Part 59

Definition. An infectious disease of turkeys, especially destructive to the young, due to a protozoön (amœba meleagridis), and characterized by inflammatory thickening of the walls of the cæca, diarrhœa, brownish, yellowish or greenish areas of degeneration of the liver, and congestion with blackish discoloration of those portions of the head which are uncovered by down or feathers.

Microbiology. The microörganism (amœba meleagridis) is found in the thickened walls of the cæca, in the exudate, in the lumen, and in the degenerating patches of the liver. The most common and simple form is that of a rounded body, varying slightly in form, and containing a group of very minute granules situated somewhat eccentrically. They may be enclosed in lymph spaces or less frequently in giant cells, or have portions of broken up cells adherent. Their size varies from 10 to 15μ. They may be stained by the following process: Harden in 95 per cent. alcohol saturated with mercuric chloride, then in the same with an equal amount of a 5 per cent. solution of bichromate of potash, and finally in Hemming’s solution. After a day in these solutions they are washed for a day in running water, then treated with ascending strengths of alcohol, dried by passing through alcohol and chloroform, imbedded in paraffin, sectioned dry, and stained in Delafield’s hæmatoxylin and eosin. The spherical or slightly oval amœbæ have a homogeneous, bluish red tint, feebler and therefore distinct from the tissue nuclei. Near the centre in most a blue circular line shows the outlines of the nucleus.

Th. Smith compares this affection with the amœbic dysentery affecting the large intestine and liver of man, and notes these differences, that amœbic movements have not been observed in amœba meleagridis, and that hepatic abscess does not occur in the turkey. The indisposition of the bird to suppuration may perhaps account for the latter distinction. Smith found rounded organisms in the tubules of the cæca and flagellates in the lumen of the gut, but did not attach any importance to their presence. Bacteria were only found in the lesions in the solid tissues where the subject had not been killed and immediately examined, but left over night for examination in the morning. There was no constancy in their species as in the case of the amœbæ, all indicating that their invasion was post mortem.

Symptoms. The disease is most frequent and fatal in the young (1 to 4 months, exceptionally 6 to 10 months), and the symptoms vary much in different cases, according to the intensity of the disease and the relatively extensive implication of the different organs. Among the general symptoms are those of general suffering and ill health, dulness, spiritlessness, drooping of the head between the wings, a pendent condition of wings and tail, erection of down or feathers, separation from the flock, the bird moping alone and sitting much of the time. The more characteristic phenomena which are rarely sufficient to identify the disease unless it is known to be prevalent, are loss of appetite, a greenish diarrhœa, yellowish or brownish discoloration of mucosæ, emaciation which becomes extreme if the subject survives long enough, and more or less blackish discoloration of the gobble and bare portions of the skin covering the head.

Lesions. These are characteristic, the cæca being greatly enlarged, the walls thickened by a yellowish submucous exudate, the epithelium disintegrated and desquamating, and the mucosa covered by a solid yellowish gelatinoid exudate arranged in superposed layers, while the contents are soft, pasty or of a greenish liquid appearance. The comparative stagnation of the contents as in the appendix of man appears to favor microbian infection. Amœbæ are especially abundant in the exudate into the submucosa and in the lymph spaces. The liver changes show infective inflammation in the spots of mottling, followed by degeneration, and necrosis, the liver cells disappearing under the compression of the giant and round cells and the amœbæ, the surface over the affected parts is depressed, and the mottling may show a variety of colors, as brown, brownish red, or yellow, pale yellow, grayish or dirty white. The degenerating tissue may become caseated, but abscess appears to be unknown, though so common in amœbic dysentery of man. In the skin of the head the blackish color predominates; there is more or less congestion, capillary embolism, and tissue degeneration.

Diagnosis. Th. Smith notes three cases of diseased cæcæ without great thickening of their walls, and an exudate in the lumen having the general appearance of that seen in the amœba disease but with no amœbæ, only the bacillus coli communis. The odor was strongly feculent. In all three cases the liver was healthy. In one there was an abundance of tapeworms in the bowels. Manifestly the absence of liver lesions may be held to indicate the absence of the protozoan disease. VonRatz (Budapest) gives two similar cases, with many nematodes, those in the exudate being 8 to 14 mm. long.

Zurn describes the presence of the diphtheria of fowls in the intestines of hens, turkeys and palmipeds and sometimes confined to the cæca. It is characterized by great prostration and debility, and an offensively smelling diarrhœa at first pultaceous and mucous, later bloody, and followed by constipation, in which case the cæca and rectum are ulcerated and blocked with the yellow croupous exudate. It lasts 2 to 3 weeks or even months, is subject to relapse, and sometimes occurs as a sequel to the diphtheritic affection of the head and throat. The absence of marked thickening of the cæcal wall, and of the protozoön, the presence of the diphtheritic exudate in the lumen, and the croupous condition or congested appearance of the head and throat are distinctive. Th. Smith, however, refers to two cases, supposed to be of this kind, in which the walls of the cæca were greatly thickened, the result of reparatory inflammation following a slough of the mucosa. Siedamgrotzky also describes thickening of the walls of both cæca in a hen, the mucosa being covered with a thin pseudo-membranous exudation, without ulceration.

It would seem that the cæca of birds, like the vermiform appendix of man is very subject to invasion microbes, bacterian and protozoan, and should always be carefully examined in case of intestinal or hepatic disorder.

Treatment would be in the line of intestinal antisepsis with carbolic acid, salol, sulphurous acid, or the sulphites, with a laxative of castor oil, to carry these agents unchanged to the cæca, but no success has attended attempts in this direction, and the danger that comes from preservation of the infected animal, and consequent multiplication of the microbe would as a rule far more than counterbalance any probable recoveries.

Prevention. Moore has shown that the amœbæ, passed with the fæces, contaminate the food and water and thus actively propagate the disease, so that preventive measures must be mainly directed toward the purification of these infecting media. To be thorough new ground must be secured on which no diseased turkeys have been, and through which no water from contaminated or suspected land can flow; if necessary this must be closely fenced to prevent all ingress or egress, and on this ground we can place, as soon as they leave the shell, young turkeys hatched from eggs obtained in noninfected localities, or the eggs carefully washed of the turkeys living on infected ground. In this way the heredity and quality of the flock can be preserved without risk of contamination from the parents. The amœba is not known as a parasite of other birds, but if it should eventually be found to be so or to occupy any other animal body as an intermediate host, the local extermination of such host will become a necessary precaution.

When a new flock has been started in this way, the birds of the old flock may be fattened, killed and marketed, and as suggested by Cooper Curtice the grounds they have occupied may be secluded by fencing for one or two years, in the hope that the amœba will perish by this break in the chain of its life history. If this should prove successful with the land, the infection might be easily exterminated in the whole infected district or state.

The poultry buildings will require thorough disinfection. All manure and droppings must be carefully removed and the building whitewashed, using freshly burned quicklime and ¼ lb. of chloride of lime to the gallon of the mixture. The litter should be burned, and all nests, roosts, drinking vessels and troughs soaked with a mixture of sulphuric acid ½ gallon, carbolic acid ½ gallon, and water 20 gallons, (Th. Smith). The agents are mixed slowly in a vessel set in cold water. The same may be liberally applied on the surface, fences, etc., of the yards. Or quicklime, freshly burned, may be used freely on the yards holding the infected flocks (Moore). Mercuric chloride is dangerous. When the infected flock has been finally disposed of, the buildings and yards should be again thoroughly disinfected, and together with the field runs, abandoned for at least one year.

ASTHENIA IN CHICKENS.

Microbiology: bacillus of colon group. Pathogenesis to Guinea pigs: rabbits, pigeons and chickens refractory to artificial cultures. Treatment.

Synonym. “Going Light,” Bacterial Infection of the Duodenum.

C. F. Dawson, in investigating a wasting disease of well fed Brahma fowls in Maryland in which there was no appreciable symptom except the gradual and extreme loss of flesh and weight found in all cases a catarrhal duodenitis, with the presence in the contents of a bacterium in pure cultures, and apparently allied to bacillus coli communis.

Bacteriology. The bacterium is 1 to 1.3μ long, by .5μ wide, with rounded ends, often in pairs. It does not stain in acid nor alkaline methylene blue, carbol fuchsin, nor alcoholic dyes, but stains easily in aqueous solutions of the same stains and by Gram’s method. It is ærobic, facultative anærobic, grows at 50° to 120° F. in acid or alkaline beef bouillon, with fœtor; in glucose, saccharose, or lactose bouillon with the production of acid; in milk causing coagulation; on gelatine, agar and potato. Growth in Bouillon ceased at 131° F. and sterilization took place at 135° to 140° F. Vitality was not lost under freezing nor drying. It was killed by a 1 per cent. solution of carbolic acid in five minutes, or by formaldehyde gas, but not by lime water.

Pathogenesis. Inoculated subcutem, in a Guinea pig caused death in 24 hours, with a necrotic œdematous condition of the adjacent tissues like malignant œdema, and containing the microbe. It was further found in the liver, spleen, abdominal exudate, heart, blood and lungs, but not in the kidneys.

It proved harmless to rabbits when injected subcutem, but fatal in 24 hours when thrown into the peritoneum. The lesions were severe duodenitis and omental inflammation, and the bacterium was found in the liver and duodenal wall.

Pigeons, rats and mice proved refractory to the artificial cultures, also chickens. The latter were injected subcutem, intraabdominally and intravenously. Yet in view of the constancy of the lesion in hens with the microbe in pure cultures and the absence of all other morbid conditions, Dawson felt justified in attributing the disease to this microörganism. It is possible that his experimental hens had become immune from a previous attack, or failed in some condition of food or environment which is essential to pathogenesis, or finally there may possibly be some other infinitesimal microbe present which escaped observation, but which furnished the occasion for the coincident development of the colon bacterium.

Treatment. The indications are: the expulsion of the offending bacterium to be followed by nutritious, easily digested food, pure water and tonics. Dawson advises castor oil in dose of two teaspoonfuls, or calomel ¼ grain repeated till purgation occurs; and to be followed by powdered fennel, anise, coriander, cinchona of each 30 grains; powdered gentian and ginger of each ½ dram; powdered copperas 15 grains. The addition of bismuth, pepsin, or orexin may be suggested.

APOPLECTIFORM SEPTICÆMIA IN CHICKENS.

Streptococcic infection in hens. Most violent in pullets and hens; less so in capons and cockerels. Found dead, or sick 24 hours, ruffled, prostrate, neck limp, head drooped, indisposed or unable to rise, liquid icteric fæces, blood-stained skin of neck and breast, death without agony. Lesions: Soiled anal feathers, plump carcass, skin pallor save neck and breast, extravasation of blood subcutem and intramuscular, mucosæ anæmic, peritoneal engorgement and effusion, enlarged, engorged liver, cell proliferation, degeneration, coagulation necrosis, gall bladder full. Enlarged congested spleen, degeneration. Congested swollen kidneys, epithelial degeneration, casts, streptococcus. Congested, consolidated bronchioles, alveoli, lungs, with microbe. Meningeal congestion, exudate. Bacteriology: Streptococcus, pure cultures in lesions, size, chains, tetrads, staining qualities, culture media, colonies, action on sugars, acid, no gas, on milk no coagulation, on gelatine no liquefaction. History: Stagnant water; no evident source of infection, buzzards, etc. Pathogenesis: Inoculation, intravenous or intramuscular, feeding. On duck, pigeon, rabbits, mice, dogs. Guinea pigs and sheep immune. Immunization by injection of sterilized cultures.

Under this name Norgaard describes a hæmorrhagic streptococcic infection which prevailed in 1901 in a flock of 200 to 250 Plymouth Rocks in Loudon County, Va. Forty birds died within six weeks, and later the mortality reached 200, death often occurring suddenly while feeding, or the birds would drop from their roosts in the night and be found dead in the morning.

Symptoms. In the majority, the pullets which died suddenly, no symptoms whatever were observed, yet a certain number of the capons and cockerels were noticeably ill for 12 to 24 hours. In these the feathers were ruffled, the prostration extreme, the head drooped between the wings, the neck was weak and wobbling (limber neck), the wings and tail drooped, and the animal lay on its breast often unable to rise. Sometimes there was a passage per anum of liquid bile-stained mucus. Close examination of the neck and breast might detect hæmorrhagic discoloration of the skin, though the skin elsewhere was pale and smooth. Death takes place without a struggle.

Lesions. The anal feathers were usually stained, indicating diarrhœa; the picked carcass was plump and fat, with pale, healthy looking skin, except on the neck and breast, where it was discolored by extravasated blood; at such points the connective tissue and muscles were infiltrated with blood in areas of an inch in diameter, more or less, and with irregular outlines. The buccal mucosa was clear, pale and bloodless. The cavity of the body contained an abundance of sero-sanguinolent exudate, and the mesenteric veins were engorged. The liver was greatly enlarged and congested, the greater part of its substance being apparently composed of the distended blood vessels. The hepatic cells were granular and fatty, and if death had been delayed over twenty-four hours their outline became indistinct and the nucleus stained only faintly. In the foci of disease were clumps of round cells and leucocytes in and between the acini, and in still more tardy cases points of coagulation necrosis. The streptococcus was abundant in the necrotic centres, among the clumps of leucocytes, in the parenchyma and capillaries. The gall bladder was usually distended with bile. The spleen had the large size and well developed Malpighian bodies that characterize the well-fed bird, but it showed still greater enlargement, combined with sanguineous congestion and circumscribed blood extravasations. With a hand lens were seen numerous round, semi-transparent points, the size of pin holes, which the microscope revealed to be centres of coagulation necrosis, surrounded by embryonic tissue. The centres consisted of a granular debris with abundance of the streptococcus. The kidneys were congested and swollen, and in cases that had survived two or three days there was granular degeneration of the epithelium of the tubules, and the lumen of the tubes contained casts with leucocytes and streptococci. The organism was also present in the capillaries. The lungs presented areas of congestion and consolidation, exudation into the walls of the bronchioles and the alveoli, and an abundance of streptococci in the lesions. In the cranium were a subdural exudate and meningeal congestion. For examination of the tissues they were hardened in specimens of alcohol of encreasing strengths, embedded in paraffin and stained with carbol fuchsin with a counterstain of methylene blue.

Bacteriology. The streptococcus was found in pure cultures in all the diseased centres except in the intestinal contents. Smear preparations were made from the blood, the abdominal exudate, the intestinal contents, the bone marrow, the cerebral exudate and the sanguineous effusions into the muscles.

The coccus is .6 to .8μ in diameter, in short chains of 2 to 8 cells, or in some media much longer. Involution forms are common, and Norgaard claims to have seen indications of fission in two directions to form tetrads. The organism stains in the usual aniline dyes, as well as by Gram’s and Gram-Weigert’s method. It is nonmotile, ærobic, facultative anærobic, grows in solid and liquid media that is neutral, or slightly acid or alkaline (not if strongly acid), best at 98.6° F., and slower at the room temperature. In alkaline peptonized beef bouillon in 24 hours it forms threads and balls on the sides and bottom of the tube, leaving the liquid clear. On agar there are formed small shining, grayish colonies 1.5 mm. in diameter with brownish centre and bluish periphery. With all the sugars it produces acid, but no gas. It does not coagulate milk. On gelatine colonies are formed in four days, and there is no liquefaction.