PSEUDOMEMBRANOUS STOMATITIS OF PIGEONS AND CHICKENS.
Contagious and destructive nature of the disease. Mode of extension from the mouth and pharynx. Causes: bacillus diphtheriæ columbarum; its characters: pathogenesis to birds, mice, rabbits, Guinea pigs; dogs, rats, and cattle immune; diagnosis from bacillus diphtheriæ. American disease. Incubation. Symptoms: prostration; wheezing breathing; sneezing; difficult deglutition; false membrane on fauces; necrotic changes in mucosa; perforations; lesions of internal organs; blood infection; nostrils stuffed; bill gapes; lesions on eye, tongue, gullet, crop, intestine; diarrhœa; vomiting. Skin lesions. Course, acute, chronic. Paralysis. Mortality. Prognosis. Diagnosis from coccidiosis, from croupous angina of Rivolta, from aspergillus disease. Treatment: isolation; destruction of carcasses; hatching; destruction of dead wild birds and rabbits; exclusion of living; quarantine of new birds; disinfection; locally, antiseptics by inhalation, swabbing, and internally, iron in water.
This affection prevails in certain countries and causes heavy losses among young pigeons, so that it might with great propriety be included among animal plagues, which should be dealt with by the State. The malady is a local inflammation leading to the formation of false membranes and its usual course is to progress from the mouth and pharynx, to the nasal passages, lachrymal ducts and sacs, the larynx, trachea, bronchia, intestines and skin.
Causes. The essential cause of the disease is held by Löeffler to be the bacillus dipththeriæ columbarum, which is a short bacillus with rounded ends, a little longer than the bacillus of fowl cholera and not quite so broad. It is usually found in irregular clusters, especially in the interior of the hepatic capillaries. It is ærobic, non-motile, non-liquifying, and grows on nutrient gelatine, blood serum or potato. In gelatine it forms a white surface layer, and spherical colonies along the line of puncture, which show a yellowish brown tint under the microscope. On blood serum and potato it forms a grayish white layer.
Pathogenesis. The bacillus is inoculable on other pigeons and as it usually appears in the young birds in the nest, still fed by the parent bird, it is probable that no inflammation nor abrasion is necessary to make it take. Pure cultures inoculated in the mouth gave rise to the usual local type of the disease. When inoculated subcutem it caused a local necrotic inflammation.
In mice subcutaneous injections proved fatal in five days with general dissemination of the bacillus. There are congested and hemorrhagic spots on the lungs, enlarged spleen, and the liver is marbled by numerous necrotic white masses, in the centre of which the capillaries are found to be blocked with the bacilli. This is so pathognomonic that Löffler looks on the inoculation of mice as the best means of diagnosis.
Inoculated rabbits showed inflammation in the seat of inoculation and sometimes fibrinous peritonitis and enlarged spleen. Inoculation on the cornea produced a false membrane.
In Guinea pigs induration and ulceration occurred in the seat of inoculation but recovery followed in 14 days.
Sparrows inoculated in the pectoral muscles died in three days with yellowish necrotic tissue highly charged with bacilli.
Inoculation of the chicken by Löffler and Megnin produced a circumscribed redness which soon disappeared. On the other hand Krajewski, Colin, Loir and Ducloux seem to have inoculated chickens successfully, and Cadeac says that the cultures are infecting for sparrows, pigeons, turkeys, chickens and ducks. It rests uncertain therefore whether the pseudomembranous pharyngitis of hens is a distinct disease as alleged by Löffler and Megnin or if the chickens used by these observers were not already immune by reason of a prior attack.
Löffler’s experiments showed that dogs and rats were immune. Loir and Ducloux failed to infect cattle.
In infected dove-cots a comparative immunity is attained by the older pigeons, which continue to harbor the germ, but do not suffer materially from its presence. They however communicate it to the susceptible young in the milky secretion produced in the crop and with which they feed them, and these accordingly perish in large numbers. Thus pigeons that are themselves in fine condition become the propagators of the bacillus to the more impressible.
Sparrows and other small birds are also held to be common propagators of the germ, and if they too can secure an individual immunity and yet harbor the bacillus, their passage from yard to yard may be attended with great danger. The grains soiled by their bills and not swallowed are common media of transmission.
Loir and Ducloux found the affection transmissible between man and pigeon. The identity of the bacillus with that of genuine diphtheria in man appears to have been thoroughly disproved by the observations of Roux and Yersin.
The following differential characters have been noted:
| Bacillus Diphtheriæ (Klebs-Löffler). | Bacillus Diphtheriæ Columbarum | ||
|---|---|---|---|
| 1. | In gelatine cultures grows only above 23°C. | 1. | In gelatine cultures grows at 15–17°C. |
| 2. | Kills Guinea-pig and dog. | 2. | Guinea-pig and dog nearly immune. |
| 3. | Mice immune. | 3. | Mice usually die with hepatic necrosis. |
| 4. | Does not grow on potatoe. | 4. | Grows luxuriantly on potatoe. |
It may be accepted as demonstrated that the common diphtheria of birds is essentially distinct from the genuine diphtheria of man, and that when such diphtheria of the bird is conveyed to man as has been often alleged (Richter, Gips, Bonig, Gerhart, etc.), it is one of the forms of pseudo diphtheria that is produced, and not that which is caused by the Klebs-Löffler bacillus. Dr. V. A. Moore, who has cultivated specimens of the bacillus diphtheriæ Columbarum obtained from Germany, considers the germ as belonging to the group of the bacillus coli communis, and as not the cause of the chicken diphtheria in America. Further investigation must settle whether the bacillus diphtheriæ Columbarum is the one cause of this affection in Europe, and what is the microbian cause or causes of the disease in America.
Incubation. This is very variable. False membranes may form in twenty-four hours in some cases; in other cases they may be delayed from four to fourteen days (Colin, Babes, Puscarin, Marinescu).
Symptoms. There is dullness, prostration, sunken head, ruffled feathers, altered hoarse voice, drooping wings, wheezing breathing, difficult deglutition, sneezing, and patches of dark red congestion in the fauces covered with a thin film, at first translucent, but soon becoming dense, adherent, opaque, whitish or yellowish. As it becomes older this deposit becomes granular, wrinkled, dry and friable. It is more adherent in chickens than in pigeons and causes bleeding when detached. Necrotic changes may take place in the mucosa leading to considerable loss of tissue, and even to perforations of the soft palate, pharynx or œsophagus. It may remain circumscribed by the region of the mouth and end in an early recovery, or it may extend to the organs of the chest and abdomen, or the germs may proliferate largely in the blood and induce fatal results. On the other hand it may become subacute or even chronic, and, as already noted in the case of the parent pigeons, it may persist as an infecting disease without materially injuring the general health of a comparatively immune animal.
The affected nasal passages become filled by frothy liquid and blocked by false membranes, so that the bird is driven to breath through the open mouth. The skin around the nares, and eyelids and the cavity beneath the eye may be covered with the false membrane, by the increase of this product the bones may be driven out of place, so that the palatines press downward, the eyeball is pressed outward and the root of the beak may seem swollen. The false membranes that form on the skin or reach the surface are soft, creamy, cheesy, or dry, granular and friable.
When the eye is specially affected there are swelling of the lids, profuse lachrymation, closure of the lids by adhesion, and formation around their borders or on their inner surface and on the membrana nictitans of false membranes which press the lids outward more or less unevenly, and may be easily recognized when the lid is everted. The cornea and even the interior of the eye may suffer, leading to perforation, internal tension, and in some cases atrophy, with permanent blindness.
The tongue may suffer on the tip as in pip, or on its dorsum, from which the disease extends to the larynx, trachea and even the air sacks, which become filled with false membranes, that are coughed up, and decomposing in the mouth, add to the infection and fœtor. Dyspnœa and cyanosis of comb and wattles are marked features.
The extension may take place downward along the alimentary track, the false membranes forming on the gullet or crop and interfering with swallowing or digestion, or on the intestine and determining a fœtid, often greenish or bloody diarrhœa with indications of false membranes. Vomiting may be a marked symptom.
The skin is usually attacked secondarily around the margin of the beak, the eyelids, the nares, the ears, the comb, the wattles, the anus, but it may develop at any point where the infecting material has touched an abraded surface.
Trinchera found that in acute cases the acme was reached in fifteen days after which improvement might be looked for. A chronic form affecting the gullet might however persist indefinitely in pigeons without proving incompatible with good health.
Paralysis of the wings or limbs may remain after the healing of the local lesions.
Mortality. Prognosis. The disease is very fatal to both pigeons and chickens, 50, 70 or even 100 per cent. perishing when a flock is attacked for the first time. In flocks that have previously suffered, on the other hand, a large number are practically immune, and even if they contract the disease it assumes a mild form, and they survive but may retain the germ and continue to communicate it to others. Even the young of such immune flocks suffer less severely, coming as they probably do from less susceptible and therefore surviving birds, or having already perhaps contracted a mild (non-fatal) type of the disease from their parents.
Differential Diagnosis. From psorospermosis (coccidiosis) it is distinguished by its origin on the mucous membranes, and not on the skin, the skin lesion being a secondary one. In psorospermosis the primary lesion is usually on the skin, from which it extends to the mouth and especially along its floor. In psorospermosis the morbid deposit assumes the form of rounded warty-like masses, on comb or wattles; is easily propagated by inoculation, is promptly checked by antiseptics, does not tend to produce internal extension nor generalization, and on microscopic examination shows numerous spheroidal coccidia intermingled with the epidermic cells and possessing amœboid movement. By virtue of this automatic movement they make their way between and into the epidermic cells in which they multiply.
From the croupous angina of Rivolta it is distinguished by the absence of the infusoria (monocercomonas gallinæ) to which he, Delprato and Pfeiffer attributed that affection. The monocercomonas is a flagellate organism 14 μ to 25 μ in length and 5 μ to 7 μ in breadth. Its rounded end bears one flagellum as long as the body, and its acute end three flagella which give it active motions. These are found in the yellowish white swellings of the mucosa, which vary in size from a millet seed to a pea, covering a hyperæmic spot and composed of epithelial cells, blood globules—white and red,—leucocytes, granules and the infusoria. The false membrane is remarkable for its lack of consistency and its tendency to invade the mouth and gullet rather than the air passages. These infusoria are not colored by picrocarminate of ammonia, but stain by methyl-violet and then appear as round or slightly irregular hyaline bodies.
From aspergillus disease of pigeons, by the absence of the characteristic, miliary, white nodule of that disease showing caseated contents intermixed with an abundant mycelium of aspergillus fumigatus. The aspergillus disease attacks especially the mouth but may also implicate the gullet, lungs, liver, intestine and kidneys. The microscopic examination of the exudate is conclusive, by reason of the presence of the bacillus diphtheriæ columbarum, and the comparative absence of the filamentous mycelium.
Treatment. This is mainly prophylactic. The first step must be to separate the sick and healthy, destroying the former, or shutting them up in a special enclosure apart from all other birds. In the case of valuable chickens, their eggs may be set under other hens and the young raised apart from the suspected flock. This may even be attempted in pigeons, the common eggs being removed and the valuable ones put in their place under a healthy sitting dove. In the case of pigeons that have been recently through the disease they should be kept strictly by themselves, even though they may appear to have regained perfect health. The dead bodies must be burned or deeply buried. Sparrows and even rabbits dying in the vicinity must be similarly disposed of, and where the disease prevails sparrows and small birds may be exterminated as probable bearers of infection.
The purchase of strange birds must be carefully guarded, none being taken that show weeping eyes, nasal discharge, labored or wheezing breathing, and all new birds should be placed by themselves in quarantine for ten to fifteen days. Finally a thorough disinfection of the place where the sick have been is of first importance. Thorough cleaning of the poultry house, followed by a coat of white-wash, every gallon of which contains four ounces of chloride of lime, or one drachm of mercuric chloride will usually prove effective. The poultry runs should be liberally sprinkled with a solution of sulphuric or hydrochloric acid, one part to 1000. The same may be used on the building, which may further be fumigated by burning sulphur.
Poultry shows should be kept under the most rigorous sanitary supervision.
Curative treatment is only profitable in the case of specially valuable birds, and even then only, as a rule, when the disease is confined to the nose, mouth, larynx and pharynx. The affected parts may be brushed with a solution of chloride of iron (1 dr. of the tincture to 1 oz. water), nitrate of silver (2 grs. to 1 oz. water), sulphide of calcium (½ dr. to 1 oz. water), tannin (10 grs. to 1 oz.). Tincture of iodine may be applied direct, or a solution of carbolic acid or of creosote or creolin (1 part to 50) will often succeed. Thomassen recommends the removal of the false membranes and the application of boric acid followed by dry sulphur. Benoist says the majority recover when made to inhale the fumes of oil of turpentine evaporated at a gentle heat twice a day.
As internal medication, or to correct the intestinal affection, sulphate of iron may be dissolved in the drinking water, or salicylic acid may be given in pill form with molasses.