Synonyms. Definition. Historic notes. Resemblance to black quarter.
Bacteriology; saprophytic cocco-bacillus, nonmotile, ærobic, related
to microbe of swine plague, chicken cholera, and rabbit septicæmia.
Pathogenic to deer, buffalo, cattle, horses, swine, rabbits, rats,
mice, goats, and sheep. Variability. Vitality: great in soil, dies in
6 to 20 days when dried, and quickly in antiseptics, resistant to
heat. Accessory causes: rise of soil water in winter or in spring,
drying of marshes in summer, wet, rich, swampy, mucky soils; youth,
gregariousness, carnivorous habit, insects, vermin, wild animals and
birds, epizoa, entozoa, wire fences, wounds of all kinds, hard, woody
provender; inoculations in wounds the most fatal. Symptoms:
superficial with hyperthermia, functional disorder; muscular tremors;
violet mucosæ; segregation; swelling in intermaxillary space, tongue,
throat, neck, dewlap, or elsewhere, not pitting on pressure. Petechiæ.
Death in six hours to four days; thoracic form kills in four to eight
days; abdominal form with colics, and bloody often frothy fœtid fæces.
Chronic forms usually pulmonary. Lesions: straw-colored exudations
subcutem or intramuscular; blood extravasations; in lungs resembles
lung plague; on bowels blood effusions, and exudates; softened,
blood-stained lymph glands. Spleen usually normal in size. Blood
black. Petechiæ extensive. Chronic lesions. Bacillus in exudate, blood
and bronchial mucus. Diagnosis: from anthrax, black quarter, lung
plague, rinderpest, and malignant œdema. Mortality 50 to 80 per cent.
Prevention: isolate and kill affected; destroy or disinfect carcasses
and infected things and places, feeding and drinking troughs and
manure. Close and drain infected fields. Immunization, by three
inoculations with cultures made at a high temperature (86° to 90°) in
free air; or with virus that has been grown in pigeon. In case of
deer, drive a few days into a noninfecting enclosure, and then on to a
sound range. Treatment.
_Synonyms._ Wild—und Rinderseuche (Bollinger), Buffalo Disease, Barbone
(Oreste and Armanni), Cornstalk Disease (Billings, Moore), Sporadic
Pneumonia (Smith), Pneumo-enteritis (Galtier.)
_Definition._ An acute bacteridian disease of domestic and wild
herbivora and swine, characterized by sudden onset, rapid and fatal
course, marked hyperthermia, accelerated breathing and pulse, and
extensive gelatinoid or sanguineous extravasation in the intermaxillary
space, tongue, skin, subcutaneous or intermuscular connective tissue,
lungs, pleura, pericardium or intestine.
_Historic Notes._ It is almost certain that in earlier times this
affection was often mistaken for gloss-anthrax, blackquarter, or even
lung plague. Metaxa, in 1816 in Italy, manifestly describes it. Oreste
and Armanni, in 1882 and 1887, traced Italian cases to the microbe. In
1854 it destroyed many cattle and deer in England (Veterinarian). In
1878 Bollinger records its great fatality among the deer, wild boars,
cattle and horses in and near the royal parks at Munich, and for a
number of years after in Bavaria. Friedberger records its presence in
Schlüchtern, Prussia, in 1885–6, Condamine in Cochin China in 1868, and
Guillbeau and Hess in Switzerland in 1894. In America, what appears to
be the same affection is noted as corn-fodder disease in Nebraska
(Billings), as Wildseuche in Tennessee (Norgaard), and as hæmorrhagica
septicæmia in Minnesota (Reynolds). I have repeatedly met with the
affection in New York in cows arriving from the west, and in the
indigenous cattle on wet, mucky, undrained land in spring, about the
period of the melting snows.
_Bacteriology._ The essential cause of the disease is a saprophytic
cocco-bacillus, ovoid, with rounded ends, about 1μ long by 0.3 to 0.6μ
broad, but showing involution forms and a variable size. It is nonmotile
(Kitt claims motility), ærobic (facultative anærobic), takes a polar
stain with clear centre in aniline colors, bleaches in Gram’s (1)
solution, shows neither spores nor flagella, grows readily in bouillon,
on gelatine, (a bluish transparent layer without liquefying), serum at
98° F., milk (without acidifying or coagulating), and alkaline potato
(not on the acid). The cultures have a peculiar odor and yield no indol.
The microbe shows a very close relationship with those of swine plague,
chicken cholera and rabbit septicæmia, but it sometimes differs in
showing little or no pathogenesis for the Guinea-pig.
_Animals susceptible._ It is pathogenic to deer, buffalo, cattle,
horses, swine, rabbits, rats, mice, and to a lesser extent to goats and
sheep.
The _pathogenesis_ varies with the immediate source of the microbe. When
obtained from cattle a drop of blood kills rabbits in twelve to twenty
hours, with intense hæmorrhagic laryngitis and tracheitis. Guinea pigs
die in forty to eighty hours. When obtained from the buffalo it killed
horse, ox, or pig in twenty to forty-eight hours. That obtained from
barbone (buffalo) appears to be more potent than that from septicæmia
hæmorrhagica (cattle).
_Vitality of the microbe._ Simple drying destroys virulence in six to
twenty-two days. Virulence is retained for nine days in putrid flesh. It
is preserved, and the microbe multiplies in soil or water containing
organic matter and nitrates. It is easily destroyed by ordinary
antiseptics 1:5000 of mercuric chloride destroying its vitality in one
minute (Hueppe). On the contrary it shows a great resistance to changes
of temperature. It grows in the soil at 55° to 60° F. (Hueppe), and in
old cultures may resist for an hour a temperature of 175° to 195°
(Oreste and Armanni).
_Accessory Causes._ These are such conditions as favor transmission of,
or receptivity to the microbe. In Southern France the disease is most
common in the winter months, probably because the soil water rises then;
on the Roman marshes on the other hand, it prevails especially from May
to October, when the water is lowest and most impure. In New York I have
seen it especially at the breaking up of the winter frosts, when the
water, pent up in the rich organic soils, is suddenly released. It is
pre-eminently the disease of wet soils, rich in the debris of
decomposing organic matter, of the rich prairies and bottom lands of the
Mississippi Valley, of springy, swampy or mucky soils elsewhere, of the
Pontine marshes at Rome, of the Delta of the Nile, of the rich virgin
soils in Asia. Youth has the greatest receptivity, the older animals
having probably acquired immunity through an earlier attack. The animals
that live in herds infect each other by contact, fighting, licking,
etc., others are affected by eating the vegetation or drinking the water
soiled by the diseased, wild boars by eating the carcasses, and all
animals by the attacks of biting or blood-sucking insects which have
just come from the diseased. It is claimed that the infection is carried
by men and animals, and by the sale in villages of the flesh of infected
animals. Dogs, wolves, foxes, and other carnivorous animals and birds
will also carry the infection for long distances. Finally, it will
travel to a greater or lesser distance with running water.
The entrance of the microbe by wounds must always be counted on, and
explains the casual inoculations, by bites of dogs, insects, worms, by
barbed wire fences, by wounds with horns, tusks, or feet, by nails,
etc., and in winter by hard, woody aliment scratching the lips, mouth,
fauces or pharynx. Shedding of teeth, diseased teeth or gums, and
everything that causes abrasion of the alimentary mucosa must be
admitted into the list of causes. Infected traumatisms of any kind, like
intratracheal and intravenous inoculations usually prove fatal, while
infection by ingestion is not necessarily so. The pathogenic potency
appears to be impaired in the stomach or intestines.
_Symptoms._ These vary widely according to the subject, the seat of
infection and the violence of the attack. They may be classed under
three principal heads: _superficial_, _thoracic_ and _intestinal_, and
in addition into _acute_ and _chronic_ cases.
In the _superficial_, _external_ or _cutaneous form_ there is usually a
sudden onset with high fever (104° to 107° F.), accelerated pulse, (70
to 90), and breathing (24 to 50), anorexia, suspended rumination,
muscular tremors or shivering, staring coat, dry, hot muzzle, burning of
ears, horns and hoofs, suppression of milk, and more or less stringy
salivation. The visible mucosæ are of a deep red or violet tinge, and
the patient will often remain apart by himself when the herd has moved
elsewhere. Soon there develops a tense, hard, hot, painful swelling of
the intermaxillary space, tongue, throat, neck, dewlap or elsewhere,
amounting to perhaps six inches in thickness, extremely resistant and
not usually indented on pressure with the finger. The breathing becomes
stertorous and deglutition difficult or impossible. The mouth is hot and
filled with tenacious saliva, and the tongue may hang pendant while on
its borders and lower surface are projections of the mucosa swollen by
infiltration, yellowish and semi-transparent, or blood-stained. At other
points petechiæ are more or less abundant.
Death may take place from pharyngeal obstruction or closure, or as the
disease advances, there may be indications of implication of the
viscera, of the chest or abdomen: encreasingly difficult breathing, a
mucous or suffocative cough, colicy pains, tenesmus, and the passage of
moulded glazed fæces, of pseudo-membranous casts, or of profuse liquid
stools. The animal may move the hind feet uneasily, lie down and rise
alternately, may remain persistently recumbent until death, or he may
stand up until he falls to perish of asphyxia. Death may occur in six
hours, or may be delayed four days.
In the _thoracic form_ the extreme hyperthermia is complicated by early
lesions in the lungs, while the muscular or cutaneous ones are omitted
or deferred. So long as the lesions are confined to the chest, they are
betrayed by hurried and even oppressed breathing or dyspnœa, a frequent,
moist, suffocative cough, persistent standing to favor respiration, and
there are the percussion and auscultation indications of consolidated
lungs or hydrothorax. The mucosæ are usually of a darker red, than in
the external form, cyanotic indeed, and the peculiar asphyxial position,
with legs apart, head extended, dilated nostrils and open mouth may be
very significant. These symptoms are likely to be modified or
supplemented before death, by those caused by intestinal or renal
disorder. In the thoracic form in young animals death by suffocation may
occur in a few hours, but more commonly the disease progresses slowly
and a fatal result is not reached until the fourth day or even the
eighth. This form is common in the deer, and less so in cattle.
In the _intestinal_ or _abdominal form_ the usual sudden onset and high
fever, are complicated by inappetence, tympany, rumbling of the bowels,
uneasy movements of the hind feet, perhaps twisting of the tail, looking
at the flanks, and even lying down and rising. There is frequent,
violent straining with the passage of fæces at first glazed, later
streaked with blood, or mixed with pseudo-membranous casts, and very
soon soft, watery, frothy and fœtid. These are usually black or reddish
black from contained blood.
The urine may also be blood-stained.
Before death, complications on the lungs or skin will often come in to
assist in diagnosis.
In the _chronic_ and _subacute types_ the lesions are often concentrated
on the lungs, and there are a moderate fever cough, hurried breathing
under exertion, dulness on percussion over limited pulmonary areas,
blowing sounds, mucous râles, crepitations and more or less
muco-purulent expectoration. These phenomena are all the more
significant if complicated by digestive disorders, costiveness, fœtid
mucous diarrhœa, tympany, or by the eruption of the superficial
swellings.
_Lesions._ The swellings on or _under the skin_ or among the _muscles_
show extensive straw-colored exudations, colored at points with blood,
with enlargement, infiltration and staining of the adjacent lymph
glands. On the chest walls the sero-sanguineous exudate may extend from
the root of the lungs, through the intercostal spaces to the skin in the
breast, the axilla and behind. The tongue is often enormously swollen
and black, charged with extensive blood extravasations in addition to
the yellowish exudate. Along its sides and on its lower surface, the
mucosa stands out in projecting masses of yellowish infiltration, which
may show equally on the fauces, pharynx, larynx, trachea and bronchi.
In the _lungs_ the pleuræ and subpleural and interlobular tissue are
extensively infiltrated and thickened by a profuse yellowish serous or
sero-sanguineous exudate, so that the appearance may closely resemble
that of lung plague. The lung tissue is consolidated, hepatized and dark
red, with at some points emphysema. The pleural sac is usually filled by
a serous or bloody effusion (2 to 25 quarts) and there is often
extensive implication of the pericardium. The tracheo-bronchial mucosa
and bronchial glands show extensive infiltration and thickening.
In the _abdomen_ are found extensive infiltrations and blood
extravasations in the mucosa and submucosa of the stomachs and
intestines, softening and shedding of the epithelium, infiltrations of
the peritoneum, diaphragm, and sublumbar adipose tissue, and softening
and degeneration of the liver and kidneys. The intestinal gastric and
mesenteric glands are usually infiltrated, softened and blood-stained.
Engorgement of the spleen is exceptional.
The _blood_ is very black but not usually materially changed in
consistency nor coagulability. Petechiation of the different serosæ and
other tissues is a prominent feature.
In _chronic cases_ the lesions are mostly shown in the lungs and lymph
glands. The lungs show circumscribed lobular islets of congestion,
induration or caseation, offering a suggestion of tubercle, which is all
the more deceptive when cretifaction has set in. The caseous centres may
vary in size from a pea to a walnut, and some may have ruptured to form
a vomica discharging into a bronchium. Bronchia leading to affected
lobules are blocked with muco-purulent matter, yellowish, thick and
tenacious, and their mucosa is thickened and puckered. The enlarged
lymph glands are especially those of the bronchia, trachea, mediastinum,
bowels, mesentery and sublumbar region.
The bacillus is present in the exudate but is especially abundant in the
blood, and in the chronic cases in the bronchial mucous.
_Diagnosis._ From _anthrax_ (gloss-anthrax) this affection is easily
distinguished by the absence from the blood and exudates of the large,
square ended anthrax bacillus, by the absence of enlargement and blood
engorgement of the spleen, and of the softness and diffluence of the
blood clot which characterize anthrax. Swine which are with difficulty
inoculated with anthrax are very susceptible to hæmorrhagic septicæmia.
Sheep which are very receptive to anthrax are somewhat refractory to the
disease now in hand. Pigeons resist anthrax but readily contract
septicæmia hæmorrhagica.
From _black quarter_ it is readily distinguished by the absence of
emphysema and crepitation and of a secondary cooling in the external
swellings, by the presence of the germ in abundance in the blood, by its
smaller size, its bipolar staining, and its lack of motility and of
spores. Inoculation with black quarter bacillus kills the guinea pig,
but spares the pigeon.
From _lung plague_ it is distinguished by the suddenness of its attack
and rapidity of its progress to a fatal issue; by the usual coincidence
of skin and bowel lesions, while the lung plague affects the chest only;
by its communicability to pigs, sheep, pigeons, and even horses, which
are all immune from lung plague; and by the usual absence of lung
lesions of different ages, which are so characteristic of lung plague.
The abundance in the blood of the cocco-bacillus with bipolar staining
in hæmorrhagic septicæmia is characteristic. _Lung plague_ spreads
slowly to exposed cattle, but spares all other domestic animals.
From _Rinderpest_ it is differentiated by the history of its advent, by
the presence of the surface œdematous swellings, by the absence of the
whitish epithelial concretions on the mouth or vulva, and of the deep
dark portwine discolorations of the mucosæ of the mouth, rectum and
vulva, and by the fact of its inoculability on domestic animals
generally. Rinderpest spreads rapidly to all exposed ruminants, but
spares pigs, rabbits, Guinea pigs, horses and birds.
From _malignant œdema_ it differs in its inoculability on the surface in
place of subcutaneously only, in the presence of the cocco-bacillus in
the blood during life, whereas in malignant œdema the germ is confined
to the local lesion, in the absence of crepitation, which may be present
in the swelling of œdema, in the greater facility with which cultures
can be made of the septicæmic cocco-bacillus and in the absence of gas
production in such cultures. The malignant œdema comes from a single
accidental deep inoculation from almost any rich soil, and is not a
malady spreading widely and generally on given limited damp, rich lands
which have become infected. Finally the cocco-bacillus of septicæmia
hæmorrhagica is found singly in the blood or exudate, whereas the
microbes of malignant œdema may be found in form of sporeless filaments
intermingled with the bacilli.
_Mortality._ The hæmorrhagic septicæmia of cattle cuts off from 50 to 80
per cent. of the animals attacked.
_Prevention._ The first consideration is to isolate and kill all the
affected animals, to destroy the carcasses by burning or boiling and to
burn or disinfect all objects that may have become contaminated. The
buildings, yards, and fences, must be disinfected, and as the bacillus
is very resistant a solution of corrosive sublimate and sodium chloride,
a drachm of each to the gallon of water may be freely used after
thorough cleansing. Or a whitewash containing ¼ lb. chloride of lime to
each gallon may be substituted. Feeding and drinking troughs may be
burned. Manure may be freely treated with sulphuric acid. Infected
fields should be closed for years and if possible drained.
_Immunization_ of buffalo and sheep has been secured by making cultures
of the microbe in free air at 86° to 90° F. and inoculating the animals
with the weakened virus, on three successive occasions with intervals of
several days. It induces a transient fever, with no serious phenomena
(Oreste and Armanni). A second available method is to pass the virus
through the system of the pigeon and inoculate with the pigeon’s blood,
on three successive occasions, the animals to be protected. It is
manifestly impossible to put such immunizing methods in force on wild
deer, and for these probably the best course is to drive them from the
infected range, to an uninfected one, having retained them for a few
days interval in a confined area, to allow of any already infected
animals developing the disease. A similar avoidance of waters running
from the infected tract is imperative.
_Treatment_, has been unsuccessful. Friedberger failed with hypodermic
injection of carbolic acid, and internal administration of salicylic
acid. Gal gave subcutem 5 per cent. solution of creolin, and doses of 1½
oz. of the same agent by the mouth. Five buffaloes out of seventeen
recovered. Friedberger suggests deep incisions of the swellings so as to
admit the air, and treatment of the wounds with strong antiseptics.