanotaenia infundibulum, Davainea echinobothrida,
D. crassula, Bertiella delafondt.

Duck: Hymenolepis anatina, H. gracilis, H. sinuosa, H. coronula,
H. parvula, H. megalops, H. lanceolata, Choanotaenia infundibulum,
Davainea crassula, Fimbriaria fasciolaris.

Goose: Hymenolepis lanceolata, H. setigera, H. gracilis, H.
fasciata, H. sinuosa, H. tenuirostris, Fimbriaria fasciolaris.

Neumann considers tapeworms as occurring infrequently in pig-
eons and rarely present in sufficient number to cause trouble. In
ducks they exert feeble pathogenic action. I/ymenolepis setigera and

184 DISEASES OF DOMESTICATED BIRDS

H. lanceolata, singly or together cause injury among geese in Europe.
Davainea friedbergert causes great losses among pheasants.

Life history. Krom time to time the tapeworm in the intestine
of the chicken discharges ripe segments filled with eggs, which are
voided in the feces. To maintain the life cycle it is necessary that
the tapeworm eges be taken with the food into some creature known
as a secondary host. In this host the embryos escape from the eggs
and migrate to some organ where they form a cyst-lke structure
known as a ecysticercoid. The life cycle is completed in case the
intermediate host is eaten by a chicken in which event the cysticercoid
develops into the adult form.

Comparatively little is known about the secondary hosts of tape-
worms of poultry. Of the five species of tapeworms that have been
reported in chickens in the United States, the intermediate host of
but one has been discovered. It has been determined that the inter-
mediate host of Choanotenia infundibulum is the common house
fly, Musca domestica.

The intermediate hosts of a number of tapeworms of birds re-
ported as occurring in other countries have been discovered. ‘Thus
a slug is necessary for the life cycle of Davainea proglottina, a
chicken tapeworm. ‘The intermediate hosts of certain tapeworms
of the duck have been found to be various species of fresh water
crustaceans.

In general, the intermediate host is to be sought among the various
insects and other forms of animal life to which the infested birds have
access such as snails, insects, crustaceans or worms.

Symptoms. These vary to some extent in different birds ac-
cording to age and the degree of infestation. A few worms are not
harmful to the bird and can hardly be noticed. Young birds are af-
fected more seriously than old ones. In moderate infestation the
bird is always hungry and experiences excessive thirst. Restless-
ness is marked and doubtless accounts fur the lean condition of the
bird. Heavily infested birds show such symptoms as drooping
wings, emaciation, ruftled feathers and isolate themselves from the
flock.

The condition of the feces is more or less altered in tapeworm in-
festation. Heavy infestation causes inilammation of the intestine
and diarrhea with mucous droppings. ‘The secretion is at first clear,
transparent, semi-liquid and slightly wiitisi in eolcr. Later the
mucus becomes brownish yellow in col » .ue to hemorrhage caused
by the worms, and this coloration cons ituies one of the most char-

INTERNAL PARASITES 185

acteristic symptoms. When the bird is very heavily infested, gas
bubbles are observed in the droppings, and remain visible for some
time.

Segments of tapeworms may be found in the feces by careful
search, and microscopic examination may be utilized for detecting
the presence of tapeworm eggs.

Tapeworm infestation in geese has been reported in Germany as
causing very marked nervous symptoms. The birds walk very lit-
tle and assume an upright position like that of the penguin.

Morbid anatomy. In excessive infestation the carcass is anemic
and emaciated. On slitting the intestine, worms will be found in
greater or less number
throughout its whole ex-
tent between the gizzard
and the ceca. They are
attached to the mucosa by
their heads and may cause
more or less inflammation.

: _ The most serious patho-

Fic. a Gravid segment of Davainea echino- loreal chanecs ace (Gansed
othrida. Enlarged. (Ransom) 5 5

by infestation with Davat-

nea echinobothrida which results in the
formation of nodules in the intestine.
This condition has been described by
Moore under the name of nodular teenia-
sis. The nodules are most numerous in
the lower third of the small intestine.
Exceptionally they oceur in the duode-
num and colon. In severe infestation
the presence of nodules causes numerous
protuberances from the serosa, varying
in size from those barely perceptible, to

(00m,

elevations 4mm. high. The color varies Fig. 26. Head of Davainea
from pale or dark yellowish in the larger ee eal

(Ransom)
ones, to the normal gray of the serosa

shown by the smallest ones. Similar elevations are observed on the
mucosa of the intestine. Small tapeworms occur attached to the
mucosa over the nodules. Over some of the nodules there are areas
in which the mucosa has sloughed, leaving ulcers.

The contents of the larger nodules consist of greenish yellow, ne-
crotic material which on section has a glistening, homogeneous ap-

186 DISEASES OF DOMESTICATED BIRDS

pearance. Surrounding this, there is a thin layer of infiltrated tis-
sue. The smaller nodules contain a substance more resembling pus,
and in these the microscopic study of sections most readily reveals the
presence of tapeworm heads. The penetration of the intestinal wall
by the heads induces infiltration and eventually results in the forma-
tion of nodules.

Diagnosis. The chief points to be relied upon in diagnosis are
emaciation, excessive appetite and thirst together with the character-
istie yellowish-brown color of the droppings. The detection of tape-
worm segments in the feces is best done by immersing the suspected
white mass in water. If it consists of urates alone, it will be dissi-
pated in fine granules, while the worm segments will be recognized as
firm masses. Some of the general symptoms of unthriftiness are
also indicative of nematode infestation, but in this case the birds
often pass blood. Ultimate decision will rest upon the information

ery may

i Mh HA LS is
| | mn sav AAO
iu 1 a HN fyi
i ut auygnanaguaggaciit al Ta

Th PAT TAMAR NEAR

Fic. 27. Hymenolepis lanceolata. Natural size, in a medium state of extension.
(Railliet )

yielded by an autopsy. The intestine should be opened while im-
mersed in warm water, to facilitate recognition of the worms. They
will be found attached to the mucosa, and vary in size from micro-
scopic objects to worms four or five inches long.

Treatment. Turpentine is held in high repute as a teniafuge
and has the additional advantage of expelling round worms also.

The fowls are fasted for twenty-four hours during which time
they should receive a dose of Epsom salts. One teaspoonful of salts
is allowed for each bird, the whole being dissolved in warm water and
mixed with mash. Greater accuracy of dosage will be assured if the
dose is administered directly to each bird. The most convenient sys-
tem of carrying out the vermifuge treatment is to withhold food in
the morning and give the salts in the evening. The following morn-
ing the turpentine should be given in a dose of from one to two
teaspoonfuls per fowl. Owing to the offensive qualities of turpen-
tine it is not possible to give it in food, but it must be administered
to each bird individually. The most expeditious method is to inject
the dose directly into the crop with a hypodermic syringe. <A slower

INTERNAL PARASITES 187

method is to introduce the dose into the crop by means of an oiled
rubber tube inserted through the oral cavity and esophagus. The
turpentine, diluted with an equal amount of olive oil may be ad-
ministered by the mouth. If the mixture is given slowly with a
spoon or medicine dropper the bird will swallow it naturally and will
cause very little trouble. Three or four hours after giving the tur-
pentine, the birds should receive another laxative dose of salts ad-
ministered in a mash as before.

Owing to the habit of burying their heads in the intestinal wall,
tapeworms are very resistant to treatment. Consequently it is ad-
visable to repeat the vermifuge treatment in about three weeks.

Gutberlet reports favorably upon the use of lye for expelling tape-
worms. <A tablespoonful of concentrated lye was added to one gal-
lon of a mixture of wheat and oats ;
which was cooked slowly for two
hours. Fifteen birds, after fasting
for about fifteen hours, were allowed
to eat the mixture. A second dose
is given twelve hours after the first
one.

A number of other substances are
employed to expel tapeworms, but
some fail on account of having lost ae nen ile ag eee
their active properties. Areca nut 100 times; B, egg enlarged 300
in doses of 30 to 45 grains may be times. (Railliet)
administered to fowls in the form of a pill, but turkeys do not tol-
erate this remedy well.

Powdered pomegranate root bark may be fed to fowls in a dose of
one teaspoonful to each 50 birds. It may be followed by a purgative
dose of 2 or 3 teaspoonfuls of castor oil per bird. Male fern in a
dose varying from 30 grains to 1 dram of the powder may be given
morning and evening before feeding.

Méenin recommends treating pheasants for tapeworm with kamala,
mixed into a paste with hard boiled eggs and bread.

Prophylaxis. An accurate knowledge of the secondary host for
each species of tapeworm, might suggest very effective preventive
measures but in the absence of much of this information, such
measures must be of a general nature. It is desirable to collect
the droppings and treat with lime. Lime or ashes may be scattered
over the droppings under the roosts. General sanitary measures
are of value, and particularly, the practice of moving birds to new

188 DISEASES OF DOMESTICATED BIRDS

ground should be encouraged. The knowledge that the house fly is
the intermediate host of a chicken tapeworm suggests the advisability
of combating that insect. It breeds commonly in bird or horse ma-
nure and any decaying vegetable matter. These breeding places
should be eliminated as far as possible besides using fly traps.

ROUND WORMS

General nature. Round worms or nematodes are common para-
sites of the intestines and are capable of inflicting considerable
damage. They are long, slender and thread-like in form. Mouth,
alimentary canal and anus are present. ‘The female worm is gener-
ally larger than the male.

Species of round worms. There are two principal species in
fowls. Ascaridia (Heterakis) perspicillum occurs in the small in-
testine. The male is 3 to 8 em. long, while the female is 6 to 12 cm.
in length. The color of the body is yellowish white. They are often
present in numbers sufficient to occlude the lumen of the intestine.
The same species is found in the turkey and guinea-fowl. Heter-
akis papilosa, a much smaller worm with white body, is very com-
mon in the ceca. The male is from 7 to 13 mm. long while the fe-
male varies from 10 to 15 mm. in length. This species is found
also in the turkey, guinea-fowl, peafowl, and pheasant. Five other
less important species, Heterakis lineata, H. brasiliensis, H. compar,
H. compressa and H. differens have been reported by Neumann as
occurring in fowls. This writer lists other nematodes of the intes-
tine as follows:

Pigeon: Heterakis columbe.

Duck: Ascaris crassa, Heterakis dispar, H. vesicularis, H.
lineata, Strongylus tenuis.

Goose: Heterakis dispar, H. vesicularis, Strongylus tenuis, Tri-
chosoma anatis.

Life history of Ascaridia perspicillum. Eggs are deposited by
the worms within the intestine and are expelled in the feces. The
length of time worm eggs will remain alive in the droppings is not
fully determined, but there is evidence that they are viable up to a
year. The life cycle of the worm is completed by eggs gaining access
to a fowl through contaminated feed or water. Ordinarily, eggs do
not hatch until they are taken into the alimentary canal of a fowl.
The worms require three to four weeks to develop into sexually ma-
ture forms.

INTERNAL PARASITES 189

Symptoms of Ascaridia infestation. Affected birds appear un-
thrifty and emaciated. ither diarrhea or constipation may occur.
The affection is most severe in young birds.

Treatment. Beach conducted experiments with a number of
remedies to determine their value in causing the expulsion of the
worms and came to the conclusion that tobacco stems are most ef-
ficient. or one hundred fowls he takes one pound of finely chopped
tobacco stems and steeps them for two hours in enough water to keep
the mass covered. The liquid and the stems are mixed with half
the amount of ground feed usually allowed the birds for one feed-
ing. On the evening before the day of administering the remedy,
the birds should be fed only half a ration and they should be kept
without feed until afternoon of the following day. Then the mixture
of tobacco and feed is given and under the circumstances is sometimes
readily eaten. Occasionally, fowls refuse the mixture. Two hours
later, the birds are given a quarter size ration of ground feed mixed
with water containing eleven ounces of Epsom salts for each hundred
birds. No difference of dosage to correspond to birds of different
ages is attempted, for the matter is adjusted by the amounts of the
mixtures that the birds can eat. teasonable care should be exercised
to make certain that birds have equal opportunity to eat. . The treat-
ment is calculated to cost about ten cents per hundred fowls.

The same procedure should be repeated in two weeks which has
been found to be sufficient to free the birds entirely from parasites.
Difficulty in administering the treatment is sometimes encountered
because the birds will refuse to eat the mash containing the tobacco.

Theobald recommends thymol as an agent against nematodes. The
dose for the fowl is .06 gram given in the form of a pill. Two or
three hours after giving the thymol, a teaspoonful of olive oil is
administered.

Mégnin recommends administering santonin in the food in a dose
of 4 to 5 grams for every ten birds.

Klee recommends 5 to 10 drops of anise oil in 1 to 2 teaspoonfuls
of olive oil, also 4 to 6 drops of benzol with oil.

Prophylaxis. Thorough disinfection of the yards and quarters
is necessary in order to minimize the possibility of reinfection from
worm eggs that have been deposited in the feces. Herms and Beach
have determined that worm eggs are found only in the top two inches
of the soil of infected yards. After sweeping the yard and removing
rubbish the area was treated with a 1: 1000 solution of bichloride
of mereury. About one gallon of solution to each ten square feet of

190 DISEASES OF DOMESTICATED BIRDS

soil was found necessary to secure penetration of the fluid to a depth
of two inches. A trial of the effectiveness of the treatment in pre-
venting the reinfection of birds that had been freed of worms yielded
evidence of its value. Such birds increased in size rapidly and post
mortem examination of the poorest specimens after three weeks
yielded no evidence of worms. Other fowls on a control area, not
disinfected, became seriously infested in a similar length of time.

Bichloride treatment of roosting houses and other buildings to
which birds have access, is indicated. Netting under the roosts is of
value in keeping birds from contact with feces.

Round worms in the pigeon. Heterakis columbe occurs in the
intestines of pigeons in enormous numbers. As many as 400 to 500
worms have been observed in one individual. The infestation causes
loss of appetite, periodic mucous diarrhea and emaciation which is

AYR particularly marked in the pectoral muscles. At
autopsy the worms are observed packed closely to-
gether. The mucosa is distended in patches which
are engorged with blood and ulcerated. These
areas are covered with thick mucus. Occasionally
the parasites perforate the wall of the intestine and
are found in various parts of the thoracic and ab-
dominal cavities. Treatment advised by Ziirn con-
sists of administering 6 centigrams of calomel in

Bes 29. Hetera- the form of pills with bread or with butter. More
is columbe. A, : : E
male; B, female. Serious cases may be treated with areca nut in 1
Natural size. oram doses, given in the same manner. Two hours
(Railliet ) 5 Sats : : : p 3
after administering the pills, each bird is given a
teaspoonful of castor oil. The affected birds may be given a weak
decoction of garlic to which one-half per cent of sodium salicylate
has been added.

Strongylus quadriradiatus has been observed by Stevenson in the
intestine of the pigeon. The presence of a few worms causes no
harm, but large numbers cause harm attributed to injury of the wall
of the intestine permitting subsequent invasion by bacteria.

TRICHOSOME INFESTATION OF CHICKENS

Several worms of the genus T’richosoma have been described as
harmless inhabitants of the intestines of fowls. However, Freese
has observed that T’richosoma retusum is capable of causing great de-
struction among chickens. The same parasite has been reported in
the guinea-fowl. The worms vary from 13 to 19 mm. in length

INTERNAL PARASITES 161

and from .06 to .07 mm. in breadth. Other species reported in the
fowl are 7. collare, T. dubium, T. caudinflatum and T. gallinum.

Symptoms. The chickens become less lively, allow the wings to
droop and show diarrhea. The appetite is at first very good but later
becomes poorer. ‘There is increased thirst. The bird becomes more
and more emaciated and finally can hardly move because of loss of
strength. Without treatment the disease usually ends fatally. The
duration of the disease varies from three to ten days according to the
resistance of the victim.

When old hens are affected, they show similar symptoms. At the
beginning of sickness egg laying drops off and soon stops entirely.
The disease in hens runs a course of 2 to 4 weeks.

Morbid anatomy. The carcass is greatly emaciated and
anemic. All organs with the exception of the intestinal canal, are
free from lesions. The mucosa of the small intestine throughout
its whole extent is covered with a grayish yellow exudate. The mu-
cosa is thickened and reddened on the surface by short streaks and
points. The contents of the ceca and rectum are thin and viscid.
Innumerable trichosome worms are present on the mucosa of the
small intestine throughout its whole extent, and a few also occur in
the ceca.

Diagnosis. The disease caused by the trichosomes can be recog-
nized with certainty only by autopsy. On account of the hair-like
fineness cf the worms they can only be discovered after the closest
scrutiny. The contents of the intestine are teased with a needle, or
the needle is stroked over the mucosa. If the worms are present, it is
likely that several will adhere to the needle. Another method is to
remove a portion of the exudate from the mucosa and mix with
water. The hair-like worms may be detected with the naked eye.
In any event it is desirable that microscopic examination be made.

Treatment. Freese recommends the administration of oil of
anise in early stages of infestation. On each of two successive days
each chicken is given a dose of 5 drops of etherial oil of anise in 1
teaspoonful of olive oil. Old hens require twice as much anise oil.

Trichosomes in the pigeon. T'richosoma columbe is fre-
quently found in the large intestine of the pigeon. It is capable of
causing an intense intestinal catarrh. It may be present in colossal
numbers in the intestine causing the mucosa to show tumefaction, in-
filtration, petechiz and red streaks.

192 DISEASES OF DOMESTICATED BIRDS

FLUKES

General nature. Trematodes (flukes) are hermaphroditic worms
possessing suckers by which they become attached to the mucosa of
the intestine of the host. The intestinal tract ends blindly without
an anus. In the temperate zone they are generally harmless and
uncommon parasites.

Species and hosts. Routan states that EHchinostomum echin-
atum occurs in the fowl, duck, goose and swan; H. conoideum in the
fowl, duck and goose; H. recurvatum in the fowl and duck; Clino-
stomum commutatum in the fowl, turkey and pigeon; Notocotyle ver-
rucosa in the fowl, duck and goose. Bunodera linearis has been re-
ported in the fowl alone, Cyclocelum mutabile in the turkey alone,
while Holostomum gracile and H. sphewrocephalum occur in the
duck alone.

THORN HEADED WORMS

Three species of the genus Hchinorhynchus occur in ducks but only
one has been reported as causing injury.

Echinorhynchus polymorphus is fusiform in shape and colored or-
ange red. ‘The anterior extremity of the worm is provided with an
ovoid proboscis armed with eight rows of hooks. The male worm
measures 4 to 6 mm. in length while the female varies from 15 to 25
mm. in length. The worms usually are fixed firmly to the wall of the
intestine.

Before opening the intestine the serous surface of the same is
seen to be covered with numerous nodules, the centers of which are
orange colored. On opening the intestine the mucosa is found
studded with worms of the same color attached by their anterior ex-
tremities. Their presence sets up a severe inflammation of the mu-
cosa and causes the formation of the nodules on the serous surface.
The condition described often causes diarrhea, emaciation and
anemia.

The same species occurs in the swan. J. filicollis and EH. spero-
cephalus are found in the duck.

FLAGELLATES

Flagellated protozoan organisms constitute a small number of
forms parasitic in the intestines of birds. These are nucleated
bodies provided with one or more flagella and sometimes possess an
undulating membrane. Neumann lists the following species: T'ri-
chomonas eberthi has been observed in the glands of Lieberkuhn of
a duck and in a goose. It is little known ‘and without pathogenic

INTERNAL PARASITES 193

importance. J. columbe has been reported as causing the forma-
tion of caseous foci in the liver of the pigeon with fatal result.
Monas (Monocercomonas) anatis has been reported as occurring in
the small intestine of the duck. Martin and Robertson have studied
the flagellates of the ceca of fowls dividing them into the four
species: Chilomastix gallinarum, Trichomonas gallinarum, ie
eberthi and Trichomastia gallinarum.

Hadley observes that the intestinal fauna of any young turkey
after it has been on the ground for a few days will contain a variety
of protozoan parasites. Among these, the most common are flagel-
lates, certain sporozoa and amebas. At least three types of flagellates
are usually present, T'richomonas, Chilomastiz and Lamblia. He
considers that Trichomonas plays a pathogenic réle in cecal and he-
patic infection in birds comparable to intestinal and hepatic ame-
biasis as observed in mammals. Hadley considers the flagellates de-
scribed by him as identical with bodies described by Theobald Smith
under the name Ameba meleagridis and the cause of blackhead in
turkeys. He regards 7'richomonas as a facultative parasite in that
under certain conditions it exists as a harmless, ever-present intes-
tinal parasite. According to this view the 7’richomonas under cer-
tain unknown circumstances invades the tissues and causes disease.

Trichomoniasis of chicks. Weinzirl has described a highly fa-
tal disease of chicks attributed to a new species designated T'richo-
monas pullorum.

Symptoms. Chicks under a month old only are attacked. The
disease most commonly appears about the tenth day after hatching.
The affected birds droop, they huddle together, the wings drag, the
eyes are closed and the skin of the head is pale. Acute cases suc-
cumb in a day or two without showing diarrhea. Other cases be-
come chronic, in which stage diarrhea is present. The temperature
is subnormal and is usually abcut 102° F. The disease is not ob-
served until late spring and summer.

Morbid anatomy. Autopsy reveals no lesions except a gen-
eral anemic condition. The ceca may be slightly enlarged and the
contents thin and slimy. The parasites collect in the crypts of the
mucosa frequently in pure culture. When diarrhea exists, the pro-
tozoan may be found in the intestine and in the voided mucus.

Etiology. The flagellate Trichomonas pullorum regarded by
Weinzirl as the cause of the chick disease occurs in two forms. One,
the pear shaped type moves about actively by means of flagella and
also exhibits active ameboid movements. This type varies from 3.5

194 DISEASES OF DOMESTICATED BIRDS

by 7 microns to 5.5 by 9 microns, and is the only form occurring in
the cecal crypts. The globular form occurs in the lumen of the ceca.

Control of disease. Feeding of sour milk is favorably regarded
as a means of saving life.

PARASITES OF THE LIVER

The liver of birds is rarely subject to parasitism, if entero-hepatitis
of the turkey be excepted.

A flagellate Cercomonas hepatica has been reported in the liver
of squabs, causing yellowish nodules.

Echinococcus polymorphus, the cystic phase of the tapeworm of
the dog, occurs sometimes in birds, and exhibits a preference for the
liver. Kchinococci have been reported in the goura, the peafowl and
the turkey. The liver becomes enlarged by the presence of the
eysts until it occupies a large part of the abdominal cavity. The
hepatic tissue is reduced to thin pieces between the cysts.

Three species of flukes, Opisthorchis simulans, Metorchis xantho-
somus and Bilharziella polonica have been found in the hepatic
canals or biliary vesicles of the domestic duck. The latter species
occurs in the blood of a large number of species of wild ducks.

Heterakis columbe, normally a parasite of the intestines of pigeons,
has been reported as occurring in nodules in the liver.

Blastomycosis. Martin and Daille have described lesions in the
liver of the goose, due to Blastomyces (Cryptococcus) anseris. The
parasites are contained in small sacs about the size of a pea, attached
to Glisson’s capsule. These sacs are yellowish white in color, fluetu-
ate on pressure and are connected with one another by narrow chan-
nels. The contents of the saes consist of a yellowish white gelatinous
material enclosing the blastomyces. These latter consist of round or
oval nucleated refractile bodies surrounded by a distinct membrane.

PARASITES OF THE BURSA OF FABRICUS

According to Neumann, the bursa of Fabricus harbors species of
flukes of the genus Prosthogonimus. They are encountered there but
rarely, for that pouch disappears in the adult. The parasites conse-
quently are obliged to leave that diverticulum and enter some of the
other canals connecting with the cloaca. Sometimes they enter the
rectum, or they may penetrate the oviduct and become enclosed in an
egg. Probably all the forms found in the oviduct and the egg also
occur in the bursa of Fabricus.

. INTERNAL PARASITES 195

Prosthogonimus ovatus occurs in the bursa of Fabricus of a large
number of birds. It has been found in the oviduct of the hen and
many observers have found it in hen’s eggs. Pr. pellucidus and Pr.
japonicus have been found in eggs. Pr. cuneatus has been reported
as occurring in the oviduct of a pea hen.

COCCIDIA

Coccidia occurring in the intestines are discussed under the head-
ing coccidiosis, page 127.

PARASITES OF THE NASAL CAVITY

A species of mite of the genus Rhinonyssus infests the nasal cavity
of fowls, causing a sort of coryza. The mites also occur in squabs
which sometimes succumb to the parasite.

Sternostomum rhinolethrum occurs in the nasal fossee of the duck.

A leech Hemiclepsis tessellata oecurs in the nasal and oral cavi-
ties of geese and ducks, attached to the mucosa. The parasites also
attach themselves in the eyes, esophagus, larynx and trachea. The
affected birds are tormented by the presence of the parasites and
rapidly become emaciated. Mégnin recommends applying a two per
cent salt solution to cause the detachment and death of the parasites.

A fluke Cyclocelum arcuatum is reported as a harmless parasite
of the infraorbital sinus of the domestic goose.

GAPE WORMS

Gapes is caused by the roundworm designated Syngamus trachealis
which attaches to the mucous membrane of the trachea and causes
severe inflammatory changes. These lesions and the additional
factor of mechanical blocking of the air passages may cause death.
The air sacs are sometimes infested.

Species affected. The fowl, pheasant, turkey, peafowl, pigeon,
certain cage birds and a considerable number of wild birds have been
reported as hosts of Syngamus trachealis. ‘The adult turkey appears
to be very much more frequently infested than the adult fowl. Ran-
som found about 23 per cent of a number of turkeys infested when
no parasites were found in 635 chickens examined. A related species
S. bronchialis occurs in the trachea, air sacs and bronchi of young
geese.

196 DISEASES OF DOMESTICATED BIRDS

General character. The female worms are about four-fifths of
an inch in length and reddish in color. In most cases, the male,
about a quarter of an inch long, is in copulation, attached to the
female near the anterior extremity. Thus the appearance of a
forked worm is induced.

Symptoms. The presence of the worms is indicated by the
peculiar wheezing cough, gasping and the expulsion of frothy saliva
from the beak. The birds appear dull with ruffled feathers, lose
appetite, breathe with difficulty and display cachexia. Spontaneous
recovery is rare, and in the absence of treatment the parasites cause
heavy mortality. Only young birds experience harm from their
presence.

Morbid anatomy. The presence of the parasites in the air
passages enveloped in foamy mucus is the most important feature
observed at autopsy. The point at which the parasites adhere often
consists of an abscess filled with yellow colored pus of caseous con-
sistency. Such an abscess may cause asphyxia.

Life history. The sexually ripe females are expelled by cough-
ing, whereupon the eggs are disseminated by the disintegration of
the female. Thus water and soil become contaminated with the
larvee hatching from the eggs. It is not believed that an intermediate
host is necessary in the life eycle of the parasite, even though it has
been shown that the feeding of earthworms will induce the disease
among chicks otherwise protected against infection. Undoubtedly
earthworms may contain larve in the intestinal tract, due to earth
ingested by them, without however, playing the réle of a host. It has
been demonstrated repeatedly that chicks may be infected by drink-
ing boiled water artificially infected with ova and young gape worms.
The young worms may live for some time in water, and the per-
sistence of the infection is favored by a wet soil. Infection undoubt-
edly occurs through ingestion. The embryos probably make their
way from the gullet or crop, to the trachea by perforating the walls
of the organs in question.

Treatment. The practice of dislodging the worms by the appli-
cation of various remedies applied by inserting the tip of a feather
into the trachea and twisting, is widespread. The small size of the
trachea in young chicks and the fact that some worms are located at
its lower extremity out of reach, makes the operation painful and
uncertain in its results. Among the remedies applied are oil of
cloves, oil cf turpentine thinned with double its volume of olive oil
ond kerosene oil. The feather also acts mechanically in dislodging

INTERNAL PARASITES 197

the parasites, whereupon they are expelled by coughing. A coiled
horse hair is frequently employed for the same purpose, but like the
feather its use is dangerous to the chick. A few worms may be
caught with tweezers if the larynx is raised high enough.

It has been asserted that pounded garlic in the proportion of one
bulb per day added to the food of ten birds would result in the ex-
pulsion of the worms. Asafcetida has been administered in the food
with the idea that the agent, eliminated through the air passages,
would kill the parasites.

Fumigation with various agents has been employed. Exposure to
sulphur fumes has been used to induce coughing and expulsion of
the worms but is dangerous. Affected birds may be exposed to
tobacco smoke until they become almost insensible, after which they
are allowed to recover in the open air. Fumes of heated carbolic
acid have been employed.

Klee has great confidence in intra-tracheal injection which re-
quires no more time than other more dangerous kinds of individual
treatment and is regarded as more effective. The affected bird is in-
jected in the trachea with 1 ¢.c. of a 5 per cent aqueous solution of
sodium salicylate, administered with a hypodermic syringe. This
fluid simultaneously loosens all the parasites occurring there and a

Fie. 30. Apparatus for making injections in trachea. a, Syringe; b, Straight
eanula; ec, Curved canula. (Klee)

198 DISEASES OF DOMESTICATED BIRDS.

violent cough will expel them. The operation in question can be
performed by one person, for a syringe with two rings on the barrel
can be guided easily with one hand. The sick bird is held between
the knees with the breast in front. The neck is bent up and back
with the left hand and the trachea lies between the thumb and index
finger. Next, the syringe lying conveniently, is grasped with the
right hand. The needle is placed near the trachea, after which with
necessary care it is inserted into the trachea slanting downwards and
the injection made quickly. The introduction of a dull canula into
the glottis through the beak is even more suitable than the foregoing
method. After the injection the bird suffers a light attack of
choking but soon recovers.

A very safe but a somewhat less effective remedy is to cause the
affected birds to breathe air containing finely powdered chalk and
camphor. Theobald recommends a mixture of two parts by weight
of powdered chalk and one part of powdered camphor. ‘This is
dusted into a closed box in which the chickens are confined.

Prevention. Contaminated water and soil are to be regarded as
the chief sources of infection. Infectious larve have been kept alive
for a year in moist soil. Chicks raised on board floors and thus iso-
lated from the soil with separation from older birds until a month
or six weeks old, will escape infection provided the water and food
supply are not infected. Rotation in the use of land to which chicks
are allowed access is a valuable practice in avoiding the use of con-
taminated soil from year to year. Above all, chickens should not be
kept on soil that has been occupied by turkeys within a year or so.
Disinfection of drinking vessels and of soil, so far as possible, de-
serves consideration. Salicylate of soda, 3 drams to the quart of
drinking water is said to kill the embryo worms. Contaminated soil
may be disinfected by drenching with a one per cent solution of sul-
phuric acid. Wet areas should so far as possible be dried by drain-
ing.

The isolation of the sick and thorough disposal of the dead are
obvicus precautions.

THE AIR SAC MITE

Cytoleichus (Cytodites) nudus has a wide distribution in the
United States and Europe affecting a large number of gallinaceous
fowls and also pigeons. The mites are barely large enough to be de-
tected by the unaided eye. They have been observed in the trachea,

INTERNAL PARASITES 199

lungs, air sacs, hollow bones and the peritoneum. They have been
reported as occurring exceptionally in the heart, liver and kidneys.
Their presence within tissues is
not readily explainable since
their structure is not adapted to
the penetration of tissue. They
are most commonly noted in the
air sacs. Hens apparently in
perfect health may be heavily in-
fested, so that the economic im-
portance of the parasite seems to
be not very great. The method
of transmission has not been thor-
oughly explained. Their exit
from the body could occur
through the trachea by expulsion
during coughing.
Fic. 31. Cytodites nudus. Male, ven- A few writers have observed
ee Enlarged 100 times. cases in which the parasites ap-
pear to be of pathological impor-
tance. Gerlach regarded them as the cause of enteritis as did also
Zundel. Williams attributed high importance to them as a parasite

Fic. 32. Cytodites nudus. Ovigerous female, ventral aspect. Enlarged 100
times. (Railliet)

200 DISEASES OF DOMESTICATED BIRDS

of fowls in Montana, a view that Wilcox was not able to confirm.

Among the later observers Walker has reported upon two autopsies
of fowls in Grahamstown, Cape Province, in which lesions occurring
in the lungs, were in his opinion, the cause of death. The owner
reported that the comb turned purple, appetite was lost and the birds:
seemed fretful and weak in the legs. Birds were noticed to be sick
for a week, when sudden collapse occurred. Observations by Walker
follow.

Morbid anatomy. Cytodites are frequently found in the thorax
and peritoneal cavity, fairly frequently on the mesentery and in the
trachea. The lungs are mottled in appearance by some purple
patches .2 to .8 em. in diameter. On section, hyperemia is observed
and serous fluid exudes from the cut surfaces. Small milary
tubercles of a gelatinous consistency are scattered through the af-
fected portion of the lung, and parasites are visible in the midst of
each of these. The larger bronchi and some of the bronchioles con-
tain an exudate in which the parasites are imbedded. Other organs
and blood appear normal. The conditions observed warrant the
pathological anatomical diagnosis of hyperemia and edema of the
lungs, and bronchial pneumonia.

Microscopie examination of sections of stained tissue, under 300
magnification shows that the lung tissue surrounding the invaded
air passages is infiltrated with leucocytes and red blood corpuscles.
The blood vessels are congested. Some of the
parasites have wandered from the air conduits
into the surrounding parenchyma _ breaking
down the regular network conformation of the
latter. In some of the invaded air passages,
the parasites have lodged themselves in the
inner lining and have broken it down. In
places eytodites are to be seen in the inter-
lobular fibrous tissue. The larger bronchi
contain an exudate.

Fic. 33. Dithyridiwm
variabile, from a fowl.
Enlarged 10 to 12 CESTODE CYSTS IN THE LUNGS
times. (Neumann )

Neumann has deseribed a case in which the
encysted parasite known as Dithyridium variabile occurred in great
numbers in the lung of a fowl. These represent the cystic stage of
a tapeworm, which has not been identified with the adult form. The
cysts were observed in the inferior surface of the lungs in the an-

INTERNAL PARASITES 201

terior and posterior diaphragmatic reservoirs. They were globular
or ovoid bodies 3 to 4 mm. in diameter, somewhat transparent and
filled with a colorless liquid containing a parasite. Some were free,
and others adhered slightly to adjoining tissues. The dithyridium
has a milk-white body, varying in length from 1.5 to 2.5 mm. It is
sometimes as broad as long and sometimes much longer than broad.
An invaginated cestode cunlee is present.

MANSON’S EYE WORM

At least 38 species of nematode worms have been reported as
parasitic in the eyes of birds throughout the world. However, only
one, Oxyspirura mansont, is known to affect com-
mon domesticated birds. This has been found in =
fowls and peafowls. Ransom has reported upon its _ °

i i Fic. 34. Manson’s
presence in the United States, and upon the preva-> “eye worm (0e-
lence of nematodes in wild birds. yspirura — ‘man-

General description. The parasite known as oe we eee
Oxyspirura mansoni or Filaria mansoni or Spi- below. Natural
roptera emmerzii is a small white, thread-like 17% (Ransom)
worm slightly over half an inch in length and about as thick as a fine
sewing needle. It is thickest in the middle and tapers toward the
ends. ‘The number present in the eyes may vary from a few located
beneath the nictitating membrane to as many as 200.

Symptoms. In some cases the worms are present in the eyes
without causing apparent inconvenience. In more severe infesta-
tion, symptoms of irritation become evident. The affected bird ap-
pears uneasy and scratches the eyes. The latter show acute inflam-
mation with abundant lachrymation. Subsequently white cheesy
exudate collects within the conjunctive and upon the edges of the
lids, causing them to adhere together. The inflammation extends
to the tissues surrounding the eye and to the infra ocular sinuses.
Eventually the whole eyeball becomes affected, with consequent de-
struction of the organ. Catarrhal changes also involve the nasal
cavities. In severe cases the subject dies.

Treatment. The first requisite to successful treatment consists
in removing the worms. ‘This may be done by the use of forceps or
by irrigating the eyes with some solution such as bicarbonate of
soda or a two per cent solution of creolin. When the worms are
partially dislodged by the fluid, they may be entirely removed with
a soft cloth. The inflammation may be alleviated by instilling into

202 DISEASES OF DOMESTICATED BIRDS

the eyes a few drops of saturated solution of boric acid. Ransom
recommends anointing the eyes with a mixture of lard 9 parts and
iodoform, 1 part or with carbolized vaseline.

Life history of the worm. Very little is known of the life his-
tory of the parasite. It seems probable that the embryos pass a
portion of their existence either free or in a secondary host. The
reports of the presence of the worm in chickens are, so far as known,
limited to sea coast regions. This suggests the possibility that some
conditions peculiar to the sea coast are necessary to the development
of the parasite.

LEECHES IN THE EYE

One incomplete report exists of the occurrence of leeches in the
eyes of geese in Ireland. Intense irritation of the eye occurred,
with symptoms of severe pain. The birds had access to a pond
teeming with leeches.

MITES PARASITIC IN CONNECTIVE TISSUE

Laminosioptes cysticola, accord-
ing to Neumann, is a mite occur-
ring in gallinaceous birds such as
fowls, pheasants and turkeys. The
parasites live on the surface and
in the thickness of the skin caus-

Wing the formation of scurf. They
“hy are encountered rarely except in
the subcutaneous tissue especially
in the places where it is very loose,
such as the flanks, the vent, on the
thighs, the breast and the neck.
They are able to penetrate the deep
connective tissue. Microscopic ex-
amination of fragments of subeu-
taneous connective tissue permits
all phases of their development to
Fic. 35. Lamin. be observed. When they die, the

osioptes cysti- carcass acts as a foreign body and
cola. Male, 7 z
ventral aspect.
Enlarged 200 nodule about it. This promptly
times. (Rail- :
liet )

F se Fic. 36. Laminosi-
causes the formation of a miliary optes _cysticola.
Ovigerous female,
: . ventral aspect.
undergoes calcareous infiltration. Enlarged 200

On treating these nodules with times. (Railliet)

INTERNAL PARASITES 203

acidulated water, the remnants of the parasite may be recovered.
The nodules are yellowish in color, oval in shape and may become as
large as 1 mm. in diameter. They may be very numerous in an
individual and are very common in old cachectic birds. These para-
sites are not injurious to health except perhaps when they are present
in excessive numbers.

Two other connective tissue parasites occur in the pigeon. A
feather mite, Falculifer rostratus, spends a portion of its life cycle in
the subcutaneous connective tissue. ilaria clava is located in the
subeutaneous connective tissue of the pigeon. Neither have any
effect upon the health of the host.

TRYPANOSOMIASIS OF BIRDS

The blood of a very large number of wild birds is infested with
trypanosomes which apparently do not exert much pathogenic effect.
Gray lists nine species of these parasites occurring in birds. Among
domesticated birds, they have been observed in the fowl and pigeon.

FILARIA IN THE BLOOD

Filaria anatts has been observed in the heart of a duck. Embryos
of filaria have been observed in the blood of a pigeon.

PARASITE OF AVIAN MALARIA

Symptoms. The parasite of Danielewsky, Hemoproteus danie-
lewskyi has also been designated Hamomeba danielewskyi, Halter-
idium danielewskyi and Plasmodiwm danielewskyt.

General nature. The parasite of avian malaria, one of the
hematozoa of birds, has many points of resemblance with the parasite
of malaria of man.

Distribution. The parasite occurs in a large number of wild
birds. Cardamatis examined the blood of 38 species of birds in
Greece, including 936 specimens. Of 724 local birds, 21.79 per cent
were affected. Of 212 migratory birds, 32.07 per cent were infected.
The domestic pigeon is the only domesticated bird reported as in-
fested by the parasite. Aragiio refers to the parasite of the pigeon
as a separate species, H. columbe.

Symptoms in wild birds. Cardamatis observes that birds in-
tensively infected appear less lively, the plumage is dull and emacia-
tion causes them to appear smaller.

204 DISEASES OF DOMESTICATED BIRDS

Lesions in wild birds. The organs according to Cardamatis,
show characteristic alterations resembling those caused by malaria in
man. ‘The blood of sick birds is sometimes watery, less abundant
than normal, pale, and coagulates slowly. The spleen is colored like

Fic. 37. Hemoproteus danielewsky in blood of the pigeon under different as-
pects. 1, 2, red blood corpuscles containing small parasites; 3, red blood
corpuscle containing a large female parasite; 4, red bluod corpuscle contain-
ing a large male parasite; 5, corpuscle with a female and a male parasite;
6, parasite after rupture of the corpuscle which had contained it (The nu-
cleus of the cell is still seen coupled with the parasite); 7, male parasite
with four flagella; 8, female parasite into which a flagellum is penetrating
(fecundation) ; 9, a free flagellum. Enlarged 1500 diameters. (Neumann)

chocolate or darker and is always swollen to twice the normal size.

This writer found turtle doves and lanners most susceptible. Iturbe

and Gonzales note that while the hematozoa frequently have no ef-

fect upon the host, the mortality may reach 90 per cent in Mytozetes
texensis, Chlorophonia pretti and Sycalis flaveola.
Transmission. Aragao observes that the natural transmittors of

H. columbe in Brazil are Lynchia livicolor and Microlynchia persilla ;

in Algeria, DL. maura; in the Transvaal, L. capensis. Direct inocula-

tion from pigeon to pigeon fails.

LEUCOCYTOZOA

Leucocytozoa are blood parasites which so modify the appearance
of the host cell that the identity of the latter is in controversy. - Fan-
tham inclines to the view that small mononuclear leucocytes are the
cells invaded. Leucocytozoa have been observed in a large number
of wild and domesticated birds. Among the latter, fowls, pigeons,
ducks, ostriches and turkeys are known to be infested. In general
they are of slight importance as disease producers.

INTERNAL PARASITES 205

LEUCOCYTOZOON INFECTION IN DUCKS

Wickware observed an outbreak of disease among young ducks
under circumstances that led him to suspect that leucocytozoa were
responsible. Bacteria could not be excluded as a cause, for it was
not possible to seed culture media.

Symptoms. The affection runs a rapid and fatal course, with
few symptoms to indicate its onset. Impaired appetite is first no-
ticed in that the birds refuse to respond to the call for feeding. In
some cases ducks succumb during the first paroxysm, while others
survive a series of exacerbations. Affected ducks lie in a semi-
comatose condition with the neck bent backwards and the head resting
upon the dorsal portion of the spinal column. When roused from
this stupor the bird experiences a period of intense excitement during
which remarkable movements are made. The head is held in various
positions, or describes circles in the air, or at other times swings to
and fro. In some cases the neck is completely turned on itself with
the head resting on the ground in an upright position. The power
of equilibrium is lost and the bird turns over backwards until ex-
hausted. In recovered birds, there is lameness and consequent
difficulty of locomotion. Purulent ophthalmia with adherent lids
is a quite constant symptom. The mortality is about 65. to 70 per
cent.

Etiology. The leucocytozo6dn present in the blood of ducks in
two outbreaks of disease is designated by Wickware as Leucocytozoin
anatis. The shape of the parasites is fairly uniform although there
appears to be considerable pleomorphism in the gamete forms. The
predominant type is a spindle shaped organism 35 microns to 60
microns in length by 10 microns in width, showing an oval elongated
or irregularly shaped nucleus, with dark chromatic band extending
along one border. With Giemsa, the nucleus stains a dark blue and
has a granular appearance. In the center there may be observed a
small chromatin staining body varying slightly in shape. The
cytoplasm appears almost transparent or at most stains a faint pink.
At each end it terminates in an acute angle. Considerable varia-
tion occurs in the staining characteristics of the mature forms.

Morbid anatomy. Other than acute hemorrhagic inflammation
of the large intestine behind the ceca, no abnormality of the visceral
organs was cbserved. The blood in all cases of infection showed an
increase of eosinophiles, besides the leucocytozoa.

206 DISEASES OF DOMESTICATED BIRDS

REFERENCES

1. Aragiio. Pesquizas sobre o “ Hemoproteus columbe.” Brazil-Med-
ico. 4 et 11 Nov., 1916. Abs. in Bull. de ? Inst. Pasteur, T. 15, p. 300.

2. Cardamatis. Le paludisme des oiseaux on Gréce. Etude biologique
et histologique du parasite de Danielewsky. Centralbl. f. Bakteriol.
(Etc.), 1 Abt. Orig., Bd. 59, 1909, S. 351. 4

8. Ciurea. Nematoden aus dem Pharynx und Osophagus des Haushuhn.
Ztschr. f. Infektionskr. d. Haustiere., Bd. 15, 1914, S. 49.

4. Freese. Ueber die durch den Strongylus nodularis hervorgerufene
Magenwurmseuche bei jungen Ginsen und die durch Trichosomen
(Trichosoma retusem Railliet) verursachte Darmwurmseuche. Deutsche
tierirztl. Wehnschr., Bd. 16, 1908, S. 713.

5. Gage and Opperman. A tapeworm disease of fowls. Md. Agr. Exp.
Sta. Bull. 139, 1909.

6. Gutberlet. Studies on the transmission and prevention of cestode in-
fection in chickens. J. Am. Vet. M. Ass., Vol. 2, 1916, p. 218.

1. Hadley. The role of the flagellated protozoa in infective processes
of the intestines and liver. Rhode Island Agr. Exp. Sta. Bull. 166.

8. Hadley. The avenue and development of tissue-infection in intes-
tinal trichomoniasis. Rhode Island Agr. Exp. Sta. Bull. 168.

9. Hadley. The case of trichomonas. Amer. Nat., Vol. 51, 1917, p. 209.

10. Hadley. The part played by the goblet cells in protozoan infections
of the intestinal tract. J. Med. Research, Vol. 36, 1917, p. 79.

11. Herms and Beach. Round worms in poultry-life history and con-
trol. Univ. Cal. Agr. Exp. Sta. Circ. 150.

12. Iturbe and Gonzales. El paludismo de las aves en Venezuela. Lab.
du Dr. Iturbe, Caracas, 1916.

13. Martin et Daille. Sur une blastomycosis Hepatique de | Oie.
Rev. Vet., T. 7, 1912, pv. 129:

14. Martin and Robertson. Further observations on the cecal para-
sites of fowls, with some reference to the rectal fauna of other verte-
brates. Quart. J. of Micr. Sc., Vol. 57, 1912, p. 53.

15. Moore. A nodular teniasis in fowls. U.S. Dep. Agr. Bureau Ani-
mal Indust. Cire. 8.

16. Neumann. Parasites et maladies parasitaires des oiseaux domes-
tiques. Paris: Asselin et Houzeau. 1909.

17. Ransom. Manson’s eye worm in chickens. U.S. Dep. Agr. Bureau
Animal Indust. Bull. 60.

18. Ransom. A new nematode (Gongylenoma ingluvicola) parasitic in
the crop of chickens. U.S. Dep. Agr. Bureau Animal Indust. Circ. 64.

19. Ransom. The tapeworms of American chickens and turkeys. U. 8S.
Dep. Agr. Bureau Animal Indust. Cire. 85.

20. Robertson. Notes on ostrich parasites. Agr. Jour. Cape of Good
Hope, Vol. 33, 1908, p. 583.

21. Stiles. Report upon the present knowledge of the tapeworms of
poultry. U.S. Dep. Agr. Bureau Animal Indust. Bull. 12.

22. Theobald. The gape worm and the white intestinal worms of poul-
try. Jour. Bd. Agr., Vol. 6, 1899, p. 157.

INTERNAL PARASITES 207

23. Theobald. Parasitic diseases of poultry. London: Gurney & Jack-
son, 1896..,

24. Walker. <A short note on the occurrence of a leucocytozoén infec-
tion. Host the ostrich. Union of So. Africa. Dep. Agr. Ann. Rpts. Dir.
Vet. Res., 2, 1912, p. 384.

25. Weinzirl. Trichomoniasis of chicks: a new and highly fatal dis-
ease. J. Bact., Vol. 2, 1917, p. 441.

26. Wickware. Intestinal parasites of poultry, their prevention and
treatment. Dominion of Canada, Dep. of Agr. Health of Animals Branch.
Bull. 25, 1917.

27. Wickware. Is Leucocytozoén anatis the cause of a new disease in
ducks? Dep. Agr. Canada. Rept. Vet. Dir. Gen., 1915, p. 95.

28. Wilcox. The internal chicken mite. Montana Agr. Exp. Sta. Bull.
22, p. 30. (Bibliography.)

29. Williams. The air sac mite of the fowl. Am. Vet. Rev., Vol. 22,
1898, p. 8.

CHAPTER XVII

EXTERNAL PARASITES
LICE

General nature. Bird lice are wingless parasitic insects with
mouth parts adapted to biting, not sucking. Lice in general perma-
nently infest the host bird except when moving to other individuals.
Opportunity exists for this migration on the roost, the nest, during
copulation or while a hen is hovering chickens. Occasionally lice
which are normally parasitic for the hen, guinea-fowl or turkey
will be found on another species in close contact.

Lice feed on epidermal products such as feathers,
scales and the skin itself. Blood dried on the skin
may be eaten but lice are not blood suckers.

Injury caused by lice. Their presence causes
pruritis set up by their claws and mouth parts.
Excessive infestation undoubtedly is a serious hin-
drance to normal growth and development. Brood
hens are annoyed in some eases to such an extent
that there is interference with incubation. In the
Fic. 38. Head Southern States, there is a heavy mortality among

ee cece chicks hatched by hens after April 1, which may be

enlarged. (Bish- attributed to the heavy infestation by lice. Bishopp

SRP end Weed)” ond Wood regard symptoms of lice infestation as
consisting of droopiness, lowered wings and ruffled feathers. In
grown fowls heavy infestation may be tolerated without causing ill
effect. In other cases there is reduction in ege yield and loss of
weight.

Species of lice. More than 40 species of lice occur on domesti-
cated birds. Some species are restricted to one host, while others
infest several different, host species. Bishopp and Wood state that
seven species are very commonly found on chickens in the United
States, four or five on pigeons, two or three each on geese and ducks,
three on turkeys and several each on guinea fowl and peafowl.
These are: On chickens, the head louse (Lipeurus heterographus),
the body louse (Menopon biseriatum), the shaft louse (Menopon

pallidum), the wing louse (Lipeurus variabilis), the fluff louse
208

EXTERNAL PARASITES 209

(Goniocotes hologaster), the large hen louse (Goniocotes abdomi-
nalis), the brown chicken louse (Goniodes dissimilis) ; on turkeys,
the large turkey louse (Goniodes stylifer) and the slender tur-
key louse (Lipeurus meleagridis). The common body louse and
the shaft louse of chickens sometimes are found on the turkey.
On ducks Docophorus icterodes and LInpeurus temporalis are com-
mon; on geese a variety of D. icterodes; on pigeons the slender
pigeon louse (Lipeurus baculus) and the broad pigeon louse (Gon-
ocotes compar) cause most of the harm from lice.

Neumann lists 6 species as occurring on the pheasant as follows:
LIipeurus variabilis, Goniodes colchicus, G. truncatus, Goniocotes
chrysocephalus, Menopon productum, and M, biseriatum; on the pea-
fowl, Goniodes falcicornis, G. parviceps,
Goniocotes rectangulatus and Menopon
pheostomum ; on the guinea-fowl, Lipeurus
numide, Goniodes numidianus, Goniocotes
rectangulatus, Menopon numide and Lipeu-
rus variabile of the fowl. In addition to
the two species listed by Bishopp and Wood
as important lice on the pigeon in the United
States, Neumann mentions Gontodes minor, Tedsiad uae ec eae
G. damicorns, Menopon giganteum, M. jouse (Lipeurus hetero-
longicephalum, Inotheum longicaudum and coer, a eee Se
M. biseriatum of fowls as occurring on opp and Wood)
pigeons ; on geese, Lipeurus crassicorms, L.
anseris, Trinoton anseris and T. lituratum; on ducks, L. anatis, T.
luridum and Menopon obscurum; on swans, Ornithonomus cygnt,
Philopterus cygni and Trinoton anseris of the goose.

The terms head louse, body louse, wing louse, ete., as applied to
the lice of fowls indicate where the various species are found in
greatest numbers and where their structure best adapts them to live.
Thus the head louse exhibits a preference for the head but is ocea-
sionally found on the feathers of the wings. Some lice are adapted
to live on the skin only, while others cceur on the feathers as much
as an inch from the skin.

Life history. In general, lice spend their whole life on one host.
All the finer details of the life history of lice have not been worked
out. The eggs, attached to the feathers are commonly known as nits.
In the case of the head louse they hatch in four or five days. The
young, after molting the skin several times, reach the adult stage in
17 to 20 days.

AAlig) DISEASES OF DOMESTICATED BIRDS

Combating lice. Owing to the habit of lice of
remaining upon the host, the most direct method of
combating them consists of the application of an in-
secticide to the bird.

Bishopp and Wood favor starting a campaign
against lice in the late summer or early fall. The
weather conditions are favorable and the amount of
stock to be treated is the lowest of any time in the
year. There is no reason to prevent a flock from
being entirely freed from lice and kept free.

These writers conclude that the commercial grade
a a 40. __ Body of sodium fluorid is the most satisfactory agent to

ouse (Menopon a i y - é ss A

biseriatum): use against lice. It kills lice in all stages including

Cais cieee those Gaching subsequent to its applieation. They

(Bishopp and apply the agent in two ways. When applied in the

Weed) powdered form, the bird is held in a pan to catch
superfluous powder. They apply one pinch on the head, one on the
neck, two on the back, one on the breast, one below the vent, one on
the tail, one on either thigh and one scattered on the inner side of
each wing when spread. They recommend this method of applica-
tion for newly hatched birds and sick birds exclusively. The action
of the powdered sodium fluorid is comparatively slow, but it remains
on the bird, and in four or five days all lice will disappear. The
dust is somewhat irritating to the air passages and the operator
should wear a dust protector over the mouth and nostrils. The
powder causes a transitory effect only on the air passages of the
treated birds. The method costs about $1.25 per hundred fowls,
calculating the man’s time at 20 cents per hour.

Applying the agent in solution by dipping has the advantage in
reducing cost of materials and is more rapidly done, without discom-
fort to the operator. Furthermore, the lice die very promptly after
being touched by the fluid. The first requisite is a warm, sunny day
so that the fowls will dry quickly. The solution is prepared in a tub
in the proportion of three-fourths to one ounce of commercial sodium
fluorid to each gallon of tepid water. In dipping the birds, the wings
are held over the back with the left hand while the bird is sub-
merged in the solution with the head out. The feathers are thor-
oughly ruffled with the right hand to secure penetration of the fluid
to the skin all over the body. The head is ducked once or twice, the
bird is drained a few seconds and is released. The work of dipping
should be stopped sufficiently early in the afternoon to permit the

Soe So

a
ya
a
Hit a
pe

EXTERNAL PARASITES 211

birds to become dry before night. By the dipping method the cost
for material is 58 cents per hundred birds. For material and labor
both, it is 71 cents.

Bishopp and Wood note that several other agents are effective in
destroying lice, but are more expensive than so-
dium fluorid. Flowers of sulphur applied with a
dust can in an amount of about 6 pounds per hun-
dred fowls is effective in about four days. Dip-
ping fowls in a solution of 1 ounce of laundry soap
to a gallon of water, repeated in ten days is ef-
fective.

Herrick strongly recommends the Cornell or
Lowry dusting powder made as follows: Two and
one-half pounds of plaster of Paris is spread in a Fic. 41. Mass of

shallow pan or tray. One-fourth pint of crude — body Touse eggs
carbolic acid is poured into a cup, and into this is feather. Greatly
poured three-fourths pint of gasoline. The mix- enlarged. (Bish-

i i : d Wood
ture of acid and gasoline is poured over the plas- ees

ter of Paris and thoroughly mixed. It is then rubbed through a
wire window screen on a piece of paper and allowed to stand for
from one and one-half to two hours or until thoroughly dry. It
must not be placed near a flame or any heat. The powder should be
kept in a closed can or jar, where it will retain its strength for a long
time. The powder is applied by means of
an ordinary sifter or with the fingers. It is
worked in among the feathers about the vent,
in the fluff, and under the wings. Two and

perhaps three applications should be made. A

small pinch of the powder is sufficient for a

fowl. The rooster should receive especial care

in being kept free from lice, as he is an im-

portant factor in spreading the parasites.
The expense of this treatment including la-

bor should not exceed 32 cents per hundred
fowls.

Fic.42. Largehen louse. he effectiveness of this method of dusting
(Goniocotes abdomi- . , 2 : , e
nalis): Male, top birds for lice has been called into question by
view. Greatly en- several observers.
larged. (Herrick) :

Lamson and Manter recommend the appli-
eation of a dilution of either mercurial ointment or blue ointment.

Mercurial ointment was considered cheaper when judged on the basis

212 DISEASES OF DOMESTICATED BIRDS

of content of metallic mereury. The mercurial ointment is mixed
with one or two parts of vaseline. One ounce is sufficient to treat
about seventy-five hens. In the case of chickens it is desirable to
place a piece of ointment the size of a pea, under the wings or around
the vent. In older stock the best place is on the skin just beneath
the vent. The treatment seems to remain effective for some time,
so that lee hatching after the application are also killed. It is not
clear that the use of mercurial ointment is cheaper or more effective
than sodium fluorid. Bishopp and Wood find that when used as
recommended, the mercurial product has little effect upon head and
wing lice. Used in larger amount it is more expensive and injurious.

The dust bath constitutes the natural defense of fowls against lice
and should be considered in connection with the measures against
them. It is desirable that the box be located in the sunlight, and if
covered, will prevent widespread dissemination of dust in the poultry
house. The finer and lighter the material available, the better.
Fine siftings from coal ashes is a desirable addition to the dust, as
also are snuff, sulphur and dry slaked lime. The dust bath, while
desirable, cannot be depended upon to the exclusion of more aggres-
sive measures. It has only a temporary effect upon the numbers
of lice on the fowls. Some birds seldom or never use the dust box.

In a flock infested with lice special care must be taken to free the
sitting hen from these parasites and to protect young chicks in like
manner.

THE BIRD FLEA

The common bird flea, Pulex avium, attacks a large number of
species of birds including fowls and pigeons. The parasite is pro-
vided with piercing mouth parts with which it penetrates the skin and
extracts blood. ‘The irritation produced by the fleas causes pruritis
and loss of rest.

Life history. The eggs are laid in hens’ nests or on manure on
the floor of the poultry house.
These nits after a week or ten days
hatch into white larve which are

nearly a quarter of an inch in

Hre.43., Larva, of hen’ fea, enlarged Jength. Che larvalataee lastaerom
20 times. (Railliet)

ten days to three weeks, depend-

ing upon the temperature. The fully developed larva becomes

secreted in some crevice and spins itself a cocoon. In this structure

the larva develops into the adult stage during a period varying from

EXTERNAL PARASITES 213

ten to twenty-one days. Fleas are temporary rather than permanent
parasites, and are nocturnal feeders. During the day they hide in
various protected places about the poultry house. Sitting hens suffer
severely from their attacks.

Combating fleas. Repression of fleas is accomplished by the
spraying necessary for combating mites. The use of whitewash con-
taining a small percentage of kerosene oil destroys larve, fills up
lurking places and drives adults away if it does not kill them. Wood
shavings is a desirable material for making nests, as it is repellent
to fleas. Simple construction of interior fixtures to facilitate re-
moval and cleaning is as necessary in connection with combating
fleas as in combating mites.

CHIGOE

A second true flea, the chigoe, Sarcopsylla gallinacea, causes in-
jury in quite a different manner. The male penetrates the skin,
while the female becomes fixed to the skin so it is not detached
quickly. Fowls, ducks and various animals are subject to attack.
The parasite is found in great numbers about the eyes and neck.
It is widely distributed, having been reported as occurring in Ceylon,
Florida, South Carolina, Italy, Turkestan and various portions of
Africa.

FLIES PARASITIC UPON PIGEONS

A fly, Ornithomyia avicularia, is parasitic upon a number of wild
birds and has been reported as occurring on pigeons in France. It
moves between the feathers and draws blood from the host. Lynchia
maura 1s a closely related species parasitic upon pigeons in Sicily
and Algeria. These flies are especially abundant upon squabs before
the plumage has developed. Their attacks cause emaciation and
sometimes also a fatal anemia. Sitting birds are disturbed by
the parasites and make quick movements which may result in break-
ing the eggs. Sometimes the birds are so tormented that they
abandon the dovecote. Sergent reports this fly as the secondary host
of the blood parasite Hamoproteus danielewskyi. L. capensis has
been reported as parasitic upon pigeons in Teneriff.

BED BUGS
The common bed bug Cimex (Acanthia) lectularia occasionally in-
fests fowls and pigeons at night for the purpose of sucking blood.

During the daytime they inhabit cracks and sheltered places about
the poultry house.

214 DISEASES OF DOMESTICATED BIRDS

NEST BUGS

The nest bug or dovecote bug Cimex (Acan-
thia) columbara is a species closely related to
the bed bug and which also attacks pigeons and
fowls. Sitting hens suffer severely. Both this
species and bed bugs are held in check by the
routine measures recommended in combating
mites. C. tmodorus occurs in Mexico, New
Mexico and Texas.

LARVAL BEETLES ATTACKING HENS AND PIGEONS

A
RK Tenebrio molitor is a beetle the larve of
which have been reported as attacking sitting
ee ai ee hens and pigeons. Pigeons have been reported
size; B, enlarged. a8 Subject to the attack of larve of Dermestes
(Railliet ) lardaritus and other larvee of the genus Necro-

phorus and genus Silpha. These coleopterous larve develop in the
manure of the dovecote, attack the skin of the squabs on the neck and
abdomen and even the superficial muscles. The wounds become in-
fested with fly maggots and are frequently fatal. The presence of
the larvee may be prevented by cleanliness. Wounds may be treated
with antiseptics.

RED MITES

Synonyms. Poultry mite, chicken mite, roost mite.

Hosts. Pigeons, fowls, turkeys, pheasants, domesticated mam-
mals and man are subject to attack by the parasites.

General nature. The common poultry mite, Dermanyssus gal-
line in general, infests birds only temporarily while they are on
the roost. It is a blood sucker, and be-
sides causing loss of blood, induces intense
irritation.

Individual mites are barely visible to
the unaided eye, but owing to the habit of
collecting in masses, they are easily de-

rs : k i Fic. 45. Egg of the
tected, especially when engorged with clieken (mate | Deane
blood and colored red. When not en- sus galline). Greatly

: enlarged. (Bisho and
gorged, they are gray in color. Wood) a

EXTERNAL PARASITES 215

The parasite is widely distributed throughout the world. Its
depredations are more serious in warmer countries because of favor-
able climatic conditions.

Habits. During the daytime the mites collect in cracks, or under
droppings and rubbish. ‘They make their way at night to the birds
on the roost where they cause annoyance
while engorging with blood. Occasion-
ally mites will attack hens on the nest
during the daytime. When engorged,
the mite leaves the bird. Some mites
that fail to become engorged the same
night they gain access to the bird, will
remain on the host during the following
day or so. Thus hens have been found
to carry as many as a hundred mites dur-
ing the daytime. Eggs are laid in the
places sheltering the mites, and hatch in
two days or more depending upon 12) eae ae Han beuenes
temperature. The larve hatching from — of the chicken mite, unfed.
the eggs shed their skins in about two Greatly enlarged. (Bishopp

and Wood)
days and become nymphs. After several
engorgements and molts, the parasite reaches maturity. The whole
life cycle is complete in a week. The parasites are not active in cold
weather. In the absence of poultry, mites will remain alive in in-
fested houses for four or five months. Moisture seems to favor their
longevity.

Injury caused by mites. Excessive mite infestation has been
held responsible for increase in cost of maintenance, decrease of
egg laying and general unthriftiness. Sitting hens have been
driven by the irritation, to abandon the nest. The attack of the
mites rarely leaves a trace on the skin. |

Combating mites. In combating the pest, it is recommended
that all interior fittings be removed so as to minimize the number of
cracks in which mites could escape the action of the spray. If the
house is of the older type, with built-in accessories such as perches and
nests, everything should be torn out leaving merely the four bare
walls. The whole house should be thoroughly swept and all rubbish
removed. Kerosene oil, or kerosene emulsion constitute suitable
agents for killing mites.. One of these agents should be applied with
a spray pump, particular care being taken to force the fluid into
cracks. Since it is quite likely that some mites and eggs will

216

DISEASES OF DOMESTICATED BIRDS

escape being hit by the fluid, it is necessary to repeat the applica-
tion in a week and perhaps a third time may be necessary.
Bishopp and Wood recommend crude petroleum as the most ef-

fective agent and one that retains its killing power for weeks.

Fic. 47. Female chicken mite before
feeding, greatly enlarged. Mouth
parts at right highly magnified.

(Bishopp and Wood.)

the water is hot it is
oil is added, and the mixture is agi-
tated or churned violently until
emulsion is formed. The best way
to produce the emulsion is to pump
the liquid back into the same con-
tainer through the pump until the
mixture becomes creamy. To
make a ten per cent emulsion, 17
gallons of water are added to the 3
gallons of stock mixture ; to make a
fifteen per cent emulsion, 101% gal-
lons of water are added to the 3
gallons of stock mixture.
Subsequent to spraying with
kerosene emulsion it is desirable to
dust the entire interior of the
houses with a mixture of air slaked
lime, 3 parts and sulphur, 1 part.

removed from the fire,

To
improve its spraying quality it
may be thinned with one part of
kerosene to four parts of crude
oul. They likewise find arseni-
eal dip such as used for dipping
cattle to be fairly satisfactory in
killing mites when applied sev-
eral times.

Repp recommends preparing
kerosene emulsion as follows:
One-half pound of laundry soap
or whale-oil soap is shaved fine
and dissolved in 1 gallon of
water. The soap is best dis-
solved if the water is nearly
or quite at the boiling point.
When the soap is dissolved and
2 gallons of kerosene

after
( Bish-

Female chicken tick
feeding. Greatly enlarged.
opp and Wood)

Fic. 48.

A further measure against mites consists in painting the perches

EXTERNAL PARASITES 217

with a mixture consisting of three parts of kerosene to one part of
erude carbolic acid.

The presence of all sorts of rubbish affords lurking places for
mites and decaying matter such as broken eggs attracts them par- _
ticularly.

When fowls are moved to fresh quarters from infested quarters it
is desirable that they be left for three days in a pen so that all mites
will have opportunity to leave the birds.

Mites are disseminated not only by live birds bearing them, but
by all such articles as crates and other objects that have been in
poultry houses. The introduction of mites by pigeons or sparrows is
quite possible.

Infestation of man. People in close contact with infested hen
roosts are liable to be attacked by the mites. They cause an
ephemeral itching lesion on the back of the hand and other exposed
portions of the body. However, they may affect any portion of the
body.

Occurrence on horses. When poultry roosting quarters are near
or in the stable, horses are subject to infestation. They cause severe
pruritis during the night. The mites cause the formation of small
vesicles single and grouped together. These vesicles are rubbed off,
accompanied by depilation, but the areas soon become covered with
new epithelium. ‘This gives the skin a characteristic flea-bitten ap-
pearance. To these changes are added others resulting from ex-
cessive rubbing.

Mites in the external ear. Mites have been observed in the
outer ear of chickens and ducks. In the case of the latter, unusual
movements of the head occurred. The mites were considered by the
observer to be D. galline but Neumann expresses doubt concerning
the identification.

HARVEST MITES

Harvest mites are first stage larvee of certain species of the genus
Trombidium. They are commonly known as chiggers, a name which
is evidently a corruption of the term chigoe, used to designate a
species of flea. The harvest mites attack a wide variety of hosts,
including poultry. They attach themselves in groups to the skin
beneath the wings and on the breast and neck. Their presence causes
areas of severe irritation and suppuration. Young chickens are most
susceptible and their death has been attributed to the result of the
presence of the parasites.

Mites occur in a wide variety of places such as in damp locations

218 DISEASES OF DOMESTICATED BIRDS

along the borders of streams, in trees and shrubbery and on the
borders of forests.

In the United States they are most numerous in the South but are
well distributed in Kansas, Indiana and Iowa. In England and
Scotland they are known popularly as gooseberry bugs.

Chickens should, so far as possible, be kept from ranging in areas
known to be infested. Dusting the feathers with sulphur is useful
in keeping the mites off. The application of sulphur ointment or
kerosene and lard for killing the mites on the skin is recommended
by Bishopp and Wood. Eroded areas may be treated antiseptically.

SCALY LEG OR FOOT MANGE

The mite designated Cnemiodocoptes mutans (Sarcoptes mutans)
affects the legs of fowls below the tarsal joint.
Other domesticated birds are affected more rarely.
The first evidence of infestation consists of the ap-
pearance of grayish white areas which gradually
coalesce and thicken. The parasites burrow in the
skin and set up cellular proliferation with exuda-
tion. This thickens the skin and causes the natu-
ral scales of the leg and toes to protrude. In an
advanced case the skin is covered with thick gray-
ish white crusts which appreciably increase the
size of the leg and toes. The enlargement of the
leg interferes with
Fic. 49. Cnemio- the motion of the

docoptes (Sar- .. é :

coptes) mutans. joints. The skin 1s

Male, dorsal as- inflamed and raw.

pect enlarged : ‘
100 times. (Neu- Examination of some
mann) of the crusts will re-

veal the presence of mites. Itching is
present as indicated by the pecking of
the lesion by the bird. In extremely
advanced cases the bird may become
lame, arthritis may develop, toes may
be lost, and the bird may squat continu-
ously. The infestation may be accom-
panied by loss of condition and even 2
cachexia terminated by death. Fid.B0.’ “Chemiodoeopeetinar
Treatment.. The legs of the af- coptes) mutans, ovigerous
fected. bird should! be soaked. im warm \ mts se

larged 100 times. (Rail-
soapy water and be thoroughly cleaned _liet)

EXTERNAL PARASITES

a9

by serubbing with a brush. The most effective remedy consists of
the application of an ointment consisting of one part of caraway oil

and four parts of lard or of white vaseline.

Another remedy con-

sists of sulphur ointment made of 1 part of sulphur and nine parts

of lard. Crude petroleum is effective.
Plain kerosene oil sometimes employed is
somewhat effective but will become smeared
on the thighs as soon as the bird perches, and
will blister the skin. The application of
any remedial agent should be repeated.
Prophylaxis. Removal of infected

birds from the flock, and general disinfec-_

tion should be carried out immediately fol-
lowing the discovery of the disease.

DEPLUMING SCABIES

The
(Sarcoptes) levis may occasion

‘Fig. 52.
levis, larva, ventral aspect, enlarged

Cnemiodocoptes (Sarcoptes)

200 times. (Railliet)

mite designated Cnemiodocoptes

Fig. 51. Sarcoptes mutans.
Ovigerous female. Dorsal
view. Enlarged 100 times.

ieneok (Railliet )

feathers in fowls, pigeons and

pheasants during the spring and

summer. It infests the portion
of the quill that lies beneath the
surface of the skin. The affec-
tion usually appears first on
some spot on the body, and pro-
gresses gradually to the neck,
thighs and head, or the head and
neck may be affected first. The
frequency with which the back
is first affected suggests that
treading may be the principal
means of dissemination. The
large feathers of the wing and
tail are not generally involved.

The feathers are either shed
entire, or the quills break off
close to the level of the skin.

Sometimes the stumps are

eracked and are surrounded by

epidermal scales.

220 DISEASES OF DOMESTICATED BIRDS

The mites may be observed on the stumps of broken off quills or of
feathers drawn from the border of the bald area. The irritation set
up by the mites at the root of the feathers often causes the bird to
pluck its feathers, or even sets up the habit of pulling the feathers
of other birds.

The skin is generally normal in appearance but occasionally ap-
pears red and nodular. In severe cases, egg laying may be inter-
fered with, and the birds become emaciated and die.

Treatment. Treatment consists in the repeated application of
essentially the same remedies as recommended for sealy leg, such as
sulphur ointment. Salmon recommends two liquid preparations, a
solution of balsam of Peru in alcohol (1:3) or a mixture of cre-
olin, 1 dram; glycerine, 2 ounces; alcohol and water, 4% ounce each.
Schleg’s solution has been recommended for treatment. This con-
sists of white arsenic and potassium carbonate each 1 dram, 3 pints
of water and 3 pints of vinegar.

OTHER MITES AFFECTING SKIN AND FEATHERS

The mites Hpidermoptes bilobatus and Epidermoptes bifurcatus
have been found associated with a form of scabies affecting the skin.
The beginning of the infestation is indicated by the appearance of
fine yellowish scales which eventually develop into thickened brown-
ish crusts. The parasite in question is frequently found on birds
without the presence of lesions, so their presence in a lesion does
not necessarily indicate that they are the cause. Treatment is
similar to that suggested for scaly leg and depluming scabies.

Other mites parasitic upon the skin and feathers and of less eco-
nomic importance are listed by Neumann as follows: On the fowl,
Pterolichus obtusus, Dermaglyphus minor, D. elongatus, Megninia
cubitalis and M. columbe; on the turkey, Freyana chanayi, D.
minor and M. cubitalis; on the guinea-fowl, D. minor and D. va-
rians; on the pheasant, P. obtusus, P. uncinatus, M. cubitalis and M.
ginglymura; on the peafowl, M. cubitalis and M. ginglymura; on the
pigeon, Falculifer rostratus, F'. cornutus, M. columbe, Analges bifidus
and Ptlerophagus strictus; on the goose and swan, I’. anserina; on the
duck, £. anatina and M. velata.

OTHER PARASITIC MITES

Mites parasitic in parts of the body other than the skin, occur
in the nasal cavities, air sacs and connective tissue. These are dis-

cussed in Chapter XVI.

EXTERNAL PARASITES 221

THE FOWL TICK

Designations. Argas miniatus (A. Americanus). In various
sections of the country the tick is designated by such popular names
as tampan, blue bug or blood sucker. It has been referred to in
the literature as the miana bug, from whence its specific name is
derived.

Hosts. Besides infesting fowls, it attacks turkeys, geese, pig-
eons, ostriches and canaries.

Fie. 53. Distribution of the fowl tick (Argas miniatus) in the United States.
The large dots indicate localities where this tick has been collected by the
Bureau of Entomology. The small dots show the normal distribution of
the species within the United States. (Bishopp, Bureau of Entomology,
U. S. Dept. Agr.)

Injury produced. Bishopp summarizes the ways in which harm
is done as follows: (1) Through death which may occur in poultry
of all ages; (2) by the lowering of the vitality of the fowl so as to
make it readily susceptible to disease; (3) by greatly reducing egg
production; (4) by stunting the growth of chickens; and (5) by
disturbing sitting hens. He further observes that death may be
caused by gross infestation which drains the fowl of blood and

222 DISEASES OF DOMESTICATED BIRDS

produces intense irritation. This ceeurs when fowls are placed
in coops which have not been occupied for months and which harbor
hungry ticks. The infested birds appear paralyzed, the wings droop,
the feathers are ruftled and appetite is lost. Death may occur within
a few days after such heavy infestation, but if removed from the
ticks, the birds will recover.

The discussion of the subject of harm induced by tick infestation
alone, is complicated by the fact that in most countries ticks are.
the carriers of spirochetosis, which is described on p. 185. In the
absence of positive information as to whether or not the fowl
ticks of this country carry spirochetosis, it is not possible to state
just how much injury is done by ticks alone and how much by a
disease transmitted by them.

Distribution. The tick occurs in the western half of Texas and
in a zone extending westward along the southern part of New Mex-
ico, Arizona and California. In the latter state the area extends
northward along the western half of the state to a point slightly
north of San Francisco. The area involved is indicated in Fig. 53.
The distribution of the tick is thus seen to be confined to the warm
portions of the arid and semi arid regions. In Texas it does not
extend into areas where the annual rainfall exceeds 30 inches, which
apparently prevents its extension into the eastern part of the state
or eastward on the Gulf coast. Ticks may occasionally be shipped
to northern states and find favorable conditions for a limited period.
Elsewhere it occurs in Persia, Australia, Africa, South America, the
West Indies, Mexico, Panama, India, Southern Russia and Rou-
mania.

Life history of the tick. The habits of the fowl ticks resemble
those of bed bugs in that they are night feeders and spend the day in
eracks and other protected places. Thus considerable injury may be
inflicted to poultry without the knowledge of the owner.

Eggs are deposited in secluded places and in the summer, hatch
in from 10 to 15 days. In the winter the hatching period may ex-
tend over three months. The young seed ticks soon make their way
to a fowl and attach themselves to the skin of the breast, thighs, or
elsewhere and engorge:with blood. This period of feeding, during
which the ticks are constantly attached to the fowl occupies from
3% to 10 days. When it is completed the ticks drop from the host.
Before feeding they are light gray in color but after feeding they
become dark blue, and are about one-tenth of an inch in length.

After 4 to 9 days the seed ticks undergo a molt and develop into

EXTERNAL PARASITES 223

Fie. 54. Female fowl tick, as seen from above and beneath. Greatly enlarged.
(Bishopp )

nymphs. The feeding habit of nymphs is different in that they re-

main attached to the fowl for but a short time, at night. Nymphs

molt two or three times, alternating with feeding periods before

they become adults. The adult female tick is shown in Fig. 54.

Contrary to the habits of many ticks the adult female does not
die after depositing eggs. She may alternate feeding periods on
the fowl with egg laying for three, four, or even seven times.

Ticks display a remarkable ability to exist for long periods with-
out food. Seed ticks have lived for 5% months without food, those
in the first nymphal stage for nine months, those in the second
nymphal stage for 15 months, and adults for 24% years.

Combating ticks. The difficulties associated with eradicating
ticks frcm a hen house are so great that in case the building is of
little value, burning the structure would save time and trouble.
Under ecnditions forbidding the employment of this extreme and
effective measure, various substances may be sprayed on the wood-
work and in the cracks. Crude Beaumont petroleum, carbolized
whitewash, boiling water, strong kerosene emulsion and various creo-
sote disinfectants have been recommended. Hot tar eliminates
cracks and imprisons ticks. Ticks are very resistant to substances
such as insect powder, kerosene and even fumigation with hydro-

224 DISEASES OF DOMESTICATED BIRDS

cyanic acid gas. No one application of any substance should be de-
pended upon to kill all ticks, because of their ability to secrete them-
selves, and because eggs secreted in cracks may escape destruction and
hatch.

In an infested flock, control measures must not be limited to the
buildings, because first stage larvee remain attached to birds for
days. To deal with these it may be quite sufficient to isolate the
birds in other than the usual quarters, until the crop of larvee be-
come engorged and drop off. An application of kerosene and lard
to the breast and underneath the wings will destroy larve. Dipping
the birds in a 10 per cent solution of one of the coal tar dips is
effective, but in general dipping is not recommended.

Since ticks must crawl to the birds and do so only at night, suit-
able isolation of the roosting perches is a valuable measure in pro-
tecting birds. The construction of the roosting poles should be
such as not to afford harboring places. The poles may be suspended
from the ceiling by rods passing through cans of kerosene or sup-
ported from beneath by a similar device. Such measures are et-
tective until the fluid becomes bridged over with dust or other ma-
terial.

Tick-proof construction. The secretive habits and resistance
of ticks are such that the menace occasioned by them can effectively
be met in the long run only by providing special building construc-
tion. A poultry house built of painted corrugated iron or of gal-
vanized iron over a framework of piping solves the tick problem.
Cracks are reduced to a minimum and the extreme heat attained
by the building during the daytime, is destructive to ticks. ur-
thermore, ticks may be destroyed by building a fire inside the build-
ing, or by the use of a gasoline torch. Tick-proof perches and nests
may be secured by setting the supports in vessels of kerosene.

If it is not possible to provide all-metal construction, the wooden
building should be put up with reference to avoiding cracks. In
any event a shingle roof should be avoided.

THE PIGEON TICK

The pigeon tick (Argas reflecus) occurring in Europe is a species
closely related to the fowl tick. It is somewhat rare in England,
Germany and other northern countries. Its habits are similar to
the fowl tick. This species is a serious pest of pigeons, while fowls,
ducks and geese are also attacked.

EXTERNAL PARASITES 225

REFERENCES

1. Bishopp. The fowl tick. U. S. Dep. Agr. Bureau Entomol. Cire.

170.
9. Bishopp and Wood. Mites and lice on poultry. U. S. Dep. Agr.

Farmers’ Bull. 801.
8 Fuller. <A fowl infesting tick. Agr. Gaz. N. 8. Wales, Vol. 7, 1896,

p. 590.

4, Haidub. Die Fussriude des Geflugels. Inaug. Diss. Giessen.

5, Hassall. Note on the chicken tick. U. S. Dep. Agr. Bureau Animal
Indust. 16th Ann. Rept., 1899, p. 496.

@. Herrick. The chicken mite. Miss. Agr. Exp. Sta. Bull. 78.

”, Herrick. Some external parasite of poultry. Cornell University Agr.

Exp. Sta. Bull. 359.
8. Lamson and Manter. Some lice and mites of the hen. Connecticut

(Storrs) Agr. Exp. Sta. Bull. 86.
9. Laurie. The poultry tick. Dep. Agr. So. Australia, Bull. 74, 1912.
10. Lounsbury. The fowl tick. Agr. Jour. Cape of Good Hope, Vol. 23,
1903, p. 261.
41. Repp. The chicken mite. Iowa Agr. Exp. Sta. Bull. 69.
42. Robertson. Fowl tick experiments. J. Dep. Agr. West Australia,

Vol. 12, 1905, p. 561.

CHAPTER XVIII

INFECTIOUS DISEASES AND PARASITES OF THE OSTRICH
ANTHRAX IN THE OSTRICH

Characterization. Anthrax of the ostrich is an acute febrile in-
fection caused by Bacterium anthracis.

History. The disease was first reported by Henning in the Cape
of Good Hope in 1894, and later by Robertson. Theiler in 1912 also
has described the disease.

Etiology. Anthrax of mammals and of the ostrich is identical,
the causative agent being B. anthracis.

Pathogenicity. The disease is transmissible from ostrich to os-
trich by inoculation with heart blood. It is also communicated from
the ostrich to the sheep and goat by inoculation. A strain of anthrax
occurring originally in cattle was inoculated into a sheep, with fatal
result, and blood of this animal when inoculated into an ostrich
caused death from the same disease.

The susceptibility of man to anthrax constitutes an important
reason for care in conducting autopsies.

Symptoms. According to Theiler anthrax occurs in the ostrich
in two forms: the peracute or apoplectic form and as anthrax fever.
The peracute form attracts most notice for it invariably ends in
death. In natural cases the birds are generally found dead in the
morning, or in a moribund condition, comatose, paralyzed and ap-
parently insensible. A bird may present the picture of health one
moment and be dead of the disease a few minutes later. In such a
sudden attack, the feathers become erect and the whole body is shaken
with tremors. The bird staggers, hes down on the side and kicks con-
vulsively, while the neck twists and untwists spasmodieally.

More chronic cases have been designated anthrax fever. The
birds show symptoms of a general illness and do not feed well for a
few days. The attack results in death, or more commonly in re-
covery.

Morbid anatomy. In the apoplectic cases the carcass is fre-
quently in the best of condition and rigor mortis usually is absent.
The blood escaping from the distended cutaneous and subcutaneous

veins is usually dark in color and coagulates badly.
226

DISEASES AND PARASITES OF THE OSTRICH 227

A smaller or greater amount of liquid is present in the pleuro-
abdominal cavity and is occasionally colored red.

Petechiz, ecchymoses or larger diffuse patches of hemorrhagic
infiltration are observed on the ribs, on the pericardium, the per-
itoneum and mesentery. Gelatinous infiltration of tissues also is
observed.

The pericardial fluid may be increased in amount. Hemorrhages
and extensive hemorrhagic infiltrations occur on the endocardium
and epicardium. ‘The blood in general is black in color, tarry in con-
sistency and is either coagulated not at all or only partially.

The lungs, proventriculus and gizzard are usually normal in ap-
pearance.

The small intestines usually show more or less intense infiltration
with blood throughout the mucosa, which structure shows a uniform
reddish discoloration. In some eases the hyperemia is irregularly
distributed in patches and streaks throughout the length of the in-
testines. The condition is visible from the serous surface of the in-
testine. The acute inflammation may be found to be more pro-
nounced in the colon where the mucous membrane is yet thicker.
The surface of the mucosa is corroded, the submucosa is gelatinous
and studded with hemorrhages, or softened and containing necrotic
patches. The contents of the colon may include blood.

The liver shows acute congestion, is enlarged and bluish in color.
Blood escapes freely when the liver is incised.

The spleen sometimes is normal in size and condition. However,
usually it is enlarged and dark colored. The kidneys may be normal
or congested, dark in color and friable in texture.

Treatment. Theiler recommends carbolic acid diluted in water,
in doses varying from one dram for a three months old bird to four
drams for a two year old bird.

Prevention. The preventive measures of isolation of sick and
disinfection are very similar to those indicated in outbreaks of the
disease among mammals. Carcasses preferably should be burned
without opening or if this is impossible, should be buried in quick-
lime at a good depth. All blood spilled at an autopsy as well as all
excreta of infected birds should be burned. Abandonment of in-
fected runs is desirable, but if this is impossible, the use of the
Pasteur type of anthrax vaccine may be undertaken.

Anthrax infection of soil constitutes practically a permanent con-
dition. Opportunity for direct infection from the soil by contam-
ination of feed, or by wounds will vary with seasonal conditions of

228 DISEASES OF DOMESTICATED BIRDS

moisture. Inundations and extension of irrigation systems may
spread the infection to new foci. On some of the infected farms
cited by Theiler the infection seems to have first attacked cattle. In
one case the infection had been introduced by cattle. In other out-
breaks, ostriches died occasionally, while horses and cattle escaped.

Every precaution should be taken to prevent the exposure of an-
thrax-infected blood to the air. Under such conditions spores form,
which are capable of remaining alive in the soil for an indefinite
period.

ASPERGILLOSIS IN ADULT OSTRICHES

Walker has observed that in adult birds, marasmus is the only
sign of aspergillus infection. When the lungs are affected, respira-
tion is accelerated and the beak is kept partly open. There is pro-
nounced loss of condition when the liver is involved. The disease
usually runs a sub-acute or chronic course.

The lesions are found to be more or less generalized, the liver and
respiratory tracts being. most generally involved. Degenerative
changes in the tubercles and destructive changes in the surrounding
tissues are marked. The tubercles may exhibit the various changes
in the evolution of a tubercle, such as miliary granulations, caseous
degeneration and fibrous transformation. ‘The lesions in the liver
usually consist of extensive caseous areas caused by the degenera-
tion of agglomerated tubercles and by necrosis of adjoining liver
tissue.

Aspergillosis in the adult ostrich as reported by Jowett may pre-
sent a condition very closely simulating miliary tuberculosis of the
lungs. The lungs are consolidated, dark red in color, and are filled
with yellowish-white miliary tubercles about the size of a pinhead,
which stand out prominently against the background of congested
and hepatized lung tissue. ‘he tubercles are not readily removed
for the periphery of each is united to others. They are fibrous and
shot-like in consistency. They show no evidence of caseation nor
calcification. There is shght thickening of the pleura, and a few
nodules are present, but no lesions are observed in the mucosa of the
trachea and bronchi.

Examination for tubercle bacilli yields negative results, but mi-
croscopic examination of crushed nodules in caustic potash reveals
the true nature of the infection.

Study of sectioned specimens shows that each nodule is composed
of: (1) an unstained or very faintly stained central area, (2) sur-

DISEASES AND PARASITES OF THE OSTRICH 229

rounding this an intensely stained peripheral zone, and (3), sur-
rounding all, a zone in which the air cells show inflammatory
changes but are still pervious. The center of the nodule has under-
gone coagulation necrosis and contains filaments and free spores.
The next zone contains leucocytes, endothelioid or epithelioid cells
together with many filaments.

The fungus undoubtedly is an aspergillus, and quite likely fumv-
gatus, although no cultures were made.

The source of infection was regarded as moldy food.

Archibald has reported upon aspergillosis in the Sudan ostrich, in
which quite different lesions were observed. On opening up the res-
piratory passage a peculiar lesion of the bronchioles is observed. The
upper portion of a bronchus is lined by dark granular masses which
project into its lumen. The masses are friable, but are closely ad-
herent to the wall. The portion of a bronchiole next to the lung
shows several “ plaques ” raised from the surface. These are grayish
in color with a nodular center and vary in size from a millet seed to a
pea. Most of them are discrete, but a few have coalesced. Their
surface is thrown into ridges and depressions. Microscopic examina-
tion reveals the nature of the infection.

Aspergillosis in other birds is discussed in Chapter X.

ASPERGILLOSIS IN OSTRICH CHICKS

Synonyms. Yellow liver, chick fever.

Characterization. Aspergillosis in the ostrich chick is a highly
fatal affection caused by aspergillus fungi, of which Aspergillus
fumigatus is the most common.

History. The disease was mentioned by Douglas in 1881 who ob-
served that it was so destructive that on some farms in Cape Prov-
ince every chick died.

We are indebted to Walker for making a useful experimental study
of the various aspects of the affection, which has elucidated the
problems of etiology and prophylaxis.

Symptoms. In young chicks a few days old the first symptom is
a disinclination to feed. The bird may go through the motions of
picking, without swallowing. food. The chick appears dull, weak,
the eyes are half closed, it moves about slowly or stands, and occa-
sionally utters a plaintive note. The neck is commonly flexed and
the head is lowered and kept close to the body. The abdomen feels
less tense and full than that of a healthy chick. The respiration is

230 DISEASES OF DOMESTICATED BIRDS

sometimes accelerated. The beak may be kept continually open, or
only kept open during a long inspiration. The temperature is irreg-
ular, there being a variation of 3° to 5° F. between the morning and
evening temperatures. In healthy birds the temperature varies
about two degrees, that is between 102° and 104° F. Sub-normal
temperature precedes death.

In some cases whitish nodules, about the size of a pin head may be
detected on the buccal mucous membranes and the epiglottis.

Destructive outbreaks of the disease occur among chicks varying
in age from a few days to 3 or 4 weeks. It is much more prev-
alent among artificially reared chicks than among those raised nat-
urally.

Death occurs within a few days after the appearance of symp-
toms and it is seldom that an affected bird recovers.

Morbid anatomy. In young chicks naturally infected the le-
sions are chiefly confined to the lungs and air sacs. Less commonly
nodules are observed on the buceal mucosa. A close examination
of the lungs will usually reveal more or less rounded nodules aver-
aging 1.2 mm. in diameter, and yellowish white in color. Rarely
caseous foci or pneumonic patches are observed in the lungs. The
lesions on the walls of the air sacs consist of either small tubercles
or fibrinous exudate.

The tubercles are composed of epithelioid cells, leucocytes and
some eosinophile cells, mixed with mycelium. The duration of the
disease in chicks is so short that caseous degeneration and fibrous
transformation of the tubercles do not usually oceur.

Etiology. The ostrich is susceptible to several species of asper-
gillus fungi but the one most pathogenic, and more commonly en-
countered is Aspergillus fumigatus. A. asper also is pathogenic for
the ostrich. The fungi are widely distributed among substances of
importance in connection with the artificial rearing of ostriches.
Straw may be naturally infected as also lucerne (alfalfa), and the soil
upon which lucerne is growing. The feces of an ostrich fed upon
lucerne are infective.

Pathogenicity. Intravenous injection of ostrich chicks with
spores produces a more or less generalized infection in which the
lungs and liver particularly contain tubercles. Death oceurs in from
2 to 7 days. Inhalation of spores produces lesions in the lungs con-
sisting of dirty white colored nodules isolated or agglomerated, and
lesions in the air sacs consisting of nodules. Chicks varying in age
from a few days to 31 days die in from one to ten days after the

DISEASES AND PARASITES OF THE OSTRICH 231

introduction of spores into the trachea. Ingestion of cultures ad-
ministered in a gelatine capsule causes the formation of tubercles,
but no marked intestinal changes. The chicks die in from 5 to 18
days.

Dosing with the fungus in a gelatin capsule produced no effect
upon one bird 41 days-old, and upon one adult.

Transmission. Chicks are susceptible to infection by both in-
halation and ingestion. Opportunity for infection exists even be-
fore hatching, for the aspergillus fungus often infects the air sac
of the egg. It is capable of penetrating unbroken shell and can thus
pass from infected to non-infected eggs. Thus chicks become in-
fected before or during hatching, and the incubators become con-
taminated, constituting a menace to later hatches. Infected straw
used as bedding in chicks’ sleeping boxes is a serious source of
infection.

Diagnosis. Aspergillosis may be identified by microscopic ex-
amination of nodules after treatment with potassium hydrate, in
which case the mycelium and fruiting heads may be recognized. No-
dules planted on potato and incubated for 24 to 36 hours at 35° C.
produce small whitish growths visible to the naked eye. After in-
cubation for a day more the growth appears bluish in color and still
later turns dark bluish green.

Control. Prophylaxis of aspergillosis concerns securing non-in-
fected eggs for incubating, non-infected incubators, non-infected bed-
ding and safe feed for the chicks.

Treatment. No medicinal treatment is available and all efforts
against the disease must be centered upon prevention.

PARALYSIS OF THE OSTRICH

Synonym. Leg-weakness.

History. In 1900 Marx observed the disease among Sudan os-
triches in the Frankfurt Zoological gardens. Robertson in 1909 de-
scribed a form of paralysis occurring among ostriches near Cape
Town. The disease is of considerable economic importance and
seems to be becoming more common.

Symptoms. The disease is abrupt in onset. There is sudden
inability to rise, the interference apparently being in the toes, which
are flexed, on fierelre, at right angles. The birds make futile and
persistent efforts to rise, and in consequence stagger along on the hock
joints. After a few days, effort to rise is abandoned and the paraly-

232 DISEASES OF DOMESTICATED BIRDS

sis eventually involves the wings and neck. Appetite remains good
and there is no evidence of pain. Marx noted the presence of
marked lachrymation in every case. Affected birds have been ob-
served to live for seven months and no instance of complete recovery
has been noted. Young birds are most commonly affected, but the
disease may be encountered among those of any age. The fice oc-
curs at irregular intervals in certain areas.

Morbid anatomy. The one constant lesion as observed by Rob-
ertson is the congestion or inflammation of the duodenum and the
reddened appearance of the mucosa, accompanied by a deposit of
exudate thereon. ‘This lesion is present in some degree in all cases,
whether early or of long standing. The sub-mucous layer of the in-
testine is thickened and infiltrated with a clear straw colored fluid.

Marx observed more or less peritonitis and purulent foci in the
spleen in each case. In some cases there was enteritis with necrotic
patches on the mucosa.

Bacteriology. Robertson obtained from the inflamed mucosa, a
short rod which does not stain by the Gram method. It grows fairly
well on the common culture media under aerobic or anaerobic condi-
tions. There is copious white growth on plain agar, glycerine agar,
agar, gelatin and malachite green agar. On the latter the color is
discharged along the needle track. Gas is evolved in sugar agar
stab cultures. Growth occurs in plain bouillon, glycerine bouillon
and sugar bouillon causing turbidity and foul odor. A brownish col-
ored raised growth occurs on potato. Milk is not coagulated nor does
liquefaction occur in gelatin. In natural cases, besides the organism
in question, Staphylococcus pyogenes aureus almost invariably is pres-
ent in cultures from the sub-mucosa of the duodenum.

Marx isolated a non-motile, non-spore bearing, Gram negative, oval,
bipolar staining rod, which is killed by exposure to 68° C. for an
hour. It grows readily on the ordinary culture media. Coagulation
of milk occurs, growth on gelatin resembles that of B. coli, and a
brownish viscid layer is produced on potato. Glucose is fermented
and no indol is produced. After 24 hours on agar there appear gray-
ish white colonies, iridescent by transmitted light which eventually
develop into a moist greenish white layer. Bouillon becomes turbid
in a few hours and a deposit of sediment forms in the tube. Marx
regards the organism as belonging to the hemorrhagic septicemia
group.

Pathogenicity. Subcutaneous injection of 25 ¢.c. of a 24 hour
culture of Robertson’s organism into a cock ostrich resulted in the

DISEASES AND PARASITES OF THE OSTRICH 233

appearance of the typical symptoms in seven days, followed by death
in about a month. Similar results were obtained with a number of
other ostriches. The organism injected can be recovered from the
lesions induced in the duodenum. Robertson regards the symptoms
as indicative of a poisoning. He holds the opinion that the or-
ganisms do not invade the general tissues, but remain localized as in
the case of diphtheria and tetanus. The poison is elaborated by the
organism in the intestine and carried to the spinal cord and thus
induces paralysis.

The organism isolated by Marx was found to be pathogenic for the
‘gray mouse, pigeon, and various small birds. Guinea pigs and rab-
bits were insusceptible.

Control. The common source of infection is regarded as con-
taminated food and water. Robertson advises that infected birds be
killed, and that the birds be shifted to bare veld and fed by hand with
cut green crops. The continuous breeding of birds on one spot seems
to be a factor contributing to the occurrence of the disease.

Treatment. Gray suggests the trial of intestinal disinfection
with eyllin, beta-naphthol, sodium salicylate, quinine or bismuth.

WIREWORMS IN OSTRICHES

The wireworm, a nematode designated Trichostrongylus douglasi,
synonym Strongylus douglasi, is a parasite infesting the mucosa and
glands of the proventriculus of the ostrich. Adult birds, if well fed
tolerate the parasite comparatively well but ostrich chicks frequently
succumb. This parasite occasions great losses in the ostrich farming
industry of South Africa.

Comparatively little was known of the life history of the wireworm
and remedial measures until the publication of the work of Theiler
and Robertson from which we have drawn largely in discussing the
problem.

Life cycle of the wireworm. The parasite undergoes four
molts corresponding to four different stages. Two stages are en-
countered in the life cycle outside the host and two inside the host.
The cycle may thus be divided into a parasitic and a non-parasitic
period.

The wireworm in its non-parasitic stages is free living. Its fu-
ture propagation and dissemination depend upon gaining access to
the body of an ostrich. This phase of its life history is of great
practical interest in connection with the application of measures to
prevent the infection of clean birds.

254 DISEASES OF DOMESTICATED BIRDS

The egg of the wireworm is expelled from the body in the feces
of the bird in about three days after expulsion from the worm. Ex-
amination of feces of a number of birds has shown that one dropping
of feces may contain from 24,000 to 600,000 eggs. A bird isolated
under conditions preventing it from becoming reinfected has con-
tinued to discharge worm eggs for a period of nine months without
showing decrease in number. The limit to the time a bird will dis-
charge eggs has not been determined. The worm eggs in fresh drop-
pings are non-infective. If fed to an ostrich they will be passed in
the feces so long as they are fed, but autopsy of the bird after an
interval will show that no worms are present.

The worm eggs hatch only outside the body of the bird and the
larve undergo four molts before reaching maturity. Hatching
and the development of the larve are sharply controlled by tempera-
ture and other conditions. Ata temperature of 98° F. ova hatch and
the larve reach maturity. At 100° to 101° F. hatching occurs, but
only the older larve reach maturity. The same is true of a tempera-
ture range of 102-102.5° F. <A temperature of 104° F. does not
permit the development of larve. Ova and larve in the first stage
may be kept dry at room temperature for two years and develop to
maturity when moistened. Ova and first stage larvee cease develop-
ment when dried over calcium chloride, but remain alive for at least
three years. Eggs retain their vitality in water but cannot reach ma-
turity at a depth of two or three inches. The vitality of eggs is not
destroyed by a temperature of 32° to 46° F. for three months.
Droppings kept under natural outdoor conditions for fifteen months
contain live mature larve and first stage larvee.

Larve in the first stage and immature larve of the second stage
do not develop in the stomach of the ostrich. Mature second stage
larve alone are capable of becoming established there. Liquid is
undoubtedly a suitable medium for these larve and they are very
active in such an environment. A temperature below 38° F. checks
their movement under these conditions. When droppings and sec-
ond stage (mature) larve are left exposed on soil where grass
is growing, the larvee crawl to the tip of the grass blades where they
are more numerous than on the portion below. They have been ob-
served to remain alive on green grass for six months and for two
months more after the grass dried up although in diminished num-
ber. On a second crop of grass, larve were observed at a height
never exceeding three inches. From one infection of the soil larvee
were found on grass up to 14 months and at 17 months in the drop-

DISEASES AND PARASITES OF THE OSTRICH 235

pings originally placed on the soil. The propensity of larve for
climbing vegetation results in rendering infective, any ostrich fodder
raised on land contaminated by the droppings of infected birds.
Mature larve will remain alive in a moist atmosphere at room tem-
perature for fifteen months. They will remain alive in water at a
low temperature for 13 months. After being kept in ice at a tem-
perature of 16° to 28° F. for 11 days and released by melting the
ice, they revive. Larve will travel through soil, so no benefit can
result from plowing infected ground.

The possibility that mature larve pass through the skin of the
ostrich to reach the stomach has been tested by experiment, with neg-
ative conclusions. Sheep and fowls do not serve as hosts for the
wireworm.

Mature larvee outside the ostrich may be killed by a liberal ap-
plication of carbolic acid or lysol in 5 or 6 per cent solution. Sul-
phurie and hydrochloric acids are effective.

On gaining access to the ostrich, the larve pass through the third
and fourth larval stages and develop into the adult worm after the
fourth molt.

Ostrich chicks may succumb to infestation by these larvee in the
parasitic stages, before they develop into adult worms.

Adult birds can tolerate an excessive infestation with wireworm
provided they are well fed. Once infested, an ostrich will remain
infective for years and constitute a source of contamination of the
soil. An infected pasture or pen will remain infected for years by
reason of the presence of eggs and larve.

Morbid anatomy. The wireworms are found in the proventric-
ulus in the lumina of certain deep glands or lying between superficial
tubular glands or in the depths of the mucosa of certain areas of the
organ near the entrance of the esophagus. They are demonstrated
in the fresh stomach by scraping off the mucous layer of the mucosa.
They are very rarely on the surface but proceed thence upon reach-
ing maturity. The effect of infestation becomes evident after about
the 24th day after infection, and subsequently. The layer of mucus
becomes detached in parts and hemorrhagic infiltration of the mu-
cosa appears. When the worms are numerous and mature, the mu-
cosa appears swollen and is covered by a copious amount of mucus.
This condition designated “ vrotmag” (rotten stomach) by the Boers,
causes anemia and emaciation of the birds.

Diagnosis. The presence of worms may be determined by worm
cultures, that is by placing fresh droppings in a wineglass which is

236 DISEASES OF DOMESTICATED BIRDS

covered to prevent evaporation. If the bird is infected, larve recog-
nizable with the naked eye, will after a time be seen on the glass.
The number present furnishes a rough indication of the extent of the
infection.

Prevention. It is possible to raise ostrich chicks free from in-
fection when suitable precautions are carried out. Small runs 50 by
150 feet are quite large enough. If clean ground over which os-
triches have not run is not available, it is possible to render an area
safe by removing the soil to a depth of three inches. The runs should
be so located that there is no contact with infected birds, and so that
there is no possibility of infection through drainage into them. ‘The
runs should be stocked with incubator chicks, or chicks removed from
the nest immediately after hatching. The feed will be of the usual
character, derived from land that has not been contaminated by in-
fected birds. If hens are kept with the chicks, all feces of the adult
birds should be picked up daily. These precautions will permit
raising ostrich chicks to such an age that wireworm infestation is
no longer dangerous to the birds, and has the additional advantage
of preventing sclerostome and tapeworm infestation.

Treatment. No treatment has been discovered which can be de-
pended upon to expel all the worms from an infected bird. The lo-
cation of the worms in the mucosa and glands is such as to dis-
courage belief that a successful treatment will be found. A num-
ber of substances when tested in vitro are undoubtedly effective in
killing the parasites. A number of methods of treatment have
been tested by Theiler and Robertson, who judged the effect by ob-
serving the influence of the treatment on the numbers of eggs in the
feces both by microscopical observation and by worm cultures.

Carbolie acid in a dose of 300 ¢.c. of a 2.5 per cent solution caused
the eggs to become rare for 14 days after which they became as
numerous as they were before treatment. Several trials with this
agent led to the conclusion that the dose employed, which is equiva-
lent to 7.5 grams of pure carbolic acid, checks the laying of eggs for
a while without killing all the worms.

A treatment was tried which consists of administering 300 c.c. of
paraffin (kerosene), followed after 24 hours by 1 ounce each of slaked
lime and of sal-ammoniac. It has been claimed that the paraffin dis-
solves the mucus-like layer over the worm infested area, and that the
ammonia resulting from the reaction between the drugs administered
later kills the worms. However, the trial failed to demonstrate any
effect upon the worms.

DISEASES AND PARASITES OF THE OSTRICH 237

Dosing with thymol in quantities as large as 12 grams had only
a temporary effect in checking the laying of eggs for a few days.

Beta-naphthol in repeated enormous doses and followed after sev-
eral days with 250 grams of magnesium sulphate merely checked the
laying of eggs for a few days.

Santonin in 10 gram doses produced some influence on the num-
ber of eggs present after treatment.

Kamala in doses of 20 and of 40 grams produced no apparent ef-
fect. Flores koso in doses of 50 and of 100 grams merely produced
some influence on the number of eggs.

Liquid ammonia proved ineffective and even harmful to birds re-
ceiving the treatment. Carbon bisulphide in a dose of 30 ec. in
170 c.c. of olive oil or in a dose of 20 ¢.c. in a gelatin capsule, proved
ineffective.

Apart from the fact that the worms are well protected in their
location in the mucosa, certain anatomical considerations prevent
drugs from acting unless the fluid fills the whole stomach and raises
the fluid to the level necessary to bring it in contact with the areas
infested with worms. ‘This is almost impossible to accomplish since
the intestinal opening is so low as to drain out fluid.

TAPEWORM OF THE OSTRICH

The tapeworm of the ostrich is known as J'enia struthionis, and
is chiefly a parasite of the young. Chicks may become infested
when only three weeks old and from that age until two years, tape-
worms constitute a very common parasite. The worms reach two
or three feet in length and may almost plug the intestine. Robert-
son reports having observed in one ostrich nine months old, over two
hundred tapeworms with a weight of nearly three, pounds. The
ageregate harm done by these in abstracting nutriment and in in-
juring the mucosa at the point of attachment, must have been con-
siderable. On the other hand, the occurrence of tapeworms in the
adult ostrich, is rarely observed. ‘The intermediate host of the os-
trich tapeworm is not known.

Symptoms. Under good conditions an ostrich may tolerate a
heavy infestation without showing symptoms. If food becomes
scarce, climate becomes unfavorable, or the chick becomes ill from
some cause, the bird exhibits evidence of the presence of the worms.
There is general ill health, and the mucose of eyes and mouth are
pale. The presence of ripe segments of tapeworm in the droppings is

238 DISEASES OF DOMESTICATED BIRDS

the one certain symptom. The segments are always found on the out-
side of the dung pellets.

Treatment. Robertson recommends the use of petrol or motor
car spirit, Pratt’s green label (gasoline). It is advisable to fast the
chicks a little before dosing, but if weak and thin, they should not
be starved before the first dose. The dosage for various ages as
recommended by Robertson, is

1 and 2 months old birds receive 1% oz.
3 months old birds receive 1 oz.

4 months old birds receive 2 oz.

5 months old birds receive 3 oz.

6 months old birds receive 4 oz.

7 to 11 months old birds receive 5 oz.
12 months old birds receive 6 oz.

Full grown birds receive 8 oz.

The petrol is given pure and not mixed with water. It volatilizes
at a temperature below that of the body of the bird, and consequently
permeates the whole intestinal tract in a short time.

Care must be taken in drenching, for even a little fluid gaining
access to the trachea may be followed by serious or even fatal con-
sequences. In drenching birds, the entrance to the windpipe should
be covered with the fingers of one hand while the bottle of petrol is
passed over them. The head of the bird should be held up for a
few minutes after drenching to prevent the possibility of regurgi-
tation.

Hutcheon has employed liquid extract of male fern in a dose
varying from a teaspoonful for a young ostrich three or four months
old, to a tablespoonful for a full grown bird. He has also used
turpentine in a dose varying from a dessertspoonful to two table-
spoonfuls. It is more effective when combined with a purgative such
as linseed or castor oil.

FILARIA OF THE OSTRICH

A gigantic nematode of the ostrich, designated Filaria spicularia
occurs in the subperitoneal connective tissue and also in the sub-
lumbar region. The parasites vary in length from a quarter of a
meter to a meter and are coiled together in such a complex manner
that it is difficult to secure a whole specimen. The presence of
the parasite appears to have no effect upon the health of the birds.

DISEASES AND PARASITES OF THE OSTRICH 239

LEUCOCYTOZOON INFECTION IN OSTRICH CHICKS

Walker has observed a leucocytozodn infection in ostrich chicks
varying in age from 4 weeks to 7 months.

Symptoms. There is a disinclination to feed, loss of condition,
stunted growth and paleness of the buccal mucous membrane. ‘The
skin of the body and around the eye is bluish colored. When the
chicks are driven, the affected ones are unable to keep up with the
rest of the flock. Sickness is noted several days before death.

Morbid anatomy. Microscopic examination of the organs shows
no constant lesions. Examination of the blood frequently reveals the
presence of a leucocytozodn. The observations lead Walker to the
conclusion that it will be necessary to ascertain whether the leucocy-
tozoon enters into the etiology of diseases of ostrich chicks.

Etiology. The organism is designated Leucocytozoén struthionis.
It oceurs in young chicks but has not been found in adult ostriches.
In dried blood smears fixed with methyl aleohol and stained with Gi-
emsa, two main types of parasites are observed which apparently cor-
respond to male and female gametocytes.

The female gametocyte occurs most frequently. The shape is more
or less rounded but may be irregular, due to distortion brought about
in preparing the smears. The organism varies from 11 to 15 microns
in length and from 9 to 13 microns in width. The protoplasm stains
deeper than does that of the male gametocyte and scattered through
the pretoplasm are a number of metachromatic granules. These ap-
pear more distinctly in some of the parasites than in others. A num-
ber of small clear spaces occur throughout the protoplasm. The nu-
cleus is represented by an aggregation of small chromatin granules
generally at the center or near the edge. In most instances a large
chromatin granule stands out distinctly. It is situated in the mass of
granules, or at the side of them, or at some distance from them. The
nucleus of the host cell is always altered in shape. In most eases it is
elongated and located at the margin of the parasite.

The male gametocyte is usually more or less rounded and is smaller
than the female. The protoplasm stains less densely than that of the
female. The chromatin granules of the nucleus are generally scat-
tered throughout the cell. Sometimes they are larger and widely sep-
arated and are observed very distinctly. The nucleus of the host cell
is irregular in shape and is found at the edge of the parasite. It is
less elongated and smaller than in the case of the cell invaded by the
female.

“’

240 DISEASES OF DOMESTICATED BIRDS

No spindle shaped formation of the host cell has been observed in
smears from ostriches.

ACORN POISONING IN THE OSTRICH

Robertson has observed a number of cases in which acorns have
killed ostriches. These when consumed in moderation constitute a
safe and excellent feed. However, when birds have access to a boun-
tiful supply, they will gorge themselves with fatal result. The in-
jury is caused by the astringent action of the tannic acid.

Symptoms. The birds lie down persistently, seem constipated,
strain and appear giddy. They stagger on tiptoe balancing them-
selves with their wings. The feces consist of nearly cylindrical pel-
lets of very hard material. The urine closely resembles green paint.
Some birds twist their necks as if in pain.

Morbid anatomy. Lungs, heart, liver and spleen appear normal.
The stomach contains undigested acorns. The intestines show evi-
dence of constipation with subsequent congestion. The duodenum is
swollen, thickened and congested with blood. The mucosa shows
acute inflammation and is covered with a dirty, grayish white deposit
or slime. On scraping this off the mucosa is seen to be very red.
The colon is packed with pellets of hard dung which are black in
color and covered with a gray slime with traces of blood. The mucosa
of the colon is also highly reddened. ‘The ceca are packed with
masses of hard dung.

Treatment. . The affected bird is given 25 ounces of raw linseed
oil to which is added 4 drams of powdered Barbadoes aloes which
previously has been dissolved in a little warm water. Twelve hours
later each bird is given one ounce of bicarbonate of soda dissolved
in water. Birds that refuse to eat may be drenched with gruel, raw
eggs and brandy several times a day.

REFERENCES

1. Archibald. Aspergillosis in the Sudan ostrich. J. Comp. Path. and
Therap., Vol. 26, 1913, p. 171.

2. Jowett. Pulmonary mycosis in the ostrich. J. Comp. Path. and
Therap., Vol. 26, 1918, p. 258.

3. Marx. Ueber ein Infectidse Krankheit der Strausse. Centralbl. f.
Bakteriol. (Hic.), 1 Abt. Orig., Bd. 27, 1900, S. 822.

4. Neumann. La filaire de l’autruche (Filaria spicularia). Rev. Vét.,
T. 66, 1909, p. 544.

5. Robertson. Paralysis in the ostrich. J. Comp. Path. and Ther.,
Vol. 23, 1910, p. 182.

DISEASES AND PARASITES OF THE OSTRICH 241

6. Robertson. Notes on ostrich parasites. Agr. J. Cape of Good
Hope, Vol. 33, 1908, p. 583.

". Theiler. Anthrax in the ostrich. Agr. J. Union of So. Africa, Vol.
4, 1912, p. 370.

8. Theiler and Robertson. Investigations into the life history of the
wire-worm in ostriches. Union of So. Africa, Dep. Agr., Ann. Rpts. Dir.
Vet. Res., 8-4, 1915, p. 215.

9. Walker. Aspergillosis in the ostrich chick. Union of So. Africa,
Dep. Agr., Ann. Rpts. Dir. Vet. Res., 3-4, 1915, p. 535.

CHAPTER XIX

INFECTIOUS DISEASES OF GEESE AND DUCKS
GOOSE SEPTICEMIA

History. Curtice in cooperation with Smith described several
outbreaks of hemorrhagic septicemia among geese in Rhode Island.
The disease occurred in one establishment among geese kept in lots
of 300 each in fattening pens. The birds were assembled from
various farms in numerous small lots, any one of which might have
contained infected birds. Subsequent handling of the birds in the
fattening pens involved separating them according to condition, which
practice brought about extensive intermingling of birds.

Etiology. The etiological agent is a member of the hemorrhagic
septicemia group which has become well adapted to waterfowl, geese
in particular. ;

Pathogenicity. Geese are susceptible to infection by feeding cul-
tures while ducks and hens are not. Geese, ducks, rabbits, mice and
pigeons are susceptible to subcutaneous injection and hens are not.
After exposure by feeding or by subcutaneous inoculation, death oc-
curs in less than thirty-six hours. Feeding culture to a goose may
cause death in less than seventeen hours.

Symptoms. It is characteristic of the disease that birds are
found dead at feeding time, mornings or evenings, without having
shown sickness. Symptoms occasionally are observed during. the
last hour or so before death and largely concern the death struggles.
The gait becomes uncertain, the head is burrowed in the dirt and
is twisted.

Morbid anatomy. There is considerable mucus in the throat
and mouth, and very tenacious mucus in the nasal cavity. The veins
of the head seem congested as if the bird had died of asphyxia. The
mucosa of the intestine is studded with ecchymoses or larger hem-
orrhagic areas. In about half of the cases, the liver is studded with
necrotic foci. Epicarditis and pericarditis are present occasionally
as also is involvement of the lung.

Treatment. Medicinal treatment is unavailing.

Prophylaxis. Preventive measures will include precautions
242

INFECTIOUS DISEASES OF GEESE AND DUCKS 243

such as restricting the number of birds in contact with one another
and other similar precautions aimed at restricting the spread of in-
fection.

EXUDATIVE SEPTICEMIA OF GEESE

Synonyms. Ansteckende Luftsackentziindung der Giinse, Giinse-
Influenza.

Characterization. Exudative septicemia is an infectious septi-
cemic disease of geese distinguished by the formation of fibrinous
exudate upon the pericardium, liver and intestines and caused by
Bacillus anserwm exudative.

History. The disease has been observed by Frosch and Birn-
baum, Loffler and also by Riemer. Bugge studied a similar disease
and while he does not give details concerning the organism present, it
is possible that he encountered the same infection.

Geographic distribution. The disease seems to have been recog-
nized unquestionably only in Germany. The occurrence of the dis-
ease among geese imported into Germany from Russia would indicate
that it exists in the latter country also. M’Fadyean has described a
septicemia observed in geese in England which resembles the disease
in question in several particulars.

Symptoms. ‘The existence of the disease is first indicated by loss
of appetite. The breathing may be accelerated, with the beak open
and accompanied by a snoring sound. Coughing and choking may
occur. The bird separates from the flock, squats frequently and rises
with difficulty. Diarrhea oceurs within 24 hours of death. The
bird becomes progressively weaker and dies in from two to five days.

Morbid anatomy. ‘The most striking lesion is the presence of a
fibrinous exudate upon various structures in the body cavity. The
surface of the liver is covered by a thin, fibrinous, yellowish white
layer which is easily detached. The exudate may extend between
loops of the intestines, the air sacs, the pericardium and the epi-
eardium. J luid exudate may also be present. The pericardial sac
contains serous, cloudy fluid. The bronchi in some cases are
plugged with yellowish, fibrinous, purulent material. The liver
is usually slightly enlarged and may contain small spots. The
spleen and kidneys are also enlarged. The mucous membrane of
the intestine is.swollen, reddened and contains small hemorrhages.

Etiology. The infection is caused by Bacillus septicemia an-
serum exudative described by Riemer. This is a small slim rod
varying in length from .5 to 1.5 microns and .5 to 1. micron broad.

244 DISEASES OF DOMESTICATED BIRDS

The cells frequently lie in pairs, so that they appear like diplococci.
The organism is always found in great numbers in the heart blood,
the pericardial fluid and in the fibrinous exudate. It is stained
readily by the common anilin dyes, and best by carbol fuchsin. The
organism is Gram negative, non-motile and does not form spores.
Indol production is not observed except perhaps in traces in old
cultures.

Frosch and Birnbaum succeeded in growing the organism at first
only on medium containing hemoglobin. The first generation out
of the goose grew on plain agar and bouillon when plenty of blood
was carried over to the medium in making the inoculation. Pigeon
blood agar induced growth but after many transfers failed. A
medium rich in hemoglobin made as follows was more successful.
Defibrinated horse blood is mixed with equal parts of distilled
water to cause the liberation of the hemoglobin. About 1 ce. of
this solution is added to each tube of melted, cooled agar. The
agar is then shaken and is subjected to fractional sterilization at
70° C. for three days. On hemoglobin agar so prepared, the organ-
isms form a luxuriant grayish white growth. In smears from such
cultures the rods appear somewhat larger than in smears from the
animal body and very frequently long thread-like forms are ob-
served.

On common agar of slightly alkaline reaction it forms in 24 to
36 hours a luxuriant grayish white, transparent, slightly opalescent
layer, which in older eultures becomes brownish yellow in color.
The condensation water contains considerable sediment. The
optimum growth temperature is 387° to 88° C. No growth occurs on
acid agar.

The period of life of a culture is limited. By holding at room
temperature, transfers succeeded at 14 days, but many transfers
fail sooner. The cultures in the incubator nearly all die within 8
days.

A slight uniform clouding occurs in bouillon, which after some
days contains a limited amount of sediment which on twisting, forms
a spiral column. In some cultures a pellicle is formed of thread-
like growth. .

In gelatin stab cultures held at 21° C., a slight non-characteristic
growth is observed in the vicinity of the line of inoculation, and on
the surface. After some time a funnel-shaped area of liquefaction
forms slowly, and complete liquefaction eventually occurs. Growth
on gelatin plates is accompanied by liquefaction and offers no char-
acteristic features.

INFECTIOUS DISEASES OF GEESE AND DUCKS 245

Glucose and lactose bouillon are uniformly clouded but gas forma-
tion does not occur. In lactose there is no change in reaction, but
in glucose there is a slight reduction of alkalinity.

A luxuriant growth occurs in the form of a whitish yellow layer
on Léffler’s serum. On potato a thin shiny, yellowish white layer is
observed at 24 to 48 hours, which later becomes brownish in color.
Growth does not occur on Drigalski-Conradi nor Endo plates. Milk
is not coagulated. Riemer and Léffler both regard the organism as
belonging to the influenza group.

Pathogenicity. The organism is markedly pathogenic for
geese, which are infected most certainly by intramuscular injection.
The musculature in the vicinity of the point of inoculation is colored
erayish white over a large area. An attempt by Frosch and Birn-
baum to infect a grown goose by feeding with organs of a goose dead
of the disease, failed, as did a similar experiment by Riemer in
which bouillon culture was used. In neither case were goslings
available.

The latter author observed that either intramuscular or subecu-
taneous injection caused sickness followed by death in from 36 to
72 hours. In artificially infected birds the fibrinous exudate on
the liver may not be found, due to the unnatural rapidity of the
course of the disease.

Rabbits, gray and mixed rats, mice, white mice, hens, and pigeons
are refractory to inoculation. Guinea pigs have succumbed to an
intraperitoneal inoculation of a suspension of the growth from one
agar culture. They withstand smaller amounts, such as 1 to 3
loops.

Riemer succeeded in infecting an 8 weeks old duck by intra-
muscular injection of a suspension from an agar culture. Of three
grown ducks, only one became infected by intramuscular injection.

M’Fadyean in England examined a few geese dead from a septi-
cemic infection. Smears from the blood contained great numbers
of organisms which were cylindrical rather than ovoid in outline.
Beyond a slight inflammation of the intestine, no lesions were ob-
served. Agar tubes seeded from the heart blood failed to show
growth, and cultures kept under anaerobic conditions likewise failed.
The organism was Gram negative, and was not pathogenic to the
mouse, the rabbit, the hen, the guinea pig, the pigeon or to one duck.
Transmission to a goose by feeding failed, but succeeded when sub-
cutaneous inoculation was employed. The writer concluded that
the disease was not fowl cholera. None of the observations made
deny the possibility that the infection was exudative septicemia.

246 DISEASES OF DOMESTICATED BIRDS

Prevention. Individual isolation of birds is the most effective
means of preventing the spread of the infection. General disinfec-
tion is indicated.

OSTEO ARTHRITIS IN YOUNG GEESE AND DUCKS

Synonyms. Ostéo arthrite aigue des jeunes oies, French; osteo-
arthritis be: jungen Gansen und Enten, German.

Characterization. The affection consists principally of a serous
or sero-fibrinous arthritis, hemorrhagic inflammation of the bone
marrow and intestinal catarrh.

Geographical distribution. Outbreaks have been reported in
France, Germany and in the latter country among birds that had
recently been imported from Russia. It is reported as generally
distributed in Germany.

History. The disease was first described by Lucet in France in
1892, by Freese in Germany in 1903, and by Hasenkamp and
Sachweh in the same country in 1914.

Etiology. Pus from all joints examined bacteriologically yields
pure cultures of Staphylococcus pyogenes aureus which, however,
forms but little pigment. The organism is recognized microscopi-
cally in pus in great numbers and a few are observed in smears from
heart blood.

Pathogenicity. Only young geese and ducks are susceptible, of
which 90 per cent become affected. Old geese and ducks, hens and
pigeons are immune. Hasenkamp and Sachweh report one instance
of finding a dead hen in an establishment where ducks were infected,
but made no bacteriological examination.

The hen, pigeon and rabbit injected subcutaneously with blood
of an infected bird, remain healthy. The hen and pigeon likewise
are not affected by subcutaneots injection of pus from the joint of
an affected bird. Hasenkamp and Sachweh have infected hens and
pigeons by intravenous inoculation.

The disease is transmitted to young ducks by intravenous inocula-
tion with culture of S. pyogenes aureus. Subcutaneous inoculation
or ingestion have failed to induce infection.

Mortality. lLéffler observed an outbreak of the disease among
346 geese, of which 43 were old, and 313 young ones. Of the 346
geese, 191 became sick. Of these latter 5 were old and 186 were
young. One old one and 159 young died. The mortality among
the young ones was 85.5 while that of the old ones was 20 per cent.

INFECTIOUS DISEASES OF GEESE AND DUCKS 247

Symptoms. In general the disease is manifested in two forms,
either as a pure acute type with rapidly fatal result, or as a chronic
form terminating in death or recovery after a long time.

In the acute type as described by Freese, young geese and ducks
appear apathetic and eat less. When driven it is seen that they are
very lame in one or the other leg. The joints of the legs are swollen,
fluctuating, hot and very painful. Usually only a few joints are in-
volved, among them most frequently the hock and single toe joints.
The wing joints may also be involved and of these frequently the
elbow is involved. In this case, the affected wing droops. Besides
symptoms of arthritis one observes severe diarrhea and often a
slight mucous catarrh of the conjunctive. Birds showing the acute
symptoms die in from two to four days.

In the chronic form of the disease the arthritis is the most promi-
nent feature of the clinical picture while the general symptoms are
less marked. ‘There is a slight diarrhea during the first few days
and appetite does not entirely disappear. The birds do not appear
quite apathetic but frequently make efforts to walk. They become
greatly emaciated. These symptoms may last for various lengths
of time, on the average, 14 days. Then, either death occurs or the
birds improve with gradual disappearance of symptoms of acute
arthritis. Nevertheless in many cases a painless swelling of cer-
tain joints remains for weeks. In this case the birds walk stiffly for
a long time. They remain halted in development so that they are
not suitable for fattening. In isolated cases during the chronic
course, an acute relapse may occur followed by death.

Lucet describes two types of the disease. One, designated as the
peracute type, is rapidly fatal. In this, the osseous lesions are
slightly pronounced or sometimes inappreciable. The other type,
the acute, is accompanied by epiphyseal osteitis and arthritis. The
duration of the disease is much longer and is terminated by death
after a variable time or by recovery.

In the acute type as observed by Lucet there is depression, the
head is bowed, the feathers are ruffled, dirty and dull. The mucose
are pale, diarrhea occurs, there is no appetite and the rectal tempera-
ture is markedly elevated. The infected subjects lag behind the
others, walk with difficulty, limp and assume a crouching position
frequently. All these symptoms rapidly become aggravated. The
upright position becomes impossible, the members are incapable of
movement and the collapse is extreme. The head rests on the
ground by the beak. Death occurs in one, two or three hours.

248 DISEASES OF DOMESTICATED BIRDS

The acute form is much more common and because of its slower
development is much better defined. First there is depression,
ruffling of the feathers, diarrhea, elevation of the rectal temperature
and loss of appetite all of which are common to serious diseases.
This period of development more or less accentuated has a somewhat
irregular duration. Sometimes it precedes the local symptoms by
several days, at other times it is hardly appreciable. Walking be-
comes difficult and painful. There is lameness in one or both legs.
The patient lags behind its fellows, sits on the ground and assumes
the upright position with difficulty. At this stage the important
joints, especially the tibio metatarsal joints, singly or together are
the site of precise pathological manifestations. They are enlarged,
doughy, very painful and execute very limited movements. Some-
times they are completely immobilized. The temperature reaches
36° to 38° C. when under normal conditions it would be 30° or
34° C.

Incapable of moving, the geese remain in the sternal position for
entire days with the feet underneath them or extended behind or even
sideways. ‘The wings droop, the bird is depressed, holds the beak
down and eats with pain. Sometimes one which is less ill attempts
to flee when approached. With neck stretched out, with beak
opened, and whistling it flaps the wings and drags itself along for
several steps before stopping exhausted.

In such a condition, two terminations are possible. There may
be increase of depression, diarrhea and pallor of the mucous mem-
branes. The cutaneous parasites become more numerous, the
emaciation and cachexia increase and death follows after one, two
or three weeks. On the other hand, the general symptoms diminish
in intensity, the appetite returns, the movements become easier and
recovery occurs after a variable time.

Complete recovery is rare. The affected joints never return to
their normal size nor their former mobility. Ankyloses, thick-
enings and irregularities of the joints interfere with movement.

Morbid anatomy. The carcass is greatly emaciated. The
mucosa of the beginning and end portions of the intestine is greatly
swollen and diffusely reddened or slate gray in color. The abundant
contents of the intestines are viscid and possess a reddish gray color.
The intestinal inflammation is most marked in the pure acute type
in which case, dark red petechiz occur in the mucosa. The spleen
is hypertrophied and the liver is always enlarged.

The affected joints are more or less swollen and filled with either

INFECTIOUS DISEASES OF GEESE AND DUCKS 249

a pure serous fluid or a sero-fibrinous exudate. The fibrin occurs
mostly as a yellowish, transparent layer on the joint cartilages and
on the inner wall of the joint capsule.

The exudate is present in various amounts. The synovial mem-
brane of the joint capsule is swollen and reddened in the acute cases.

The bone marrow is very shiny, dark red in color and the consist-
ency is strikingly soft, often fluid.

In the chronic form the joint cartilage is involved in spots and is
easily lifted from the tissues beneath. Under these spots, the bone
has a porous, rough consistency. In the epiphyses of the bone are
noted cavities of various sizes which are filled with dry, crumbly,
grayish yellow masses. These when rubbed between the fingers feel
granular and are regarded as bone pus. Freese observes that pus
in birds has this consistency instead of the creamy-like character
of that occurring in mammals. In other epiphyses there are holes
in the joint cartilage which communieate directly from the joint to
the cavities in the bone described above. In such cases the joints
contain more or less of the bone pus. The bone of the altered epi-
physes is covered on the outer surface with a cartilage-like deposit,
which is easily overlooked.

Prevention. Prophylactic measures should include separation
of the sound birds from infected ones, disinfection of the quarters,
proper disposal of the dead and of the manure.

Treatment. The advisability of local treatment with counter
irritants and disinfection might be considered.

SEPTICEMIA OF DUCKS

Lisi has described a fatal septicemia of ducks in which all birds
exposed to the infection succumbed.

Etiology. The causative organism is present in the various
exudates, organs and in small numbers in the blood. It is somewhat
larger than that of fowl cholera. The organism grows on gelatin,
causing slow liquefaction and forms a brown colored layer on potato.

Pathogenicity. Inoculation of ducks with culture causes death
in ten or twelve hours. Rabbits and guinea pigs succumb in three
days. The fowl is refractory. The white rat is somewhat suscept-
ible and an area of caseous infiltration forms at the point of inocula-
tion,

Symptoms. The advent of symptoms is abrupt, the eyes are
closed and lachrymating. The bird appears depressed and remains

250 DISEASES OF DOMESTICATED BIRDS

in one position a long time without moving. Death occurs in from
one to four hours.

Morbid anatomy. The eyelids are closed with a purulent secre-
tion, the cornea is covered with white spots, the aqueous humor some-
times is opaque. The pericardium contains a gelatinous exudate
and the heart muscle is pale. The liver is softened, the intestines
and mesentery are congested. A fibrinous exudate occurs on the
peritoneum of some birds.

DUCK CHOLERA

Cornil and Toupet described a disease of ducks which resembles
fowl cholera very closely. The authors differentiate it from that
disease on the basis of the non-susceptibility of fowls and pigeons
to cultures of the organism isolated from the ducks.

SEPTICEMIC INFECTION OF WATERFOWL

Willach observed a cholera-like infection among waterfowl. The
outbreak involved Pekin ducks, swans and geese.

Symptoms. The affected birds show dullness, apathy, inap-
petence, marked thirst, difficulty in swallowing and_ hoarseness.
They die suddenly without spasms.

Morbid anatomy. Autopsy reveals lesions of fowl cholera.

Etiology. Examination of the blood reveals an organism resem-
bling that of fowl cholera. However, it differs from it in several
particulars.

Pathogenicity. Hens, ducks, pigeons and mice succumb to the
infection.

REFERENCES

1. Bugge. Ansteckende Luftsackentziindung der Ginse. Zeitschr. f.
Infektionskr. d. Haustiere, Bd. 3, 1907, p. 470.

9. Curtice. Goose septicemia. Rhode Island Agr. Exp. Sta. Bull. 86,
1902.

3. Cornil et Toupet. Sur eine nouvelle maladie bacterienne du canard
(choléra des canards). Compt. rend. Soc. de biol., T. 106, 1888, p. 1747.

4. Freese. Ueber eine durch den Staphylococcus pyogenes aureus
hervorgerufene Osteo-Arthritis bei jungen Ginsen und Enten. Deutsche
tierirztl. Wchnschr., Bd. 15, 1907, S. 322.

5. Frosch u. Birnbaum. Ueber eine durch den Bacillus septicemiz
anserum exudative (Riemer) bedingte Ginseseuche, Zugleich ein Beitrag
zur Frage dere Pseudoinfluenzabacillen. Centralbl. f. Bakteriol. (Etc.),
1 Abt. Orig., Bd. 52, 1909, S. 433.

INFECTIOUS DISEASES OF GEESE AND DUCKS 201

6. Hasenkamp und Sachweh. Staphylokokken-Erkrankungen beim
Geflugel. Tierdrztliche Rundschau, Bd. 20, 1914, S. 85.

7. Lofiler. Ueber eine in Jahre 1904 in Klein-Kiesow bei Greifsweld
beobachtete Ginseseuche. Arch. f. Tierheilk., Suppl. Bd. 36, 1910, S. 289.

8. Lisi. Infezzione setticoemia in una branco di anatrini. J] moderno
zooiatio, 1896, p. 415.

9. Lucet. De Vosteo-arthrite aigue infectieuse des jeunes oies. Ann.
de l’ Inst. Pasteur, T. 6, 1892, p. 841.

10. M’Fadyean. A remarkable outbreak of goose septicemia. J. Comp.
Path. and Therap., Vol. 15, 1902, p. 162.

11. Riemer. Kurze Mitteilung iiber eine bei Ginsen beobachtete ex-
sudative Septikiimie und deren Errger. Centralbl. f. Bakteriol. (Etc.),
1 Abt. Orig., Bd. 37, 1905, S. 641.

12. Willach. Eine Cholera unter dem Wassergefliigel in Schwetzingen.
Deutsche tierdrztl. Wchnschr., 1895, No. 51. Abstracted in Centralbl.
f. Bakteriol. (Etc.), 1 Abt. Orig., Bd. 20, 1896, S. 187.

CHARTER 2X

INFECTIOUS DISEASES OF CANARY BIRDS

Infectious diseases of canary birds cause heavy losses in breeding
establishmenis where hundreds of birds are kept in close contact
with one another. These conditions, and the occasional introduction
of breeding stock furnish favorable circumstances for the spread of
disease, and severe losses occur. The literature contains references
to a number of infections chiefly observed in Germany where canary
breeding attains considerable importance. Careful comparison of
the descriptions of canary bird infections indicates that most of those
described fall into one of two groups. One, designated infectious
necrosis is caused by a member of the hemorrhagic Spare ae: group,
and another is caused by B. paratyphosus B.

INFECTIOUS NECROSIS OF CANARIES

Synonyms. Bird fever, canary fever, septic fever and bird
plague.

Characterization. The disease is an infection chiefly distin-
guished by the presence of necrotic lesions in the spleen and liver.

History. The disease has been described by a number of writers
including Rieck, Wasielewski and Hoffman, Pfaff, Zwick, Miessner
and Schern, Zeiss, and Binder. The last two writers independently,
have thoroughly reviewed the literature of canary bird diseases.
Doubtless the diseases observed by Kinyoun and by Ziirn are the
same, and in the opinion of Zeiss the one observed by Kern is
identical. On the other hand, Binder withholds decision as to
whether or not Kern’s disease is really the one in question. Most
of the writers have refrained from giving the disease a name, but
Miessner and Schern suggested the name infectious necrosis.

Etiology. The organism causing the disease is a non-motile rod
measuring from 1.5 to 2.5 microns long and .5 to 1. micron broad.
Occasionally larger forms are observed. The organism is Gram
negative and shows bipolar staining. Surface colonies on agar are
grayish in color, appear distinctly granular and are about the size
of a pinhead. No growth occurs on plain potato, but when this

medium has been rendered alkaline a slight brownish colored layer
252

INFECTIOUS DISEASES OF CANARY BIRDS 253

forms. Bouillon becomes slightly clouded and abundant sediment
accumulates. Milk is not coagulated and no gas is formed in sugar
agar. Gelatin is not liquefied. Blue colonies form on Drigalski
plates. A trace of indol was observed by one writer.

Several writers who have worked with the organism regard it
as a member of the hemorrhagic septicemia group. Miessner and
Schern name the organism Bacillus canariensis necrophorus.

Pathogenicity. The organism induces disease in canaries when
introduced subcutaneously and per os. The disease must progress
for at least three days in inoculated birds before the characteristic
necrotic lesions develop. Mice, sparrows, finches, guinea pigs and
rabbits are also susceptible. Pigeons vary in susceptibility while
hens are resistant.

Symptoms. There is nothing characteristic about the behavior
of birds harboring this infection. The birds lose appetite, become
less lively and finally squat in a corner of the cage. Death occurs
after a sickness of from 24 to 36 hours.

Morbid anatomy. The characteristic feature observed at
autopsy is the presence of metastatic foci in the spleen, liver and
oceasionally in other organs.

The liver is enlarged and contains numerous yellow foci the size:
of a pinhead and larger as seen by the unaided eye. The use of a
hand lens reveals smaller punctiform foci. These areas present a
great variety of shapes, and do not separate readily from the sur-
rounding tissue. They are sometimes leathery in texture, some-
times crumbly in structure. The larger ones when cut, are seen to
consist of a homogeneous central mass surrounded by an opaque,
gray colored zone.

The spleen is swollen into a cylindrical form and contains similar
nodules. These distend the capsule and cause the surface of the
organ to have an irregular, undulating appearance. The spleen
contains so many nodules and is so fragile in consequence, that it
breaks apart when grasped with tweezers. The mucous membrane
of the pharynx occasionally contains yellowish nodules which may
be detached with the tweezers. The walls of the pleural cavities oc-
easionally are covered with yellowish exudate, and the lungs may be
involved. Intestinal inflammation is sometimes observed.

The necrotic lesions closely resemble those of avian tuberculosis,
but tubercle bacilli are not demonstrable.

Stained sections of the nodules in the organs reveal the fact that
the smaller ones consist of great clumps of bacteria which have

254 DISEASES OF DOMESTICATED BIRDS

multiplied at the places in question. The larger ones consist of
clumps of bacteria surrounded by necrotic cells. The largest
nodules consist of a number of smaller ones united together.

The presence of the organism in the heart blood is not always
demonstrated microscopically or by culture.

Diagnosis. The disease can be recognized only by the char-
acteristic lesions observed at autopsy.

Treatment. No medical treatment is available.

Prevention. General sanitation and isolation as recommended
in paratyphoid B infection is suggested.

INFECTION IN CANARIES CAUSED BY B. PARATYPHOSUS B

Synonyms. Septic fever in cage birds.

Characterization. The disease is characterized by enlargement
of the spleen with enteritis and is caused by B. paratyphosus B.

History. The disease was described by Joest in 1906 and has
been encountered later by Gilruth, Pfeiler, Adam and Medler, Man-
ninger and by Binder. The latter writer and also Zeiss have sum-
marized the work of earlier students of canary bird infections.

Etiology. The organism isolated from the birds is a short
plump rod 2 to 4 microns long and % to 1 micron broad with
rounded ends. It is actively motile and Gram negative. Flagella
may be demonstrated by Léoffler’s method, but with all care, it 1s pos-
sible to demonstrate one flagellum only on the end of the rods. The
organism in fresh smears from heart blood or organs often shows
bipolar staining.

Growth on agar, gelatin, bouillon, blood serum and potato is the
same as that of cultures of B. paratyphosus B and B. supiestifer.
Neither can differences be discovered between the growth of these
cultures and the canary strains on Drigalski and Conradi or on
Endo’s fuchsin agar plates.

In all strains, milk becomes brightened and yellowish colored
after 8 days. After 14 to 20 days it becomes markedly vellow and
transparent. After standing in the incubator for a longer time it
becomes thickened, viscid and yellowish brown in color. Acid and
gas are produced in dextrose, arabinose, rhamnose and zylose but not
in lactose, saccharose, and raffinose. Indol is not produced.

The organism agglutinates to B. paratyphosus B serum and para-
typhoid B cultures of human origin agglutinates to serum prepared
from the canary strain. :

INFECTIOUS DISEASES OF CANARY BIRDS 255

Pathogenicity. The organism is highly virulent for canary
birds, mice, guinea pigs and rabbits.

Symptoms. In the beginning of the disease the bird is not so
lively as usual and sits on the perches with ruffled feathers. Later
the head is turned backward between the wings, which latter droop.
Occasionally the bird hops about briskly and eats. As the disease
progresses the bird becomes more depressed, appetite ceases en-
tirely, the droppings become thin, the eyes are kept half closed and
respiration becomes quickened to 150 per minute. Occasionally the
bird peeps hoarsely. Movements become uncertain, the bird falls
down, loses consciousness and dies in a spasm.

Morbid anatomy. Rigor mortis is pronounced. The legs are
most often extended from the body. There is more or less marked
inflammation of the intestines. The spleen always shows hyperemic
enlargement, twice to five times its normal size. There is
hyperemia of the liver and kidneys. Smears from heart blood and
organs, contain great numbers of short, thick rods in pure culture.

Prophylaxis. The first measure should consist of separating
the sound from the diseased birds. Further the healthy ones should
be isolated in separate cages so far as possible. The droppings
should be removed daily and be burned. eed and water containers
should be removed from the cages daily and be disinfected.

Treatment. Sick birds may be supplied with drinking water
containing 3 to 5 grams of sulphate of iron per liter. It is best to
separate them so that there will be one or at the most two to a cage.

DISEASE OBSERVED BY FREESE

Freese has described a septicemic disease of canary birds sub-
stantially as follows:

Symptoms. The bird at first ruffles the feathers occasionally
and is not so lively as usual. On the next day it sits quietly on the
perch, peeps now and then and shows a certain degree of dyspnea.
There is somewhat more thirst than usual but the appetite is not
changed. In addition, there may be slight diarrhea. It is char-
acteristic that the sick birds at frequent intervals hop around in the
cage like healthy birds. The symptoms become more marked and
the birds die in a day or so. Some hours before death they sit with
ruffled feathers, on the perch or in the corner of the cage. The eyes
are half closed and the head is turned backwards and held in the
feathers. At this time there is a great increase in the frequency

256 DISEASES OF DOMESTICATED BIRDS

of respiration. It is noteworthy that the birds often continue to
eat, up to a few hours before death. The duration of the disease is
from two to three days.

Morbid anatomy. The blood is coagulated and dark red in
color. The mucosa of the duodenum is swollen and diffusely red-
dened. The liver is either very much congested or fragile and yel-
lowish in color. In most cases the spleen is without microscopic
lesions but occasionally there is a hyperemic swelling of that organ.

Etiology. In smears from the heart blood stained with the com-
mon anilin dyes there are seen small rods 0.5 micron to 1.5 microns
long which stain uniformly. In some cases an organism can only
be found after long search. Bacteria are found very sparingly in
smears from liver, spleen, and kidneys of fresh carcasses. In car-
easses which have lain for several hours the bacteria are found in
larger numbers. ‘That these are not post-mortem invaders is shown ©
by the fact that pure cultures of the organism in question may be
obtained from such material. The organism is Gram positive in
culture as well as in smears from tissues and is non-motile. It
grows on all the common culture media at incubator and at room
temperature but somewhat more slowly under the latter condition.
The organism thrives best with access to air and less well anaerobi-
cally.

After twelve hours on slanted agar at incubator temperature the
organism forms sharp bordered, distinctly prominent, shiny colonies
about the size of a poppy seed. These are thickest in the center and
become uniformly thinner toward the border. By reflected light
they are grayish white in color. By transmitted light they are
bright, transparent and have a bluish shimmer. On long standing
these colonies do not become larger and do not change in appearance.
Such isolated colonies develop after a light seeding of material such
as heart blood from a fresh carcass. After rich seeding of material
and after transfer from a culture a more uniform layer forms, espe-
cially in the vicinity of the condensation water, which however, by
close examination is seen to consist of colonies shaped like fine dew
drops. After about twenty hours, growth ceases. At room tem-
perature, growth is observed after twenty hours and stops at about
thirty-six hours.

The organism grows in a similar manner on four per cent glycer-
ine agar, one per cent glucose agar, and on blood serum. On the
latter medium growth appears first after twenty-four hours at in-
cubator temperature and continues about three days. After this

INFECTIOUS DISEASES OF CANARY BIRDS 207

time there has formed a very shiny, thin layer, the border of which
appears finely toothed.

The organism remains living on agar for six weeks without trans-
ferring and on blood serum for eight weeks.

On agar plates after fourteen hours at incubator temperature
there are formed sharply defined, gray-white colonies about the size
of a poppy seed which lie partly on the surface and partly within the
medium. They do not change in appearance after a longer time.

On gelatin plates one observes with the unaided eye, after forty
hours, fine gray-white points. By reflected light under the micro-
scope with low magnification colonies are seen to have a brownish
yellow color, have sharp borders and are circular or oval in form.
In the center of these are a number of dark brown granules and on
this account the center appears darker than the periphery. After
two days a bright, transparent area forms about each colony and
after three days one observes distinct liquefaction. This advances
until the whole plate is liquefied after five days, reckoned from the
time that the culture was planted. Similar growth is observed on
one per cent glucose gelatin plates.

On slanted gelatin a distinct liquefaction occurs along the line of
inoculation after forty-eight hours. On the bottom of the tube there
is observed a large amount of cloudy fluid which has run down from
the surface of the gelatin leaving a trough-like depression. In
gelatin stab cultures after forty-eight hours punctiform colonies are
observed along the line of the stab. There is a depression on the
surface the size of a pinhead, which represents the beginning of
liquefaction.

The liquefaction progresses and in about fourteen days the whole
of the medium becomes liquefied. Then there is observed a gray-
white viscid mass in the bottom of the test tube which when shaken,
ascends and forms a dense cloudiness. The organism remains alive
on gelatin without transfer for about six weeks.

In bouillon in the incubator after fourteen hours, the organism
causes a uniform clouding and on shaking, a viscid sediment rises.
The clouding continues till the third day and the sediment increases
at the same time. After five days the upper part of the bouillon be-
comes somewhat more clear and after fourteen days it becomes en-
tirely clear. In the bottom of the test tube at this time there is an
accumulation of brownish gray, thick sediment which on whirling
the tube appears granular and stringy. No pellicile forms on the
surface of the bouillon. Similar growth is observed in glycerine

208 DISEASES OF DOMESTICATED BIRDS

bouillon and in glucose bouillon. At room temperature growth in
bouillon is somewhat more slow. The organism remains alive in
bouillon for about four weeks.

After 18 hours, growth occurs on potato in the form of prominent,
sharply outlined grayish-white colonies about the size of a poppy
seed. In the middle of the inoculated area these coalesce into a
uniform layer. After two or three days the culture frequently be-
comes brownish yellow in color in the thicker parts. The organism
grows on potato at incubator and at room temperature equally well,
and remains alive on this medium for six weeks.

In whole milk at incubator temperature after 15 hours a marked
separation of the whey occurs. ‘The casein is coagulated in large
flakes. After 36 hours the coagulation process is completed. <At
room temperature coagulation occurs first at 32 hours. In spite of
the lactic acid, the organism remains alive four weeks without
transfer.

The organism forms no gas in the culture media employed and no
acid, with the exception of that formed in milk. It develops no
specific odor.

Indol is not detected in bouillon cultures four days old.

It is to be noted that in general the organism, in fresh cultures
on the various media has the same form. In these, however, it
appears shorter than in smears from tissues. Occasionally short,
plump rods and very rarely, division forms occur. Among these
may be observed many which are similar to a diplococcus. The
organism appears somewhat smaller on blood serum than upon the
other media. The organisms when grown on potato are the largest
and longest.

Pathogenesis. Hens, pigeons, rabbits and guinea pigs are in-
susceptible to subcutaneous injection of culture or to injection of
heart blood of a canary bird dead of the disease. In these birds
it causes only a straw yellow focus about the size of a pea, at the
point of injection.

The infection may be transmitted to canary birds by inoculation
and by feeding. Sparrows and mice are also susceptible.

Freese compares the disease found by him with fowl cholera and
with the diseases described by Rieck, Kern and Pfaff. He con-
cludes that it differs from all of them. The one deseribed by Kern
‘shows the greatest similarity. The two practically agree in symp-
toms, lesions and pathogenesis, but cultural characters show some

INFECTIOUS DISEASES OF CANARY BIRDS 209

marked differences. No subsequent writer seems to have encoun-
tered the disease described by Freese.

SEPTIC ENTERITIS OF CROSS BILLS

Tartakowski has described a disease occurring in cross bills (Lowia
curvirosa and pityopsittacus), gold finches (Carduelis elegans),
green finches (Chrysonitris spinus) and rarely in canary birds.

Symptoms. The bird exhibits periods of dullness alternating
with periods of apparent complete health. There are frequent at-
tacks of weakness, somnolence with impairment of appetite, and in-
creased thirst. The disease causes death in from 10 to 12 days.
During the last few days the bird sits on the bottom of the cage
with eyes closed.

Morbid anatomy. When the disease has been of long duration
the carcass shows great emaciation. ‘There are no ecchymoses or
exudates in the serous cavities. The breast muscles are always
yellow as if cooked. Spleen and liver are always enlarged. Kad-
neys and heart muscle are yellow and clouded. Rarely there is
marked hyperemia of the intestinal canal. Organs of respiration
are normal. ‘The brain is anemic.

Etiology. There is constantly found in the spleen, liver and
blood a rod which measures from 2. to 2.5 microns long and varies
from .6 to 1. micron thick. The organism is actively motile and
Gram negative. There is nothing distinctive about the growth on
agar and gelatin. Gas formation occurs. There is no liquefaction
in the latter. Milk is not coagulated. Tartakowski has designated
the organism as Bacillus loxiacida.

Pathogenesis. The organism is fatal to cross bills when ad-
ministered in drinking water, and when injected subcutaneously or
intramuscularly. In guinea pigs a local swelling is induced at the
point of inoculation together with transient fever. Intraperitoneal
inoculation causes a sero-fibrinous peritonitis and death in from one
to two days. Rabbits injected the same way do not always die from
peritonitis.

REFERENCES

1. Adam u. Medler. Ueber Paratyphus-B-Infektionen bei Kanarien-

végeln und Untersuchungen iiber das Vorkommen yon Bakterien der Koli-

Typhusgruppe im normalen Kanarienvogeldarm. Centralbl. f. Bakteriol.
(Etc.), Orig., Bd. 62, 1912, S. 569.

260 DISEASES OF DOMESTICATED BIRDS

2. Binder. Ueber die infektiose Nekrose der Kanarien. Ween. tierarztl.
Wehnschr., Bd. 1, 1914, S. 337.

3. Gray. Disease in canaries. Vet. Rec., Vol. 22, 1910, p. 753.

4. Gilruth. Diseases of canaries. Vet. J., n. s. Vol. 17, 1910, p. 655.

5. Joest. Eine durch Bakterien der Enteritisgruppe verursachte
Kanarienvogelseuche. Ber. ii. d. k. Hochschule zu Dresden, Bd. 1, 1906,
Selo:

6. Kern. Eine neue’ infectidse Krankheit der Kanarienvdégel.
(Kanariencholera) Deutsche Ztschr. f. Tiermed., Bd. 22, 1896, S. 171.

7. Kinyoun. Vogelpest. Preliminary note. Centralbl. f. Bakteriol.
(Ftc.), 1 Abt. Orig., Bd. 38, 1906, S. 329.

8. Miessner u. Schern. Die infektidse Nekrose bei den Kanarienvégeln.
Arch. f. Tierheilk., Bd. 34, 1908, S. 132.

9. Pfaff. Eine infektiése Erkrankung der Kanarienvigel. Centralbl.
f. Bakteriol. (Htc.), 1 Abt. Orig., Bd. 38, 1905, S. 275.

10. Manninger. Ueber eine durch den Bacillus paratyphi B. verursachte
Infektionskrankheit der Finken. Centralbl. f. Bakteriol. (Etc.), Bd. 70,
191308, 12.

11. Pfeiler. Ueber ein seuchenhaftes, durch Bakterien aus der Para-
typhusgruppe verursachtes Kanariensterben. Berl. tierarztl. Wehnschr.,
Bd. 27, 1911, S. 953.

12. Rieck. Eine infectidse Erkrankung der Kanarienvoégel. Deutsche
Ztschr. f. Tiermed., Bd., 15, 1889, S. 68.

13. Tartakowski. Ueber eine Infektionskrankheit der Kreuzschnabel und
anderer Zimmer-und Singvogel. Arch. d. Veterindrwesenschaften, 1898.
(Russian.) Abstracted in Centralbl. f. Bakteriol. (Htc.), 1 Abt. Orig.,
Bd. 25, 1899, S. 89.

14. Wasieliewski u. Hoffmann. Ueber eine seuchenhafte Erkrankung bei
Singvégeln. Arch. f. Hyg., Bd. 47, 1903, S. 44.

15. Zeiss. Beitrag zur Frage der Erreger von Kanarienvogelseuchen.
Arch. f. Hyg., Bd. 82, 1914, S. 1.

16. Zwick. Untersuchungen iiber eine Se ana SE Nan, Ztschr. f.
Infektionskr. d. Haustiere., Bd. 4, 1908, S. 33.

CHAPTER XXI

TUMORS IN FOWLS

Tumors in fowls hardly constitute a serious economic problem.
However, in view of their great similarity in structure to those of
man, they have received considerable attention.

FREQUENCY OF OCCURRENCE OF TUMORS

Curtis has reported upon the frequency of occurrence of tumors
of fowls based upon autopsies of 880 birds. Of these 79, or 8.96
per cent had tumors. This percentage corresponds to 90 cases of
tumors per 1000 birds. No significant difference was noted in fre-
quency of occurrence of tumors, between birds which died from nat-
ural causes, and apparently normal birds which were killed. There
is a significant correlation between age and the occurrence of tumors.
Of the birds under 2% years of age, only 7.37 per cent had tumors,
while they were present in 19.17 per cent of birds over that age.
In birds which died from natural causes, and showed tumors, these
were directly or indirectly the cause of death in from one-third to
one-half the cases. There was a decided tendency for the associa-
tion of hypertrophy of the liver, spleen or kidney, with the presence
of tumors in other organs. The hypertrophy was apparently due to
cell infiltration. Death often resulted from internal hemorrhage
originating in the tumor, the underlying tissue or the hypertrophied
liver or spleen. Data as to the character of the tumors were classi-
fied with reference to whether the tumors were cystic or of solid
tissue structure. Those of cystic structure comprised 22.78 per
cent and solid tumors constituted 74.68 per cent. Three cases fell
in both classifications in that cysts were attached to solid tissue
tumors. In females the genital organs were most frequently in-
volved. In 87.76 per cent of all, the tumors were in the ovary and
18.36 per cent involved the oviduct and oviduct ligament. Too
few males were examined to warrant drawing conclusions. In most
cases the tumors were confined to one organ. In 15 cases metastasis
had evidently occurred since tumors of similar nature were found

in from two to four organs.
261

262 DISEASES OF DOMESTICATED BIRDS

Ehrenreich collected data on the frequency of the occurrence of
tumors in fowls. Arrangement was made with a hotel to have sent
to him the organs of all birds noticed to contain tumors. From
nearly 2000 mature hens he obtained 7 malignant tumors of which
5 were surely carcinomata. Doubtless the hotel employees over-
looked many small tumors. It should be noted that the birds ex-
amined were in apparent health and the discovery of carcinomata
was purely accidental. Under more favorable conditions, the per-
centage of carcinomata would have been higher. Among 3000
pullets under a year old, no carcinomata were found, which confirms
the belief that carcinoma is associated not with youth, but with
maturity.

CARCINOMA

One carcinoma described by Ehrenreich was about the size of a
hazel nut and had developed between the gizzard and the spleen. It
was in contact with the upper end of the small intestine which
showed stenosis at that point. The consistency was soft, the surface
uneven and covered with shiny serosa. The color was gray and on
section showed a few yellow points. Microscopic examination
showed the tumor to be an adeno-carcinoma.

Two more highly differentiated adeno-carcinomata were obtained
from the ovary. They were about the size of a small apple or a
man’s fist, were of solid consistency, had rough surfaces and were of
a reddish gray color. In both cases a seeding of small metastatic
tumors on the peritoneum had occurred.

Ehrenreich and Michaelis described three malignant tumors of
the hen, of which two were adeno-carcinomata and one was a sar-
coma-like tumor.

SQUAMOUS CELL CARCINOMA

Pick described a squamous cell carcinoma located beneath the
floor of the mouth of a hen and which caused a marked deforma-
tion of the region. The subject was a hen about seven years old.
The tumor was observed at New Year’s as a small lump and by
September had grown to a mass measuring 4 by 3 by 3 em. when the
bird was killed. The tumor was located in the rear half of the floor
of the oral cavity and bulged out on each side. It extended down-
wards to the sparsely feathered area between the wattles. The sur-
face was smooth except for a small ulcerated spot near the beak.
On section it was observed that the tumor was necrotic near the

TUMORS IN FOWLS 263

mouth cavity. Microscopic examination showed the tumor to be a
typical squamous cell carcinoma.

Koch describes a squamous cell carcinoma (cancroid) of a hen.
The subject belonged to the Brahma-Putra breed, which is noted for
its longevity. The bird had been in the Berlin Zoological Gardens
for seven years and was full grown when brought there. Thus it
was concluded that the bird must have been at least eight years old.
The tumor was located in the roof of the oral cavity close to the back
wall of the pharynx. It is to be noted that the other squamous cell
carcinoma reported by Pick was located on the floor of the oral
cavity and occurred in a seven year old hen.

According to Koch’s description, the internal organs present no
noteworthy features. On opening the oral cavity by a cut through
the left commissure of the beak there is revealed a somewhat solid
mass which completely fills the pharnyx and exerts such pressure on
the larynx that it contains a depression corresponding to it. The
surface of this yellowish mass is spotted with bright red blood clots
which may well have caused death by strangling.

The yellow mass is so large that the disfigurement of the tracheal
region would have been discovered in life but for the fact that it
was covered with feathers. The tumor is very lightly attached and
can be raised easily. It involves only soft tissue and no alteration
of bone is observed. Microscopic examination shows the tumor to
be a typical squamous cell carcinoma.

CYSTO-ADENOMA

Pickens has reported upon a cysto-adenoma in a fowl. The sub-
ject was a rather large Plymouth Rock and appeared to be in rela-
tively good condition. The abdominal cavity was found to con-
tain a pint of very thin straw colored fluid. After being collected in
a flask, and after standing, a small amount of sediment was precipi-
tated. The proventriculus, gizzard, liver, spleen, intestines and
peritoneum were covered with numerous white lobulated tumor-like
masses. These varied greatly in size, some measuring 1-2 mm. in
diameter while others measured 5 to 6 em. in diameter. They were
either sessile or attached to the serosa by means of a very short
stalk. The stalk seemed to be a continuation of the capsule of the
nodule, and was easily broken, leaving the tumor free. The capsules
of the nodules were smooth and resembled the peritoneum very
closely. Many of the larger of these nodules contained small sacs

264 DISEASES OF DOMESTICATED BIRDS

or cysts attached to them. The cysts contained a small amount of
serous fluid similar to that found in the abdominal cavity. Only
one cyst occurred on a nodule. The proventriculus and gizzard
showed only a few nodules. These were small varying from 2 mm.
to 2 em. in diameter. No cysts were found on the nodules of these
organs.

Only a few nodules were attached to the liver and spleen. Those
on the spleen were of the smaller variety and did not show cysts.
There were several large nodules on the liver, the largest one meas-
uring 6 cm. in diameter and contained a cyst. The stalk of this
tumor seemed to extend down through the capsule into the liver
tissue proper. ‘The serous coverings of the small and large intestines
were affected alike and showed the attachments of many tumors
of varying size. Section of a medium sized nodule showed it to
contain several cysts containing thin, straw colored fluid. The cut
surface of the tumor was white in color, tinged with pink. It was
firm in consistency and numerous blood vessels were seen.

Histological examination of the tumors shows them to be made up
of rather loose fibrous connective tissue stroma, relatively scarce in
cells. Scattered irregularly through the stroma, and occupying
approximately one-fourth of the area of the tumor are numerous
alveoli, varying in size from a solid cord made of two or three.
epithelial cells to large cysts 5 mm. in diameter, in the larger
nodules. The alveoli are lined with epithelium which range from
squamous to columnar in type. The alveoli vary greatly in shape.
Some are irregularly oval, while others are much elongated and com-
paratively narrow, resembling thé duct of a gland. Still others are
found where numerous branching has taken place, giving the tumor
the appearance of a papillary adenoma. ‘The epithelium is, as far
as can be determined, attached to a very thin basement membrane
and the cells are only one layer thick. The connective tissue stroma
of the tumor is exceedingly well supplied with blood vessels. The
serous covering or capsules of the tumors are composed of rather
dense fibrous connective tissue, which serves as the connection of
the tumor to the serosa of the intestine. At the point of contact of
the tumors with the liver, the liver cells have been replaced to a con-
siderable extent with connective tissue stroma like that of the
tumor.

TUMORS IN FOWLS 265

FEATHER CYSTS

Koch observes that feather cysts (cystomata pennifera) occur in
hens and geese, which are analogous to the dermoid cysts of mam-
mals.

LYMPHOMA

Tyzzer and Ordway observe that lymphomata occur both with and
without lymphatic leukemia. They regard the latter condition as
due to the presence in the circulating blood of tumor cells having
the characteristics of the cells of the lymphoid series. ‘The only dis-
tinction made by them between a leukemic lymphoma and lymphoma
with lymphatic leukemia is that in the former the tumor is ex-
travascular while in the latter the tumor is intravascular. ‘Tumors
observed by them occurred as definite primary growth either with or
without secondary nodules or were so disseminated that the site of
origin could not be determined. Some of the tumors have a more
or less alveolar structure while others grow diffusely by infiltrating
normal structures. Examples are given of a few cases observed by
Tyzzer and Ordway.

Lymphoma associated with lymphatic leukemia. Lympho-
matous tumors are disseminated throughout the liver, the kidneys
and the peritoneum; lymphatic leukemia. The subject is a hen at
least one and possibly two years of age. ‘The liver is greatly en-
larged and presents many distinct rounded nodules of pale pink
color distributed through its substance. Many of these nodules are
apparent in the surface of the liver. Some present slightly de-
pressed central areas, and elongated rounded borders. The largest
measures 3 cm. across. The spleen is several times its normal size
and is rather soft. The cervical lymph glands are enlarged. The
kidneys are enlarged and studded with rounded pink nodules, some of
which are 4 mm. in diameter. Distributed over various portions of
the peritoneal surface are elevated plaques of tissue from which
small blood vessels radiate into the surrounding normal tissue.

The tissue of this case being poorly preserved it is impossible to
determine the finer histological features of the cells. It is apparent,
however, that the nodules in the liver, the kidneys, and the peri-
toneum are composed of cells somewhat larger than the lymphoid
cells of the circulating blood of the fowl and possess a more or less
spherical, eccentrically situated nucleus. They correspond quite
closely in their morphology to the plasma cell, and are evidently

266 DISEASES OF DOMESTICATED BIRDS

closely related to cells of the lymphoid series. The blood found in
the vessels of various organs and tissues contains large numbers of
these cells, so that the proportion of white cells in the circulating
blood is very great. In addition to the nodules of tumor tissue
found in the liver and kidneys, these organs are to a large extent
infiltrated with tumor cells.

A case of lymphoma of the neck with metastasis to the lungs and
the liver without lymphatic leukemia is described by the same
writers. The cervical tumor appears as an oval flattened mass with
an elevated rounded edge and a thick central crust. It measures 5
by 6 cm. across and 2 em. in thickness. On section it is found to be
composed of rounded cells which vary considerably as to size, and
which contain rounded, somewhat irregular nuclei. The liver is
ereatly enlarged. The right lobe presents a rounded nodule, 1 cm.
in diameter consisting of tissue of similar appearance to that of the
primary tumor. The entire liver is infiltrated with this tissue
which appears to augment the size of the lobules and in places grows
diffusely in areas 2 to 5 mm. in diameter. The tumor involves both
lungs, and only a small portion of one lung contains air. Near the
roots of the lungs are two rounded nodules of tumor tissue. The
tumor consists of cells with little supporting tissue. The latter
consists for the most part of a delicate reticulum of connective tissue
which apparently does not develop to any considerable extent within
the tumor, but represents preéxisting tissue into which the tumor
has grown. There are also a few coarser bands of fibrous tissue.
The tumor is rather vascular throughout, and the connective tissue
reticulum is more distinct around the vessels than elsewhere. The
tumor cells vary in size. Many are no larger than the lymphocytes
of the circulation but some are equal in size to large connective tissue
cells. They are apparently not concerned in the formation of in-
tercellular fibrils.

Another case reported presented a primary tumor of the nature
of a lymphoma, situated on the neck, with secondary nodules on the
sternum, in the lung and in the liver. The sternum and adjacent
muscles are infiltrated with the tumor, but the tumor occurs as dis-
crete nodules in the lung and liver. The spleen is not involved and
the blood appears normal.

Warthin observed several cases of leukemic lymphocytoma in
fowls in which there were observed tumor-like nodules and infiltra-
tion of lymphoid cells in all the organs, particularly in the liver,
spleen, kidneys, bone marrow, and hemolymph nodes. He observes

TUMORS IN FOWLS 267

that aleukemic and leukemic forms of lymphocytoma occur and is
of the opinion that the two conditions appear to be genetically re-
lated if not different stages of the same process. He interprets the
two conditions as malignant neoplasms.

LEIOMYOMA

Tyzzer and Ordway describe a leiomyoma of the mesentery of a
hen. The specimen consists of a loop of hypertrophied intestine
30 em. long and 8 to 4 em. in circumference. Within the mesentery
and covered on both sides by peritoneum is a large rounded tumor
of firm, flesh-like consistence, which measures 7 by 5 by 5 cm. This
is of a general reddish pink color. On section the coloring is simi-
lar, and the surface is traversed by firm, glistening bands of some-
what lighter color. On scraping the surface, these stand out
prominently and no soft tissue comes away. Between this tumor
and the intestine is a tumor mass of similar character measuring
2 by 1.5 em. On histological examination the tumor is found to
be composed of typical smooth muscle fibers running in various
directions. Sections stained by the Van Gieson method for con-
nective tissue show only a few small strands of fibrous tissue be-
tween the masses of smooth muscle fibers. The tumor is composed
chiefly of smooth muscle fibers and is in many respects similar to
the leiomyoma of mammals.

OSTEOCHONDROSARCOMA

Rous, Murphy and Tytler have described an osteochondrosarcoma.
The fowl bearing the original growth was a Plymouth Rock hen in
good condition and apparently about a year old. On the lower
portion of the keel of the sternum was an irregularly spherical mass,
so symmetrically disposed that the keel passed almost through its
center. The tumor measured 6.6 by 5.7 by 4 cm. The growth was
smooth, nearly as hard as bone and the skin over it was slightly
stretched but not firmly attached. The tumor was well encapsu-
lated. In the gross specimen the sternal keel could be traced to
the center of the growth, but here it was lost in a mass of red,
spongy, bony tissue which radiated from it for a distance of one to
one and one-half em. Peripheral to this, the tumor was hard and
white with fine strands of opaque, fibrous tissue separating more
translucent, homogeneous areas.

268 DISEASES OF DOMESTICATED BIRDS

Microscopically the capsule of the tumor was found to consist of
fibrous connective tissue containing isolated muscle bundles. The
growth itself was made up of a zone of what may be called pre-
chondral tissue, enclosing and grading into a mass of hyaline carti-
lage through which ran the sternal keel. From this latter numer-
ous irregular, bony trabecule radiated into the cartilage.

A brief recapitulation of the microscopic observations indicates
that the outermost, youngest zone of the tumor is made up of cells
of fibroblastic type scattered sparsely in a collagenous intercellular
substance. In its deeper portions this tissue is undergoing a trans-
formation to cartilage, its cells taking the character of cartilage cells,
while the ground substance becomes homogeneous and basic staining.
The original tumor is well encapsulated, and seems nearly, if not
quite, stationary.

The growth is readily propagated in other birds by transplanting
small bits of fresh, peripheral, neoplastic cartilage. By means of a
trochar, the grafts are placed deep in the pectoral muscles. In
erowth resulting from the transplantation, cartilage is laid down,
followed later by bone if the bird lives long enough. Death results
from the tumor but rarely and in such instances the host gradually
becomes emaciated. The tumor is not transferable to the pigeon.

The growth may also be induced by the filtrate of a Berkefeld
filter. The tumor tissue is ground up with sterile sand. The re-
sulting mass is suspended in Ringer’s solution at blood heat and
centrifugalized to free from tissue fragments. The supernatant
fluid is passed through a Berkefeld filter of fine enough grade to re-
tain B. fluorescens-liquefaciens. ‘The percentage of tumors caused
by the injection of filtrate is considerably higher when sterile in-
fusorial earth is included. This material apparently causes a cell
derangement favorable to tumor formation.

SPINDLE CELL SARCOMA

Rous observed a spindle cell sarcoma in a Plymouth Rock hen
about fifteen months old. A large irregularly globular mass pro-
truded from the right breast. It had developed slowly and without
apparent involvement of the health of the host. The bird was
anesthetized and nearly all of the growth was removed. When
sliced it was found to have undergone a widespread coagulation
necrosis at the center, but there was a rim of translucent, rather
friable, yellowish pink tissue of glistening, finely striated surface.

TUMORS IN FOWLS 269

Autopsy of the bird reveals the presence of about 20 ¢.c. of a thin
straw colored fluid in the peritoneal cavity. Attached to the lower
margin of the liver, to the oblique membrane, and to the parietal
peritoneum are many firm, pale yellow, ovoid globular nodules, the
largest about 1 cm. in diameter. On section these resemble the
nodule in the left breast, except that in them the necrosis is irregu-
larly distributed. At the pelvic region, where several of the masses
have coalesced, softening and necrosis are extensive. No growths
are visible in the other organs.

Microscopic examination of the tumor reveals it to be a spindle-
celled sarcoma. In a typical section there are observed loose bundles
of spindle cells coursing in every direction, and separated from the
lesser blood vessels only by endothelium. Where such a bundle is
cut transversely, the appearance is that of a group of round cells of
varying sizes.

Transplantation of the tumor was accomplished by the use of
fowls from the small, intimately related stock in which the growth
appeared originally. Young chickens were more susceptible than
adults. Market fowls of similar variety proved insusceptible as did
pigeons and guinea pigs. During the first four generations, the
tumor remained true to type and was infiltrative and destructive.
Metastasis to the heart was observed once.

The tumor has been found to be transferable by the filtrate of a
Berkefeld filter.

Rous has shown that ultraviolet light rapidly kills the cells of this
transplantable sarcoma of the fowl without notably injuring the
etiological agent associated therewith. The Roentgen ray has little
effect on either cells or agent.

He observes that fowls manifest two sorts of resistance to the
avian tumor, one directed against the implanted tumor cells as such,
the other against the action of the etiological agent to cause a neo-
plastic change. In the individual fowl the two resistances appear
to be independent of one another, though they may exist together or
may both be absent. A recognition of them will perhaps explain
some features in the biology of other tumors.

Rous and Murphy observe that variations have from time to time
occurred in the structure and behavior of this tumor. After a long
series of transfers the growth frequently gave rise to fatal hem-
orrhages from its substance. In some of the later, rapidly growing
tumors the cells tended to be spherical, showing only a very tardy
and imperfect differentiation to the spindle form. A giant-celled

270 DISEASES OF DOMESTICATED BIRDS

form of the growth was sometimes met with. Despite their diversity,
the tumors graded into one another and in the final analysis, all are
to be considered as spindle-celled sarcomata.

Attempts to obtain an action of the etiological agent upon cells
other than those it usually affects have failed, as have attempts to
bring about changes in the histology of the sarcomata by attenuating
the agent.

Some of the lesser morphological variations in the sarcomata are
undoubtedly due to local conditions of the host, and of the more im-
portant changes some have been associated with an increase in the
malignancy of the growth. For others the determining conditions
have yet to be discovered. On the whole the variations described are
not more marked than those occasionally manifested by the trans-
plantable mammalian tumors, and traceable to the changes in a single
strain of tumor cells during their propagation in successive hosts.
In mammals the ultimate reason for these changes is not known.
In the case of the chicken tumor some of them are undoubtedly the
expression of changes in the causative agent of the growth.

Rous and Lange describe a spontaneous chicken sarcoma. The
subject was a mongrel brown Leghorn hen which was rendered lame
by swellings on the left leg. The growth regarded as the primary
one was located in the gizzard. It occupied nearly the whole right
anterior portion of the organ and projected irregularly under a cover-
ing of mesentery in which were located several small nodules. The
mass was roughly spherical and was about 4.3 em. in diameter. The
tumor was surrounded by muscle and encroached on the gizzard
cavity. The tumor had no capsule but was sharply defined by its
pale pinkish white color as contrasted with the wine color of the
muscle. The tumor was made up of many irregular, tightly com-
pressed subdivisions separated by minute, irregular fissures, and
bulged on the cut surface. <A localized soft yellow area of necrosis
was located to one side, but in general the growth was translucent
and appeared sound though poorly vascularized. The liver was en-
larged, congested and mottled with ill defined, pale areas. Two
small stellate depressions making irregular gray areas in the paren-
chyma, were located on the surface of the organs. These proved to
be composed of tumor tissue. The other viscera appeared normal.

An oblong smooth mass 4.5 by 3 by 3 em. was located in the ex-
tensor muscles of the left thigh. A similar one was located in the
muscles below the knee. The upper mass was attached to the peri-
osteum for about 2 cm. above the patella and also to the joint capsule.

TUMORS IN FOWLS 271.

A prolongation extended from it to the back of the joint. The lower
growth was attached to the joint capsule but the bulk of it lay in the
muscle. These growths were extremely firm, more so than the one
in the gizzard. ‘They were pinkish white in color and nearly blood-
less. They consisted of finely striated tissue in part solid and in
part divided into irregular lobuli, like the tumor in the gizzard.
Some of the lobuli had a central, semigelatinous depression and in a
tew the center was yellow, firm and opaque, evidently necrotic. The
growths were not encapsulated and were poorly defined from the
muscle sheaths, periosteum and tendons which they involved.

The knee joint was full of translucent, gristly papillary pro-
liferations attached to the capsule or joint surface. These were ex-
tensions from the growths on the outer surface of the capsule.
Within the lower end of the femur and lying in the red marrow was
a translucent tumor mass about .4 em. in diameter. Tumors were
also located in the muscle of the chest wall near the ribs, in the an-
terior muscles of the neck and elsewhere.

Microscopically, the tumor was found to consist of spindle-celled,
sarcomatous tissue fissured and subdivided by many flattened sinuses,
and often intracanicular in its growth.

Transplantation was carried through eight successive groups of
fowls. The development of the first few series of transplantation
tumors was very slow. They exhibited the histological structure of
the original growth and showed the same tendency to form metastatic
foci in the skeletal muscles. Later the tumor grew more rapidly
and underwent a simplification of structure to that of a pure spindle-
celled sarcoma. Plymouth Rock fowls proved to be quite as satis-
factory hosts as the brown Leghorn breed in which the tumor oc-
curred originally. The agent causing the tumor was capable of
passing through a Berkefeld: filter.

Goérig reports multiple sarcomata in a Plymouth Rock hen about
three or four years old. During life the subject displayed difficult
breathing, was greatly emaciated as a result of difficulty in eating
caused by two tumors, which hung from the lower side of the neck.

There is a tumor the size of a pigeon’s egg suspended from the
neck below the wattles. It is located in the subcutaneous connective
tissue, has a solid consistency and the surface appears finely rough-
ened. The skin is for the most part attached only loosely to the
tumor and only in a small spot is there a close union between the
two. This is marked from without by an excoriated spot on the
skin. The tumor measures 5 by 3% em. It is gray white in color

272 DISEASES OF DOMESTICATED BIRDS

and the cut section has a slight shiny appearance. There are ob-
served whitish threads of connective tissue between which there are
darker islands of tissue. Blood vessels seem somewhat scarce. No
lesions are observed in the internal organs. Microscopic examina-
tion leads to the diagnosis of small spindle-cell sarcoma.

LYMPHO SARCOMA

Regenbogen has described a case of multiple sarcomata of the
skin of a hen two years old. The subject is in good condition, dis-
plays good appetite and is active. A number of tumors are located
on the head, neck, and back. These are of various sizes; one involv-
ing the left eye is 4 em. in diameter. The surface of this tumor
is uneven. The center appears dark brown as a result of the pres-
ence of scabs and crusts. The periphery of the tumor shows the
color of the skin and is thrown up in a circular ridge. The tumor
extends above to the comb, below to the ear wattle, forward to the
corner of the mouth and deep in the orbit. The other tumors move
freely within the skin and are sharply defined from surrounding tis-
sues. On the cut surface they are grayish white in color, smooth
and fatty. The center of the surface of the larger tumors has under-
gone an ulcerative degeneration.

Microscopic examination shows round cells for the most part.
Between these is a scanty and delicate reticular foundation struc-
ture. The vessels appear throughout as thin walled canals between
the cell masses. rom this it is seen that the tumor is a small round
cell sarcoma, for instance, a lymphosarcoma.

Ziirn and Pauly have observed diffuse round cell sarcomata in the
liver of hens, and Watson has reported upon a round cell sarcoma in
the heart of a fowl.

MELANOSIS

Lewin described a case of general melanosis in a young slaughtered
hen. The bird had coal black feathers, beak and legs. The comb
was dark red, the tongue and oral mucosa, black. After removing the
feathers, the whole body appeared bluish black, the musculature shone
bright through the skin and after removal of the skin, appeared un-
altered. The loose tissues between the muscle groups contained
black patches of various sizes and shapes. After opening the body
cavity the serous surface was observed to be completely black, as was

TUMORS IN FOWLS 273

the intestinal canal. Black patches were present on the gizzard and
heart. After removing the flesh from the bones, the periosteum was
observed to be wholly black as were also the cartilages of the joint
surfaces. After scraping the periosteum the bone was seen to be
black in places.

A specimen exhibiting generalized melanosis in a fowl is included
in the pathological collection of the New York State Veterinary
College at Cornell University.

MYXO-SARCOMA

Tyzzer and Ordway describe a myxo-sarcoma of the thigh of a
hen in part as follows. The tumor was situated on the outer aspect
of the thigh of an adult hen, and appeared as a turban-shaped mass
with a depressed central area and an elevated rounded edge. It
measured 5 em. across and 2 cm. in thickness. On section it was
found to consist chiefly of a translucent, soft tissue almost gelatinous
in consistence. The tumor is found to be composed of lobules of
tissue which consist of cells widely separated from one another by a
relatively large amount of intercellular material. The lobules are
to a large extent limited by connective tissue which in places forms
a definite capsule. In certain places, however, the tumor is without
capsule of any sort and appears to be infiltrating the subcutaneous
fat. The central portions of many of the lobules are necrotic, and
the cells in the surrounding tissue are somewhat degenerated. The
connective tissue around the lobules is loose and vascular in places,
and, since there is in such places a marked infiltration with leu-
cocytes, it resembles closely granulation tissue. In it are found
large numbers of lymphoid and plasma cells, and large phagocytic
cells.

The cells of this tumor present the characteristics of connective
tissue cells, and are associated with intercellular material consisting
in part of a fibrillar reticulum, in part of a homogeneous substance
which reacts to staining reagents like mucin. The fibrillar material
is probably closely related to collagin, although it is stained some-
what atypically with alum hematoxylin. The tumor is malignant
in that it is rapidly growing, and in that it infiltrates normal tissues
such as fat and nerves. Although blood vessels of considerable size
are found within many of the lobules, the tumor tissue is not every-
where well vascularized, and is prone to necrosis. No metastases
were found.

274 DISEASES OF DOMESTICATED BIRDS

MYXO-FIBROMA

Koch observed tumors in a partridge which closely resembled
avian tuberculosis. Both ceca were studded with numerous tuber-
cules some as large as a pea. However the larger ones had a glazed
appearance resembling cysts with gelatinous contents, while the
smaller ones had an opaque, whitish gray appearance. Some of the
larger tubercules showed a similar characteristic. Some of these’
were located in the intestinal wall protruding in the lumen as a
hemisphere, without perforating the mucosa.

Microscopic examination showed the large tubercles to be myxo-
fibroma and the smaller ones to be a pure fibroma.

REFERENCES

1. Curtis. Frequency of occurrence of tumors in the domestic fowl. JU.
S. Dep. Agr. J. Agr. Research, Vol. 5, 1915, p. 397.

2. Ehrenreich and Michaelis. Ueber Tumoren bei Hiihnern. Ztschr.
Krebsforch., Vol. 4, 1906, S. 586.

3. Ehrenreich. Weitere Mittheilungen itiber das Vorkommen malignes
Tumoren bei Hiihnern. Med. Klin., Berlin, Bd. 3, 1907, S. 614.

4. Gorig. Multiple Sarkome beim Huhn. Deutsche tierirztl. Wehn-
schr., Bd. 8, 1900, S. 54.

5. Jones. A myxo-chondro-carcinoma of the testicle of a fowl. Rept.
N.Y. State Vet. College, 1912-1913, p. 160.

6. Koch. Demonstration einiger Geschwulste bei Tieren. Verhandl.
Deutsche Path. Gesellsch., Bd. 7-8, 1904, S. 136.

7. Lange. On certain spontaneous chicken tumors as manifestations of
a single diesase. II. Simple spindle-celled sarcomata. J. Exper. M., Vol.
19, 1914, p. 577.

8. Lewin. Ueber einen Fall von allgemeiner Melanose beim Huhn.
Ztsch. f. Veterinark., Bd. 22, 1910, S. 455.

9. Murphy and Rous. The behavior of chicken sarcoma implanted in
the developing embryo. J. Hxaper. Med., Vol. 15, 1912, p. 119.

10. Petit et German. Le cancer de l’ovaire chez la Poule. Bull. Soe.
Cent. de Méd. Vet., T. 63, 1909, pp. 341 and 386.

11. Pick. Zur Frage vom Vorkommen des carcinoms bei Vogeln:
Grosser Plattenepithelkrebs des Mundhéhlenbodens bei einem Huhn.
Berl. klin. Wchnschr., Bd. 40, 1903, S. 669.

12. Pickens. A cysto-adenoma in a fowl. Rept. N. Y. State Vet. Coll.,
1913-1914, p. 261.

13. Regenbogen. Multiples Sarkom in des Haut eines Hahnes. Berl.
tierdrztl. Wchnschr., Bd. 19, 1907, S. 328.

14. Rous. Resistance to a tumor-producing agent distinct from re-
sistance to the implanted tumor cells. J. Exper. M., Vol. 18, 1913, p. 416.

15. Rous. A transmissible avian neoplasm (Sarcoma of the common
fowl). J. Exper. Med., Vol. 12, 1910, p. 696.

TUMORS IN FOWLS 275

16. Rous. On certain spontaneous chicken tumors as manifestations of
a single disease. I. Spindle-celled sarcomata rifted with blood sinuses.
J. Exper. Med., Vol. 19, 1914, p. 570.

17. Rous and Lange. The characters of a third transplantable chicken
tumor due to a filterable cause. A sarcoma of the intracanicular pattern.
J. Exper. Med., Vol. 18, 1913, p. 651.

18. Rous and Murphy. Variations in a chicken sarcoma caused by a
filterable agent. J. Exper. Med., Vol. 17, 1913, p. 219.

19. Rous and Murphy. On the causation by filterable agents of three
distinct chicken tumors. J. Hxper. Med., Vol. 19, 1914, p. 52.

20. Schlegel. Maligne Neoplasmen. Ztschr. f. tiermed., Bd. 17, 1913,
S. 387.

21. Tytler. A transplantable new growth of the fowl producing car-
tilage and bone. J. Hxuper. Med., Vol. 17, 1913, p. 466.

22. Tyzzer and Ordway. Tumors in the common fowl. J. Med. Re-
search, Vol. 21, 1909, p. 459.

23. Warthin. Leukemia of the common fowl. J. Infect. Dis., Vol. 4,
1907, p. 369.

24. Watson. Malignant disease of a heart of a fowl. Vet. J., Vol. 9,
1904, p. 182.

CHAPTER XXII

TOXICOLOGY

It is a well established fact that considerable variations in toler-
ance to drugs of a toxic nature exist in animals of different species.
While these variations have been pointed out in the case of mam-
malian species, little information is found in toxicologic literature
on the toxicity to fowls of drugs or poisonous substances which may
be of value in the treatment or control of avian diseases.

The experiments described in this chapter were undertaken by
Gallagher for the purpose of determining the toxic doses for
fowls of the more commonly used medicinal agents and of poisonous
substances to which fowls not infrequently have access. No attempt
was made to fix the toxic dose in certain instances where the sub-
stance on test proved non-toxic when given in comparatively large
quantities. A few tests only were made with each substance. The
results of these are summarized in the doses indicated under the name
of each drug. In a few instances reference has been made to obser-
vations by other writers.

In each experiment, unless otherwise stated, fluids were admin-
istered directly into the esophagus or crop by means of a pipette and
solids were given in gelatin capsules per os.

Medium sized healthy mature hens weighing between 3 and 4
pounds were usually employed. Those of larger size are designated.
All doses were given while the crop contained a normal amount of
food.

From the results of the experiments it may be concluded that in
general fowls may be considered as having approximately the same
susceptibility to toxic substances as medium sized dogs. They are
more resistant than dogs to such substances as calomel, strychnine
and tartar emetic, and less resistant to carbolie acid, salicylic acid
and potassium cyanide.

In treating outbreaks of disease in fowls, it is of great advantage
to employ the drinking water as a vehicle for medicinal agents. It
is shown that fowls are not visibly affected by drinking solutions of

bichloride of mercury 1—6000, carbolic acid 1-1000, permanganate
276

TOXICOLOGY 277

of potash 1-500, and crude catechu 1-500 for periods of 18 to 21
days.

It is interesting to note that the crop not only serves as a reservoir
for food, but that absorption through its wall is very rapid, symptoms
appearing in from two to five minutes after the administration of
such substances as ammonium chloride in solution, potassium cy-
anide and strychnine sulphate.

AMMONIUM CHLORIDE

Lethal dose. 60 grains.

45 grains in solution (15 cc. of 20 per cent so-
lution).

Toxic dose. Same as lethal.

Non-toxic dose. 15 to 45 grains.

Experiments. (1) July 8, 1918, 2 p.m. Fowl received 60
grains of ammonium chloride. July 9. Fowl droopy, weak in legs,
sitting. July 10. Same as July 9. July 11. Fowl died before
8 a.m. Autopsy notes. No lesions were apparent.

(2) February 20, 1918, 11.05 a.m. Fowl received 45 grains of
ammonium chloride in 12 ¢.c. of water (15 ¢.c. of a 20 per cent solu-
tion). Stimulating effect observed almost immediately. Fowl had
not been very active previously. After administration of the chlo-
ride, bird began scratching energetically and singing more than the
neighboring untreated fowls. Would drop wing on one side in imi-
tation of a rooster and would crowd up against the side of the cage
which separated her from another hen. Would peck at her through
the cage. 11.20a.m. Sameasabove. 11.25 .4.m. Drinking con-
siderable water. 11.30 a.m. Excitement has passed. 1.00 p.m.
Fowl has a sleepy appearance. Bunches up somewhat when not dis-
turbed. 4.30pr.m. Notactive. Bunched up. February 21, 1918,
9 a.m. Fowl sleepy and bunched up. Stands erect but wabbles
when disturbed. 4.30P.m. Fowl droopy. Bunchedup. Feathers
ruffled. February 22. Above described condition intensified. Feb-
ruary 23. Fowl died before 8 a.m. Autopsy notes. Crop filled
with food. Lungs pale. Other organs apparently normal.

(3) June 25,1918, 10 a.m. Fowl received 45 grains of ammon-
ium chloride. Result. No effect was apparent.

(4) February 28, 1918, 10.05 a.m. Fowl received 15 grains of
ammonium chloride. Result. No effect was apparent.

278 DISEASES OF DOMESTICATED BIRDS

ARSENIOUS ACID

Lethal dose. 5 grains.

Toxic dose. 5 grains.

Non-toxic dose. 1 to 3 grains.

Experiments. (1) June 10, 1918, 10 a.m. Fowl received 5
grains of arsenious acid. 4.00 p.m. Fowl somewhat droopy.
Droppings greenish. July 11, 9.00 a.m. Fowl droopy. Drop-
pings greenish and watery. 12 m. Fowl weak. Comb dark.
1.30 p.m. Fowl dead. Autopsy notes. Food in crop and gizzard.
Catarrhal exudate in the proventriculus. Internal membrane of the
gizzard is necrosed and separated from wall at entrance of pro-
ventriculus. Contents of gizzard greenish. Duodenum shows a ca-
tarrhal condition and is pale in color. Contents of intestines are
fluid and of greenish tinge. Liver is mottled. Rigor mortis is
marked 1 hour after death.

(2) July 8, 1918, 2 p.m. Fowl received 3 grains of arsenious
acid. Result. No effect was apparent.

(3) June 25, 1918, 10.00 a.m. Fowl received 1 grain arseni-
ous acid. Result. No effect was apparent.

Reinhardt fed .2 gram of arsenic and observed no symptoms up
to the sixtieth hour. He then gave .4 gram more and the hen died
40 hours after the last dose was administered. A second hen died
64% days after receiving .2 gram of arsenic.

Reinhardt observes that arsenic poisoning in hens causes lesions
which are characteristic with reference to location and character.
The horny epithelial layer of the gizzard is raised from the under-
lying muscles by a gelatinous or sero-fibrinous exudate and in con-
sequence is easily peeled off. The exudate lying beneath the epi-
thelium, in places reaches a thickness of 1 em. Sometimes this
exudate consists of a serous, yellowish, clear fluid, which spurts out
when an incision is made in the tissues. In ease the epithelial layer
has been perforated, only a small amount of gelatinous exudate may
be present. On removing the epithelial layer, highly reddened
areas due to corrosive action, may be observed. The proventriculus
shows no lesions. The mucosa of the crop is somewhat reddened,
the vessels of the intestines are injected and the contents of the in-
testines are thinly fluid. The liver is usually yellowish brown in
color and fragile, due to fatty degeneration. The fat, especially on
the gizzard is somewhat edematous and soft. Frequently the fat is

TOXICOLOGY 219

orange colored. The blood is well coagulated and brownish red in
color.

BICHLORIDE OF MERCURY (MERCURIC CHLORIDE, CORROSIVE
SUBLIMATE)

Lethal dose. 4 grains.

Toxic dose. 4 grains.

Non-toxie dose. 3 grains.

1—6000 solution as drinking water for 18 days without harm.

Experiments. (1) June 10, 1918, 10 a.m. Fowl received 5
grains of bichloride of mercury. 10.45 a.m. Spasmodic move-
ments of the crop for several minutes. 11.45 a.m. Droopy. 2
p.M. Sitting. Legs weak. Drooping. 4p.m. Sitting. Cannot
stand. Marked depression. June 11, 1918, 9 a.m. Fowl found
dead. Autopsy notes. No food in crop. Gizzard filled with food.
Mucous membrane of dependent portion of crop is whitened and thick-
ened as a result of coagulation necrosis. Proventriculus shows severe
catarrhal condition. Mucosa at entrance to gizzard is necrosed.
Membrane of posterior portion of gizzard is separated from the giz-
zard wall, the space being filled with clear fluid. Mucosa of first
third of intestine is exfoliated and remainder of small intestine shows
a severe catarrhal condition. Other organs apparently normal.

(2) August 12, 1918, 2.20 p.m. Four pound fowl received 4
grains of bichloride of mercury. 4.30 p.m. Nochange noted. Au-
gust 138, 9 a.m. Legs very weak. Bird cannot walk. Sits down.
Otherwise looks bright and normal. August 14,9 a.m. Fowl can-
not stand. August 15,9 4.m. Fowl dead. Autopsy notes. Small
amount of oats in crop. Crop wall is thickened, pale; mucosa is
coagulated. Subcutaneous tissue surrounding crop and esophagus
is infiltrated with a greenish gelatinous exudate. Proventriculus
shows several hemorrhagic points on mucosa. Gizzard contains a
considerable quantity of greenish colored food. Mucosa of small in-
testine is pale. Kidney is very pale and studded with minute white
spots. Air sac membranes in abdominal cavity are thickened. The
abdominal cavity contains 6 ounces of a thick somewhat viscid fluid
with a slight greenish tinge.

(3) February 28, 1918, 10 a.m. Fowl received a tablet contain-
ing 3 grains of bichloride of mercury and 3 grains of ammonium
chloride. Result. No effect was apparent.

280 DISEASES OF DOMESTICATED BIRDS

(4) May 27, 1918, 10 a.m. Gave fowl 1.4 grains of bichloride
of mercury in feed. Fowl had not been fed for 24 hours, crop nearly
empty. 8 p.m. Gave fowl another 1.4 grains of bichloride of
mercury in feed. Result. No effect was apparent as a result of
fowl consuming 2.8 grains of bichloride of mercury in feed in one
day.

(5) June 14, 1918. Gave three fowls a 1-6000 solution of bi-
chloride of mercury as drinking water. Fowls drank solution for
a period of 18 days consuming about 2500 e.c. each. No other
water was given. Result. No effect was apparent.

(6) June 12 to 14,1918. Several fowls which had not received
drinking water for 24 hours were given bichloride of mercury solu-
tions of 1-2000 and 1—4000 as drinking water. FT owls tasted solu-
tions and refused to drink. Solutions were clear. At intervals the
solutions were again placed in the fowls’ cages with the same result
as above. After taking 1 to 3 swallows of solution the fowl shakes
its head, rubs beak in the litter and elevates the feathers on the neck
for a few moments. Gave fresh water and fowls drank eagerly.

Ward, adopting a suggestion by Ritzler, employed corrosive sub-
limate in the drinking water of a large flock of birds during an out-
break of fowl cholera, without harmful result. The period during
which the sublimate was used to disinfect the water covered 16.
days. or the first two days a solution of 1: 1000 was employed.
Since the fowls did not drink the solution readily, the bichloride was
diluted to 1 part to 2000 parts of water.

BISMUTH SUBNITRATE

Non-toxic dose. %4 ounce +
Experiment. (1) February 20, 1918, 9.50 a.m. Fowl received
7% ounce of bismuth subnitrate. Result. No effect was apparent.

CALCIUM OXIDE (QUICKLIME)

Toxic dose. 1% drams.

Non-toxic dose. % dram.

Experiments. (1) August 15, 1918, 9.40 a.m. Gave 3 pound
fowl 1% drams of calcium oxide. August 16. Fowl is somewhat
droopy. Droppings are greenish in color. August 17. Fowl is
dull in appearance. August 18. Fowl is dull in appearance.
August 19. Fowl appears normal.

TOXICOLOGY 281

(2) August 27, 1918, 10.30 a.m. Gave 34% pound fowl % dram
of calcium oxide. Result. No effect was apparent.

CALOMEL (MERCURIOUS CHLORIDE)

Non-toxic dose. 30 grains.

Experiment. (1) February 7, 1918, 10.30 a.m. Fowl received
30 grains of calomel. February 8, 9 a.m. Evidence of purging.
Droppings greenish. Fowl has not been visibly affected otherwise.

CARBOLIC ACID

Toxic dose. 5 grains in solution (11 ¢.c of 3 per cent solution).
3.75 grains in solution (12.5 cc. of 2 per cent solu-
tion).

Non-toxic dose. 2 grains in solution (13 ce. of 1 per cent solu-
tion).

1—1000 solution as drinking water for 18 days.

Experiments. (1) August 12, 1918, 2.20 p.m. Five pound
fowl received 11 cc. of 3 per cent carbolic acid solution (5 grains
earbolic acid). 2.22 p.m. Crop puffed out somewhat. 3.00 P.M.
Fowl has shown some droopiness since receiving the solution. 3.45
p.M. Fowl apparently normal. 4.30 p.m. Fowl apparently nor-
mal. August 13. Fowl appears normal.

(2) February 2, 1918, 10 a.m. Three pound fowl received 12.5
e.c. of 2 per cent carbolic acid solution (3.75 grains carbolic acid).
11 a.m. Fowl shows dullness. 2 p.m. Fowl appears normal.
February 3. Fowl is apparently normal.

(3) August 27, 1918, 10.30 a.m. Gave 4 pound fowl 13 e.c. of
1 per cent carbolie acid solution (2 grains earbolic acid). Result.
No effect was apparent.

(4) June 14, 1918. Gave three fowls a 1-1000 solution of car-
bolic acid as drinking water for a period of 18 days. Each fowl
consumed about 2500 ¢c.c. No other water was given. Result. No
effect was apparent in any of the fowls.

(5) June 14, 1918. Several fowls were given carbolic acid solu-
tions of 1-250 and 1-500 as drinking water. Fowls refused to
drink the solutions. Gave fresh water and fowls drank eagerly.

282 DISEASES OF DOMESTICATED BIRDS

CASTOR OIL

Non-toxic dose. 6% drams +

Experiment. (1) February 7, 1918, 10.30 a.m. Fowl received
6% drams of castor oil. February 8, 1918. 9 a.m. Evidence of
moderate purging. Droppings greenish. Fowl was not visibly af-
fected otherwise.

CATECHU (CRUDE)

Non-toxic dose. 1-500 solution +

Experiment. (1) June 10, 1918. Gave fowl a 1-500 solution
of crude catechu as drinking water. Fowl drank solution freely.
July 1, 1918. Fowl drank 3000 ¢.c. of above solution in 21 days.
No other water was given. No constipation was observed. No
change in fowl was apparent.

CHLORIDE OF LIME

Non-toxie dose. %4 to 1% drams.

Experiments. (1) August 15, 1918, 10.30 a.m. Five pound
fowl received 1% drams of chloride of lime. Result. No effect
was apparent.

(2) August 13, 1918, 2.30 p.m. Five pound fowl received %
dram of chloride of lime. Result. No effect was apparent.

COPPER SULPHATE (BLUE STONE)

Lethal dose. 20 grains.

15 grains in solution.

Toxie dose. Same as lethal.

Non-toxie dose. 5 to 15 grains.

Experiments. (1) July 8,1918,2P.m. Fowl received 20 grains
of copper sulphate. 4 p.m. No change apparent. July 9. Fowl
droopy. Sitting. July 10. Same as July 9. July 11, 9a.M.
Fowl dead. Autopsy notes. Pharynx and esophagus show coagula-
tion of the mucosa. Mucosa of crop exfolated. Crop filled with
water and greenish catarrhal exudate. Lower esophagus shows co-
agulation necrosis of mucosa. Proventriculus shows severe catarrhal
gastritis. Catarrhal enteritis. Entire intestine is filled with green-
ish catarrhal exudate.

TOXICOLOGY 283

(2) February 2, 1918, 10 a.m. Fowl received 15 grains of cop-
per sulphate in solution (10 cc. of 10 per cent solution). Fowl
drank water continuously for 15 minutes then became restless for
about three minutes. 12 m. Dull. 2 p.m. Dull. 430 p.m.
Dull. February 3, 1918, 9 a.m. Fowl is droopy. 9.30 a.™.
Convulsions developed and fowl died. Autopsy notes. Crop nor-
mal. Distended with water. Considerable food in crop and giz-
zard. Mucosa of proventriculus intensely inflamed. Horny mem-
brane of gizzard loosened near opening of proventriculus. Hem-
orrhagic points in submucosa. Catarrhal enteritis is quite marked.
Intestine contains considerable bluish fluid. Mesenteric fat and
peritoneum are petechiated. Heart is in systole.

(3) June 25, 1918, 10 a.m. Fowl received 15 grains of copper
sulphate. Result. No effect was apparent.

(4) February 28, 1918, 10.10 a.m. Fowl received 5 grains of
copper sulphate. Result. No effect was apparent.

ERGOT. F. E.
Non-toxic dose. 2% drams F. E. equivalent to 2% drams of ergot.
Experiment. (1) February 8, 1918, 10.30 a.m. Fowl received

2% drams of fluid extract of ergot with 24 drams of water. Result.

No effect was apparent.

FERROUS SULPHATE (COPPERAS)
Non-toxic dose. 30 grains +
Experiment. (1) February 7, 1918, 10.30 a.m. Fowl received
30 grains of ferrous sulphate in solution (10 ¢.c. of 20 per cent solu-
tion). Result. No effect was apparent.

IPECAC. F. E.

Lethal dose. 1 to 2 drams.

Toxic dose. 1 dram.

Non-toxic dose. % to %4 dram.

Experiments. (1) August 19, 1918,1.10 p.m. Gave 474 pound
fowl 2 drams fluid extract of ipecac. August 20. No apparent
change. August 21,9 a.m. Greenish fluid droppings. August 22,
9 a.m. Fowl dead. Autopsy notes. Crop and gizzard filled with
food. Mucosa of crop pale, slightly thickened. Lower esophagus

284 DISEASES OF DOMESTICATED BIRDS

and proventriculus show a catarrhal condition. Several hemor-
rhagic points in proventriculus. Small area of internal lining of
gizzard at entrance of proventriculus separated from gizzard wall.
Mucosa of duodenum pale. Liver pale.

(2) August 19, 1918, 1.10 p.m. Gave 3 pound fowl 14 drams
fluid extract of ipecac. August 20, 9 a.m. Fowl dead. Autopsy
notes. Some food in crop. Proventriculus shows a catarrhal con-
dition. Hemorrhagic near entrance to gizzard. Membrane of giz-
zard easily separated near opening of proventriculus. Liver is
banded with light and dark stripes.

(3) August 27, 1918, 10.30 a.m. Gave 4% pound fowl 1 dram
of fluid extract of ipecac. August. 28. No change apparent.
August 29. Fowl dull. August 30. Fowl dead at 9 a.m. Aw
topsy notes. Crop and gizzard filled with food. Mucosa of pro-
ventriculus thickened and catarrhal. Submucosa of gizzard near pro-
ventricular opening hemorrhagic. Liver pale in spots and streaked
with darker bands. Heart in systole.

(4) August 12, 1918, 2.20 p.m. Gave 5 pound fowl 1% drams
fluid extract of ipecac. August 14, 9 a.m. Fowl has shown no
change. August 15. Somewhat dull. August 16. Same as Au-
gust 15. August 17. Apparently normal.

(5) August 30, 1918, 10.30 a.m. Gave 4 pound fowl % dram
of fluid extract of ipecac. Result. No effect was apparent.

(6) August 30, 1918, 10.30 a.m. Gave 4 pound fowl % dram of
fluid extract of ipecac. Result. No effect was apparent.

LEAD OXIDE (LITHARGE)

Non-toxic dose. 1% drams.
Experiment. (1) August 15, 1918, 9.40 a.m. Five pound fowl
received 1% drams of lead oxide. Result. No effect was apparent.

MAGNESIUM SULPHATE

(Epsom Salts)
Non-toxie dose. 1 dram in solution +
Experiment. (1) February 7, 1918, 11 a.m. Fowl received 1
dram of Epsom salts in 4% drams of water. February 8, 9 a. M.
Evidence of moderate purging. Droppings fluid and brownish.
Fowl] was not visibly affected otherwise.

TOXICOLOGY 285

MALE FERN. F. E.

Toxic dose. 2% drams, F. E.

Non-toxic dose. 1% drams, F. E.

Experiments. (1) April 25, 1918, 11.15 a.m. Fowl received
2% drams of fluid extract of male fern. 11.30 a.m. Fowl sleepy.
Droopy. 11.45.a.m. Fowl sleepy. Sitting. 12 m. Legs very
weak. 1 p.m. Very weak. Can raise itself on its feet with dif-
ficulty. 2.45 p.m. Sitting. Has great difficulty in attempting to
stand. 4 p.m. Standing but legs are still weak. April 26, 1918,
9 a.M. Fowl has recovered.

(2) July 8, 1918, 2 p.m. Fowl received 1% drams of fluid ex-
tract of male fern. Result. No effect was apparent.

PHOSPHORUS

Poisoning with this substance may occur as a result of eating rat
poison. ‘The writers have observed a case of phosphorus poisoning
induced by eating the debris left after a display of fireworks among
which was fine gravel employed in “ torpedoes.”

Birds exhibit depression, weakness, trembling, diarrhea, thirst
and sometimes emphysema of the skin. Death may occur within a
period varying from one hour to several days.

At autopsy, care should be taken in opening the crop, proven-
triculus and gizzard in looking for the so-called phosphorus vapor
which appears as a transient cloud on opening the organs or when the
contents are moved. The phosphorus in the crop and gizzard may
be detected by the characteristic odor and by: faint luminosity when
in the dark, especially if the material is rubbed. The more pres-
sure exerted, the more luminous it appears. The most marked le-
sions occur in the proventriculus and are characterized by hem-
orrhages and erosions in the mucosa. Inflammation is also present
in the upper portions of the intestines. Eechymoses may be pres-
ent on the heart and in various organs. In cases of long standing
there may be fatty degeneration of the liver and other organs, and
yellow colored liver.

286 DISEASES OF DOMESTICATED BIRDS

POTASSIUM CYANIDE

Lethal dose. 1 to 2 grains.

Toxic dose. 740 to % grains.

Experiments. (1) February 20, 1918, 10.15 a.m. Gave fowl a
2 grain crystal of potassium cyanide per os. Symptoms appeared in
4 minutes. Fowl had difficulty in maintaining its balance.
Dropped to the floor. After several minutes it fluttered around the
cage for about five seconds, went down again, became comatose and
was dead in 12 minutes after swallowing the cyanide.

(2) February 20, 10.30 a.m. Gave fowl a 1 grain crystal of
potassium cyanide per os. Symptoms appeared in 2 minutes.
Fowl became droopy, stood for several minutes with head dropped
to floor (limber neck), fell to floor in a comatose state and was dead
13 minutes after swallowing the cyanide. Did not struggle at any
time.

(3) July 8, 1918, 2 p.m. Gave fowl a % grain crystal of po-
tassium cyanide per os. 2.02 p.m. Fowl jumped suddenly strik-
ing top of cage. Stands very erect. Breathing more rapidly.
Mouth open. 2.05 p.m. Unsteady on legs. Wings drooped. Dis-
tressed expression. 2.20 p.m. Fowl lying down. Continues
breathing through mouth. 3p.m. Sameasabove. Fowl can stand
when foreed up. 4p.M. Fowl has recovered.

(4) February 28, 10.15 a.m. Gave fowl 7% grain of potassium
cyanide in gelatin capsule per os. 10.23 a.m. Fowl breathing rap-
idly through the mouth. 10.25 a.m. Wings drooping. Has at-
tempted to pass droppings four times, each time a very small amount
has been passed. 10.45 a.m. Same as above. Getting sleepy. 11
A.M. Same as above. Sleepy. 12 m.. No change except that
breathing is not as rapid. 1.30 p.m. Fowl has recovered.

(5) August 12, 2.23 p.m. Gave 3 pound fowl ‘Ao grain potas-
sium cyanide in small piece per os. 2.26 p.m. Breathing rapidly.
2.30 p.m. Sitting. 82.m. Has depressed appearance. Drowsy.
Half sitting posture on being placed on feet. Sits again. Breath-
ing not so rapid. 3.45 p.m. Standing. Some droopiness appar-
ent. Breathing is normal and fowl is recovering. 4.30 p.m. Ap-
parently normal. August 13, 9 a.m. Fowl is apparently normal.

POTASSIUM PERMANGANATE

Lethal dose. 30 grains.
Toxic dose. 30 grains.

TOXICOLOGY 287

Non-toxic dose. 15 grains.
15 “im sohution.
1-500 solution as drinking water.

Experiments. (1) June 25,1918,104.m. Gave fowl 30 grains
of potassium permanganate. 4.30 p.m. No symptoms noticed.
June 26, 9 a.m. Fowl died during night. Autopsy notes. Crop
filled with oats and some water. Dependent portion of crop charred
and softened. Apparently the mucous membrane was eaten through.
Submucosa blackened, also skin on lower surface of crop and ad-
jacent breast. Thick coating of moist black material on lower
mucosa of crop. Probably remains of permanganate. Several blood
clots in crop. Remainder of crop mucosa normal. All other organs
normal. Permanganate had not left crop as far as could be deter-
mined. Apparently hemorrhage had occurred in subcutaneous tissue
and blood had been oxidized.

(2) February 2, 1918, 10 a.m. Gave fowl 15 grains of potas-
sium permanganate in solution (30 cc. of 3% per cent solution).
Result. No effect was apparent.

(8) July 8,2p.m. Gave fowl 15 grains of potassium permanga-
nate. Result. No effect was apparent.

(4) June 10,10 a.m. Gave fowl a 1-500 solution of potassium
permanganate as drinking water. Fowl drank solution freely. July
1. Fowl drank about 3000 ¢.c. of above solution in 21 days. No
other water was given. Result. No effect was apparent.

ROSE CHAFERS

Lamson has observed poisoning of chickens due to eating rose
chafers (Macrodatylus subspinosus).

When opportunity affords, chickens eat rose chafers ravenously.
Within an hour after feeding the birds assume a dozing attitude.
Later, weakness is apparent and death usually occurs within 24 hours.
Convulsions occur in less than five per cent of the cases.

At autopsy the crop is usually found to be so full of insects as to
give the impression that death has been due to “ crop bound” but no
abnormal condition of other organs is observed.

Feeding experiments have shown that 15 to 20 rose chafers are
sufficient to kill a chicken one week old. From 25 to 45 are neces-
sary to kill a three weeks old chicken. Ten weeks about marks the
age limit of susceptibility. The damage is not merely mechanical,
for an extract of crushed rose chafers in distilled water, after filter-

288 DISEASES OF DOMESTICATED BIRDS

ing, will cause death when fed to chickens. The rose chafers ap-
parently contain a toxin affecting the heart.

Preventive measures should consist in keeping chickens on mowed
fields and away from grape vines and flowering shrubs during the
month when rose chafers are prevalent.

SALICYLIC ACID

Lethal dose. 30 to 75 grains.

Toxic dose. 30 grains.

Non-toxie dose. 15 grains.

Experiments. (1) June 10,1918,104.m. Gave fowl 75 grains
of salicylic acid. 11.30 a.m. Wings dropped. Fowl sleepy.
Droopy. 12M. Condition growing worse. 1.30 p.m. Bird dead.
Autopsy notes. Crop filled with oats. No trace of the three gela-
tin capsules. At least half of the salicylic acid administered re-
mains in the esophagus. Mucous membrane of mouth, esophagus,
crop and lower esophagus is white from action of the salicylic acid.
Protoplasm is apparently coagulated. Not so severe in lower esopha-
gus and crop as in upper esophagus and mouth. No other lesions ap-
parent.

(2) June 25, 1918, 10 a.m. Gave fowl 30 grains of salicylic
acid. 4p.mM. Fowl droopy. June 26,9a4.m. Fowl lying on side
in comatose condition. 2.30 p.m. Fowl died. Autopsy notes.
Crop filled with food and some white material probably salicylic acid.
Dependent portion of wall of crop thickened, wrinkled and coagulated,
white in color. Mucosa of lower esophagus and proventriculus
whitened. Intestine mildly hemorrhagic throughout its length. Wall
congested. Liver dark, capsule thickened in one place. Spleen soft.
Ovary shows B. pullorum infection.

(3) July 8,2 p.m. Gave fowl 15 grains of salicylic acid. Re-
sult. No effect was apparent.

SANTONIN

Non-toxic dose. 5 to 15 grains.

Experiments. (1) June 25, 10 a.m. Gave fowl 15 grains of
santonin. Result. No effect was apparent.

(2) June 10,10 4.m. Gave fowl 5 grains of santonin. Result.
No effect was apparent.

TOXICOLOGY 289

SODIUM CHLORIDE (COMMON SALT)

Lethal dose. 2% drams.

2% drams in solution.

Toxic dose. Same as lethal.

Non-toxic dose. 1% to 1% drams.

Experiments. (1) February 2, 10 a.m. Gave fowl 24% drams
of sodium chloride in solution (40 ¢.c. of 25 per cent solution). 11
a.M. Fowl is dull. 12 m. Same. 2 p.m. Same. Droopy.
Sleepy. 4.30 p.m. Fowl is sitting. Sleepy. February 3, 9 a.m.
Fowl found dead. Autopsy notes. Considerable food in crop and
gizzard. Crop, proventriculus and gizzard are normal. Small in-
testine normal. Rectum slightly inflamed. Liver darkened. Kid-
ney congested. Heart is systole.

(2) June 25,10 a.m. Gave fowl 2% drams of sodium chloride.
June 26, 9 a.m. Fowl droopy. 1 p.m. Paralyzed. 4 P.M.
Paralyzed. Shows condition known as wry neck. June 27, 9 a. M.
Paralyzed. Lying on side. Wry neck. 11a.m. Died. Autopsy
notes. Crop gorged with food. Mucosa of crop white, cooked ap-
pearance, thickened. Severe catarrh of proventriculus, tenacious
mucous exudate. Horny membrane of gizzard easily removed.
Duodenum shows slight congestion. Catarrh of duodenum. Liver
darkened.

(3) July 8, 2 p.m. Gave fowl 1% drams of sodium chloride.
Result. No effect was apparent.

(4) February 28,10 a.m. Gave fowl 1% drams of sodium chlor-
ide. 10.30 a.m. Fowl shows a moderate thirst. Result. No ef-
fect wag apparent.

Suffran observes that fatal poisoning is induced in the hen by a
dose of 4 grams of common salt per kilo of body weight, while the
pigeon succumbs to 5 grams per bird.

The clinical picture of intoxication by salt gives the impression
that it acts as a poison of the muscles. The gradual weakening of
the contractile power induces progressive difficulty in walking and
at last falling down. It is not a true paralysis for sensation and
movement continue until death. Pricking, and the point of a
thermo cautery produce response by contraction. The weakening
of the muscles of respiration causes a progressive asphyxia which
leads to death.

The toxic action of salt is exercised also in a certain measure on

290 DISEASES OF DOMESTICATED BIRDS

the nervous centers. A proof of that influence is seen in the phenom-
ena of somnolence which dominate the morbid scene, in the hyper-
esthesia which is manifested by the transitory crises and last by the
interference with locomotion.

The lesions are chiefly in the digestive canal. The buccal mucosa
is covered with a yellowish brown layer which is viscid and adherent.
When this is removed, marked congestion is seen, with hemorrhages
at some points. The mucosa of the crop shows traces of a violent
irritation with numerous hemorrhages and superficial ulceration.
The mucosa of the esophagus shows general congestion with super-
ficial erosions. The intestinal mucosa is hyperemic, hemorrhagic
and ulcerated. The principal visceral organs such as liver, spleen,
kidneys, lungs, heart and nervous centers such as brain and cord
show more or less marked congestive lesions. The blood possesses
a characteristic bright red color.

Edwards found that doses of salt as high as 2.5 grams per kilo-
gram of body weight administered to pigeons by injecting into the
crop, produced no effect. A dose of 4.5 grams per kilogram of body
weight caused great depression, followed by death in eighteen hours.
A similar dose of 3.33 grams per kilogram caused death in twenty-
three hours. No lesions other than acute congestion of the mucous
membrane of the lower portion of the esophagus were observed.
Only about 25 per cent of the salt was absorbed from the crop.

SODIUM NITRATE

Lethal dose. 2% drams.

Toxic dose. 1% drams.

Non-toxic dose. %% dram.

Experiments. (1) February 20, 9.50 a.m. Gave fowl 2%
drams of sodium nitrate. 11 a.m. Fowl dull and droopy. 12 m.
Fowl shows increased dullness, droopiness and sleepiness. Sitting.
1p.m. Fowl is wide awake but dull. Is ina sitting posture. Legs
paralyzed, cannot stand. 3 p.m. Fowl lying on its side, cannot
move, legs paralyzed. Greatly depressed. Death appears imminent.
4.30 p.m. No change from above. February 21, 9 a.m. Fowl
died during night. Autopsy notes. Crop wall and skin covering it
dehydrated. These membranes were transparent, dry and tough.
Proventriculus shows marked catarrhal exudate. Inner membrane
of gizzard separated from submucosa. Considerable fluid beneath
inner membrane. Catarrhal enteritis. Duodenal mucosa congested

TOXICOLOGY 291

somewhat. Liver dark. Spleen pale. Pancreas enlarged and in-
filtrated. Heart is systole. Considerable food in crop.

(2) February 28, 1918, 10 a.m. Gave fowl 174 drams of sodium
nitrate. 1.830 p.m. No change is apparent. 3.30 p.m. Fowl
bunched up and sleeping. On being aroused displays marked thirst.
Becomes droopy and sleepy again. 4.30 p.m. Fowl droopy and
shows thirst. March 1, 9 a.m. Fowl quiet. Sits down. Comb
and wattles dark red. 12 m. Same as above. 1.30 p.m. Fowl
paralyzed, no use of feet, prostrated. 3.30 p.m. Same as above.
Comb blackening at the tips. 4.80 p.m. Same as above. March
2, 9 a.m. Fowl up, normal in appearance but quiet on being
‘handled. Comba bright red. 3 ~.m. Fowl apparently normal.

(3) June 25,10a.m. Gave fowl % dram of sodium nitrate. Re-
sult. No effect was apparent.

STRYCHNINE SULPHATE

Lethal dose. 2 grains to 3% pound fowl.
Toxic dose. 2 to 3 grains to 5 pound fowl.
1.5 grains to 3 pound fowl.
8 c.c. F. E. nux vomica = 1.2 grains to 3 pound fowl.

Non-toxie dose. 2 grains to 5 pound fowl.

Experiments. (1) August 12, 2.22 p.m. Gave 3% pound fowl
2 grains of strychnine sulphate in gelatin capsule per os. 2.30 Pp. M.
Breathing more rapidly. Some unsteadiness of legs. 2.31 P.M.
Convulsion lasting 10 seconds. Fowl down on side. 2.32 P.M.
Slight convulsion. Rapid breathing. 2.35 p.m. Slight convul-
sion. 2.36 p.m. Fowl stretched out at length. Rapid shivering of
legs. 2.40 p.m. Fowl dead. Autopsy notes. Fowl stiff. Con-
siderable fluid in crop. Heart in systole. Liver slightly congested.
Comb, wattles and face darkened.

(2) August 12, 2.23 p.m. Gave 5 pound fowl 3 grains of strych-
nine sulphate in gelatin capsule per os. 2.45 p.m. Breathing
rapidly. Unsteady on legs. 2.50 p.m. Sitting. 2.55 p.M.
Standing. Breathing 180 per minute. 3.45 p.m. Breathing con-
siderably decreased. Some unsteadiness on legs through lack of
normal powers of balance. 4.30 p.m. Appears improved. August
13, 9 a.m. Fowl’s legs straddled. Cannot stand up. When dis-
turbed clonic spasms lasting 4 or 5 seconds are set up. August 14,
9 a.m. Fowl paralyzed. August 15, 9 a.m. Fowl stands fairly
erect for a short time but is unsteady on its feet. Diarrhea present.

292 DISEASES OF DOMESTICATED BIRDS

August 16. Fowl stands but is unsteady on feet. Much improved.
August 17,9 a.m. Fowl appears normal.

(3) July 8, 1.55 p.m. Gave 5 pound fowl 2 grains of strychnine
in gelatin capsule per os. 2.10 p.m. Fowl unsteady on feet. 2.15
p.M. Sways over backwards. Weak in legs. 4 p.m. No other
change observed. Fowl apparently normal.

(4) February 19, 2.10 p.m. Gave fowl 1.5 grains of strychnine
sulphate in gelatin capsule per os. 2.30 p.m. Fowl suddenly af-
fected. Delay due to slowness of liquefaction of the capsule. Fowl
staggers, legs spread, bird drops on her side. Several severe spasms
in first 5 minutes, breathing rapidly. 2.40 p.m. Fowl sleepy, dozes
for a moment and then starts suddenly, breathing rapidly, no spasms.
3p.M. Breathing less labored, fowl still prostrated. 4 p.m. Bird
in sitting position. Can rise slightly from the floor but cannot stand
erect. Breathing normal and fowl appears bright and normal other
than the leg weakness. February 20, 9 a.m. Fowl is apparently
normal except for incoordination of movement. Unsteady on its feet
and lifts them higher than normal in walking. February 21. Fowl
improving in ability to control legs but still unsteady. February 23.
Fowl apparently normal.

(5) February 8, 10.80 a.m. Gave fowl 8 c.c. of fluid extract of
nux vomica (1 per cent strychnine) with 8 cc. H,O by tube into
crop—1.2 grains of strychnine. 10.35 a.m. Fowl nervous. .
Breathing very rapidly. 10.40 a.m. Fowl wabbles, difficult to
maintain balance, legs weak, bird does not stand erect. Severe spasm
of muscles of body and wings lasting 10 seconds. 10.50 4.m. Fowl
in sitting position from leg weakness or partial paralysis, breathing
rapidly. Has had three violent convulsions. Comb and wattles red-
der than normal. 11 a.m. Breathing much slower. No more
spasms. Bird is recovering. 11.20 a.m. Fowl can stand. 12 m.
Fowl appears normal. 4.30 p.m. Fowl normal.

(6) June 25, 10 a.m. Gave 5 pound fowl 2 grains of strych-
nine in gelatin capsule per os. No effect apparent except a slight
increase in activity for several moments one hour after administra-
tion.

Schneider determined the therapeutic and lethal doses for strych-
nine nitrate for various birds. His results presented in tabular form
below refer to doses in milligrams per kilo of body weight.

TOXICOLOGY 293

Subeutaneous Internal per os.
Therapeutic Lethal Therapeutic Lethal
Geese A 1.0-2.0 6 2.5
Ducks .5-.6 1.0-1.1 1.5-2.0 3.0— 4.5
Hens 1.0 3.0-5.0 2.0-38.0 30.0-140.0
Pigeons 5-75 1.0-1.5 6.0 8.5— 11.0

It will be observed that pigeons are least susceptible to internal
therapeutic doses, while hens, ducks and geese are more so. How-
ever, with reference to lethal doses per os, hens are most resistant,
and pigeons, ducks and geese less so.

The therapeutic doses expressed above in milligrams per kilo of
body weight, are given below on a basis of milligrams per bird.

Therapeutic doses

Subcutaneous Per os.

Geese 1.4 QAG—2.22

Ducks “7 — .96 2.5 -3.8

Hens “7 -1.5 2.0 —5.0

Pigeons .16— .26 9.0 -2.4
SULPHUR

Non-toxic dose. ™% ounce +

Experiment. (1) February 20, 9.45 a.m. Fowl received 4
ounce of sulphur. Result. No effect was apparent. Fowl re-
mained as active as it was previous to administration of the sulphur.

TARTAR EMETIC

Lethal dose. 10 to 15 grains.

Toxie dose. 10 grains.

Non-toxic dose. 5 grains.

Experiments. (1) February 20, 9.40 a.m. Gave fowl 15 grains
of tartar emetic. 12 mM. No special change except that the bird is
quieter than normal. 1p.m. Bird quieter than normal. Sits down
a good deal. 4.30 p.m. Quiet but shows no special symptoms.
February 21, 9 a.m. Fowl died during the night. Autopsy notes.
Comb normal. Heart in systole. Crop contains considerable food.
Proventriculus shows catarrhal condition. Intestine catarrhal.
Duodenum petechiated. Heart petechiated. Liver pale. Kidneys
congested.

(2) June 25,10 4.m. Gave fowl 10 grains tartar emetic. June
26. No apparent change. June 27. No apparent change. June

294 DISEASES OF DOMESTICATED BIRDS

28,9 a.m. Fowl dead. Autopsy notes. Considerable food in erop.
Mucosa of dependent portion of crop shows a number of small necrotic
patches and erosions. Mucosa of duodenum hemorrhagic. Liver
congested and pale in spots. Heart in systole.

(38) February 28, 10.15 a.m. Fowl received 5 grains of tartar
emetic. Result. No effect was apparent.

TURPENTINE

Non-toxic dose. 2% drams +

Experiment. (1) February 7, 10.30 a.m. Fowl received 2%
drams of turpentine with 2% drams of linseed oil. Result. No ef-
fect was apparent.

REFERENCES

1. Edwards. Salt poisoning in pigs and poultry. Jour. Compar. Path.
and Ther. Vol. 31, 1918, p. 40.

2. Gallagher. Experiments in avian toxicology. J. Am. Vet. Med. Ass.,
Vol. 7, 1919, p. 337.

3. Lamson. The poisonous effects of the rose chafer upon chickens.
Science, n. s. Vol. 48, 1916, p. 138.

4. Reinhardt. Beitrage zur Kenntniss der Gefliigelkrankheiten. Berl.
tierdrztl. Wehnschr., Bd. 30, 1914, S. 214.

5. Schneider. Toxikologische Versuche mit Strychninum nitricum bei
Ginsen, Enten, Hiihnern und Tauben. Monatschr. f. prakt. tierh., Bd. 11,
1899-1900, S. 245.

6. Suffran. Sur Vempoisonnement des volailles par le sel de cuisine.
Rev. Gén. Méd. Veét., T. 18, 1909, p. 698.

CHAPTER XXIII

SURGICAL DISEASES
ANESTHETIZING FOWLS

Occasions demanding the administration of a general anesthetic
are limited largely to serious operations undertaken in connection
with the study of the functions of certain organs. Pearl and Surface
have pointed out that by the ordinary method of administration of an
anesthetic, ninety per cent of the subjects will die under the anes-
thetic. If less of the drug is administered, reflex excitability is not
lost, and the bird will struggle. It is likely that the explanation of
the high mortality lies in the fact that the air sac system of birds
furnishes opportunity for the storage of a large amount of anesthetic
which is wholly absorbed in a short time and not eliminated by ex-
piration as in mammals. The excessive amount of anesthetic prob-
ably affects the vagus center which causes cardiac inhibition, respira-
tory failure and death.

These writers obviate fatal results in anesthetizing hens by inject-
ing subcutaneously in the axilla 1-200 grain of atropine sulphate dis-
solved in 1 ¢.c. of warm normal salt solution. Administration of
ether follows immediately and the bird will be ready for operation
in fifteen to twenty minutes.

ARTHRITIS IN PIGEONS

Arthritis of the wing joints of pigeons, preventing flight, may be
eaused by a number of infectious diseases such as tuberculosis or
diphtheria; by gout or by mechanical injury. Klee observes that
carrier pigeons are subject to the disease under such circumstances
as to indicate the existence of a common cause. In affected birds
one wing usually droops, for involvement of both wings is rare.
On examination the shoulder and elbow joints will be found to be
somewhat swollen, reddened and painful. In undertaking treat-
ment, isolation of the bird is absolutely necessary to ensure rest for
the joints. He recommends applying a woolen bandage to the wing
in such a way as to secure immobility and applying lead water to the

same at frequent intervals. The bandage should be changed every
295

296 DISEASES OF DOMESTICATED BIRDS

two days. When heat and swelling disappear after 8 to 14 days, the
bandage is removed permanently and the bird is still confined in a
cage. The joints may then be painted with tincture of iodine.
Cases that do not recover in three weeks may be regarded as hope-
less. When caseous masses form in the joints and neighboring tis-
sues they may be removed by operation. Birds thus operated upon
seldom fly again and their future usefulness is limited to breeding.

BUMBLEFOOT

Bumblefoot is a suppurative condition of the feet of walking
birds. It consists of an inflammatory condition involving the burss,

Sea? NN
Dn:

Fic. 55. Bumblefoot. (Klee)

tendon sheaths, and tendons of the foot. It is reputed to occur most
often in the heavy breeds and in cocks more often than in hens.

The diseased feet are swollen and hot to the touch. In extreme
cases the swelling becomes so large as to interfere with locomotion.

SURGICAL DISEASES 297

In some eases fluctuation occurs and in others the tumor remains
hard.

Surgical treatment involves incising the bottom of the swelling to
allow the escape of the grayish semi-fluid contents. Sometimes the
swelling contains a caseous mass of a lamellated structure.

The eavity may be packed with gauze wet with perchloride of iron
as a hemostatic and the whole foot bandaged. The bird is confined
to an area not provided with a perch. The wound may be dressed
every few days, some disinfectant being substituted for the per-
chloride of iron. Likely the wound will continue to slough, and dis-
charge an ill smelling secretion. In this event the foot may be bathed
in a warm solution of compound solution of eresol. Iodine, zine chlo-
ride or lunar caustic may be applied to the interior of the wound.
Often treatment may require months, and necessitate trouble out of
proportion to the value of the bird.

Bumblefoot has been attributed to injury resulting from jumping
from high perches or to roosting on perches of an unsuitable, angular
character.

CUTANEOUS EMPHYSEMA

Emphysema of the skin designates a condition in which there
is an abnormal amount of air in the subcutaneous region. The
cause is either a wound or
spontaneous rupture of the or-
gans containing air, such as
the trachea, or the various air
sacs and passages communicat-
ing between them. The air
imprisoned beneath the skin
may so distend the skin that
the bird appears almost like a
ball.

The condition occurs in
young canary birds and has
Fie. 56. A young canary bird with em- been reported in fowls, turkeys

physema of the skin. (Klee) and pigeons.

Radical correction of the trouble by preventing the leakage is not
possible, but relief of the condition may be accomplished by slitting
the skin to prevent accumulation of air.

298 DISEASES OF DOMESTICATED BIRDS

CUTANEOUS HORNY GROWTHS

Horny growths on the skin of birds are not rare. They result from
a proliferation of the epithelial cells and subsequent hardening of the
tissue causing deformity. The growths have no effect upon the
general health. When the location interferes with function as on
the beak, operative treatment is indicated.

In parrots cutaneous horny growths occur, which are of tuberculous
origin. Klee reports that skin horns occur in about 50 per cent of
parrots affected with tuberculosis.

DUBBING OR CROPPING

The removal of the comb and wattles is commonly practiced in pre-
paring game birds for the ring. It is also performed upon male
breeding birds of some breeds where the comb and wattles are abnor-
mally developed. The removal of these structures is said to improve
the condition of the bird and increase the percentage of fertile eggs.
The operation is indicated in bad cases of frost bite and in the in-
fectious disease known as edema of the wattles.

In removing the comb, the bird is held by an assistant who grasps
the two legs with one hand and the wings with the other. The
operator grasps the comb firmly and cuts with a knife from the base
forward to the beak as close to the head as possible. Hemorrhage
may usually be controlled by pouring cold water upon the head, but
if not, the actual cautery may be applied. Curved surgical scissors
may be employed in removing the wattles, which operation does not
cause such severe hemorrhage. Antiseptic dusting powders may be
applied to the wounds. ‘The bird should be kept secluded until the
wounds have entirely healed, before being turned loose among other

birds.

FRACTURED BONES

Broken bones are not rare among fowls as a result of accidents,
fighting and mistreatment. Pigeons frequently break wing bones by
colliding with objects during flight. Bones of the feet may be frac-
tured when the bird becomes entangled and struggles while hanging
by the feet.

A cure is possible and probable if the break is fresh and uncom-
plicated by splinters, if the soft tissues are not lacerated and if the
skin is not punctured. Cure is most probable in simple fractures

SURGICAL DISEASES 299

of the bones of the leg and feet. The bird is laid upon the back and
the feathers are clipped from the region of the break. The skin is
cleaned of blood by washing with three per cent solution of com-
pound solution of cresol. The two broken ends are brought into the
correct position. A strip of adhesive tape of the proper dimension
is wrapped about the broken bone so that there is formed. an en-
veloping band. Care should be taken not to draw the tape too tight.
Pigeons and most sorts of hens do not require a special splint, for
the adhesive tape is stiff enough. In the case of very heavy boned
fowls, ducks and geese it is preferable to use thin strips of wood or
an envelope of stiff paper as a foundation for the bandage. Goose
quills, softened in hot water and split from end to end, are useful as
splints. In the case of weak bones, one quill is enough, but larger
ones need two quills, one on each side. The softened quill fits itself
to the bone and is held in place by a bandage. These quill splints are
at the same time light and strong and consequently are decidedly
preferable to other material.

Fractures of wing bones of pigeons are mostly followed by an im-
pairment of the ability to fly so that treatment is only indicated in
valuable individuals which can be utilized as breeders. An adhesive
tape bandage is applied after removal of the feathers as in the case
of a fracture of a leg bone, only it is useful to make the bandage
broader and longer. As soon as the bandage is applied, but while
yet soft, it is pressed with the fingers into a flat shape correspond-
ing to that of the wing. The bird is then wrapped with bandages so
that both wings lie close to the body and the use of even the sound
one is impossible.

The bandages are kept in place for about two weeks and in that
time healing has mostly taken place. To hasten recovery the bird
is isolated in a cage without perches or in a crate with planer shav-
ings. In such cases when a bird is confined for a long time, the
feathers and cage should be thoroughly dusted with insect powder.
The torments suffered by such a bird from blood sucking insects are
severe and the restlessness ensuing, retards recovery.

After removal of the bandages, the bird is to be kept isolated for a
time from others of his kind for fear that the bone will be broken
again.

Swelling of the extremity after bandaging a broken bone indicates
that the bandage is too tight and that it must be replaced by a better
fitting one. Often in this case it is too late, and it is better to kill

300 DISEASES OF DOMESTICATED BIRDS

the patient because in birds dry gangrene occurs very quickly in parts
from which the circulation is cut off. (Klee. )

FROZEN COMB AND WATTLES

When freezing of the appendages of the head occurs, thawing may
be accomplished by smearing with vaseline, and manipulating with
the fingers. In case of serious injury of the comb or wattles, they
may be removed as described under dubbing.

INCISION OF THE CROP

This operation is frequently necessary in order to evacuate the
contents of the organ when impaction is present, and is comparatively
harmless in fowls. After removing the feathers from the operative
area, an incision is made parallel to the axis of the neck, and as
long as the circumstances require. The material is removed by
kneading, and the use of forceps. Healing occurs in about a week
after suturing. Feeding must be restricted for a few days to bread
and milk but water may be given without limit after 36 hours.

PREVENTION OF FLIGHT

It is sometimes necessary to deprive birds of the power of flight
either temporarily or permanently. To arrive at this result it may
be necessary only to cut off the large feathers on one wing, or to pre-
vent the extension of the member by some mechanical device. What-
ever the method employed it should be applied to but one wing. The
effect in preventing flight is accomplished more by destroying power
of maintaining equilibrium than in reducing wing surface.

Permanent elimination of the primary wing feathers may be ac-
complished by severing the region of the wing corresponding to the
hand. <A cut is made with scissors on a line so as barely to leave
intact the bone corresponding to the thumb. The proper location for
the amputation may be determined by making the cut barely include
the primary feathers. Hemorrhage may be arrested by cauterizing
or by applying perchloride of iron.

The operation is very simple and quite harmless. Very little
trace is left, for the stump is covered by the feathers of the thumb.
When the wing is folded, the absence of the primary feathers is not
noticeable.

SURGICAL DISEASES 301

WOUNDS

Fowls are lable to be wounded by fighting, by bites of dogs, by
birds of prey, ete. Treatment consists of clipping off the feathers
in the vicinity to expose the wounded area. The wound may be
washed in a three per cent solution of compound solution of cresol.
Hemorrhage may be controlled by the application of perchloride of
iron with a pledget of cotton. Shght hemorrhage may be treated
with styptie collodion. Since the blood of birds, especially of pigeons,
clots very readily, hemorrhage is usually controlled without difficulty.
Extensive wounds of the skin may be sutured. Tattered portions of
muscle may be clipped off smooth with scissors.

Treatment is more difficult if the wound includes a tear of the
crop. In such a case the organ must be first emptied of its food
contents by flushing out with fluid introduced by means of a rubber
tube. Treatment then is carried out in the same manner as in
closing an incision of the crop.

In general, wounds of birds, except the most severe ones, heal
readily. Suppuration of wounds as in mammals, does not occur in

birds.
REFERENCES

1. Klee. Die hauptsichlichsten Gefliigel-Krankheiten. Leipzig. 1905.

2. Mégnin. Medecine des oiseaux. Vincennes: Au Bureaux de I-
Eleven. 1906.

3. Pearl and Surface. The use of atropine sulphate in anesthetizing
birds for surgical experiments. J. Am. M. Ass., Vol. 52, 1909, p. 382.

CHAPTER XXIV

CAPONIZING
CAPONIZING THE FOWL

The operation of caponizing or castration of the male fowl is de-
scribed by Slocum as follows:

TIME TO CAPONIZE

In so far as the effects of the operation and the rapidity and ease
of healing are concerned, the time of year when the operation is per-
formed is of little importance. The capons seem to recover and do
well at any time. Certain other considerations, however, do influ-

Fie. 57. Barred Plymouth Rock cockerel of suitable size to caponize. (Drawn
from photograph by Slocum)

ence the time. The age and size of the cockerel are very important.
As soon as the cockerels weigh 1% to 2% pounds, or when 2 to 4

months old, they should be operated upon. The lower age and weight
302

CAPONIZING 303

limits apply particularly to the American breeds, while the higher
apply to the Asiatics. If smaller than this, their bodies do not give
room enough to work handily. On the other hand, they should never
be over 6 months old, as by this time the testicles have developed
to a considerable extent, the spermatic arteries carry greater amounts
of blood, and the danger of pricking these arteries and causing the
fowl to bleed to death is greatly increased. The fact that capons
are in greatest demand and bring the best prices from the Christmas
season until the end of March, and that it takes about 10 months to
grow and finish them properly, makes it important to hatch the
chicks in early spring so that they will be of proper size for caponiz-
ing in June, July, and August. These are by far the most popular
months for the operation, though in some cases it is performed still
later.

CAPONIZING INSTRUMENTS

There are several sets of instruments for performing the operation.
These differ principally in the type of instrument used in getting
hold of and removing the testicle. One type is the cannula (Fig. 58,
a). This consists of a hollow tube, the lower end of which is com-
pressed and closed except for two small holes through which to run the
horse hair or wire comprising the other part of the instrument.
This type requires two hands to operate. Another type is the twist-
ing scoop (Fig. 58,6). This is a spoon-like scoop slotted in the center
and mounted upon a slender rod. It is designed to slip under the
testicle, allowing the spermatic cord to pass through the slot. By
twisting the cord is severed. This type has the advantage of requir-
ing only one hand to operate, but is more liable to produce “ slips ”
(see p. 809) than the cannula. A third style of instrument (Fig 58,
2) is also in the form of a spoon or scoop, but instead of being in one
piece has two jaws regulated by a slide. The testicle is caught in
the scoop with the spermatic cord between the jaws, and by tighten-
ing the jaws and gently moving the instrument the cord is severed and
the testicle removed. Still another type, not now in common use, is
the spoon forceps. With this the testicle is simply grasped with the
forceps and detached by a twisting movement. Here one hand can
be used also, but the liability of slips is rather greater than with the
other methods.

Figure 58, k, shows a type of forceps, consisting of two hinged
arms, one of which terminates in a broad, flat surface, and the other
in an end of similar shape from which the center has been removed,

304 DISEASES OF DOMESTICATED BIRDS

Instruments used in caponizing. (Slocum)

leaving only a narrow rim. ‘These two ends are held closely pressed
together by means of a rubber band passing across the handles. In
use, the ends of the forceps are separated, the solid one slipped under
the testicle and the rim then allowed to settle down over it. The
cord is thus caught and the testicle can be removed. Careless or too
rapid use of this instrument is likely to cause ships. Figure 58, 7 and
m, shows two additional types of testicle removers. The type shown
in / has a curved handle which brings the hand out of the line of
vision, making it easier to see into the body cavity when using the
instrument. A knife for making the incision into the body eavity is,
cf course, necessary. Almost any sharp-pointed, thin-bladed knife
will answer the purpose well (see Fig. 58, c). Some sort of spreader

CAPONIZING 305

to spring apart the ribs far enough to allow the instruments to be
inserted into the body must be used. A plain spring spreader, as
shown in figure 58, d, or a sliding spreader (Fig. 58, e), allowing the
pressure to be gauged, will answer the purpose. A sharp-pointed
hook (Fig. 58, h), for tearing away the thin membranes, and a blunt
probe, of which figure 58, g, is one type, for pushing aside the intes-
tines, complete the necessary equipment. <A pair of small tweezers
or nippers (Fig. 58, f) is also useful in removing any foreign matter
from the body.

THE OPERATION OF CAPONIZING

Before beginning the operation two conditions are absolutely essen-
tial. If these are not favorable, do not attempt to operate. The
first of these is that the intestines of the fowl should be completely
empty, so that they will fall away and expose the testicle to view.
This can be accomplished by shutting up the fowls and withholding
all food and water for 24 to 36 hours before the operation. With-
holding water tends to make the blood thicker and consequently to
decrease the amount of bleeding. Thirty-six hours is better than 24,
especially for a beginner. The second condition is a good, strong
light, so that the organs of the fowl may be clearly and easily dis-
tinguished. Direct sunlight is best for this, and in consequence it is
well to operate out of doors on a bright day. Some operators have
substituted the physician’s head reflector and artificial ight with
good success. An ordinary incandescent electric bulb fastened to a
gooseneck standard and provided with a reflector can be used to good
advantage when caponizing indoors. It has been suggested that a
probe consisting of a small electric bulb on the end of a slender rod
and operated by small dry batteries, so that it can be introduced into
the body cavity, could be manufactured and used with good success.

METHODS OF HOLDING THE FOWL

When ready to operate, catch the bird and pass a noose of strong
string about the legs. Do the same with both wings close to the
shoulder joints. To the other end of the strings are attached weights
of sufficient size to hold down and stretch out the bird when placed
upon the head of a barrel or box of convenient height, which is to
serve as operating table. These weights are allowed to hang on oppo-
site sides of the barrel or box (Fig. 59). A table, if so desired, may

306 DISEASES OF DOMESTICATED BIRDS

be arranged by boring holes through its top at proper distances from
each other, allowing the strings to pass through these, and hanging
the weights underneath. Still other ways of holding the fowl in
place have been devised, but these are unimportant so long as the
fowl is held securely stretched out.

DETAILS OF THE OPERATION

Having fastened the fowl, be sure that all the instruments are at
hand. It is also well, though not necessary, to have ready some
absorbent cotton and a dish of water to which have been added a few
drops of carbolic acid or some other antiseptic. Having once started,
carry the operation through as quickly as possible. Moisten and
remove the feathers from a small area over the last two ribs just in

iN .
pega
PN
"
' \
\

Fic. 59. Feathers plucked away to make ready for incision. (Drawn from
photograph by Slocum)

front of the thigh (Fig. 59). With the left hand slide the skin
and flesh down toward the thigh. Holding it thus, make the incision
between the last two ribs (Fig. 60), holding the edge of the knife
away from you as you stand back of the fowl. Lengthen the incision
in each direction until it is 1 to 1% inches long. Now insert the
spreader into the incision, thus springing the ribs apart, as shown in
figure 61. The intestines will now be visible, covered by a thin
membrane called the omentum. Tear apart this membrane with
the hook, and the upper testicle, yellow or sometimes rather dark
colored and about the size and shape of an ordinary bean, should
be visible close up against the backbone. By pushing aside the in-
testines this can easily be seen, and the lower one also, in a similar
position on the other side of the backbone. Expert operators usually
remove both testicles through one incision: This is a desirable prac-

CAPONIZING 307

Fie. 60. The incision made. Before making the cut, the skin over the last two
ribs is pulled down toward the thigh and held there while the incision is made.
When the bird is released after the operation, the skin slips back into its
natural position. The cut in the skin is then not directly over the incision
in the body, with the result that the wound is closed and protected. (Drawn
from photograph by Slocum)

\

Fic. 61. The spreader in place. Tearing open the membranes. (Drawn from
photograph by Slocum)

tice, as it saves time and is not so hard on the bird. Inexperienced
operators will usually find it well to attempt the removal of the
upper or nearer testicle only and to make a second incision on the
opposite side of the body for the removal of the other testicle.

If both testicles are to be removed through the same incision,
remove the lower first, as the bleeding from the upper might be suffi-

308 DISEASES OF DOMESTICATED BIRDS

Fic. 62. Spreader in place. The testicle can be observed lying between the
jaws of the spreader. (Drawn from photograph by Slocum)

Fic. 63. Removing the testicle. (Drawn from photograph by Slocum)

cient to cbscure the lower. ach testicle is enveloped in a thin mem-
brane. This may be and probably is best removed with the testicle,
though some operators tear it open and remove the testicle only.
The delicate part of the operation is now at hand, owing to the close
proximity of the spermatic artery, which runs just back of the testicle
and to which the testicle is in part attached. If this is ruptured the
fowl will bleed to death. The cannula, threaded with a coarse horse-

CAPONIZING 309

hair or fine wire, or one of the other forms of instrument previously
described, now comes into use. If the cannula is used, allow the hair
or wire protruding from the end to form a small loop just large
enough to slip over the testicle. Work this over the testicle, being
careful to inclose the entire organ. Now tighten up on the free ends
of the hair or wire being careful not to catch any part of the
artery. If the spermatic cord does not separate, saw lightly with

Fria. 64. The spreader removed and the weights taken off the wings. Notice
how the skin slips back over the incision so as to close it. (Drawn from
photograph by Slocum)

the hair or wire. When the testicle is free, remove it from the body.
The method of removing the testicle is shown in figure 63. If only
the upper testicle has been removed, turn the bird over and proceed
in exactly the same manner upon the other side.

After removing the testicle, if the bleeding is at all profuse it is
well to remove a portion of the blood by introducing small pieces
of absorbent cotton into the body by means of the hook or nippers,
allowing them to become saturated and then removing them. Be sure
to remove all blood clots, feathers, or foreign matter. After the
testicles and all foreign matter are removed, take out the spreaders,
thus allowing the skin to slip back over the incision.

LOSSES DUE TO CAPONIZING

Even experts are sure to kill some birds, but the loss is small,
seldom exceeding 5 per cent where any considerable number are
caponized, and usually not more than 2 or 3 per cent. With be-
ginners, of course, the percentage is much larger, but with a little

310 DISEASES OF DOMESTICATED BIRDS

practice and care this is soon overcome. Any fowls which may be
killed in this way are perfectly good to eat and are therefore not
wasted.

A great deal of practice is required to become expert enough to
operate rapidly. Consequently it is quite common in localities where
many capons are grown to hire experts to do the work. These men
are able to caponize a fowl every two to five minutes, and charge
from 3 to 6 cents a fowl for the service. It is most humane for the
beginner to make his first trials upon dead fowls.

SLIPS

Many times, particularly with beginners, while the operation seems
to be entirely satisfactory, the bird will turn out to be what is known
asa “slip.” A “slip” is neither cockerel nor capon, but is between
the two, possessing the mischievous disposition and the appearance
of an ordinary cockerel, but, as a rule, being unable to reproduce.
This condition is due to the fact that a small piece of the testicle is
left in the body. This piece often grows to a considerable size. As
the “ slips ” possess the same restless disposition as the cockerels, they
grow and fatten little if any better, while they do not bring as good a
price in the market as the capons. Consequently it is well to use
every precaution in order to avoid “ slips,” as they are unprofitable
as compared with capons. With the greatest care, however, “ slips”
are more common than are deaths due to the operation. ‘The per-
centage varies all the way from 50 per cent with beginners down to
2 or 3 per cent with experts.

CARE OF FOWLS AFTER THE OPERATION

Upon being released from the operating table the capons are
usually put in a closed yard where they can find shelter, food, and
water and can be kept quiet. No roosts are provided, as the less fly-
ing and jumping they do the sooner will the wound heal. The
capons seem to be very little inconvenienced by the operation, and
water and soft feed mixed with sweet skim milk can be given imme-
diately. Some feeders give this in unlimited quantity, while others
feed more sparingly for a time. Some growers observe no precau-
tions whatever, giving the birds their full liberty immediately after
the operation and allowing them to have any sort of feed.

For a week or 10 days the newly made capons should be carefully

CAPONIZING ~ 311

observed to see whether they become “ wind puffed.” This is a con-
dition caused by air gathering under and puffing out the skin near the
wound. When observed it can be readily relieved by pricking the
skin with a needle or knife and pressing out the air. In about 10
days or 2 weeks the incision into the body should be entirely healed,
and, although no special antiseptic methods are employed in the
operation, blood poisoning or any other trouble seldom results.

CAPONIZING THE MALE OSTRICH

According to Elley, whose description of the operation is given
below, the best age for castration of the ostrich is from eighteen
months to two years. ‘The testes are then beginning to develop, are
easily located, but are not yet so vascular as to occasion any prob-
able risk of hemorrhage. .

Preparation for operation. “Have the birds brought into
the pen on the afternoon of the day before it is intended to operate,
so that they may have no food whatever for say twenty hours before
the operation, as the less ingesta in the stomach and bowels, the bet-
ter and easier it will be. If possible there should be three adjoining
pens; the first in which to catch the birds, the second or middle for
operating in, and the third in which to place the birds after the opera-
tion. The operating pen should be well sprayed with a disinfectant
solution before commencing. The first bird is caught and brought to
the operating pen and the chloroform bag placed on his head with
rather less than half an ounce of chloroform (2-3 teaspoonfuls) on
the cotton wool. One good boy can then hold him until he is properly
under the influence of the anesthetic. A little more chloroform can
be added after he is down, and if necessary once or twice during the
operation. One ounce, or at the most one-and-a-half ounces, should
be sufficient for the whole operation. Ascertain by moving the wings
or striking him, if he is properly under, then place him on his left
side. A boy now grasps the right leg and brings it slightly further
forward than at right angles to the body. The seat of the operation
is now exposed. It lies in the angle formed by the leg and the lower
edge of the innominate bone, about three inches behind the former
and one-and-a-half inches below the latter. The innominate bone
can be felt as a distinct ridge running backwards and slightly down-
wards, about the middle of the body immediately behind the leg; it
corresponds to the lowest part of the body on which any feathers
are found. It is immediately below this ridge that the incision is

312 DISEASES OF DOMESTICATED BIRDS

made. The operator should now wash his hands and the seat of the
operation with a disinfectant solution.
The operation. Make an incision about four inches long, cut-
ting from before backwards, in a line parallel with the ridge men-
tioned above. Cut down until the peritoneum or thin membrane
covering the bowels is reached. Care is required at this point.
Having reached the peritoneum grasp it with the forceps, taking care
not to include any of the gut, and draw it slightly towards the ex-
ternal wound, then make an opening through it just large enough
to admit the hand. Pour a little carbolic oil over the right hand and
force it gently through the opening into the abdominal cavity. The
testes are easily located about three to four inches further forward
than the incision, almost exactly between the upper extremities of
the two legs, situated on and closely attached to the middle of the
roof of the abdominal cavity, immediately below the kidneys. In
birds of an age which I have recommended for the operation they
are felt as two elongated firm structures, about one-and-a-half inches
long by a quarter of an inch broad, somewhat the shape of a 303
bullet. They lie about two inches apart, the left usually slightly
more forward than the right. Having located them, the tissue round
about them is easily broken down by the fingers, and a few twists
liberate them and they fall into the palm of the hand. Both testes
should be located before either is removed. With care the one can
be liberated and held in the palm of the hand whilst the fingers
free the other one. It is then only necessary for the hand to enter
the abdominal cavity once and be once withdrawn, containing both
testes. If the birds are in very good condition there will be a certain
amount of fatty tissue round the testes which may give a little
more trouble in removing them. Having withdrawn them it only
remains to suture the wound. Thread a needle with fine cat-gut and
put two or three stitches through the peritoneum or membrane tak-
ing care not to prick the gut in doing so. Then stitch the external
wound with three or four stitches including the skin and muscle.
Dress the external wound with a little iodoform and the operation
is complete. Whilst the last stitches are being put in, the chloro-
form bag should have been removed. Allow the bird to lie quietly
until he wakes up and let him take his own time about rising, on
_no account frighten him up or he will invariably attempt to rise be-
fore the effects of the chloroform have quite passed off and in fall-
ing or struggling the stitches may be broken. Watch the breathing
throughout the operation, it should be steady and regular. Should

CAPONIZING 313

it become jerky or irregular, at once open the end of the chloroform
bag and admit more air.

After treatment. Jor the first twenty-four hours after the op-
eration the birds should be placed in as quiet a camp as possible,
where they are not likely to be frightened or made to run. Green
alfalfa is the best food both before and after the operation.

Instruments. All the instruments required by any one operat-
ing by this method are: (a) chloroform bag, such as the one I have
had made, (b) sharp knives, (c) needles and eat-gut, (d) needle
holder. This latter will be found useful for the deep stitches in the
peritoneum.

Advantages resulting from the operation. Having described
the operation I will briefly enumerate the advantages which it is
claimed will result from it.

1. It is claimed that with the increased condition of the bird which
is sure to follow the operation, there will be increased weight of
feathers.

2. That owing to the quieter life of the bird the feathers will
be less damaged by fighting or scraping on the ground than in the
entire bird.

3. In droughts or when food is scarce, castrated birds will keep
in fair condition where entire birds would starve.

4. I believe the flesh of a capon will prove an acceptable article
of human food. I am quite prepared for this idea to be ridiculed
today, but in time to come it may be considered.”

REFERENCES

1. Elley. Castration of ostriches. Agr. J. Cape of Good Hope, Vol.
29, 1906, p. 349.

2. Slocum. Capons and ecaponizing. U. 8. Dep. Agr. Farmers’ Bull.
849, 1917.

CHAPTER XXV

KILLING POULTRY

Results of bad bleeding. The manner in which fowls are
slaughtered and bled out has an important bearing upon the ap-
pearance and keeping quality of the product. Poorly bled fowls
often show red dots where the feathers have been removed, espe-
cially in areas over the thighs and wings. Also, veins are seen to
stand out prominently over the breast, angles of the wings, or on
the neck. In poorly bled birds the neck is the first part to discolor.
At first it is red, later bluish red or purple and still later, green.
The bad appearance of poorly bled carcasses detracts from their
value and their keeping qualities are very much impaired.

Pennington and Betts have made an anatomical study of the
blood vessels of the head and neck of the chicken with reference to
determining the most satisfactory method of securing complete bleed-
ing. ‘Their description of proper methods of killing, and discussion
of faulty methods are quoted as follows.

“ oUTTING” TO BLEED AND ‘“ STICKING” TO BRAIN

When the feathers are removed by scalding, the bird is killed by
bleeding alone, hence the cuts to sever the veins are the only ones
attempted, and if the attempt fails bad bleeding will surely result.
Tf, on the other hand, dry picking is to be practiced, the birds are cut
to bleed and are also stuck through the brain to paralyze the feather
muscles. The latter operation is sometimes performed by running
the knife under the eye at such an angle that its point. will touch the
skull midway between the eyes and a little behind them; or the
braining is accomplished by placing the knife about halfway down
the groove in the roof of the chicken’s mouth, and then thrusting it
up until the knife reaches the top of the skull. The knife, as in
sticking under the eye, should touch the brain in the back part of
the skull. The point of the knife should then be twisted slightly, so
that enough brain tissue may be destroyed to paralyze the bird and
cause the feathers to loosen. If the “ outside-stick”” method is prac-

ticed, practically no blood escapes. If, on the other hand, braining
314

KILLING POULTRY 315

inside of the mouth is adopted, the blood vessels in the brain which
are cut find an outlet for their contents through the knife hole.
Bleeding from these vessels is, under any circumstances, of assistance
in obtaining the best results, and where the neck vessels are missed
the condition of the chicken is often greatly improved by the bleed-
ing from the brain.

DISCUSSION OF THE ILLUSTRATIONS
LOCATION OF VEINS

The location of the principal veins in the neck of the chicken,
their relation to the skull, and the point at which it is desirable
to make the cut for bleeding, are shown in the accompanying illus-
trations. Figure 65 shows the head and neck of a young cock about
a year old. Two large veins (heavily
lined with black in the figure) run the
whole length of the neck, one on each side,
and unite by a “ bridge-vein” which is
just below and behind the ear. This vein,
which connects the two others, does not
run straight across but at an angle, so that
it is farther front on the left than on the
right side. If the feathers on the neck of
a chicken are pushed aside, or, better still,
if a molting chicken with but a few
feathers is observed, these veins can be
seen at each side of the neck while the
bird is alive, especially if a little pressure
is used at the lower part of the neck so that
the blood collects and distends them. It
is important that the position of these
veins be exactly located on the neck of the
live bird, since upon this information will
depend very largely the proper guiding of
the knife to the blood vessel.

Fig. 66 shows two sketches of a chicken’s
head from which the lower jaw has been re-
moved. The lower jaw of the chicken is
Fie. 65. External view of much longer than the beak. It runs back

head and neck showing +> g point just below the ear, where the

position of veins. (Pen- aA. : A
nington and Betts) hinged joint can be felt. The skin which

‘a im

uae iV

we

316 DISEASES OF DOMESTICATED BIRDS

makes the corner of the mouth and limits the length of the beak ends
is indicated in the anatomical drawing marked “ A.” The skin and
lower jaw have been cut away in order that the position of the veins
which lie far back on the roof of the mouth and just below its surface
may be seen. The groove which occurs in the roof of the chicken’s
mouth is a guide to the position of the blood vessel which it is desir-
able to cut, this point being behind and to the left of the end of the
groove when the chicken is held head down and with the lower side
of the head uppermost. The direction and position of the cut which

CORRECT CUT CORRECT CUFT

GROOVE -/N
ROOF OF MOUTH

EYE = EYE
ENO OF BEAK

Fie. 66. Lower jaw removed, showing position of veins, anatomy of skull, and

location of cut. (Pennington and Betts)
is to sever the veins is shown in Fig. 66 to be on the left side of the
chicken’s head when in the position just described. Because the
short blood vessel connecting the two long veins, which we have
termed the “ bridge,” does not run straight but at an angle, the point
just indicated is farthest front and the most easily reached by the
knife. As stated before, these veins lie just below the skin of the
roof of the mouth, hence a deep cut is not needed, neither is any
amount of strength required for the operation.

It will be observed that just in front of the line which indicates the
point at which these veins are to be cut they divide into two small
branches, the course of which is not further shown. This is because
they very soon pass through small holes in the bone and go into the

KILLING POULTRY O17

inside of the skull, and into the deep tissue, where they are quite
safe from the killer’s knife. If, then, these large veins are to be sev-
ered, the cut must be made far enough back to reach them before
they penetrate the bones of the skull. On the other hand, if the cut
is made too far back and over the edge of the skull, as will be dis-
cussed in connection with Fig. 66, B, much of the blood will settle in
the loose tissue of the neck instead of running out of the mouth,
thereby clogging the vessels and preventing complete bleeding, as
well as moieae juetiie discolored areas on the neck near the head.
It is better to make one cut as shown in this plate rather than to
cut the “ bridge ” in the middle or to cut each side vein separately,
since this sometimes results in the clotting of the blood at the ends
of the veins before the bleeding is completed.

ANATOMY OF THE SKULL

From what has been said concerning the necessity of cutting far
back in order to reach the point desired, it will be seen that it is
necessary to know something of the position and shape of the bones
of the chicken’s skull and their relation to the external parts of the
head. This information is given in Fig. 66, B. Dotted lines
around the drawing of the skull show the position of wattles, comb,
ete. In this sketch, too, is shown clearly the length of the chicken’s
jaw, as before mentioned. Its hinge will be found on the head of
the live bird just below the ear. Still farther back there is a
U-shaped depression in the skull into which fits the upper part of the
spinal column. ‘The spine is not shown in the sketch, but the bridge
vein connecting the two large veins of the neck hes directly across the
U-shaped eae seto

It can be seen by studying this drawing how a back the knife
must go if the veins are to be cut at the angle, and it will also be ob-
served that when they are cut in this “od ae the knife will have a
bony backing which will prevent it from going too deep, thereby
obviating in spongy mass of blood in the naele tissues which was dis-
cussed in connection with Fig. 66, A. This illustration also shows
where the fingers can grasp the head of the chicken firmly and yet
not press against the soft parts of the neck. Just above the angle of
the jaw — that is, about at the chicken’s ear —there is a smooth,
strong area of bone large enough to support the thumb on one side

and the forefinger on the other, and this is where the head should be
held while killing.

318 DISEASES OF DOMESTICATED BIRDS

POSITION OF HAND AND KNIFE

Figure 67 shows the position of a chicken ready for killing and
held by the feet in a U-shaped shackle. Notice that the thumb of
the killer is pressed firmly down on the head just below and behind

Fig. 67. Correct grasp of head at angle of jaw and position of small knife when
cutting vein. (Pennington and Betts)

the ear in the space to which attention was called when discussing
the bones of the skull. Here, too, is the hinge of the jaw. Pressure
of the thumb on one side of this portion of the skull and on the other
side at the same place with the forefinger, or with the forefinger and
second finger, will result in opening the chicken’s mouth and holding
it open while the operator makes the cut to bleed. Held in such
fashion, there is nothing to constrict the blood vessels, thereby pre-
venting the blood from escaping even though these vessels be cut.
The pressure against the jaw makes accurate cutting of the veins
easier, since the bird can not close its mouth until the pressure is
removed. Of course, care must be taken not to stretch the neck
unduly, else the vessels will be pulled to such a narrow diameter
that they are more difficult to find and also more difficult to empty.

The position of the knife in the mouth, which is shown by the
dotted line, needs no further explanation. The knife itself, how-
ever, is very different from that ordinarily used in the bleeding of

KILLING POULTRY 319

hw i y i : e
Cae

iy ii
a {{ |
a i" i :

ESS

Fie. 68. Location of cuts in mouths of badly bled chickens (lower jaw removed),
(Pennington and Betts)
chickens. The knife in common use is much too large, both too
long and too broad for the most successful work. Generally it is
provided with a heavy handle, large enough to be grasped easily
by a large, strong hand. As has already been observed in this dis-
cussion, the heavy slashing inside the bird’s mouth is not only fre-
quently futile so far as cutting the veins goes, but is really harmful
in that it makes a pathway for the entrance of bacteria and the con-
sequent hastening of the bird’s decomposition. The operation calls
for accuracy rather than for strength, and therefore it is desirable
that the knife should have a smaller handle, which can not be gripped
so hard. The blade of the knife should be about 2 inches long and
one-fourth of an inch wide and of a heavy piece of steel, so that it
will not bend. It is advisable, therefore, to have the back of the
blade about one-sixteenth of an inch thick. It should be made of
good hard steel and ground to a sharp point with a straight cutting
edge, the slope for the point being taken from the back rather than

320 DISEASES OF DOMESTICATED BIRDS

from the edge. The working space in the back part of the mouth of
the chicken where the blood vessels lie is very small. Often the
knife which is used by the killer is too broad to go into this space
without cutting the sides of the mouth, and as for turning and guid-
ing it, that is quite out of the question.

EXAMPLES OF BAD CUTTING

Ineffectual cutting, due to lack of knowledge of the structure of
the chicken’s neck and head, the use of force rather than skill on the
part of the operator, and a knife ill adapted to the work which it has
to do, is illustrated in Figs. 68 and 69 which show some of the most
common types of cuts in badly bled chickens. A study of these illus-
trations indicates very plainly why these chickens are badly bled.
The lower jaws from these heads were removed so that the position
of the cuts could be noted. Head A has had two cuts. One has run

CUTS

Fic. 69. Attempts at “cross cutting,’ showing veins untouched. (Pennington
and Betts)

KILLING POULTRY 321

parallel with the connection between the two veins and very close to
it but has not cut it, and another has run from the angle of the
mouth to close to the point where the blood vessel on the left side
of the head breaks into the two smaller vessels and penetrates the
bones of the skull. The only vessels which were cut in this chicken
were the small superficial veins supplying the roof of the mouth and
from which the bleeding amounted to almost nothing. Head B
shows a cut in the right direction but it did not go quite far enough
back to reach the veins at their junction. Head A, in Fig. 69, shows
the cross cut which is advocated by so many killers. In this case it
was made too far front. Both of the large veins escaped and only
the small vessels of the roof of the mouth were disturbed. “B”
is a good illustration of indiscriminate cutting by a badly directed
knife, which in all probability was far too large, since the upper cut
extends all the way across the roof of the chicken’s mouth and almost
as far front as the beak. Another cut which partly follows the groove
in the roof of the mouth would indicate that the killer had tried to
make a cross cut.

Such examples of bad cutting might be multiplied indefinitely.
Yet the general principle is the same and the result is the same —
namely, a fowl which is not completely bled, which is unsightly, even
in the packing house, and which deteriorates as a food stuff more
rapidly than does the well-bled chicken under similar conditions.

SUMMARY

The facts which have been stated in the foregoing pages may be
summarized as follows:

(1) Grasp the chicken when killing by the bony part of the skull.
Do not let the fingers touch the neck.

(2) Make a small cut inside the mouth on the left side of the
throat just where the bones of the skull end, using a narrow-bladed
sharp-pointed knife. The direction of the knife is upward and to-
ward the left when the bird is held head downward with the throat
toward the operator while killing.

(3) Brain for dry picking by thrusting the knife through the
eroove which runs along the middle line of the roof of the mouth until
it pierces the brain in the back part of the skull, causing a loosening
of the feathers.

(4) For chickens use a knife the blade of which is 2 inches long,

322 DISEASES OF DOMESTICATED BIRDS
one-fourth inch wide, with a thin, flat handle, a sharp point, and a
straight cutting edge. For turkeys the blade may be 2% inches long.
Keep knives very sharp.

REFERENCE

1. Pennington and Betts. How to kill and bleed market poultry. JU. 8.
Dep. Agr. Bureau Chemistry Circ. 61, Revised.

AUTHOR INDEX

A

Adam and Medier, 254, 259
Aragiio, 141, 144, 203, 206
Archibald, 229, 240

B

Balfour, 118
Beach, 109, 189
Beach and Halpin, 118
Beach, Lother and Halpin, 108, 109
Belfanti and Ascoli, 86
Bertegh, 97, 109
Bevan, 136, 144
Binder, 252, 254, 260
Bishopp, 221, 225
Bishopp and Wood, 208, 209, 210, 211,

212, 216, 218, 225
Bordet and Fally, 107, 109
Borrel, 97
Boyce and Warrington, 19
Bradley, 19
Bugge, 250
Burnet, 19, 109
Burnett, 98
Bushnell and Maurer, 79
Butterfield, 146

C

Cardamatis, 203, 206
Centanni, 86
Chauveau, 19

Ciurea, 206

Claussen, 61, 65
Cobbold, 63

Cogny, 39

Colucci, 178
Cominotti, 82, 86
Cornil and Toupet, 250
Curtice, 50, 65, 121, 126, 242, 250
Curtis, 261, 274
Cushman, 126

D

Dammann and Manegold, 30, 33

323

Danielewski, 203
Dawson, 50, 64, 143, 144
Dickson, 154, 177

Dodd, 140

Douglas, 229

Dubois, 86, 143, 144
Dupuy, 65

E

Eastwood and Griffith, 89
Edwards, 290, 294

Ehrenreich, 262, 274

Ehrenreich and Michaelis, 262, 274
Ehrhardt, 142, 144

Ellenberger, 19

Ellenberger and Baum, 19

Ellerman and Bang, 146, 149
Elley, 311, 313

F

Fantham, 127, 134, 204

Fiorentini, 46, 47, 48

Freese, 83, 86, 190, 246, 247, 250, 255
Friedberger and Frohner, 97

Frosch and Birnbaum, 243, 250

Fuller, 225

G

Gage and Hyland, 79

Gage and Martin, 79

Gage and Opperman, 160, 206
Gage and Paige, 80
Gallagher, 16, 39, 48, 109, 163, 276, 294
Gerlach, 199

Gilruth, 254, 260

Gorig, 271, 274

Gray, 203, 233, 260

Greve, 31, 33

Gutberlet, 187, 206

H

Hadley, 36, 48, 65, 120, 126, 193, 206
Hadley and Beach, 109

324

Haidub, 225

Halasi, 97, 109

Haring and Kofoid, 98, 103, 109
Harrison and Streit, 107, 109
Hasenkamp and Sachweh, 246, 251
Hassall, 225

Hastings and Halpin, 95

Hauer, 140, 144

Hausser, 107, 109

Hebrand and Antoine, 150, 177
Herms and Beach, 189, 206
Herrick, 211, 225

Hertel, 86

Higgins, 48

Hindle, 144

Hutcheon, 238

I
Iturbe and Gonzales, 204, 206
J

Jackley, 108, 109

Joest, 86, 254, 260

Jones, 75, 77, 80, 274
Jowett, 43, 48, 134, 144, 240

=

Ke

Kaupp, 19

Kern, 260

Kinyoun, 252, 260

Kionka, 151

Kitt, 39, 48

Klee, 177, 189, 197, 295, 298, 300, 301
Klein, 50, 62, 65

Kleine and Moellers, 87
Koch, 263, 265, 274

Koch and Rabinowitsch, 95
Kon, Yutaka, 146

Kraus and Schiffmann, 87

L

Lamson, 287, 294

Lamson and Manter, 211, 225
Landsteiner and Berliner, 87
Lange, 274

Laurie, 225

Leclainche, 45, 48, 87
Leichtenstern, 54, 65

Lewin, 272, 274

Ligniéres, 61, 66

AUTHOR INDEX

Ligniéres and Petit, 119
Ligniéres and Zabala, 59, 66
Lipschutz, 87

Lisi, 42, 249, 251

Lode and Gruber, 87

Loer, 18, 19

Loffler, 243, 246, 251
Lounsbury, 225

Lucet, 43, 48, 119, 246, 247, 251

Me
M’Fadyean, 43, 48, 243, 251
M

Mack, 109

Mack and Records, 48, 109

Maggiora and Valenti, 87

Magnussen, 28, 33

Mane, 87

Manegold, 31

Manninger, 254, 260

Manteufel, 109

Marchoux and Salimbini, 141, 144

Martel, 61, 66

Martin and Daille, 194, 206

Martin and Robertson, 193, 206

Marx, 231, 232, 233, 240

Marx and Sticker, 97, 98

Matruchot and Dassonville, 119

Mazza, 44, 48

Mégnin, 65, 157, 187, 189, 195, 301

Meyer and Crocker, 134

Miessner and Schern, 252, 260

Milks, 126

Mohler and Buckley, 119

MolWhoff, 143, 144

Moore, 50, 53, 56, 66, 95, 96, 107, 126,
185, 206

Morse, 63, 66

Murphy and Rous, 274

N

Neumann, 119, 183, 188, 192, 194, 200,
202, 206, 209, 220, 240

Nocard and Leclainche, 42, 48

Noguchi, 135, 145

Norgaard and Mohler, 28, 33

O

Ostertag and Bugge, 87

AUTHOR INDEX

Ostertag and Wolfhiigel, 87
Ottolenghi, 81, 87
Owen, 19

P
Palamidessi, 66
Pasteur, 39, 48
Pearl and Surface, 295, 301
Pearl, Surface and Curtis, 27
Pennington and Betts, 314, 322
Pereira, 145
Petit and German, 274
Pfaff, 252, 260
Pfeiler, 254, 260
Pfeiler and Rehse, 66
Pfeiler and Roepke, 50, 66
Pick, 262, 274
Pickens, 146, 149, 263, 274

R

Rabieaux, 42, 49

Ransom, 179, 183, 195, 202, 206

Regenbogen, 272, 274

Reinhardt, 278, 294

Reinholdt, 60, 66

Reischauer, 98

Repp, 216, 225

Rettger, 80

Rettger and Harvey, 68, 80

Rettger, Hull and Sturges, 80

Rettger, Kirkpatrick and Card, 80

Rettger, Kirkpatrick and Jones, 80

Rettger, Kirkpatrick and Stoneburn, 80

Rettger and Koser, 66

Rettger and Stoneburn, 80

Rieck, 252, 260

Riemer, 243, 251

Ritzler, 280

Robertson, 206, 225, 231, 232, 233, 238,
240, 241

Rous, 268, 269, 274, 275

Rous and Lange, 270, 275

Rous and Murphy, 269, 275

Rous, Murphy and Tytler, 267

Russ, 87

Sabouraud, 119

Sabouraud, Suis and Suffran, 119
Salmon, 27, 220

Sanfelice, 62, 66

Schantyr, 161

325

Scherago and Benson, 79
Schlegel, 275

Schmid, 97

Schneider, 292, 294
Seddon, 41, 49

Sigwart, 97, 107

Slocum, 302, 313

Smith, 120, 126, 193, 242
Smith and Ten Broeck, 66, 69
Steen, 19

Stevenson, 190

Stiles, 206

Suffran, 289, 294

iy

Tartakowski, 259, 260

Taylor, 50, 66

Theiler, 226, 241

Theiler and Robertson, 236, 241
Theobald, 189, 198, 206, 207

Tretop, 45, 49

Tytler, 275

Tyzzer and Ordway, 265, 267, 273, 275

U

Uhlenhuth, 140
Uhlenhuth and Manteufel, 97

Vv

Vages, 39
Van Es and Schalk, 92, 94, 95

Ww

Walker, 200, 228, 229, 239, 241
Ward, 34, 36, 49, 95, 280
Ward and Gallagher, 80
Warthin, 146, 149, 226, 275
Wasielewski and Hoffmann, 252, 260
Watson, 275

Weil, 40

Weinzirl, 193, 207

Wickware, 205, 207

Wilcox, 200, 207

Willach, 250, 251

Williams, 199, 207

= YZ

Yutaka Kon, 146
Zeiss, 66, 252, 254, 260

326 AUTHOR INDEX

Zeiss and Schlegel, 61 Ziirn, 252
Zingle, 57, 66 Ziirn and Pauly, 272
Zundel, 199 Zwick, 260

SUBJECT INDEX

A

Abdomen, drooping, 173
Acanthia columbara, 214
Acanthia lectularia, 213
Acetabulum, 4
Acorn poisoning in the ostrich, 240
Ageressin for fowl cholera, 40
Air sacs, 15
Air sac mite, 198
Alimentary system, 10
tract, diseases of, 154
Aloes, Barbadoes, 240
Ammonia, 237
Ammonium chloride, 277
Ameba meleagridis, 120, 193
Ameebotenia sphenoides, 183
Analges bifidus, 220
Anesthetizing fowls, 295
Anatomy, 1
Anise oil, 191
Anthrax in the fowl, 143
in the ostrich, 226
vaccine, 227
Apoplectiform septicemia, 28
Areca nut, 187, 190
Argas americanus, 221
miniatus, 221
reflexus, 224
Arsenious acid, toxicity, 278
Arteries, 6
Arthritis in pigeons, 295
Ascaridia perspicillum, 169, 188
Ascaris crassa, 188
Ascites, 173
Aspergillosis in the fowl, 111
in the ostrich, 228
Aspergillus fumigatus, 111, 230
eandidus, 112
glaucus, 112
nigressens, 112
Asthenia of fowls, 64
Atropine sulphate, 295
Autopsy directions, 25
Avian diphtheria, 96
salmonellosis, 59
tuberculosis, 88

B

Bacillary white diarrhea, 68

327

Bacillus avicida, 34
avisepticus, 34
bipolaris septicus, 34
canariensis necrophorus, 253
cholere gallinarum, 34
coscoroba, 45
enteritidis, 60
gallinarum, 50
loxiacida, 259
paratyphosus B, 57, 58, 60, 252, 254
septicemia anserum exudative, 243
suipestifer, 56
Bacterium anthracis, 226
asthenie, 64
diphtheriz, 108
pullorum, 52, 68
pullorum infection in grown fowls, 74
sanguinarium, 50
tuberculosis, 88
typhi gallinarum alcalifaciens, 50
Balsam of Peru, 220
Bed bugs, 213
Bertiella delafondi, 183
Bichloride of mercury, disinfectant, 23,
40
toxicity of, 279
Bilharziella polonica, 194
Bird fever, 252
flea, 212
pest, 81
plague, 81
pox, 96
Bismuth subnitrate, toxicity, 280
Blackhead, 120, 193
Blastomyces anseris, 194
Blastomycosis, 194
Blood, 7
platelets, 8
spots in eggs, 169
Blue stone, toxicity, 282
Bones, broken, 298
Boracic acid, 105
Bothriotenia longicollis, 183
Brisket, 3
Bronchitis, 162
Brooder pneumonia, 111
Bumblefoot, 296
Bunodera linearis, 192
Bursa of Fabricus, 13
distention of, 161
parasites of, 194

328 SUBJECT INDEX

Cc Copperas, toxicity, 283
Copper sulphate, toxicity, 282
Calcium oxide, toxicity, 280 Coracoid, 3
Calomel, toxicity, 281 Corrosive sublimate, disinfectant, 23
Camphor, powdered, 198 toxicity, 279
Canary birds, infectious diseases of, 252 Coryza, 96
fever, 252 Coscoroba swans, 45
Canker, 96 Cotugnia diagonopora, 183
Caponizing cockerels, 302 Creosote oil, 23
ostrich, 311 Cresol, compound solution, 22
Caraway oil, 219 Crop, anatomy, 10, 12
Carbolic acid, disinfectant, 23 eatarrh of, 155
toxicity, 281 impaction of, 156
vermifuge, 236 incision of, 300
Carcinoma, 262 inflammation of, in pigeons, 156
Carpal bones, 4 parasites of, 178
Caruncle, 18 Cropping wattles, 298
Castor oil, toxicity, 282 Crude carbolic acid, 23
Catarrh, 96 petroleum, 216
contagious, 96 Cryptococcus anseris, 194
of crop, 155 Cutaneous emphysema, 297
Catechu, 133, 282 horn, 298
Ceea, 13 Cyclocelum arcuatum, 195
Cercomonas hepatica, 194 mutabile, 192
Cerebellum, 9 Cysto-adenoma, 263
Cestodes, 182 Cytodites nudus, 198
Chalk, powdered, 198 Cytoleichus nudus, 198
Chicken cholera, 34 D
Chiggers, 217
Chigoe, 213 Daphnia pulex, 181
Chilomastix gallinarum, 193 Davainea cantaniana, 183
Chloride of lime, disinfectant, 23 cesticillus, 183
toxicity, 282 erassula, 183
Chlorinated lime, 23 echinobothrida, 183
Choanotenia infundibulum, 183, 184 friedbergeri, 183, 184
Cholera-like septicemias, 42 proglottina, 183, 184
Choléra des poules, 34 tetragona, 183
Cimex columbara, 214 Depluming scabies, 219
inodorus, 214 Dermaglyphus elongatus, 220
lectularia, 213 minor, 220
Circulatory system, 6 varians, 220
Clinostomum commutatum, 192 Dermanyssus galline, 214
Cloaca, 13 Dermestes lardarius, 214
Cloacitis, 167 Diaphragm, 56
Cnemiodocoptes mutans, 218, 219 Diarrhea, simple, 159
Coal tar disinfectants, 23 Digits, 5
Coccidiosis, 127 Diphtheria, avian, 96
Coccidium avium, 127 Discolored yolks, 170
Colds, 96 Diseases of the alimentary tract, 154
Colibacillosis tetraonidarum, 63 of the oviduct, 164
Collodion, styptic, 301 of the peritoneal cavity, 172
Colon bacilli, septicemias caused by, 61 of the respiratory tract, 162
Comb, 18 Disinfectants, 22, 23, 24
frozen, 300 Disinfecting buildings, 22
Compound solution of eresol, 22 Dispharagus hamulosus, 178
Congestion of lungs, 162 laticeps, 178
Connective tissue, mites in, 202 ~ nasutus, 178
Constipation, 160 spiralis, 179

Contagious catarrh, 96 uncinatus, 181

SUBJECT INDEX

Distention of the bursa of Fabricus, 161

Dithyridium variabile, 200

Docophorus icterodes, 29

Double-yolked eggs, 171

Drooping abdomen, 173

Dropsy, 173

Dubbing wattles, 298

Duck cholera, 250

Ducks, infectious diseases of, 242
septicemia of, 249

Duodenum, 12, 13

E

Echinococcus polymorphus, 194
Echinorhynchus polymorphus, 193
Echinostomum conoideum, 192
echinatum, 192
filicollis, 192
recurvatum, 192
sperocephalus, 192
Edema of wattles, 41
Egg, blood spots in, 169
bound, 165
double yolked, 171
eating, 176
soft shelled, 171
structure of, 168
Eimeria avium, 127
Epsom salts, 160, 186
Emphysema, cutaneous, 297
Enteritis, 158
Entero-hepatitis of turkeys, 120
Eosinophiles, 8
Epidermoptes bifurcatus, 220
bilobatus, 220
Episternal process, 3
Epithelioma contagiosum, 96
Epizootic dysentery of fowls and tur-
keys, 43
pneumo-pericarditis in the turkey,
3

Ergot, toxicity, 283

Esophagus, parasites of, 178
External parasites, 208

Exudative septicemia of geese, 243

F

Faleulifer anatina, 220
anserina, 220
cornutus, 220
rostratus, 203, 220

Favus, 116

Feathers, 17

Feather cysts, 265
pulling, 176

Femur, 4

Ferrous sulphate, toxicity, 283
Filaria anatis, 203

clava, 203

cygni, 182

mansoni, 201

spicularia, 238
Fimbriaria fasciolaris, 183
Flagellates, 192
Flea, bird, 212
Flight, prevention of, 300
Flukes, 192
Foot and mouth disease, 142
Foot mange, 218
Formaldehyde gas, 22
Formalin, 22
Fowl cholera, 34

fever, 135

plague, 81

tick, 221

typhoid, 50
Fractures of bones, 298
Freyana chanayi, 220
Frozen comb, 300
Fureculum, 3, 4

G

Gangrene of ovary, 75
Gape worms, 195
Gasoline, 211, 238
Gastritis, 157
Geese, infectious diseases of, 242
Gefliigelpest, 81
General diseases, 150
Generative system, 16
Gizzard, 12
parasites of, 178
Gonglyonema ingluvicola, 179
Goniocotes abdominalis, 209
chrysocephalus, 209
compar, 209
hologaster, 209
rectangulatus, 209
Goniodes colchicus, 209
damicornis, 209
dissimilis, 209
falcicornis, 209
minor, 209
numidanus, 209
parviceps, 209
stylifer, 209
truncatus, 209
Gout, 150
Grouse disease, 62

H

Habits, vicious, 175
Hemomeba danielewskyi, 203

330

Hexmoproteus columbe, 203
danielewskyi, 203
Harvest mites, 217
Heart, 6
Hematozoa, 203
Hemiclepsis tessellata, 195
Hemorrhagic septicemia of fowls, 34
of geese, 242
of the ring dove, 45
of the swan, 46
Heterakis brasiliensis, 188
columbe, 188, 190, 194
compar, 188
compressa, 188
differens, 188
dispar, 188
lineata, 188
papillosa, 188
perspicillum, 188
vesicularis, 188
Holostomum gracile, 192
spherocephalum, 192
Horn, cutaneous, 298
Hiihnercholera, 34
Hiihnerspirillose, 135
Hiihner typhus, 50
Humerus, 4
Hymenolepis anatina, 183
cantaniana, 183
earloca, 183
coronula, 183
fasciata, 183
gracilis, 183
lanceolata, 183, 184
megalops, 183
meleagris, 183
musculosa, 183
parvula, 183
setigera, 183
sinuosa, 183
tenuirostris, 183
Hygiene, 20
Hystrichis cygni, 181
elegans, 181
tricolor, 181

Tleum, 13
Tlium, 4
Impaction of crop, 156
Incision of crop, 300
Incubating periods, 18
Indigestion, 157
in parrots, 158
Infectious diseases of geese and ducks,
242
enteritis of pheasants, 47

SUBJECT INDEX

Infectious entero-hepatitis of turkeys,
120

necrosis of canaries, 252

Inflammation of crop in pigeons, 156
of the oviduct, 164

Infraorbital sinuses, 14

Internal parasites, 178

Intestines, 12

Ipecac, toxicity, 283

Ischium, 4
J
Jejunum, 13
K
Keel, 3
Kerosene emulsion, 215
oil, 213

Kidneys, 16
Killing poultry, 314

L

Laminosioptes cysticola, 202
Large mononuclear leucocytes, 8
Larynx, 14
Lead water, 295
Leg weakness, 153
Leiomyoma, 267
Leucocytes, 7
Leucocytozoa, 204
Leucocytozodn anatis, 205
infection in ducks, 205
infection in ostrich, 239
struthionis, 239
Leukemia, 146
Lice, 208
Limberneck, 154
Linseed oil, raw, 240
Liotheum longicaudum, 209
Lipeurus anatis, 209
anseris, 209
baculus, 209
erassicornis, 209
heterographus, 208
meleagridis, 209
numidez, 209
temporalis, 209
variabilis, 208, 209
Liver, 14
complaint, 88
parasites of, 194
Lophophvton galline, 116
Lungs, 15
congestion of, 162
Lymphatiecs, 7
Lymphocytes, 8

SUBJECT INDEX dol

Lymphoma, 265

Lympho sarcoma, 272

Lynchia maura, 204, 213
livicolor, 204

M

Macroblasts, 8
Maladie du somneil, 30
Malaria, avian, 203
Male fern, toxicity, 285
Malta fever, 143
Manson’s eye worm, 201
Mast cells, 8
Megninia cubitalis, 220
columbe, 220
ginglymura, 220
velata, 220
Megrims of pigeons, 57
Menopon biseriatum, 208, 209
giganteum, 209
longicephalum, 209
numide, 209
obscurum, 209
pallidum, 208
pheostomum, 209
productum, 209
Mercurial ointment, 212
Mercurie chloride, toxicity, 229
Metroliasthes lucida, 183
Metorchis xanthosomus, 194
Microblasts, 8
Micrococcus melitensis, 143
Microlynchia persilla, 204
Mites, 214
in connective tissue, 202
Monas anatis, 193
Monocerecomonas anatis, 193
Mouth, 10
Muscular system, 5
Myelogenous leucocytes, 9
Myxo fibroma, 274
sarcoma, 273

N

Nasal cavity, parasites of, 195
Nervous system, 9

Nest bugs, 214

Nodular teniasis, 185

Nostrils, 14

Notocotyle verrucosa, 192

O

Oidium albicans, 155
Opisthorchis simulans, 194
Ornithonomus eveni, 209
Ornithomyia avicularia, 213

Osteo arthritis in geese and ducks, 246
Osteochondrosarcoma, 267
Ostrich, caponizing, 311
diseases of, 226
Ovary, 16, 17
Oviduct, 16
diseases of, 164
Oxyspirura mansoni, 201

Pr

Palate, 1
Pancreas, 12, 13
Paralysis of the ostrich, 231
of bursa of Fabricus, 194
Parasites, external, 208
internal, 178
of nasal cavity, 195
Parrot septicemia, 54
Parrots, indigestion in, 158
Pasteurella avium, 34
Pasteurellosis avium, 34
Patella, 4
Pectoral muscles, 5
Pelvic bone, 4
Perchloride of iron, 297, 301
Peritoneal cavity, diseases of, 172
Peritonitis, 174
Permanganate of potash, 105
Peste aviaria, 81
Petrol, 238
Petroleum, crude, 216
Phalanges, 5
Pheasants, infectious enteritis in, 47
Phenol, 23
Philopterus cygni, 209
Phosphorus, toxicity, 285
Physaloptera truncata, 178
Pip, 101, 154
Plasmodium danielewskyi, 203
Pneumo-mycosis, 111
Pneumonia, 163
brooder, 111
Poisons, 276
Polymorphonuclear leucocytes, 8
Polyneuritis, 153
Pomegranate root bark, 187
Post-mortem examination, 25
Potassium permanganate, 24, 72
toxicity, 286
Poultry houses, 21
Pox, bird, 96
Prevention of flight, 300
Prolapse of oviduct, 167
Prosthogonimus cuneatus, 195
japonicus, 195
ovatus, 195
in eggs, 169
pellucidus, 179, 195

3a2 SUBJECT INDEX

Proventriculus, 12
parasites of, 178

Pseudo leukemia, 146

Psittacosis of parrots, 54

Pterolichus obtusus, 220

Pterophagus strictus, 220
uncinatus, 220

Pubis, 4

Pulex avium, 212

Pulse rate, 18

Pygostyle, 3

Quail disease, 63
R

Rabies, 142

Rachitis, 152

Red blood corpuscles, 7

Respiration frequency, 19

Respiratory system, 14
tract, diseases of, 162

Rheumatism, 88

Ribs, 3

Ring dove, 45

Rose chafers, toxicity, 287

Round worms, 188

Roup, 96

Rump gland, 17

Rupture of the oviduct, 165

s

Saccharomyces albicans, 155

Salicylic acid, 288

Salmonellosis, avian, 59

Sanitation, 20

Santonin, toxicity, 288

Sarcopsylla gallinacea, 213

Sarcoptes levis, 219
mutans, 218

Sealy leg, 218

Seapula, 3

Schlafkrankheit, 30

Schlafsucht, 30

Schleg’s solution, 220

Sclerostomum anseris, 181

Septie enteritis of cross bills, 259
fever of the canary, 252

of the parrot, 54

Septicemia of ducks, 249
caused by colon bacilli, 61

Shadow cells, 8

Simple diarrhea, 159

Skeleton, 1

Skin, 17

Skull, 1

Sleeping disease, 30

Small mononuclear leucocytes, 8

Sodium chloride, toxicity, 289
fluorid, 210
nitrate, toxicity, 290
salicylate, 197

Soft-shelled eggs, 171

Soil, relation to health, 20

Soor, 155

Spinal cord, 9

Spindle cell sarcoma, 268

Spirocheta anserina, 135
gallinarum, 135

Spirochetosis, 135

Spiroptera emmerzii, 201
pectinifera, 179

Spotted liver, 88

Spur, 5

Staphylococcus pyogenes aureus, 232,

246
Sternostomum rhinolethrum, 195
Sternum, 3
Stomoxysis calcitrans, 99
Streptococcus, 28
eapsulatus gallinarum, 31
Strongylus douglasi, 233
nodularis, 180
quadriradiatus, 190
tenius, 188
Strychnine sulphate, toxicity, 291
Styptie collodion, 301
Suborbital sinuses, 14
Sulphur, flowers of, 211
ointment, 219
toxicity, 293

Swan, hemorrhagic septicemia in, 46

Syngamus bronchialis, 195
trachealis, 195
Syrinx, 15

Tenia exilis, 183
fasciolaris, 183
struthionis, 237

Teniasis, 182

Tapeworm of the ostrich, 237

Tapeworms, 182

Tarso-metatarsal bone, 5

Tartar emetic, toxicity, 293

Temperature, normal, 19

Tenebrio molitor, 214

Thrush, 155

Thorn-headed worms, 192

Thymol, 237

Tibia 4e05

Ticks, 221

Tobacco, vermifuge, 189

Toe pecking, 175

SUBJECT INDEX

Toxicology, 276

Trachea, 15

Trematodes, 192

Treponema gallinarum, 135

Trichomastix eberthi, 193
gallinarum, 193

Trichomonas, 120
columbe, 192
eberthi, 192
gallinarum, 193
pullorum, 195

Trichomoniasis, 193

Trichosoma anatis, 188
annulatum, 179
eaudinflatum, 191
eollare, 191
columbe, 191
econtortum, 181
dubium, 191
gallinum, 191
nodularis, 179
retusum, 190
strumosum, 179

Trichostrongylus douglasi, 233
pergracilis, 63

Trinoton anseris, 209
lituratum, 209
luridum, 209

Tropisurus fissipinus, 181

Trypanosomiasis, 203

Tuberculin, avian, 91
test, 91

Tuberculosis, avian, 88

Tumors, 261

Turbinated bones, 14

Turpentine, 186, 294
U

Ulna, 4

Ureters, 16
Urinary system, 16
Uropygium, 17

V

Veins, 7

Vent gleet, 167
Ventriculus bulbosus, 12
Vertebre, 1

Vertebral column, 1
Vicious habits, 175
Visceral gout, 150
Vitamines, 153

W

Wattles, 18

Weisser Kamm, 116

White blood corpuscles, 7
White comb, 116

White diarrhea, 68
Whitewash, 24

Wireworms in the ostrich, 233
Wishbone, 3

Wounds, 301

ve

Yolks, discolored, 170

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ning the study of microbiology. It is the outgrowth of a lecture course which
has accompanied the laboratory work in bacteriology and protozoology. The
author has endeavored to choose the material that will be of most help to the
student of animal diseases and to avoid as much as possible matters of contro-
versy. In its preparation, the purpose has been to point out the place and role
of micro-organisms in nature; to give the methods for their study and identifi-
cation; to indicate the relation of certain species to animal diseases; to give a
description of the more important species pathogenic for animals; and a brief
discussion of the reaction of the tissues to microbian invasion and the theories
of immunity. In order that the volume be of further aid as a key to the entire
subject, numerous references to the literature are given where the student can
obtain at first hand the results of original research.

THE MACMILLAN COMPANY
Publishers 64-66 Fifth Avenue New York

Medical and Veterinary Entomology

By WILLIAM B. HERMS

Associate Professor of Parasitology in the University of California;
Consulting Parasitologist for the California State
Board of Health, etc.

Cloth, 8vo, illustrated, $4.00
A work of interest to physicians, veterinarians, health officers, and
sanitarians as well as to students. Herein is contained a discussion
of all the more important insects and arachnids relating to disease and
irritations of man and beast. The author has placed special emphasis
on control and prevention. He has aimed to familiarize the student
with the specific parasite treated in a chapter, its identity, life history,
habits, relation to disease transmission or causation, and to indicate
methods for its control and prevention. There are 228 illustrations in

the text, largely made from original photographs or drawings.

General Surgery

By DR. EUGEN FROHNER
Professor in the Royal Veterinary College in Berlin
Third Revised Edition
Authorized Translation by D. HAMMOND UDALL, B.S.A., V.M.D.
Professor of Medicine and Hygiene, N. Y. State Veterinary College,
Ithaca; Major, Veterinary Reserve Corps, U. S. Army
Cloth, 8°, $3.00

The new third edition of general surgery is improved and enlarged
in many respects. The chapter on etiology of tumors has been re-
written, and many additions made. The chapter on botryomycosis has
been newly written to harmonize with the most recent investigations
on this subject. The chapter on tuberculosis has been retained and
even enlarged. The important chapter on chronic deforming ar-
thritis has been supplemented with the results of recent investications
made in D. Frohner’s clinic upon ring-bones, chronic gonitis, and omar-
thritis. Recent investigations on myositis, neuritis, healing of frac-
tures, necrosis bacilli, pseudo-edema bacilli, and foal-lameness have also
been considered.

THE MACMILLAN COMPANY
Publishers 64-66 Fifth Avenue New York

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