TRANSCRIBER NOTES:
Words in italics are indicated with an underscore (_) at the begining
and end. Words in bold are indicated with an equal sign (=) at the
begining and end. Subscripts contained in chemical notations are
indicated as _{ }.
The table on page 32 has been modified to fit by the use of
keys to replace some of the information.
U. S. DEPARTMENT OF AGRICULTURE.
BUREAU OF PLANT INDUSTRY--BULLETIN NO. 129.
B. T. GALLOWAY, _Chief of Bureau_.
BARIUM, A CAUSE OF THE
LOCO-WEED DISEASE.
BY
ALBERT C. CRAWFORD,
PHARMACOLOGIST, POISONOUS-PLANT INVESTIGATIONS.
ISSUED AUGUST 22, 1908.
[Illustration]
WASHINGTON:
GOVERNMENT PRINTING OFFICE.
1908.
BUREAU OF PLANT INDUSTRY.
_Physiologist and Pathologist, and Chief of Bureau_,
Beverly T. Galloway.
_Physiologist and Pathologist, and Assistant Chief of Bureau_,
Albert F. Woods.
_Laboratory of Plant Pathology_,
Erwin F. Smith, Pathologist in Charge.
_Investigations of Diseases of Fruits_,
Merton B. Waite, Pathologist in Charge.
_Laboratory of Forest Pathology_,
Haven Metcalf, Pathologist in Charge.
_Cotton and Truck Diseases and Plant Disease Survey_,
William A. Orton, Pathologist in Charge.
_Plant Life History Investigations_,
Walter T. Swingle, Physiologist in Charge.
_Cotton Breeding Investigations_,
Archibald D. Shamel and Daniel N. Shoemaker, Physiologists in
Charge.
_Tobacco Investigations_,
Archibald D. Shamel, Wightman W. Garner, and Ernest H. Mathewson,
in Charge.
_Corn Investigations_,
Charles P. Hartley, Physiologist in Charge.
_Alkali and Drought Resistant Plant Breeding Investigations_,
Thomas H. Kearney, Physiologist in Charge.
_Soil Bacteriology and Water Purification Investigations_,
Karl F. Kellerman, Physiologist in Charge.
_Bionomic Investigations of Tropical and Subtropical Plants_,
Orator F. Cook, Bionomist in Charge.
_Drug and Poisonous Plant Investigations and Tea Culture
Investigations_, Rodney H. True, Physiologist in Charge.
_Physical Laboratory_,
Lyman J. Briggs, Physicist in Charge.
_Crop Technology and Fiber Plant Investigations_,
Nathan A. Cobb, Crop Technologist in Charge.
_Taxonomic and Range Investigations_,
Frederick V. Coville, Botanist in Charge.
_Farm Management Investigations_,
William J. Spillman, Agriculturist in Charge.
_Grain Investigations_,
Mark Alfred Carleton, Cerealist in Charge.
_Arlington Experimental Farm_,
Lee C. Corbett, Horticulturist in Charge.
_Vegetable Testing Gardens_,
William W. Tracy, sr., Superintendent.
_Sugar-Beet Investigations_,
Charles O. Townsend, Pathologist in Charge.
_Western Agricultural Extension Investigations_,
Carl S. Scofield, Agriculturist in Charge.
_Dry-Land Agriculture Investigations_,
E. Channing Chilcott, Agriculturist in Charge.
_Pomological Collections_,
Gustavus B. Brackett, Pomologist in Charge.
_Field Investigations in Pomology_,
William A. Taylor and G. Harold Powell, Pomologists in Charge.
_Experimental Gardens and Grounds_,
Edward N. Byrnes, Superintendent.
_Foreign Seed and Plant Introduction_,
David Fairchild, Agricultural Explorer in Charge.
_Forage Crop Investigations_,
Charles V. Piper, Agrostologist in Charge.
_Seed Laboratory_,
Edgar Brown, Botanist in Charge.
_Grain Standardization_,
John D. Shanahan, Crop Technologist in Charge.
_Subtropical Laboratory and Garden, Miami, Fla._,
Ernst A. Bessey, Pathologist in Charge.
_Plant Introduction Garden, Chico, Cal._,
W. W. Tracy, jr., Assistant Botanist in Charge.
_South Texas Garden, Brownsville, Tex._,
Edward C. Green, Pomologist in Charge.
_Farmers' Cooperative Demonstration Work_,
Seaman A. Knapp, Special Agent in Charge.
_Seed Distribution_ (Directed by Chief of Bureau),
Lisle Morrison, Assistant in General Charge.
_Editor_, J. E. Rockwell.
_Chief Clerk_, James E. Jones.
POISONOUS-PLANT INVESTIGATIONS.
SCIENTIFIC STAFF.
Rodney H. True, _Physiologist in Charge_.
C. Dwight Marsh, _Expert in Charge of Field Investigations_.
Albert C. Crawford, _Pharmacologist_.
Arthur B. Clawson, _Expert in Field Investigations_.
Ivar Tidestrom, _Assistant Botanist, in Cooperation with Forest
Service_.
LETTER OF TRANSMITTAL.
U. S. DEPARTMENT OF AGRICULTURE,
BUREAU OF PLANT INDUSTRY,
OFFICE OF THE CHIEF,
_Washington, D. C., April 10, 1908_.
SIR: I have the honor to transmit herewith the manuscript of a technical
bulletin entitled "Barium, a Cause of the Loco-Weed Disease," prepared
by Dr. A. C. Crawford, Pharmacologist, under the direction of Dr. Rodney
H. True, Physiologist in Charge of Poisonous-Plant Investigations, and
to recommend that it be published as Bulletin No. 129 of the series of
this Bureau.
For many years the stockmen in many parts of the West have reported
disastrous consequences following the eating of so-called loco weeds
characteristic of the regions involved. While many have doubted any
causal relation between the plants in question and the stock losses, the
reality of the damage has remained and has seemed to require a
thoroughgoing sifting of the evidence concerning the part played by the
plants. Accordingly, in the spring of 1905 a station for the
experimental study of the problem was established at Hugo, Colo., in
charge of Dr. C. Dwight Marsh, Expert, in cooperation with the Colorado
Agricultural Experiment Station. Later a further feeding experiment was
undertaken at Imperial, Nebr., in cooperation with the Nebraska
Agricultural Experiment Station. Parallel with the feeding work in the
field, laboratory work, designed to test under laboratory conditions the
poisonous action of the plants from given areas, was undertaken at
Washington by Dr. A. C. Crawford, Pharmacologist. A further phase of his
part of the work was an attempt to ascertain the nature of such
poisonous substance or substances as might occur in the loco plants.
In both of these lines of work Doctor Crawford has been successful, and
the technical results of his work are here collected.
Respectfully,
B. T. GALLOWAY,
_Chief of Bureau_.
Hon. JAMES WILSON,
_Secretary of Agriculture_.
INTRODUCTORY STATEMENT.
A scientific understanding of the so-called loco-weed disease has been
demanded and sought after for several decades for most practical
purposes, but, in spite of the great amount of attention which this
problem has received, no general agreement has been found among the
results obtained. The field investigations have given such contradictory
evidence that until the Bureau of Plant Industry of the Department of
Agriculture turned its attention to the matter the whole subject of the
loco disease was regarded by many as a kind of delusion and the
existence of a distinct entity was freely doubted. Not only did this
confusion characterize the field aspect of the matter, but the situation
viewed from the standpoint of laboratory study was also much obscured.
Some investigators claimed to have separated poisonous substances of
various sorts from the loco weeds, while others of equal scientific
standing denied the presence of any poisonous substance in the plants
under general suspicion--the so-called loco weeds.
In view of the great seriousness of the loco situation from the
standpoint of the stock interests, an active campaign both in the line
of feeding experiments in the field and laboratory study at Washington
was undertaken by the Office of Poisonous-Plant Investigations of the
Bureau of Plant Industry.
The feeding experiments carried out at Hugo, Colo., in cooperation with
the Colorado Agricultural Experiment Station, before the close of the
first season developed evidence that there was in reality such a thing
as a loco disease. The investigator in charge was enabled to describe
the disease in its most important manifestations and made it possible to
sift the facts from the large number of contradictory statements in the
literature.
The laboratory work, undertaken and carried on simultaneously, consisted
of a pharmacological study, under laboratory conditions and with the
usual laboratory subjects, of the action of plant material sent in from
the field. The acute phase of loco-weed poisoning, as well as a more
prolonged type of the disease, was studied. In plants found in this
preliminary feeding to be harmful, the poisonous principle was sought,
with the very striking results fully described in this paper. The
demonstration of the presence of barium in the plants was followed by
barium feeding, with the production of symptoms which agreed with those
produced in the laboratory with loco extracts and in the field
experiments with the loco plants as seen growing on the range. By
comparing these laboratory results with those produced in connection
with the field work, it became possible to sift the wheat from the chaff
in the mass of contradictory evidence detailed in the literature of this
subject.
The practical importance of the discovery of the true nature of the
active poisonous principle of the loco weeds is very great. It not only
sheds light on the loco situation and enables one to explain many
hitherto inexplicable things, but it also adds much to our knowledge of
barium in its medical bearings. It opens up most important problems
concerning the soils and the relation of the flora to them. It should be
borne in mind that although barium is shown to be chiefly responsible
for the poisonous properties of loco weeds in eastern Colorado, it is
entirely possible that in other regions other substances may be equally
or even more significant. This discovery also seems likely to provide a
basis for a rational treatment of locoed stock. Unfortunately, the
discovery of the fact that barium is the poisonous constituent of loco
weeds came too late to aid in the search for remedial measures on the
range during the period covered by this report, but those empirically
arrived at have received additional support from these laboratory
results.
Thus the work in field and laboratory, undertaken after repeated
attempts and discouraging failures by others, has yielded results to
persistent scientific research and promises practical aid to the now
suffering live-stock interests. The results of the laboratory work are
presented in this bulletin.
RODNEY H. TRUE,
_Physiologist in Charge_.
CONTENTS.
Page.
Geographical distribution of the loco-weed disease and
allied conditions 9
Plants associated with the locoed condition 10
Clinical symptoms of locoed animals as described in literature 12
Conditions similar to loco-weed poisoning in other parts
of the world 16
Pathological conditions in locoed animals as described on
the range 18
Historical sketch of loco investigations from a pharmacological
standpoint 19
Notes on various members of the loco-weed family 35
Laboratory experiments--physiological 36
Experiments on rabbits 36
Acute cases 36
Chronic cases 38
Pregnant animals 42
Subcutaneous injections 43
Summary of feeding experiments on rabbits 44
Experiments on sheep 44
Laboratory experiments--chemical 46
Effect of the aqueous extract of ashed loco plants 49
Total ash determinations of loco plants 54
Barium determinations in the ash of loco plants 55
Analysis of soils 57
Feeding experiments with barium salts on animals in the
laboratory 57
Barium poisoning in man 62
Pathological lesions in experimental barium poisoning 65
Toxicity of various aqueous extracts of loco plants 66
Theoretical antidote for loco-weed poisoning 71
Action of barium on domestic and farm animals 72
Application of the results of these investigations to
the range 74
Conclusions 75
Index 77
BARIUM, A CAUSE OF THE LOCO-WEED
DISEASE.
=GEOGRAPHICAL DISTRIBUTION OF THE LOCO-WEED DISEASE AND ALLIED
CONDITIONS.=
In our Western States there is a marked annual loss of stock due to
various causes. Some of these animals die in a condition known as
"locoed," a term derived from the Spanish word "loco," meaning foolish
or crazy.
This disorder extends from Montana to Texas and Mexico, and from Kansas
and Nebraska to California.[1]
In 1898 the United States Department of Agriculture sent out, under the
immediate direction of Mr. V. K. Chesnut, a request for information
concerning the ravages of the loco disease. It was found that in the ten
States of California, Colorado, Kansas, Montana, Nebraska, New Mexico,
North Dakota, Oklahoma, Texas, and Wyoming the loss in 1898 was
$144,850. Of this amount, $117,300 was attributed to Colorado alone; in
fact, the disorder spread so that this State expended more than $200,000
in two years and over $425,000 in a period of nine years in attempts to
eradicate the loco plants, the supposed cause of the trouble.[2]
The loss in one area of 35 by 120 miles in southwestern Kansas amounted
to 25,000 cattle in 1883.[3] This loss in stock has been so great that
the raising of horses has of necessity been abandoned in certain areas
on account of the prevalence of these loco weeds.
It is difficult to obtain accurate data, as the ranchmen believe that
any information as to the prevalence of the disorder would interfere
with the value of their stock.[4]
Dr. James Fletcher, of the Central Experimental Farm, Ottawa, Canada,
testified before the Select Standing Committee on Agriculture and
Colonization that he had never seen a case in the North-west of a
Canadian bred animal being locoed, although the loco plants were
prevalent. He explained this absence of loco disease by the abundance of
grass on the range, because of which the animals do not acquire the
habit of eating loco plants.[5] Cases have been reported, however, in
Manitoba.[6]
* * * * *
FOOTNOTES:
[1] Stalker, M. The "Loco" Plant and Its Effect on Animals.
Bur. Animal Industry, 3d Ann. Rept. (1886), p. 271. 1887.
[2] Bur. Animal Industry, 6th and 7th Ann. Repts. (1889 and
1890), p. 272. 1891.
[3] Day, M. G. Loco-Weed. In F. P. Foster's Reference-Book of
Practical Therapeutics, vol. 1, p. 587. 1896.
[4] O'Brine, D. Progress Bulletin on the Loco and Larkspur.
Colo. State Agric. Coll. Bul. 25, p. 18. 1893.
[5] Fletcher, J. Evidence Before the Select Standing
Comminttee on Agriculture and Colonization. Ottawas, 1905, p.
53.
[6] Fletcher, J. Experimental Farms Reports for 1892, p. 148.
1893.
=PLANTS ASSOCIATED WITH THE LOCOED CONDITION.=
The condition known as "locoed" is popularly believed to be due to
eating various plants, especially the members of the Astragalus and
Aragallus genera of the Leguminosæ, or pea family, but particularly to
_Astragalus mollissimus_ and _Aragallus lamberti_. These plants have
therefore received the name "loco plants,"[7] or crazy weed. But others,
as _Astragalus mortoni_,[8] _A. hornii_, _A. lentiginosus_, _A.
pattersoni_,[9] _A. nuttallianus_, _A. missouriensis_, _A. lotifloras_,
_A. bisulcatus_, _A. haydenianus_,[10] _A. tridactylicus_,[11]
_Crotalaria sagittalis_, _Lotus americanus_,[12] _Sophora sericea_,
_Caprioides aureum_, _Aragallus deflexa_,[13] _A. campestris_,[14] _A.
lagopus_,[15] _Malvastrum coccineum_, _Amaranthus graecizans_, and
_Rhamnus lanceolata_, are considered by some as loco plants.[16] In
other places _Stipa vaseyi_, _Leucocrinum montanum_, _Fritillaria
pudica_, _Zygadenus elegans_,[17] and even species of Delphinium are
considered loco plants, so widely has this name been used.
In Mexico the term "locoed" embraces a condition due to the action of
_Cannabis sativa_ and various members of the nightshade family. This
term has been much abused and has been made to embrace many groups of
symptoms. In fact, if an animal dies while showing more or less stupor
it is said to be locoed.[18] The early Spanish settlers seemed to be
unfamiliar with the disease, or at least of any causative relation
between the plant and the disease. The Spanish name for _Astragalus
mollissimus_ was "Garbanzillo," from its resemblance to Garbanzo (_Cicer
arietinum_), which is used in Spain as a food.[19] The term as applied
to this condition seems to be of comparatively recent origin.[20]
A somewhat similar condition to the loco in stock is sometimes
attributed by the ranchmen of our Western States to eating various
sages.[21] In Texas the loco disease is known as "grass staggers."[22]
Hayes[23] has described as follows a condition known as grass staggers,
which apparently has little resemblance to loco and is supposed to be
due to eating overripe grass, especially rye.
The symptoms, generally, take two or three days to become
developed. The animal gradually becomes more or less unconscious
and paralyzed and staggers if forced to walk. Although he may have
great difficulty in keeping on his legs, he is extremely averse
from going down and leans for support against any convenient
object. He breathes in a snoring manner. The mucous membranes are
tinged with yellow. Convulsions, or spasms, like those of tetanus,
may come on.
Recovery may be expected in cases which are not marked by extreme
symptoms.
If animals are not regularly salted, they visit salt deposits and eat
the alkalis. This some sheepmen believe to be the cause of the locoed
condition, but this is disproved by the occurrence of locoed animals in
ranges without salt. Others modify this view by claiming that the
vitiation in taste from eating these alkalis leads to a desire for the
loco weeds and thus to the locoed condition.[24]
* * * * *
FOOTNOTES:
[5] Fletcher, J. Evidence Before the Select Standing
Committee on Agriculture and Colonization. Ottawa, 1905, p.
53.
[7] Sayre, L. E. Loco Weed. Amer. Vet. Rev., vol. 11, p. 555.
1887.--Stalker, M. The "Loco" Plant and Its Effect on
Animals. Bur. Animal Industry, 3d Ann. Report. (1886), p.
271. 1887.
[8] Eastwood, A. The Loco Weeds. Zoe, vol. 3, p. 53. 1892.
[9] Chesnut, V. K. Preliminary Catalogue of Plants Poisonous
to Stock. Bur. Animal Industry, 15th Ann. Rept. (1898), p.
404.
[10] Williams, T. A. Some Plants Injurious to Stock. S. Dak.
Agric. Coll. and Exper. Sta. Bul. 33, p. 21. 1893.
[11] Givens, A. J. Loco or Crazy Weed. Med. Century, vol. 1,
p. 22. 1893.
[12] Eastwood, A., l. c. 1892.
[13] Sayre, L. E. Loco Weed. Amer. Vet. Rev., vol. 11, p.
555. 1887.
[14] Amer. Pharm. Assoc. Proc. for 1879, vol. 27, p. 611.
1880.
[15] Kelsey, F. D. Another Loco Plant. Bot. Gaz., vol. 14, p.
20. 1889.
[16] Sayre, L. E. Loco Weed. Kans. State Board Agric., 5th
Bienn. Rept., p. 209. 1887.
[17] Anderson, F. W. Poisonous Plants and the Symptoms They
Produce. Bot. Gaz., vol. 14, p. 180. 1889.--Pammel, L. H.
Loco Weeds. Vis Medicatrix, vol. 1, p. 44. 1891.
[18] Stalker, M. The "Loco" Plant and Its Effect on Animals.
Bur. Animal Industry, 3d Ann. Rept. (1886), p. 275.
1887.--Anderson, F. W. Poisonous Plants and the Symptoms They
Produce. Bot. Gaz., vol. 14, p. 180. 1889.
NOTE.--The symptoms described in Janvier's interesting story,
"In Old Mexico" (Scribner's Magazine, vol. 1, p. 67, 1887),
would coincide with those due to some member of the
nightshade family (probably _Datura stramonium_). See also
Pilgrim, C. W., Does the Loco Weed Produce Insanity? in Proc.
Amer. Medico-Psycholog. Assoc., vol. 5, p. 167. 1898.
[19] Sayre, L. E. Loco Weed. Kans. State Board Agric., 5th
Bienn. Rept., p. 209. 1887.
[20] Stalker, M. The "Loco" Plant and Its Effect on Animals.
Bur. Animal Industry, 3d Ann. Rept. (1886), p. 272. 1887.
[21] Mayo, N. S. Loco. The Industrialist, vol. 30, p. 473.
1904.
[22] Science, vol. 9, p. 32. 1887.
[23] Hayes, M. H. Veterinary Notes for Horse Owners, London,
1903, p. 425.--Compare Woronin, M. Ueber die Taumelgetreide
in Süd-Ussurien. Bot. Zeit., vol. 49, p. 80. 1891.
[24] Chesnut, V. K., and Wilcox, E. V. Stock-Poisoning Plants
of Montana. U. S. Dept. Agric., Div. Bot., Bul. 26, p. 88.
1901.
NOTE.--The wide distribution of these plants is claimed to be
partly due to the buffalo. See Blankinship, J. W., The Loco
and Some Other Poisonous Plants in Montana, in Mont. Agric.
Exper. Sta. Bul. 45, p. 79. 1903.
=CLINICAL SYMPTOMS OF LOCOED ANIMALS AS DESCRIBED IN LITERATURE.=
The animals usually affected are sheep, horses, cattle, mules,[25]
donkeys,[26] and goats. It is claimed that practically all herbivorous
animals are liable to the disease, even antelopes being affected.[27]
Hogs are said to be unaffected,[28] but definite information is lacking.
Cows seem to be less sensitive to this form of intoxication.[29] The
condition is usually a chronic one, although acute cases are said to
occur at times. The symptoms consist of digestive disturbances,
associated with emaciation and various symptoms suggesting lesions in
the nervous system, central or peripheral. The animals lose their
appetite from the first, begin to emaciate, and show symptoms of
malnutrition and starvation. The head trembles, the gait becomes feeble
and uncertain, the eyes become sunken and have a "flat, glassy
look."[30] There is a general sluggishness, muscular incoordination, and
difficulty in motion; finally all control of the limbs is lost and the
animal is unable to stand; the coat becomes rough and loses its luster,
and, in fact, all the typical symptoms of starvation appear. In some
cases diarrhea is also present.
All of Nockolds's animals, however, were constipated and the stools were
covered with mucus.[31] The dependent portions of the body may swell,
simply as an expression of the anæmia.[32] Sometimes there are symptoms
indicating acute pain,[33] the animals running about as if affected with
colic. They may belch and their abdomens swell. Some claim that the
animals are markedly salivated so that the saliva trickles from their
mouths. In other cases the mouth may be dry.[34] The eyes may be rolled
up so that the whites alone show. In some cases the pupil has been noted
to be dilated, as in atropine poisoning,[35] but Wilcox states that
they are contracted as after the use of eserine.[36] The temperature of
the animal falls from 1/2 degree to 1-1/2 degrees F. below normal.[37]
Tetanic symptoms may occur,[38] or the muscles of the mouth and tongue
becoming paralyzed may interfere with mastication. When water is offered
to the animal, it gazes stupidly at it and may not drink for days. One
of the symptoms noted is the loss of power to back properly.[39] Cows
during the first two or three months of gestation are almost sure to
abort.[40] This is claimed by Knowles, however, to be due to
malnutrition. As a result of these observations, suggesting some uterine
action, the drug has been proposed as an emmenagogue.[41]
The psychical symptoms are shown by errors of judgment. The animal
becomes dull and spiritless and wanders about half dazed. The mental
dullness passes into stupor. This dull, stupid condition has been
compared to intoxication with opium. If the locoed horse is led across a
stick lying on the ground he often jumps high as if it were a great
obstacle. The animal may now have maniacal attacks, during which he
rears and may fall backward,[42] and makes unreasonable jumps and other
unexpected movements, thus rendering himself dangerous to man.[43] Other
symptoms due to disturbances of the central nervous system are
hallucinations of various sorts. Though the optic nerve itself is
apparently not affected, the animal will stare at an object for a long
time without any apparent comprehension of its nature. This disturbance
in the visual function McCullaugh claims to be one of the first symptoms
of this disease. The animal seems to lose all idea of distance, as he
will butt against an obstruction as if oblivious of its presence. Any
sudden or violent motion made before him may cause him to fall.
According to some, the animal loses the sense which guides him in
finding water. A cow may fail to recognize her calf.[44] There is more
or less loss of control of the limbs[45] and tremors;[46] the feet are
lifted abnormally high when trotting, and, if crowded, the animal falls
headlong and will jump over little hollows as if they were wide
ditches.[47] The horse may shy without apparent cause and kick at
imaginary objects,[48] and, in fact, the reasoning powers seem to be
lost. These attacks are brought on by sudden excitement or when crossing
water.[49] There may be cutaneous hyperæsthesia.
The animals may remain with the herd, but they often wander away.
Stalker records the following observations:
I have seen a single animal miles away from any other individual of
the herd, carefully searching as if for some lost object, and when
a loco plant is found he would devour every morsel of it with the
greatest relish. As soon as one plant was eaten he would
immediately go in search of more, apparently oblivious to
everything but the intoxication afforded by his one favorite
article of food.[50]
All of Nockolds's animals which were locoed were mares more than 6 years
of age.[51]
According to Stalker there is a passive type in which the animal shows
symptoms only on being disturbed; the animal then becomes unmanageable.
This happens even with old, well-broken saddle horses.[52]
There are few published reports as to the symptoms occurring in sheep
which are locoed. Stalker[53] says sheep "become loco-eaters, grow
stupid, emaciated, and eventually die." One of the few descriptions of
the symptoms is that of Ruedi,[54] in which he claims that the symptoms
in sheep are those comparable to the symptoms of cerebro-spinal
meningitis except that there is an absence of fever. Ruedi speaks of
sheep "lying flat on the ground, not able to stand, and not able even to
lift their heads to drink the offered water; the head and the vertebra
in opisthotonus position; the four legs stretched out and stiff;
breathing was stertorous, pulse slow, abdomen much distended, diarrhea
present. * * * The heart * * * was very slow and insufficient." The
teeth (in sheep) may blacken and fall out.[55]
It is mainly the young animals, such as lambs and colts, that are
affected, probably due to the fact that their attention is more easily
directed to the flower of the loco[56] plants. It is claimed (on slight
evidence) that men have become locoed. The symptoms in them are nausea
and headache.[57]
Schuchardt[58] has called attention to the resemblance of the symptoms
in locoed animals to those which occur in so-called lathyrism, but most
observers in this country have especially marked the resemblance of the
symptoms to those induced by the habitual use of narcotic drugs.[59]
As a rule the loco plants are refused by animals save when there is lack
of other food, although at times animals have shown the keenest relish
for these plants, rejected all other forage, and devoted their whole
attention to searching for the loco plants.[60]
Stalker says that animals not too long addicted to the use of these
plants, if confined, soon lose their taste for them (after two or three
months),[61] although old loco eaters do not readily lose the habit.
Stalker also says that "it is to be presumed that the plant is possessed
of some toxic property that has a specific effect on the nervous
centers, and that these effects have a marked tendency to remain
permanent."[62]
The fundamental character of the disorder seems to be a progressing
anæmia. The interpretation of psychical symptoms in herbivora, and
especially on the range, must often be fallacious.
* * * * *
FOOTNOTES:
[25] Kingsley, B. F. The Loco Plant. Daniel's Texas Medical
Journal, vol. 3, p. 522. 1888.
[26] Schwartzkopff, O. The Effects of "Loco-Weed." Amer. Vet.
Rev., vol. 12, p. 162. 1888.
[27] McCullaugh, F. A. Locoed Horses. Journ. Comp. Med. &
Vet. Archives, vol. 13, p. 435. 1892.
[28] Eastwood, A. The Loco Weeds. Zoe, vol. 3, p. 57. 1892.
[29] Vasey, G. Plants Poisonous to Cattle in California.
Report of Commissioner of Agriculture for 1874, p. 159. 1875.
[30] Vasey, G., l. c., p. 159.
[31] Nockolds, C. Poisoning by Loco Weed. Amer. Vet. Rev.,
vol. 20, p. 570. 1896-7.
[32] Patterson, A. H. Starvation OEdema. Med. Rev., vol.
56, p. 715, 1899.
[33] Vasey, G. Botanical Notes, Monthly Reports of Dept.
Agriculture for 1873, p. 504. 1874.
[34] Anderson, F. W. Poisonous Plants and the Symptoms They
Produce. Bot. Gaz., vol. 14, p. 180. 1889.
[35] Schwartzkopff, O. The Effects of "Loco-Weed." Amer. Vet.
Rev., vol. 12, p. 161. 1888.
[36] Wilcox, T. E. Treatment of "Loco" Poisoning in Idaho
Territory. Med. Rec., vol. 31, p. 268. 1887.
[37] Mayo, N. S. Some Observations Upon Loco. Kans. State
Agric. Coll. Bul. 35, p. 118. 1893.
[38] McCullaugh, F. A. Locoed Horses. Journ. Comp. Med. and
Vet. Archives, vol. 13, p. 436. 1892.
[39] O'Brine, D. Progress Bulletin on the Loco and Larkspur.
Colo. State Agric. Coll. Bul. 25, p. 12. 1893.
[40] Knowles, M. E. Loco Poisoning. Breeders' Gaz., vol. 39,
p. 973. 1901.--Sayre, L. E. Loco Weed. Kans. State Board of
Agric., 5th Bienn. Rept., p. 211. 1887.--Ruedi, C. Loco Weed.
Trans. Colo. State Med. Soc., p. 422. 1895.
[41] Miller, C. H. The Loco Weed: Its Probable Usefulness as
an Emmenagogue. Southern Clinic, vol. 11, p. 269. 1888.
[42] Vasey, G. Botanical Notes. Monthly Reports of Dept.
Agriculture for 1873, p. 504. 1874.
[43] Parker, W. T. The Loco-Weed. Science, vol. 23, p. 101.
1894.
[44] Vasey, G. Botanical Notes. Monthly Reports of Dept.
Agriculture for 1874, p. 513. 1875.
[45] Anderson, F. W. Poisonous Plants and the Symptoms They
Produce. Bot. Gaz., vol. 14, p. 180. 1889.
[46] Sayre, L. E. Loco Weed. Proc. Amer. Pharm. Assoc., vol.
36, p. 111. 1888.
[47] Nockolds, C. Poisoning by Loco Weed. Amer. Vet. Rev.,
vol. 20, p. 570. 1896-7.
[48] Knowles, M. E. Loco Poisoning. Breeders' Gaz., vol. 39,
p. 972. 1901.
[49] Vasey, G. Botanical Notes. Monthly Reports of Dept.
Agriculture for 1873, p. 504. 1874.
[50] Stalker, M. The "Loco" Plant and Its Effect on Animals.
Bur. Animal Industry, 3d Ann. Rept. (1886), p. 272.
1887.--Nockolds, C. Poisoning by Loco Weed. Amer. Vet. Rev.,
vol. 20, p. 570. 1896-7.--Maisch, J. M. Poisonous Species of
Astragalus. Amer. Journ. Pharm., vol. 51, p. 239. 1879.
[51] Nockolds, C. Poisoning by Loco Weed. Amer. Vet. Rev.,
vol. 20, p. 570. 1896-7.
[52] Stalker, M., l. c., p. 273.
[53] Stalker, M., l. c., p. 274.
[54] Ruedi, C. Loco Weed (Astragalus Mollissimus): A
Toxico-Chemical Study. Trans. Colo. State Med. Soc., 1895, p.
417.
[55] Blankinship, J. W. Loco and Some Other Poisonous Plants
in Montana. Mont. Agric. Exper. Sta. Bul. 45, p. 81. 1903.
[56] Blankinship, J. W., l. c.
[57] Day, M. G. Loco-Weed. In F. P. Foster's Reference Book
of Practical Therapeutics, vol. 1, p. 588. 1896.--Pilgrim, C.
W. Does the Loco-Weed Produce Insanity? Proc. Amer.
Medico-Psycholog. Assoc., vol. 5, p. 167. 1898.
[58] Schuchardt, B. Die Loco-Krankheit der Pferde und des
Rindviehs. Deutsch. Zeits. f. Thiermed., vol. 18, p. 405.
1892.--Parker, W. T. Loco-Weed. Science, vol. 23, p. 101.
1894.
[59] McCullaugh, F. A. Locoed Horses. Journ. Comp. Med. and
Vet. Archives, vol. 13, p. 435. 1892.
[60] Stalker, M. The "Loco" Plant and Its Effect on Animals.
Bur. Animal Industry, 3d Ann. Rept. (1886), p. 272. 1887.
[61] Stalker, M. The "Loco" Plant and Its Effect on Animals.
Bur. Animal Industry, 3d Ann. Rept. (1886), p. 272.
1887.--See also Linfield, F. B. Sheep Feeding, in Mont.
Agric. Coll. Exper. Sta. Bul., 59. 1905.--Special Report on
Diseases of Cattle. Bur. Animal Industry, 1904, p.
66.--Wilcox, E. V. Plant Poisoning of Stock in Montana. Bur.
Animal Industry, 17th Ann. Rept., p. 115. 1900.
[62] Stalker, M., l. c., p. 275.
=CONDITIONS SIMILAR TO LOCO-WEED POISONING IN OTHER PARTS OF THE WORLD.=
According to Maiden[63] a condition similar to loco is met with among
animals in Australia and is there believed to be due to eating various
species of Swainsona.[64] As Maiden says, "Its effect on sheep is well
known; they separate from the flock, wander about listlessly, and are
known to the shepherds as 'pea-eaters' or 'indigo-eaters.' When once a
sheep takes to eating this plant it seldom or never fattens, and may be
said to be lost to its owner." Horses, after eating this herb, "were
exceptionally difficult to catch, and it was observed how strange they
appeared. Their eyes were staring out of their heads and they were
prancing against trees and stumps. The second day two out of nine died,
and five others had to be left at the camp."
Martin[65] experimentally studied these cases of intoxication and sums
up his work as follows:
1. That one can by feeding sheep upon Darling pea reproduce all the
symptoms which are attributed by pastoralists to this cause.
Briefly stated these symptoms are: Stupidity, loss of alertness and
an agonized expression, followed by stiffness and slight staggering
and frequently trembling of the head or limbs. Later, clumsiness
and unsteadiness ensue, which slowly advance until the animal often
falls down. In this stage, the action of the animal in running over
small obstacles is characteristic. It jumps over a twig as if it
were a foot in height. When first it commences to tumble about, it
is able more or less readily to regain its feet, but in the
advanced stage of the disease this is impossible and, after
exhausting itself in efforts to do so, it remains lying down until
it dies. During the whole time the sheep become progressively more
bloodless, and in advanced cases the blood when shed appears to the
naked eye lighter in color. It contains fewer red blood-cells
(about two-thirds to one-half the usual number). (The corpuscles
were estimated in several cases by means of a hæmocytometer.) All
these symptoms are much aggravated by driving. Thus, an animal in
which the symptoms are little marked may exhibit them in a striking
degree after being driven. In addition to the above the teeth
(especially in young sheep) frequently become loose, and
consequently displaced or even dislodged.
2. That the time which elapses before the onset of definite
symptoms is three to four weeks in sheep of 2 to 3 years old. (It
is probable, however, that with younger animals the time is
shorter.)
3. That under the conditions of the experiment, the animals
survived about three months. They lived, however, an invalid's
life. Everything was brought to them, and it is improbable that if
feeding exclusively upon the pea, and left to shift for themselves
in the paddocks, they would survive more than two months.
4. That if a sheep be returned to proper fodder after one month to
six weeks feeding upon the pea, and before the symptoms are fully
established, it may recover completely.
5. That when once the paralytic symptoms are established it will
not recover; but if returned to proper food, will remain in much
the same condition, becoming neither better nor worse.
6. That Darling pea contains a very fair amount of nourishing
material so that animals may, provided they eat it readily, retain
their condition on it for some weeks, until the poisonous principle
contained has had time to exert its effects.
These plants, if fed with other herbage, do not seem to be injurious and
apparently lose their harmful action upon being cultivated.[66] As long
as salt is properly fed the animals will not eat this plant[67] and are
said to suffer no effects from it. Physiological study has shown the
presence of a body with marked sudorific power which causes rapid
emaciation in frogs.[68]
It has been claimed that these symptoms are due to the presence of a
narcotic poison in the plant.[69] Post-mortem examinations were negative
save for the presence of a peripheral neuritis.[70]
* * * * *
FOOTNOTES:
[63] Maiden, J. H. Plants Reputed to be Poisonous to Stock in
Australia. Dept. Agric., New South Wales, Misc. Pub. No. 477,
pp. 15, 16. 1901.
[64] Notes on Some American and Australian Plants Injurious
to Stock. Agric. Gaz., New South Wales, vol. 4, p. 677.
1894.--Notes on Weeds. The Darling Pea. Agric. Gaz., New
South Wales, vol. 3, p. 330. 1893.
[65] Martin, C. J. Report on an Investigation into the
Effects of Darling Pea (Swainsona Galegifolia) upon Sheep.
Agric. Gaz., New South Wales, vol. 8, p. 366. 1898.
[66] Woolls, W. On the Forage-Plants Indigenous in New South
Wales. Linn. Soc., New South Wales, Proc., vol. 7, pp.
315-316. 1882.
[67] Guthrie, F. B., and Turner, F. Supposed Poisonous Plant.
Agric. Gaz., New South Wales, vol. 4, p. 86. 1894.
[68] Bailey, F. M., and Gordon, P. R. Plants Reputed
Poisonous and Injurious to Stock, Brisbane, 1887, p. 25.
[69] Guthrie, F. B., and Turner, F. Supposed Poisonous Plant.
Agric. Gaz., New South Wales, vol. 4, p. 87. 1894.
[70] Martin, C. J. Report on the Investigation into the
Effects of Darling Pea (Swainsona Galegifolia) upon Sheep.
Agric. Gaz., New South Wales, vol. 8, p. 367. 1898. (Further
literature on the indigo disease will be found in Bailey, F.
M., and Gordon, P. R. Plants Reputed Poisonous and Injurious
to Stock, Brisbane, 1887, p. 25).
NOTE.--In Canada a chronic disease associated with cirrhosis
of the liver results from eating ragwort, or _Senecio
jacobaea_. See Dept. of Agriculture, Canada, Rept. of
Veterinary Director General, 1905, Ottawa, 1906, p. 31.--In
South Africa a disorder known as nenta appears in goats after
eating certain plants, especially _Cotyledon ventricosa_. See
Hutcheon, D., Nenta, in Agric. Journ. Cape of Good Hope, vol.
14, p. 862. 1899.
=PATHOLOGICAL CONDITIONS IN LOCOED ANIMALS AS DESCRIBED ON THE RANGE.=
The pathological features as described by previous writers are a
softening and ulceration of the stomach walls[71] and a degeneration of
the walls of the intestines with or without perforations. The peritoneum
may be found inflamed.[72] The peritoneum and omentum in one case (cow),
reported by Sayre, were covered with small nodules. These were probably
tubercular in origin. The colon in one horse was found enormously
distended, while the coecum and small intestines were normal,[73] save
that the walls appeared thin.
Ulcers have been found at times in the kidneys, but were probably
secondary in origin, as other cases are reported with normal kidneys.
Faville has found in some cases amyloid degeneration. The pancreas and
spleen are reported normal. The abdominal cavity may contain a slight
effusion.[74] The liver has been found cirrhotic, and at times shows
tubercular lesions of a secondary nature. The inner coat of the bladder
has been found softened, and in sheep the bladder may be markedly
distended at the autopsy. The cerebral membranes are congested and
perhaps adherent,[75] and there may be blood clots over the longitudinal
sinus or at the base of the brain. Effusions have been especially noted
around the medulla. The arachnoid has also shown slight congestion, and
in other cases the membranes showed a slight thickening. The middle
ventricle was found filled with yellow serum, while the fourth ventricle
contained a hemorrhagic effusion,[76] and the base of the brain was
covered by a clot. The hemorrhage may become organized and the brain be
held to the membranes by tough organized fibers. In many cases serous
effusion is present in the lateral ventricles. The arachnoid space is
also in some cases similarly filled. Microscopic examination of the
brain in the case of a steer showed atrophy of Purkinjie's cells.[77]
In sheep the post-mortem examination showed paleness, anæmia of the
muscles, and great distention of the abdomen. The intestines were found
filled with gases, and the mesenteric blood vessels filled with blood.
No peritonitis, or ascites, or ecchymoses in the mucous membranes were
noted in the autopsies made on sheep by Ruedi. The liver has been seen
enlarged. In sheep the brain was anæmic. Microscopically the brain
showed atrophy and the Purkinjie's cells disappeared or their processes
atrophied. In these sheep the brain was so anæmic that the distinction
between the gray and the white matter was hard to define.[78] The
membranes of the cord have been found inflamed and adherent, but the
spinal cord was usually normal.[79] In some cases, however, the spinal
cord has been found softened[80] and oedematous. The arteries of the
limbs were gorged with blood,[81] and at the same time there was a
collection of serum in the abdominal cavity. Death is thought to be due
to starvation.[82] In other words, the pathological condition, according
to published accounts, shows little that is characteristic save some
action on the gastro-intestinal tract.
* * * * *
FOOTNOTES:
[71] Anderson, F. W. Poisonous Plants and the Symptoms They
Produce. Bot. Gaz., vol. 14, p. 180. 1889.
[72] Sayre, L. E. Loco Weed. Amer. Vet. Rev., vol. 11, p.
558. 1887.
[73] O'Brine, D. Progress Bulletin on the Loco and Larkspur.
Colo. State Agric. Coll. Bul. 25, p. 12. 1893.
[74] Faville, in O'Brine, D. Progress Bulletin on the Loco
and Larkspur. Colo. State Agric. Coll. Bul. 25, p. 11. 1893.
[75] Sayre, L. E. Loco Weed. Amer. Vet. Rev., vol. 11, p.
559. 1887.
[76] Stalker, M. The "Loco" Plant and Its Effect on Animals.
Bur. Animal Industry, 3d Ann. Rept. (1886), p. 274.
1887--Sayre, L. E. Loco-Weed. Amer. Pharm. Assoc. Proc., vol.
38, p. 108. 1890.--O'Brine, D. Progress Bulletin on the Loco
and Larkspur. Colo. State Agric. Coll. Bul. 25, pp. 16, 17.
1893.
[77] Mayo, N. S., l. c., p. 118.
[78] Ruedi, C. Loco Weed (Astragalus Mollissimus): A
Toxico-Chemical Study. Trans. Colo. State Med. Soc., 1895, p.
418.
[79] Sayre, L. E. Loco Weed. Amer. Vet. Rev., vol. 11, p.
559. 1887.
[80] O'Brine, D. Progress Bulletin on the Loco and Larkspur.
Colo. State Agric. Coll. Bul. 25, p. 12. 1893.--Klench, J. P.
Rattleweed or Loco Disease. Amer. Vet. Rev., vol 12, p. 399.
1888.
[81] Anderson, F. W. Poisonous Plants and the Symptoms They
Produce. Bot. Gaz., vol. 14, p. 180. 1889.
[82] McCullaugh, F. A. Locoed Horses. Journ. Comp. Med. and
Vet. Archives, vol. 13, p. 436. 1892.
=HISTORICAL SKETCH OF LOCO INVESTIGATIONS FROM A PHARMACOLOGICAL
STANDPOINT.=
During the western immigration of 1849 the Indians along the Missouri
River described to the immigrants a plant (_Astragalus mollissimus_)
producing death in horses and cattle, which was preceded by various
forms of excitement.[83]
The attention of the United States Department of Agriculture was first
called to the toxic action of the loco plants in 1873, when specimens of
the plants, which were identified as _Astragalus hornii_ and _A.
lentiginosus_,[84] were sent from California by Mr. O. B. Ormsby, with
the statement that they were poisonous to stock, especially to horses.
Mrs. J. S. Whipple also corroborated this information. The botanist of
the Department, Dr. George Vasey,[85] published a note and requested
further information concerning the plants. These notes were enlarged by
a similar contribution by Dr. P. Moffat on _Aragallus lamberti_.[86] The
following year Vasey reported with more fullness, and his description of
the action of the plants is substantially what we find in most of the
books of to-day.
In 1876 Lemmon[87] noted that _Astragalus mortoni_ was "a deadly sheep
poison." At the same time Rothrock,[88] botanist of the United States
Geographical Survey under Lieutenant Wheeler, described these plants,
and Kellogg,[89] a botanist in California, reported that _Astragalus
menziesii_ was causing great losses in horses, sheep, and cattle and
claimed that the stockmen had been familiar with this disorder for at
least ten or fifteen years. This report of Kellogg was followed by that
of Rothrock[90] in 1877.
In 1876 a specimen of _Aragallus lamberti_ was sent from Colorado to
Professor Prescott, of the University of Michigan, under the name of
"crazy weed," with the statement that it was poisonous to horses and
cattle and that, while the Mexicans often used it in making beer, it
sometimes caused symptoms in men. His pupil, Miss Watson, undertook a
study of its chemical properties. She failed to isolate any pure
chemical compound, but claimed that in the root there was a body giving
alkaloidal reactions and that there was also a resinous body present.
Another of his pupils, W. R. Birdsall, took the ground-up root himself
in doses of 20 grains at various intervals for several days and later
40-grain doses in one and a half hours, but without experiencing any
marked symptoms except colicky pains. A kitten also was given about one
and a half ounces of the fluid extract without effect. Prescott[91] sums
up by saying that "it would seem that the dried ground root possesses no
poisonous properties." The work of Miss Watson was considered of
sufficient importance to be abstracted in the Annual Report of the
Commissioner of Agriculture for 1878 (1879), page 134.
Gradually the Department of Agriculture became more and more interested
in this subject, and Peter Collier, chief chemist, in 1878, examined the
roots and leaves of _Aragallus lamberti_ for alkaloids, but found
none.[92]
In 1880 Peter Collier published a proximate analysis of _Astragalus
mollissimus_ made by Francis A. Wentz, of Kansas. His investigations
showed it to have an ash content of 6.76 per cent, while the _Aragallus
lamberti_, analyzed by L. F. Dyrenforth, of Chicago, showed an ash
content of 4.32 per cent. Collier[93] sums up by saying:
From the additional work done at this Department it seems probable
that the deleterious effects observed from animals eating this
plant may be due principally to the fact that the sweet taste
causes cattle to reject more nutritious food and strive to subsist
upon the Oxytropis only. This plant is mechanically a very unfit
substance for food, being of a tough, fibrous, and indigestible
character. It is possible that, when the animal becomes somewhat
enfeebled by lack of proper nourishment, the small amount of
alkaloid may have a direct poisonous action. Again, it seems
probable that the plant may contain much larger proportions of
alkaloid at certain stages in its development than at others, or
the seeds may prove to be the most injurious portion.
The departmental work was continued by further short notices by
Vasey[94] in 1884, 1886, and 1887, and by the report of Stalker in 1887.
This report by Stalker is still the best description on the clinical
side of the question.
Rothrock,[95] meeting the loco plants in his survey work, describes
their effects on animals as follows:
Certain it is, however, that, once commenced, they continue it,
passing through temporary intoxication to a complete nervous and
muscular wreck in the later stages, when it has developed into a
fully marked disease which terminates in death from starvation or
inability to digest a more nourishing food. The animal toward the
last becomes stupid or wild, or even vicious, or, again, acting as
though attacked with "blind staggers."
Under the name of Crotalaria, H. Gibbons,[96] in 1879, refers to a plant
growing in California which it was claimed was producing characteristic
symptoms of poisoning in horses and sheep. This plant Professor Maisch
afterwards identified as _Aragallus lamberti_.
Dr. Isaac Ott[97] undertook the physiological study of the question and
used an alcoholic extract of _Astragalus mollissimus_. He found from its
action on frogs, rabbits, and cats that the plant had decided
physiological action, as follows:
(1) It decreases the irritability of the motor nerves.
(2) Greatly affects the sensory ganglia of the central nervous
system, preventing them from readily receiving impressions.
(3) Has a spinal tetanic action.
(4) Kills mainly by arrest of the heart.
(5) Increases the salivary secretion.
(6) Has a stupefying action on the brain.
(7) Reduces the cardiac force and frequency.
(8) Temporarily increases arterial tension, but finally decreases
it.
(9) It greatly dilates the pupil.
Doctor Stockman, in England, about this time tried the action of the
aqueous and alcoholic extracts of the dried _Astragalus mollissimus_
sent from Texas. He experimented with frogs and rabbits in increasing
doses, but without result.[98]