Definition. Historic notes. Bacteriology: Bacterium choleræ
gallinaceæ, nonmotile, with polar stain, bleached by iodine,
non-liquefying, causes septicæmic lesions. Lignieres’ bacillus,
culture features non-gasogenic, acidifies dextrose; vitality in
disinfectants; survives drying. Accessory causes: new birds in flock,
or eggs for hatching, mingling of flocks, manure, watershed, streams,
ponds, dust, wild birds, buzzards, rabbits, insects, infected soil.
Susceptible animals: hens, doves, peafowl, pheasants, parrots, ducks,
small birds, guinea pigs, rabbits, white and gray mice. Effect on
sheep, horse, man, cow, frog. Incubation 18 to 48 hours. Symptoms: in
fulminant cases rarely seen, in acute, anorexia, depression, debility,
apathy, ruffled feathers, sunken head, neck, wings, tail, tremors,
nasal and buccal discharge, hyperthermia, sighing, violet comb and
wattles, thirst, pultaceous fæces, later glairy, green and fetid.
Temperature becomes subnormal, inability to rise, stupor, convulsions,
death in 1 to 3 days. Mild cases last 7 days. Cases caused by one
microbe have slough only. Lesions: congested, petechiated, hæmorrhagic
intestinal mucosa; contents of bowels watery, frothy, bloody;
epithelial degeneration and desquamation; abrasions, croupous
exudates, enlarged congested lymph glands, fermenting contents of
crop. Petechiæ general, spleen and liver swollen, congested, friable;
kidneys congested; lungs hyperæmic or blood gorged. Blood diffluent
with microbe. Anæmia. Emaciation. Arthritis. Diagnosis: by rapid
spread, infection origin, early excessive mortality, hæmorrhagic
lesions, microbe in blood and liquid ingesta. Prognosis: Mortality 90
to 95 per cent. at outset. Prevention: Quarantine new birds, inside
screens in summer; burn or acidify manure; exclude buzzards, vermin,
wild birds, and visitors; separate sick, kill, burn, disinfect; divide
infected flock in small lots; prevent wandering in fowls, destroy
insects. Phenic acid subcutem. Immunization: inoculate in breast with
one microbe (Salmon): or with weakened virus (Pasteur). Limitations.
Treatment: gastric and intestinal disinfection—copperas, mineral
acids, carbolic or salicylic acids, aromatics, quinine, naphthol, tar,
phenic acid subcutem.
_Definition._ A febrile hemorrhagic septicæmia of chickens and other
fowls (pigeons, ducks, geese, parrots, etc.) communicable to certain
rodents and other animals, and characterized by a short incubation,
rapid progress, great prostration, violent diarrhœa usually greenish,
and a high mortality (90 to 95 per cent.).
_History, Geographical distribution._ It is quoted as prevalent in
Lombardy in 1789, in East India in 1817, in France in 1825, and
generally in Europe and America in the last half century.
The _losses_ from the ravages of this disease are far greater than the
average value of the individual animal would lead one to suppose, but
with domestic fowls numbering 300,000,000 and a yearly egg crop
bordering on a billion dozens it may well be called enormous.
_Bacteriology._ Chicken cholera is caused by a very small ovoid
bacterium (B. Choleræ gallinaceæ) about 0.3 to 1.8μ long, as found in
the blood and tissues of the fowl. It has the general characters of the
groups which cause hemorrhagic septicæmia, thus: 1. It fixes, above all
at the poles, the ordinary anilin colors; 2. It is decolorized by the
methods of Gram and Wiegert (iodine solutions); 3. It grows on gelatine
without liquefying it; 4. It produces acute septicemic lesions; 5. It
tends to polymorphism when grown under different conditions. In the
peritoneum of the guinea pig it forms cocco-bacilli tending in acute and
violent cases to diplococci. Fed to rabbits it appears in the fæces as a
minute bacillus. Even the mode of staining causes a difference in
appearance. Fixed in alcohol-ether, and then stained in Ziehl’s phenated
preparation, coloring is polar, and the central area clear. If in place
of Ziehl’s fluid, hot fuchsin solution is used warm for ½ a minute,
bacillus or cocco-bacillus is shown (Lignieres). It is nonmotile, though
some observers have been misled by Brownian movements. There are no
flagella. In old bouillon cultures short chain forms are met with. No
spores are formed.
From fresh cultures, in flask or in animals, the bacterium grows readily
in alkaline culture media. In _bouillon_ a turbidity ensues, and after
some days pellicles form on the surface and walls, and the liquid slowly
clears. The addition of a little blood serum, sugar or glycerine
encreases and hastens the growth, while acid retards or prevents. This
is common also to other septicemic germs. In _gelatine_ growth is tardy,
but in two or three days there are whitish glistening colonies, becoming
opaque later, and appearing granular if slightly magnified. In punctures
minute colonies form along the line of culture and one at the surface,
at first translucent; later opaque. On _agar_ the colonies grow faster
with similar appearance. On _gelose_ at 37° C. the colonies are blueish
and iridescent, at first, and later opaque. If the germ has been
repeatedly passed through the Guinea pig, they are more translucent. On
_potato_ with alkaline surface, there is a delicate grayish yellow
growth after 48 hours; if acid, growth ceases. In _milk_ there is no
coagulation nor acidification for four weeks; then it becomes slowly
clear and opalescent. With _sugars_ it is not gas producing. With
dextrose it forms an acid solution; with saccharose or lactose an
alkaline one. Cultures in peptone gave a strong _indol_ reaction (V. A.
Moore). Lignieres found no indol in cultures in pancreatic bouillon.
The bacterium perishes when heated to 58° C. for fifteen minutes. It
dies in carbolic acid solution (1:100) in five minutes; in sulphuric
acid solution (0.25:100) in ten minutes; in lime water in ten minutes;
and in sulphur fumes in three hours. Easily destroyed by disinfectants,
it remains potent for months in flasks or buildings that are not
subjected to disinfection. It is not killed by drying (T. Smith and V.
A. Moore) nor by zero temperature maintained for seventeen hours.
The cultures, especially those made in agar have a very characteristic
odor.
_Accessory Causes._ Birds sent to poultry shows will often contract the
disease and introduce it into the home flock on their return. It may
also be imported in newly purchased birds, or on eggs obtained for
hatching. It is even alleged that it has been propagated by feeding
healthy hens on the eggs of diseased ones. When chickens run at large it
passes easily from flock to flock in the immediate vicinity. The
infected manure is, however, the most common channel of infection.
Carried on the feet or bill this contaminates the food and drinking
water, and washed into streams and ponds, it finally in any case reaches
the alimentary canal of the susceptible bird. Or drying up and raised as
dust it is inhaled into the lungs. Or finally from any such source it
infects any open sore. As granivorous birds, wild and tame, suffer from
fowl cholera, it is often introduced by the wild, especially coming from
infected poultry yards. Predatory birds, like hawks and buzzards, but
the latter especially, are common bearers of infection. Rabbits, which
contract the affection so readily, transmit it equally with birds, but
man or beast, soiled by the manure will convey it. Insects are among the
most prolific bearers, hence, as noted by Salmon, the infection may fail
to overstep a close fence in winter, but is subject to no such
limitation during the fly season. In this respect chicken cholera agrees
with Asiatic cholera, typhoid fever and other affections in which the
virus abounds in the alvine discharges. The sale and transportation of
the guano from the infected poultry yard is a direct cause of new
outbreaks. Feeding on the carcasses or offal of the infected birds is a
further cause. It must not be forgotten that the microbe is largely
saprophytic, living indefinitely in the organic matter in soils, and
determining new outbreaks when brought in contact with susceptible
animals. Thus a period of immunity may be followed by infection when new
birds are brought in or when young and susceptible ones grow up.
_Susceptible Animals._ Fowl cholera is preëminently a disease of
chickens, but the microbe is successfully transferred to pigeons,
peafowl, pheasants, parrots, ducks, canaries, sparrows and other small
birds, also to Guinea pigs, rabbits, white and gray mice. Guinea pigs
have abscesses in the seats of inoculation (Pasteur); the same is
alleged of sheep and horses (Kitt), and man (Marchiafava, Celli).
Injection into a cow’s teat caused chronic catarrhal mammitis in which
the microbe persisted for a long while (Kitt). Like other members of the
group of microbes causing septicæmia hæmorrhagica, the pathogeny and
even the morphology are liable to material modification as grown in
different environment (genera). Some of the forms of cholera occurring
among domesticated birds and held to be distinct diseases may find in
this an explanation. Rabieaux claims that under favorable conditions it
has been transmitted to the frog.
_Incubation._ This varies from 18 to 48 hours, the usual being 24 hours.
_Symptoms._ In some _fulminant cases_ the animal is found dead a few
hours after apparently blooming health; it may even have died on the
nest or fallen dead from the roost. Cadeac speaks of transient symptoms
even in such cases—extreme dulness, prostration, somnolence, seclusion
in a cool, dark place, ruffling of feathers, sinking of the head between
the wings, drooping, trailing wings and tail, violet comb, gaping,
discharge of glairy mucus from the bill, convulsions and death. These
symptoms last from two to five hours.
In _acute_ but less fulminant forms there is loss of appetite,
depression, debility, apathy, erection of the feathers, sinking of the
head, swaying when made to walk, drooping wings and tail, sitting on the
breast, convulsive tremblings, discharge of filmy or frothy mucus by the
nose or mouth, vomiting, hyperthermia (108° to 111° F. ), sighing,
breathing, inflation of the crop, violet colored comb, wattles and
mucosæ, great thirst and diarrhœa, at first pultaceous and light yellow,
later glairy, green and fetid. The feathers round the anus become soaked
and matted with the discharge. Temperature becomes subnormal, the
patient falls and is unable to rise, and finally dies in a stupor or
convulsions, the illness having lasted 1 to 3 days.
_Milder cases_ occurring chiefly towards the end of an outbreak when the
less susceptible animals only are left, or when the microbe has become
less virulent, show a larger ratio of recoveries. These show a lack of
spirit and vigor, impaired appetite, diarrhœa, emaciation, dulness,
prostration, moping, ruffling of the plumes, dark discoloration of the
comb, and often swelling of one or more important joints (femoro-tibial,
etc.). These may burst and discharge a reddish pus, or simply form dark
or grayish swellings. These cases may drag along for a week or more and
finally die in marasmus. The minute bacillus is not obtainable from
these (Lignieres).
Cases inoculated in the pectoral muscles with only one or two microbes
usually have only a circumscribed slough, with loss of condition, and
after the elimination of the slough and the healing of the sore the bird
proves immune.
_Lesions._ The alimentary canal is the main seat of morbid changes. The
intestinal walls, and especially the mucosa, have points and patches of
blood extravasation, extensive areas of congestion with ramified
redness, exudation and thickening. The intestinal contents are watery,
frothy, browned or blackened by effused blood, and swarming with
ferments including the specific bacterium. The mucous surface is
brownish or blackish, and epithelial degeneration and desquamation with
abrasions are not uncommon especially on the summits of the duodenal
folds and villi. Croupous exudates and swelling or ulceration of the
follicles are met with. The lymph glands at the base of the cæcum are
often enlarged and congested. The crop is full of watery, pulpy, frothy
or slimy contents, and its mucosa and that of the pharynx may be deeply
congested.
Elsewhere the lesions suggest rather the action of destructive toxins
and the profound changes in the blood. Pericardium and endocardium are
usually studded with dark petechiæ, and congestion and even slight
exudation may be present. The spleen is enlarged, soft, and gorged with
blood. The liver is swollen, congested, extremely friable, and mottled,
grayish white from degenerations. The kidneys are dark red, and friable.
The lungs may show slight hyperæmia only, or a blood engorgement and
consolidation, and are then easily reduced to a dark red pulp.
Friedberger and Fröhner say that respiratory changes are most frequent
in land birds; and intestinal and cardiac in water fowl.
The blood is diffluent coagulating loosely if at all, of a brownish red
color, reddening slowly and imperfectly in contact with air, and like
the tissues contains an abundance of the characteristic bacterium
staining deeply at the poles and clear in the center.
In birds that survive a few days there are marked anæmia and emaciation,
and the muscular system is of a grayish red color, with fatty
degeneration. In acute and fulminant cases on the other hand the muscles
may be full and of the normal red color.
In arthritic cases the congestion and thickening of the soft tissues,
and the excess of synovia, are supplemented by destruction of the
articular cartilage and by areas of bone abrasion. In the more tardy
cases collections of caseous matter are found.
_Diagnosis._ This is based on the demonstrably highly contagious
character of the disease, its rapid spread in a flock, and from the
first to nearby adjoining flocks in summer, the short period of
incubation, the constancy and nature of the diarrhœa, the speedy and
great mortality, and the hemorrhagic lesions of comb, bowels, heart,
lungs, liver, kidneys, spleen, and serous membranes. The demonstration
of the bacterium in the blood and affected tissues is conclusive. Kitt
points out that inoculation of a pigeon kills the bird in 12 to 48
hours, with dry yellow exudate in patches of from ½ to ¾ inch in
diameter on the surface of the muscles, and yellow discoloration and
nodular induration beneath.
_Prognosis._ The mortality reaches 90 to 95 per cent. The negative
chemiotaxis exerted on the leucocytes by the microbe, precludes
defensive phagocytosis, and the progress of the deadly microbe is
comparatively unhindered. Toward the end of a severe outbreak, and in
certain mild epizoötics the recoveries are much greater.
_Prevention._ All birds bought or otherwise acquired and all birds
returning from shows should be quarantined for one week before being
allowed to mingle with the flock. In summer this should be conducted
inside fly screens. The manure should be burned, carefully secluded, or
treated with dilute sulphuric acid. Buzzards and vermin as possible
bearers of the infection should be excluded from poultry yards. So with
human beings, dogs, etc., coming from infected places. In an infected
flock the sick should be at once separated, killed and burned or treated
with sulphuric acid. All manure should be treated in the same way.
Buildings, yards and runs should be thoroughly cleaned and liberally
sprinkled with a dilute sulphuric acid (2:100). If the birds can be
divided up in small groups (say of 5) the appearance of the disease will
only endanger that group. In small flocks or with very valuable birds it
may even be well to take the body temperature morning and night and
separate at once any bird showing a rise. Any diseased or suspected
flock should be kept where its manure will not be washed into wells,
running streams or ponds to which other birds have access. In a locality
where the disease exists fowls should not be allowed to run at large. In
winter this is very effective; in summer owing to the danger from insect
bearers, it must be supplemented by the most scrupulous cleanliness of
poultry houses and yards, and by a liberal sprinkling with dilute
sulphuric acid, or other disinfectant, to be made especially abundant
and frequent on the manure. Nocard cuts short the disease by injections,
subcutem of a 5 per cent. solution of carbolic acid.
_Immunization._ With valuable birds it may be desirable to secure
immunization by non-fatal inoculations. Salmon secured this by first
estimating the number of microbes in an mm. of the blood, then diluting
until five drops would contain but one, or at most two of these
organisms, and injecting this amount into the pectoral muscles. A
sequestrum forms in the muscle and is gradually sloughed out, and the
cavity heals, with resulting immunity.
Pasteur produced a weakened virus by exposing the artificial bouillon
cultures to air for from three to ten months, the strength decreasing
with the length of exposure. The weaker form produces slight illness
only, from which recovery is prompt. A second and stronger virus is used
ten or twelve days later and produces a real immunity.
The drawbacks to these methods are: 1st; that fowls are of too little
value, to warrant inoculation in healthy flocks; 2d; that in infected
flocks, where it is employed, the more susceptible birds are usually
already contaminated, and a large proportion die in spite of it; and 3d;
that it becomes a means of planting the infection in new localities
(Kitt).
_Treatment._ The disease is so deadly that little can be hoped from
medicinal treatment. It has been directed mainly to gastric and
intestinal disinfection. Copperas and sulphuric or hydrochloric acid in
the drinking water ½ to 1 per cent. of each is at once prophylactic and
curative. Friedberger and Fröhner add fennel or peppermint, and give a
tablespoonful every hour to an affected chicken. Other agents
recommended are: carbolic acid (5:100) by the mouth or subcutem
(Nocard), salicylate of soda, quinia (Cadeac), tannic acid (2:100),
salol, naphthol, tar water, etc.