Chapter VI: Part 6

This appears at times in many horses in the same locality, as in New York in 1850 (Large), in Denmark since 1852 (Stockfleth, Bagge), and in Egypt in 1876 (Apostolides). In Cairo alone about 6,000 horses, mules and donkeys perished. Hence the disease is known as _epizootic cerebro spinal meningitis_. But again it is often seen in scattering or sporadic cases. Add to this that no evidence has ever been adduced that the disease is communicated from one animal to another, and in these days of the parallelism of _epizootics_ and _pathogenic microbes_, we may well hesitate about continuing to use such a qualifying term. Friedberger and Fröhner claim “that a large number of clinical facts have been erroneously reported under the name of spasm of the neck. Rabies, tubercular basilar meningitis, apoplexy, simple encephalitis, and certain poisonings have been confounded with that disease.” They assure us that “cold, damp, chilly weather, hot stables, clipping and overfeeding are of but secondary importance,” but they fail absolutely to tell us what is of _primary importance_ in a causative sense. American writers who have attempted to account for the disease have groped somewhat blindly for causes in the idea of poison. Large charged it on insanitary conditions, poisonous gases, and defective sewerage in cities, and lack of drainage and deficient stable ventilation in the country. J. C. Michener attributes it to foods undergoing fermentation and considers it as a paralysis due to toxic fungi. W. L. Williams, in Idaho, found the greatest number of cases in winter had been fed hay made from alfalfa (lucerne) and timothy, though some had small grains and native grasses. The soil was dry, porous, gravelly, devoid of humus, and lying on lava rock. The altitude and clearness of the atmosphere were supposed to exclude the idea of cryptogams, yet the crops generally were raised by irrigation. The water was from clear mountain streams. Stables were generally low and full of manure, with thatched roofs, but hardly tight enough to be called close. In these cases the defective stable room, the irrigation, the leafy hay (lucerne), and the probable presence of ferments (bacteria), are the only suggestive conditions. In a fatal outbreak which I saw among the Wilkesbarre, Pa., pit mules, rain-soaked and badly fermented timothy hay, overwork in view of a strike, and a Sunday’s holiday in an unshaded yard under a hot July sun, in contrast with the previous darkness and coolness of the pits, coincided to disturb the general health. In several of the Southern States it is attributed to worm-eaten corn. Trumbower thinks it should be traced to the parasitic fungi that grow on plants, grains, and vegetation. In many instances the disease has appeared simultaneously with the feeding on certain specimens of brewer’s grains, oats and hay, so that to use Trumbower’s words these were the carriers if not the prime factors of the disease.

In recognizing how much cryptogams and bacteria vary under different conditions of life, and what various products they elaborate at different stages of their growth, we can theoretically explain the absence of the disease at one time and its presence at another under what seem to be identical circumstances, as also the variety of symptoms shown in different outbreaks. While this causation cannot be said to be absolutely proved, it is not antagonistic to the facts in many of the best observed outbreaks, and may serve as a hypothetical working theory until actual demonstration can be furnished. The affection suggests a narcotic poison introduced from without, rather than a disease due to a germ propagated in the system.

This need not, however, exclude the operation of attendant conditions such as overwork, plethoric feeding, excitement, close stables, heat exhaustion, etc., which tend to bring about cerebro-spinal congestion. Even the electric tension of Idaho, of the United States generally, and of Egypt, in connection with their comparatively dry atmosphere, should not be overlooked in considering the possible causative factors.

In all probability as we learn more of the true pathology of the disease, we shall come to recognize not one, but several toxic principles, and several different affections each with its characteristic phenomena in the somewhat indefinite affection still known as cerebro-spinal meningitis.

The malady has been described in horses, oxen, sheep, goats and dogs, attacking by preference the young, which are not yet inured to the unknown poison, and by preference in winter and spring, the periods of close stabling, dry feeding and shedding of the coat.

In the absence of bacteriological data from the horse, it may be noted that in man cerebro-spinal meningitis, has been commonly found to be associated with the presence in the meningeal exudates of the _micrococcus pneumoniæ crouposæ_, (Micrococcus lanceolatus encapsulates). This is frequent in the mouths of healthy persons so that some additional accessory cause must be invoked to increase the susceptibility or lessen the protective power of the tissues. This has been thought to be found in the concurrent presence of other bacteria, the staphylococcus pyogenes aureus, pneumobaccillus of Friedländer and the streptococcus pyogenes. Mosny appears to have established this for the staphylococcus in the case of rabbits. With a given dose of the micrococcus pneumoniæ death was always delayed for a fortnight, while with the same dose thrown into one thigh, and the staphylococcus aureus in the other, the rabbit died in one day. This enhanced potency resulting from the presence of the golden staphylococcus has been invoked to account for the germ making its way from the mouth to the brain in cases of otitis, suppuration of the Eustachian tube, tonsilitis or nasal catarrh. These remarks are intended to be suggestive, rather than conclusive, as we have as yet no certainty that cerebro spinal meningitis in the horse is caused by the same germ as it is in man.

_Lesions._ The lesions are usually those of leptomeningitis, or congestion of the brain and spinal cord and often effusion into the ventricles, with a serous exudation under the pia mater or into the arachnoid cavity. This may be transparent and yellowish, or grayish and turbid, or milky. In the sheep, Roloff has found purulent products under the pia mater, around the roots of the spinal nerves, and in the surface layers of cerebral gray matter. The marked hyperæmia on the surface of the gray matter is a striking feature, and circumscribed areas of necrotic nervous tissue and softening are not uncommon. Petechiæ are frequent on the meninges, the brain, heart, lungs and kidneys. Granular and fatty degenerations are also met with in these parenchymatous organs. The blood may be dark and liquid or diffluent.

_Symptoms in the_ =Horse=. The mildest attacks are manifested by paresis, or loss of perfect control over the limbs, or loss of power over the tail, impairment of appetite and some difficulty of swallowing, together with some congestion or reddish brown discoloration of the orbital and nasal mucosæ. In other cases paralysis of one or more limbs may supervene but without marked fever or coma.

The more severe forms are ushered in by violent trembling, or by stupor, apathy, and extreme muscular weakness, or actual paralysis. In such cases the animal may stagger or fall. Dysphagia or inability to swallow is often a marked symptom, the saliva falling in strings from the lips. Another common phenomenon is the rigid contraction of the muscles of the neck, back and loins, the parts becoming tender to the touch and a more or less prominent oposthotonos setting in. Twitching of the muscles of the shoulders and flanks may be noticed. Trismus also is sometimes seen. The breathing is usually rapid and catching and the temperature 104° to 106°. The pulse may be accelerated and hard, or weak and soft, or alternating. The eyes are violently congested, of a brownish or yellowish red color, and the eyeballs may be turned to one side. Paroxysms of delirium may set in, when the animal will push against the wall, or perform any of the disorderly movements described under meningo-encephalitis. Sooner or later coma and paralysis supervene, and death occurs in from five to forty-eight hours. In the most acute (fulminant) cases the animal falls and dies in convulsions. On an average the disease lasts from eight to fifteen days. In the more favorable cases, without any supervention of coma, recovery may begin on the third or fourth day.

_Symptoms in the_ =Ox=. These are largely those of encephalo-meningitis. If they do not come on with the customary violence, there may be at first difficulty in prehension, mastication and swallowing of food; a rigid condition of the muscles of the neck, back, and sometimes of the jaws, and twitching of the muscles of the limbs, neck, lips, or eyes. For a time there may be hyperæsthesia, restlessness and irritability, stamping of the feet or shaking of the head, then there is liable to follow, dullness, apathy, stupor, coma and paralysis. As in the horse, the distinction from ordinary encephalo-meningitis will at times rest on the prevalence of the epizootic disease in the locality.

_Symptoms in_ =Sheep=. The attack is described as coming on with weakness, dullness, lethargy, salivation, convulsions, oposthotonos, grinding of the teeth, succussions of the body and limbs, heat of the head, and stupor or paralysis unless death ensues during a paroxysm. The congestion of the head and of the encephalic mucous membranes, and the deviation of the eyes are constant features. Wischnikewitsch describes an extended outbreak in sheep in which the brain lesions were complicated by hepatization of the lungs, and bacilli were found in the various exudates. This reminds one of the presently accepted cause in man, which is, however, a micrococcus rather than a bacillus.

_Symptoms in_ =Dogs=. These are described as some aberration of the senses, which gradually merges into stupor, coma and paralysis. While the animal is able to keep on his feet he sways and staggers, runs unconsciously against objects, or walks in a circle. There is heat of the head, injected eyes, sometimes drawn back or squinting, oposthotonos, and general spasms occurring in paroxysms. The duration of the disease is about the same as in the horse.

_Differential Diagnosis._ From other forms of meningitis this is easily distinguished. Fulminant cases almost all belong to this type, the fact of the coincident implication of brain and spinal cord is strongly suggestive of this form, and the occurrence of many cases at once, without any demonstrable toxic or thermic cause, is tolerably conclusive. From tetanus there is this added distinction, that the disease does not set in so slowly, the spasms of the neck and back are not so persistent, and stupor sets in early, in a way that is unknown in lockjaw. Rabies is recognized by the slow onset, the characteristic prodromata, the mischevious disposition, the depraved appetite, and by the history of its local prevalence. Tubercular meningitis in cattle has a similar association with tuberculous animals in the same family or herd, and often by the local indications of tubercle elsewhere, emaciation, unthriftiness, cough, flocculent and gritty nasal discharge, enlarged lymph glands, pharyngitis, mammary disease.

_Treatment._ With a disease so fatal _prevention_ should be the first consideration and especially when it appears in an enzootic form. Even in the absence of a definite knowledge of its germ or toxin, it is logical to avoid the locality, condition, food or water by which such germ or toxin has presumably entered the system, together with every unhygienic condition, which may have reduced the resistance of the system and laid it open to the attack. The animals should be removed to a clean, airy, building and the old one should be thoroughly emptied, purified and whitewashed, the lime-wash containing 4 ozs. of chloride of lime, or 1 dr. of mercuric chloride to the gallon. Drains and gutters should have special attention and the animals should not be returned until the stable is thoroughly dry. A change of feed is imperative when there is any suggestion of damp, mustiness or fermentation, and even in the absence of such indications, since the ferments and their products may still be present in a dried condition. It should also be an object to correct any morbid or pyogenic condition of the pharynx, Eustachian pouch, nose or ear, by appropriate measures and the inhalation of sulphurous acid or chlorine may be resorted to with advantage.

As medicinal treatment Large advises to give at the outset 1 oz. aloes with one or two drs. of solid extract of belladonna and as an eliminant, derivative and nervous sedative there is much to be said for it. In case the difficulty of swallowing should prove a serious barrier a hypodermic injection of ½ dr. barium chloride, 1½ to 2 grs. eserine, or 2 grs. hydrochlorate of pilocarpin together with ¼ grain of atropin, may be employed. As a substitute for atropin, ergot, potassium bromide, chloral hydrate, chloroform, or phenacetin have been tried in different cases with varying results. Iodide of potassium has been employed with advantage in the advanced stages and in convalescence, and may be usefully employed in the early stages as a sedative to the nervous system, a deobstruant and an eliminant, if not as a direct antidote, to the toxins.

Bleeding is generally condemned, yet in acute cases where there are indications of active brain congestion, threatening convulsions or coma it may tend to ward off a fatal result.

Cold applications to the head are generally commended. Bags of ice or snow, irrigation with cold water, or cooling by running water at a low temperature, through a pipe coiled round the head or extended along the spine, will meet the purpose. Applied continuously this constringes the blood-vessels within the cranium as well as on its surface, lessens the exudation, and controls the pain and spasms. This may be advantageously associated with warm fomentations to the feet and limbs, friction, or even the application of stimulating embrocations to draw the blood to these parts. In the smaller animals even warm baths may be resorted to as a derivative, cold being meanwhile applied to the head and spine. This not only lessens the vascular pressure within the cranium, but secures elimination of toxic matters by both skin and kidneys. Cold pure water should be constantly within reach.

A most important thing in the horse is to put him in slings, if he is at all able to stand with their assistance. In decubitus he rests on his side, with the head on the ground, and lower than the splanchnic cavities. The result is a gravitation of blood toward the head. In the sling, with the head fairly raised the gravitation is the other way and the head is depleted. If the patient is too ill to be maintained in the sling, he may be packed up with bundles of straw on each side, so that his breast may lie on a thickly littered bed, and his head may be elevated.

When convalescence sets in care must be taken to nourish with non-stimulating, easily digested food, gruels, soft mashes, pulped or finely sliced roots. In vomiting animals rectal alimentation may become necessary. The rise of cranial temperature or the aggravation of brain symptoms should be met as needed by the local application of cold, and potassium iodide and iron or bitter tonics may be given if they do not interfere with digestion.

ABSCESS OF THE BRAIN.

Infection, in traumas, meningitis, encephalitis, strangles, etc.
Symptoms: evidence of trauma, chill, hyperæsthesia irritability,
drowsiness, giddiness, stupor, spasms, paresis, coma, dilated pupils,
congested mucosæ, vomiting. Location indicated by muscular groups
involved. Treatment: As in meningitis: trephining in hopeful cases.

The formation of abscess in the cranial cavity has been referred to in connection with injuries to the cranium and meningo-encephalitis. It may here be said in general terms that this abscess is a product of infection. In the horse the most common cause is strangles, and especially such cases as run a tardy or irregular course with imperfect softening and limited suppuration in the submaxillary or pharyngeal region. It is to be looked on as an extension of the purulent infection so as to cause a secondary abscess. The same may occur in case of ordinary abscess in any distant organ. In the brain as elsewhere suppuration may result from direct local injury as in the case of blows by clubs, or yokes, running against walls or posts, falls, the effects of butting, injuries by bullets and otherwise. In these cases, as noticed under concussion, there may be two points of injury (and two abscesses) one, in the seat of the injury, and one in a deeper part of the brain, at the opposite wall of the cranium. Again abscess may result in the brain from extension from a similar process going on in the vicinity. Thus otitis extends through the middle and internal ear to the brain, and its starting point may have been more distant, namely, in the Eustachian tube, or pouch, or in the pharynx.

The _symptoms_ vary according to the size of the abscess, the rapidity of its formation and the amount of attendant congestion. In the common cases resulting from strangles, I have usually found the animal down, unable to rise, blind, amaurotic, with dilated pupils, congested mucous membranes, and occasional spasmodic movements of the limbs, neck and head. The symptoms may, however, vary through hyperæsthesia, irritability, drowsiness, giddiness, stupor, local or general paralysis with occasional spasms or convulsions. There may be an initial shivering, and a rise of temperature, yet as pressure on the brain increases it may become normal or subnormal. In circumscribed abscess the symptoms may be much less severe, not perhaps exceeding irritability, drowsiness, and some paresis or local paralysis.

In some such cases one can trace the connection to some primary disease, (traumatic injuries to the cranium, abscess of the diplöe or sinus, parasites in the sinus, otitis, or pharyngeal disease) which serve as an indication of the true state of things. In others there may be circumscribed local manifestations, (anæsthesia, hyperæsthesia, hemiplegia, paralysis of special muscular groups, or spasms of the same ) which may indicate more or less accurately the exact seat of the lesion. When well defined, this localization of the resultant phenomena, serves to distinguish this and other local lesions, from meningitis which is apt to be much more general in its diffusion. In the carnivora and omnivora vomiting is a marked symptom.

_Treatment_ of brain abscess is usually hopeless, yet the attendant inflammation may be met as in other cases of meningitis. If the seat of abscess can be ascertained surgical interference is fully warranted.

TUBERCULAR MENINGITIS.

Little seen in cattle. Acute and chronic cases. Miliary tubercles in
pia. Hydrocephalus. Progresses slowly. Irritability, hyperæsthesia,
photophobia, congested conjunctiva, grinding teeth, spasms, squinting,
dilated pupils, congested disc, drowsiness, stupor, coma, palsy.

Tubercle of the encephalon has been little noticed in the lower animals, partly because it is especially a disease of early life, while animals usually contract tubercle later in life, and partly because subjective symptoms are inappreciable, and the cranium is seldom opened in post mortem examinations. As the affection usually appears as a secondary deposit, the tubercles elsewhere go a long way toward identifying the nature of the disease in the brain. It has usually been found consecutive to pulmonary tuberculosis.

In a case reported by Fischœder as seen at the Bromberg abattoir, in a 350 lbs. calf, the animal had shown weakness, stupor and a tendency to fall toward the right. The brain lesions consisted of small foci of tubercle on the posterior pillars of the fornix (trigone) and adjacent parts. The left eye had on its inner aspect, near the junction of sclerotic and cornea, a firm mass with tubercular centres, extending inward as far as the retina. The bronchial mediastinal, prepectoral, brachial and precrural glands were tuberculous.

In a case in a cow reported by Lesage there were unsteady gait, impaired vision, and great timidity. Necropsy showed a suboccipital tubercle extending into the frontal sinus and cranium, and invading the brain near the parietal lobe for more than an inch. There were retro-pharyngeal and pleural tubercles as well.

In a case of Routledge’s, with extensive recent exudate, the condition advanced from apparent health to extensive paralysis in three days, while in a case which the author obtained in slaughtering a tuberculous herd no special nervous symptoms had been noticed during life. Much therefore depends on the rapidity as well as the seat of development.

The primary lesions in the brain are of the nature of miliary tubercles in the pia mater which becomes congested, rough, granular, and throws out a free serous secretion. Thus hydrocephalus is a usual concomitant of the affection.

The disease is characterized by its slow advance in keeping with gradual increase of the tubercle and is thus distinguishable from the more acute congestions and inflammations. The earlier stages are usually marked by nervous irritability, hyperæsthesia, intolerance of light, closed eyelids, congested conjunctiva, grinding of the teeth and even spasms partial or general. The second stage shows somnolence, deepening into stupor or coma, or there may be going in a circle or other irregular movement. Squinting usually convergent, dilated pupils and congestion of the optic disc frequently occur. The sleep, stupor, paralysis or coma may set in early and is usually largely due to the amount of exudation and the rapidity of its effusion.

TUMORS OF THE BRAIN. NEOPLASMS.

Existence inferential with similar external tumors. Cholesterine
tumors on plexus of lateral, third or fourth ventricle: pea to egg: in
old; concentric layers with abundant exudate. Symptoms: slight, or
excitability, dullness, vertiginous paroxysms with sudden congestions,
as in encephalitis, sopor, stupor, paresis, coma. Melanoma: mainly
meningeal; pea to walnut; with skin melanomata in gray or white
horses. Cases. Pigmented sarcomata. Diagnosis, inferential. Psammoma:
advanced cholesteatoma, melanoma, fibroma, etc.: osteid tumors.
Nervous irritation, delirium, spasms, nervous disorder, and paroxysms.
Myxoma: contains mucin: cells (in homogeneous matrix) round,
spindle-shaped or stellate. Changes to fat (cholesterin). Œdematous
connective tissue, neoplasm. Myxolipoma. Myxo-cystoid. Symptoms.

Tumors in the brain are not marked by distinct pathognomonic symptoms, so that their presence is to be inferred as a probability rather than pronounced upon as a certainty.

The most common forms in the horse are cholesterine (cholesteatoma), melanotic (melanoma), sandy, gritty (psammoma), and fibrous (fibroma).

CHOLESTEATOMA.

These are tumors formed largely of the peculiar fat which is found in bile and brain matter, and that crystallizes in flat oblong scales with a notch at one corner. The tumors are usually connected with the choroid plexus and developed beneath the pia mater, and may be of any size from a pea to a hen’s egg, or in exceptional cases a sheep’s kidney. As a basis there is a stroma of connective tissue permeated by blood vessels from the plexus. Groups of spherical or polygonal cells fill the interstices while fusiform cells are found in the stroma. There is a variable amount of phosphate or carbonate of lime which in oldstanding cases may give a cretaceous character to the mass. These constitute sandy tumors (psammomata).

Cholesteatomata are especially common in old horses and are manifestly connected with congestion of the choroid plexus and exudation. In a recent case or in a case which has shown a recent cerebral hyperæmia, we may find a central mass of yellowish cholesterine, and surrounding this an abundant yellow gelatinoid exudation. This latter is rich in cholesterine which fails to dissolve along with the rest of the exudate on the occurrence of resolution, and is therefore laid up as the solid fatty material. For the same reason the fatty element is usually laid on in layers, one corresponding to each access of local hyperæmia and exudation. The great tendency to calcareous degeneration has been attributed to the abundance of phosphate of lime in the cerebral exudate.

The _symptoms_ of these tumors are exceedingly uncertain. Many such tumors of considerable size have been found after death in animals in which no disease of the brain had been suspected during life. In these it is to be inferred that the accretions were slow, gradual, and without any serious congestion. In other cases the tumor is attended by paroxysms of vertigo, or indications of hyperæmia or meningitis, which will last for several days and gradually subside. It is reasonable to suppose that the tumors are largely the result of such recurrent attacks of encephalitis, and are no less the cause of their recurrence. The intervals of temporary recovery correspond to the subsidence of hyperæmia and the reabsorption of the liquid portion of the exudate. The manifestations during an access correspond directly to those met with in encephalitis. As in that affection there is usually an initial period of excitement and functional nervous disorder tending to more or less somnolence, stupor, paralysis or coma, with long intermissions of apparently good health. In other cases the stupor or paretic symptoms may persist up to the fatal issue.

MELANOMA OF THE ENCEPHALON.

Black pigment tumors have been found in connection with the brain and especially the meninges, varying in size from a pea to a walnut, and as a rule, secondary to similar formations elsewhere. They are most common in gray horses which have turned white, and may give rise to gradually advancing nervous disorder. Bouley and Goubaux record a case of this kind attended with general paralysis. W. Williams reports the case of an aged gray stallion with melanomata on the meninges and in the brain substance which were associated with stringhalt of old standing. Mollereau in a vertiginous horse found a pigmented sarcoma in the right hemisphere between the gray and white matter, and like an olive in size and shape. There were melanomata around the anus. (Annales de Medecine Veterinaire, 1889). So far as such have been examined they follow the usual rule in melanomata in having a sarcomatous structure.

While it is impossible to make a certain diagnosis without opening the cranium, the condition may be suspected, in gray horses, when melanotic tumors are abundant in the usual external situations (anus, vulva, tail, mammæ, sheath, lips, eyelids, etc.), and when brain symptoms set in and progress slowly in such a way as to suggest the gradual growth of a tumor.

_Treatment_ is hopeless, since if they have invaded the brain, the tumors are likely to be multiple in the organ, and numerous and widely scattered elsewhere.

PSAMMOMATA (GRITTY TUMORS) OF THE BRAIN.

As already noted these sandy tumors are often the advanced stage of cholesteatomata, the abundance of the phosphate of lime leading to its precipitation in the neoplasm. The same cretaceous deposit often takes place in old standing tumors of other kinds, as in melanoma, and fibroma so that the sandy neoplasm may be looked upon as a calcareous degeneration of various forms of intracranial tumors. The same tendency to calcareous deposit is seen in the tuber cinereum (pineal body) of the healthy brain which has taken its name from the contained gritty matter. This tendency to the precipitation of earthy salts may be further recognized in the osteid tumors which occasionally grow from the dura mater.

The gritty tumors are especially found in the older horses in which the tendency is greatest to extension of ossification and calcic degenerations.

Like other tumors these may attain a considerable size before they give rise to any very appreciable symptoms, but having attained a given development—often the size of a walnut, they become the occasion of nervous irritation, delirium and disorder, as indicated under encephalic hyperæmia and inflammation, cholesteatomata, etc. There may, however, be drowsiness, stupor, coma, or paralysis as the exclusive symptom, or there may be spasms and convulsions.

MYXOMA OF THE BRAIN.

Myxoma is a tumor in which mucoid elements or a gelatinoid degeneration and infiltration containing mucin is a prominent feature. The _mucous tissue_ which constitutes the tumor may differ little from ordinary connective tissue except that the intercellular spaces contain mucin. Histologically the tissue consists of cells embedded in a homogeneous matrix. The cells may be of various forms, round, (in recent formations) and spindle-shaped or star-shaped, but especially the latter, in the older. When incised a fluid containing mucus escapes in greater or less abundance. While this has properties resembling albumen it is distinguished by the fact that the precipitate thrown down in it by alcohol is softened and redissolved on the addition of water. The precipitate thrown down in an albuminous liquid is insoluble in water.

The formation of this mucous exudate is liable to be followed by fat so that Virchow considered it as antecedent to fat formation. This is especially noticeable in the early stages of the cholesteatomata of the choroid plexus of the horse, in which, as observed by Fürstenberg, Lassaigne, and Verheyen, the new formation is at first a myxoma, which later becomes filled up with cholesterine.

Recent observations tend to discredit the alleged distinctive character of myxoma. The meshes of all connective tissue contain a perceptible amount of mucin. Œdematous subcutaneous connective tissue contains this mucin in greater proportion and approximates to the condition of mucous tissue. The umbilical cord, which has been long advanced as the physiological type of mucous tissue, has been shown to consist of ordinary connective tissue with an abundance of fluid in its meshes.

Koster denies that the myxoma is a special type of tumor, and holds that it is only a condition that may arise in any tumor which contains connective tissue. In other words, myxoma is only an œdematous condition of the connective tissue neoplasm—fibroma, sarcoma, carcinoma, etc.—due to passive congestion or other circulatory disturbance.

As seen in the brain of the horse the formation is usually of the nature of a myxo-lipoma, as the final outcome is usually the cholesterine bearing mass. In other cases the connective tissue spaces become further distended with the viscous, gelatinoid liquid and form veritable cysts—myxoma-cystoides.

In tumors of this kind affecting the choroid plexus the chain of symptoms is essentially the same as given under cholesteatoma and the prognosis is nearly equally grave. It need only be said that in recent cases in which there is as yet little permanent tissue, measures may sometimes be hopefully adopted, to secure the reabsorption of liquid constituents, and even perchance to remove some obvious cause of passive congestion upon which the effusion depends.

ACROMEGALY. HYPERTROPHY OF THE PITUITARY BODY.

Like other portions of the brain the pituitary body is subject to degenerations and diseases of various kinds. This is particularly mentioned here because of the occasional association of its hypertrophy with the trophic processes of different parts of the body. Along with an over-development of the limbs, and less frequently of the body, an enormous increase of the hypophysis has been found, and the one condition has naturally been set down as the result of the other. In some such instances, of overgrowth, however, some other blood glands, such as the thyroid or thymus, have been found to be hypertrophied, so that at present it is difficult to do more than notice the association observed between the two conditions.

CEREBELLAR DISEASE.

Cerebellum and coördination. Pressure on adjacent parts renders
results uncertain. Generic symptoms, ataxia, titubation. Marked
symptoms with rapid morbid progress. Treatment: tonic, hygienic.

Whatever functions are exercised by the cerebellum there is no doubt of its control over muscular coördination. It is quite true that disease of any other part of the brain causing effusion, exudation or intracranial pressure will more or less completely arrest the functions of the cerebellum just as disease of the cerebellum producing intracranial pressure will derange the functions of other parts of the encephalon. The general symptoms produced in this way cannot therefore be accepted as indicating the precise localization of an intracranial disease. Dullness, stupor, coma, dilated pupils, choked discs, optic neuritis, and vomiting, are in this sense generic symptoms, which may in the absence of fever indicate dropsy, exudation, apoplexy, tumor, concussion or other lesion, and with hyperthermia may indicate encephalitis or meningitis. But if in the absence of these symptoms and of aural disease there should appear ataxia, swaying unsteady gait, and staggering, there is a strong presumption of cerebellar disease. This may also be manifested by the other and generic symptoms already mentioned only the diagnosis is not then so certain. Again cerebellar disease may exist without the ataxia and lack of balance, but probably only in cases in which the progress is slow and the organ has had ample time to accommodate itself to the as yet comparatively restricted lesions. The result may be a mere defect of muscular tone, or it may extend to an almost absolute loss of contractility, or it may be of any intermediate grade.

_Treatment_, which is eminently unsatisfactory, consists in improving the general health and tone, by corroborant medicines and conditions of life, and training the muscles by carefully graduated exercise and even electricity.

BULBAR PARALYSIS. DISEASE OF MEDULLA OBLONGATA.

Impaired innervation of bulbar nerves. Paresis of lips, tongue, and
larynx. Roaring. Rapid pulse. Glycosuria, albuminuria. Ptosis.
Twitching eyelids. Dysphagia. Paralysis. Treatment, rest, cold to
head, laxatives, nerve stimulants, tonics, electricity.

The bulb is intimately connected with the origin of the hypoglossal, glosso-pharyngeal, spinal accessory, vagus, facial, and trifacial nerves and active disease in the bulb is therefore likely to entail impairment of the function of several of these nerves. In man this is recognized in _chronic progressive bulbar paralysis_, which almost always affects the lips, tongue and larynx advancing steadily though slowly to a fatal termination. In degenerative lesions there is modified voice, difficulty of swallowing, rapid pulse, and laryngeal paralysis (especially of the arytenoid muscles). The implication of the root of the vagus may be inferred from the arrest of inhibition of the heart, and from glycosuria or albuminuria. Occasionally the ocular and palpebral muscles are involved causing ptosis, or twitching of the muscles. When the facial (7th) nerve is implicated, paralysis of one or both sides of the face may be marked, including often the ears. When the glosso-pharyngeal, the difficulty of swallowing is a prominent feature, and when the spinal accessory, spasm or paralysis of the neck. In the worst cases death supervenes early, by reason of interference with the respiratory and cardiac functions.

The _treatment_ of these affections is usually very unsatisfactory, though in meat producing animals it may sometimes be desirable to preserve them in preparation for the butcher. Rest, in hyperæmic cases, cold to the head and purgatives, and in those in which fever is absent, small doses of nerve stimulants (strychnia) and tonics (phosphorus, phosphates, ammonia-sulphate of copper, zinc sulphate, silver nitrate) may be tried. A course of arsenic and carefully regulated electrical stimuli may at times give good results.

LOCO POISONING. OXYTROPIS LAMBERTI. ASTRAGALUS MOLLISSIMUS

Astragalus Hornii: A. Lentiginosus: A. Mollissimus: Oxytropis
Lamberti: O. Multifloris: O. Deflexa: Sophora Serecia: Malvastrum
Coccinium: Corydalis Aurea. In dry regions. Cause, a psychosis.
Emaciation. Lassitude. Impaired sight. Illusions. Vice. Refuses other
food. Contradictory views. Experiments by Dr. Day.

The term _loco_ is of Spanish origin and has come to us through the Spanish speaking residents on the cattle raising plains and the Pacific Coast. The word is defined to mean _mad_, _crazy_, _foolish_. It has been applied indiscriminately to a disease in stock manifested by these symptoms, and to a variety of leguminous plants, found growing on the western lands and supposed to cause the disease in question. The plants complained of are Astragalus Hornii, and A. Lentiginosus (Griesbach) in California, A. Mollissimus (Torrey) and Oxytropis Lamberti (Purshiana) in Colorado and New Mexico. Other allied species, and like these found also in the other Rocky Mountain States, Sophora Serecia, Oxytropis Multifloris, O. Deflexa, Malvastrum Coccinium, and Corydalis Aurea var. Occidentalis have been less confidently charged with producing the disease.

These plants grow on poor, dry, sandy or gravelly soils, and having great power of resisting drought, are often in fair growth, and present an abundant mass of leaves when surrounding vegetation is withered up. Hence, it is alleged, the animals are driven to use it when nothing else is obtainable and once accustomed to it, the desire for more becomes a veritable craze or neurosis, and the victim searches for it and devours it to the exclusion of other food.

The following quotations may serve to illustrate the effects alleged:

Among the symptoms first noticed are loss of flesh, general lassitude and impaired vision; later the animal’s brain seems to be affected; it becomes vicious and unmanageable and rapidly loses both flesh and strength. Frequently when approaching some small object it will leap into the air as if to clear a fence. The patient also totters on its limbs and appears as if crazy. After becoming affected it may linger many months, or a year, but usually dies at last from the effects of the complaint. (Dr. Vasey. Report of Dept. of Agriculture, 1884).

“I think very few if any animals eat the loco at first from choice; but as it resists the drought until other food is scarce they are first starved to it, and after eating it a short time appear to prefer it to anything else. Cows are poisoned by it as well as horses, but it takes more of it to affect them. It is also said to poison sheep. As I have seen its actions on the horse, the first symptom apparently is hallucination. When led or ridden up to some little obstruction, such as a bar or rail lying in the road, he stops short, and if urged, leaps as though it were four feet high. Next he is seized with fits of mania in which he is quite uncontrollable and sometimes dangerous. He rears, sometimes even falling backwards, runs or gives several successive leaps forward, and generally falls. His eyes are rolled upward until only the white can be seen, which is strongly injected and as he sees nothing, is as apt to leap against a wall or a man, as in any other direction. Anything which excites him appears to induce the fits, which, I think, are more apt to occur in crossing water than elsewhere, and the animal sometimes falls so exhausted as to drown in water not over two feet deep. He loses flesh from the first and sometimes presents the appearance of a walking skeleton. In the next and last stage he only goes from the loco to water and back, his gait is feeble and uncertain, his eyes are sunken and have a flat, glassy look, and his coat is rough and lustreless. In general the animal appears to perish from starvation and consequent excitement of the nervous system, but sometimes appears to suffer acute pain, causing him to expend his strength in running wildly from place to place, pausing and rolling, until he falls and dies in a few minutes.” (O. B. Ormsby, Report Dept. of Agriculture, 1874.)

“Animals are not fond of it at first, or don’t seem to be, but after they get accustomed to the taste they are crazy for it and will eat little or nothing else when loco can be had. There seems to be little or no nutrition in it as the animal invariably loses flesh and spirit. Even after eating of it they may live for years, if kept entirely out of its reach, but if not, they almost invariably eat of it until they die.” (Mrs. T. S. Whipple, San Luis, Cal. Report Dept. of Agriculture, 1874).

“Cattle, after having eaten it,” Oxytropis Lamberti, “may linger many months, or for a year or two, but invariably die at last from the effects of it. The animal does not lose flesh apparently, but totters on its limbs and becomes crazy. The sight becomes affected so that the animal has no knowledge of distance, but will make an effort to step over a stream or an obstacle while at a distance off, yet will plunge into it or walk up against it on arriving at it.” (Dr. Moffat, U. S. Army.)

“The term _loco_, simply meaning foolish, is applied because of the peculiar form of dementia induced in the animals that are in the habit of eating the plant. Whether the animals (horses chiefly) begin to eat the plant from necessity (which is not likely) or from choice, I am unable to say. Certain it is, however, that when once commenced, they continue it, passing through a temporary intoxication, to a complete nervous and muscular wreck in the latter stages, when it has developed into a fully marked disease, which terminates in death from starvation or inability to digest more nourishing food. The animal, toward the last, becomes stupid or wild, or even vicious, or again acting as though attacked with blind staggers.” (Dr. Rothrock, Report of Dept. of Agriculture, 1884).

Dr. Isaac Ott, of Easton, Pa., gives the following as the physiological action of the Astragalus Mollissimus: “It decreases the irritability of the motor nerve, greatly affects the sensory ganglia of the central nervous system, preventing them from readily receiving impressions. Has a spinal tetanic action. It kills mainly by arrest of the heart. Increases the callory secretion. Has a stupifying action on the brain. Reduces the cardiac force and frequency. Temporarily increases arterial tension, but finally decreases it. Greatly dilates the pupil.” (_Amer. Jour. of Pharmacy_, 1882).

In opposition to these statements Professor Sayre, of Kansas, after an extended observation, arrived at the conclusion that “it is a grave question whether loco weed is a poison at all; upon chemical examination no poisonous principle of any kind was discovered; no toxic effect was observable when administered to frogs, cats, dogs, or the human species, ... the point cannot be accepted as a settled one whether loco is poisonous to cattle or not.”

Dr. G. C. Faville found in _locoed_ sheep in Colorado bunches of tapeworms in the gall ducts. Dr. Cooper Curtice, who subsequently studied the subject, found the tænia fimbriata, and believes that to these the symptoms are exclusively due. “The affected lambs are large headed with undersized bodies and hidebound skins. Their gait is slightly like that of a rheumatic. They seem to have difficulty in cropping the shorter grass; they also appear to be more foolish than the other sheep, standing oftener to stamp at the sheep dogs or the herder than the healthier ones. Others do not seem to see as well, or are so affected that they seem to appreciate danger less. In driving, they are to be found at the rear of the flock.” (Animal Parasites of Sheep.)

It is altogether probable that the tæniasis of sheep has been mistaken for _loco_, but this can hardly account for the remarkable symptoms found in other genera of animals, as a concomitant of an acquired and insatiable fondness for these leguminous plants. The tænia fimbriata has been found in sheep and deer, but there is no record of it as a parasite of cattle and horses.

Dr. Sayre’s failure to find any poisonous principle in the plants, or any toxic action on frogs, dogs or cats, cannot be received as conclusive in face of the results reached by others. Perhaps Dr. Sayre’s specimens were not grown under the proper conditions, or were not collected in the proper season to secure the toxic ingredient.

Miss C. M. Watson, of Ann Arbor, Mich., succeeded in separating a small amount of alkaloid from the root of Oxytropis Lamberti, but did not apply the crucial test of physiological experiment. In the Report of the Department of Agriculture for 1879, are given analyses of Oxytropis Lamberti, Astragalus Mollissimus and Sophora Speciosa, in each of which a small amount of alkaloid was found.

In 1888–9, Dr. Mary Gage Day, of Wichita, Kansas, made careful experiments on cats and rabbits, under the supervision of Dr. Vaughan in the Michigan Laboratory of Hygiene. She used a decoction of roots, stems and leaves of plants gathered in September and gave 60 to 70 c.c. of this to a half-grown vigorous kitten daily, along with abundance of milk and other food. In two days the kitten became less active, showed rough coat, increased desire for the _loco_, with partial loss of appetite for other food, diarrhœa came on, and retching and vomiting occasionally occurred. The expression became peculiar and characteristic. These symptoms increased, and emaciation advanced, and on the 18th day periods of convulsive excitement supervened. These were sometimes tetanic, the head being thrown backward and the mouth frothing. At other times the kitten stood on its hind limbs and struck the air with its fore paws, then fell backward and threw itself from side to side. There were short intervals of quiet, life being indicated by breathing only. After 36 hours of these intermittent convulsions paraplegia set in, and the kitten died in two hours. There was no apparent loss of consciousness before death.

Post mortem examination revealed gastric and duodenal ulcers, some of which were nearly perforating. The heart was in diastole; brain and myel appeared normal; the entire body anæmic.

To a _vigorous adult cat_ 60 c.c. to 70 c.c. of a more concentrated solution were given with other food. The results were essentially the same. By the twelfth day the cat was wasted to a skeleton and very weak. Paralysis of the hind limbs came on and the cat died on the thirteenth day.

As a test experiment, two strong young cats were confined in the same place, fed from the same dish, and treated in every way the same, except that the one was fed daily a decoction of the _loco_. The one fed _loco_ acquired the _loco_ disease with the symptoms described above while the other, eating ordinary food only, remained healthy.

Subcutaneous injections of the concentrated decoction thrown into frogs and chickens at the Michigan Laboratory of Hygiene, under direction of Dr. Victor C. Vaughan, caused nervous twitching and in large doses, death in 1 or 2 hours from heart paralysis. The same symptoms were produced in frogs by injection of an alcoholic extract of the residue left after evaporation to dryness of the decoction.

The loss of appetite, acquired liking for the “_loco weed_”, rough coat, emaciation, peculiar expression, rearing, plunging, and a staggering uncertain gait are among the symptoms given in the earliest published observations on the loco disease, and agree with the statements universally made by ranchmen. An ulcerated condition of the intestines was also pointed out by Professor Sayre in a locoed cow upon which he made a necropsy (Dodge City Times, July, 1887): but the diarrhœa which was so marked a symptom in the cats experimented on, is not mentioned as a characteristic symptom in horses and cattle.

“From the close agreement of the symptoms in the cats with those universally recognized in locoed horses and cattle, I conclude that the cases described above were genuine cases of the “loco disease” and are, so far as can be ascertained, the first that were ever experimentally produced.”

“The craving for the “loco” is soon acquired. The kittens would beg for it as an ordinary kitten does for milk, and when supplied would lie down contented. To determine whether a herbivorous animal would easily acquire the “loco habit” a young “jack” rabbit was captured and fed a few days on milk and grass; then fresh “loco” was substituted for the grass. At first the “loco” was refused, but soon it was taken with as much relish as the grass had been. After ten days of the milk and “loco” diet the rabbit was found dead, with the head drawn back and the stomach ruptured.”

“With reference to the character of the plants at the different seasons of the year, I am convinced by numerous experiments, on material gathered in different months, that the greatest amount of poison is present in the autumn and winter.” The scarcity of other food at that period of the year is only a partial explanation of the number of deaths occurring at that season.

Conclusions:

“1st. There is some poison in “loco weed” which may cause the illness and, if sufficient quantity is taken, the death of an animal.”

“2d. This poison is contained in the decoction obtained from the plants, and by systematically feeding it to healthy cats cases of “loco” disease may be produced.”

“3d. Taste for the green “loco weed” may be experimentally produced in the jack rabbit.”

“4th. From the large quantity of the plant or the decoction required to produce the disease, the poison must be weak, or if strong, it must be in very small amount.”

LEAD POISONING. PLUMBISM.

Physiological action on nervous system. Sources: near smelting
furnaces on vegetation; paints; paint scrapings in manure and on
soils; lead packing of pumps, engines, etc.; sheet lead; bullet spray;
wall paper lead; leaden water pipes or cisterns; lead acetate; painted
buckets; painted silo; lead compounds in arts. Experiments on animals.
Accidental poisoning: =horse=, fever, gray nasal discharge,
salivation, convulsions, paralysis, dyspnœa. =Cattle=, emaciation,
dyspnœa, palsy, tonic spasm of flexors of limbs, swollen carpus, death
in a few months. Young worst. =Sheep=, lambs paretic. =Swine= in pens
escaped, those at large suffered. Post mortem; lead or lead compounds
in stomach, or shown by analysis, in gastric contents, liver, spleen,
kidney, etc. Tests. Treatment: hydrosulphuric or sulphuric acid,
sulphate of magnesia or soda, antispasmodics; in chronic cases,
potassium iodide, bitters.

The physiological action of lead is exerted on the nervous system, so that lead poisoning may be appropriately enough treated of as a disease of the nervous system.

_Sources._ The sources of lead as a poison for animals are extremely varied. In England in the vicinity of lead mines and smelting furnaces it is deposited from the air in a fine powder, and consumed with the vegetation. Herapath found that the deposit, in dangerous amount, began half a mile from the chimney of the smelter and extended about half a mile further.

A second source is in lead paints used about farms and the scrapings of paint pots thrown out with manure and spread upon the fields. These lead combinations will last for years in the soil or on the surface, being plowed under one year and turned up again the next when the occasion of their presence has been completely forgotten. In one case I found the red lead paint marked by the tongues of cattle at the back of an abandoned cottage the fence around which had been broken down. In another the scrapings were found in an orchard which had been near and convenient for throwing them out. In a third case a paint can hung on the branch of an apple tree, well out of the way of the stock as the owner fondly supposed, showed in its contents the marking of the barbed tongues of the cattle. In a fourth case a barrel of paint was set under the barn where there was not height enough to admit the matured cattle, but it bore the marks of licking by the young stock, and they alone died but in such numbers that the owner concluded it must be the “Rinderpest.”

The lead packing from the joints of pumps, engines and other machinery, thrown away around works and mines, is a common source of the trouble. I once found large quantities in the gastric contents of cows that had died around a coal mine in Ayrshire, Scotland.

Sheet lead—tea-chest lead—is another common source of the poison. This is thrown out, scattered with the manure on the field, and will resist the elements for years but dissolves when taken into the acid stomach of the animal.

The spray from bullets in the vicinity of rifle butts is another common cause of the poisoning.

In one instance I have seen a cow poisoned by eating some lead-impregnated wall paper which had been carelessly left in the stable.

Less frequently the poisoning comes from drinking water carried in leaden pipes, or left to stand in a leaden cistern. The softest waters—rain, snow, distilled water—are the most liable to this impregnation. The hard waters containing carbonates, sulphates or phosphates, tend to be decomposed, the acid uniting with the lead to form comparatively insoluble carbonates, sulphates or phosphates of lead, which protect the subjacent lead against solution. The hardness of the water is not, however, a sufficient safeguard, as iron, solder, and other agents present in the lead as an impurity or merely resting upon it, are sufficient to set up a galvanic action resulting in solution.

The salts of lead may find direct access to the animal, as in the case reported by Gamgee in which a farmer used a barrel which had contained acetate of lead for mixing the feed given to his stock. A somewhat similar source of poisoning is found in the use of buckets or silos which have been painted inside, and scale off in contact with hot water, etc.

Blythe enumerates the following compounds of lead as employed in the arts:

1st. Hair dyes which have a basis of litharge, acetate or carbonate of lead in combination with lime and other agents.

2nd. White lead in its various forms is carbonate of lead.

3rd. Newcastle white is white lead made with molasses vinegar.

4th. Nottingham white is white lead made with sour ale.

5th. Miniature Painter’s white is lead sulphate.

6th. Pattison white is an oxychloride of lead.

7th. Chrome Yellow is impure chromate of lead.

8th. Turner’s Yellow, Casella Yellow, Patent Yellow is oxychloride of lead.

9th. Chrome Red is a bichromate of lead.

10th. Red Lead is the red oxide of lead.

11th. Orange Red is an oxide obtained by calcining the carbonate.

12th. Nitrate of Lead is much used in calico printing.

13th. Pyrolignite of Lead is an impure acetate used in dyeing.