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.