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 2μ long and 0.3 to 0.4μ 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.
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.
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.
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.
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.
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).