Grows in milk; Acidifies and clots Acidifies milk growing
acidifies, often milk in 8 to 10 days freely
coagulates it
Thermal death point Thermal death point Thermal death point
(moist) 58° C. in 10 (moist) 60° C. in 10 (moist) 56° C. in 10
minutes minutes minutes
Loses virulence rapidly
when dried
Dies in water in 18 to
20 days
Lives and even Lives and grows in
multiplies in rich fæces
soils, manure, etc.
Loses virulence slowly
in light and air
Pathogenic to swine,
pigeons, sparrows,
rabbits, white and
house mice, white
rats
Guinea pigs, field mice
and hens immune
=Hog Cholera.= =McFadyean’s.= =Swine Plague.=
Hen or pigeon has Hen or pigeon dies in
slough where 48 hours, after
inoculated, diarrhœa, drowsiness, drooping
ruffled plumage, wings, sunken head,
somnolence ruffled plumage,
liquid stools, soft
black comb and
wattles, prostration
Rabbits getting 0.1cc. Rabbits getting 0.5 to Rabbits getting 0.01cc.
virulent culture 1cc. culture subcutem culture subcutem die
subcutem die in 5 to had tumor like walnut in 16 to 20 hours,
7 days with enlarged but recovered with inflamed serosæ
spleen and necrotic and lung; Petechiæ
liver foci
Weaker culture kills in Weak cultures kill in 4
10 to 20 days with to 10 days, with
enlarged spleen, or inflamed serosæ and
recovery ensues suppuration
Guinea pigs die in 7 to Not pathogenic to Guinea pigs die in 1 to
12 days Guinea-pig 4 days
Swine inoculated Swine inoculated have
subcutem have often local lesions only,
local lesions and only exceptionally
bacilli, also in fatal
lymph glands, only
exceptionally fatal
Ingestion of virulent Ingestion of 30cc. by Ingestion of virulent
cultures by fasting pigs proved always cultures by pigs is
pig causes bowel fatal usually harmless
lesions and death
Intravenous inoculation Intravenous inoculation
in pig causes causes septicæmia and
septicæmic lesions death in 1 or 2 days
and death, or chronic
diseases and typical
bowel ulcers
Intrapulmonary
infection causes
pleuro-pneumonia
Swine erysipelas kills inoculated pigeon in 3 to 8 days, and rabbit in
4 to 8 days.
_Accessory Causes._ These are especially those conditions which favor
the transmission of the germ from animal to animal. They include the
reprehensible habit of allowing swine to run at large so that herd
mingles with herd; the freedom to wander along the lines of railroad by
which hogs are carried, and where the infected excretions fall on the
ground; the scattering of infected litter or manure from a car or boat;
the use of the same cars, boats or trucks for the conveyance of infected
and sound pigs in succession, without intermediate disinfection; the use
of the same loading banks, chutes, runways, yards, pens and feeding and
watering troughs by strange pigs from all sources in succession, without
constant disinfection; the purchase of stock swine at public markets;
the return of swine from public fairs and exhibitions; the feeding and
watering of pigs on the line of streams that have drained pig pens or
pastures higher up; the use for pigs of premises that have harbored
infected ones at an earlier (even distant) date; the supply of food or
litter from barns where pigs have recently died; the admission to the
pens or yards of butchers, dealers or others who are likely to carry
infection on their persons; the admission even of wagons, dogs or other
animals, including birds, tame and wild, which are liable to carry
infection. Of all birds the buzzard is the most to be shunned as having
presumably just come from infected carrion, but barnyard fowl and small
birds that feed from the same trough with the pig are to be feared as
well. The same remark applies to rats and mice, squirrels, skunks,
woodchucks and rabbits which may easily carry the infection on their
paws. If the infection is near, flies and other insects, in the warm
season, will convey it for some distance from herd to herd. A common
cause is the feeding of swine about abattoirs where they devour the
offal and waste in a raw condition. Another is the feeding of boarding
house, hotel or other kitchen slops, raw, or without the most exhaustive
precautions in the way of cooking. Many outbreaks can be traced in this
way to the consumption by the animals of the products of infected swine.
Some indeed are fostered by the utter neglect of the parties in charge
of an infected herd, in leaving the infected carcasses exposed so that
they are eaten by wandering hogs, or portions are carried away by
buzzards, carrion crows, dogs and other animals. In some cases a strong
wind will carry the infection on dust, straw or other light object into
sound herds at a distance. The introduction into a hitherto healthy herd
of an apparently sound pig may be the occasion of a deadly outbreak. The
strange new pig may have already had the disease, and in a condition of
immunity, may without hurt to itself, carry the germ which becomes so
fatal to the susceptible.
This susceptibility is one of the most important factors. It may be
inherent in a given family or strain of blood. It may be enhanced by a
constitutional weakness, engendered by too close breeding, by breeding
from the young and immature, or from the old and worn out. It may be
favored by a general debility from starvation, faulty or injudicious
feeding, as exclusive feeding on corn (maize), an unbalanced ration,
feeding cotton seed, irregular feeding, etc. It may result from
parasitism, as round worms in the lungs, bowels, muscles, fat, kidneys
or liver, from trichinosis, from cysticerci, echinococci, or from
distomatosis. These not only lessen the force of constitutional and
phagocytic resistance, but they also in many cases open the way for the
entrance of the microbe by the wounds which they inflict. Perhaps
nothing operates more effectively in this way than the attacks of other
pathogenic microbes. The treatment of the domestic hog is often such
that it would almost appear as if it were designed to destroy health and
vitality. He is used to clear up the soiled and spoiled provender which
has been rejected by other animals. Decayed vegetables and flesh of all
kinds, which is no longer fit for other use, is supposed to be good for
him and is furnished raw. Worse still, this is conveyed in barrels that
are never washed, but are sent for each new supply reeking with
abominations which render them a nuisance on the highway. It is left
standing till wanted in these barrels, or in still larger receptacles,
which are never emptied nor cleaned, but are allowed in the hottest
weather, to continue a hotbed of the foulest fermentations. On a smaller
scale the kitchen swill barrel becomes a similar centre of
decomposition. Even at the creamery and cheese factory the surplus or
waste products often remain in a common tank breeding larvæ, toxins and
ptomaines, before they are fed to the hogs. In the hog pen, or yard,
corn in the ear is thrown on the ground, already filthy with the solid
and liquid excretions and is eaten with the rotting, if not infecting,
filth in which it has been rolled. From grubbing in this filth with his
snout, the pig plunges the latter in the liquid food in his trough and
too often he gets his feet into the food as well, and further charges it
with the injurious ferments. Again the kitchen swill is liable to
contain various inorganic poisons and notably the carbonates and
bicarbonates of potash and soda which are used to excess in the form of
_powdered soaps_ and, as shown by experiment, are deadly poisons to
pigs.
The gastro-intestinal disorders caused by these poisons; (it may be
botulism from stale or decomposing flesh, fish or fowl, the poisoning by
mouldy bread or musty grain, or meal, or by the toxins of the many and
varied saprophytic fermentations), often prove as deadly as outbreaks of
genuine hog cholera, and are habitually mistaken for them. They do not,
however, as a rule extend beyond the particular herd which has been
exposed to the faulty management, and introduce no risk of a general
spreading infection. The careless owner suffers and adjacent herds
escape, unless exposed to similar causes. But if the hog cholera germ is
present these pave the way for its destructive advance and tend to
enhance the mortality. It may even be that the combination of the two
factors is a condition of the eruption of a severe attack. The faulty
feeding or food or poison by itself could be resisted, and the
comparatively non-virulent hog cholera bacillus might have been
resisted, but with the weakened system and digestive apparatus, the
microbe finds a specially inviting field in which it can multiply
destructively, and where it can gather a virulence which will enable it
to invade and sweep away herd after herd in a deadly epizoötic.
I may add, as a prominent factor in the great modern extensions of hog
cholera, the habitual aggregation of swine in large herds. This with the
rapid steam transit of modern times, and the great aggregations of hogs
in one common market, probably contributes more than anything else to
the extraordinary diffusion of the infection. By accident, purchase or
otherwise, a large herd becomes infected, and the owner, knowing that
delay is ruin, at once ships the apparently healthy animals to market;
these infect anything they or their excretions come in contact with; if
sold in smaller lots they carry infection into every locality where they
go, and along the route; if sold for slaughter, they still diffuse
infection through the herds that receive their butcher and kitchen
trimmings.
Finally other domestic animals may bring in an infection which becomes
manifested by symptoms similar to those of hog cholera, and which if
really different, yet serves to pave the way for such an outbreak.
Galtier’s remarkable experience with a _pneumo-enteritis_ in sheep,
introduced into five separate flocks by infected pigs from the same
market, is significant in this respect. It is further significant that
the hog cholera bacillus is a very protean microbe. Th. Smith, to whom
we owe more than to any one else the identification of the germ, gives
seven varieties, which showed well-marked distinctions in their
morphology, in their modes of growth on culture media, in the amount of
gas they respectively produced in a glucose bouillon, or in their
pathogenesis for rabbits. One of these modified germs which has largely
parted with its virulence for pigs and some other animals, may under
specially favorable conditions, resume its former potency and proceed on
a new career of infection.
_Lesions in the Acute or Septicæmic Form._ The skin and subcutaneous fat
are the seats of diffuse blotches or spots of a deep red varying from
dark purple to light red, confined it may be to the inner sides of the
arms and thighs the belly, the ears, eyelids, and muzzle, or it may be
all but uniformly diffused over the body. When pressed so as to expel
the blood, the greater part of the surface may be momentarily whitened,
but red points remain representing the minute extravasations. Under the
microscope the red points show tortuous and enlarged capillaries with
here and there a rupture and minute clot. The visible mucosæ may show
similar petechiæ, as may also the serosæ of the chest, cranium and
abdomen. In the latter blood extravasations are liable to be more
extensive. The spleen and lymph glands (particularly those of the bowels
and omentum, the sublumbar and subdorsal regions) are usually enlarged,
gorged with blood and softened. Many of the lymph glands may escape, and
in others the congestion is largely confined to the cortical portion.
The lungs may show petechiæ and even extensive hæmorrhages into their
substance. The kidneys may show petechiæ in the glomeruli, the medullary
substance, the papillæ or the pelvic mucosa, or there may be larger
circumscribed hæmorrhages.
The stomach in its greater curvature especially is usually deeply
congested and petechiated, with small submucous extravasations, and
these conditions are liable to be still more marked in the small
intestines and especially in the large, which may have a dark red or
port wine hue. Blood may be present in clots among the contents.
Necrotic ulcers are absent.
_Lesions in the Protracted and Chronic Forms._ The lesions of the skin
are usually less extensive than in the acute type, and may be almost
entirely absent. The lymph glands are enlarged and congested, though the
discoloration may be largely confined to the cortical layer. The spleen
is as a rule normal in size. The liver is firm, but it may show
softening of the secreting acini and encrease of the fibrous framework.
Petechiæ or circumscribed hæmorrhages may or may not be present on or
under the serosæ or in the tissues.
The characteristic lesions belong to the gastric-intestinal organs.
Congestions and ulcers may be found on the gastric mucosa, on that of
the small intestine, and rectum, but they are above all common on the
ileocæcal valve, cæcum and first half of the colon. In the earlier
stages of these lesions the mucosa and submucosa are the seat of a
congestion and exudation, but later the round button-like ulcer usually
stands out prominently with its necrotic centre dirty white, brown or
black, and composed of superposed layers, the whole resting on a
congested and thickened submucosa. This contains small round and giant
cells and may show considerable encrease in connective tissue. The
ulcers may be seated on the agminated or solitary glands but do not show
the same predilection for these parts which is seen in typhoid fever.
_Incubation._ This varies according to the dose and susceptibility from
two or three to as many as thirty days. With the short incubation the
disease tends to assume its most acute and deadly type, while the
prolonged incubation bespeaks a milder form. During ordinary outbreaks
from six to fourteen days represent the average interval between
exposure and the onset of active symptoms. During the extreme heats of
summer and the excessive cold of midwinter in our northern states
incubation tends to be shortened.
_Symptoms in Fulminant Type._ In violent outbreaks some pigs are found
dead without observed preliminary symptoms, and have been set down as
fulminant examples of the disease. When these occur during very hot
weather, in open yards or fields, there is reason to believe that
insolation, acting on a system rendered specially susceptible by the
toxic fever, has much to do with the early death. Though seldom observed
during life, it has been said that such cases, show extreme dulness,
prostration, stupor, weakness, unsteady gait, thirst, hyperthermia,
persistent recumbency, and at times red blotching of the skin and even
convulsions.
_Symptoms in Acute Type._ In contrast with erysipelas these may advance
slowly and insidiously, there is a lack of the customary life and
vivacity, the tail droops, appetite is impaired, the pig creeps under
the litter and lies there, preferably on its belly, a great part of its
time, there may even be tremors suggestive of slight chill, when moved
it shows weakness, may stagger, or it may have difficulty in rising on
its hind limbs and there is encreased thirst and heat of the skin. Even
in the absence of shivering or chill, the skin is usually tender to the
touch, calling out plaintive grunting or squealing, and the same is
often true of manipulation of the belly. The temperature is raised, yet
this must be compared with the previous temperature under the conditions
in which the pig has been kept. That may have been anywhere from 100° F.
in a confined, cold, draughty pen, to 104° F. in a warm, dry pen and
with plenty of exercise. In hog cholera it may rise 1° to 3°. The
patient is breathless under exertion, the circulation is accelerated and
the mucosæ congested.
Sooner or later, (usually by the second or third day) the skin shows an
erythematous blush, especially on the ears, breast, belly and inner
sides of the thighs and forearms, in greater part effaceable by pressure
but promptly reappearing and complicated by darker spots of
extravasation which retain their color under pressure. The blush may
appear in spots of ⅒ to ⅓ inch in diameter, or it may cover the region,
or indeed the whole body uniformly. At first of a brighter red it tends
to pass in succession through the different shades of purple and violet.
Appetite becomes more and more impaired, and in exceptional cases
vomiting may occur, but often the pig will drink liquid food to the
last. A marked symptom is the enlargement of the inguinal lymph glands,
which may even be tender. An early symptom is watering of the eyes, and
later a muco-purulent exudate may form, and drying, gum the lids
together. An abundant exudate appears on the skin as the disease
advances, most abundantly about the eyelids, roots of the ears, axillæ
and groins, but often covering the whole body, forming a foul greasy
inunction, and later a black scaly covering.
The bowels may be costive at first, with fæces, firm, moulded, and
covered with mucous, and this may continue to the end. In most cases,
however, about the second or third day they become soft, pultaceous and
finally liquid, profuse, fœtid, and mixed with abundance of mucous or
even blood. The color varies, they may be whitish, yellowish (on maize
diet), red, or black (on swill).
Petechiæ usually form on the mucosæ and small sloughs and ulcers may be
found on the lips, tongue or elsewhere on the buccal mucosa.
A cough may be present but is by no means a marked symptom.
Emaciation advances with great rapidity, the patient arches the back,
tucks up the abdomen, moves weakly and unsteadily or is unable to rise,
and dies in one or several weeks, it may be quietly or in a state of
coma, but usually without convulsions.
_Symptoms in Subacute and Chronic Forms._ In this type the disease may
be obscure, and even overlooked, so that infected animals carry the
microörganism into fresh herds, without rousing a suspicion as to its
true source. In other cases, after a slow and progressive development,
it takes on such a distinct pathognomonic character that its diagnosis
becomes more easy.
In the slightest cases there may be only a capricious or irregular
appetite, drooping tail, enlarged inguinal glands, and a progressive
emaciation, with loss of life and strength and occasional irregularity
of the bowels. The greasy exudation on the skin and black scaly
encrustation is not uncommon. Such patients usually survive but they are
liable to prove unthrifty and unprofitable.
In other cases the pig becomes dull and listless, leaves its fellows,
creeps and lies much under the litter, has impaired or irregular
appetite, some costiveness followed by a fœtid diarrhœa, abdominal
tenderness, enlarged inguinal glands, progressive emaciation, arched
loins, hollow flanks, skin exudation, and oftentimes in the end
erythematous eruption with petechiæ and black scaly exudate on the skin.
It is in these protracted cases especially that the formation and
detachment of the necrotic intestinal sloughs take place and these may
pass in the fæces as flattened rounded masses or more extensive plaques.
Necrotic ulcers are also liable to show on the buccal mucous membrane or
skin. The patient may finally die of colliquative diarrhœa, of
exhaustion and marasmus, in a state of coma as in the more acute cases.
The mortality may be high and the survivors are liable to prove
unthrifty and unprofitable.
_Diagnosis._ With a group of plagues in swine bearing a strong family
resemblance, and maintained by microörganisms, which, though maintaining
distinct characters, yet show so much in common that it seems not
impossible that they may have been originally derived from a common
ancestor, and in face of the not infrequent complication of two of these
microbes in one patient, it becomes a task of great difficulty to
diagnose at once the particular outbreak that is met with in the field.
In some outbreaks, however, the differential features are clear enough
to allow the veterinarian to pronounce at once on the true nature of the
disease. In others he must withhold his diagnosis until he can put it to
the test of microscopic examination, bacteriological culture, the Widal
test, or inoculation.
_Hog Cholera_ may be decided upon, when upon wholesome food, in healthy
environment, without any change of food, and in six to fourteen days
after the introduction of pigs from outside, or the arrival of strange
pigs in the near vicinity, or higher up on the watershed, sickness
appears tardily, taking one or two daily, with or without a sudden
hyperthermia, petechiæ on nose, eyes, belly, axilla, or groin, a general
soreness of the skin and abdomen, stiffness or weakness, hiding much
under the litter, enlargement of the lymph glands, costiveness with dark
red rectum and glazed dung, followed by a profuse, watery, fœtid,
bloody, black or yellow diarrhœa, and death mostly after one or two
weeks or more. The absence of cough, and the presence of ulcers bearing
necrotic sloughs on the lips, mouth or skin, and above all the presence
of the button-like necrotic ulcers on the mucosæ of the cæcum, colon or
ileum may be accepted as conclusive evidence on this point. So also its
prompt fatality to rodents, but not to pigeons.
Swine erysipelas has a much shorter incubation, more rapid and violent
onset, deeper, darker congestion of visible mucosæ, more extensive
petechiæ of skin, mucosæ, serosæ, and tissues generally, a comparative
absence of inflammatory and necrotic lesions of bowels, a very early and
high mortality in swine, rabbits and pigeons, and a harmlessness toward
the inoculated Guinea pig.
_Swine plague_ also shows a shorter incubation, a speedy elevation of
temperature, more mucous congestion, less indication of abdominal
tenderness or of diarrhœa, more cough, dyspnœa, wheezing and objective
symptoms of pulmonary consolidation, less congestion or engorgement of
the spleen, or ulceration of the bowels, and finally is very much more
fatal to pigeons, and spares neither rabbits nor Guinea pigs.
_Widal test._ The cessation of movements and the agglutination of the
bacilli of hog cholera, noted by Dawson, is a valuable test, but as in
the case of typhoid fever in man is not to be implicitly relied on in
all cases. Some of the forms of bacillus coli commune and other allied
microbes act in a similar way. It necessitates the maintenance of fresh
(24 hours) active, artificial, agar cultures of the hog cholera bacillus
and is thus virtually reserved for the bacteriological laboratory. A
drop of blood is drawn from the suspected pig smeared very thinly on the
cover glass and about 10 times the amount of sterile water added. Then
the smallest possible addition of the agar culture of the bacillus is
made. Immediately, or in ½ hour the bacilli cease their active motility
and mass together in clumps in which they can be seen individually clear
and distinct but absolutely still and crossing each other in all
directions forming a kind of network. A few isolated bacilli remaining
in the intervals between the clumps and even showing a slight motility
are not to be considered as invalidating the reaction.
The table on the next page will serve to place in contrast the
differential phenomena of the diseases caused by bacilli of hog cholera,
swine plague and swine erysipelas in uncomplicated infections.
_Prevention._ As in all other contagious diseases, effective preventive
measures imply the destruction of the pathogenic germ and all sanitary
measures should aim at the early and final extinction of this organism
and its subsequent exclusion from the country. This, however, entails an
outlay and governmental control which it seems idle to expect in the
very near future so that palliative measures, and those looking toward
success over limited areas must still be resorted to. It should be here
distinctly stated, however, that the extinction of a plague, though
often the most expensive at the start, is in the end by far the most
economical resort.
_Removal of accessory causes._ The _health_ and _vigor_ of the animal
exposed is not without its influence in case of attempted invasion by a
virus of diminished potency.