Part 12

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 Bacillus Diphtheriæ Columbarum (Klebs-Löffler).

1. In gelatine cultures grows only 1. In gelatine cultures grows at above 23°C. 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.