The Diseases of the Sweet Pea

THESIS

Pines Nie Omen bACUEIY OF Mie GwADUAREe SCHOOL OF
THE UNIVERSITY OF PENNSYLVANIA IN PARTIAL FUL-
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DEGKEE TOR DOCTORS OF se HiIkOSOREY

J. J. TAUBENHAUS

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PHILADELPHIA
1914

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BULLETIN NO. 106 NOVEMBER,

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Delaware College

Agricultural

xperiment Station

The Diseases of the Sweet Pea

BY J. J. TAUBENHAUS

Newark, Delaware

1914

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Root nov CRhvelavaa tasicola, Zopit)) sia... ot se ee 12—21
Rhizoctonia root rot (Corticium vagum B. & C.) ...... 21—27
Chaetomium root rot (Chaetomium spirochaete Patt.).. 27—30
Fusarium root rot (Fusarium lathyri Taub.).......... 31— 34
Root Knot (Heterodera radicicola [Greef] Muller)...... 30—36
Stem or collar rot (S. libertiana Fckl.) ....... Deeg oo 4 36—41
Powdery mildew, (Oiduim sp:)) saogse eee ee ee 4143
Anthracnose (Glomerella rufomaculans) ...........--. 43—d5
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Diseases not known to be present in this country........ 64—65

Pea blight (Peronospora trifoliorum De By.) ...... 64— 65
Pea spot (Ascochyta prs Wib))) 23322 -o eee 65
Diseased: seed si jie aj akin t ee tenner ence Creer ees 65— 68
Streak disease (Bacillus eee Me 6c Tee) Ga Aa oes cee 68—72
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THE DISEASES OF THE SWEET PEA’

BY J. J. TAUBENHAUS

—

THE HOST
TAXONOMY AND BOTANY

The sweet pea (Lathyrus odoratus Ll.) belongs to the family
Leguminosae, the sub family Papilionaceae, the tribe Vicieae. The
sweet pea (Lathyrus odoratus L.) is a herbaceous vine with rough
stems, hairy and winged. .The leaves are alternate, pinnately com-
pound with terminal tendriliform leaflets. The leaflets are oval or
oblong, mucronate. Peduncles 2-4 flowered, much longer than the
leaves. The calyx teeth are broad, longer than the tube. The flowers
are large, and showy in shades of blue, red, yellow and white. The
standard is large, expanded, hooded, or wavy. The legumes are com-
pressed, linear, 1-3 inches, hairy. The seeds are round, sometimes
angled, black, white or mottled.

HISTORY OF THE SWEET PHA

Origin, Improvement and Distribution,**. The word ‘‘Lathy-
rus’’ is from the Greek La. la (augmentative) and thouros, anything
exciting, having reference to the qualities of seeds of certain species.
In Europe the species of Lathyrus are known as ‘‘Gesse,’’ the sweet
pea being known as Gesse odorante. The French know the plant under
this name, or as Pois Odorante, or Pois de Senteur.”’

The earliest mention of the sweet pea is found in ‘‘Sillabus Plant-
arum Sicilla-nuper detectarum a P. F. Franciscus Cupani’’
(Panormi, 1695). The sweet pea is spoken of as ‘‘Lathyrus distoplat-
yphyllos hirsutis mollis, magno et peramoeno flore odore.’’ Father

*Also presented to the Faculty of the Graduate School of the University of
Pennsylvania, June 1913, as a major thesis in partial fulfillment of the require-
ments for the degree of Doctor of Philosophy.

Acknowledgements.—The writer isindebted to Dr. John W. Harshberger,
under whose direction the work was conducted, for helpful suggestions and erit-
icisms. Acknowledgements are also due to Dr. T. F. Manns for helpful sugges-
tions and advice. Thanks are also due to the many American seedsmen for finan-
cial support in carrying out the field experiments.

** All references will be found on pp. Sto 93.

2

Cupani was very enthusiastic about this flower and in 1699 sent seed
to Dr. Uvedale at Enfield, England, and to Caspar Commelin at Am-
sterdam, Holland. Commelin described and illustrated the plant in
his ‘‘Hort.-Medici Amstelodamensis’’ (1697-1701). Commelin also
adopted Cupani’s name for the plant.

In his ‘‘Almagesti Botanici Mantissa’’ (1700) Dr. Leonard
Plukenet also gives a description of the sweet pea. A dried specimen
preserved in Plukenet’s Herbarium, which now forms part of Sir
Hans Sloane collection, is the oldest specimen of the sweet pea in ex-
istence.

Mention is made of the sweet pea by Petiver in the ‘‘Botanicum
Hortense III’’ (1713). Petiver calls the plant Lathyrus Siculus, a
native of Sicily which has large broad sweet smelling flowers. H. B.
Ruppu in ‘‘Flora Jenensis’’ (Frankfort, 1718) places Lathyrus
Siculus Ravini in a class of plants with irregular flowers. It is thus
seen that all authorities place Sicily as the home of the sweet pea.

Linneus, 1753, in his great ‘‘Systema Plantarum Europe,’’
classifies the sweet pea as follows:

‘‘Odoratus II. Lathyrus peduneulis bifloris, cirrhis
diphyllis, foliis ovato-oblongis, leguminibus hirsutis. Hort.
Cliff. 368, Hort. Upsal. 216, Roy. lugd. 363.

‘*Siculus a. Lathyrus Siculus. Rupp. jen., 210

Lathyrus distoplatyphyllos hirsuitis mollis, magno et per-

ameceno flore odoro. Comm. Hort. 2, p. 219, t. 80.

‘““Zeylanicus b. Lathyrus Zeylanicus. Odorato flore amcene

ex albo et rubro vario. Burm. Zeyl., 138.

““Habitat: a. in Sicilia; b. in Zeylona.”’

Here then is the first use of the term ‘‘odoratus’’ as a distinctive
name.

Kniphof in his ‘‘Botanico in originali’’ (1757-1763) gives a col-
ored illustration of Painted Lady sweet pea. In the catalog of W.
Malcolm (1778), seedsman of Kensington Turnpike, we find offered
for sale, white, purple and Painted Lady sweet peas. The first evi-
dence of improvement is noticed in the catalog of John Mason (1793).
He offered black, purple, scarlet, white and Painted Lady sweet peas.
Between 1845 and 1849 the firm of Messrs. J. Carter & Co. introduced
a new striped sweet pea and a new large purple sweet pea. In 1850
Messrs. Nobel, Cooper and Bolton introduced a new large dark pur-
ple variety. In 1860 Mr. Carter offered several new varieties of sweet

3

peas. In James Vick’s ‘‘Illustrated Catalog and Flower Guide’’
(1870), nine varieties of sweet peas are mentioned.

Beginning with 1880, great strides have been made in the im-
provement of the sweet pea in England. Thomas Laxton and Henry
Eekford (about 1880) were the moving spirits. Mr. Laxton intro-
duced several new varieties obtained by crossing. Mr. Eckford was
responsible for one hundred and fifteen new varieties. In America,
Hdward Sayers in his book ‘‘The American Flower Garden Com-
panion’’ Boston, 1838), gives a list of five varieties of sweet peas. Of
the American pioneers and breeders of the sweet pea, those who should
be mentioned are D. M. Ferry & Co. who in 1889 introdued the
Blanche Ferry; W. Atlee Burpee & Co., Messrs. C. C. Morse & Co.,
J. C. Vaughn and Peter Henderson.

During the first one hundred years of sweet pea culture only three
varieties, or colors, were known, 1. e., purple with blue wings, pale red
with white wings (Painted Lady) and white. The black and the scar-
let appeared in the last years of the eighteenth century. At the pre-
sent time there are more than a hundred and fifty varieties in cultiva-
tion with promising new ones appearing every year. ‘his shows the
great popularity of the sweet pea and the extent to which it is grown.
Whenever a crop is grown extensively and for a long time under cer-
tain soil and climatic conditions, as is the sweet pea, diseases are sure
to appear, making it difficult for the crop to succeed unless precau-
tionary measures are taken. The cultivation of the sweet pea in Eng-
land is at a erisis, the disease factor being the one obstacle to its cul-
tivation. In America sweet pea growers are confronted with several
important diseases.

ECONOMIC IMPORTANCE

I have been unable to obtain statistical data concerning the sweet
pea crop. Messrs. C. C. Morse & Co. furnished us with the following
information :

‘‘Your favor of the 8th inst. was duly received and I shall be very
glad to answer the questions you have asked, as well as I can.

‘“However, our Sweet Peas will be practically a failure this year
and my statistics will apply only to past seasons, probably more ac-
curately to the crop of 1911, which was the best we have had in recent
times. Even last year’s crop was very poor.

4

1. So far as seed is concerned, the Sweet Pea crop is
worth about $250,000 annually to the grower.

2. There are about 1700 acres of land planted to Sweet
Peas for seed in California annually. I have no knowledge
of what acreage is devoted to flowers for market.

3. Practically no Sweet Pea seed is imported and about
one-half of the California acreage is exported.

4. Fully 90 per cent. of the export business is done with
Great Britain; the balance with Holland, Germany and
France.

5. No other country, so far as we know, produces Sweet
Pea seed to amount to anything.
Respectfully yours,
C. C. MORSE & CO.”’’

According to Bailey,, California, in 1902, supplied the world’s
market with 125 tons of sweet pea seeds. As a cut flower the sweet
pea is a great favorite and is extensively grown for that purpose.

CULTIVATION AND CARE

In this connection we will consider only those points of culture
which directly influence the disease factor.

Climate. The sweet pea does best in a temperate region. It
will not stand too warm a climate, as the plants there soon dry up
and die, or they are so weakened as to succumb readily to all sorts of
fungous diseases. California seems to be its ideal home, nevertheless
the sweet pea is known to thrive under various climatic conditions. It
is less susceptible to cold than to heat and in hot dry climates irri-
gation is essential.

Site. The sweet pea requires an open, sunny location so as
to get plenty of light and air. Plants grown in too shady a place
will be spindly, weak, and open to the attacks of diseases.

Sow. All light sandy soils should be avoided for the reason

already referred to above. A good loamy soil is preferred provided,
of course, its subsoil is well underdrained, otherwise the plants will
grow poorly and be constantly open to the attacks of disease.

Fertilzer. In order to be at their best, sweet peas must be
provided with sufficient available plant food in the soil. However,

5

fertilizers should be used very judiciously. The aim should be to apply
a food that is well balanced, i. e., it should contain the proper amount
of nitrogen, phosphorus, potash and lime. Too much of one of these
elements and too little of the other will produce disturbances in the
metabolism of the plant as will be seen later under the discussion of
physiological diseases. For an ordinary garden land, the following
is a well balanced fertilizer devised by Prof. T. F. Manns of the Del.
Expt. Station. Before plowing a surface application of well rotted
manure at the rate of 6 tons per acre is first applied to the soil. After
plowing and harrowing the soil, it is furrowed and 5 tons of rotted
manure per acre is applied in the furrows. The manure is worked in
deep with a spade and the following fertilizer is applied in the
furrows:

*Sodium nitrate 200 lbs. per acre
Dried blood 7x0) MOSS
Acid phosphate WAU) Hose Se 928
Potassium sulphate ZAM Se cs
Rock phosphate 400 sites
Hydrated lime 200 ribs ce oa
Carbonate of lime COOAbs:

The fertilizer is well mixed up with the soil and the seeds are
planted on top and covered to a depth of about two to three inches.

Care of the Seeds and Depth of Sowing. Most of the white-
seeded varieties are subject to decay in the soil. Most of the black-
seeded varieties are more resistant to soil decay but they do not ger-
minate evenly. In order, therefore, to hasten germination, it is ad-
visable to place the seed in tepid water over night. With this treat-.
ment the seeds swell and are ready to be sown the next day. The Rev.
W. T. Hutchins, a well-known sweet peas specialist in America, advises
the placing of the seed in moist earth for seven or eight days. They
are then taken out and examined. The swollen seeds are planted and
the hard seeds cut with a knife to hasten germination. Whatever
method is used the aim should be to hasten germination in order to
prevent the seed from laying too long in the ground and thereby caus-
ing decay. The depth of sowing the seeds varies from two to three
inches according to the nature of the soil. As to distance, five feet

*“This mixture was recommended for a very heavy acid soil deficient in or-
ganic matter.

apart between the rows and three inches in the row will insure ine de-
sired amount of air and light.

Care of the Growing Plants. Frequent cultivations with the
hoe or with the cultivator will provide sufficient aeration of the roots
to insure a vigorous growth of the vine. It is in baked and ill-drained
soils that saprophytic fungi assume the nature of semi parasites, since
it ig in these soils that the plants are often weak and consequently
yield readily to the attacks of disease. Moreover, frequent cultivations
destroy the weeds which may act as disease carriers or disease trans-

A convenient way of trailing sweet peas

mitters. Irrigation wherever possible will no doubt benefit the plants,
but irrigation should not replace cultivation. The plants should
be kept free from the insect and the fungus pests. This will be dis-
cussed under methods of control. With the sweet pea, contrary to
many other flowering plants, the blooms should be gathered freely as
the more we do this the longer the vines will continue to flower.

SWEET PEAS UNDER GLASS

The following notes on cultivation are by Mr. William Sim, Clif-
tondale, Mass., and are extracted from a paper read by him before
the Gardeners’ and Florists’ Club of Boston on April 21, 1908:

‘No grow the sweet pea to perfection under glass you must have
a greenhouse suitable for the purpose. It should be at least eight feet
high on the sides, four and a half feet being glass. My houses are
seven feet, and I find the side rows strike the glass when the vines are
about half grown, thereby giving me half a crop. My center rows are
about right; they are twelve to fifteen feet high. The higher the vines
grow the more and better flowers you get. We plant the rows five
feet apart and in a line with the supports of the greenhouse. The up-
rights are twelve feet apart, so in supporting we run twine from one
support to the other on each side of the row. This I have found the
best method of supporting. I have tried wire netting; it is only a
nuisance, as the vines do not cling to the wire, which causes just as
much tying as if it were not there. It also causes injury many times
to the vines, as a sweet pea stretches many times more than a foot in
developing; if held back by anything in growing the growth looks
like a spiral spring, and the picking of the blooms is made very dif-
ficult. The side rows are planted five feet from the sides of the house;
and all the heating pipes are on the sides. The vines are very suscep-
tible to red spider and as they will not stand syringing, the further
you ean afford economically to have them from the pipes the better.

‘“We have not changed the soil in the houses since they were built
four and five years ago, and we find the vines are getting more vig-
orous each year. In the same soil a crop of tomatoes and of violets
is harvested each year. The soil was originally eighteen inches deep,
but by the application of manure each year the depth is now two and
a half feet. The tomato crop is on the wane the middle of August.
When these are cleaned out we trench the house over as deep as the
soil, bringing the bottom soil to the surface. In the bottom of the
trench we put three inches of decomposed cow manure; one foot from
the surface we put on three inches more of the same material. The
house is allowed to remain in this state until nearly time for sowing
the seed. The soil is then usually very dry, so we dampen it down
enough to cling together while the house gets another forking over.
This time we go down one foot and mix the top layer of manure with
the surface soil. We then make the surface as nearly level as pos-

8

sible and thoroughly water the soil, giving enough to penetrate the
entire mass, with a strong dose of liquid horse manure. In about
three days, depending on the weather, the house will be ready to plant.
We sow the seeds about one and a half inches apart. We make the
drills one inch deep and do not allow more than one inch of soil over
them. We do not pull any more soil toward the roots, as is often
recommended, but let it remain level. If more soil is pulled around
the base of the plant, stem rot is sure to follow. We do not water the
plants again until they are up about three inches.

‘‘Of course, you can grow them on a bench with a few inches of
soil, but the results will be just what you make them—a weak growth
and a crop of short-stemmed flowers. These soon play out, as there is
not enough soil or food for the vines to live on.

‘(They may be made to flower any time you wish by increasing
the temperature, but the best results are obtained by growing at a
temperature just above freezing until the buds can be felt in the
crowns of the plants. Then the temperature should be gradually in-
ereased, say one degree a night, until you reach 48 degrees. This, I
think, is about right, although in midwinter I think they move a little
better at 50. As the days lengthen a little cooler temperature seems
to suit better. A rise of 10 to 15 degrees should be given during the
day in sunny weather. In spells of cloudy weather 55 degrees is high
enough during the day. If a high temperature is given in dark
weather the growth gets soft and wilts when the sun comes out bright
again. While the plants are young they should be regularly fumigat-
ed so there will not be a sign of lice when the plants commence to
flower. If they are clean at this stage it will not be necessary to fumi-
gate while they are in bloom. It is impossible to sell sweet peas that
smell of tobacco. Tobacco also bleaches the flowers of some varieties,
and makes them look like some other variety.

‘(We sometimes hear of someone having trouble with the buds
dropping. This is more the case in midwinter than at any other time,
and is caused by a too cool temperature or a sudden chill, or too much
water. Should a house be allowed to go near the freezing point in
midwniter the wholesale dropping of buds will be sure to follow.”’

9

DISEASES OF THE SWEET PEA
HISTORICAL

The literature on the subject of sweet pea disease previous to 1966
is mostly of a fragmentary nature. In 1896 Cuthbertson, first recoris
a bud and blossom drop of the Cupid sweet pea in Scotland SELON
the cause to cold and damp weather at that time.

In 1906, Massee, gave the first brief scientific account of some
sweet pea diseases, mentioning the following fungi: Peronospora tri-
foliorum, P. viciae, Erysiphe polygoni, and Ascochyta pisi.

In 1906, Weston, was first to describe the ‘‘Streak’’ as a new dis-
ease of the sweet pea in England (the cause not given). In 1907, Wes-
ton, again calls attention to the serious nature of the ‘‘Streak.’’

In 1907, an anonymous note, mentions the following diseases:
eelworm (Tylenchus devastatrix and obtusa), Peronospora trifolio-
rum,, sclerotia of some species of Sclerotinia, Erysiphe martii, and
Botrytis cinerea.

In 1909, in a brief note, Massee, also mentions the ‘‘Streak’’ dis-
ease which he thinks is induced by an excess of manure in the soil.
This excess produces a deleterious effect on the soil flora which in turn
brings about physiological disturbances resulting in the ‘‘streak.’’? In
1912, Massee, again mentions a disease of sweet pea seedlings and of
other plants as due to Thielavia.

In the same year (1912) Chittenden,, before the London Sweet
Pea Society and in an article in the Royal Horticultural Society Jour-
nal reports on the “‘Streak’’ disease, which according to him, was
found to be due to Thielavia basicola.

In 1912, W. Dyke,,, an amateur scientist and gardener, calls
attention to the ‘‘streak’’ disease which he believes is induced by a
species of Fusarium and Macrosporium. It will be seen from the
above reference that the only ones of scientific importance are those
of Massee and Chittenden, because both of these investigators base
their facts on research. However, as it will be shown later, both
Massee and Chittenden mistook Thielavia as the cause of the ‘‘Streak’’
disease.

In American literature, Sheldon,, was the first one to eall atten-
tion to the anthracnose of the sweet pea (Glomerella rufomaculans. )

The diseases of the sweet pea have received no other attention at
the hands of American plant pathologists.

10

For the past three years the writer has been investigating the dis-
eases of the sweet pea, and as a result three papers have already been
published,,.

It is the purpose of the present thesis to bring together all the re-
sults obtained in my investigations. The subject is by no means ex-
hausted, as yet, and we hope to devote many more years to the study
of the diseases of the sweet pea.

THE DISEASES OF THE SWEET PHA

The diseases treated in this thesis are as follows:

J. Fungous Diseases.

II. Bacterial Diseases.

III. Physiological Diseases.

IV. Animal or Insect Pest (Of the animal pests I will only con-
sider the Heterodera radicicola and will discuss it under ‘‘root dis-
eases.’’ Of the insect pests I will only consider the green aphids and
these will be discussed in relation to the ‘‘mosaie.”’

I. Fungous Diseases

A. Root Diseases.
B. Diseases of the Aerial Paris of the Plants.
C. Diseased Seeds.

A. Root Diseases

All root troubles of the sweet pea are caused by fungi which live
primarily in the soil. They can, therefore, also be designated as soil
diseases. Diseased roots invariably indicate an infected soil. All
soil parasites are not necessarily confined to the roots of the sweet
pea only, as we shall have occasion to show later. Of the soil organ-
isms which attack the roots, the following have been investigated:

Root rot. (Thielavia basicola Zopf.)

Root rot. Rhizoctonia (Cortictum Vagum B. & C.)

Root rot. (Chaetomium spirochaete Patt.)

Root rot. (Fusarium lathyri n. sp.)

Root galls Eel worms (Heterodera radicicola. )

ROOT ROT (Thielavia basicola Zopf)

Historical, Synonymy and Relationship. Thielavia basicola
belongs to the ascomycetous family Perisporiacez. The fungus was

11

first described by Berkeley and Broome,, in 1850, who gave it the name
of Torula basicola; they found it growing at the base of affected pea
plants. The torula or chlamydospore stage is the most conspicuous
and it is abundantly found on the host. In 1875, Zopf,, found the
fungus on roots of Senecio elegans in Berlin, and in 1876, Sorokin,,
found it on the roots of Cochlearia armoracia (horse radish) in
Russia, and named it Helminthosporium fragile. Zopf, however, made
a more thorough study of the fungus, and he discovered the perfect
stage, placing it in the Perisporiacex, creating a new genus Thielavia
after Prof. F. von Thielav of the University of Berlin.

In 1886 Sacecardo ,, found the same fungus. Noting the observa-
tions of Sorokin, he did not agree with him in ealling the fungus Hel-
minthosporium, and he placed it in the genus Clasterosporium. Sac-
cardo thus failed to identify Sorokin’s Helminthosporium fragile with
the chlamydospore stage of Thielavia and with Berkeley and
Broome’s Torula basicola. It was to the credit of Sorauer,, who dis-
covered the relationship of these different stages to belong to one and
the same fungus. The name of the fungus with its synonomy is as
follows:

Thielavia basicola (B. & R.) Zopf.
Torula basicola (B. & R.)
Helminthosporium fragile Sor.
Clasterosporium fragile (Sorok.) Sace.

Thielavia a Parasite on Other Hosts. The table on page 12 will
show the list of hosts parasitized by Thielavia together with the au-
thority for the same.

Thielavia Attacking Sweet Peas. In 1912, Chittenden,, was
asked by the National Sweet Pea Society of England to investigate the

dreaded ‘‘Streak’’ disease ofthe sweet pea. In his report before that
society Chittenden gives an accurate description of the ‘‘Streak,’’
so that there can be no doubt but that he had the disease well in mind,
that is, he described it as a stem disease. Chittenden found Thielavia
basicola to be the cause of ‘‘Streak’’ as he states, ‘‘careful micro-
scopic examinations of the brown patches of the roots, and one must
insist on the need for care; hasty examination may fail to reveal any-
thing showing that they were attacked by a fungus wheih turned out
to be Thielavia basicola. The same fungus was present in practically

12

Name of Plant Authority
Avralliaranmnciule kolilayen ai aectee ivoire Selby
Beconiasrulbease ecco aces een er err yoe Ong

Cy Ua ih (=) Cla eesena oe er Ye Woe resits enn os Arc rAueipie Rtn aA Zopt
Catalpartspectosa sess nenrecien cee. era. ee Selby
Cochledriavarmoracian ware mance eae rae Sorokin
Cyclamen Le ete ik Ae ras co rae ie ene Sorokin
Gossyyomuuam lnewoeeswnin sos 550508 bocce s0000ce Smith, HE. F.
eayomatns calli WS ere tmeree re cae ay skowine: ack ea aa es cere tees Zopt
IDIMMENETA), CAMAGCAINGIS; dob osooeeoocGu0ob5 0b on d~O Gilbert
Nema inary aunreuila ta ino: rae erase aoe Berkeley and Broome
INGUCOMNANAE, GAO CULI 5 wea etn ob Soo o coma w oc Selby, Gilbert, Clinton
Omobrychisrerista—— Callies sneer saree Zopt
Oxhisneormmicuilaibar en. set omenet epee acceso serene Gilbert, Stewart
J ETSTUN AMS Ye RNA Nk peR une ee eas nS corsa racy Bic ies eR Berkeley and others
nase Oluis: vile arise e..e Me temmtcr ie erctecne cose Zopt
Mrniloonelllar COCrULER hes. n) naar cokeee aes oe nieme chan ee
VAST GSTAER ISU aKe) CVS) [S\N eene eran ree neuen Srila in Nearer 5 fp Smith, E. F.
Wallepro dora wats: retin sie. aerate Jan aR e aie Thaxter and others
pl Greiticollinnaa’, Ge CN Sets ihe even cree re ares emote Gilbert and Stewart
Bratnvass OMOr aus! 2.5.52 Casual Meera ue ua toe ane acto Taubenhaus

every case, sometimes abundantly fruiting, sometimes with only a few
spores.”’

I will show later where Chittenden has erred in his investigations,
and that the ‘‘streak’’ is not a root but a stem disease which is in-
duced by a bacterium and not by Thielavia. In every case where
Thielavia hag been reported as a parasite on other hosts, it hag been
found on the roots and not on the stem. This same holds true for the
sweet pea. Moreover, Chittenden in his artificial inoculation with the
fungus, has succeeded in reproducing the typical root rot and not the
‘“streak’’ on the stems. Massee,, too made the same mistake as Chit-
tenden, for he too considers Thielavia to be the cause of the ‘‘Streak.’’
I have seen the Thielavia root rot on half an acre of sweet peas at the
trial grounds of one of our commercial seed men. The plants on that
infested area were carefully examined, and no signs of streak could be
found on,the stems. On the other hand, the trouble was seen to be
plainly localized at the roots.

Symptoms of Thielavia Root Rot on Sweet Peas. Plants severely
infected have practically little or no root system since the latter is
destroyed by the fungus as rapidly as the roots appear. (Figs.
land 2). Whatever root system is present is of a stubby nature and

= < Wii bewiinitae sn

4
|

es

Fig. 1*. Root rot caused by Thiclavia. Contrasting a healthy with a diseased

eeWios ah 325, ob
icle (England).

plant of the same age.
7, 33, 34, 35, 37, 39, 40 anc 42, Hlectrotype, Gardener
Photographs by the author.

’s Chron-

14

charred in appearance. The fungus sometimes works upon the stem
to a distance of two to three inches above ground, but never to the
extent of invading the entire stem. It is probably due to this that
some workers have mistaken this disease for the well-known ‘‘streak.”’

eee ay

Fig. 2. Root rot caused by Thielavia. Comparing root systems of healthy plants
with diseased plants of the same age.

15

Sweet peas infested with Thielavia have a dwarfed and sickly appear-
ance. The fungus does not seem to kill it, but merely to produce an
arrested development. The infected plants are useless for commer-
cial purposes, as they fail to set flowers.

Pathogenicity. Chittenden,, seems to have been unable to in-
fect healthy sweet pea seedlings with the fungus Thielavia basicola
under normal conditions of growth. It was only when his plants were
overwatered that the fungus became an active parasite.

In my own inoculation experiments, healthy sweet pea seedlings
have been readily infected by placing a pure culture of the fungus on
the roots of the plants growing in sterile soil. In two to three weeks
the roots were thoroughly diseased. Overwatering was not found nec-
essary to bring about infection, although such treatment as well as
injury to the roots favor the fungus in its activity. Another method
adapted for proving the pathogenicity of the fungus was to sow pure
cultures of the fungus together with sterilized seed (seeds treated in
a solution of formaldehyde, 5 parts in 100 of water for 1-2 hr.)
in sterile pots and soil. Checks were also sown with sterilized seeds
in sterile pots and soil but without the fungus. Six days after sow-
ing both lots of seeds germinated and both check and infected seed-
lings apparently grew equally as well. Beginning with the third
week, infected seedlings ceased growing, whereas the checks made con-
siderable progress. After six weeks the infected seedlings were seen
to be decidedly dwarfed and pale green in color reproducing the typ-
ical symptoms of the disease as observed in the field. The check seed-
lings have by this time made decided growth. An examination of the
roots of the infected seedlings revealed a diseased condition as found
in the field, namely, absence of a well developed root system, and a
blackening of the affected parts. The infection experiments were re-
peated five times always with the same result. In no case was the Thie-
lavia seen to kill the host, but in each case a dwarfed condition of the
plant was the result.

Infection of Sweet Peas with Thielavia from Other Hosts. It
was found desirable to determine whether there existed any racial
strains or physiological species of Thielavia basicola. Accordingly,
pure cultures of the fungus obtained from cowpea, violets, parsnip and
tobacco, were inoculated on sweet peas, using the same method of in-
oculation as previously described. In connection with this experiment

16

a parallel series of inoculations was also run, using the Thielavia basi-
cola from the sweet pea. The results obtained were the same, 1. e. the
Thielavia fungus when taken from other hosts than the sweet pea will
readily infect the sweet pea, thus showing the absence of physiological
strains or species.

Morphology of Thielavia basicola. Our studies and observa-
tions on this fungus have brought out facts found by other investiga-
tors. The mycelium of the fungus is hyalin, septate and branched.
The hyphe average from 3-4" in width. The mycelium becomes more
or less greyish with age. There are three kinds of spore forms pro-
duced. 1. Endospores, so called because they are formed inside a
special thread of the mycelium. This is the spore form that is most
commonly met with in pure cultures of artificial media. The endo-

Fig. 3. Endospores.

Figs. 4, 5. Chlamydospores breaking up into individual spores.
Fig. 6. Chlamydospores, unbroken.

Fig. 7. Ascospores.

Fig. 8. Ascus.

spore case is formed on terminal branches. It has a somewhat swol-
len base and a long tapering cell (Fig. 3). The endospores are form-
ed in the apex of this terminal cell and are pushed out of the rup-
tured end by the growth of the unfragmented protoplasm of the base.
They are hyalin, thin-walled, oblong to linear 10-25x4-5u.

The second kind of spores formed are the chlamydospores (Figs.
4-6). These are thick-walled dark brown bodies, born on the same
mycelium as the endospores, and average from 20-50"x10-184, and
correspond to the Torula stage of Berkeley’s classification.

ny

The third kind of spores are the ascospores (Fig. 7.) These are
lenticular in shape 12x5u and are born in asci which in turn are born
in spherical black perithecia. We have not as yet found the asco-
spore stage (Hig. 8) on the affected host, altho it is said to appear
quite commonly on other hosts affected by this fungus.

Peglion,, in 1897 was apparently the first to grow the fungus
in pure culture. Aderhold,, in 1903 reports to have grown the fun-
gus in pure culture. Clinton,, and Gilbert., experienced considerable
difficulty in obtaining a pure culture of the fungus, due to the fact
that the chlamydospores when taken from old diseased roots fail to
germinate by being overrun with bacteria. At no time did the writer
experience any difficulty in obtaining a pure culture of Thielavia from
diseased sweet pea tissue. The following method was adapted from
Manns,;. Portions of the diseased roots are placed in a test tube in a
solution of 1-1000 HgCl, in a 50 per cent. alcohol and thoroughly
shaken for thirty seconds. This will kill all surface contaminations.
The disinfectant is then poured out and the material is rinsed three
times in sterile water, the object being to remove all traces of mer-
curie chloride. Hach tissue fragment is then taken separately and
crushed with a sterile forceps in a tube of medium which has been melt-
ed and cooled to the proper temperature. The crushed tissue is now
mixed with the medium in the tube, and the whole poured into a petri
dish. After five or six days a pure growth of the fungus appears in
the petri dish. The growth in this case resulted from the mycelium:
which has been crushed and liberated from the deeper tissue.

The fungus will grow on a variety of media. It grows well on
sterilized vegetable plugs as those of potato, beet, carrot, sweet potato,
corn stalks, and parsnip and particularly well on corn meal. Both
endospores and chamydospores are produced on these media, but in no
case did I obtain the perfect stage, although it was often looked for.
Previous investigators too have never succeeded in obtaining the asco-
Spore stage on pure culture.

Pathological Conditions of the Diseased Host. Reference has
been previously made to the fact that the disease produced by Thie-
lavia is confined to the root system. Infected plants have little or no
root system at all, or if present it is charred and invaded by the fun-
gus. The question arises, how do the plants persist such a long time
without collapsing? It was observed that sweet peas affected with

18

Thielavia, constantly make an attempt to produce new roots, but as
fast as they are formed they are invaded by the fungus. It is possi-
ble, therefore, that these new rootlets help the host to persist so long,
and yet not long enough to enable it to make any growth. It is also
probable that there is a close symbiosis between host and parasite with
the latter getting the upper hand. As far as observed from cross sec-
tions of that part of the stem which hes closest to the roots, the fun-
gus is seen to invade all parts of the tissue with the exception of the
xylem vessels. This fact, that the fungus does not enter the conduct-
ing vessels permits an upward movement of the water, and this is suf-
ficient to prevent the host from dying.

ROOT ROT, Corticium vagum B. & C.

Historical data, European literature. The first mention of
Rhizoctonia can be traced to Duhamel,, who in 1728 described a dis-
ease of Saffron (Crocus sativus). He considered the sclerotia to be a
special plant and the hyphe its roots, and named it Tuberoides. In
1782 Fougeroux de Bondaroy,, found asparagus plants which grew
near a diseased saffron field to be likewise affected with Tuberoides.
The first attempt to place the fungus in a systematic position was made
by P. Builliard,, who referred it to the Truffles-as Tuber parasiticum.
Persoon,, placed it in the Genus Sclerotium, and called it Sclerotium
crocorum. De Candolle,, was first to use the name Rhizoctonia. He
at that time distinguished three species, R. crocorum, R. medicaginis,
and R. mali. Nees,, in 1817 refers to a fungus disease of the crocus
which he calls Thanatophytum crocorum. From an examination of
his figures there can be no doubt but that it is Rhizoctonia. In 1830,
Duby, described a fungus disease of Allium ascalonicum and named
it Rhizoctonia allii. In 1843 Leveilleé,, describes Rhizoctonia as at-
tacking Rubia tinctorum, Solanum tuberosum, Phaseolus, and other
plants. (The species of Rhizoctonia is not stated.) In 1851 the
Tulsane,, Brothers placed all the known forms of Rhizoctonia in one
species which they called Rhizoctonia violacea. However, from Kuhn S
eritical work a few years later, it seems advisable to maintain the dis-
tinction between R. solani and R. medicaginis. In Kukn’s,, work
which was published in 1858, a brief account is given of the smooth
sclerotia of R. solani contrasted with the wooly sclerotia of R.
medicaginis. Distinction is also made of R. crocorum and R. medi-
caginis, the latter is stated to attack beets and carrots. In 1903

19

Hrikson;, concerns himself chiefly toward the discovery of biologie
forms of the fungus.

In 1905, Gussow,;, described the disease on potato and lucern, and
he considers R. solani and R. violacea as one and the same.

In 1912 Shaw,, investigated the morphology and parasitism of
Rhizoctonia with a view of obtaining a better understanding of the
supposed different species. Shaw concludes that the name R. violacea
should be retained for all the non-fruiting forms with macrosclero-
tia, and the name Corticium vagum be given to the fruiting stage of
the macrosclerotia of R. violacea, while the forms with microsclerotia
should be identified as R. solani Kuhn.

American Interature on Rhizoctonia. The American references
to Rhizoctonia are as follows:

In 1891 Pammel,, describes a rot of the beet root which he at-
tributes to Rhizoctonia betae Kuhn.

In 1892 Atkinson,, found a sterile fungus causing a damping-off
of cotton, which he ealled ‘‘sore shin.’’ The fungus can no doubt be
referred to as Rhizoctonia. Later, Stone and Smith,, give an account
of a lettuce disease due to Rhizoctonia.

In 1901 Duggar and Stewart,, describe extensively a list of hosts
attacked by Rhizoctonia. However, the species of the fungus is not
given.

In 1904 Rolfs,, reports on a potato disease due to Rhizoctonia, in
which he found the fertile stage Corticium vagum B. and C. Speci-
mens were sent by Rolfs to Dr. E. A. Burt, who pronounced it a va-
riety of Corticium vagum B. and C. and for which he has suggested
the name Corticium vagum B. and C. var. solani Burt.

In 1909 Stevens and Hall,, described a disease of the apple, pear
and quince, which they attributed to a sterile fungus Hypochnus och-
roleuca Noack. The fungus is described as having small sclerotia and
there is no doubt but that it is a Rhizoctonia. Several workers have
claimed to have connected different fruiting stages with that of
Rhizoctonia. In 1869 Fuckel,, stated that the Ascomycete Byssothe-
cium circinans F'ckl. was the perfect form of Rhizoctonia, both stages
were found on decaying stems of Medicago sativa. Prunet,, also ob-
served this association of Rhizoctonia on lucern with an ascomycete.

Haritig,, found a Rosellinia associated with a Rhizoctonia on the
roots of oak.

20

Frank,, reports Rhizoctonia violacea on grapes to be associated
with Thelephora, which he named Th. rhizoctoniw. However, none of
the above authors have carried on any cultural work to prove the val-
idity of their claims, hence none of the statements can be accepted
as valid.

Rolfs,, found a basidiomycete associated with Rhizoctonia on
potato. Pure cultures obtained from spores of the basidiomycete
always gave a Rhizoctonia, thus proving definitely the relationship of
the two forms. Rolfs basidiomycete is already known as Corticium
vagum B. and C.

American, European and East Indian Hosts Subject to the
Attacks of Rhizoctoma.

Name of Host

SUDEEPNSY [OY(0) eee rere nen ae aaes Meme Nne A rerekt te Ta Duggar

SAMO AT ets tesees, Seue hoses oko ee ‘¢ ,Leveille

CMRI OG tee Mae siete beeline i i iatee a mee eR ae sf

Celera ti teat eargsr eyes Oe date a eae Mey eee ns ee a a

COIL WPS eRe ees a Cen aoe Oi, Ota RN Ey oa hea ae

NSN UNC CEC tet ates oN GE Naga sles anor na CeO is

[OOUA Osean Seaetra nie rohan ena a ear als Uist ‘¢ , Leveille, Rolfs.
KOTO. CUS otis e erie ata Cerin euies Re MRC eR cin Gene ann Duhamel, Bulliard, Pers.
ONS) OB Ce MEAD IS teenie pee aati eae My AM. “A i 25 Fougeroux

ERNOBOHESS Op meee, cermin. Tmeniata an Wey gamer sh arg WG Duby

ROUGE Grate rape cre ca men fee eter aat inne Penni We Kuhn

SrreOuMN Ge TANT aise asta eet sil atc seer eaten ee nO Shaw

cowpea. ..... Sey Sah RN Pra gine aM can 3

ph lat vee irs Meas cok rey fe me gaat ir A oe

SOV iv.ot coed ail inhine yl aoe a benyaainin e Sy waegke eer ost

TOOT OMe ersac A ONL Gat ee ciel age cele cs oe ee peg ae

SIWECTRDCA. Cue siae a aks ine cone | gerne ene erage Taubenhaus

Rhizoctonia Attacking Sweet Peas. As far as could be ascer-
tained no mention could be found in literature of a Rhizoctonia dis-
ease of sweet peas. I have observed it during winters of 1911 and
1912 on greenhouse specimens sent in by different sweet pea growers.
In the fall of 1913, diseased sweet pea seedlings attacked with Rhiz-
octonia were collected in the greenhouse of the University of Penn-
sylvania. From correspondence with Plant Pathologists, A. D. Selby
reports it in Ohio, W. G. Sackett in Colorado and E. C. Stackman in
Minnesota. There seems no doubt but that the Rhizoctonia root rot
of sweet pea is much more widespread than is reported.

21

Symptoms of the Disease. Severely infected plants have prac-
tically no root system (Fig. 9). In less infected plants only one or two
rootlets may be destroyed. The fungus produces a browning effect of

f

Fig. 9. Root rot caused by Rhizoctonia. (A) healthy. (B) diseased.

the root before total destruction sets in. In very early stages of infec-
tion the seedlings are seen to have a wilted appearance; as the disease
progresses the infected seedlings fall over and collapse. The fungus
is not often confined to the roots alone. It is often seen to work its
way up the stem and this may produce a constricted area which marks
it off from the healthy part. The fungus being a soil organism, it is
usually introduced with manure; infection can take place at any part

22

of the roots, or at the stem near the roots. When the latter is the case
reddish sunken spots are observed at the base of the stem. It seems
that only young seedlings can be quickly destroyed by the fungus
whereas older plants seem to linger for considerable time altho such
plants remain dwarfed, sickly looking and valueless for commercial
purposes.

Pathogenicity. The pathogenicity of the sweet pea Rhizoc-
tonia is readily proven by planting sterilized seeds in sterile soil and
pots which were inoculated with a pure culture of the fungus. The
best material to use is somewhat old cultures which have well devel-
oped sclerotia. It is from the latter that the fungus begins to vegetate
and to spread in the soil. Five pots were inoculated with the fungus
and two were kept as checks. The checks germinated and grew well,
whereas none of the seeds germinated in the infected pots (Fig. 9a).
In digging out some of these seeds they were found to be invaded with
the fungus hyphe of the Rhizoctonia. A pure culture may be readily
obtained from these seeds, thus proving that the Rhizoctonia is a path-
ogenic organisms. Young seedlings may likewise be infected by the
fungus, but as already indicated older plants are more resistant as
they can live for some time with the fungus on them.

Morphology and Identity of the Sweet Pea Rhizoctonia. So
far as my studies have gone, only two stages have been found of the
sweet pea Rhizoctonia.

1. The Rhizoctonia stage—This consists of long and narrow
hyphal branches varying in color from hyalin to reddish brown (Fig.
10). These hyphe are either aerial or are embedded in the substratum,
varying according to the media on which it is grown. It is this hyphal
growth which is most active in the parasitism of the fungus.

2. The Sclerotial stage.—In cultures which are from three to four
weeks old numerous sclerotia are formed. These sclerotia are made
up of closely interwoven short barrel-shaped hyphae (Fig. 11).

According to Shaw,, Rhizoctonia solani Kuhn produces only mic-
rosclerotia while Corticium vagum B. and C. produces macrosclerotia.
After repeated attempts the corticium stage of the sweet pea Rhizoc-
tonia could not be obtained on artificial media. This accords with the
findings of Shaw and Rolfs who could not obtain the perfect stage on
culture media but found it several times on the affected host. How-
ever, as the sweet pea Rhizoctonia produces macrosclerotia and as

23

Fig. 9A. Root rot caused by Rhizoctonia. To the right the soil was inoculated
with the fungus, resulting in no germination. At the left the soil was free from
the fungus, resulting in good germination.

already pointed out by Shaw the maerosclerotia produce the Corticium
stage: the sweet pea organism is therefore referred to as Corticium
vagum B. and C.

Pathological Conditions of the Host. The Rhizoctonia fungus
when attacking other hosts, is known to be confined primarily to the
cambium layer of the plant. With the sweet pea, conditions are sim-

24

ilar. The fungus attacks the phloem of the bundles and makes its way
into the parenchyma cells as well as to the epidermal cells. The ef-
fect produced is loss of turgidity, wilting, and early collapse of the

11

Fig. 10. Young hyphae of Rhizoctonia from sweet pea.
Fig. 11. Barrel shaped hyphae from sclerotium of the same fungus.

host. Infection may take place in the base of stem first and in this
case the fungus invades both stem and root, or it may start at the roots
first, then gradually work up to the stem. In either case death of the
seedling is a natural consequence. In cases where the roots are first
attacked by the fungus, the former deteriorates so rapidly that when
pulling out a plant, it is found to be without any root system.

CHAETOMIUM ROOT ROT, Chaetomium spirochaete Patt.

Historical. In the fall of 1912 Prof. A. C. Beal of Cornell Uni-
versity sent me specimens of diseased sweet peas grown in the green-
house for diagnosing the cause of the trouble. The disease was readily
located in the roots. A fungus was found invading the interior tis-
sue of the latter but no fruiting stage of any kind could be found
which would help to identify the fungus. Crush cultures were made
at once from the diseased tissue, the method employed being the same

29

as that described for Thielavia basicola. Some forty poured plates
of nutrient agar were made in all. In 5 days a pure culture of a
fungus appeared in all the plates with the exception of one which
showed a Fusarium. The cultures were watched closely and in two
weeks perithecia-like bodies developed in abundance but no spores
were formed. The fungus proved to be an ascomycete belonging to the
genus Chaetomium, and determined by Mrs. Flora Patterson as C.
spirochaete Patt. In mid-winter of that same year, more diseased
specimens were sent to me from a florist in Illinois. These specimens
showed the same symptoms as those observed on Prof. Beal’s material
and in this case, too, the trouble was confined to the roots. As pre-
viously stated, no fruiting stage was found on the affected tissue.
Cultures made from this material gave a pure growth of Chaetomium
spirochaete. A search through the literature failed to show the re-
cord of any of the known Chaetomiums to be parasitic on living plants.
It is known for instance that C. arachnoides Massee, C. simile Massee,
C. bostrychoides Zopf and C. murorum Cda., all grow on dung of
various animals.

Reinke and Berthold, in their studies of the fungous diseases of
the potato report to have found Chaetomium bostrychoides Zopf and
C. erispatum Fekl. growing on rotted tubers. The above authors
state that when germinated spores are placed on a cut surface of a
healthy tuber they fail to penetrate the same, indicating the sapro-
phytic nature of the fungus. Its presence on the decayed potatoes
must have been secondary. The present thesis gives the first record
of the parasitic nature of Chaetomium.

Pathogenicity. The fact that a pure culture of C. spirochaete
was obtained from numerous platings of diseased material obtained
from two different states at once led to the supposition that the organ-
ism was the cause of the disease. In order, therefore, to test out the
pathogenicity of the fungus, the following experiments were tried.
Out of ten sterilized pots and soil, five were sown with sterilized seeds
(these were soaked in a solution of formaldehyde, 5 parts in 100 of
water for one-half hour) inoculated with a pure culture of the fungus
broken up in sterilized water. In the remaining five pots sterilized
seeds were sown without the fungus to serve as checks. Both lots of
seeds germinated and the seedlings of both the inoculated and the
check pots seemed to grow well for about three weeks. After that time

26

the seedlings in the inoculated lots appeared to lose their green color
and to become paler and yellow. The infected plants could be readily
pulled out from the soil and the rootlets appeared to be half rotted
by the fungus, whereas the check seedlings did not exhibit such
symptoms. Cultures made by surface sterilizing the affected rootlets
readily gave pure cultures of Chaetomium spirochaete. The experi-
ment was repeated once more and this time, both checks and inocu-
lated seedlings were watered frequently, care being taken to keep the
soil very moist or even wet. This was accomplished by allowing the
dish to remain filled with water in which the pots stood. In this case
the checks again remained healthy, but after three weeks the inocu-
lated seedlings had their roots mostly destroyed by the fungus; the
infected seedlings could be readily pulled out from the soil. This
time the greatest part of the root system was destroyed. Cultures
made from parts of the remaining infected roots readily gave pure
cultures of the fungus.

From these experiments it is shown that Chaetomium spirochaete
altho perhaps a saprophyte will, under certain conditions, assume a
parasitic nature on sweet peas. It was further shown that in poorly
drained soils the viruient nature of the organisms becomes more pro-
nouneed.

Morphology and Physiology of the Fungus. The mycelium of
the fungus is hyalin, closely septate and branched (Fig. 12) when
grown in the substratum of the media. The aerial mycelium consists
of long unbranched filaments and vary in color from very light %o
deep lemon. This seems to be produced within the fungous hyphae
and later the yellow color is also transmitted to the media in which
it grows.

Reinke and Berithold,, report to have found a conidial stage con-
nected with C. crispatum. In our work we have as yet not found any
conidial stage of C. Spirochaete. As previously stated, we have not
found any fruiting stages of the fungus on the affected host. In pure
culture in artificial media perithecia appear in two weeks from the
time of planting and in three weeks mature asci with spores are also
formed. The perithecia are covered with darkish brown hair-like
appendages, thus giving it a bristly appearance. The hairs are coiled
at the apex and septate at different intervals; they are covered with
very minute pointed warts (Fig. 13). The asci are very evanescent

27

Figs. 12-15. Showing (12) mycelium of Chaetomium spirochaete. 13, hairs. 14
and 15, asci. 16, ascospores.

and can only be seen in young cultures. In old cultures the ascus
wall readily breaks so that it is difficult to make out the arrangement
of the ascospores. There are 8 ascospores to an ascus (Fig. 14-15).
The ascospores are apiculate (Fig. 16) at both ends. The wall of the
ascospore is smooth, light brown when young and dark when old. The
ascospores readily germinate in a sweet pea broth which is made up
as follows:

Take 15 grams of ground sweet pea seeds to 1000 ee of water.
Bring to a boil, filter, then add 15 grams of agar; bring to a boil,
then filter, tube and sterilize in the autoclave for 15 minutes at 15
pounds pressure.

\

FUSARIUM ROOT ROT, Fusarium lathyri n. sp.

Historical. It seems that Tulasne,, was the first to recognize
the parasitic nature of Fusarium. In 1883 Hansen,, describes a dis-
ease on oats which is attributed to Fusarium graminum Corda. In
1884 Worthington Smith,, describes a wheat disease due to Fusispor-

28

jum (Fusarium)’culmorum W. Sm., and another disease on barley due
to Fusarium hordei W. Sm. In 1889 EH. F. Smith,, mentions different
related Fusaria isolated from the soil which play the role of plant
pathogens. The species of the Fusarium are not given. In the same
year, in their excellent report on the loose smut of wheat, Kellerman
& Swingle,, report on a Fusarium which lives as a parasite on the loose
smut of wheat and which they named Fusarium ustilaginis K. & Sw.
In 1892 Frank,, reports Fusarium heterosporium Nees, a parasite on
several graminaceous hosts. In the same year Atkinson,, reports on a
cotton disease due to Fusarium vasinfectum. In 1893 Rostrup,, de-
scribed an oat disease due to Fusarium avenaceum. In 1899, Smith,,
describes a disease of cotton, watermelon, cowpeas, and melons as
due to a Fusarium whose perfect stage was believed to be Neocosmo-
pora vasinfecta. In 1899 Woods,. reports on a disease of Chinese
asters due to a Fusarium. In 1900 Manguin,, reports on the parasitic
nature of Fusarium roseum. In 1901 Prillieux and Delacroix,, report-
ed on a carnation disease due to F. dianthi. In 1901 Bolley,., reports
on a flax disease due to Fusarium lini. In 1901 Sorauer,, reports on a
rye disease due to Fusarium nivale. In the same year Pammel,, re-
ports on a wheat disease due to Fusarium roseum Lk. In 1902 Smith,,
reports extensively on a wilt of Chinese Aster the same disease as pre-
viously reported by Woods, . In 1902 Hennings,, describes a disease
on the black locust which he attributes to Fusarium vogelii. In 1903
Van Hall,, describes a pea disease which he attributes to Fusarium
vasinfectum Atk. var. Pisi. In 1904 Smith and Swingle,, reports on
the dry rot of potatoes due to Fusarium oxysporum. In the same year
Osterwalder,, reports on a fruit rot due to F. putrefaciens. In 1905
Owen,, reports on a tomato disease which he attributes to Fusarium
erubescens Appel. and v. Oven. This fungus is claimed to be differ-
ent from Fusarium solani, F. putrefaciens and F. Lycopersici. In
1906 Appel and Schikarra,, report on different species of Fusaria
which induce disease in plants. In the same year Heald,, reports
on a bud rot of carnations due to a species of Fusarium. In 1906
Hedgeock,, in his extended studies of chromogenic fungi reports
Fusarium roseum as capable of discoloring wood. In 1907 Chifflot,,
reports on a pelargonium disease due to Fusarium pelargonii. In 1909
in their extended studies on corn rots, Burrill and Barrett, report on
three species of Fusaria which attack the ear of corn. In 1910 Wolf,,
reports on a pansy disease as due to Fusarium. In ‘the same year

29

Smith ,, reports on a banana disease due to Fusarium, and Cook,, re-
ports on the double blossom due to Fusarium rubi. In 1911 Bubak,,
describes a rot on ears of corn due to Fusarium maydiperdum. In
1912 Gifford,, reports extensively on a damping off disease of con-
iferous seedlings due to Fusarium, the species not stated. There are of
course many more Fusaria described, but the aim in this brief his-
torical sketch is to mention the literature which bears more or less
directly on the parasitic nature of Fusarium. In a very recent paper
Wollenweber,, describes several species of Fusaria parasitic on the
potato. He also emphasizes the importance of morphological studies
as well as infection experiments as the basis of classification in Fusaria.

Fusarium Root Rot of Sweet Pea. There is no record in the
literature of a Fusarium disease of the sweet pea. Several complaints
from florists have shown that they could not grow sweet peas under
greenhouse conditions because of a root rot which developed early and
in some eases destroyed the entire planting. Cultures made from the
infected material or from the infected soil, and from seedlings sown
in the laboratory on the infected soil, gave in each case a pure cul-
ture of Fusarium.

Symptoms. ‘The first symptom of the disease is a sudden flag-
ging of the leaves accompanied by general wilting and collapse of the
seedling. Usually upon sowing the seeds a fair percentage germinate
and reach the height of about 8 to 10 inches when they are attacked
by the fungus. If the collapsed seedlings are allowed to remain on
the ground, the stems will soon be covered with the sickle shaped
spores. Eventually the decayed tissue rots and disintegrates and is
soon invaded by small fruit flies which now begin to distribute the fun-
gus from place to place by carrying its spores.

Pathogenicity. The pathogenicity of this fungus is readily -
proven by inoculating with a pure culture of the organism sterilized
seeds planted in sterile soil. The seed germinate and reach a height of
7 to 8 inches but soon succumb to the attacks of the fungus. The fun-
gus can be reisolated from the artificially infected seedlings and the
disease induced at will (Fig. 17). The checks remain healthy pro-
vided of course all means of contamination are guarded against.

Morphology of the Fungus. The mycelium of the fungus is
hyalin, septate and branched. At an early age the hyphae begin to

30

Fig. 17. Fusarium wilt or root rot. At left, healthy; at right, infected.

form chlamydospores. These are round hyalin bodies often filled
with oil globules and are formed in the center of the hypha (Fig. 18),
in this case the contents of the former collect into the chlamydospores.
Usually also the chlamydospores are born at the tip end of the hyphae
in chains of twos, threes and even fours (Figs. 19-22). Old cultures
are practically one mass of chlamydospores. There are also two
spore forms present and these appear as early as the third day in the
pure culture. These are microconidia which are fairly abundant and
macroconidia, varying from two celled to four celled. The average
form is the three celled. Both micro- and macro- conidia are hyalin
and smooth (Figs. 23-31). In old cultures the macroconidia shrink
so that the septa become slightly pronounced (Figs. 25, 28-29). These
old macroconidia soon lose their protoplasm or the latter breaks up

dl

presenting a granular appearance. In young cultures the outer wall
of the chlamydospore is smooth, but in old cultures it becomes slightly
warty or covered with minute points (Fig. 19). No perfect stage has
been found to accompany this fungus either in pure culture or on
the host.

Figs. 18-32. Fusarium lathvri. showing chlamydospores and conidia.

Identity of the Fungus. There is no doubt but that the fun-
gus belongs to the genus Fusarium. It produces its micro- and macro-
spores (sickle shaped) as well as chlamydospores which according ‘%o
Wollenweber,, are true characteristics of the genus Fusarium. The
fungus has been grown in pure culture (Fig. 32) and on different
media for two years and no perfect stage has ever appeared. Unless
further studies prove differently it seems that the present Fusarium
is a new species and the name Fusarium lathyri n. sp. is tentatively
given to it. A description of the fungus follows:

Sporodochia slightly erumpent to superficial on the host, but not
always present on culture media. Macroconidia sickle-shaped, slight-
ly curved and fitting into the section Martiella of Wollenweber, 2 to
4 septate, the majority being three septate, 15.8x4.2u—30.8x5.6".
Microconidia elliptical to oval 9.8x2.8u—14x3.50¥. Chlamydospores
spherical, thick walled and spinulate when old, 7.3"-9¥ borne singly or
in chains of twos, threes and sometimes in fours.

ROOT ROT OR EEL WORM, Heterodera radicicola (Greef) Muller

Altho not belonging to the domain of this thesis the eel worm is
here considered, first because of the important root knot disease it

32

produces, and the second, because it opens the way to several fungous”
parasites.

Heterodera radicicola attacking many hosts. The eel worm is
of an omnivorous nature. Marcinowski,, gives a list of 235 species
of plants affected with the pest. Almost all of the more important
families of flowering plants are present in the list, as well as one gym-
nosperm and a fern. The plants include both Monocotyledons and
dicotyledons, herbs, woody plants, annuals and perennials. Many of
our garden plants and field crops are attacked by the pest.

Of the plants said not to be affected by Heterodera, Bessey,, cites
the following hosts: Crab grass (Syntherisma sanguinalis), redtop
(Agrostis alba), Johnson grass (Andropogon halepensis), some varie-
ties of oats (Avena sativa), Bromus schraderi, Eustachys petrea,

=

lon

Fig. 32. Pure culture of Eee lathyri. the cause of sweet pea
wi

some varieties of barley (Hordeum vulgare), perennial rye grass,
Lolium perenne, Hchinochioa frumentacea, Panicum miliaceum, Pen-

nisteum sp. timothy (Phleum pratense), rye (Secale cereale), Andro-

pogon sorghum, Triticum, maize (Zea mays), Huchlaena luxurians,

Bidens leucantha, B. bipinnata, Gnaphalium purpurem, Helenium

cenuifolium, some species of Solidago and Zinnia.

e

33

Heterodera attacking sweet peas. In his excellent work on
the root knot Bessey,, mentions the sweet pea as attacked by Heier-
odera radicicola. Chittenden,, found the eel worm associated with
Thielavia root rot.

In my own investigations I have found the eel worm capable of
producing the root knot. I have often found this pest to be asso-
ciated with Rhizoctonia. It seems very probable that the Heterodera
worm in the case of the sweet pea opens the way to the attacks of
Rhizoctonia and several other fungi. Heterodera radicicola often
produces the greatest amount of damage in light sandy soil, but seems
unable to thrive in heavy elay soils. In every case where seen by the
writer or where reported by florists and seedsmen the eel worm was
most troublesome where sweet peas have been grown on too light soils
in the greenhouse. No sweet peas have been reported to be attacked
by the eel worm out of doors.

Symptoms. The disease is characterized by swellings on the
roots. These are either small swellings formed singly, in pairs, or in
strings, thus giving the affected root a beaded condition (Fig. 33) or
the swellings may be very large so as to be mistaken for root nodules.
However, these galls cannot be mistaken for the normal root nodules,
because the latter are lobed and are attached at one end (Fig. 34),
whereas the root gall produces a swelling of the entire surface of the
part affected. Infected plants usually linger for a long time, but they
can be distinguished by a thin growth and yellow sickly looking leaves
and stems.

B. Diseases of the Aerial Parts of the Plant

STEM OR COLLAR ROT, Sclerotinia libertiana Fckl.
Synonomy.

Sclerotinia libertiana Fckl.
Peziza sclerotiorum Lib.
Sclerotinia libertiana Fekl.
‘* Kaufmanniana
> _Postuma Bo & W:.
‘* ~~ Coemansii Kick.

‘“ selerotiorum Br.

Sclerotinia sclerotiorum Ad.

34

History of Sclerotinia libertiana Fckl. as a Plant Disease Pro-
ducer. In 1860 Coemans,, was the first to record a disease of carrots
and ‘turnip which he attributed to Sclerotinia libertiana (Peziza
sclerotium). In 1886 De Bary,, also reports on a disease of turnips

t

ey

as

E:

hades Me ay Pk a
33 : 34

Fig. 33. Sweet pea roots affected with eel worm.

Fig. 34. Sweet pea nodules formed by nitrogen fixing bacteria.

and carrots due to S. libertiana. In 1887 Cohn,, reports on a potato

disease due to the same fungus. Smith,, in 1890 reports on a holly-

hock disease due to Sclerotiana libertiana. In 1891 Behrens,; reports

on a hemp disease due to this fungus. In 1892 Humphrey,, reports

30

on a lettuce disease which he thought was due to Botrytis cinerea, the
then supposed conidial stage of Sclerotinia libertiana. Humphrey
again in 1893 reports on a cucumber disease due to Selerotinia lib-
ertiana. In 1897 Prillieux and Delacroix,, report on an important
mulberry disease due to this same fungus. In 1900 in his extended
studies on Sclerotinia, Smith,, reports on the omnivorous nature of
S. libertiana. Hedgecock,, in 1905 reports on a serious disease of cab-
bage and cauliflower due to S. libertiana. In the same year Parisot,,,
reports on a disease of Jerusalem artichokes in the western part of
France and due to this same fungus. He also mentions the potato,
bean, corn, carrot, turnip, rutabaga and flax as all being subject to the
same disease. In 1906 Appel and Bruch,,, also report on a similar
disease of turnip and parsnips. Masseron,,, in 1907 reports this fun-
gus to produce a serious disease on the garden and field pea. In 1911
Westerdijk,,, reports a wide range of hosts to be attacked by the fun-
gus such as rape, cabbage, cauliflower, kohlrabi, sesame, bean, pea,
vetch, clover, lettuce, Jerusalem artichoke, dahlia, zinnia, sugar beets,
carrots, turnips, parsnips and beets.

Sclerotinia libertiana Fekl., a Fungous Disease of the Sweet
Pea. As far as I could ascertain there is no mention in literature
of S. libertiana attacking the sweet pea. I have first noticed this dis-
ease on greenhouse specimeng sent in by a grower in Pennsylvania.
My first record of the disease appeared in the Florist Exchange,,,.
Observations so far seem to show that the disease is limited to sweet
peas under greenhouse conditions only. A special effort was made
to find this disease out of doors but without success. It is well known
that under certain conditions unfavorable to the host the fungus can
attack a variety of hosts which grow in the open. That the fungus has
not been found so far to attack sweet peas out of doors does not limit
its appearance in the field at any time that climatic conditions are un-
favorable to the host.

Symptoms. This is usually a seedling disease (Figs. 35-36)
altho it may attack plants of all ages (Fig. 36).* And it is most severe
in poorly ventilated houses or in beds which are overwatered and
which lack proper drainage. The disease when present does its work
quickly. Affected plants first show a wilting of the tip and flagging

*Figs. 36, 41. Electrotype, Florists’ Exchange. Photographs by the author.

36

of the leaves and then the seedlings fall over and collapse. The fun-
gus Sclerotinia libertiana, altho a soil organism cannot attack the roots
of its host. The fungus penetrates the collar of the stem and complete-
ly invades the vessels of the host, thus checking the upward flow of the
water from “he roots. Freshly collapsed plants have a watersoaked

(b and ¢)

(a) healthy plants.

infected seedlings.

a
Fig. 35. Sclerotinia wilt of sweet pea se edlings.

~ Aas

appearance, later to be overrun with a white weft of fungus mycelium,
finally to be followed by selerotia which are found here and there on or
within the affected stems.

37

Pathogenicity. In order to establish definitely the relation-
ship of the fungus to this disease of sweet peas under glass, sterilized
seeds were planted in sterilized pots and soil in the laboratory. All
the seeds germinated and the plants were allowed to grow for three
weeks, in a perfectly healthy state. Then the pots were divided in

"——S = =

Fig. 56. Damping off caused by sclerotinia.

two lots; one lot was left as a check and the other lot was inoculated
with the pure culture of the Sclerotinia by introducing pieces of the
fungus in the soil. Both lots, check and infected plants, were covered
with bell jars to imitate the moisture conditions of the greenhouse.

08

After four to six days, wilting of the inoculated seedlings began,
whereas the checks remained healthy. This was repeated several
times with always the same results. This conclusively shows that the
fungus Sclerotinia libertiana is able, when present in the soil, to pro-
duce a disease on sweet peas under glass. The fungus is usually
brought into the greenhouse with the soil, or with the manure. Cross
inoculation with the fungus from the sweet pea, lettuce, turnip and
cucumber on the sweet pea produced typical cases of wilt, thus proy-
ing conclusively that the fungus from the sweet pea is the same as
the Sclerotinia libertiana of the hosts mentioned above.

Identity of the Fungus. The fungus from the sweet pea was
run on artificial media with parallel cultures of S. libertiana from let-
tuce, cowpea and cucumber. There was no difference observed in the
manner of growth nor of sclerotial formation of these strains. Under
pathogenicity, I have shown that cultures of S. libertiana obtained
from hosts such ag lettuce, turnip and cucumber readily produced
the typical wilt of the sweet pea similar to that obtained when inocu-
lations are made with the fungus from the sweet pea on the sweet pea.
In order to further verify the identity of the fungus, sclerotia from
cultures three months old were placed in small flat covered chambers
containing sterile moist sand. These were placed outdoors in the cold
for four weeks, then brought in the laboratory and kept at room tem-
perature. The moisture was maintained by adding every three to
four days some sterile water. In nine weeks the sclerotia germinated
by sending out from each a number of grayish stalks, and in two
weeks the apothecia developed at the tip of the stalks. In shape and
measurement of asci and ascospores the fungus answered in every de-
scription that of Sclerotinia libertiana.

Morphology of the Fungus. In my work I find no conidial
stage of a Botrytis type or of any other type to be connected with
Sclerotinia libertiana of the sweet pea. This is in accord with the
studies made by Smith, R. E.,,.. There seems no doubt but that Bot-
rytis cinerea which is often found to accompany S. libertiana is in no
way connected with the former.

POWDERY MILDEW, Erysiphe polygon?
The sweet pea mildew was first described by Massee,,, as
being prevalent in England. Erysiphe polygoni was attributed
as the cause, both of sweet pea mildew and that of the edible

39

garden pea. In this country Stewart,,, was the first to record
a powdery mildew on the sweet pea. However, Stewart did not
find the perithecial stage, and hence the fungus was not deter-
mined. The powdery mildew is a very prevalent disease on

"eee eae ae

|
|
|
Bee eee peste pa a

Fig. 37. Anthracnose disease of sweet pea on stem and peduncles,

40

greenhouse sweet peas, and on irrigated fields or where they are plant-
ed on a large scale for seeds. Ordinarily, however, in small garden
lots, and especially where the plants do not receive any water, the dis-
ease is practically unimportant since the attack is usually very mild
during the active growing season, but becomes somewhat more abun-
dant when the plants have passed all usefulness. The writer had the
opportunity of collecting specimens at random from six large houses,
and from three acres of out-door sweet peas in Mass. and from
a similar three acre plantation in Pa. Like Prof. Stewart, the
writer has only met with the conidial or Oidium stage. On our own

Fig. 38. Anthracnose disease of pods and seeds.

sweet pea field, we have carefully watched for a perithecial stage but
without suecess. Late in the fall, badly infected leaves have been col-
lected and put away to winter over, but that material up to date,
April, 1913, has failed to develop perithecia.

le

4]

ANTHRACNOSEH, Glomerella rufomaculons (Berk.) S. & V. Sch.
A very serious anthracnose disease of the sweet pea on the Dela-
ware Experiment Station farm was ealled to the attention of the
writer during ‘he latter part of July, 1910. This disease proved to be
the same or very similar to the one reported by Sheldon,,, from Wes%

Fig. 39. Anthracnose disease affecting the sweet pea leaf.

Virginia in 1905, and is very probably the so-called ‘‘wilt’’ which
has been so often referred to in old seed catalogues and treatises on
sweet peas.

42

Symptoms. The disease occurs on the stems, leaves (Fig. 39),
flowers and pods but is most severe on the latter. There is a general
wilting of the affected parts followed by dying, which begins at the
tips of the younger shoots and works downward (Fig. 37). The older
parts of the plants are not killed immediately but may persist for
some time after being attacked by the fungus. The dead paris shrivel,
become brittle, and are soon covered with minute acervuli. The af-
fected pods are at first a dirty white in appearance but assume a dull
color, which is due to the presence of the acervuli. A definite canker,
which is so characteristic of the bean anthracnose is not produced.
Although the disease on the stems seems to be restricted to the young-
est growths, the pods may be infected at any stage of their develop-
ment. The seeds of the diseased pods are always infected, become
shrivelled and frequently do not reach maturity (Fig. 38.)

Pathogenicity. Sheldon ealled attention to the identity of the
Gloesporium of the sweet pea with Glomerella rufomaculans (Berk.)
Spauld. & von Sch. which is the cause of the bitter rot of the apple.
With this in mind, the writer made the following experiments in the
autumn of 1910. Sweet pea seeds, which to all appearances were per-
fectly healthy, were carefully selected, sterilized by immersion for 15
minutes in a 5% solution of formaldehyde, and planted in pots in
soil which had been sterilized by heating for one hour in the autoclave.
The seeds germinated in 5 days and the seedlings were allowed to
grow for three weeks. Fifty plants were allowed to grow in each pot.
The temperature of the room ranged as high ag 72° F.. during the day
and several degrees lower during the night, but not low enough to
injure the plants. All the seedlings grew well and were perfectly
healthy. The day before inoculation the pots with the seedlings were
covered with bell jars thus forming moist chambers. These covers
were removed one day after inoculation. Two methods of inoculation
were employed: (1) the introduction of spores into the hving stems
through punctures made with a sterilized needle; (2) by liberally
spraying the surface of the plants by means of an atomizer with
spores suspended in sterilized water. Fruits of apples and pears on
the trees in the orchard were also treated in the following manner:
Healthy frutts on the trees were first washed with a 5% solution of
formaldehyde and then rinsed with distilled water. They were then
inoculated through sterile needle punctures and covered with paper
bags. For the inoculation, pure cultures were used of Gloeosporiums

43

from various sources as indicated below. The results of these experi-
ments are given in Table I.

The data in Table I show: (1) that the original organism of the
sweet pea is pathogenic to the sweet pea, and also to the apple in which

TABLE I
Source of Number and kiud Method of | Date of
. Gloeospor- of plants nee aa inocula- ima Checks
lum culture inoculated tion
50 sweet pea seed- i :

Sweet Pea | lings, 3 weeks old Punctr € | Sept. 26 | Oct. 2, alll dead 50 all
86 66 Same Atomize |Qct. 26|Noy. 7. “« << healthy
6G WG Same_ a0 Nov. 14 | Nov. 21, 6G. 6G oe
Apple Same Puneture | Oct. 10 | Oct. 18, «6 « o

ce 50 sweet pea seed- a 66 66 ee
lings 4 weeks old Oats 2, a
es Same Atomizer |Nov. 20 | Nov. 29,44 <«¢ a
aS Same Puncture |Oct. 26|Nov. 1,31 <‘¢ ‘6
ie Same a Nov. 14) Nov. 20,all <é “
o6 Same Atomizer |Oct. 5 |Oct. 14,37 ‘ ce
ce 50 sweet pea seed- ce Og, 7 kG
lings 8 weeks old 0 Gee Ui a4
Oct. 17, typical

Sweet Pea |12 apples on tree} Puncture |Oct. 7 bitter rot KH 66
oe 66 16 66 oe 66 Oct. 8 ce 66 (a3 12 o¢
Apple 15 (a3 66 oe 66 66 ce (m4 66 16 (a9

(a4 a1 pears on tree oe (5 66 66 (m4 oe 8 » 66

Sweet Pea 18 (a4 66 oe oe (a9 oo (a4 oe i 66

oe (3 16 66 66 6 Cr (a3 66 66¢ (a3 12 66

it causes the typical bitter rot; (2) that Gloeosporium fructigenum
Berk. from the apple causes a disease on the sweet pea which is sim-
ilar to the disease caused by the original sweet pea Gloeosporium.
This definitely proves that Glomerella rufomaculans (Berk.) Spauld.
& von Sch. is the cause of the anthracnose disease of the sweet pea.

Relation of other Gloeosporiums to the Sweet Pea Disease.
While working on the question of the identity of the bitter rot of the
apple and the anthracnose of the sweet pea, it was considered desir-
able to determine whether other species of Gloeosporiums could pro-
duce an anthracnose of the sweet pea similar to that caused by the
bitter rot organisms of the apple. Therefore, sweet pea seedlings were
inoculated with spores from pure cultures of five different Gloed,
sporiums then in stock in the laboratory. The results of these experi-
ments are given in Table II.

TABLE II

: Number and Date of
eci 1 H ‘
Gisecoperramn | I Oe let es artice lh mccm es hear on Check
Gloeosporium | 50 sweet pea | Puncture | Oct. 26 | Nov. 7, 42 50 all healthy
gailarum seedlings dead
oe Oe ae Nov. 14 | Nov. 25, 41 a
dead
rz v< Atomizer | Nov. 30 | Dec. 12, 8 x
dead
6 6G e Dec. 2] Dec. 14, 19 nS
dead
GG G6 is Oct. 26 | Nov. 7, 34 ‘e
dead
Gloeosporium 66 Puncture | Nov. 14 | Nov. 25, 43 oe
officinale a dead
ae au a Nov. 30 | Dee. 12, 50 oe
dead
ie a Atomizer | Dec. 2 Dec. 14, 50 a
dead
56 BG of Oct. 26 | Nov. 7, 50 %
dead
Species from of Puncture | Noy. 14 | Nov. 26, 42 oe
May apple dead
us BG i Nov. 30 | Dee. 12, 17 oe
dead
“< oc Atomizer | Dec. 2] Dee. 14, 19 i
dead
ce 66 6¢ Dee. 26 66 66
Glomerella 66 Puncture 66 Nov. 20 oe
psidi failure
a 66 Atomizer 66 66 GG
Species from ce a Oct. 20 o4 A
Persea
G6 GG Puncture es 6é ss
Gloeosporium | 15 pears on ze GG Nov. 15, typ- i GG
gallarum tree ical bitter rot
Gloeosporium | 12 es us ae Dis 1
Officinale
Species from | 14 a ee OG Oe
May apple Nov. 15, not
Glomerella TO es mn Be typical bitter 6a
psidii rot
Species from | 16 ‘é es Oct. 5 B6 Girvaes
Persea
Species from | 106 pole lima of Oct. 7 | Oct. 19, suc- ay
sweet pea on pods cessful
Species from | 66 ‘ os 66 a ayes
apple
Species from | 24 ‘¢ bie uG a Digs
May apple
Gloeosporium | 32 ‘¢ a a Gs a6
Officinale
Gloeosporium | 42 ‘¢ He ce a oe
gallarum
Glomerella 60 bush lima gg a a es
psidii bean
Species from | 42 ‘‘ ee “e a LO, Serge
sweet pea
Species from | 49 ‘‘ BG ce a Oc
apple
Species from | 40 ‘ Atomizer ae Oct. 26, fail- | 12 <¢
apple ure
Species from | 58 ‘‘ By ee GS 19. 26

sweet pea

oo eee

45

From Table ITI it will be seen that the Gloeosporium from the May
apple fruit (Podophyllum peltatum), G. gallarum Ch. Rich. from oak
gall, and G. officinale EH. & KH. from sassafras leaves, are able to infect
sweet pea seedlings through puncture inoculations as readily as the
sweet pea or the apple Gloeosporium. Furthermore, that G. officinale
readily infects sweet pea seedlings by atomizer inoculations, the infec-
tion being nearly 100%. While G. gallarwm and the species of Gloeo-
sporium from the May apple fruit also infect sweet pea seedlings, the
percentage of successfully inoculated seedlings is smaller with the
atomizer inoculations than when the inoculations are made by needle
punctures.

Glomerella psidii (G. Del.) Sheldon and the Gloeosporium from
Persea failed to infect sweet pea seedlings.

The apple trees in the old orchard of the Experiment Station did
not bear enough fruits to permit inoculation experiments with the
above five organisms; hence Kieffer pear trees which bore heavily were
chosen for this purpose. They were accordingly inoculated with the
five Gloeosporiums already mentioned. The results of these mocula-
tions (Table II), show that the species of Gloeosporium from the May
apple G. gallarum and G. officinale produce the typical bitter rot on
the pear, while the Gloeosporium from the guava and Persea infect
the pear, but cause dull spots in which the acervuli are black and the
spores are borne on long black conidiophores. Similar results were
obtained when pear fruits were inoculated with the same Gloeosporium
and kept in moist chambers in the laboratory. These experiments
also show (Table II) that all the Gloeosporiums here considered, ex-
cept the species from guava and Persea very readily produced an
anthracnose disease on the pods of the lima beans in the field, which
was similar to the anthracnose of the sweet pea, but quite unlike the
bean anthracnose, Colletotrichum lindemuthianum (Sace. & Mag.) B.
& C. All the Gloeosporiums referred to above attacked the pods of
the lima beans in ‘he field when the inoculations were made by means
of punctures, but not otherwise. The spots produced on the lima bean
pods by Glomerella psidii are gray with grayish acervuli and made up
of black setae very similar to those of a true Colletotrichum, but un-
like C. lindemuthianwm. None of the above species of Gloeosporiums
would infect bean or vetch seedlings. The same precautions were
taken in inoculating the bean pods and pears in the field as with the
apples.

46

Further Studies of some Gloeosporiums and their relation to the
Sweet Pea Anthracnose. The first year (1910) the inoculations were
carried on at a time when both the apples and the pears were almost
mature, and ripe fruits being a more favorable medium, since they are
physiologically less active than young ones, it was felt advisable to
start the present inoculations of the apples and pears in the orchard
at a much earlier date, this time using more organisms. The inocula-
tions were begun in 1911 when the fruits were the size of a grape, and
were repeated at various stages of their development. The Kieffer
pear and the Rubicon and Paradise Sweet apples were selected for
this purpose. The inoculations were made by means of punctures
through the cuticle. For each organism a different sterilized needle
was used. Natural infection of the inoculated fruits was prevented
by means of heavy paper bags which were tied to the limbs to which
the inoculated fruits were attached. Any inoculated fruits which
happened to drop off fell into the bags and were retained there. In
every case where infection occurred it first appeared at the point of
inoculation. For each organism eight fruits were used as checks.
These were punctured with a sterile needle and covered with paper
bags, and in all cases remained healthy. Investigations were also ear-
ried on with sweet pea, specimens of which were grown in the labor-
atory from carefully selected and sterilized seeds grown in sterilized
pots and soil. Checks were also used, fifty seedlings for each organism,
and these in all cases remained healthy, although they were punctured
with a sterilized needle. Only spores from pure cultures were used
for the inoculations. The results obtained are given in Table III.

From Table III it will be seen that Glom. rufomaculans from
apple and sweet pea, Gloe. gallarwm Ch. Rich., Glom. gossypu (South)
Edg., Gloe. diospyri BE. & E., Colletotrichum phomoides (Sacce.)
Chest., and C. nigrum Ell. & Halst. produce the typical anthracnose
disease on the sweet pea and the symptoms produced by all the above
organisms were identical with those produced by the original Gloeo-
sporium isolated from diseased sweet pea plants in the field. Many
more inoculations than are indicated in Table IV were made with the
above named organisms on the sweet pea. They were omitted from
the table, since the results obtained were similar to those given above.
The data in Table III further show that Gloe. piperatum BH. & HB.
failed to infect the sweet pea by atomizer inoculation, while infection
by puncture inoculation was fairly successful. When this organisms

47

was reisolated from seedlings infected by puncture, it regained its
virulence, and then became able to infect sweet pea seedlings by atom-
izer inoculation. Glom. rufomaculans from the fig failed to infect the
sweet pea, and, as wiil be seen later, it also failed to infect apples and

TABLE III
Species of Methods of Date of Results of _
fungus inoculation lnoculation inoculation
Glomerella rufomaculans
ane ays hoses co eoe Atomizer June 16 June 28, 99% infection
Glom. rufomaculans
from sweet pea......... ie May 21 June 2, 92% <*
Ben 86 May 25 June 6, 90% <é
~ oe June 16 June 21, 95% ‘$*
e a June 29 dimly Til, 4g oe
o 54 July 27 Aug. 10, 80% ‘<<
at Nov. 1 Nov. 10,100% ‘<‘
Gloeosporium gallarum at June 16 June 28) 91% *
Gloe. piperatum.......... cc May 25 we 1B, ag 8
ue Puncture ce June12, 2% *
Ee us June 29 July 6, 41% ‘
ie Atomizer June 4 Hiv bse ¥2)) Ws 0 (0 eas
6e ney (m4 July a7 Aug. 9, 50% Ce
Glom. gossy pul seein d.0d00 ie May 21 ya py (AY oY
: May 25 une 12, 60% ‘
es ct June 21 July 7,100% <é
ee a June 29 July 7, 80% ‘*
Gloe. diospyri....... oe oe Oct. 28 Nov. 10, 82%
Colletotrihum phomoides 36 66 Nov. 10, 80% ‘‘
CL Snir MONS SHS a6 Seo Ce OEE eG 2G Nov. 10, 92% “*
C. gloeosporioides......... 86 July 3 Vuk 4b say. SY
é * . Puncture Aug. 1 pC Cee aise ee ai, ma
lom. rufomaculans ae
9 ce (a4
INOW IGS aed 9 oi 6 OIC 0 May 21 June 2,
ce Atomizer OG Sbhaeye Pie E <a EG
Gloeosporium from ie eas
Populus deltoides....... 7 June 29 July 11,
of Puncture May 25 Suma pn ae CS
C. lindemuthianum....... 66 Aug. 1 Atoll ee ree
es Atomizer es ACU UO er aS Stig
Cioesma sar unless. sisrlets as s July 27 Aug. 10, siete
ae Puncture eG sioner ualOpec eG se BEY
Cmlacenaniuml ener aeiiee ae Nov. 1 INOW Os SS Ee
ci Atomizer ce Nove lOb ame seegece

pears on the tree. Edgerton,,, states that the above two organisms
readily lose their virulence when grown for some time on artificial
media. The Gloeosporium sp. from Populus deltoides, Colletotrichum
lindemuthianum (Sace. & Magn.) B. & C., and Gloe. musarwm Cke.

*Gloeosporium piperatum reisolated from sweet pea seedlings infected by
puncture inoculation.

48

& Mass. failed to infect the sweet pea after repeated trials both by
puncture and atomizer inoculations. In comparing Tables I and II
we see that the organisms which infect the sweet pea also infect the
apple, with the exception, however, of Gloe. gossypu, which readily
infects the sweet pea by atomizer inoculation, but always fails to infect
apples on the tree.

Fig. 40. Bitter rot of apple induced by the same fungous which causes anthrac-
nose of the sweet pea, viz.—Glomerella rufomaculans.

The data in Table [V show that none of the organisms used could
infect the Rubicon apple on the tree when the fruits were about the
size of a large grape. Later, however, by June 26, the first positive
infection was obtained with Glom. rufomaculans from the apple. At
this same date all the other organisms used failed to infect. On July
15 the same condition prevailed. By August 19, typical bitter rot
infections were obtained with Glom. rufomaculans from the apple and
sweet pea, Gloe. officinale, Gloe. gallarum, Gloeosporium sp. from
May apple fruit, and Gloe. piperatum. Negative results were obtained
with Glom. rufomaculans from fig, Glom. gossypu, Glocosporvum sp.
from Populus deltoides, Colletotrichum lindemuthianum and Gloe.

49

musarum. Further inoculations were made on the Rubicon apple
until September when the fruits were ripe and the results were the
same as mentioned above.

Field inoculations were tried on the Paradise Sweet apple with
the organisms mentioned in Table IV and with like intervals of time
between them. The results obtained were the same as with the Rubi-
con except that positive infection with Glom. rufomaculans from
apple was not obtained before Sept. 7. Inasmuch as the Paradise
Sweet is a late variety this indicates the greater resistance of late
over early varieties.

Species of No. fruits Dates of Results from
fungus inoculated |inoculation inoculation
12 species named below 6 fruits /|June 2 | June 12, all healthy
for each
organism
(a9

12 species named below

June 6 | June 21, all healthy
Glomerella rufomaculans

OWN BO ONOs »canacvme 8 June 14 | June 26, all typical bitter rot
11 other species named
elOnrg inet sees 8 nn ‘« all healthy
Glom. rufomaculans
EE OMMEA PO Clceieteeerme ste 8 June 27 | June 15, all typical bitter rot
Glom. rufomaculans
from sweet pea....... 10 of ‘< 8 fruits show small spots
Gloeosporium from ‘<2 fruits are healthy
MiaiveapDlels vo suo eco 10 ee “« same as above
9 other species named
lOXe) (Oiveteear nears sees oem 10 fruits ae ‘« all healthy
for each
organism

Glom. rufomaculans

ION: AYO DE. BS ncoo coon 8 July 7 | Aug. 2,all typical bitter rot
Glom. rufomaculans

from sweet pea....... 10 eh ‘F be
Gloeosporium officinale 10 oe oe a
Gloemscallarumis-acs os. - 10 as eG &
Gloeosporium sp. from ny xt

Wine 20) Os Sas oiteto eee 10 = Ns He
Colletotrichum phomoides 10 a ‘* all very small spots, but
Gloe. piperatum......... 10 re typical bitter rot
C. gloeosporioides....... 10 BY ‘¢ very small spots but not
Gloms 7 eOssy pila. os. =. 10 = typical bitter ro¢
Gloeosporium sp. from ‘¢ same as above

Populus deltoides...... 10 we ‘¢ all healthy
C. lindemuthianum...... 10 oe a oe

C. lagenarium.......... 10 aE ee ie

50

Field moculations were also carried on with Kieffer pear fruits.
The latter being a variety which ripens very late, positive infection
on the fruit with six of the organisms could not be obtained earlier
than Oct. 6. The above fungi which produce the anthracnose disease
of the sweet pea and the bitter rot on the apple also produce typical
bitter rot on the Kieffer pear.

The foregoing experiments have conclusively proved that the an-
thracnose disease of the sweet pea is identical with Glom. rufomaculans
which produces the bitter rot of the apple. Moreover, the six organ-
isms above mentioned, which were previously considered as distinet
species, are now shown through the above experiments to be identical
with Glom. rufomaculans, since they readily produce the typical an-
thracnose disease on the sweet pea and the bitter rot of the apple and
the pear fruits on the tree. The experiments further indicate the
saprophytic nature of Glom. rufomaculans,,, Since no infection could
be obtained on very young apples or Kieffer pear fruits on the tree.
In the Delaware bulletin just referred to an explanation is given of
the causes of the difference in resistance between different varities
of the same fruits and between young and older fruits of the same
variety. If we look for an explanation as to why Glom. gossypw in-
fects sweet peas and fails to infect apples and pears on ‘the tree but
readily infects the same fruits when they are picked and placed in
moist chambers in the laboratory, we are brought to the following
theory: It seems that the Glom. gossypw at one time was identical
with Glom. rufomaculans, but that through long association with the
cotton plant it has become so modified in its habits as to make it a phy-
siological species capable of infecting the sweet pea and possibly other
hosts, but having lost the power to infect the apple. From this it
would seem that it is the cell contents of the host which may in some
cases modify the physiological habits of an organism. To refute the
above statement it could not be argued that the sweet pea can be in-
fected by all species of Gloeosporium. This is not the case, since
experiments have proven that only the organisms which infect the
apple can also infect the sweet pea, with the above exception.

The writer hopes to continue experiments along these same lines
with the object of finding out whether certain other supposedly differ-
ent species of the Glomerella type are not one and the same.

Mode of Infection and Period of Incubation. The anihrae-
nose of the sweet pea is mainly a disease of the tender parts of the

51

plant. Infection starts at the tips and the fungus works downwards
invading both stems and leaflets until it reaches a node on the older
paris of the stem, where it is stopped in its course. It is not infre-
quent, however, to find whole branches dying, and sometimes the
entire plant is involved. In such cases it has been found that the
plant is suffering from insect attacks, either by plant aphids (Aphis
sp.), or more especially the red spider, (Tetranychus bimaculatus
Haw.). These help the fungus both by weakening the host plant and
by distributing the spores over its surface. The spores when ger-
minating have no difficulty in penetrating the oldest parts of the host
if it has been punctured by these insects. This explains why the
plants suffer most during the hot dry weather, since at that time the
aphids are most abundant. Infection often begins with the blossoms
at the junction between the flower and the peduncle, in which case
the blossom shrivels. ‘The pods, also, even those which are nearly ripe,
are often seen to be badly affected. Here, too, the aphids will be found
7~o have opened the way for the fungus. These symptoms are observed
in the field when infection takes place naturally, or in the laboratory
where the plants are artificially inoculated with Glom. rufomaculans
from the sweet pea. The same mode of infection and the same symp-
toms are observed with the other organisms which are capable of in-
fecting the sweet pea.

The spores of Glom. rufomaculans from the sweet pea usually
germinate in from six to twenty-four hours, according to the amount
of moisture in the atmosphere. The germ tubes enter the host by
breaking through the epidermal cells of either leaf or stem. In case
the spore lodges on a stomate, the germ tube grows away and avoids
entrance. It may be that the gases which are given off at the stomates
are toxic and prohibit the entrance of the germ tube, which often
breaks through the epidermal cells as soon as the spore germinates.
At other times the spore germinates by sending out a short germ tube
which forms an appressorium which attaches to the epidermal wall.
This appressorium is then seen to germinate, its germ tube breaking
through the epidermal cell.

The period of incubation varies from three to five days according
to the amount of moisture in the atmosphere. The acervuli appear
within five days after wilting begins unless the weather is dry, when
they may not appear until eight to ten days after infection. In the
field the sweet pea anthracnose is at its height during July and Aug-

52

ust. This is also the time when the bitter rot of the apple makes its
appearance in the orchard. It is thus easy to understand how readily
the natural cross inoculation may be effected.

Morphology of the fungus. The spores and mycelium of the
Gloeosporium of the sweet pea do not differ from the corresponding
structures of Glomerella rufomaculans.. Sheldon first observed endo-
spores of the Gloeosporium of the sweet pea in pure cultures, and the
writer has observed the same structures in hanging drop and plate
cultures of Glomerella rufomaculans from the apple and the sweet
pea, G. officinale and G. psidu.

The formation of endospores is as follows: In some of the mycelial
threads the protoplasmic content rounds itself into one or more cells,
resembling chlamydospores. At the tip end of these cells a filament
grows out within the empty part of the mycelial thread and at the
tip of this filament the endospore is formed in the same manner as the
conidia on the conidiophores of a Gloeosporium. The endospore is
broken off and pushed forward for the formation of a new one. Fur-
ther studies are necessary to determine the conditions necessary for
endospore formation. The spores of G. fructigenum, G. Gallarum,
and the Gloeosporiums from sweet pea and May apple, all germinate
in the same manner, by sending out a stout germ tube. On five dif-
ferent synthetic media these Gloeosporiums produce growths and
fructifications of the same character. The spores of the species from
guava and Persea germinate by sending out a very thin germ tube.
They also differ in manner of growth and fructification on the syn-
thetic media from the other organisms used. Until the perfect stages
are found, it appears from these studies that we are justified in con-
sidering G. gallarum, G. officinale and the Gloeosporium from the
May apple fruit as one and the same with Glomerella rufomaculans
(Berk.) Spaul. & von Sch. of the apple and the sweet pea.

Infe History. In order to determine whether the disease is
carried over with the seeds of the sweet pea, a large quantity of dis-
eased pods were collected and kept over winter, some in the laboratory
and some out of doors. Spores from both lots of materials were tested
Nov. 22, Dec. 22, 1910, Jan. 22, Feb. 22, Mareh 15, 20, 24, April 20,
May 21, and June 20, 1911. In all cases the spores germinated well
and produced normal colonies on bean agar. Spores of cultures ob-
tained from the sowing of June 20, 1911, readily infected healthy

53

sweet pea seedlings, wnich were grown in pots in the laboratory. This
indicates that the organism is carried over the winter as viable spores
on the pods and on the seeds, and there is very little doubt that the
disease is introduced into new localities through diseased seeds.

MOSAIC DISEASE OF THE SWEET PEA

Brief History. The first study of the disease was made by
Mayer,,, in 1866 on the mosaic of tobacco. Mayer found ‘that the dis-
ease was not induced by insufficient mineral nutrients. He also found
the disease to be distributed over large areas irrespective of soil con-
ditions and further proved that the juice of the leaves of affected
plants, when injected into healthy leaves would reproduce the disease
in from ten to eleven days. Mayer found that a temperature of 60°
C. does not destroy the infectious nature of the juice, but that a tem-
perature of 80° kills it. Mayer could not find any animal or fungus
parasite to be associated with the disease, altho he believed the true
cause to be bacteria which could not be isolated.

In 1892 Iwanowsky,,, confirmed Mayer’s work. He too was un-
able to isolate the specific germ on artificial media but states that he
saw the bacteria and proved their presence in the tissues of the affect-
ed host. In 1894 Prillieux and Delacroix,,, found this same disease
on tobacco in France.

In 1897 Marchal,,, described under the name of ‘‘La mosaique
du tabaec’’ a disease similar in appearance to that described by
Mayer,,;. Marchal claims to have obtained from diseased leaves a
motile bacillus forming chains in culture media, and capable of re-
producing the disease by inoculating with a pure culture.

In 1898 Beijerinck added considerable to our knowledge of this
disease. He apparently proved the absence of bacteria in the devel-
opment of the disease. When the juice of diseased plants is passed
through filters, the liquid, while remaining perfectly clear and free
from bacteria still retains the power of infection. He found that only
growing meristematic tissue could become diseased. Among many
other things he also found that soil from diseased plants may infect
healthy plants. He further showed that the infective material could
be transported through considerable distance without losing its vir-
ulence. He assumed the virus to be a non-corpuscular fluid like mate-
rial which has the power of growth when in contact in a sort of sym-

54

biosis with growing cells. He called it therefore ‘‘a living fluid con-
tagium.”’

In 1902 Woods,,, concludes that the disease is due to the presence
of oxidizing enzymes in the plant; these he designated as oxidase and
peroxidase.

In 1904 Selby,,, refers to the mosaic disease of tobacco as a non-
parasitic disease, he, accepting the conclusions of Sturgis and
Woods.

In a recent paper, Allard,,, has succeeded to transfer by means
of inoculation the mosaic of tobacco to other solanaceous plants of the
following genera: Nicotiana, Lycopersicum, Petunia, Physalis, Datura,
Hyoscyamus, Solanum and Capsicum. T. Allard also found aphids
to be carriers of the disease.

Mosaic Disease of the Sweet Pea. As far as known there is
no mention made before of the mosaic disease of the sweet pea. The
writer first made a study of the disease in the summer of 1912 and his
first published report appeared in the Florist Exchange,,,.

Like the anthracnose, the mosaic of the sweet pea is a very impor-
tant disease. Both owt door and greenhouse plants are alike sub-
ject to it.

Symptoms. Mosaic is readily distinguishable by a yellow dotting
or mottling of the leaf, presenting in some instances a beautiful mosaic
structure, hence its name (Fig. 41). Affected leaves seem to linger
for a time but they eventually lose all their chorophyll and goon drop
off. Another symptom of this disease is a curling of leaves (Fig. 42),
resembling the curling induced by the green aphids, but in this case the
aphids had no association with it. The disease makes its appear-
ance after the seedlings are from three to four weeks old. Often, the
disease is so bad and the curling so pronounced that the plants thus
affected cannot make any headway and remain dwarfed. An attempt
is made by these curled parts to produce a few flowers, but the later
are borne on very short peduncles as compared with the long ped-
uncles of healthy plants of the same variety. Frequently, however,
the affected plants outgrow the disease entirely, and thus a distinct
line of demarcation is observed between the previously diseased part
and the healthy part of the new growth. At other times infected
plants kecp on growme and even flowering, with the disease keeping
pace.

5d

; (c) healthy.

ing mosaic

(a) (b) leaves show

Fig. 41. Sweet pea mosaic disease.

Pathogenicity. Like peach yellows and mosaic disease of tobacco
and tomato, this disease of the sweet pea, too, can be reproduced
by a puncture with a sterile needle from the diseased leaf into

56

a healthy leaf. No organism could be obtained in culture, nor
could it be detected with the microscope. Nevertheless, this disease
is contagious, as is the peach yellows. When the disease first made
its appearance in our experimental sweet pea fieid, the diseased areas

Fig. 41 Mosaic disease causing dwarfing of the plant and rolling of the leaves.

Or
—]

were immediately located in order to learn something of its spread.
They formed two small areas, one in about the center of the field, the
other in the southeast corner. Within ten days another survey was
made and the whole field was found to be infected. Wzuth the excep-
tion of the dwarf Cupid varieties, which are seemingly immune, all
the rest were found to be affected with the mosaic. When first inves-
tigating this disease I thought that, perhaps, this mottling of the
- leaves was merely a variegated condition. We also thought that per-
haps the curling of the tender tips as well as the mosaic effect was due
primarily to the presence of aphids, which at the beginning of the
season were so plentiful. Experiments were then undertaken to de-
termine definitely these points. Accordingly, sterile pots with sterile
soil were isolated in a glass chamber and the plants were allowed to
grow for three weeks to see if any disease would develop on them.
However, these plants remained very free from any disease. The pots
with plants were then divided into four lots; into Lot I were intro-
duced a few stem mothers of aphids from affected mosaic plants in
the field. In Lot II were introduced a few stem mother aphids from
apparently healty plants in the field. The plants in Lot III were
punctured with sterile needles and by pricking a mosaic affected leaf,
and then puncturing with the same needle the healthy leaves. Lot
IV was punctured merely with the sterile needle, the plants of this
lot were designed to serve as checks. In each lot there were two pots
with plants in order to duplicate each experiment. After ten days
the lot which were inoculated with the aphids from the diseased and
healthy plants both began to show the symptoms of mosaic. This,
therefore, would appear to show that the mere puncture of aphids
would be responsible for the mosaic disease. However, this is not the
case, aS we will soon see. Moreover, it is easy to suppose, and that on
very good ground, that the aphids taken from seemingly healthy plants
in an infected field might themselves have been infected before. But
this would be no valid proof. Lot IlI, which was infected with needle
punctures from diseased leaves, began after ten days to show the
mosaic disease, while the check punctures remained all healthy to the
end of the experiment. This definitely proves that the aphids are not
the cause of the trouble but are merely the carriers of the mosaic dis-
ease. It seems, therefore, that any steps taken to control the aphids
may also serve to control the mosaic. From this, too, it is evident

58

that not only the aphids, but also any biting or sucking insect may
help spread the disease.

It has been definitely proven that the mosaic disease is contagious,
since it can be produced at will by artificial moculations. The symp-
toms produced in artificially inoculated plants are similar to those in
the field, namely, a yellowish spotting or mottling of the leaves and
a tendency of the leaves of the tips of the plant to curl.

Cause of the Mosaic Disease. Mention has been made of pre-
vious workers who with ourselves have definitely proven the infectious
nature of the disease. Attempts to prove the cause of the trouble
have resulted in failure. Mayer,,, failed ‘to find the association of ani-
mal or fungus parasites with the disease. He thought that bacteria
were the cause of the disease, but all inoculations with bacteria culti-
vated from the surface of diseased leaves, and with mixtures of dif-
ferent bacteria gave negative results.

Beijerinck,,, disproved the theory that the cause of the trouble
was bacteria, by showing that the juice of diseased plants filtered
through Chamberland filters while remaining perfectly clear and free
from bacteria still retained the power ‘of infection.

Sturgis,.. In his conelusions states as follows:

‘‘Tt (mosaic) is not caused by predaceous insects, nematodes, or
parasitic fungi.

‘‘Bacteria have not been associated with the disease but no erit-
ical method for their isolation or culture has been applied, and there-
fore the question of their influence cannot at present be answered.

Woods,,; believes the disease to be of a physiological nature and
of enzymic activity. Woods claims to have reproduced the disease
several times by merely removing the tip of a rapidly growing plant.

Suzuki,,, in his studies of the so-called mulberry dwarf troubles
in Japan (all evidence seems to show that this disease is of a similar
nature aS our mosaic), concludes that the principal cause of the dis-
ease is due to the practice of subjecting the mulberry trees to repeated
low cuttings, thus removing the reserved food which is required for
growth. Woods believes that it was the enzyme (peroxidase) of the
leaves that induced the disease because he claims that he induced the
disease artificially by injecting into a healthy plant the juice from
another healthy plant. Woods found more peroxidase in diseased
than in healthy plants. ‘‘It is through the introduction of the enzyme

59

into the infected host that pathological changes are brought about
which result in an increase of the normal enzymes of the cell and the
decrease of available reserve food. When this condition is reached,
it is very difficult for the plant to outgrow the trouble.’’ Accepting
this hypothesis, Woods is ai a losg to explain how the disease is spread.

In my investigations repeated trials failed to reveal the presence
of either fungus or bacteria in culture. Nevertheless I do not believe
with Woods that the disease is physiological and enzymic. I strongly
believe. the trouble to be either bacterial or protozoic* and the patho-
genic nature of the disease strongly points to this conclusion. That all
attempts to obtain a living micro-organism in pure culture have failed
does not argue against the possibility of its being either bacteria or
protozoa, but simply that our present cultural or filtering methods
are not suitable for its detection or retention. Previous to the discov-
ery of Bacterium tumefaciens, by E. F. Smith, no one suspected the
crown gall of plants to be of bacterial origin, cultural attempts in each
ease failed to reveal the organism.

As I have already indicated, Beijerinck showed that the juice
of diseased plants when filtered through Chamberland filters, while
remaining clear and free from bacteria still retains the power of infec-
tion. This proof too does not argue against the possibility of the bac-
terial or protozoic nature of the mosaic, because the former may be
even smaller than bacteria and readily pass through the Chamberland
filters. It is therefore possible that Beijerinck’s filtered fluid was
- contaminated with the pathogen and this is why the filtered fluid
retained its pathogenic nature. Neither can we accept Wood’s state-
ment that healthy plants when cut back develop the disease unless we
admit again of the possibility of contamination. If the mosaic path-
ogen is not present or has not made its appearance on a certain host,
the latter can be cut back time and again without the disease ever
making its appearance. Before I introduced the disease through punc-
ture inoculation with diseased tissue in the laboratory, I cut back
my experimental sweet pea plants in order to prevent them from
growing too high and altho I have practiced this very often I have
never had a case of mosaic develop from this operation. It is also
difficult to believe with Woods that the disease is of a physiological
and enzymic nature. Enzymes in plants are natural factors of im-

*The idea of the protozoic nature of mosaic was suggested to me by Dr. T.
F. Manns.

60

munity to protect that plant from disease. Diseased plants will nat-
urally possess a higher enzymic content just as much as the leucocytes
in the human blood increase in case of wounds, ete. That this per-
oxidase of Woods from diseased plants should possess the power of
infection is very possible as I have already pointed out the former
may be contaminated. That the peroxidase of healthy plants when
inoculated into a healthy plant should be able to produce the disease
as Woods claims to have done, is probable, only if we admit of pos-
sibilities of contaminations which may have been the case. As al-
ready stated, the pathogenic nature of the disease points to a living
organism as being the cause.

In Wood’s enzymic explanation we have no means of accounting
for the spread of the disease. Under pathogenicity we have shown
that green aphids carry and spread the disease from leaf to leaf and
from plant to plant. This by itself is sufficient proof that a living
organism ig the cause of the mosaic, for if as Wood maintains, the
peroxidase of a healthy plant when inoculated into a healthy host will
reproduce the disease and if there be no chemical difference between
peroxidase of healthy and diseased plants, then why is it when green
aphids from perfectly healthy plants are transferred to healthy sweet
peas the disease never develops but the mosaic readily makes its ap-
pearance by introducing green aphids from diseased plants to healthy
ones. If the aphids can carry the peroxidase from diseased plants why
do they not carry the same from the healthy plants while sucking
their juice? This to my mind is the strongest argument against
Wood’s physiological and enzymic nature of the mosaic, and on the
other hand it strongly points to the probable activity of a living bac-
terial or protozoic organism. Aphids are not the only agents capable
of carrying and distributing the disease, for there are others which
may do it. Among the biting insects we have the ‘‘corn root worm
beetle’’ (Diabrotica longicornis), the striped potato beetle (Epicanta
vittata) and several others which feed on the sweet pea and at the
same time help to distribute the mosaic.

Transmission of the Mosaic through Seed or Soil. Beijerinck
claims that soil around diseased plants may infect the roots of healthy
plants. In order to determine whether the disease is carried in the
soil, the following experiments were tried. A number of sterile pots
were taken and arranged in groups. Group A. consisted of pots filled
with sterile soil, on the level surface of which leaves infected with

61

mosaic were spread. Sterilized seeds were sown on the surface of the
leaves and the infected leaves and seeds were covered with a 2-inch
layer of sterile soil.

Group B. consisted of 2 pots filled with sterile soil but the latter
was mixed thoroughly with a quantity of mosaic infected leaves.

These pots were sown with sterilized seeds and covered with a 2-inch
layer of sterile soil.

Group C. consisted of two pots filled with sterile soil and sown
with sterile seeds and then thoroughly watered with water from a vase
in which mosaic infected plants stood for two days.

Group D. consisted of two pots filled with soil taken from the
field and from a spot where mosaic infected plants grew.

Group E. were untreated checks, that is, two pots with sterile soil
were sown with sterile seeds and placed at a distance from the infected
series. All the pots were then watered with distilled water up to the
end of the experiment. The seeds in all the groups germinated and the
plants were allowed to grow for ten weeks when they had attained
considerable size and in no case did the mosaic appear, thus appar-
ently proving that the mosaic soil is not a factor in carrying the dis-
ease. There is no evidence either that the mosaic is carried with the
seeds for in no case did the disease appear in the laboratory where
unsterilized seeds were used.

Diseases of the Sweet Pea not known to be present in
this Country

In an article in ‘‘The Sweet Pea Annual,’’ Massee,,, describes
the following diseases, which as far as known, have not as yet made
their appearance in this country on the sweet pea.

Pea Blight (Peronospora trifoliorum)

Pea Spot (Ascochyta pis!)

PEA BLIGHT, Peronospora trifohorum De By.
According to Massee, this is the most destructive disease to
peas, lupines, and to most of the pea family. The disease may
appear and spread quickly when the plants are only a few inches
high, or it may attack older plants. In dry weather the mycel-
ium of the fungus present in the tissue spreads throughout the leaf,

62

which soon assumes a sickly yellow-green color, and finally bleaches,
shrivels and dies without showing any, or only a small amount of
mould on the surface. In damp, dull weather infected leaves show
yellow patches, which soon becomes covered on one or both surfaces
with a very delicate greyish-lilac mould. The summer spores are pro-
duced on the leaves, or on any other part of the host. The winter, or
resting spores, are imbedded in the tissue of the host that has been
previously killed by the fungus. The resting spores have a very thick
smooth brown wall. Peronospora viciae is also stated to be able to
produce a disease on sweet peas.

PEA SPOT, Ascochyta yisi Inb.

According to Massee, this disease also attacks the French beans
and several other leguminous crops. The first indications of disease
on the pods is the appearance of pale green spots of variable size and
irregular shape. These blotches continue to increase in size for some
time and eventually become whitish, bordered with a dark line, and
have the surface studded with minute black points which are the
pycnidia of the fungus.

C. Diseased Seeds

Under the discussion of the anthracnose disease I have shown
that the fungus (Glomerella rufomaculans) is transmitted with the
seed. In that case infection starts at the pods and the fungus works
inwards gradually penetrating the seed coat and the seed proper
(Fig. 38). Such seeds when harvested have a shirveled appearance
and when planted with healthy seeds introduce the fungus in the soil
and then the disease begins to attack the adjacent seedlings, thus
spreading throughout the whole field.

Another disease that may be transmitted with the seeds is the
“‘Streak’’. In examining infected plants we can readily see the organ-
ism (Bacillus lathyri) invade the pods and then work into the seeds.
Pure cultures of the organism may readily be obtained by surface
sterilizing an infected pod, picking out the seed with sterile forceps
and then dropping the same into a plate of media. We have as yet
no data to prove that the organism can survive the drying when it
is only present on the surface of the seed coat. However, as is often
the case, the organism works through the seed coat and into the seed.
Under such conditions it is very probable that it may be carried over

63

winter while present in the seed tissue. Such seeds when planted
introduce the parasite into the soil and from there the disease gets
a foothold to carry on its destructive work.

Sweet pea seeds as we buy them from the seedsmen are put in
small paper packages. During my work on the sweet pea diseases
I had occasion to open two thousand of such packages. In very few

Fig. 48. Fusarium and Botrytis fungi from shriveled and non-germinated sweet
pea seeds.

cases were all the seeds plump and full. A certain percent were shriv-
eled and gave the appearance of being diseased. It was thought,
therefore, advisable to make a study of such shriveled seeds to deter-

64

mine whether or not they are disease carriers and the nature of the
pathogens. The technique employed was_as follows:

Fresh packages of sweet peas were opened and the percent. of
shriveled seeds in each package determined, labeled and separated.
The next step was to soak each lot of seed with a 5% formaldehyde
solution for 14 hr. and then to wash it three times in sterile water in
order to remove all trace of formaldehyde. Then with a sterile for-
cep, each lot of seeds thus treated was dropped into a petri dish con-
taining nutrient agar that had been melted and cooled to the proper
temperature. As the agar solidified the plates were placed in the incu-
bator and kept there for one week. Observations were made every
other day to determine the percent. of germination and to make trans-
fers into slant tubes of agar of all fungus or bacterial growth which
appeared on the shriveled seeds (Fig. 43). The results obtained are
given in Table V from which will be seen that a large percentage of

TABLE V

Name of variety
in package

Per cent of shriv-
eled seeds in

Per cent of germ-
ination of shriv-

Kind of fungi obtained
from non-germinated

package eled seeds shriveled seeds
King Edward VII 13% 33% None
Gray Friar 1/100% 0 aes
Aurora 9% 20% Botrytis cinerea
Apple Blossom 12% 6% . None
Emely Henderson 18% 100% ~ GUE
Henry Eckfort 15% 4% Fusarium sp.
Jeannie Gordon 5% 100% None
Dorothy Eckfort 138% 80% Fusarium s
Hellen Pierce 10% 80% a oe
Coccineae 6% 90% os ue
Katherine Tracy 15% 40% Alternaria
George Herbert 19% 0 Bacteria
Black Knight 4% 100% _ None
Jeannett Scott 21% 100% oe
Dobbies Mid Blue 3% 100% Be
Blanche Burpee 12% 100% -_ fof
America 9% 100% BG
Blanche’ Ferry 1% 100% ee
Mrs. A. Watkins 7% 60% Fusarium sp.
Countess Spencer 15% 18% Botrytis
Boltons Pink 1% Clanostachys sp
Countess Cadogan 12% 9% None
Agnes Hekfort 16% 8% Fusarium
E. J. Castle 3% 1% Se
Mrs. Collier 10% 50% a
Burpees Midnight 0 0 aa

65

the so called shriveled seeds readily germinated. It was further ob-
served that these before germination became plump and resembled in
every respect the germinated healthy seeds which were treated in the
Same way as the shriveled and were run as checks. It seems then
that shriveling in the seeds is merely correlated with a loss of water.
Whether shriveled seeds in the long run produce weaker plants has
not been determined. Observations so far have shown that the seed-
lings from the germinated shriveled seeds were in every way equal
in vigor to the seedlings of the germinated plump seeds.

Of the non-germinated shriveled seeds, those which remained
free from fungous growth can be classed as hard seeds and those prob-
ably would have germinated if the seed coat had been pierced. The
germinated seeds which showed growth of fungus or bacteria were at
once seen to become soft and rotted. Of the organisms isolated from
the non-germinated seeds there were two species of Fusaria, one species
of Alternaria, one species of Clonostachys, Rhizopus nigricans and
Botrytis cinerea. These after repeated trials failed to infect healthy
sweet pea seedlings, thus seemingly proving that they are saprophytes
and of secondary nature. Their presence on some of the weak and
non-germinated seeds, no doubt helped in the decay of the former, but
they fail to play the role of active parasites on growing plants.

Ii. Bacterial Diseases

So far only one kind of bacterial disease of the sweet pea has
been observed and that is the ‘‘streak’’ disease. ‘This has been deter-
mined to be caused by a newly described organism, viz. Bacillus lathyri
Manns and Taubenhaus.

STREAK IN ENGLAND

Historical. In correspondence with Mr. T. A. Weston of Or-
pington, England, the former states that the disease was first observed
by H. J. Digges of Dublin in about 1904 or 1905.

In 1906 T. A. Weston,,, gave the name of ‘‘streak’’ to the dis-
ease referred to above (the cause of the disease was not given). In
1908 Massee,,, in a letter to a correspondent who had sent in diseased
specimens replied, ‘‘the disease is of a physiological nature’’ and
‘“brought about by over feeding.’’ In 1912 Chittenden,,, believed
that the fungus Thielavia basicola was the cause of the “‘streak’’.
For the first two years of his inoculation experiments Chittenden

66

failed to infect healthy seedlings with the Thielavia fungus. It was
only by overwatering his plants that he succeeded in getting some root
infection, as he states: ‘‘To sum up, as far as our experiments go, the
‘streak’ disease is brought about by the attack of the fungus Thielavia
basicola on plants that have received some check at the root.’’ Chit-
tenden has failed to reproduce the typical ‘‘streak’’ but merely the
Thielavia root rot as I have already indicated under my description
of the above fungus. In the same year Massee,,, again studied the
disease and attributed it to Thielavia basicola.

In 1912 Dyke,,, found Macrosporium solani constantly associa-
ted with the disease, and believed it to be the cause of the trouble.

STREAK IN THE UNITED STATES

Ag far ag I know, up to 1913 there were no American references
to this disease.

Massee’s,;, Short note led me to believe that the disease was phy-
siological. Under Mosaie disease, I have shown that some workers be-
lieved it to be a physiological disease. While working on the mosaic,
and having the ‘‘streak’’ in mind, I,,, made the following statement:

‘‘In England the sweet peas suffer from a disease known as
‘streak’. This disease is very much dreaded by English gardeners,
as it causes great losses. From the description given of that disease
it seems to be similar to the new mosaic disease of this country. How-
ever, we refrain from passing final Judgement uniil we have the op-
portunity of seeing the English specimens and of making compari-
sons. In England the streak disease is attributed to a fungus Thiel-
avia basicola, which attacks the roots. In our investigations we have
not found the Thielavia fungus or any other organism associated on
the roots of mosaic affected plants. In fact, such affected plants were
found to have as normal a root with as much in the way of legume
nodules, as the healthy ones. If our mosaic disease proves to be the
same ag the streak disease of England, it will be safe to assume that
the Thielavia in England is secondary and merely follows the already
weakened mosaic affected plant.’’

The above was published on July 20, 1912, and the statement
was made before the American Sweet Pea Society at Boston early in
July of the same year.

In the middle of July of 1912, I first noticed a peculiar disease on
the stems of sweet peas grown in our experimental field. The disease

67

was characterized by dark streaks running along the stems. This sug-
gested at once the possibility of its being the ‘‘Streak’’ disease of Eng-
land. Diseased specimens were brought in the laboratory, and micro-
scopical crush mounts were made, but no organism was found that
would give any clue as to the nature of the trouble.

In submitting specimens to Prof. Manns and in consultation with
him, it was suspected that the trouble might be of bacterial origin.
We at once started to make cultures from the diseased material and a
pure culture of a yellow bacterium was obtained. Platings made from
diseased material from widely separated gardens gave a pure culture
of the same bacterial organism. Cultures made from diseased mate-
rial sent in by Wm. Sims of Boston, Mass. and by T. A. Weston of
Orpington, England, all gave an organism similar to that isolated
from the home material. Stains made of this organism revealed a
bacillus sp. In the meantime Prof. Manns recalled that he had seen
a similar streak disease on clovers in Ohio. A search for plants in-
fected in this way showed it upon clovers and upon some other
leguminous plants in the vicinity of Newark, Del.

Inoculations made with the bacterial organism on the sweet pea
reproduced the typical ‘‘streak’’ disease. That the ‘‘streak’’ is pre-
sent and widespread in the United States there is no doubt. I have
seen it in widely different localities in Delaware, in Pennsylvania, in
Massachusetts, and in New York. A letter addressed to me by C. C.
Morse & Co., of California, gives the folowing information:

‘“The ‘streak’ disease has not appeared in California as yet, and
this is accounted for by the fact that growers so far have not gotten
into methods of over-manuring their grounds.’’

As previously stated, the American literature contains no refer-
ence to the disease. Manns and Taubenhaus* published their first
account of the disease in the Gardeners’ Chronicle of England, an-
nouncing the ‘‘streak’’ ag being a bacterial disease and the parasite a
newly described bacillus, giving it the name of Bacillus lathyri.

““Symptoms.t like the Bacteriosis of beans, streak makes its
appearance in the season of heavy dew. On the sweet pea the disease
usually appears just as the plants begin to blossom; it is manifested by

*Manns, T. F., and Taubenhaus, J. J. ‘‘Streak, a Bacterial Disease of the
Sweet Pea and Clovers.’’ The Gard. Chron., London, Apr. 5, 1913.
tAbstracted from above article.

68

light reddish-brown to dark brown spots and streaks (the older almost
purple) along the stems, having their origin usually near the ground,
indicating distribution by spattering rain and infection through the
stomata. The disease becomes quickly distributed over the more ma-
ture stems until the cambium and deeper tissues are destroyed in con-
tinuous areas, when the plant prematurely dies. From the stems the
disease spreads to the petiole, flower, peduncles and pods. The symp-
toms in these cases being similar to those on the stems. On the leaves,
however, the disease appears as small roundish spots which gradually
coalesce, and eventually involve the entire leaf, which when killed
presents a brownish dark appearance.”’

Pathogenicity. The pathogenicity of the causative organism
may be proven by diluting a pure culture of the organism in sterilized
water and by spraying on the plants with an atomizer. This should
be done in the evening when the temperature is cooler and there is
less chance for evaporation of the applied infectious liquid.

The disease makes its appearance from seven to ten days after
artificial infection and the symptoms are similar to those produced
in nature. The organism may be reisolated from the artificially in-
fected plants and the disease induced again at will on healthy plants,
in each case the check remaining healthy.

Natural or artificial infection can only take place on mature
plants which have started to bloom. All attempts to inoculate plants
in all stages of growth previous to the blooming has failed. It seems
that the host possesses certain protective properties previous to the
blossoming which inhibits the growth of the parasite. Failure %o in-
fect young plants was not due to abnormal conditions or to bad tech-
nique. The disease in the field does not make its appearance until the
plants have started to blossom.

Isolation and Morphological Studies. Over 1,500 plate cul-
tures of beginning or young lesions were made from the several hosts.
The organisms may almost invariably be taken in abundance in pure
cultures from the beginning lesions in the stems of sweet peas when
the surface is properly sterilized.

The isolation work readily indicated the parasite to be a bacter-
ium; a yellow organism which grows luxuriantly upon all the nutrient
media, and especially rapid upon nutrient media containing sugars.

69

On standard nutrient glucose agar the colonies appear within 24 to 36
hours. The center becomes granular and the colonies have a marked
tendency to become stellate or auriculaie.

Morphological studies show the organisms to be a cemparatively
small rod-shaped bacillus, which in fresh cultures is rarely found in
chains, and seldom united in twos or fours. The flagella are not easily
demonstrated; they are shed so readily that usually not more than
two to five may be stained, and these are generally quite short. How-
ever, when proper material is selected, carefully fixed and stained,
the flagella may be demonstrated to be very long and delicate, and to
number 8 to 12, well distributed peritrichially*.

Ili. Physiological Diseases

By physiological diseases of the sweet pea we mean all disturb-
ances in the plants which are not induced by fungi, bacteria, in-
sects, or any other parasites but is expressed in a disturbance in the
metabolism of the plant. This disturbance seldom results in the sud-
den death of the plant. ;

Under Physiological diseases I will consider the following two
troubles: 1. Bud drop. 2. Arrested development.

BUD DROP

As the name implies the young flower buds at a very early
age turn yellow and drop off. This drop should not be con-
fused with the drop produced by the anthracnose disease. In the
latter case, the flower develops into a normal spike but it is attacked
soon by the fungus Glomerella rufomaculans which girdles it at a

point of attachment between the flower and the peduncle. In this case — ,

the flower often drops off leaving behind the beheaded peduncle. In ...°.
the latter case, however, the minute young flower bud never develops; -:
instead it turns yellow and drops off. ate

There seems no doubt that the drop is a physiological disease and’ +" >

is induced by an unbalanced condition of food elements in the soil.
This may occur in a soil that has been excessively fed or in a soil that
is lacking in plant food. ;
The following extract of a letter from a grower whose plants have
suffered severely from the drop and who gives the history of his soil

*A more detailed account of this organism will soon appear in 2 Delaware
Bulletin by Dr. T. F. Manns. ;

70

treatment will help to confirm the physiological nature of the disease.

‘“The soil is rich and is located in a valley near a creek, the sub-
soil is similarly rich but is not of a mucky nature. Before sowing the
peas the field was trenched and a thick layer of pig manure mixed
with a little hen manure was put at the bottom of the trench. The
manure was mixed up with soil in the trench and the seeds sown
thereon. After germination and when the plants reached from 8 to 10
inches, a commercial fertilizer (kind of fertilizer not stated) was
worked in at both sides of the row. A short time before blooming, a
layer of coarse stable manure was put around the plants to serve as
a mulch. During blossoming time the flower buds began to drop off
heavily and what promised to be a successful crop of blooms looked as
though it would result in total failure.’’ It is here very evident that
the plants were supplied with too much nitrogenous matter but with
little of potash and other mineral elemenis.

Cultures made from these fallen buds failed to produce an organ-
ism of any kind.

In order to remedy this trouble Prof. T. F. Manns suggested the
application of 150 ibs. muriate of potash and 600 lbs. acid phosphate
per acre. This treatment was followed out by the grower and the
drop ceased within a week resulting in a perfect crop of flowers.

On poor soils I have often seen this same ‘‘flower drop’’ and 1%
is also especially evident where sweet peas are grown in pots and in
poor, light, gravelly soil in the laboratory. An application of a bal-
anced fertilizer to these pots readily helped the plant to overcome
the bud drop.

ARRESTED DEVELOPMENT

This trouble, too, is a physiological disease and is induced by the
use of excessive fertilizers. The following facts from the letter of
a grower who has suffered from this trouble will also help to confirm
the ‘belief in the physiological nature of the disease.

The seeds were sown Nov. Ist in pots and planted Dee. 15 in
the beds in the greenhouse. Previous to the planting the beds were
well manured with horse manure which was applied six months before
planting. Besides this, wood ashes were also applied to the beds at
the rate of 1500 lbs. to 4500 sq. feet of bed space. This would be
equivalent to nearly seven and one-half tons per acre. About one

71

month after planting some of the plants turned yellow and died.
Upon examining the dead diseased specimens the plants were found
to be dwarfed with a sickly yellowish appearance. The roots pre-
sented a burned appearance suggesting the attacks of Thielavia.
Microscopical examinations and cultures made from the diseased tis-
sue did not reveal the presence of any parasite which could be asso-
ciated with the soil. In submitting some of the soil to Prof. T. F.
Manns for examination, he found it strongly alkaline. Hard wood
ashes contain about 30% caustic lime and from 5 to 12% potash. Ac-
cording to Prof. Manns it was the excess of these elements in the soil
that made it so highly alkaline, and this condition injuriously affect-
ed the plants. This kind of injury could be considered purely phy-
sical since it is brought about by the exposed surface of the roots to
an alkaline substance. Nevertheless any injury which interferes with
the metabolism of the roots is reflected in a derangement of the meta-
bolism of the plant. The resulting injury is therefore of a physical
nature.

As a remedy for this trouble Prof. Manns advises the use of acid
phosphate, followed by a good drenching of water. This will neu-
tralize the alkaline effect of the soil and also help to balance the plant
ration.

METHODS OF CONTROL

Under methods of control the following lines of investigation
have been carried on:

Resistant varieties

Seed treatment

Treatment of soil with chemicals

Studies of the fungicidal value of some chemical poisons

Formaldehyde treatment of soil

Steam treatment of soil

RESISTANT VARIETIES

To test out the resistance of different varieties of the same host
to a certain parasite, the general practice is to plant in the field the
varieties to be tested and to allow full sway to the natural causes of

72

infection. At the end of the growing season an estimate is taken of
the per cent of infection of each variety and on that basis a seale of re-
sistance is formulated. While this method by itself is fairly val-
uable, the method nevertheless is unreliable because a certain va-
riety which under the above test proves highly immune or highly sus-
ceptible to disease will, under different conditions of climate, ete. prove
the opposite of what it has promised to be in its first trial. The reason
is very obvious. No two varieties are alike as well as no two individu-
als are alike. Conditions in the field are not always ideal for every
variety of a certain host to become susceptible to disease. If this were
the case we would have all our crops ravaged by pests. In order to
make a reliable test of the resistance of different varieties it is
necessary to have the same conditions of soil and care and then to
submit the varieties to the severest test by making all conditions ideal
for the parasite to attack the plants. To carry out this idea, I planted
100 sweet pea seeds of each variety to be tested in sterile soil and pots
in the laboratory. Previous to the planting, the seeds were sterilized
by being soaked in a 5% formaldehyde for 1% hr. The seeds
of the different varieties did not all germinate evenly due to
the hardness of the seed coats in some seeds but eventually they
all germinated. When the plants were eight weeks old:each pot
with its different variety was well watered and then covered with
a bell jar. The latter was sterilized by being previously washed
with a 1-1000 mereuric bi-chloride solution and then rinsed with
distilled water. The plants remained under the bell jars for 48
hours, where all were seen to be uniformly covered with drops
of water. A large amount of moisture accumulated under the bell
jars and this was plainly visible by the drops of water standing on
their walls. Under such conditions of moisture as described above,
infection readily takes place. The infecting material chosen for this
purpose wag the fungus Glomerella rufomaculans, which causes the
anthracnose disease. Accordingly a heavy suspension of spores from
a pure culture was diluted in sterilized water and then applied to the
plants by means of an atomizer. The inoculated plants were covered
again for 48 hours. After that the bell jars were removed and the
plants left uncovered. The result of the experiment is given in
Table VI.

From Table VI it is seen that of all of the varieties tested not one
of them proved to be entirely resistant. On the other hand it is seen

73

that the percent of infection differs with the variety. This means
then that in each variety there are certain individual plants which
are resistant to this particular fungus tested. Attempts were made
to reinfect those plants which remained healthy after the first inocu-
lation and it was found that nearly 50% in each ease was infected
and ‘the rest remained resistant and continued to grow well. This con-
clusively shows that while no one variety is entirely immune to a dis-
ease yet there are nevertheless certain individuals of that variety
which have developed the power of resistance. It is well known that
if a plant is resistant to a particular disease, it may be very susceptible
to another disease. The problem, therefore, is to test the desired va-

TABLE VI
Name of variety (seed- Fungus used (spores in sus- Per cent of
lings six weeks old) pension of water) infection
King Edward VII Glomerella rufomaculans 90%
Gray Friar oe 66 80%
Aurora aS oe 93%
Apple Blossom eG Eg 90%
Emely Henderson os oe 40%
Henry Eckfort me ae 100%
Jeannie Gordon ue es 98%
Dorothy Eckfort gs ge 100%
Hellen Pierce ae oe 92%
Coccineae ae = 70%
Katherine Tracy te He 70%
George Herbert oe a 60%
Black Knight ae ie 80%
Jeanett Scott og oe 72%
Dobbie Mid Blue @e as 40%
Blanche Burpee ae Bs 90%
America ee éf 100%
Blanche Ferry oe a 100%
Mrs. A. Watkins 4 a6 100%
Countess Spencer oe a6 90%
Black Michael es ee 60%
Bolton’s pink ce ig 80%
Countess Cadogan as ne 100%
Mrs. Bieberstedt ae is 20%
Agnes Eckfort ue ee 100%
Burpees Dainty a a 100%
KH. J. Castle ra 4g 1%
Glady’s Union oe oo 4%
Captain of the Blues ee ae 60%
Duke of Westminster ze ue 80% °
Mrs. Collier Sf Ss 70%
Burpees Midnight ee he 40%

er bce ee in LS AO eater AI pel
rieties with all the known diseases to which they are subject. In these
tests all the immune individuals must be selected and by crossing and

74

selecting we will build up a strain which will possess complete immun-
ity to all or at least to most of the diseases to which that variety is
subject.

SEED TREATMENT

I have previously shown that the sweet pea seeds are capable of
carrying and of introducing one of the most dreaded diseases of the
sweet pea, namely, the anthracnose (Glomerella rufomaculans).
Sweet pea seeds were also found to carry several species of fungi
which seem to be unable to assume the role of parasites. Nevertheless,
the time may come when these fungi may become parasites of the
Sweet pea.

It was, therefore, thought necessary to devise some means of
treating the seeds which woud kill all external as well as internal
parasites, and at the same time not inhibit the germinative power of
the same. The following are the methods which have been tried:

Effect of temperature
Effect of sulphuric acid treatment
Effect of formaldehyde treatment

Effect of Temperature on Seed. In order to test the effect
of temperature the following experiments were tried. Ten differ-
ent varieties were thoroughly mixed and lots of 100 seeds each were
picked out and put in pieces of cheese cloth and tied up with a string.
The experimental temperatures of the water used were boiling water,
90°, 80°, and 60° C. The seeds were immersed in the water with the
varying temperatures and kept there for different intervals of time,
as is indicated in Table VII. In each test a duplicate series was al-
ways made, 1. e. using two packages of 100 seeds each. The per cent
of germination in each case expresses the average taken from each
duplicate series. After each treatment seeds were placed in sterilized
petri dishes containing moistened filter paper which had been pre-
viously sterilized by being placed in boiling water for two minutes.

After placing the seeds in the petri dish more sterile water was
added in order to secure the amount of moisture necessary for ger-
mination. The plates were then placed in the incubators for 10 days,
observations being made every two days. The result of the experi-
ment is given in Table VII.

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76

From Table VII it is seen that of all the temperatures tried,
placing the seeds in boiling water for one or two seconds, seems to
offer only little promise of success.

Placing the seeds in water of 90° C. for one minute insures a
somewhat higher per cent of germination. However, the growth of
seedlings seems to be weaker than either checks or those boiled for
one or two seconds.

The series treated with water at temperatures of 80° C., 70° C.,
and 60° C. did not meet our expectations of success. However, these
results are not final, as they simply open up a line of investigation
for the future.

Effect of the Sulphuric Acid Treatment on Seed. Historical.
Rostrup,,,; was one of the first investigators to use sulphuric acid
on hard seed in order to hasten germination. Todaro,;,, while
working independently, found that concentrated sulphuric acid
of a density of 1.84 acted upon hard seeds of many leguminous planis,
rendering them capable of prompt germination. Thornber,,,, %oo,
found that when certain seeds are treated with sulphurie acid, their
germination was hastened. Schneider-Orelli,,, also found the sul-
phuric acid treatment of value in hastening the germination. Bolley,,.
also found sulphuric acid to benefit the germination of seeds. In 1912
Love and Leighty,,, also found the same general beneficial results oa
germination of seeds treated with sulphuric acid.

My object in treating sweet pea seeds with sulphuric acid was to
find out tis effect on germination, and as a preventive mears in de-
stroying all possible adhering spores of pathogenic organisms. The
method was to place the seeds to be treated in glass receptacles and
then to cover the seeds with pure sulphuric acid. The time of treat-
ment was five minutes, fifteen minutes, one-half hour, one hour and one
and a half hours. After the treatment the acid was poured off and
the glass receptacle was put under running tap water for five min-
utes and then rinsed three times in sterilized water. After that the
seeds were placed on moist filter paper in petri dishes, and ‘the latter
were put in the incubator for ten days. A series of untreated seeds
were also run as checks.

The results obtained from the seeds treated five minutes, fifteen
minutes and one-half hour were practically the same, i e., in each
case the percentage of germination was much higher in the treated

77

seeds than in the checks. In the former the percentage of germination
ranged from 95% to 100%, while in the later it ranged from
60% to 85%. The seeds treated in the acid for one hour showed
50% injury, and the 114 hour treatment gave only 2% germination.

In order to test the effect of sulphuric acid on the fungus flora
of the seeds, 10 ce of the acid was put in test tubes, and the latter
were inoculated heavily with spores of Glomerella rufomaculans and
allowed to stand for five minutes, fifteen minutes, half-hour and one
hour. Transfers of the treated spores were made by means of a loop
into melted tubes of agar. These were well shaken and poured into
petri dishes, cooled, and placed in an incubator. Check cultures were
also run by using untreated spores transferred directly into agar. In
three days the check plates all showed a vigorous growth of a pure
culture of the fungus where none of the series of the treated spores
showed signs of germination even after eight days. This proves, then,
that sulphuric acid can be used with advantage in treating seed both
to inerease the per cent of germination and also to kill all spores
which adheres to the seed coat.

Formaldehyde Treatment of Seed. The method employed here
was the same as for the sulphuric acid. The strength used was 5%,
and the time of treatment was five minutes, fifteen minutes, half hour,
one hour and one and a half hours. It was found that the one and a
half hour treatment seemed to have reduced the percentage of germin-
ation, whereas, all the other treatments did not affect in any way the
germination.

Where there was no injury apparent, the formaldehyde treatment
did not seem to help the germination of the seeds as did the sulphuric
acid. However, it no doubt helps to kill the adhering fungus spores
of the seed coat. This latter advantage makes the formaldehyde
treatment a valuable preventive means.

TREATMENT OF SOILS WITH CHEMICALS

The object of this treatment was to determine: 1, the effect of the
treatment on the growth of the plant and its resistance to disease;
2, the effect on the soil flora; and 3, the effect on the nitrogen content
‘and ammonification. The method employed was to sow 50 seeds in a
pot (18 pots in all) ; the soil employed was unsterilized hight garden
leam.

78

The chemicals and the strengths used are indicated in Table VIII.
After the seed had germinated and the plant had attained three inches
in height, I began to water them twice a week with the respective
chemicals. The checks were treated with distilled water. The experi-
ment was run for two seasons, in each case up to the flowering time
of the host.

The results of the first season are not indicated in Table VIII
because with one exception as stated below there was no apparent dif:
ference between the treated and the check plants. During the first
season, the treatment did not affect in any way the fungus or bac-
terial flora of the soil. Both treated and check planis, before the
close of the first season, were inoculated with spores of Glomerella
rufomaculans. But both lots gave about the same percentage of in-
fection. This clearly indicated the wonderful power of the soil to
absorb mineral poisons and to fix them in such a way as to make them
harmless to plant growth. Ordinarily, neither plant, fungi, nor bac-
teria could grow in a solution of 1-1000 copper sulphate, for instanee. .
However, when this same solution is applied to the growing plants
through the soil, the latter fixes it so that the plants continue their
growth and reach maturity as they would if the copper sulfate were
not there. The same holds true for the soil flora.

The only injury apparent to the plants during the first sea-
son’s trial was on the series watered with 1/100 MnSO,. Altho grow-
ing fairly well, these plants were seen to lose their chlorophyll at an
early date. These plants died just before blossoming, and at that
stage they were white with no trace of chlorophyll.

The results obtained from the second season’s growth are tab-
ulated in Table VIII.

In order to determine the effect of the different chemical treat-
ments on the soil flora, the method employed for isolating the organ-
isms was the same as that recommended by Prof. T. F. Manns,,o.
Plates containing 1/1000 and 1/10,000 of a gram of soil was made.
Two kinds of media were used for this purpose, the composition of
which is given in Table VIII. The media marked X XI is purely syn-
thetic and is of value in bringing out the azotofiers. It is also valuable
in bringing out the bacterial flora of a soil and in keeping down
the saprophytic fungi. Medium II on the other hand, is more likely
to bring out the fungus growths and to keep in check the bacterial

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19

flora. The nitrogen was determined* according to the Kjeldahl
(modified) method, ,,.

Ammonification wag determined by inoculating 100 ce of nutrient
broth containing one gram of peptone with 1 ce of an infusion made
by shaking 10 grams of soil in 100 ce of water.

From Table VIII we see that the results obtained vary consid-
erably, especially during the first six days, which more nearly rep-
resents the ammonifying power. Under copper sulphate for instanee,
1/1000 killed 70% of the seedlings and the growth of the latter wag
quite stunted. The average number of bacteria per gram of soil was
also less when compared to the checks, whereas there was an actual in-
erease in the nitrifiers, which resulted in an increase of total nitrogen
and ammonia. On the other hand, copper sulphate 1/3000 produced
stimulation in plant growth; there did not seem to be an appreciable
decrease in the general bacterial flora, but there was a resultant de-
erease of ammonifiers. Again, under Hg Cl, 1/2000, the result was
a killing of all the seedlings, but an increase in the bacterial flora as
well as nitrification and ammonification. Hg Cl, 1/4000 gave stimula-
tion in plant growth, soil flora, and in ammonification.

Table VIII is extremely interesting, as it opens up so many new
phases in soil biology, soil bacteriology, and in plant pathology.

STUDIES OF THE FUNGICIDAL VALUE OF SOME
CHEMICAL POISONS

Those who are actively engaged in the study of methods of con-
trol in plant disease, will readily realize how uncertain it is to depend
upon field methods alone. In order to test out the value of a fungi-
cide the only method used consisted in spraying the particular plant
to be treated, with that fungicide, and of noting results. With such
a method one works in the dark. Moreover, a great deal of time is lost,
because each trial, or each modification of a trial means one season
of growth. In 1910 Reddick and Wallace,,, worked out a quick
method of determining the efficiency of a certain spray material. In
brief, the method is as follows:

The fungicide to be tested is sprayed on a clean slide with an
atomizer. It is then allowed to dry in order to permit any chemical

*Mr. Paul Emerson under the direction of Prof. Manns carried out this
phase of the work.

80

changes to oceur that are likely to be induced by exposure to atmos-
pheric conditions. It is supposed that the same chemical changes
which take place on the leaf previous to infection also take place on
the slide in the laboratory before the spores are placed to germinate.
This more nearly duplicates natural conditions, and the results at
time of germination practicaly indicate the relative fungicidal value
of the chemical tested. When thoroughly dry, each slide is placed in
a petri dish containing enough waver to keep the air well saturated.
Spores of the particular fungus which we wish to control are mixed
in water, and drops of this water are placed, with a dropper, on the
treated slide. The petri dish is now covered and 24 hours are allowed
for the spores to germinate. The inhibition of germination of all the
spores in the drops placed on the slide indicates the value of the fungi-
eide. While the method above described is excellent, it nevertheless
has its drawbacks. We know that in practice we do not spray our
plants every day, but this is usually done every three or four weeks.
The method employed by Reddick and Wallace cannot account for
the fungicidal value of a certain spray material during the two or
three weeks from the time of its first application. In my studies I have
supplemented this deficiency by the following method. While adopting
the method used by Reddick and Wallace of applying the fungicide
and of drying the slide, I have worked out the following modifications.
Instead of spraying only a few slides and of inoculating them at onee,
I have sprayed some fifty slides at one time with each chemical.
These slides were all dried and divided into different lots. Lot I was
used for germination at once, lot 2 used, say, after an interval of one
week, ete. This method allows the time element to have its full effect
on the fungicide concerned, and each germination test definitely indi-
cated whether that fungicide deteriorates rapidly or not. The fungi-
cide which preserves its germicidal value the longest is probably of
the greater economical value. The fungicides tested and the strengths
used are indicated in Table IX.

It will be seen from the above table, that copper sulfate at the
strength of 1/100 up to 1/500, and potassium permanganate 14% up
to 8% completely inhibited the germination of the spores of Glom-
erella rufomaculans for nearly two months. On the other hand, lime
sulphur 1/10 up to 1/50 gave most unsatisfactory results from the
very first test, and its fungicidal value rapidly weakened with age.
This was still more evident with the ‘‘Sulphurated Potassium’’ also

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82

known as ‘‘Liver of Sulphur.’’ Lime sulphur is a valuable fungicide
in controlling apple scab (Venturia inequalis) and sulphurated
potassium is a valuable fungicide in controlling mildew (Oidium sp.),
but evidently these two fungicides are of no value in the control of
the sweet pea anthracnose. On the other hand, copper sulphate and
potassium permanganate both prove very toxic to the spores of the
anthracnose. The next step therefore, was to test all the strengths
used of these two fungicides by spraying them on sweet pea plants in
field, and by watching to see if these poisons produced burning of the
leaves and stems. Copper sulphate at the strengths of 1/100, 1/200,
1/300, 1/400 and 1/500 all burned the leaves of the sweet pea. Hence
while the above strengths possess valuable germicidal properties their
use upon the sweet pea is prohibitive. This means that weaker
strengths are to be tried until the proper limit is reached, 1. e. the
limit which does not decrease the germicidal value of the copper sul-
fate and which does not produce injury to the plant. This we intend
to earry on further in the future. Potassium permanganate 144% up
to 3% does not produce any injury to the plant whatsoever. As a
matter of economy, therefore, 14% of potassium permanganate proves
a valuable fungicide in the control of the sweet pea anthracnose. It
should be applied to the plant not oftener than it is washed off by
rain. The method can be used in testing out an endless number of
chemicals and there is no doubt that a good many will prove valuable
additions to our list of fungicides.

Sort ‘TREATMENT IN THE GREENHOUSE

Growers who are troubled with Rhizoctonia or Fusarium in their
greenhouse beds, will find the following directions valuable,,,.

STEAM STERILIZATION

‘““The preventive method which promises best results to those who
have the convenience for applying it is that of sterilization of the seed
beds by steam.

“In addition to the killing of the fungus, this method, in com-
mon with surface firing, to be described later, has several advantages
over formalin treatments. The weed seeds im the soil are very largely
killed, and this alone, according to the testimony of the farmers who
have used sterilization, pays for the cost of treatment, as the beds do
not have to be weeded and thus a large amount of hand labor is ob-
viated. The physical texture of the soil is altered by the heat and

83

made more suitable to root development and, moreover considerable
plant food is made directly available to the seedlings. Furthermore,
the heating of the soil just before sowing in the spring has an ap-
preciable effect in starting the seedlings off quickly.

“With the elimination of the fungus it is possible to employ
those methods forcing the plants by extra fertilization, increased
watering, and higher temperature which would otherwise be unsafe
as favoring the development of the root-rot fungus.

“Ordinary greenhouse method—The method of sterilization to
be used will depend to some extent on the size, the location, and ‘the
permanency of beds and the cost of application.

‘“The method in general use for the sterilization of soil in green-
house benches might advantageously be employed in beds that are
to be used year after year without change of location, as the equip-
ment would be more or less permanent. This consists in placing one
foot below the surface of the soil a system of 114-inch pipes which
are perforated with 14-inch holes on their under side at intervals of
6 inches throughout their entire length. The pipes should run
lengthwise of the bed, 18 inches apart, and be connected with a steam
boiler capable of producing 80 to 100 pounds pressure. Before treat-
ment the soil should be thoroughly spaded up and pulverized to permit
ready access of the steam to all parts, and all fertilizers should be
applied at this time.

‘“The bed to be treated should be covered with several thicknesses
of old burlap or blankets to confine the heat to the soil. The steam
should be applied at a pressure of 80 to 100 pounds, as at a high
pressure it is much drier and the soil is not wet as much as when low-
pressure steam is used. A treatment of from one to two hours is
usually sufficient to thoroughly sterilize the soil to a depth of 18 inches.
A few potatoes laid in the surface will indicate the thoroughness of
the treatment by the degree to which they are cooked. The blankets
might advantageously be left on fof some time to make the treatment
‘more thorough.

‘‘While this method offers some advantages for seed beds of lim-
ited area, in that the pipes may be left in the ground and used year
after year with little extra labor and may also be used for subirriga-
tion, the initial cost of installation, especially on large seed-bed areas,
may be prohibitive.

84

““Inverted-pan method. The method which has given the best re-
sults in practice, and which because of its simplicity and small cost
recommends itself for use on large or small areas, is the invention of
Mr. A. D. Shamel, of the Bureau of Plant Industry, and was devised
by him to sterilize nematode-infested soils in Florida. The apparatus
consists of a galvanized iron pan, 6 by 10 feet and 6 inches deep, which
ig inverted over the soil to be sterilized and the steam admitted under
pressure. The pan is supplied with steam hose connections, has
sharp edges, which are forced into the soil on all sides to prevent the
escape of steam, and is fitted with handles for moving it from place to
place, the weight of the entire pan being not over 400 pounds.

‘‘The soil is prepared as in the greenhouse method, a few potatoes
being buried at a depth of a foot to gauge the degree of heat attained.
A soil thermometer may also be used if desired. The steam should be
kept at as high a pressure as possible, 80 to 100 pounds being best,
and the treatment should continue for one to two hours, depending on
the pressure maintained. In experiments conducted in the spring of
1907, one hour’s steaming at 80° C. under 100 pounds pressure gave
best results in killing ‘both the fungus and the weed seeds. When one
section of the bed is treated the pan is lifted and carried to an un-
sterilized portion and the operation repeated until the entire bed is
steamed.

FORMALDEHYDE STERILIZATION

‘“The use of a formalin solution for the sterilization of green-
house soil against Rhizoctonia has been in vogue for some time with
excellent resulis, and furnishes a very simple means of combating the
root-rot. The method is as follows: The beds are thoroughly pre-
pared the same way as for the other methods of sterilization described
and are then drenched with a formalin solution composed of 1 part
of commercial formalin to 150 to 200 parts of water, three-fourths
to 1 gallon of this solution being used to the square foot of bed space.
The solution should be put on with a watering pot with a hose and
distributed as evenly as possible over the bed, so as to thoroughly wet
the soil to the depth of a foot. It will in most eases be necessary to
put this solution on in two or three applications, as the soil will not
take in this quantity of water immediately. The beds should then be
covered with heavy burlap or a tarpaulin to keep in the fumes for a
day or so, and then aired for a week before sowing the seed.

85

‘‘Spring applications of formalin are open to the following ob-
jections: The addition of such a large quantity of water to the goil
keeps 1t wet and cold for some time longer than would naturally be
the case, thus delaying germination as well as subsequent growth; the
necessity of airing the beds to remove the formalin fumes and to allow
the soil to dry out also causes delay in seeding. To obviate this dif-
ficulty the beds should be treated in the fall, before freezing weather
sets in. In this case a stronger solution, 1 to 100, may well be used,
as there will of course be no danger then of injuring the seedlings.’’

SUMMARY

1. It has been shown that the sweet pea is subject to a number of
diseases.

2. The following classes of diseases have been investigated:
I. Fungous; II. Bacterial; III. Physiological; IV. Animal or In-
sect Pests.

3. Contrary to the statements of Massee and Chittenden, Thiel-
avia basicola does not produce the ‘‘streak,’’ but produces only a root
rot of the sweet pea.

4. The pathogenic nature of Corticium vagum B. & C. has been
established.

5. Chaetomium spirochaete has been shown for the first time to
be a plant pathogen, and especially to produce a root rot of the sweet
pea.

6. A new Fusarium root disease has been described, and the name
Fusarium lathyri Taubenhaus has been given to the fungus, and its
pathogenicity established.

7. Of the Animal parasites the eel worm (Heterodera radicicola)
has been shown to produce a root gall disease of the sweet pea. The
disease is carefully described. The eel worm has also been shown to
open the way to the attacks of several fungous diseases.

8. Sclerotinia libertiana has been shown for the first time to pro-
duce a collar rot as well as a stem disease of the sweet pea.

9. Studies on the mildew of the sweet pea have shown the disease
to be very prevalent under greenhouse conditions as well as out of
doors. The cause of the mildew is a species of Oidium. Observations
up to date have failed to reveal the perfect stage of the fungus.

86

10. Extended studies and cross inoculations have definitely proven
that the anthracnose disease of the sweet pea and the bitter rot of ‘the
apple are caused by the same fungus Glomerella rufomaculans.

11. It has been also proven that the following pathogens, namely,
Gloeosporium gallarum from oak gall, Gloes. diospyri from persim-
mon fruit, Gloe. officinale from the Sassafras, Colletotrichum nigrum
from the pepper plant, Colletotrichum phomoides from the tomato,
appear to be identical and the same as Glomerella rufomaculans, since
they can all produce the anthracnose disease of the sweet pea and the
bitter rot of the apple. Cross inoculations would no doubt reduce the
great number of our so-called different species of Gloeosporiums.

12. The mosaic has been shown for the first time to produce a dis-
ease on the sweet pea. The pathogenicity and the infectious nature
of the disease have been clearly demonstrated. Exceptions are taken
with Woods that the disease is of a physiological nature but that it is
induced by either bacteria or protozoa which neither our microscope
nor our present method of staining are able to detect. Insects and
especially the green aphids seem to be the main earriers and distrib-
utors of the disease.

13. Manns and Taubenhaus have definitely proven that the
‘“streak’’ disease is caused by Bacillus lathyri M. & T. and not by
Thielavia basicola as previously believed by Massee and Chittenden.

14. Bud Drop in one form is here shown to be induced by a high
nitrogen supply not properly balanced by phosphorie acid and pot-
ash; by addition of the latter the trouble is quickly corrected. Ar-
rested development may be due to overtreatment of soil with wood
ashes the treatment being too caustic. Such an error may be corrected
by the addition of acid phosphate.

15. Under methods of control it is shown that no one variety is
immune to the anthracnose but there are certain individuals in each
variety which are more or less immune to the disease.

16. Boiling the seeds for one or two seconds destroys the spores of
parasitic fungi, but commercially the treatment is not applicable on
large quantities of seed at a time.

17. Soaking the seeds in sulphurie acid for five minutes, fifteen
minutes and one-half hour increases ‘the per cent of germination and
at the same time kills all the spores which adhere to the seed coat.

87

18. Soaking the seeds in a 5% formaldehyde solution from five
minutes to one hour does not iincrease nor decrease the percent of ger-
mination but helps to kill the spores which adhere to the seed coat.

19. Watering soils with chemical poisons does not increase the
resistance of the plants which are grown on that soil. The latter
adsorbs and fixes some of these poisons so as to make them harmless
to plant growth.

20. A new method has been devised in determining the length of
time in which any fungicide can remain efficient in controlling plant
diseases when sprayed on the plant to be treated.

88

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