Part 2

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.