Part 23

At the same time it is only logical to conclude that any morbid condition of the cerebral circulation or of the brain or membranes which leads to a corresponding amount of ventricular effusion, or atrophy or destruction of the nerve centres already designated, will produce the symptoms characteristic of this disease. Thus the different forms of meningitis, traumatic injuries to the cranium, chronic encephalitis, cerebral softening or degeneration, sclerosis, neoplasms of all kinds affecting the brain (cysts, cholesteatoma, psammoma, melanoma, etc.), and parasites may occasion this disease.

Prognosis. The disease is essentially incurable. It may last for years with little change except the winter improvement, but it rarely subsides permanently. It is only in those cases in which the symptoms have been determined by a transient or removable cause, as a moderate exudation or a parasite with a short term of life that a favorable result may be looked for. Usually the improvements seen in cool seasons or stables, under good hygiene, are not recoveries but temporary amelioration only.

Symptoms in other animals. Corresponding conditions produce similar symptoms in cattle, sheep, swine and dogs, but the disease receives less attention in these animals because they are not called on for steady work. The animals are lazy, dull, insensible to excitement, stupid, show a lack of muscular power and control, stagger or move disorderly and show tympanies or other indications of indigestion.

Treatment. Majendie and others had a few apparent recoveries after violent counter-irritation over the spinal cord (cervical and dorsal). Coculet and Lafosse claimed recoveries from the prolonged use of nux vomica in large doses (up to 5 drachms). Hayne attempted evacuation of the fluid by puncture through the perforated plate of the ethmoid bone, but had evil results from the ensuing hæmorrhage and encephalitis. Aseptic puncture through the plate of the frontal bone would be much more promising. Klemm suggested hydrochlorate of pilocarpin (15 grains), and this would promise better than any other measure to induce absorption of the liquid. The fatal drawback to this as to other measures is that it is not applied until the slow, steady pressure has caused such extensive cerebral atrophy that, even if the liquid could be removed and its reproduction prevented, the lost functions can never be restored. If the disease could be diagnosed and treated before this change of structure had taken place, the hope of recovery would be much better founded. Even in cases which make a temporary recovery during cold weather one would be warranted in using active derivatives toward the bowels and kidneys, also pilocarpin, counter-irritation to the spine and even tapping of the ventricles.

Legal Aspect of Chronic Hydrocephalus.

To claim relief in case a horse affected in this way is sold as sound, the seller must be notified at an early date. In the different countries of Europe a limit is set after which such notification will have no legal value. The seller must be notified, in France in 9 days, in Saxony in 15 days, in Bavaria, Wurtenberg and Baden in 21 days, in Hesse and Prussia in 28 days, and in Austria in 30 days.

Diagnosis. The veterinarian called to act as expert in such cases must examine the suspected animal along the different lines in which the cerebral aberration is manifested in the disease. He will see the animal standing quietly in the stall apart from all sources of excitement. See if there is a defect in the breadth of the cranium, or a deflection backward of this region from the straight line of the front of the face, together with a heavy clumsy head. Is the head pendent, resting on the manger, with dull eye, drooping lids, lack of expression, loose hanging lower lip? Does he hold morsels unchewed projecting from the mouth or over the tongue, or in the cheek? Does he plunge both mouth and nose in the water to drink, and masticate meanwhile? Are his legs found crossed or in abnormal positions, and if put in such positions, does he fail to rectify them at once? Is the head left in an abnormal flexed, depressed or lateral position if placed in it? Does the subject find it difficult or impossible to back? Does he pay the customary attention to the going or coming of other horses, to feeding, etc.?

If no distinct symptoms are found he should then be examined under other conditions. In taking out of the stable how does he turn in the stall or back out of it, and in what way does he approach the door, clumsily or with difficulty? When moved in a circle, does he sway or stagger? Can he back when mounted or attached to a heavy carriage? Can he execute all these movements satisfactorily after the respiration and circulation have been excited by walking, trotting or galloping in hand or otherwise? In case of difficulty in backing, in the absence of the other diagnostic symptoms, he must see that this does not arise from other causes. Some untrained horses have not been taught to back and cannot be made to do so at once. Some refuse to back from indocility or stubbornness, but can perform the act if induced in other ways, as in having a narrow stall. Sometimes a sore mouth, from a hard bit may make a horse nervous and obstinate so that he will seek to escape in any other way rather than by backing under steady pressure of the bit. Sometimes he will back all right under a halter. In all such cases of simple obstinacy or fear of pain, the absence of the other symptoms is strongly suggestive. If the horse has a well-developed cranium, a full bright, alert eye, firmness of lips, intelligent expression, readiness to appreciate and respond to all noises, words, touches or other causes of excitement, plenty of fire and spirit, and an absence of any apathy, dulness, awkwardness of movement or position of the limbs, or of any other sign of failing nervous power he may be considered free from this affection, even if he refuses to back in a docile manner. In other cases there is a distinct physical incapacity quite apart from any brain disorder. Sprains or anchylosis of the back or loins or anchylosis or painful arthritis of the hocks, may hinder backing.

The diagnosis from encephalitis and other inflammatory affections associated with stupor, rests on the absence of hyperthermia, of the congestion of the orbital and nasal mucosæ, of the heat of the head and of the paroxysmal attacks of excitement which characterize these diseases.

CEREBRO-SPINAL MENINGITIS.

Definition. Epizootic manifestations. Faulty hygiene, insanitary stables, impure air, defective drainage, fermenting food, overwork, overfeeding, excitement, heat exhaustion, electric tension. Probably complex. Horse, ox, sheep, goat, dog. Microbian factors in man and rabbit. Lesions: meningeal, brain and spinal congestion, effusion, suppuration, circumscribed necrosis, softening, petechiæ. Blood dark, fluid or a diffluent clot. Symptoms: horse: paresis, anorexia, dysphagia, mucous congestion, reddish brown: in severe cases, chill, stupor, apathy, debility, palsy, tonic spasms of neck, back or loins, hyperæsthesia, twitching, trismus, hyperthermia, delirium, coma, convulsions, and early death. Duration averages 7 to 15 days. Ox, as in encephalo-meningitis. Sheep, microbes. Dog, dulled senses, stupor, coma, palsy, hyperthermia, heat of head, spasms, etc. Diagnosis: by brain and spinal symptoms; cases in groups. More sudden than tetanus, or rabies, and shows no mischievous purpose, nor depraved appetite: from tubercular meningitis. Treatment: Avoid suspected stable, food, water, or suspicious environment, disinfect, correct local diseases, unload bowels, belladonna, atropia, chloral, bromides, ergot, phenacetin, potassium iodide. Bleeding. Cold to head or back. Derivatives. Sling. In convalescence, regulated diet and tonics.

Definition. Concurrent inflammation of the meninges of the brain and spinal cord.

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.