Cockleburs (species of Xanthium) as poisonous plants

Historic, archived document

Do not assume content reflects current
scientific knowledge, policies, or practices.

Washington, D. C.

COCKLEBURS (SPECIES OF XANTHIUM) AS

By C. DwicHt Marsh, Physiologist in Charge of
oning by Plants; GLENWoop C. Ror, Assistant, a
gist, Pathological Division, Bureau of Animal

ae f
ew ‘eee re

CONTENTS
Page Page
Bueposecand seopes 2 22 st 1 | Discussion, ete.—Continued.
ASTORCa ouTaManT yeas ee = 2 Time from feeding to appearance
@hercocklepur plant = ose = 5 OFSVInp LOMc? Soe 16
PxpenimMenta ln Works —— = == oe oe 6 Murat On OLeSsiCkMeSS=—=- ae 16
Typical case of pig 18_________ 6 Effect of continued feeding____ 1/6
Discussion and general conclusions_ T¢ Animals poisoned by cocklebur_ 18
HIP LOMSe Ples=— le eee Oe 7 Part of plant poisonous_______ 18
Symptoms in sheep and eattle__ A Mechanical injury by burs__-__ 19
Symptoms tine chickens 2.2. — _ = 12 Toxicity OF Tied splat 20
AUTOPSY (ndings =! Sie ehe bs) aD, ETT ECT See aa 21
Microscopic changes in tissues_ 13 SS CLT Tey See ee See ee ee 22
Toxic and lethal dosage_______ TLS) ot pnd BU DUO RERIEER VO) ON cae ale a ee ie ee 22

PURPOSE AND SCOPE

For several years requests have come to the United States Depart-
ment of Agriculture for information in regard to the poisonous prop-
erties of the cocklebur, a well-known weed. Frequently these requests
have been accompanied with more or less detailed statements in re-
gard, to supposed cases of the poisoning of aneo ed s by these weeds.
Some correspondents have complained of heavy losses, especially of
pigs. Published statements, however, in regard to the plants have
been somewhat contradictory, and it has seemed strange that if they
were really poisonous there were not much greater losses, for cockle-
burs are widely distributed in the United States and grow with great
luxuriance. The plants are found in nearly all. parts of the world
and have become especially noxious in South Africa and Australia,
where, after being introduced, they have made themselves very
much at home.

From the stock raiser’s standpoint the question of the poisonous
properties of the plant has become very important. On this account
an experimental study of cockleburs has been made by the Depart-
ment of Agriculture. The results of this work have brought out the

96994°—24 1 4

¢

2 BULLETIN 1274, U. S. DEPARTMENT OF AGRICULTURE ~

essential facts, and, while much more work can be done, the impor-
tance of the subject makes it seem wise to issue a publication which
will discuss the subject in a definite manner.

HISTORICAL SUMMARY

In the discussion of cockleburs (species of Xanthium) as stock-
poisoning plants, no attempt has been made to distinguish the dif-
ferent species. The species are closely allied and, there is reason to
think, do not differ materially in their poisonous properties. Many
of the articles which have been written on cockleburs were not writ-
ten by technical botanists, neither were the plants submitted to
botanists for determination, so that. it is probable that the species in
many cases were incorrectly named.

The history of the species of Xanthium as stock-poisoning plants

is comparatively modern. The first statement that was found in re-
gard to the injurious effect of these plants upon domestic animals
was made by Doctor Bancroft in 1880 in a paper read before the
Queensland (Australia) Physiological Society. It has been impos-
sible for the writers to see the original paper, but the information in
regard to it was obtained from a review by Heldreich in the
Botanische Centralblatt, 1880. It is stated that, on the estate of a
Mr. Yates, a large number of cows, one horse, and a sheep had been
killed by eating the young plants of Xanthium strumarium. The
animals fell upon the ground and died very quickly. Doctor Ban-
eroft made an extract of the plant, with which he poisoned small
animals and obtained the same results with extracts of the species
Xanthium spinosum. The reviewer calls attention to the fact that
although two species of Xanthium are widely distributed in central
and southern Europe there are no reports there of cases of poison-
ing. The cocklebur in Queensland, of course, was an introduced
plant.
: Zander, 1881, quotes a letter from Heimberger to the effect that
cases of poisoning have arisen from the seeds and oil of Xanthium
strumarium. He states that the oil has been pressed out for com-
mercial purposes. All who have eaten the oil or the seeds were made
exceedingly sick and several children died. On this account an in-
vestigation had been made but no poisonous substance had been
found. He reported that he had made experiments on cats and dogs
with the oil with no results, although one of the workers was made
sick after taking about 10 of the seeds. Zander himself made some
experiments with cats and frogs with no tangible results.

Cheatham, 1884, states that cocklebur is one of the first plants that
appear in the spring, and that in some of the Southern and Western
States the swine which run at large are very fond of the young
plants and almost invariably die after eating them, and that antidotes
had not been used with any suctess. He explained some chemical
work which was done on the plant.

Goff, 1894, makes the following statement : “ It has been said that
the plant is poisonous to cattle, but this is probably a mistake. It is
at least known that cattle sometimes eat sparingly of it without
serious results.”

*
a

COCKLEBURS AS POISONOUS PLANTS 8

Maiden, 1895, speaking of the Xanthium spinosum, which in some
localities is known as “ Bathurst bur,” quotes Doctors Bancroft and
Goff, but adds nothing to preceding information. In 1896 Maiden
quotes Prof. J. C. Arthur as stating in correspondence that in the
United States the cockleburs do not have the reputation of being’.
poisonous, and goes on to say that he is convinced that whether ex-
tracts of the plant are poisonous or not it is not injurious in the
field, and that he has investigated one case of supposed poisonous
effect of Xanthium and found the trouble to be anthrax.

Lewin, 1897, states that XYanthzwm spinosum in certain stages is
poisonous and may kill 50 per cent of a herd.

Bailey, 1898, referring to the supposed poisonous results from
cocklebur, known in Queensland as “ Noogoora bur,” states that in
his opinion the plant would be dangerous only when making a rank,
succulent growth. He describes it evidently from hearsay.

Chesnut, in his preliminary catalogue, 1898, speaks of Xanthium
canadense as killing hogs in Texas, X. strwmarium as being fatal to
the same class of animals in Georgia, and XY. spinosum as being’ sus-
pected of having poisonous properties.

Halsted, 1889, says that the deaths of swine are attributed to Xan-
thium, but while the effect may be mechanical, the plant does have
poisonous properties.

Kirk, 1901, makes the following statement: “At certain stages of
growth the plant is poisonous to stock, but this is of little consequence
as it is very rarely eaten by them.”

O’Gara, 1903, says there have been no cases of cattle poisoned in
Nebraska, but one farmer lost 20 hogs averaging 160 pounds each,
and evidence showed that they had eaten a quantity of the young,
juicy burs. O’Gara adds: “The whole plant, as well as the burs, is
known to contain a poisonous principle which reduces heart action
and causes death.”

Craig and Bitting, 1904, report that a chemical examination and
a feeding test of Xanthium was negative. The young plants stripped
of the burs were fed to calves, pigs, rabbits, and guinea pigs, but no
untoward effects resulted. They state that post-mortems on animals
supposed to have died from cocklebur poisoning showed that in all
cases the death was due to the burs. “A few burs would be swallowed
with the young plants and their horny prickles would irritate the
stomach wail and cause inflammation which finally terminated in
death. In three cases the burs lodged in the throat and could not be
expelled.”

tanley Coulter, 1904, says that cockleburs “are irritant on ac-
count of the dust and hairs with which they are covered and not
because of a toxic principle.”

Mayo, 1905, reported two serious losses of hogs from cocklebur.
Out of 35 head, 25 died in one night, and 8 more during the next
day. “They would he down on their sides, kicking and pawing for
a short time and then died.”

In an article in the Breeder’s Gazette, 1908, Glint says that
cocklebur is sure death to hogs, farmers sometimes losing 40 per
cent, and that the plant will Inll cattle in the spring.

An article by King, 1909, states that young cockleburs are poison-
ous to pigs.

4 BULLETIN 1274, U. S. DEPARTMENT OF AGRICULTURE

Kinsley, 1909, tells of a case in which one hundred 6-months-old
shotes were turned into a 40-acre field on which cocklebur was just
coming up through the ground. The hogs were seen to eat the
young plants and seven of them died. He gives the details of a post-
mortem examination.

Pammel, in his Manual of Poisonous Plants, 1910 and 1911, while
quoting statements of the poisonous properties of Xanthium, says:
“The injury from this plant probably comes largely from its me-
chanical action,” and he quotes others in substantiating this belief.

In articles by Pammel in the American Journal of Veterinary
Medicine, of 1918, 1919, 1920, and 1921, quoting statements of the
poisonous properties of the plant, he gives the impression that he
still thinks the chief injuries by cocklebur are mechanical.

In Cooperative Manager and Farmer, 1917, the following state-
ment is made which apparently is based on work by the Missouri
Experiment Station: “ Cockleburs in pastures are particularly dan-
gerous for pigs and shotes. The burs. get inside the stomach of the
animal and inflame the lining, causing death, which is the usual
result. Even the plants themselves are poisonous to hogs, but most
authorities think it is the old, matured bur that does the most
damage.”

Maiden, 1918, states that a dermatitis is produced in those who
handle Xanthium strumarium. He made a similar statement in
1921.

In Bulletin 185 of the Alabama Experiment Station, 1920, occurs
the following statement by Cary: “ Young cockleburs are said to be
poisonous to pigs, but our feeding tests disprove it. We could not
kill pigs by feeding them young cockleburs. Jimson weeds grow
with cockleburs, and Jimson weeds are very poisonous.”

Hansen, 1920, makes the following statement: “ Although fatal

results are generally attributed to poisoning, there is little evidence —

to substantiate this theory. The harmful effects are largely due to
the mechanical action of the spiny burs, which are injurious in sev-
eral ways. ‘These burs may (1) irritate the walls of the stomach,
causing inflammation and sometimes death; (2) lodge in the throat
and thus choke the animal; or (38) clog the intestinal tract, fre-
quently with fatal results. Overeating the young and succulent
plants may cause bloating, which is similar in nature to bloating
caused by succulent clover, corn, etc. The hairy leaves are also said
to cause severe itching.”

Johnson and Archer, 1922, make the following statement: “The
injury from this plant most likely occurs from mechanical obstruc-
tion rather than from poison. The plant has been reported to
contain a poisonous glucoside, although Doctor Bitting was unable
to obtain any poisonous properties in the growing plant. Cases
investigated by the senior writer on post-mortem proved that the
thorny bristles were a factor in causing mechanical obstruction and
extreme irritation to the mucous surface of the intestine.”

Kinsley, 1922, gives a general description of cocklebur poisoning
in swine with symptoms and lesions. This is an excellent résumé
of the subject but apparently is not based on any definite experi-
mental evidence.

{* °

Bul. 1274, U. S. Department of Agriculture PLATE I

Fic. |.—A BRANCH OF COCKLEBUR, SHOWING THE FORM OF THE
LEAVES AND BURS

Fic. 2.—COCKLEBUR PLANTS IN THE YOUNG COTYLEDON
STAGE

PLATE II

1274, U. S. Department of Agriculture

Bul.

SLNV1d YNAAIMOOD YNNOA JO G3Ag V DNIMOHS SHVLA SYIOAYSSSY NOSINNNS 30 SYOHS SHL

COCKLEBURS AS POISONOUS PLANTS 5

In this historical sketch a bibliography has been made of those
publications which were of special significance. The Department
of Agriculture has received many letters from various sections of
the country stating conclusively that animals were killed by cockle-
burs. Most of these statements were with reference to swine, but
complaints have also been made, especially from New Mexico and
western Texas, of losses of cattle. A number of losses of this kind
were brought to the attention of the department by Dr. Harry
Grafke, inspector in charge at Fort Worth, Tex., in the spring of
1922, in which he felt certain that the deaths were due to cocklebur
poisoning.

Some of the Xanthium losses which have been reported in the
literature and in the correspondence have been rather heavy.

Pammel, 1920, says that “4 pigs were turned on Xanthium and
3 died;” Mayo, 1905, gives an instance in which 33 out of 35 head
died; one author states that in one section of the country the
farmers lose 40 per cent of their pigs.

Dr. Harry Grafke reported in 1922 one loss of 25 cattle out of a
herd of 150 and another of 20 out of a herd of 58. In the San
Antonio Express in April, 1922, was reported a loss of 15 registered
Hereford bulls out of 17.

Many statements of the same general character as those above have
been made by correspondents from different sections of the United
States.

The foregoing indicates that while many people have been con-
vinced of the poisonous properties of cocklebur this belief has by
no means been universal. Others have felt certain that the losses
occasioned by this plant, if such losses occurred, were due to mechan-
ical injury. Among those who believed that the plant was poisonous
there has been a good deal of uncertainty in regard to the part of
the plant which produced the harm. Most of those, who have
reported cases of poisoning have stated that it was due to the young
plant, but some experiments apparently have proved that the plant
was not poisonous in any stage. Inasmuch as the losses which in
some localities have been ascribed to Xanthium have been very heavy,
it was deemed cf special importance to determine positively
whether the plant was poisonous or not and if poisonous what part
of the plant was injurious, and at what age the plant should be
avoided, and also, in case the plant proved to be poisonous, to find a
remedy. The investigations detailed in this bulletin were undertaken
to answer these questions,

THE COCKLEBUR PLANT

The species of Xanthium are widely distributed throughout the
United States, growing in moist, waste places and along the shores
of rivers, lakes, and ponds. It has not seemed wise to discuss in this
bulletin the species relations of the genus, partly because there
is reason to think that all are equally poisonous and partly because
there is little doubt that in the literature of the subject there has
been much confusion in the use of specific names. Because of the
close relationships and rather wide limits of variation in the plants,
botanists are by no means agreed as to the specific limitations.

6 BULLETIN 1274, U. S. DEPARTMENT OF AGRICULTURE

The species used in the experimental work has been determined
by W. W. Eggleston, of the Bureau of Plant Industry, as Xanthium
echinatum Murr. The material was collected at Salina, Utah, and
on the shores of a large reservoir near Sterling, Utah. Considerable
material was also used that was grown in sand beds at the Salina
Experiment Station and in the Department of Agriculture green-
house in Washington, D. C., from seeds collected at Salina.

Plate I, Figure 1, is a picture of a branch of the plant, showing ~

the forms of the leaves and burs. Plate I, Figure 2, shows plants
in the young cotyledon stage. It was in this stage and a little
later, before the full development of the first pair of leaves, that
the plants were found to be most poisonous. Plate IIT shows the
shore of the reservoir, where much of the material was collected,
and is typical of many places where the plant grows in abundance.
The old burs accumulate on the shores of the reservoir, sometimes
partly buried and sometimes bunched together on the surface. The
young plants grow rapidly, forming dense masses around the shores.
As the water of the reservoir is gradually lowered during the sum-
mer, a band of young plants develops, this band varying in width
in accordance with the moisture conditions. Thus for several weeks
there is a succession of crops of the young plant.

If the plants are toxic and the trouble is confined to the young
plants, as is shown later, 1t follows that under such conditions the
dangerous season may be greatly prolonged. Where the plants
grow on the shores of temporary ponds the growth may not cease
until the ponds are entirely dried up. Each bur contains two seeds
and it is a well-known fact that ordinarily only one seed germinates
in the year following maturity, the other one germinating in the
second year or later. So, while the plants are considered as annuals
and theoretically can be exterminated if destroyed before the burs

are formed, one must expect another crop from the seeds in which

germination has been delayed.
EXPERIMENTAL WORK

The experiments on which this report is based were carried on
in the years 1920, 1921, 1922, and 1923. Most of the work was
done at the Salina Experiment Station, but a few experiments were
made at the Bureau of Animal Industry Experiment Station, Beth-
esda, Md., near Washington, D. C. There were, in all, 67 experi-
ments with swine, 11 with sheep, 12 with cattle, and 19 with chickens.
Table 1 contains a summarized statement of these experiments.

TYPICAL CASE OF PIG 18

Pig 18 was a female, 2 months old, of the Poland-China breed.
She was in good, healthy condition at the time of the experiment and
weighed 40.5 pounds. ‘To this animal was given, at 9.15 a. m., June
9, 1.496 per cent of the animal’s weight of Yanthium echinatum in
the young cotyledon stage. The plants were cut up and mixed
with garbage and bran. At 4 p. m. it was noticed a little of the
plant remained, but after the addition of more bran the animal
ate the remainder.

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COCKLEBURS AS POISONOUS PLANTS ci

At the time of feeding, 9 a. m., the pig’s temperature was 101.3° F.
and respiration 28. At 8 p. m. the temperature was 102, respiration
32. No symptoms appeared during the day. On the morning of
June 10 the temperature was 100.6° pie respiration 25, and at 8 p. m.
the temperature was 101.3°, respiration 28. During the day the
animal was given grass and bran and showed no symptoms of illness.
On June 11, at 6.15 a. m., the pig was walking about in her pen,
frothing at the mouth, and had been vomiting. “Her temperature at
6.18 was 101.4° F., respiration 26. The animal was weak, and at
6.30 she lay down and then got up and walked about the pen in
an uneasy manner. At 7.20 she was getting weaker and tottered
when attempting to walk. At 8.20 a. m. the temperature was 97° F.,
respiration 28. “At 8.30 the temperature was 97.3°. The animal was
lying down with her forefeet drawn up below her jaws. She was
gasping for breath and somewhat salivated. The legs were trem-
bling and the respiration spasmodic. At 8.35 a. m. the temperature
was 96. 1°, respiration 44. The animal continued to gasp, the body
moving ina jerky and trembling fashion and occasionally emitted
loud grunts. At 8.40 a. m. the temperature was 95.8°. The move-
ments of the legs and the gasps became more es At 9.03
the temperature was 95.7° F., the animal continually gasping, and
she died at 9.05 a. m.

Plate ILI, Figures 1 and 2, show her condition at 8.20 and 8.25
a. m.

In the autopsy the fundus portion of the stomach showed extreme
congestion. There was slight congestion in the duodenum and in the
cecum. The liver was dark and well filled with blood, but it was not
noted, as, in some other cases, that the bile was abnormal. There
was some congestion in the abdominal lymph glands.

This animal may be considered typical in the symptoms and
rapidity with which the symptoms developed, although the autopsy
was not so characteristic as in some other cases. :

The lesions, as shown in the microscopic study, were typical in
every respect.

DISCUSSION AND GENERAL CONCLUSIONS

SYMPTOMS IN PiGs

The first symptom noted in poisoned pigs, ordinarily, was depres-
sion. This was accompanied in most cases with nausea which fre-
quently resulted in continued vomiting. As the sickness progressed
the animals became so weak as to be unable to stand. In those
- that were very sick the respiration became labored, the animals fre-
quently gasping for breath. The pulse became rapid and weak. In
some cases there were spasmodic movements of the body. Oc-
casionally the animals moved their legs in what might be described
as running movements. Sometimes, however, death resulted without
these spasmodic movements. The appearance of sick animals is
shown in the pictures of pig 18, Plate III, Figures 1 and 2, and in
the series of pictures of pig 21, in Plate ine Figures £2. and 3.

1274, U. S. DEPARTMENT OF AGRICULTURE

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Bul. 1274, U. S. Department of Agriculture

Fic. 3.—SHEEP 636, SHOWING EXTREME DE-
PRESSION AND WEAKNESS

PLATE III

Bul. 1274, U. S. Department of Agriculture PLATE IV

Fic. 1.—Pic 21 AT 11.44 A. M., SHow!nNG NAUSEA
AND WEAKNESS

Fig. 2.—Piag 21 AT 11.45 A. M., SHOWING WEAK-
NESS, AS SHOWN BY DIFFICULTY IN HANDLING
ITs LEGS

Fic. 3.—Pic 2! at 12.26 P. M., WHEN COM-
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COCKLEBURS AS POISONOUS PLANTS

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12 BULLETIN 1274, U. S. DEPARTMENT OF AGRICULTURE
SYMPTOMS IN SHEEP AND CATTLE

In sheep and cattle, as in the pigs, the first effect of the plant
was depression. This was followed by extreme weakness with la-
bored respiration, gasping, and spasmodic movements of the limbs.
Plate III, Figure 3, shows this condition of extreme depression in
sheep 636. In some cases there was evidence of hyperesthesia and
in the cattle there was a peculiar trembling or quivering of the
muscles. Vomiting was not noted in either cattle or sheep.

SYMPTOMS IN CHICKENS

The symptoms in chickens were not especially characteristic. As
in the other animals there was marked depression, followed by
weakness and in one case, chicken 33, a distinct condition of coma.
There were no spasmodic movements, although in one case there
was some struggling just before death.

AUTOPSY FINDINGS

Autopsies were made on 7 pigs, 1 sheep, 2 cattle, and 2 chickens.

The pictures presented by these examinations were not of a uni-
form character in details but showed some outstanding features.
The parts especially affected were the alimentary canal, the liver,
and to a lesser degree, other glandular structures.

In the pigs the walls of the stomach were more or less congested,
the stomach congestion in the cattle being confined to the fourth
stomach. This congestion extended, in some cases, to a greater or
less degree, to the duodenum, jejunum, ileum, cecum, and colon.
Where this congestion occurred there was a tendency to thickening
of the walls with a serous infiltration.

In the sheep and pigs the liver was congested or spotted, while
in the cattle it was bluish. The walls of the gali bladder, and in
some cases those of the common bile duct, were thickened and the
bile was thick and viscid.

The spleen in some cases appeared congested and a similar condi-
tion was found in some of the lymph glands, especially those of the
abdominal cavity.

In some cases there was an accumulation of a serous infiltration
about the gall bladder and ducts and there was generally an excess
of serum in the abdominal cavity. These conditions varied in the
different animals and did not appear uniformly by any means; this
was especially true of the pigs the only abnormal condition com-
mon to a majority being the congested stomach.

The cattle presented a more nearly uniform picture, each animal
having a congested fourth stomach, bluish liver, thickened gall blad-
der, congested spleen, serous infiltration about gall bladder and ducts,
and abnormal suprarenals. It should be noted, however, that the
thickened gall bladder may have been due, in part at least, to the
flukes with which the cattle were infested.

In one of the two chickens autopsied there were no abnormal con-
ditions; in the other there were petachiz on the heart, an unusual
quantity of pericardial fluid, the serous fluid of the abdominal cavity
was bloody, the crop showed shght inflammation, and the gall blad-
der was distended.

COCKLEBURS AS POISONOUS PLANTS 18
MICROSCOPIC CHANGES IN TISSUES

At the time of the autopsies, samples were preserved of such tissues
as it was thought desirable to examine in greater detail. In this
work 142 samples of tissues were sectioned and studied.

In the sections of the livers every lobule examined was found to
be hemorrhagic, although the interlobular branches of the portal
vein did not contain an excess of blood. Usually most of the intra-
lobular capillaries and often the central lobular veins had move or
less completely disappeared, and many of the hepatic cells were
necrotic. In the most advanced cases the liver cords were broken up,
leaving a few dead hepatic cells lying in a mass of blood. In the
least advanced cases the hepatic cells were still arranged in cords,
but were compressed, and most of them necrotic. Usually two or
three rows of cells in the peripheral portion of the lobule were less
severely affected, though greatly swollen. In 6 of the 10 cases an
excess of leucocytes was found throughout the liver tissues.

The bile ducts varied considerably in their condition. As a rule
the smallest ducts were little altered. The larger ducts usually had
a swollen epithelium, a few cells of which were necrotic. A few
ducts, in four of the cases, contained exfoliated epithelial cells. In
six of the cases the interlobular connective tissue was edematous, and
in two cases the capillaries of this region were congested. In four
cases the walls of the gall bladders were necrotic and thickened by a
serous exudate. In three of these the tissues were infiltrated with
leucocytes, and in one case there were hemorrhages.

The changes in the kidneys were less severe than those in the livers.
The most pronounced alterations were in the epithelium of the con-
voluted tubules. This was swollen and often ina well-advanced stage
of granular disintegration, the granular material being scattered
throughout the lumina. In such tubules the nuclei were disarranged
and often shrunken. In some cases many cells were necrotic. Simi-
lar changes had occurred in the ascending limb of Henle. The de-
scending limb was often distended and sometimes contained hyaline
casts. The collecting tubules were much less affected, but in some
cases they had a swollen and even granular epithelium. Blood, as
a rule, was not abundant, though occasional capillaries, both inter-
tubular and those in the glomeruli, were distended, and in some cases
minute hemorrhages were present.

The sections of the walls of the fundus portion of the stomach of
the pigs, with the single exception of pig 13, showed a capillary con-
gestion or hemorrhagic condition of the mucous membrane. In the
milder cases this consisted of a pronounced distention and engorge-
ment of the capillaries near the surface of this membrane. In the
more pronounced cases severe hemorrhages had occurred. The con-
gestion and hemorrhage were confined, in all but one case, to the
portion of the mucous membrane next to the stomach cavity, and
extended through about one-third of its thickness. Usually there
was edema of the interglandular tissues, with a swelling or degenera-
tion of the cells.

No congestion or hemorrhage was found in the mucous membrane
of the sections of the abomasum of the sheep or cattle. In one of
the cattle the interglandular cells were swollen, and in this and the
other cases leucocytes in this region were slightly more abundant

14 BULLETIN 1274, U. S. DEPARTMENT OF AGRICULTURE

than normal. Other layers of the walls of the stomachs of all
animals appeared to be unaffected.

No uniform pathological change was noted in any portion of the
intestines. In very few instances did the sections show a congested
condition. In most sections from the various portions there was an
excess of lymphoid cells or other leucocytes in the mucous mem-
brane. In some instances, however, this was probably due to para-
sites. In half of the samples examined the serosa was thickened or
contained an excess of leucocytes. Some of them were of the endo-
thelial type and were on the surface of the serosa, probably due to
the presence of an irritant in the abdominal cavity.

While there was evidence of some irrritation in the spleen it was
not found uniformly in all the animals, nor was it particularly
severe. Of the 10 cases studied, 5—2 pigs, the sheep, and both cat-
tle—had congested spleens. ‘This blood, however, was very unevenly
distributed, some small areas being full of red blood corpuscles,
while in other areas there were few, if any. In 5 cases there was a
swelling of the pulp reticular cells, and in 6 cases splenic cells
seemed unusually abundant. In the sheep and in both cattle the
iymphoid cells of the germinal centers had undergone more or less
degeneration. In the most extreme case—cattle 954—the nuclei of
these cells were found in various stages of degeneration. Many of
them were fragmented, and some of the fragments had been taken
up by phagocytes.

Sections of several mesenteric and mediastinal lymph glands were

examined. ‘These were in a condition very similar to that found —

in the spleens. In 8 glands taken from 5 of the animals the reticular
cells were distinctly swollen and in 5 of these glands they were
noticeably degenerated. In 5 glands there was an excess of large
mononuclear cells of the endothelial cell type. Only rarely were the
glands congested. In 2 cases small hemorrhages had occurred in the
lymphoid areas and in 8 cases red blood corpuscles were found in
the lymph spaces. In 1 pig and the sheep polymorphonuclear leuco-
cytes were present in considerable excess. In the glands of both
cattle eosinophiles were present in excess, a condition doubtless con-
nected with the fluke infestation of the livers of the animals.

Little of significance was found in sections of the lungs or of heart
tissue. On the average there was a relatively small quantity of
blood in the interalveolar capillaries, many of them being entirely
empty. The sheep was the only animal in which a congestion was
found. Occasionally the epithelium of the bronchial tubes was
swollen and sometimes the surrounding connective tissue was some-
what congested. In the walls of the ventricles occasional areas of
capillary congestion were found, but the condition was not constant.

In general, then, it appears that the most severe and perhaps the
primary effect was in the liver, and had resulted in hemorrhages in
all the lobules and a severe necrosis of the hepatic cells. The epi-
thelium of the larger bile ducts was often injured, the change ex-
tending apparently to the gall bladder, the walls of which were some-
times necrotic. In the kidneys there was a condition of parenchy-
matous nephritis affecting mainly the convoluted tubules and the
ascending limb of Henle with less injury to other tubules. The

mucous membrane of the stomach, in the pigs especially, was con-

gested or even hemorrhagic.

Cc

©

COCKLEBURS AS POISONOUS PLANTS 15

Of the other organs the spleen and lymph glands appear to have
shown the effects of a mild irritant. The lungs were characterized
rather by a lack of blood than by congestion. This may have been
due largely to the removal, from the general circulation, of the con-
siderable quantity of blood which was accumulated in the liver.

TOXIC AND LETHAL DOSAGE

As is shown elsewhere, the plant was found to be poisonous only
in the younger stages; the largest part of the experimental work was
done, therefore, on that stage of the plant which has been designated
as the young cotyledon stage. This means the stage of the plant up
to the time the first pair of leaves is partially formed. In gathering
the plant for experimental purposes, especially during the later feed-
ings, great care was taken to get it as young as possible. Plants in
which the first pair of leaves was much developed were not ordinarily
used. In the following discussion of dosage, only plants of this age
are considered.

In the experiments on pigs the smallest toxic dose was 0.736 per
cent. of the weight of animal in pig 20; pig 10 was made sick on
0.895 per cent. The smallest. lethal dose was 1.496 per cent of ani-
mal, in pig 18. When no remedy was given and the plant was fresh,
the largest dose given without effect was in the case of pig 20, July
11, 1921, being 1.521 per cent. (Pig 12 received June 13, without
effect, 2.856 per cent of its weight. The plant in this case, however,
was probably older than the young cotyledon stage.)

In general, then, it may be stated that the lethal dose for pigs
is about 14 per cent of the weight. of the animal, and that the toxic
dose may be as small as half of that quantity.

Sheep 636 was killed by 1.543 pounds per hundredweight of ani-
mal, while sheep 631 and sheep 711 ate 1.477 pounds with no harm.
So far as these experiments go, it would appear that the plant is
about equally toxic to pigs and sheep.

Cattle 945 was killed by 2.911 pounds per hundredweight of ani-
mal, while cattle 970 received 2.801 pounds per hundredweight of
animal with no effect. It seems probable from these results that the
toxic and lethal dose for cattle is about 3 pounds per hundredweight
of animal, and that it takes about twice as much to poison cattle as
it does to affect pigs or sheep.

With the chickens the feedings gave no definite results as to the
toxic and lethal doses. Chicken 38 on two dates, a month apart, re-
ceived 6 per cent of its weight and was not affected. Chicken 33 was
fatally poisoned by two doses of 6 per cent on two successive days.

In the autopsy of chicken 383 the crop was found still distended by
a mass of Xanthium which was thought to be fully equal to the
quantity given on the second day of the feeding. While the data
are insufficient for a definite statement, these experiments indicate
that the toxic and lethal dose is between 6 and 12 per cent of the
animal’s weight, with the probability that it is much nearer 6 than
12. It is evident that chickens are much less susceptible to Xanthium
poisoning than are pigs, cattle, or sheep.

The relative toxicity of different parts of the plant is discussed on
page 20. ;

16 BULLETIN 1274, U. S. DEPARTMENT OF AGRICULTURE

TIME FROM FEEDING TO APPEARANCE OF SYMPTOMS

TABLE 2.—Time elapsed from feeding to development of symptoms

j
: Time
Animal Date of feeding before
symptoms
|
Hrs. Ms.
iN Seer eS ae ek a ae ae | Aug. 18, 1920_._______- 21 45
og LES a MPs eee ae eae Sess a SE | Max: 1, 19212 ste 24 00
Ee hee ad Ea BLS EADS TR EWU Shp Oe ES eee ee pees Ne ee Fane OS AOL st es: 38 15
ee es Pas Pe fle hae ee eos ba 2 eee | June 20, 1921_________. 43 10
a ee Re ee ae a ee ee | Sept.24, 1924. ee i9 15
Shoop Gobo 2. ents ee Aad hie a er oe ee ae | June 28, 1921_______ 16 35
SES Heyy Pde SW Sate Eee 8 oie Sh ae ee ee See, eee SUNS 20, JO22 2. eh 17_ 35
Fattlo Ot: OS 28 FE Pe ee ae pe A ae Eee Se ee Avg! 21 W822. ses ss 14 55
GS EL ae ee ee Se ee ee ae eS ee ee Sept..8, 1922). -) 8 35
JERE HOTT oO et Sy Pe A LE a a eS eee July 2051923 See 17 5
Ghicken 37 + © ee en ee bee heel e oe ee eee Ee SA ys eee 16 50

Table 2 is far from giving the exact time which elapsed between
the feeding and the development of symptoms. In some eases the
feeding continued over a considerable period, so that there may
have been some poisonous effects even before the conclusion of the
feeding. The time is computed from the end of the feeding. There
is some indefiniteness in the time at which symptoms developed.
The animals were not, in all cases, under constant observation, and
in some the first symptoms were noted when the animals were ob-
served in the morning, and it is possible that they had been sick for
a considerable period before that time.

The shortest time noted was in the case of cattle 945—8 hours and
55 minutes. The longest period was in the case of pig 20—43 hours
and 10 minutes. In most cases, however, the time was a little less
than 24 hours. :

In general, a period of several hours elapses before symptoms ap-
pear, and this time, in some cases, may be between one and two days.

It should be noted that the chickens quoted in Table 2 received
seeds, while the other animals, with the exception of pig 10, August
18, received plants in the young cotyledon stage. This difference in
material apparently did not affect the time elapsing between the
feeding and the development of symptoms.

DURATION OF SICKNESS

Table 3 shows the duration of illness in cases of animals that either
were sick or died.
TABLE 3.—Duration of sickness

Animal * Date of feeding pag Result
H. M.

| 4 || SE Pe Se 2 Se See ee 1 2 8 July 8,192). 24 6 00] Recovery
Je et Ea Seer merseeee CF See Fae 3 ed) Sere eres | Aug: 18. 1990-< oN 2 10} Death
gE et Be re eee SS I Mee) fel se Py |e eo 2 26 Do.
Big 18 2.4. A gees hee es Se ee Jane 9; 1920 cere wets 2 50 Do.
ie ae a. Sere De RR Oe i ae Se ee Jane 16; 1981 23 40] Recovery.
5p SERS tee a oe ae Semmot ioe, oe hs 2} Sa SE -) Sept. 14, 1921_-___. 2 25] Death.
(ay lS a SR Le re es Rd oT OT ily, |, June 20; 1028. 2 ss 1 35] Recovery.
Sheep 636______- ae Re ae Naas Laelia de BA Jane 25,1921 oe eee 13 00] Death.
OaMBO Os «= Wo. aps ce ee ee ee SD | Aug. 21, 1922___....... 3 19 Do.
Cattle SOL er gs a a es ae -2| Sept. 8; 2922522" = a 0 40 Do.
Chicken 39. _ ._- ey MS ACS INY SiR ee eee ees | Joly 20, Tew 2 Ae (fag Do.
a oh (hes Rae ae eee ee oe Auy. 10,193 5. Se 24 00} Recovery.
CRUGIBIN Gol see cee cutee kt ee he a a oe Sept. 6,(:192382 ae 13 10] Death.

OC

COCKLEBURS AS POISONOUS PLANTS bE

In Table 3 the time was computed from the first to the last-
noted symptom. It is evident that in many cases this does not show
the actual duration of illness. Inasmuch as the animals were not.
under constant observation, they were in some cases undoubtedly
sick before the first symptom was noted, and doubtless in many
cases the illness continued after the last-noted symptom. In some
the first symptom was noted in the morning after a night during
which no observations were taken. This accounts for the very
short time of cattle 945 because when the first symptom was noted
in the morning the animal was already very sick. Table 3, however,
gives in a general way a fair indication of the time during which
the animals were sick. Excluding cattle 945, the shortest period of
illness was in the case of pig 26 which was sick 1 hour and 35
minutes and recovered. The longest period which any animal
was sick was in the case of chicken 87, which recovered after an
illness of 24 hours.

If the time of symptoms recorded is compared with the dosage
which the animals received it will be seen that there is no clear
correlation between them.

EFFECT OF CONTINUED FEEDING

Three pigs were fed Xanthium daily for a considerable period.
Pig 12 was fed from June 13 to July 9, with the exception of four
days, receiving daily doses varying from 0.313 to 2.856 per cent of
its weight. On June 23 it received 2.125 per cent, June 24, 1.966,
June 25, 1.574, and June 26, 1.574. On June 28 and June 29, and
on July 4, 5, and 6, it received daily 1.574 per cent of its weight.

Pig 10, from July 13 to 20, with the exception of one day, received
the plant daily in doses varying from 0.378 per cent of its weight
to 1.749 per cent. On July 17 it received 1.512 per cent of its weight
and on July 18, 1.749 per cent, with no effect.

Pig 32 from August 25 to August 26 received daily doses of
1.102 per cent of its weight, and on September 5, 6, 8, 10, and 11
received 1.333 per cent.

It has been found, as shown on page 15, that the minimum
toxic dose of the plant, in the young cotyledon stage, is 0.786 per cent
of the pig’s weight, and the minimum lethal dose is 1.496 per cent.
These animals then, in some cases, received on successive days not
only more than the toxic dose but more than the lethal dose. With
the exception of pig 12, which received on the first day 2.856 per
cent of its weight, all the animals received in the first feedings less
than the toxic dose. All these feedings were of the plant in the
young cotyledon. stage. After it was found that the plant was
most poisonous before the growth of the leaves, great care was
used to: collect for the routine feeding only the very young plants.
Less attention was paid to this in the early part of the work; while
the notes are incomplete in regard to the collections used, it is
known that some of the material used for pigs 10 and 12 was in the
2 and 4 leaf stages. This probably explains the failure to poison
pig 12 on 2.856 per cent of its weight. Making some allowance for
the indefiniteness in regard to the age of the plant in some of the
feedings, it is still noticeable that pigs 10 and 12 on successive days
could receive such large quantities with no resulting symptoms.

18 BULLETIN 1274, U. S. DEPARTMENT OF AGRICULTURE

In the case of pig 32 it is known that all the feedings were of the
young plant, before the development of the leaves, and this animal
repeatedly received a quantity slightly less than the minimum lethal
dose, with no ill effect. Twice on two successive days it received a

total of 2.645 per cent of its weight, while, with the exception ~

of pig 12 on June 9, as has been explained, no other pig received
more than 1.521 per cent without toxic effects. These cases make it
fairly evident that Xanthium is not a cumulative poison, but that,
on the other hand, it is rather rapidly eliminated.

Inasmuch as several times, after a series of daily feedings, a single
feeding much greater than the minimum lethal dose produced no
symptoms, it seems probable that some toleration was acquired. The
experiments were not sufficiently numerous so that a positive state-
ment can be made of this fact, but it seems probable that this is the
case.

ANIMALS POISONED BY COCKLEBUR

The experimental work described in this bulletin was on swine,
sheep, cattle, and chickens and demonstrated conclusively the poi-
sonous effect of cocklebur on these animals. There was no work done
by the writers on horses, but others have reported such eases of poi-
soning. It is presumable that they wouid be affected if they ate the
plant. Asa matter of fact, horses are less liable than other domestic
animals to be injured by any poisonous plants, because they select
their feed with more care. The dosage would indicate that while
chickens may be poisoned, under ordinary circumstances such occur-
rences are rare.

PART OF PLANT POISONOUS

Experimental feedings were made not only of the whole plant in
the young cotyledon stage but of seeds, roots, cotyledons, stems and
roots, and plants with the cotyledons removed. It was found that
plants above the young cotyledon stage were only shghtly poisonous
and these are therefore of no practical importance from the stand-
point of the toxicology of the plant. Moreover, as the plants in the
young cotyledon stage have no disagreeable taste, they are eaten quite
readily. As the plants grow older the leaves develop a very bitter
taste, and animals generally refuse to eat them.

It was found that the seeds, removed from the burs and fed to
some of the pigs, were much more toxic than other parts of the
plant. Pig 10 was killed by 0.275 per cent of animal weight. Pig
12 received 0.2535 per cent of animal weight with no effect. It seems
probable from the experiments with pig 10 that the minimum toxic
and lethal dose is not far from 0.275 per cent of animal weight, al-
though an animal may receive as much as 0.2535 per cent with no
apparent effect.

Chicken 57 was made sick on 0.22 per cent of its weight, and chicken
39 died from the same dosage. So far as these few experiments go
the seeds appear to be more toxic to chickens than to pigs. |

The feeding of plants having 2, 4, and 6 leaves was not attended
with harmful result, showing that the plant loses its toxie proper-
lies very rapidly as it develops from the cotyledon stage. So far as
ihe experiments indicate it would appear that the cotyledons have
about the same toxicity as the whole plant in the young cotyledon

stage.

9

ee ee ee r 2

COCKLEBURS AS POISONOUS PLANTS 19

ARE THE POISONOUS PROPERTIES OF THE COTYLEDONS DERIVED FROM THE
SEEDS?

Since the seeds are by weight much more poisonous than the young
plants, and as the plants, early i in their growth, lose their toxic prop-
erties, the question has arisen whether the young plants derive their
toxicity solely or largely from the seeds. If the plants contain sim-
ply the toxic material from the seeds, animals should be poisoned by
a number of plants equal to the number of seeds which produce a
poisonous effect. Counts were made in 5 experimental feedings to
pigs of seeds, in 11 feedings of the whole plant in young cotyledon
stage, and in 6 feedings of cotyledons.

The results were as shown in Table 4:

TABLE 4.—Number of sceds, plants, and cotyledons producing toxic and nontoxic
effects to pigs

Number of

seeds per

Part of plant hundred-

weight of

animal

Secds2 steer. st Raant eve ta aM et des ke Ne itr ot BR Haballe sees ea 2, 200
Nalababonb egal = Ses 2s INOnTOMCseess oat 1, 800
NVA OLS aii ieee etre te ser ein ie lh ae IMbvanianyeea ee fy SR AIG aE ees Sha as 900
MMigparonbanls soo =e INOnMtOxXIGM ee esis 1, 200
iPairsolscotyJledonse se erat ye eT IMEI Mees ee HBG». aK Clie o aies A AW a 1, 600
Miaxeimiumie 2 = sae INODCOx! Chlae ete Ie Siva 1, 600

Since in the case of the seeds no effect was produced by 1,800, it
may be assumed that 2,200 is not only the lethal dose but is not far
from the toxic dose.

Of the whole plant, as there were 11 feedings, 9 of which were
between 900 and 1,200, it seems probable that 900 is very close to the
minimum toxic and lethal dose.

With the pairs of cotyledons, 1,600 produced symptoms and in
another case the same number had no effect, so here, too, the dosage
must be close to the minimum. While too much reliance must not
be placed on the comparatively small number of experiments, never-
theless the results have some significance, but do not show the ex-
pected correlation. On the contrary, considering numbers only, the
whole plant is most toxic, the cotyledons next, and the seeds least
of all, the proportionate toxic doses being 9, 1G, and 22. As the -
writers have no knowledge of the chemistry of the plant, it is 1m-
possible to explain this fact. It is possible, of course, that the toxic
substance is not actually greater in the plant, but is in a more avail-
able form, but it is also possible that a greater quantity is secreted
in the plant. These figures also show quite clearly that the cotyle-
dons do not contain all the toxic substance, as it takes 1,600 cotyledons
to equal the effect of 900 whole plants.

MECHANICAL INJURY BY BURS

As stated in the historical résumé, some writers claim that. the burs
injure animals either by irritation caused by the spines, or by ob-
struction of parts of the alimentary canal, or by both. There was
ttle evidence in the experiments made by the writers either in sup-

20 BULLETIN 1274, U. S. DEPARTMENT OF AGRICULTURE

port or in refutation of this claim. In one case, pig 10, July 6, 1920,
six fruits of the Xanthium were eaten with no deleterious results.
Presumably they were digested.

The experimental feeding of fruit to chickens may have some bear- —

ing on this question. Six mature burs coated with a stiff mixture
of white flour and water were given to chicken 37. The dough was
used to cover the spines in order to protect the chicken’s throat.
During the first 18 hours after feeding, 4 of the burs had disap-
peared from the crop. Of the two remaining burs one had gone in
90 hours, while the other did not move on for 186 hours.

The first morning following the feeding the chicken was slightly
depressed, but by evening the depression was almost entirely gone.
At the end of the first 96 hours the animal’s weight had dropped 250
grams. After this time it rose slightly, but still remained about 200
grams below the weight at the beginning of the feeding. After the
last bur had gone the weight increased. The autopsy showed no
effect of the burs.

Chicken 32 was given 12 mature burs which were likewise coated
with dough. Eighteen hours after feeding there still remained a
mat of burs in the crop, possibly 8 or 9 in number; the clump was
too large for counting. Forty-two hours after feeding, the clump of
burs was still present, but a few were separated from the main ball.
Sixty-six hours after feeding, 6 burs could be counted. These were
separated from one another. Ninety hours after feeding, 4 burs
still remained. In 97 hours only 1 bur remained and that one had
disappeared in 114 hours. At the end of 42 hours the animal was
slightly stupid, and the points of his comb were dark. There was a
drop in weight of about 70 grams for a week following the feeding.

No serious consequences resulted from these two feedings, but in
each case it seems likely that there was a slight disturbance of a
general nature. As soon as the cause of the trouble was removed
there seemed to be prompt improvement.

While the feces of these animals were not collected, they were un-
der constant observation and it is believed that the burs were di-
gested.

To sum up the present state of our knowledge in regard to in-
juries to animals from the use of the whole fruit, the statements
made by other authors, quoted on pages 2—5, seem to be based on
actual experience, and must be taken at their face value. It must
be presumed, then, that swine may be injured by the fruit. The
experience of the authors, however, indicates that swine do not.
readily eat the burs and that injuries from this source, if they oc-
cur, are somewhat rare. So far as chickens are concerned it is im-
probable that, when left to themselves, they would ever take as many
burs as were given in the experiments, and as these animals were not
injured it may be fairly concluded that burs, under ordinary cir-
cumstances, do not harm chickens.

TOXICITY OF DRIED PLANT

There were four experimental feedings of dried plant. In these
feedings, estimating the material as green plant, pig 21 was killed
with 1.74 per cent of its weight of cotyledons. Pig 23 received of the
plant in the young cotyledon stage at one time 1.54 per cent of its

COCKLEBURS AS POISONOUS PLANTS 21

weight, and at another 4.514 per cent, and pig 22 received of the
plant in the same stage 2.2 per cent; these feedings to pigs 23 and 22
produced no toxic effect. As 1.512 per cent was the largest quantity
of the fresh plant which failed to produce symptoms, it seems prob-
able that the plants lose some of their toxicity in drying.

REMEDIES

To avoid losses from Xanthium, the most important thing is to
prevent animals from eating the weed. Very hungry animals will
eat almost anything available. If there is a shortage of good forage,
and animals find the young plants of cocklebur, they may easily eat
enough to cause serious results.

Pigs are attracted to the margins of shallow ponds, where cockle-
burs’ grow in profusion, and are especially hable to be poisoned,
and other animals may eat the succulent young plants when there is
a lack of other forage. These young plants, as stated, do not have
the bitter taste which is found in later growth, and it is not strange
that they are eaten in considerable quantity. |

In regard to medicinal remedies, considerable work has been done,
and the results apparently indicate methods of treatment which may
be used successfully. Mrs. A. Creecy, of Raton, N. Mex., told the
senior writer that her people had found that if pigs were given whole
milk they were not poisoned by cocklebur. Acting on this sugges-
tion, several experiments were made. Pig 28, on September 12, was
given 1.653 per cent of animal weight of the young cotyledon stage
of cocklebur. It received 14 quarts of fresh milk, part immediately
after the feeding of cockleburs and part the next morning, and
showed no symptoms of poisoning. On September 18 the same pig
received 1.873 per cent of animal weight of cockiebur. Immediately
after the feeding it was given 1 quart of fresh milk and another
quart the next morning. Again it showed no symptoms. This ex-
periment was repeated with pig 29, with the same result.

Remembering that 1.5 per cent of animal weight may be con-
sidered as the toxic or lethal dose, and that, as stated, the largest
quantity of the plant in the young cotyledon stage which was eaten
with no toxic results, when no remedy was given, was 1.521 per cent
of animal weight, it would seem that the milk must have had a
beneficial effect. :

Assuming that the beneficial effect of the milk was due to the
contained fats, it was thought that similar results might be obtained
by the use of other fats or oils. Pig 30, February 27, received 1.873
per cent of animal weight of Xanthium, this as before being con-
sidered a toxic dose, and immediately after the feeding was given 60
grams (2.1 ounces) of lard and the same quantity the next morning.
That quantity of lard was used, although it is about double the
quantity of the fat in a quart of rich milk. The animal showed no
symptoms of poisoning.

The same animal in another experiment, March 28, received the
same quantity of Xanthium, and after feeding was given 60 cubic
centimeters (2 fluid ounces) of raw linseed oil and the same quantity
next morning. As in the use of lard, the dosage of oil was estimated
‘as being about twice the quantity of fat in a quart of milk. In this
case, too, no toxic effect followed.

99 BULLETIN 1274, U. S. DEPARTMENT OF AGRICULTURE

Chicken 37 was given 0.3 per cent of its weight of mature seeds
and immediately after the feeding received 5 grams (0.2 of an ounce)
of bacon grease; no symptoms followed. As 0.22 per cent produced
symptoms in a preceding feeding, and the same quantity in the case
of chicken 39 resulted in death, it is probable that the grease was
instrumental in preventing poisoning.

The uniformly successful results of these experiments make it
probable that in fats and oils, like milk, bacon grease, lard, and
linseed oil, we have a distinctly valuable remedy.

SUMMARY

While there have been many reports of the poisoning of animals—
more especially of pigs—by the cocklebur, there has been little
experimental proof of the toxic character of these plants.

Experimental feedings have shown conclusively that cocklebur
plants are poisonous to swine, cattle, sheep, and chickens.

While the burs may produce some mechanical injury and the seeds
are very poisonous, stock poisoning is caused by feeding on the
young plants before the development of the leaves.

The toxic dosage has been worked out together with the symptoms
and lesions produced by the plant.

It has been shown that beneficial remedial effects may be produced
by the use of milk, oils, or fats.

: BIBLIOGRAPHY

This bibliography of Xanthium includes only those papers which refer
to its poisonous properties.
BANCROFT, JOSEPH.
1880. The newly introduced poisonous bur, Xanthium strumarium. (Read
before the Queensland Philosop. Soe. 22nd Jan., 1880) Brisbane
(Beal) 1880.
Battey, F. M.
1898. Plants reputed poisonous to stock. Queensland Agr. Jour. Vol. 3,
pp. 356-357.
1906. The weeds and suspected poisonous plants of Queensland. p. 82.
BAKER, EUSTACE THURMAN.
1920. Sheep Diseases. Vet. Med. Series No. 12, See. Edition. p. 253.
3ESSEY, C. EH.
1902. A preliminary account of the plants of Nebraska which are reputed
to be poisonous, or suspected of being so. Sixteenth ann. rep. of
the botanist of the Neb. State Board of Agriculture, p. 123.
Cary, C. A.
1915. Alabama Ex. Sta. Bulletin No. 185, p. 55.
CHEATHAM, M. V.
1884. Xanthium strumarium, Linné. Am, Jour. of Pharmacy, Vol. LVI,
4th series, p. 134.
CHESNUT, V. K.
1898. Preliminary catalogue of plants poisonous to stock. Ann. rep.
Bureau of Animal Industry for 1898, p. 417.

1917. Cockleburs poison hogs. Coop. Manager & Farmer, Minn., vol. 7,
p. 87.
COULTER, STANLEY.
1904. The Poisonous Plants of Indiana. Proc. Ind. Acad. of Science, 1904,
pp. 55-63.
Craic, R. A., and A. W. BITTING.
1904. Diseases of Swine. Purdue Univ. Agr. Exp. Station, Bull. No, 100;
Vol. XII, Sept., p. 88.

a Pe eee

COCKLEBURS AS POISONOUS PLANTS 93

Davy IB:
1902. Stock ranges of northwestern California. U.S. Dept. Agric, B. P. I. -
Bull. 12, p. 74.
Guint, E. E.
1908. Cocklebur injurious to swine. Breeder’s Gaz., vol. 54, p. 433.
GLovER, G. H.
1915. Colorado plants injurious to live stock. Colo. Exp. Sta. Bull. 211,
p. 68.
Gorr, HE. 8.
1894. Noxious weeds. Wisconsin Agr. Exp. Sta. Bull. No. 89, pp. 16-17.

HAtstep, B. D.
1899. The poisonous plants of New Jersey. N. J. Agr. Exp. Sta. Bull. 35,
p. 19
HANSEN, ALBERT A.
1920. Cocklebur. U.S. Dept. of Agr. Cir. 109.
JEPSON, WILLIS LINN.
1911. A fiora of Western Middle California. Second Edition, p. 456.
JCHNSON & ARCHER.
1922. The Principal Stock-Poisoning Plants of New Mexico. New Mex.
College of Agr. & Mechanic Arts, Extension Cir. 71, p. 38.
KANNGIESSER, F.
1910. Weiterer Beitrag zum Kapitel der Phytonosen. Naturw. Wochens.,
vol. 25, 1910, p. 412.
Kine, F. G.
1909. The Brood Sow and Her Litter. Mo. State Rd. of Agr. Monthly
Bull., vol. 7, No. 10, p. 26.
KInsLEy, A. T.
1909. Gastro-Enteritis in Hogs. (Caused by eating young cockleburs,
Aanthium canadense.) Am. Vet. Rey. 35; 5, p. 576.
1922. Cocklebur poisoning in swine. Vet. Med. XVII, No. 6, pp. 282-283.
Kirk, T. W.
1901. Report of T. W. Kirk, F. L. 8. (Lond.), Ete., Government Biologist.
Sth Ann. Rept. New Zealand Dept. Agr. 1900, App. VII, Division
of Biology and Pomology, p. 309-810.
LANDER, G. D.
1912. Veterinary Toxicology, pp. 222-223.
MAIDEN, J. H.
1895. The Bathurst Burr (Xanthiwm spinosum, Linn.). Agr. Gaz. N. S. W.,
Vol. VI, pp. 44547.
1896. The cocklebur a serious weed pest which threatens the colony.
Agr. Gaz. of New South Wales, vol. 7, pp. 421-428.
1899. The Noogoora-burr,. or Cockle-birr. The Agricultural Gazette of
New South Wales. Vol. X. Part 10, Oct:, pp. 1048-1048.
1917. Weeds of New South Wales. The Bathurst Burr (X. spinosum
Linn.). Agri. Gaz. of New South Wales, Vol. XXVIII, part 7,
pp. 489-497. }
1918. Plants which produce inflammation or irritation of the skin. Agr.
Gaz. of N. S. W., vol. 29, pp. 844-345.
1921. Plants which produce inflammation or irritation of the skin. Agr.
Gaz. of N. 8. W., Vol. XXXII, part 3, p. 206.
LEWIN, L.
1897. Lehrbouch de Toxikologie, p. 314.
MarsH, C. D., G. C. Ror, and A. B. CLAwson.
1923. Livestock Poisoning by Cocklebur. U.S. Dept. of Agr. Cir. 283.
Mayo, N. S.
1905. Accidental Stock Poisoning. 14th Biennial Report, part V, Kansas
State Board of Agr., pp. 632-633, 685.
1917. Poisonous plants. The Vet. Jour., vol. 73, No. 7, p. 252.
O’GaRA, P. J.
1903. Poisonous Weeds. 16th Ann. Rep. Agr. Exp. Sta. Nebraska, p. 50.

~ Paw™et, L. H.

1910 Manual of Poisonous Plants, Part 1, pp. 67 and 137.
1910. Poisonous and Medical Plants of Missouri. Missouri State Board of
Horticulture, Bull. No. 14, p. 46.
PAMMEL, L. H. :
1911. Manual of Poisonous Plants, Part II. pp. 768-770.
1918. ae Cockleburs Poisonous. Am. Jour. Vet. Medicine, Vol. 13, p.

1919. Cocklebur injurious. Am. (Ae of Vet. Med.
1920. Hogs Poisoned by Young Cockleburs. Amer, |
XV, No. 8, August, pp. 385-6. eae
1921. Young cockleburs and frozen alfalfa supposed to be > poi s
Med. Vol. XVI, No. 9, p. 48. r ;
1928. Young Cockleburs Poisonous to Swine. Veterinary Medic 1e, J
VIEL, ‘p. 630. ;< ;
PyPar, PW: J:
1913. Cocklebur. Purdue Univ. Dept. Agr. Extension Bull. 24. |
1923. Symptoms of Cocklebur Poisoning in Swine. Vet. Med. « ;
Vol. XVIII, No. 10, p. 960. a ia
ZANDER, ARTHUR.
1881. Chemisches iiber die Samen von Xanthium strumarium.
maceutische Zeitschrift fiir Russland, Vol. 20, pp. 661-668, a 682,
693-704.

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