CRYPTOGAMIC POISONING IN SOLIPEDS.
Prominent symptoms, asthenia and vertigo. Vary with cryptogam, merge into zymotic diseases. Causes: grain harvested damp and moulded, bluish or greenish, hay greenish white, brown or black, clover reddish, musty fodder, and diuresis, indigestion, gastric intestinal and systemic paresis, somnolence, delirium. Rusts, spring and summer, their evolution. Bunt, smut, produce fever and paralysis, spasms, abortions and dry gangrene, buccal erosions; evolution of ergot, honey dew on leguminous plants causing skin disease, bacterial ferments, diplococcus, streptococcus from foul water, causing enteritis. Symptoms: adynamic, dullness, blunted sense, pendent head, ears, eyelids, congested, yellow, ecchymosed conjunctiva, fever, tympany, colic, constipation, dung small, round, coated masses, vertigo, sometimes fatal diarrhœa, or colliquative diuresis; vertiginous: fever, anorexia, yellow mucosæ, tardy breathing, costiveness colics, stupor, somnolence, giddiness, heavy steps, stumbling, delirium, push head against wall, clinch jaws, grind teeth, make walking or trotting or plunging motions, or pull on halter and fall, amaurosis, paralysis, coma. Remissions. Death in one day or upward. Resumption of functions and recovery. Diagnosis: from meningo-encephalitis. Lesions: gastro-intestinal congestion, infiltration, ecchymosis, fermenting ingesta, congestion of mesenteric glands, liver, brain and meninges. Leucin and tyrosin in urine. Treatment: stomach pump, antiferments, potassium iodide, purgatives, enemata; for brain, bleeding, sedatives, ice, snow, elevation, derivatives, prevent mechanical injury.
The most prominent features of cryptogamic poisoning in these animals are asthenia and vertigo. In dealing with such poisoning, however, we must bear in mind that we have in hand, not one particular disease but a group, differing among themselves according to the cryptogam and its products which may be present:—a group moreover which overlaps more or less the true zymotic diseases.
Causes. Oats, barley and other grain or fodder which has been put up damp, and especially ground feed, becomes speedily overgrown and permeated with moulds, especially penicillium glaucus, aspergillus flavus and glaucus, mucor racemosus, and ascophora mucedo which give a bluish or greenish color and heavy odor, rob it of its nutritive constituents and charge it with toxic products. On mouldy hay it is common to find aspergillus candidus, botrytis grisea, torula herbariorum, and eurotium herbarium which form a greenish white or brownish dust. The spœria herbarium is characterized by small black or brown spots with yellowish, brown or black spores. The peronspora trifolium attacks growing clover (clover sickness) and isaria fuciformis the fescue grasses. The latter has a red color and mucous consistency and is charged with producing fatal poisoning in cattle.
Mouldy or musty oats, or other grain or fodder have long been notorious for producing diuresis in horses with excessive elimination of phosphates, extreme emaciation, weakness and death. In other seasons, and probably because of a difference in the fungi or their products they have caused widespread enzootics of indigestion with paresis of stomach and bowels, and of the systemic muscles. Paraplegia is a common manifestation, suggesting lesions of the spinal cord, and in other cases there are general paresis, somnolence and delirium suggesting cerebral lesions, (Staggers).
Gillespie records an enzootic of gastro-intestinal indigestion and tympany among the horses of a battery of artillery in Afghanistan from eating mouldy grass. Fröhner, Martin and Varnell have seen cases of poisoning by moulds without digestive, urinary or febrile troubles.
Of rusts growing on grain crops there are two chief varieties; the spring rust (uredo rubigo vera) which commences as light yellow patches on the leaves and stems, which change to black as the fungus approaches maturity; and the summer rust (uredo linearis) which grows to a larger size and assumes a browner color. Each of these passes through an evolutionary cycle, the small preliminary patches (uredo) passing into the mature fungus (puccinia rubigo vera and puccinia graminis.) Then it must pass through an alternate generation on another family of plants before it can again grow on the gramineæ.
Bunt produced by the tilletia caries attacks the grasses and small grains. The growing seed (wheat especially) is changed into a black or olive colored powder, having a fishy odor. If the stems are attacked the leaves become pale, withered and dry. It can only be detected by carefully examining the individual seeds.
Other forms of smut are the ustilago carbo and ustilago maidis the familiar black smuts of small grains and maize. These develop by preference in the growing seeds, but also in the stem and leaves. The tilletia caries is as a rule more poisonous than the ustilago the effects being mainly hyperthermia and paralysis. There is, however, a tendency to spasmodic contractions, and abortions, and dry gangrene will occur from smut. The author has seen a large herd of cattle attacked with gangrenous sores around the coronet, which were promptly stopped when the light, smutty ears of corn were no longer given. In other cases the hoof was in part separated from the quick and creaked when the animal walked.
In connection with the gangrenous ergotism of cattle, the author has found on the same farms and feed, horses with ulcers on the buccal mucosa and gastro-intestinal indigestion. Ergot affects the seeds in nearly all the small graminaeæ and is produced by the claviceps purpurea which first attacks the ovary of the seed (sphacelia stage), then it invades the whole seed which grows out from the glumes as a hard, dark or purple spur-like process (ergot stage), then falling on the ground it grows up as a minute stalk with rounded head containing spores.
Honey dew growing on leguminous plants is reputed to cause skin disease in white horses and on the white spots of dark horses, from which those not eating the diseased plants escaped.
Bacterial ferments have an equally bad reputation. Bastin records the poisoning of five foals by fermented rye; Dieckerhoff describes an acute gastro-enteritis with congestion and swelling of liver, spleen and kidneys, as the result of microbes and their products in the fodders. Galtier traced a pneumoenteritis in the horse to two cocci, a motile diplococcus and non-motile streptococcus. Both stained in aniline colors, and were bleached by iodine. They grew in ordinary culture media above 50° F. but most freely at 98° F. The animals were infected by drinking putrid water or spoiled fodders in which the microbes were contained. The change to boiled water in the former case led to their prompt disappearance. Reynal, Cailleux and Foucher have also adduced instances of severe enteritis in the horse from drinking putrid water. These animals showed active congestion of the intestinal mucosa with abundant infiltration of the submucosa.
Bouley found 14 cases in one stable, the owner of which had marketed the good fodder and kept the spoiled for home use. Barthelemy, Alasonniere, Lombroso and Hausmann, Clichy, Rey, Gamgee and others give similar examples.
A large number of observations show the dangerous results on the horse of mouldy bread, inducing colics, vertigo, profuse sweating.
Symptoms. When Adynamia prevails there is great dullness and depression, the senses are blunted, the head depressed resting on the manger, the eyes sunken, weeping and half covered by the drooping upper lid, the conjunctiva is congested, sometimes yellow or marked by petechiæ. The mouth is hot, the lower lips pendent, the tongue furred, the abdomen somewhat tympanitic, with slight colics, but with little rumbling or indication of peristalsis. There is a primary constipation, a few small, hard pellets being passed with effort. The temperature may be 102° to 104°, breathing short, pulse small, weak; the walk unsteady, the animal preferring to stand, completely apathetic. In some cases a profuse diarrhœa sets in and may prove fatal.
In the cases attended by diuresis, the weakness is extreme, emaciation advancing rapidly, but the other symptoms of nervous depression are less marked, the poisons being apparently eliminated by the kidneys (see diuresis).
In the Vertiginous form the disease may set in with more or less hyperthermia, anorexia, a dislike particularly of the spoiled fodder, yellowness of the visible mucosæ, slow breathing, small accelerated pulse, costiveness, tympany, colics more or less intense, tenderness of the belly, and sooner or later marked nervous disorder. This may be in the form of stupor, the head resting in the manger, the senses are manifestly clouded, the animal walks unsteadily, staggers, steps heavily, striking the feet against obstacles, and stumbling. At the end of a variable number of hours (2 to 6 or 8 after feeding) nervous excitability and vertigo may supervene. He may push the head against the wall, the jaws clenched, grinding the teeth, the eyes fixed, pupils dilated, facial muscles contracted, respirations hurried, heart palpitating and the skin perspiring. He may continue in this position, moving his feet as if walking, or he may rear plunging his feet into the manger or fall back over, and rising push anew against any object he may come in contact with. Coulbaux speaks of rabiform symptoms such as attempts to bite but any such deliberate purpose is rare.
There may follow complete amaurosis, insensibility to pricking of the skin, and even paralysis or coma. Hyperæsthesia may also be temporarily present.
Course. Remissions and exacerbations usually alternate, the duration of the former furnishing some criterion by which to establish a favorable prognosis. Death may take place in 24 hours or it may be delayed for several days. Recovery is usually heralded by the resumption of defecation and urination, and the return of appetite. It is liable to be at first only partial, some of the senses remaining dull, or a general stupor persisting.
Diagnosis. In all such forms of poisoning there is the history of the ingestion of the toxic matters, and in any suspicious looking cases a careful examination of the food should be made. From meningo-encephalitis the presence of the abdominal disorder will serve to identify and to incriminate the food.
Lesions. These vary much with the poison. There is always, however, inflammation of the gastro-intestinal mucous membrane, usually with ecchymosis, and infiltration of the submucosa. The contents of the bowels are imperfectly digested, the mesenteric glands congested and enlarged, the liver congested and softened, and the brain and its meninges hyperæmic or infiltrated. The leucine and tyrosine present in the urine during the acute attack is said to disappear when improvement sets in (Pellagi, Azzaroli).
Treatment. The first object must be the removal or neutralizing of the poison. In some instances the stomach pump or tube might be tried. Usually one must fall back on antiferments such as naphthol, naphthalin, salol, salicylic acid, and above all iodide of potassium. The last checks the growth of the fungi or bacteria and favors elimination of the toxins. It may be given freely to act on the kidneys. Creolin, 1¼ drachm, repeated three times a day has been found effective (Albrecht). In addition the action of the bowels may be solicited by full doses of sulphate of soda and abundance of water.
When the brain is implicated Cadeac recommends bleeding as an eliminating as well as a sedative measure. In any case use cold water, snow or ice to the head, elevation of the head, and purgatives which may as a rule be doubled. Potassium iodide or other antiseptics should be pushed, and diuresis as well as a relaxed condition of the bowels maintained. Counter-irritants such as mustard may be applied to the abdomen, and enemata used at frequent intervals. It is important to fix the patient to a ring in the centre of a box stall or barn to keep him from injuring himself.