Chapter XI: Part 11

_Symptoms._ The attack is usually sudden. The dog is seized with vomiting and diarrhœa and stands with head depressed, back arched and belly tucked up. The vomit is at first of alimentary matters, then of glairy mucus, or black and bloodstained material. The fæces are black, bloody, glairy, frothy, and abundant, fouling the tail and the hips. The abdomen is at first tense and extremely tender. The pulse is accelerated, the heart beats tumultuous, the breathing slow and temperature elevated. Redness of the visible mucosæ, often tinged more or less deeply with yellow, implies hepatic disorder or destruction of blood globules. Death may occur in two or three days.

The abruptness and violence of the attack, the violent vomiting and purging and the staining of the discharges with blood are to a large extent diagnostic.

_Lesions._ These are most noticeable in the stomach and intestines which are empty and of a dark blood red. The mucosa is thickened, gorged with blood, and showing deeper shades here and there where extravasation has occurred. The liver and kidneys are also deeply congested.

_Treatment_ has been almost constantly a failure. Cadeac recommends disinfection of the intestinal canal, with salol, cresyl or dinaphthol, but in the absence of contagious germs this seems the less called for. The indications would seem to point to elimination of the chemical poisons, the soothing of the irritation and the tiding the animal over the period of weakness. Agents that will at once eliminate the poisons and sustain the heart’s action appear to be called for, hence digitalis 2 grs. or tincture of strophanthus 10 drops are particularly indicated. Laxatives are rather hopeless considering the congestion and paralysis of the bowels, and yet if they can be made to operate on any comparatively healthy part of the intestine they will serve a good purpose in eliminating the poisonous contents, in securing secretion and elimination of poison from the blood, and in depleting from the overcharged portal system. Glauber salts by mouth and anus, or jalap, or castor oil may be resorted to. In the absence of these a free use of watery enemata and the ingestion of water by the mouth may be resorted to. A damp compress around abdomen and loins will be at once soothing and stimulating to the secretions of both kidneys and bowels.

To counteract congestion and extravasation Cadeac advocates ergotine 2 grs. subcutem, or iron perchloride, 2 ozs., to 1 quart of water to be given in doses of two or three tablespoonfuls every two hours. It might also be used in enema.

CATARRHAL ENTERITIS IN BIRDS.

Causes: microbes, diagnosis from fowl cholera, less virulent rapid and
deadly, and comparatively harmless to the rabbit, debility, youth,
age, unsuitable food, ill health: bacillus gallinorum, bacillus coli
communis, bacillus of duck cholera, spirillum Metchnikowi. Symptoms:
dullness, fever, langor, inappetence, thirst, pale comb, greenish
fæces, erect plumage, drooping wings and tail, sunken head, gaping,
staggering, somnolence, bloody fæces, violet comb, low temperature,
death in one to three weeks. Diagnosis: by restriction to one flock,
or species, and immunity of rabbits. Mortality 80%. Prevention:
separation of sick and healthy, disinfection of roosts and yards, pure
food and water boiled or acidified, immunization. Treatment: boiled
food with antiseptics, antiseptic enemata, stimulants, tonics.

_Causes._ A number of different microbes are implicated in producing and maintaining catarrhal enteritis in the domestic poultry. All forms of the disease are therefore closely related to the well known fowl cholera, which is however to be differentiated, by its more intense virulence, rapid progress, and its deadly effect when inoculated on the rabbit. As in other forms of microbian enteritis, that of fowls is undoubtedly favored by general and local debility, youth, old age, unsuitable food and other health depressing causes, yet as the specific pathogenic microbe has been in many cases identified, it is well to consider some of the different species.

=Bacillus gallinorum= found by Klein (1889) in the blood of chickens suffering from an infective diarrhœal enteritis, is ovoid, with rounded ends, from 0.8 to 2_μ_ long and 0.3 to 0.4_μ_ thick; often in pairs. Stains in the aniline colors. Ærobic (facultative anærobic) non-liquifying, non-motile, asporogenous. Culture easy in neutral, alkaline or slightly acid media at room temperature, or better in thermostat. On gelatine plate films, it forms grayish white, superficial colonies, becoming flat homogeneous white discs, brownish under transmitted light. The deeper colonies are small spherical and brown or yellowish by transmitted light. On agar it forms a thin gray layer with irregular margins, which extends over the entire surface. In bouillon it causes turbidity and in 24 hours a precipitate of bacilli to the bottom.

=Pathogenesis.= Chickens inoculated hypodermically or intravenously die in 1 to 5 or 6 days with peritonitis and intense intestinal congestion. Fed in vegetable food it is harmless, but with animal food virulent. Rabbits and pigeons are immune.

Pond water is a common source of casual infection, also dung heaps in which carcasses of little chicks have been buried. Summer is the period of greatest prevalence, as there is the best opportunity for the multiplication of the germ, and the drying of the ponds concentrates the product.

The bacillus is found on the intestinal mucous membrane, and in the mucus and in advanced stages, in the blood, spleen, liver and kidneys.

=Bacillus Coli Communis=, the familiar bacillus of the healthy bowel, is charged by Lignieres with causing a fowl enteritis and probably does so as in mammals when the mucosa has become diseased and non-resistant. At the same time there are so many closely allied forms or varieties of this bacillus found in different intestinal diseases, that it may well be that the pathogenic agent is a modified form or “sport” from the parent microbe, though no clearly defined peculiarities can be established by cultures.

The typical colon bacillus is 2 to 3 _μ_ long by 0.4 to 0.6 _μ_ broad, with rounded ends, but it may be ovoid or even round, or it may be 5 _μ_ long. It stains readily with aniline colors, bleaches with iodine. It is ærobic, facultative anærobic, non-motile, non-liquifying, and asporogenous. It ferments all sugars producing gas, acidifies its culture fluids, and coagulates milk. It grows freely at room temperatures in peptonized gelatine, agar and bouillon and on potato. Stab cultures in gelatine have a moss-like tufted appearance.

=Pathogenesis.= Injections subcutem, and into the veins and ingestion with food all failed to infect the chicken, while the pigeon died in 24 hours from intravenous injection and in 12 to 18 days from 1 c.c. given subcutem. In rabbits and guinea-pigs hypodermic injection caused abscess, while pleural and peritoneal injections killed in 24 to 48 hours. Rabbits are unaffected by intravenous injection, while guinea-pigs die in 1 to 3 days.

=Bacillus of Duck Cholera= found by Cornil and Toupet in the blood of ducks suffering from a diarrhœal enteritis, is 1 to 1.5μ long, by 0.5μ broad, with rounded ends. It is ærobic, non-liquifying, non-motile and asporogenous. Stains in the aniline colors and bleaches in iodine.

=Pathogenesis.= In morphology and cultures it resembles the bacillus of fowl cholera, but it fails to infect chicken, pigeon or rabbit. It infects ducks readily by ingestion or hypodermic inoculation.

=Spirillum Metchnikowi= was found in 1888, by Gamaleia in the ingesta of chickens dying in Russia of a choleræic enteritis. It resembles the cholera spirillum, but is shorter, broader and more curved. Its size varies, being twice as broad as the cholera spirillum, when found in pigeons. It may be 0.8μ long, by .5μ broad, furnished with one polar flagellum and very motile. It stains in aniline colors and bleaches in iodine. Grows readily in common media at room temperature, and is killed in five minutes by 122° F.; renders milk strongly acid, coagulating it, and perishes in the acid. In eggs turns the albumen yellow and the yolk black. In gelatine it forms transparent colonies and in potato pale brown.

=Pathogenesis.= By inoculation it infects chickens, pigeons and guinea-pigs, while rabbits and mice are refractory except to large doses. By ingestion it infects chickens and guinea-pigs but not pigeons. Infection takes place easily by the air passages. In all cases alike the lesions are concentrated in the intestines.

_Lesions._ These are very similar in the different forms. The intestine is violently congested and contains a quantity of yellowish green mucopurulent or serous fluid. The mucosa is infiltrated, softened and even abraded by the desquamation of epithelium. The liver is greatly enlarged and softened and gorged with blood, and the gall bladder filled. The spleen is enlarged and pale, contrary to what is seen in fowl cholera, and the kidneys are congested. The heart is flaccid, soft, petechiated, and the pericardium is the seat of serous effusion.

_Symptoms._ In the _acute form_ there is dullness, langor, inappetence, ardent thirst, pale comb, and greenish fæces. Later the feathers are erect, the wings and tail droop, the head sinks, the patient gapes frequently, walks unsteadily, and a liquid bluish green diarrhœa sets in, which later becomes yellow and bloody. The somnolence increases, the walk becomes more unsteady, or the patient sinks down with eyes half closed and refuses to rise. As the disease advances the comb becomes violet, the dark shade constantly increasing and a glairy grayish mucus is discharged from the nose and bill. The temperature which was at first raised 1° or 2°, falls 2° or 3° below the normal prior to death, which may be deferred to near the end of the second week.

In the chronic cases the disease may drag along for three weeks, the emaciation, pallor and weakness constantly increasing and the feathers around the anus soiled and matted together by the fœtid liquid discharges. There may be remissions which go on to complete convalescence but more commonly an exacerbation occurs which proves fatal in a day or two.

_Diagnosis._ From fowl cholera this may be distinguished by the fact that it is confined to one farm or flock of turkeys, chickens or ducks, proving most deadly in early summer, to the broods of the same spring, and at the commencement of the epizootic, and proving less and less so as time passes. The immunity of rabbits even when inoculated is a further distinguishing feature. From intestinal parasitism it is distinguished by the color of the discharges, and the absence of worms and their eggs from these liquids.

_Mortality_ is often very high. Klein found it 80 per cent.

_Prevention._ Remove the infected from the flock (with ordinary fowl it is often best to kill and burn or bury them), keep the poultry house and yard scrupulously clean of droppings and sprinkle it occasionally with a 3 per cent. solution of sulphuric acid. The poultry house may be fumigated with sulphur (1 ounce to the cubic yard), or the walls and roosts may be washed with a solution (1:12) of bisulphide of carbon in liquid vaseline. The diseased must be removed as soon as they are detected and food and water must be given pure. If pure water is not available, boil it or render it acid by sulphuric acid (1:33), and feed grain, cooked roots, bran and bread with more or less green food.

In the case of valuable birds immunization may be secured by inoculating with the virulent blood or culture so diluted that not more than one or two of the germs shall be inserted in each case or the virulent liquid may be heated for 20 minutes to a temperature of 55° C (121° F) and then injected in a dose of 2 drops.

_Treatment._ If it is decided to treat the sick they should be placed together in safe seclusion from all others. Feed with mush or cooked roots or vegetables adding salol ½ dr. naphthol 1 dr. and quinia 1 dr. to the food of 15 or 20 fowls. Nitrate of bismuth and powdered charcoal may be added in moderate quantities. As drink give water containing 2% of sulphuric acid. Antiseptic enemata may be added in the case of very valuable birds, salol, naphthol, boric acid, salicylate of soda, or solution of carbolic acid or creosote. Stimulants and tonics are highly esteemed by some, and Cadeac recommends the free use of the following mixture: powdered fennel, anise, coriander and quinia of each 5 drs., gentian 10 drs., ginger 12 drs., ferric sulphate 2½ drs.

COCCIDIAN ENTERITIS IN CATTLE. COCCIDIOSIS. RED DYSENTERY.

Definition. Distribution: Switzerland in summer. Causes: weakness,
debility, youth, cold, heats, spoilt fodder, protozoa, coccidium
oviforme, coccidium perforans. Lesions: reddening, thickening and
desquamation of alimentary mucosa and lungs, congested mesenteric
glands, liver and spleen, coccidia in discharge and epithelium,
staining, anæmia. Symptoms: chill, fever, grinding teeth, fœtid
diarrhœa becoming bloody, tenesmus, stiffness, red ulcerated rectum,
emaciation, false membranes. Duration: death in one to fourteen days
or more. Complications. Diagnosis by coccidia. Prevention: avoidance
of affected soils, water and fodder. Treatment: antiseptic, by mouth
and as enemata, demulcents. Flesh safely eaten by man. Coccidium
bigeminum in dogs, coccidium oviforme in rabbits, coccidium tenellum
and gregarina avium intestinalis in birds.

_Definition._ Enteritis affecting chiefly the colon and rectum, and due to the presence of the protozoa, coccidium oviforme, and coccidium perforans.

_Distribution._ This affection was found in 1885 in the cantons of Berne, Lucerne and Argovi where it attacked 5 per cent. of the cattle and destroyed from 2 to 4 per cent. of those that suffered. It prevailed mainly in the summer (May to October) on the pastures, though not unknown at other seasons. Sucking calves were immune and the ages of a year to two and a half years were the main sufferers.

_Causes._ Predisposing causes embrace such as induce weakness or debility, youth, low condition, cold intemperate weather, extreme heats, musty or spoilt fodders.

The essential cause, the coccidium, appears to be taken in with food or water as sucking calves are largely exempt. The parasite is found in the gastric and intestinal epithelium of the diseased animals, in numbers proportionate to the severity of the attack, being very abundant when the disease is at its height, diminishing during convalescence, and disappearing entirely on recovery. Two species are found in this disease.

=Coccidium Oviforme= is 40 to 50μ long by 22 to 28μ thick, ovoid, with a double outlined limiting membrane enclosing a refrangent protoplasm with a nucleus two or three times as large as that of an epithelial cell, and staining with hæmatoxylon or aniline colors. The young coccidia appear as round granular protoplasmic masses, without a capsule but provided with a nucleus. At first of a diameter of 9 to 10μ they increase to 26μ retaining the spherical form and acquiring the membrane of the mature parasite. As it grows the protoplasm separates from the wall and forms a globular nucleated mass, which after fifteen days divides into two and later into four masses or sporoblasts. Each sporoblast in its turn divides into two falciform corpuscles lying in contact but in an inverse sense to each other. Each of these under favorable conditions becomes a new amœboid individual capable of invading an epithelial cell and passing through the same stages of development as its predecessor.

The coccidium oviforme is found in the epidermis in cutaneous psorospermosis of birds, and in the coccidian hepatitis in rabbits.

=Coccidium Perforans.= In its mature form this is 25μ to 35μ long, by 14μ to 20μ broad. Its different stages of evolution are essentially the same as for the Coccidium Oviforme. It is a cause of intestinal Coccidiosis in both dog and rabbit as well as in cattle, usually killing the rabbit in from eight to ten days.

_Lesions._ In the first reported cases in calves in 1877 (Proger and Zurn), there was catarrhal inflammation of the upper air passages as well as the bowels. There was thickening, redness and desquamation of the abomasum near the pylorus of the small intestine and colon. In the intestines there were patches of thickening and softening of the mucosa and miliary ulcers with yellowish contents. The mesenteric glands, liver and spleen were enlarged, softened and ecchymosed. In all the lesions coccidia were found. In the cases reported by Hess, Zschokke, Guillebeau and Cadeac the abomasum and large intestine principally suffered. There was a diffuse inflammation of the mucosa and in the rectum and portion of the colon a great degeneration and desquamation of the epithelium. The columnar cells of the mucous glands especially suffered. A single cell would contain five or six psorosperms, in different stages of development. If the parasites have escaped, the cell walls are pressed together. Among the diseased glands others with healthy epithelium were found, their orifices plugged with mucus. Both forms of coccidia above described are found in two conditions, in the epithelial cells with granular nuclei staining in hæmatoxylon, and violet or black with iodine (Lugol’s), and outside the cells with granular nucleus or simple hyaline contents which do not stain. Zschokke considers the latter as in process of degeneration. Other organs are anæmic.

_Symptoms._ The disease is ushered in by cold extremities, weakness, dullness, suspended rumination, ardent thirst, hyperthermia, 102° to 104° and even 106°, small, weak thready pulse beating 100 to 140 per minute, sunken eyes, grinding of the teeth, and defecation in small quantity only. Toward the fourth day or earlier a fœtid diarrhœa sets in, watery, bloody and fibrinous. The bloody discharges last to the seventh day, the diarrhœa to the end of the second or fourth week. Straining may be violent, exposing or everting the irritated or ulcerated rectum, the hind parts may be stiff, the patient rises with difficulty, he winches if pressed on the back or right side of the abdomen, loses flesh rapidly and becomes a walking skeleton. when the discharges are less profuse cylindroid croupous casts are sometimes expelled.

_Course._ _Duration._ In the weak and young a violent attack may prove fatal in 24 hours. In others the malady lasts for two or more weeks and sometimes relapses, and the patient becomes very weak and anæmic. Complications of various kinds may also supervene and cut off the animal, the lesions and debility alike favoring the introduction of the germ. Thus black quarter, bronchitis, pneumonia, convulsions, paralysis, phthiriasis and ring-worm have been noted as sequelæ.

_Diagnosis_ can always be made by microscopic examination of the fresh warm fæces.

_Prevention._ This will consist in the avoidance of water and of green food from soils where the disease has been found to prevail.

_Treatment._ Antiseptics given by the mouth have proved of very little avail having as a rule lost their power through dilution in the contents of the stomachs. They may still be given to keep in check the propagation of the coccidia in the fourth stomach. Silver nitrate, iron sulphate, lead acetate, tannic acid, oak bark, carbolic acid, cresol, lysol, salicylic acid, hydrochloric acid, sulphuric acid, hyposulphite of soda have been used in this way. The same agents may be used with better effect as enemata being forced as far as is consistent with safety and frequently repeated. Quinia and iodide of potassium may also be given as parasiticides. Mucilaginous gruels and decoctions should be given at first, followed by mashes as they can be borne, but the food must be moderate and easily digestible until full convalescence has taken place.

The flesh of animals killed while suffering from this affection has been eaten by man with impunity.

COCCIDIAN ENTERITIS IN THE DOG. INTESTINAL COCCIDIOSIS.

_Causes._ Two parasites have been found in connection with this disease in the dog; the =Coccidium penetrans=, already described, and the =Coccidium bigeminum=.

=Coccidium Bigeminum, var. Canis.= This is elliptical and from 12 to 15 μ long by 7 to 10 μ broad. They are usually found in pairs lying side by side, and sometimes both in the same envelope indicating multiplication by division along the longitudinal axis.

The bigeminum is held to be harmless, but the perforans, as in the cow and rabbit is very injurious and even fatal. The _symptoms_ are those of digestive disturbance, dullness, loss of appetite, retching, vomiting, colic and fœtid and bloody diarrhœa. Irritability, and a morose disposition and loss of control over the hind limbs have been set down as rabiform indications.

_Diagnosis_ depends on the inveteracy and sanguineous nature of the diarrhœa, but especially on the discovery of the amœboid organisms in the recent, warm discharges.

_Treatment_ should be along the same line as in cattle.

COCCIDIAN ENTERITIS IN RABBITS. INTESTINAL COCCIDIOSIS.

_Causes._ In rabbits the coccidium perforans is the psorosperm which usually attacks the bowels. The coccidium oviforme which produces hepatic coccidiosis is also occasionally found in the intestines. The perforans is smaller than in cattle being 15 to 25 μ long, by 12 to 15 μ broad, approximating to the variety found in man.

_Lesions._ There is extensive congestion of the intestinal mucosa, with thickening and softening of the epithelium so that it breaks down into a pulp under pressure, also free desquamation with the formation of abrasions, sloughs and ulcers. In some instances extensive croupous casts of the intestine are found. As in the other animals the coccidium is found abundantly in the epithelial cells of the affected parts which swell up and degenerate. When the parasite has escaped from the cells it lives free in the abundant mucopurulent and sanguineous secretions of the bowels.

_Symptoms._ There are loss of appetite, swelling of the abdomen, profuse diarrhœa, the fæces yellowish in color and containing mucopurulent matters and blood. The disease may prove fatal in a few days without much loss of flesh, but if protracted it leads to extreme anæmia, emaciation and debility and the animal dies in marasmus.

_Diagnosis_ is always to be certified by the profusion of coccidia found in the fresh liquid discharges.

_Prevention_ must be secured if possible by the removal of the healthy rabbits from the infected and from the hutch or warren in which the latter have been. The greatest care must be taken to prevent them from obtaining access to the droppings of the sick, or to streams, ponds or wells, into which the drainage from such manure can have found its way. The safest course is to destroy the sick and burn up them and all their droppings, as the latter ground into powder can blow on the wind.

_Therapeutic treatment_ has proved unsatisfactory but may be attempted along the same lines as for the larger animals.

COCCIDIAN ENTERITIS IN BIRDS. INTESTINAL COCCIDIOSIS.

Two sporozoa are known to be pathogenic in the intestines of birds: the =coccidium tenellum= and the =gregarina avium intestinalis=.

=Coccidium Tenellum.= This has a nearly globular body 21 to 25 mm. long by 17 to 19 mm. broad, a very thin, delicate investing membrane, and has been found in the mucosa of the cæca of birds, producing a fatal typhlitis. The sporoblasts are developed in water outside the animal body and when taken in with the food colonize in the intestinal mucosa.

=Gregarina Avium Intestinalis.= When mature this is in form of a granular body with hollow spaces or utricles, is oval, or globular and measures 40 to 48 μ in diameter. The spores are 11 to 14 μ. They are found in the submucosa of the intestines in chickens, being taken in with food or water, and attack not the intestines only but the skin, the buccal and pharyngeal mucosa and even the liver and lungs. They traverse the mucous membrane and become encysted in the submucosa as white isolated or confluent points, disturbing the circulation and nutrition and destroying the nutritive and other functional activities of the mucosa.

_Lesions._ From the coccidium tenellum these are mainly found in the cæca and consist in intense inflammation, white lines formed by the parasitic colonies, desquamations of the epithelium and erosions and ulcers. In the early stages and in the absence of diarrhœa there may be simply thickening and induration of the mucous membrane and whitish colonies of the parasites. When there has been diarrhœa the contents are serous, or seropurulent, brick red, and filled with epithelial cells, red globules, leucocytes, fat globules and coccidia.

The gregarinæ are not confined to the cæca but scattered over the whole intestinal canal as white spots in the submucosa surrounded by congestion and degenerative changes. It has been found complicated with false membranes.

_Symptoms._ Dullness, anorexia, ruffled feathers, sunken head, trailing wings, slow uncertain gait, plaintive cries, with diarrhœa, passing through serous, brick red, and bloody. In small chicks it may be whitish and followed by constipation. Death is usually an early result.

_Treatment._ Hyposulphite of soda with carminatives (fennel anise, coriander, ginger, and gentian) has been given in boiled milk or bread. Quinia and iodine might be tried.

_Prevention._ Avoidance of infected roosts and runs, and above all of infected streams, wells and ponds, and the removal and cremation of the sick, followed by thorough disinfection, are much more promising than therapeutic treatment.

GASTRO-ENTERITIS FROM CAUSTIC ALKALIES AND ALKALINE SALTS.

Ammonia: Counter-irritation, fauces, larynx, bronchia, congestion and
softening of the gastric mucosa, loose blood clots, solution of
globules, dysphagia, salivation, in carnivora and omnivora vomiting,
diarrhœa, white fumes with muriatic acid.—Ammonia carbonate: less
corrosive, same symptoms.—Potash lye, deep corrosion, gastric
congestions, fluid, blackish red blood.—Soda lye.—Carbonates of potash
and soda, less violent, tests for potash and soda. Treatment: weak
acids, demulcents, anodynes.

=Aqua Ammonia.= Lethal dose pure, horse 1 oz. and upward; cattle 2 ozs.; dog ½ dr. There may be sudden death from abstraction of water and cauterization of the fauces and larynx including at times the bronchial mucosa. In other cases death occurs later from gastro-enteritis, the mucosa of the alimentary canal being congested, softened and covered with bloody mucus. The blood in the vessels is of a dark red, coagulates imperfectly and the blood globules are dissolved changing the color to black, and then brownish red. Prior to death there is great distress, salivation, inability to swallow, swollen tongue, frequent pulse and respiration, cough, spasms, and sometimes the odor of ammonia. Retching and vomiting may be a feature in carnivora and omnivora, and diarrhœa if the case is not promptly fatal. The urine is not rendered alkaline. White fumes with muriatic acid indicate ammonia.

=Ammonia Carbonate= gives rise to the same symptoms and lesions with the exceptions that there is less corrosion of the mucosa, and no pure ammonia exhales in the breath.

=Caustic Potash, Lye.= Lethal dose, 5 grs. dog intervenous. In strong solution this is one of the most potent caustics, which penetrates deeply into the tissues and abstracting water cauterizes everything with which it comes in contact. It therefore produces the most destructive changes on the walls of the stomach, and intestines, with violent gastro-enteritis, retching, or vomiting of alkaline matters. The congested, ashen and even black color of the tongue, and (post mortem) of the gullet, stomach and intestines, and the intense alkalinity of contents are characteristic. The blood is fluid, gelatiniform, and blackish red. Later, erosions and contractions are common.

=Caustic Soda= is only less destructive than potash, and produces the same general lesions and symptoms.

The =Carbonates of Potash and Soda= have the same general properties only they act with very much less energy. Potassium can be recognized by its purple color in an alcohol or Bunsen flame and sodium by an intense yellow.

_Treatment._ Weak acids (acetic, vinegar, citric, malic, lactic, boric, benzoic, salicylic) or the stronger mineral acids largely diluted. Mucilaginous solutions (flaxseed, elm bark, gruel, mallow). Anodynes (opium).

GASTRO-ENTERITIS FROM CAUSTIC ACIDS.

Sulphuric acid, corrodes, blackens, dysphagia, salivation, retching,
vomiting, colics, collapse. Lesions. Test, barium nitrate. Nitric
acid, corrodes, stains yellow, or brown. Test, reddish fumes with
copper and sulphuric acid. Muriatic acid, corrodes, whitens. Test,
chlorine odor, white curdy precipitate with silver nitrate. Oxalic
acid, colic, emesis of black bloody matter, gastric mucosa red or
black, blood bright red, lowered respiration, innervation,
temperature. Acetic acid, congestion, softening of gastric mucosa, may
stop heart. Treatment: weak bases, magnesia, lime or their carbonates,
soap, lime water, demulcents.

=Sulphuric Acid.= This acts on stomach and intestine as on the mouth abstracting water and blackening the tissues. It produces dysphagia, salivation, retching, vomiting in carnivora and omnivora, colics, and collapse. Sometimes the urine becomes albuminous or bloody. The post mortem blackness of the contents and walls of stomach and intestine and their intense acidity are characteristic. Nitrate of baryta will precipitate the insoluble sulphate.

=Nitric Acid.= In concentrated state this acts in the main like the sulphuric acid, but stains the lips yellow, and the mucosæ white changing to citron yellow or brown and does not precipitate baryta. It gives reddish fumes with copper and strong sulphuric acid.

=Muriatic Acid.= This is less caustic than nitric or sulphuric acid, and may be recognized by its white cauterized patches on the mucosa of the mouth, stomach and intestines, its chlorine odor, and the curdy precipitate which it throws down with silver nitrate. It does not corrode the skin. In the stomach this acid is normally present in the free state.

=Oxalic Acid.= Lethal dose, dog 15 grs., cat 2 grs. When swallowed this causes colics, emesis in vomiting animals, the rejected matters being black and perhaps bloody. After death the gastric contents and walls and those of the bowels are congested and more or less blackened, and the blood of a bright red color. Heart is arythmic, respiration slow, paresis of limbs, spasms, temperature subnormal.

=Acetic Acid.= This causes congestion and softening of the gastric and intestinal mucosa, colics, emesis in vomiting animals. It may kill by suddenly arresting the heart’s action.

_Treatment_ for the acids consists in alkaline or basic antidotes; magnesia, or its carbonate, lime, or its carbonate, soapsuds, carbonates and bicarbonates of potash and soda. Lime water is the one appropriate antidote to oxalic acid, precipitating the insoluble oxalate. Mucilaginous drinks may be added freely.

POISONING BY SODIUM CHLORIDE.

Poisonous with privation of water. Dose: horse, ox, pig, dog, hen.
Symptoms: anorexia, thirst, emesis, colics, diarrhœa, dysuria,
weakness, spasms, palsy, death in six hours to two days or more.
Lesions: gastric congestion, ecchymosis, blood fluid, bright red,
cerebral congestion. Treatment: emesis, water, demulcents, enemata,
oils, cold to head. Brine: salt, ptomaines, toxins, from salt meat and
fish. Strongest at three months old. Dose: horse, pig, dog. Symptoms:
nervous, disorder, mainly spasmodic. Lesions: congestion of
encephalon. Treatment: anodynes, stimulants, wine, camphor.

Common salt is especially irritant if given in concentrated solution and with subsequent deprivation of water. The poisonous dose for the horse is 2 to 3 lbs. (Gohier), for cattle 4 to 5 lbs. (Hertwig), for the pig 7 to 8 ozs. and for the dog 6 to 7 ozs. Chickens are poisoned by picking up broken pieces of salt instead of pebbles, or by salted food.

_Symptoms._ Anorexia, intense thirst, dullness, emesis in vomiting animals, colics, watery diarrhœa, frequent urination, muscular weakness, spasms, paralysis, weak pulse, red buccal mucosa, dilated pupils. Death may take place in six hours or it may be delayed two days or longer. In chickens giddiness and rotary movements are common.

_Lesions._ Congestion of the stomach and intestines with points of ecchymosis. The mucosa of the bladder is reddened. The blood is fluid and of a bright red. There is more or less congestion of the cerebellum and medulla and their meninges.

_Treatment._ Emetics (tepid water, tickling fauces) and the stomach pump. Abundance of water or of mucilaginous drinks. The same liquids by the rectum. Bland oils may be given as emollients and eliminating agents. Cold to the head is usually desirable.

POISONING BY BRINE.

This is partly due to the toxic effects of common salt but also to the ptomaines and toxins formed in old brine. It has been seen most frequently in hogs fed on salted kitchen waste and on the liquids from salt meats, (beef, pork, fish). Herring-brine is a common source of poisoning for hogs and dogs, also the brine from the salted meats of the butcher’s shops. Reynal found it to be especially poisonous when at least four or five months old. He gave as the fatal doses for horse 3½ pints, for pig ½ pint, for dog 6–7 ozs. The lethal dose however will vary with the concentration of the fluid and its age.

_Symptoms._ In addition to the direct irritation caused by the sodium chloride there are marked nervous symptoms, nervous irritability, spasms, rolling of the eyes, convulsive winking, dilated pupil, blindness, vertigo, staggering gait, epileptiform seizures, trismus, oposthotonos, pleurosthotonos, stupor.

_Lesions._ In addition to those of the stomach and intestines there is marked congestion of the encephalon, especially the medulla and cerebellum.

_Treatment._ In addition to that for common salt, anodynes and stimulants (wine, camphor) may be demanded.

NITRATES OF POTASH AND SODA.

Lethal dose. Symptoms: Colics, tympany, emesis, salivation, pupillary
dilatation, diarrhœa, diuresis, hypothermia, stupor, palpitations,
trembling, spasms, palsy. Lesions: Congested gastro-intestinal mucosæ,
erosions, ecchymosis, congested kidney and bladder. Blood fluid,
bright red. Treatment: Emesis, stomach pump, water and mucilaginous
liquids, stimulants.

Nitrate of soda being used largely as a top dressing for grass and other crops is more liable to be taken in toxic doses than nitrate of potash. The former is also given in mistake for common salt. The toxic dose is high. Morton gave 2 pounds saltpeter to a horse with only a temporary purgative and diuretic effect. Huzard found that 3 doses of 16 ounces each, given at intervals of 8 days sufficed to kill a horse. Cattle are said to have died from taking 5 to 6 ounces.

_Symptoms._ There are colics, tympany, emesis in vomiting animals, salivation, dilated pupil, diarrhœa, diuresis, hypothermia, stupor, palpitations, weak pulse, trembling, convulsions, tetanic symptoms, paralysis.

_Lesions._ Congestion of a cherry red, brown or purple of the gastric mucosa and that of the small intestine, erosions and ecchymosis, congestion and ecchymosis of the kidney and of the mucosa of the bladder. Blood uncoagulated and of a bright red.

_Treatment._ Favor emesis or use stomach pump according to the species of animal. Give abundance of water or mucilaginous fluids by mouth and anus. Stimulants may be resorted to in case of sinking or collapse.

ACUTE ARSENICAL POISONING, ARSENIOUS ACID, PARIS GREEN.

_Acute poisoning._ Sources. Lethal dose, horse, ox, sheep, dogs, pigs.
Endermic. Symptoms: colic, weak pulse, rapid breathing, red eyes,
dilated pupils, purging, weakness, trembling, stupor, convulsions,
paralysis, green or yellow vomit, test of urine. Lesions:
gastro-intestinal inflammation, ropy, bloody mucus, ecchymosis,
extravasation, ulceration. Treatment: emesis, stomach pump, hydrated
iron oxide, calcined magnesia.—_Chronic poisoning._ Excessive
administration, arsenical fumes from smelting furnaces. Symptoms:
indigestion, emaciation, hide-bound, depilation, red eyes, diarrhœa,
agalactia, weakness, paraplegia, salivation. Lesions: as in acute,
fatty liver, test of urine. Tests: on hot charcoal garlic odor,
Marsh’s test by zinc and sulphuric acid. Treatment: avoidance of
cause, antidotes demulcents, diet.

Arsenious acid given recklessly as medicine, rat poison, arsenite of soda made into a sheep dip and left within reach of animals, and arsenite of copper used for potato bugs, or other insect pests and carelessly left where animals can get it are the most common sources of acute arsenical poisoning. Horses die from 140 grains in solution, or 3½ drs. in the solid form, cattle from 3½ to 7 drs., sheep are killed by 2 drs., dogs may die from 2 grs., but larger doses usually cause vomiting and the animal is saved. Hogs may die from 15 grs. but they often save themselves by vomiting with much larger doses. The poisonous effects may be induced by putting arsenic on a raw sore.

_Symptoms._ Violent colic, quick, feeble, irregular pulse, hurried respiration, emesis in vomiting animals, ardent thirst, purging, tenesmus, lowered or unevenly distributed temperature, red eyes, dilated pupils, and nervous symptoms, weakness, trembling, stupor, convulsions and paralysis. The urine is albuminous and may be bloodstained. In case of Paris green, the green color of the vomit, and of arsenious acid, a yellow color may be looked for. Test urine for arsenic.

_Lesions._ Inflammation of the stomach and small intestine, with ropy, often bloody mucus. Ecchymosis, and extravasations appear in the stomach. Ulceration is not common in very acute cases, but in protracted cases, it is usually present in the stomach (abomasum in cattle). Petechiæ may be met with in different internal organs and in protracted cases, fatty degeneration of liver, heart, or kidney.

_Treatment._ In vomiting animals encourage emesis by tepid water, tickling the fauces, or giving ipecacuan. For non-vomiting animals the stomach pump may be tried. The available antidotes are hydrated oxide of iron, or a solution of calcined magnesia. To make the first, mix 100 parts sulphate of iron in solution with 250 parts magnesia in solution. This should be given liberally and often: horse or ox 1 qt., sheep or pig 2 ozs., dog 1 oz. A simple aqueous solution of calcined magnesia also forms with arsenic an insoluble combination.

CHRONIC ARSENICAL POISONING.

This comes from continuous injudicious dosing with arsenic, or from the condensing on the grass of the vapors from the smelting of ores containing arsenic.

_Symptoms._ There is chronic indigestion, emaciation, hide-bound, depilation, red or weeping eyes, chronic diarrhœa, suppression of milk in cows, muscular weakness, paraplegia, soreness of the gums, salivation.

The _lesions_ are essentially the same only less intense than in the acute form. Hugo found in the intestines of poisoned animals a slimy, serous, grayish white fluid, and a false membrane like a frog spawn streaking the intestine. Later this may be dense like a diphtheritic membrane. There was fatty degeneration of the liver and of the gall bladder epithelium. Injection of the capillary vessels of the brain and pia, and effusion into the ventricles and on the surface of the brain were found in dogs.

_Elimination._ Arsenic is eliminated mainly in the urine, but also in part in the bile and perspiration.

_Tests for Arsenic._ When taken in the solid form it may be found undissolved on the gastric mucosa.

If burned on red hot charcoal or iron it gives out the odor of garlic.

Marsh’s test consists in evolving arseniureted hydrogen from zinc and sulphuric acid to which a little of the suspected liquid has been added. A flask is taken having a cork conveying two tubes, one a funnel reaching nearly the bottom of the flask, and the other a delivery tube of some length and provided with a chloride of calcium bulb, and at its end turned up at right angles and drawn out to form a narrow orifice. Pieces of zinc are placed in the bottom of the flask, and sulphuric acid is poured upon these through the funnel. This causes the evolution of hydrogen. The suspected liquid is now added, and the gas issuing from the delivery tube having been lighted, a piece of cold white porcelain is held above and a short distance from the flame. A dark metallic spot of arsenic is obtained. The stain obtained by antimony differs in being formed more closely to the flame, in volatilizing less rapidly under heat, and in forming a black or orange instead of the canary yellow sulphide when subjected to a stream of H_{2}S. with gentle heat. Chloride of lime dissolves the arsenic stain but has no effect on the antimonial one.

_Treatment._ Avoid the causes. Employ the antidotes in small doses once or twice daily. Check the diarrhœa by mucilaginous agents, and nourish the animals well.

POISONING BY PHOSPHORUS.

From matches, rat poisons, fatal dose, horse, ox, pig, dog, chicken.
Symptoms: Anorexia, dysphagia, swelled tongue, thirst, colic, emesis,
vomit phosphorescent, or bloody, diarrhœa, icterus, agalactia,
trembling, weakness, choreic spasms, hemorrhages. Lesions:
Buccal-gastro-intestinal inflammation, fatty degeneration of
epithelium, liver, kidneys, heart and muscles, black blood,
ecchymosis, hemorrhage, phosphorescent ingesta. Treatment: Emesis,
stomach pump, oil of turpentine in mucilage.

Phosphorus is usually taken in the form of matches or more frequently as one of the pastes sold for the destruction of vermin. Almost all of the latter contain 1 to 2 per cent. of phosphorus, in combination with flour, sugar, and fatty or oily matters. The lethal dose of phosphorus is: Horse or ox 7 to 30 grains; pig 2 to 4 grains; dog ¾ to 1½ grain; chicken ⅓ grain.

_Symptoms._ Anorexia, dysphagia, swelling of the tongue, intense thirst, colic, emesis in vomiting animals, vomited matters may shine in the dark, and may be tinged with blood, diarrhœa is common though not constant, icterus, and suppression of the milk. Trembling, weakness, acceleration of the pulse and breathing and hyperthermia may be noted. Chickens have been noticed to have choreic movements in walking. Hemorrhages are common.

_Lesions._ Inflammation of the mucosa of the alimentary canal from the mouth to the stomach and intestines. Fatty degeneration of the epithelium very noticeable in the gastric glands. Enlargement and fatty degeneration of the liver and kidneys, and degeneration of the heart and muscles. The blood is black and ecchymosis and hemorrhages appear on various internal organs. The contents of stomach and bowels shine in the dark. Phosphorus may be recognized by its luminosity when distilled at a very low heat from an acid solution and received into a refrigerated condenser. This must be done in perfect darkness, and the phosphorescence will be seen in the condenser or connecting tube.

_Treatment._ Empty the stomach by emetic or stomach pump, and then give oil of turpentine in mucilaginous liquid: Horse 1 to 2 ounces; ox 2 to 3 ounces; pig ½ ounce; dog 20 to 30 drops; chicken 5 to 10 drops. This may be repeated several times and if used early enough will probably succeed.

POISONING BY TARTAR EMETIC.

Fatal doses, large in herbivora. Symptoms: vomiting, diarrhœa,
ulcerative stomatitis, salivation, thirst, colic, tremors, palsy.
Lesions: gastro-intestinal inflammations, ulcerations, lung
infarctions. Treatment: emesis, antidote tannic acid.

This is mainly seen in the smaller vomiting animals. To kill horses or cattle much larger doses are necessary than are likely to be taken. Barlow and Dun gave 4 drs. to a horse thrice a day, and in all 10 ozs. in 10 days, yet it improved in condition. Ten and a half ounces given in 6 days proved fatal. An old sow was killed by 2 drs., a 5 months pig by 80 grs., (Hertwig). Dogs were killed by 3 to 7 grs.

_Symptoms._ Vomiting, diarrhœa, ulcerative stomatitis, salivation, vertigo, thirst, dullness, cold surface, colicy pains, trembling, paralysis of the hind quarters, and early death.

_Lesions._ General inflammation of the gastric and intestinal mucosa, sometimes ulceration especially if the agent has been taken in the solid form. Congestions and infarctions of the lung are not unknown.

_Treatment._ Encourage vomiting by tickling the fauces, and by the ingestion of tepid water. The best known antidote is tannic acid in any one of its combinations. Solution of tannin, decoctions of oak bark, oak galls, catechu, kino, rumex, sumac, or even strong tea will serve to render it insoluble and non-irritant.

POISONING BY CORROSIVE SALTS OF MERCURY.

Calomel with muriatic acid, corrosive sublimate, mercuric chloride,
iodide, nitrate, cyanide. Fatal dose. Symptoms: anorexia, salivation,
thirst, emesis, colic, diarrhœa, rumbling, debility, tremors, stupor,
death. Lesions: corrosive whitening of gastro-intestinal mucosa,
congestion, ulceration, blackening, bloody, glairy ingesta. Treatment:
albumen, emesis, demulcents, chlorate of potash, bitters, iron
sulphate. Test: copper and muriatic acid.

Calomel in itself cannot be looked on as corrosive, but in ruminants in which it is retained in the system for 3 or 4 days it is largely resolved into mercuric chloride by the free gastric acid and alkaline chlorides. It has therefore been largely excluded from the materia medica of these animals. When in these or other animals it produces corrosive action, the operation is essentially that of corrosive sublimate.

The corrosive salts of mercury likely to be taken by animals are corrosive sublimate now so largely used as an antiseptic, the nitrates and iodides, and cyanides of mercury used as local applications or as antiseptics.

=Mercuric chloride= may be taken as the type. It has proved fatal to the horse in a dose of 2 drs.; to the ox in 1 to 2 drs.; to the dog in doses of 4 to 6 grs.

_Symptoms._ Loss of appetite, salivation, thirst, emesis in vomiting animals, colics, diarrhœa, often bloody, weak perhaps imperceptible pulse, hurried breathing, much rumbling of the abdomen, debility, trembling, stupor and death.

_Lesions._ Escharotic whitening in patches of the mucosa of the mouth, throat, gullet, stomach and intestines, with acute congestion, ulceration and ecchymosis, and sometimes blackening by the formation of the sulphide. The contents of the bowels may be serous or bloody and more or less glairy. Like arsenic, mercuric chloride concentrates its action on the intestinal canal by whatever channel it may have entered the body.

_Treatment._ The mercury should be precipitated in an insoluble form and then eliminated by emesis or by the stomach pump. White of eggs is usually the most available agent producing the albuminate of mercury. This is, however, still soluble in acid and alkaline liquids, in chlorides of potassium, sodium or calcium and even in excess of albumen. Vomiting may be favored by tickling the fauces, or by hypodermic injection of apomorphia. This may be followed by boiled flaxseed or copious drinks of rain water. When the mercury has been largely eliminated the salivation may be controlled by chlorate of potash, and the digestive disorder met by bitters and iron sulphate.

_Test for Mercury._ Place a few drops of the suspected solution on a clean surface of copper; acidulate with muriatic acid; then touch the copper through the liquid with a piece of zinc; a silver colored stain will be formed easily dissipated by heat.

POISONING BY SULPHUR.

Fatal dose, horse 16 ozs. Symptoms: dullness, anorexia, colic,
diarrhœa, sulphur odor. Lesions: congestion, desquamation, ulceration
of gastro-intestinal mucosa, sulphur odor in flesh, blood nearly
fluid, blackens silver. Treatment: chloride of lime, oil, puncture
rumen or colon, stimulants.

In excessive doses this is irritant. The horse is poisoned by 16 ozs. (Tabourin): violent colics follow a dose of 12 ozs. (Collaine). Cattle are less susceptible.

_Symptoms._ Dullness, anorexia, colic, pulse small and quick, skin cold and clammy. Fœtid flatus and profuse diarrhœa, are marked symptoms.

_Lesions._ Injection of the gastro-intestinal mucosa, shedding of the epithelium, ulceration, and sometimes gangrene. Sulphur is found in the ingesta and fæces and a sulphur odor is prominent, not only in the bowels but also in the flesh. Tympany from H_{2}S is common. The blood is mostly fluid, and ecchymosis is shown on heart, lungs and other internal organs. The tissues blacken silver.

_Treatment._ Chloride of lime, oleaginous laxatives, use trochar and canunla for tympany. In prostrate conditions give stimulants (alcohol, ether).

POISONING BY BROMINE AND IODINE.

Poisoning by these agents is rare in domestic animals. Bromine 2 drs. killed a dog in 5 hours: 10 to 12 drops in 1 oz. water intravenously killed a dog suddenly, and 5 to 6 drs. of iodine by the mouth killed in a few days (Orfila). A horse had colic from taking ½ oz. iodine (Tabourin), others died from the effect of 2 drs. doses intravenously (Patu).

_Symptoms._ Violent colicy pains, salivation, emesis in vomiting animals, diarrhœa, iodine or bromine odor, acute coryza, red eyes, dilated pupils, weakness, debility, vertigo, convulsions. If the patient survives the glandular system undergoes atrophy, with emaciation and scaly skin eruptions.

_Lesions._ After large doses there are congestion, ulceration, corrosion and sloughing of the œsophagus, gastric and intestinal mucosa, and more or less yellow discoloration of the parts. The odor is characteristic. With iodine there may be blue iodide of starch in the ingesta.

_Treatment._ Favor emesis by tickling the fauces and giving tepid water, or apomorphia subcutem. Boiled starch is the best antidote and may be given freely, both by mouth and rectum. Opium is often called for to relieve suffering.

POISONING BY COPPER.

Copper sulphate: Fatal dose, horse, dog. Symptoms: Dullness, colic,
blue or green vomit, diarrhœa, straining, weakness, spasms, palsy,
albuminuria, icterus, hæmoglobinuria, impaired appetite, emaciation,
spasms. Lesions: Redness, softening, ulceration, sloughing of
alimentary mucosa, methe-globinæmia, fatty liver, enlarged spleen,
ingesta give copper film on polished iron. Treatment: Albumen, milk,
mucilage, iron filings, sulphur, magnesia, laxatives, opium. Avoid
acids.

The common copper poisons are the sulphate and acetate. Copper alum, oxide or carbonate of copper and paints with a copper base are less frequently taken.

=Sulphate of copper= 1 ounce has proved fatal to the horse. In dilute solution or with mucilaginous liquids it is much less injurious. Ten grains to 2 drachms subcutem have killed the dog. (Tabourin.)

_Symptoms._ Dullness, colics, emesis of blue or greenish matter in vomiting animals, diarrhœa, tenesmus, weakness, trembling, spasms, trismus, paralysis, small, weak pulse, hurried breathing. In experimental chronic poisoning in the sheep, albuminuria, icterus, hæmaglobinuria, hæmaturia, impaired appetite and rumination, constipation followed by diarrhœa, great emaciation and weakness and finally convulsions. (Ellenberger and Hofmeister).

_Lesions._ Redness and softening of the alimentary mucosa, ulceration, sloughing, perforation. In the chronic forms methe-globinæmia, free hæmatin as crystals in liver, spleen and kidney, nephritic extravasation, fatty degeneration of the liver, enlarged spleen, and catarrhal changes in the intestinal mucosa. Polished iron placed in the gastric or intestinal contents becomes coated with copper.

_Treatment._ White of egg, milk, mucilage, iron filings, sulphur, calcined magnesia, laxatives. Opium may be required to calm suffering, but acids must be carefully avoided.

POISONING BY ZINC.

Sulphate and chloride poisonous, less potent oxide and carbonate.
Symptoms: colics, emesis, congested alimentary mucosa, diarrhœa,
cramps, weakness, paresis, anæmia, emaciation. Lesions: white,
leathery, sloughing or ulcerated alimentary mucosa, strictures.
Treatment: emesis, demulcents, tannic acid, sodium carbonate.

The =sulphate= and =chloride= are the most likely to be taken in dangerous amount, the former being mistaken for Glauber salts. Three ounces of sulphate intravenously in the horse has proved fatal, or 10 to 50 grains in the dog. In the vicinity of zinc ore furnaces the agent is taken in on the fodder as oxide or carbonate.

_Symptoms._ There is much abdominal pain, emesis in vomiting animals, quick pulse, congested mucosæ, diarrhœa, cramps, weakness, and paresis, and if the patient survives, anæmia and emaciation.

_Lesions._ The mucosa of mouth, gullet, stomach and perhaps duodenum is white, opaque, hard, corrugated, leathery, sloughing, or ulcerated. Congestion is well marked. Strictures may appear in chronic cases.

_Treatment._ Give tepid water and tickle the fauces. Use white of egg or milk freely and mucilaginous agents. Tannic acid, or carbonate of soda are antidotal by tending to precipitate insoluble compounds.

POISONING BY SILVER.

Toxic doses of silver come mostly from materials used in the arts. The photographer uses chiefly the nitrate, iodide, bromide, cyanide and chloride. Taken into the stomach the silver salts are less poisonous because they are largely precipitated as insoluble chloride or albuminate. The chloride and albuminate are, however, soluble in solutions of alkaline chlorides and hence even they may poison.

_Symptoms._ Colic, emesis in vomiting animals the vomited matters blackening in the light, diarrhœa, great muscular weakness, paresis, weak clonic spasms, and disturbed respiration. The nervous symptoms are very prominent (Rouget and Curci). Chronic poisoning produces emaciation and fatty degeneration of liver, kidneys and muscles (Bogoslowsky).

_Lesions._ Patches of congestion and of white corrosion on the buccal œsophageal and gastric mucous membrane, the presence of the curdy white chloride of silver adherent to the gastric mucosa. In chronic cases the visible mucosæ and white skin may have a slaty color.

_Treatment._ Emetics in vomiting animals. White of egg, common salt largely diluted and followed by milk as antidotal, demulcent and nutritive agent.

POISONING BY BARIUM.

Poisonous salts. Symptoms: spasms, peristalsis, defecation, urination,
restlessness, prostration, emesis, weak pulse, coma. Lesions: Moderate
congestion of gastro-intestinal mucosa. Treatment: alkaline sulphate,
anodynes, demulcents.

The salts of barium are irritant with a special action on the nervous system shown by weakened action of the heart and spasms or paresis of the muscles. The chloride is used in staining wool, the nitrate and chlorate in producing green colors in fireworks, the oxide and carbonate in glassmaking, the chromate by painters, and the sulphate for giving weight and body to various white powders. The chloride is now largely used to stimulate intestinal peristalsis in animals.

_Symptoms._ Barium chloride hypodermically produces tonic and clonic convulsions, increased peristalsis, discharges of urine and fæces, great restlessness, muscular prostration, emesis in vomiting animals, hurried, shallow respiration, weak, thready pulse, asthenia, coma, and death.

_Lesions._ There is congestion of the gastric and intestinal mucosa, but this is rarely violent, and corrosion and ulceration are almost unknown. The agent indeed seems to act more energetically upon the nervous system than on the mucosa of the alimentary tract.

_Treatment._ This consists in giving an alkaline sulphate (sulphate of soda, potash, or magnesia), to precipitate the insoluble barium sulphate, with anodynes (opium) and mucilaginous agents.

POISONING BY IRON.

Sulphate and chloride on empty stomach poisonous. Symptoms: Colic,
emesis, rumbling, purging. Treatment: Alkaline or earthy carbonates,
tannic acid, albumen. Opium.

Sulphate and chloride are the principal poisonous compounds. Both are comparatively harmless even in large doses taken on a full stomach, while on an empty stomach they may cause violent gastro-enteritis.

_Symptoms._ Colicy pains, purging, emesis in vomiting animals, more or less tympany and rumbling of the bowels, and surface coldness.

_Treatment._ Give carbonates of the alkalies, magnesia or lime to precipitate the comparatively insoluble carbonate or oxide; or tannic acid or infusion of oak bark or galls. White of egg, milk and mucilaginous agents, and opium may be required to allay irritation.

POISONING BY CHROMIUM.

Chromic acid, chromate and bichromate of potash. Corrosive. Cause:
Gastro-intestinal inflammation, albuminuria, hæmaturia, emaciation,
digital ulcers and sloughs, colic. Diarrhœa, vertigo, stiffness,
weakness. Lesions. Treatment: Emesis, stomach pump, demulcents.