country, especially in Colorado, Texas, and South Dakota, have increasingly
noted the occurrence of enzootics of "sore mouth" among the young animals
of their herds. Instead of healing, like the usual forms, of themselves,
these cases, if untreated, die. Careful study of some of them has resulted
in their identification with cases reported in 1877 by Dammann, from the
shore of the Baltic; in 1878 by Blazekowic, in Slavonia; in 1879 by
Vollers, in Holstein; in 1880 by Lenglen, in France; in 1881 by
Macgillivray, in England; and in 1884 by Lˆffler, who isolated and
described the microorganism which produces the disease. Bang obtained this
organism from the diphtheritic lesions of calves in 1890, and Kitt likewise
recovered the bacillus from similar lesions of the larynx and pharynx of
calves and pigs in 1893.
[Illustration: PLATE XLII. SECTION OF MUSCLE FROM A BLACKLEG SWELLING.
a. GAS BUBBLES.
b. CAVITIES DUE TO GAS FORMATION.]
[Illustration: PLATE XLIII. NECROTIC STOMATITIS (CALF DIPTHERIA).]
_Etiology._--The cause of necrotic stomatitis, as demonstrated by Lˆffler
and since confirmed by other investigators, is _Bacillus necrophorus_,
often spoken of as the bacillus of necrosis. This organism varies in form
from a coccoid rod to long, wavy filaments, which may reach a length of
100µ; the width varies from 0.75µ to 1µ. Hence it is described as
polymorphic. It does not stain by Gram, but takes the ordinary anilin dyes,
often presenting, especially the longer forms, a beaded appearance. A
characteristic of the organism, of great moment when we come to treatment,
is that it grows only in the absence of oxygen, from which fact it is
described as an obligate anÊrobe.
Very few organisms exhibit a wider range of pathogenesis. According to
clinical observation to the present time, _Bacillus necrophorus_ is
pathogenic for cattle, horses, hogs, sheep, reindeer, kangaroos, antelope,
and rabbits. Experimentally it has been proved pathogenic for rabbits and
white mice. The dog, cat, guinea pig, pigeon, and chicken appear to be
absolutely immune. It is not pathogenic for man.
The importance of this bacillus is far beyond even its relation to necrotic
stomatitis. Besides this disease it has been demonstrated as the causative
factor in foot rot, multiple liver abscesses, disseminated liver necrosis,
embolic necrosis of the lungs, necrosis of the heart, in cattle; gangrenous
pox of the teats, diphtheria of the uterus and vagina, in cows;
diphtheritic inflammation of the small intestine of calves. Among horses it
is the agent in the production of necrotic malanders, quittor, and
diphtheritic inflammation of the large intestine. In hogs it has caused
necrotic or diphtheritic processes in the mucous membrane of the mouth,
necrosis of the anterior wall of the nasal septum, and pulmonary and
intestinal necrosis, accompanying hog cholera. Abscesses of the liver,
gangrenous processes of the lips and nose, and gangrenous affections of the
hoof have all been caused in sheep by this organism.
_Pathology._--The principal lesions in necrotic stomatitis occur in the
mucous membrane of the mouth and pharynx. The alterations may extend to the
nasal cavities, the larynx, the trachea, the lung, the esophagus, the
intestines, and to the hoof. The oral surfaces affected are, in the order
of frequency, tongue, cheeks, hard palate, gums, lips, and pharynx. In the
majority of cases the primary infection seems to occur in the tongue. (Pl.
XLIII.)
Infection takes place by inoculation. Some abrasion or break in the
continuity of the mucous membrane of the mouth occurs. Very likely the
origin may be connected with the eruption of the first teeth after birth,
or, in animals somewhat older, the entrance of a sharp-pointed particle of
feed. Gaining an entrance at this point, the bacilli begin to multiply.
During their development they elaborate a toxin, or poisonous substance,
which causes the death, or necrosis, of the epithelial, or superficial,
layer of the mucous membrane and also of the white blood cells which have
sallied forth through the vessel walls to the defense of the tissues
against the bacillary attack. This destruction of the surface epithelium
seems to be the essential factor in the production of the caseous patch,
often called the false membrane. From the connective-tissue framework below
is poured forth an inflammatory exudate highly albuminous or rich in
fibrin-forming elements. When this exudate and the necrosed cellular
elements come in contact, the latter furnish a fibrin ferment which
transforms the exduate into a fibrinous mass. This process is known as
coagulation necrosis, and the resulting fibroid mass, containing in its
meshes the necrosed and degenerated epithelium and leucocytes, constitutes
the diphtheritic or false membrane. Did the process cease at this point it
would be properly called a diphtheritic inflammation, but it does not. A
caseating ferment is supplied by the bacilli, and this, acting upon the
fibroid patch, transforms it into a dry, finely granular, yellowish mass of
tissue detritus resembling cheese.
Frequently this caseous inflammation results in the formation of one or
more ulcers with thickened, slightly reddened borders, surmounted by
several layers of this necrosed tissue. The floor of the ulcer is formed by
a grayish-yellow, corroded surface, under which the tissue is transformed
into a dry, friable, or firm cheesy mass. In the tongue this may progress
to two fingers' thickness into the muscular portion; in the cheek it may
form an external opening, permitting fluids to escape from the mouth; upon
the palate it frequently reaches and includes the bone in its destructive
course; upon the gums it has produced necrosis of the tooth sockets,
causing loss of the teeth. In the advanced forms, caseous foci may be seen
in the lung and in the liver and necrotic patches observed on the mucous
membrane of the gastrointestinal tract.
_Symptoms._--Necrotic stomatitis is both a local and a systemic affection.
Primarily it is local. The local lesion is the caseo-necrotic patch or
ulcer developed as a result of the multiplication of the bacilli at the
point of inoculation. The general affection is an intoxication, or
poisoning, of the whole system produced by a soluble toxin elaborated by
the bacilli.
The stage of incubation is from three to five days. The first symptoms
noted are a disinclination to take nourishment, some drooling from the
mouth, and an examination of the mouth will show on some portion of its
mucous membrane a circumscribed area of infiltration and redness, possibly
an erosion. The latter gradually extends in size and depth, forming a
sharply circumscribed area of necrotic inflammation. It may measure
anywhere from the size of a 5-cent piece to that of a silver dollar or even
larger. It has the appearance of a corroded surface, under which the mucous
membrane or muscular tissue seems transformed into a dry, friable, or firm
cheesy mass. It is grayish yellow in color and is bordered by a zone of
thickened tissue slightly reddened and somewhat granulated. The necrotic
tissue is very adherent and can be only partially peeled off. It is
homogeneous, cheesy, and may extend two fingers' depth into the tissues
beneath. The general symptoms are languor, weakness, and slight fever. In
spite of plenty of good feed the calf is seen to be failing. It stops
sucking, or, if older, altogether refuses to eat. The temperature at this
time may be from 104∞ to 107∞ F. The slobber becomes profuse, swallowing
very difficult, opening of the mouth quite painful, and a most offensive
odor is exhaled. The tongue is swollen and its motion greatly impaired.
Sometimes the mouth is kept open, permitting the tumefied tongue to
protrude. One or more of the above symptoms direct the attention to the
mouth as the seat of disease; or, having noticed the debility and
disinclination to eat, an examination of the animal may show a lump under
the neck or swelling of the throat or head. The following extract from a
letter is characteristic:
I noticed my calves beginning to fail about the first week in December, but
could not account for it, as they were getting plenty of grain and hay. My
attention was first attracted by a swelling under the neck of one of the
calves. I cast the animal and found that it was feed that had collected and
the animal couldn't swallow it. I removed it, and in so doing noticed a
large ulcer on the tongue and a very offensive odor. This was the first
knowledge I had of anything being wrong with the calves' mouths. They may
have been sick for some time before this.
Out of a herd of 100 belonging to this man, 70 were affected, and the
letter emphasizes the insidious character of the onset.
The general affection at this time manifests itself by dejectedness,
extreme weakness, and emaciation, constant lying down, with stiffness and
marked difficulty in standing.
The disease frequently extends to the nasal cavities, producing a thin,
yellowish, or greenish-yellow, sticky discharge which adheres closely to
the borders of the nostrils. Their edges also show caseous patches similar
to those in the mouth. Sometimes the nasal passage is obstructed by great
masses of the necrosed exudate, thus causing extreme difficulty in
breathing. When the caseous process involves the larynx and trachea there
result cough, wheezing, and dyspnea, together with a yellowish mucopurulent
expectoration.
When life is prolonged three or four weeks, caseous foci may be established
in the lung, giving rise to all the signs of a bronchopneumonia. Many of
these cases are associated with a fibrinous pleurisy. The invasion of the
gastrointestinal tract is announced by diarrheal symptoms. This disease
principally attacks sucklings not more than 6 weeks of age, but calves 8
and 10 months old are frequently affected, and several cases in adult
cattle have been reported to this office.
In its very acute form many of the cases run their course in from five to
eight days. In these the local lesions are not strongly marked, and death
seems due to acute intoxication. In other enzootics the majority of the
affected animals live from three to five weeks. These are cases that
occasionally present the pulmonary and intestinal symptoms, and sometimes
develop also caseo-necrotic lesions in the liver.
Ordinarily cases show no tendency to spontaneous cure. Left to themselves
they die. On the contrary, if taken in hand early, the disease is readily
amenable to treatment. In the latter event the prospects of recovery are
excellent.
_Differential diagnosis._--Necrotic stomatitis may be differentiated from
foot-and-mouth disease by the fact that in the latter there is a rapid
infection of the entire herd, including the adult cattle, as well as the
infection of hogs and sheep. The characteristic lesion of foot-and-mouth
disease is the appearance of vesicles containing a serous fluid upon the
mucous membrane of the mouth and upon the udder, teats, and feet of the
affected animals. In necrotic stomatitis vesicles are never formed,
necrosis occurring from the beginning and followed by the formation of
yellowish, cheesy patches, principally found in the mouth. Mycotic
stomatitis occurs in only a few animals of the herd, chiefly the adult
cattle, and the lesions produced consist of an inflammation of the mouth
and lips and of the skin between the toes, followed in a few days by small
irregular ulcers in the mouth. This disease appears sporadically, usually
in the early fall after a dry summer, does not run a regular course, and
can not be inoculated.
_Prevention._--Prophylaxis should be carried out along three lines:
(1) Separation of the sick from the healthy animals.
(2) Close scrutiny and thorough disinfection once or twice daily for five
days of the mouths and nasal passages of those animals that have been
exposed.
(3) Complete disinfection of all stalls and sheds.
The disease appears to break out in winter and hold over to spring. It is
conceivable that exposure to cold might so disturb the normal circulation
of the oral tissues as to make the mucous membrane an excellent location
for the causative factor of the disease. There is another possibility,
however, which bears on the third line of prophylaxis. The so-called
diphtheritic inflammations of the vagina and uterus in cows are caused by
the same organism that induces necrotic stomatitis. A European writer has
recently pointed out the almost constant relation of such attacks to
previous occurrences of foul foot or foot rot in the same or other cattle
on the place.
In all likelihood, in such cases, the stalls and sheds are the harborers of
this germ. It is possible that many of these outbreaks have some relation
to preceding cases of the above-mentioned diseases and the greater use in
winter of the stalls and sheds, thus harboring the _Bacillus necrophorus._
_Treatment._--The treatment consists almost solely in careful and extensive
cleansing and disinfection of the mouth and other affected surfaces. The
mucous membrane of the mouth should be copiously irrigated with a 4 per
cent solution of boracic acid in warm water at least twice daily. As
exposure to oxygen kills the bacilli, one need have no fear about
disturbing or tearing off the caseous patches or necrotic tissue during
irrigation. The irrigation of the sores should then be followed by the
application with a brush or rag on a stick of a paste made with 1 part of
salicylic acid and 10 parts of water, or the affected areas may be painted
with Lugol's solution of iodin (iodin, 1; potassium iodid, 5; water, 200).
Frequent injections of 1 per cent carbolic-acid solution into the mouth
make an excellent treatment. The internal administration of 2 grams of
salicylic acid and 3 grams of chlorate of potassium three times a day has
also proved to be very beneficial when accompanied with local antiseptic
treatment.
MALIGNANT CATARRH.
Malignant catarrh, or infectious catarrhal fever, is an acute infectious
disease of cattle preeminently involving the respiratory and digestive
tracts, although the sinuses of the head, the eyes, and the urinary and
sexual organs are very frequently affected. It is relatively rare in this
country, being more common on the continent of Europe. Outbreaks have
occurred, however, in Minnesota, New York, and New Jersey. So far the
causal agent of the disease has never been isolated, and inoculation
experiments with the view of artificially reproducing the disease have
proved negative in every case. In spite of the foregoing statements the
consensus of opinion of eminent investigators points to malignant catarrh
as being of specific origin; that is, due to some form of microorganism the
contagious character of which is poorly developed. This accounts for the
slow transmissibility of the disease from one animal to another. In fact,
malignant catarrh is a type of that class of affections scientifically
known as miasmatic diseases; that is, they remain stationary in stables
with damp floors, low ceilings, poor ventilation, and bad sanitary
conditions in general. Such places furnish a favorable seat of propagation
for the infective material, and it will remain active for a long time,
causing the loss of a few animals each year. One European veterinarian
reports an instance in which the disease remained for 25 years on the same
farm, attacking in all 225 animals, with a mortality of about 98 per cent.
The disease is most common in late winter and early spring, at all
altitudes, and has a special preference for young, well-nourished cattle,
although older animals are not immune. The time between the entrance of the
infective principle into the body of the animal and the appearance of the
first symptoms is relatively very long, averaging, according to German
investigators, from 20 to 30 days. Fortunately, it is not a disease which
spreads to any great extent or which causes severe losses, and hence
legislative enactments do not seem to be necessary for its restriction.
_Symptoms._--These are extremely variable according to the point of
localization of the lesions. It is usually ushered in with a chill,
followed by a marked rise of temperature (104∞ to 107∞ F.). The head
droops, the skin is hot and dry, and the coat staring. Quivering of the
muscles in various parts of the body is frequently observed. Marked
dullness of the animal, passing, according to some observers, into an
almost stupefied condition later on, is quite common. The secretion of milk
stops in the beginning of the disease, and loss of flesh, invariably
associated with the disease, is extremely marked and rapid. The lesions of
the eyes may best be likened to moon blindness (periodic ophthalmia) in
horses.
There is first an abundant secretion of tears, which run down the face. The
lids are swollen and inflamed, and indeed this may be so marked as to cause
involuntary eversion, exposing the reddened conjunctiva to view. Sunlight
is painful, as is shown by the fact that the animal keeps the eyes
continuously closed. This inflammation may extend to the cornea, causing it
to assume a slightly clouded appearance in mild cases or a chalky whiteness
in more severe affection. Cases of ulceration of the cornea followed by
perforation and subsequent escape of the aqueous humor, leading to
shrinking of the eyeball and permanent loss of sight, have been recorded,
but these are relatively rare, although slight inflammation of the deeper
structures of the eye (iris) are more frequent. In mild cases this
inflammation may undergo complete resolution, but more frequently permanent
cloudliness of the cornea, either diffuse or in spots (leucoma), is the
result. The mucous membrane of the mouth, nose, sinuses of the head,
throat, and lower respiratory passages are also involved. It is first
catarrhal in character, but soon a false or diphtheritic membrane is
formed, with the production of shallow ulcers. There is dribbling of saliva
from the mouth and discharge from the nose, at first watery, becoming
thicker and mixed with blood and small masses of cast-off croupous
membrane, causing a very fetid odor. These croupous areas when they form in
the throat, larynx, or windpipe, may lead to narrowing of the passages,
with consequent difficult breathing and even suffocation. Various
respiratory murmurs may also be heard, caused by the to-and-fro movement of
mucus and inflammatory deposits along the air passages. There is also
inflammation of the horn core with consequent loosening of the horn shell,
and the horns are thus readily knocked off by the uneasy, blind sufferer.
The animal may refuse all feed from the time of the initial rise of
temperature, or in less severe cases, and especially when the lesions of
the digestive tract are not so marked, the appetite may remain until the
disease is well advanced. Constipation is quite common at the commencement
of the attack, followed by diarrhea and severe straining, the evacuations
becoming very soft, fetid, and streaked with blood. Cases of the evacuation
of desquamated patches of diphtheritic membrane from the intestinal mucosa
6 to 9 feet in length have been reported. The kidneys and bladder are
usually inflamed, the urine being voided with difficulty and the animal
evincing signs of pain. Inflammatory elements, as albumen, casts, etc., may
be seen on examination of the urine. In cows the mucous membrane of the
vestibule is congested, swollen, and may contain ulcers and an excessive
quantity of mucus. Abortion during advanced pregnancy is not infrequent,
following a severe attack. In connection with these various symptoms there
may be much uneasiness on the part of the animal, leading in some cases to
madness and furious delirium, in others to spasms and convulsions or
paralysis. A vesicular eruption of the skin may occur, seen principally
between the toes and on the inside of the flank and in the armpits, with
subsequent loss of hair and epidermis.
Like other infectious diseases, malignant catarrh pursues a longer or
shorter course in accordance with the severity of the attack. In acute
cases death is said to take place three to seven days after the appearance
of symptoms. Recovery, if it occurs, may take three or four weeks.
According to statistics, from 50 to 90 per cent of the affected animals
die.
If animals which have died of this disease are examined, in addition to the
changes of the mucous membrane of mouth and nasal cavities referred to
above, shallow ulcers in these situations will be found occasionally. These
necrotic processes may pass beneath the mucous membrane and even involve
the underlying bony structure. In severe cases membranous (croupous)
deposits are found in the throat. Similar deposits have been found upon the
mucous membrane of the fourth stomach and intestine, which is always
inflamed. There is more or less inflammation of the membranes of the brain,
kidneys, and liver, and some fatty degeneration of the voluntary muscles.
In countries where rinderpest occasionally appears it may be difficult to
distinguish between it and malignant catarrh, owing to a general similarity
of the symptoms. The principal points to be observed in differentiating
between the two are the very slight transmissibility of the latter as
compared with the intense contagiousness of the former, and the tendency of
malignant catarrh to run a more chronic course than rinderpest, which
usually results fatally in a very few days. Only a trained veterinarian who
takes into consideration all the different symptoms and lesions of both
diseases should decide in such cases.
_Treatment._--There is no specific treatment for this affection. Copious
blood letting in the earliest stages has been highly recommended, however,
as this has a tendency to deplete the system and lessen the exudation of
inflammatory products. Antiseptic washes, such as 4 per cent boric-acid
solution to the eyes and Dobell's solution applied to the nose and mouth
with ice poultices over the crest of the head and frontal region, have also
proved efficacious. Calomel should also be given in 1-dram doses twice a
day for three days, and in severe cases, involving the respiratory tract, a
powder containing ferrous sulphate, quinin, and subnitrate of bismuth,
given twice a day, will be found beneficial. At the same time it must be
remembered that much greater success is to be looked for in the preventive
treatment. This consists in the removal of the healthy from the infected
animals (not vice versa) and thorough cleaning and disinfecting of the
contaminated stables. If the floors are low and damp, they should be raised
and made dry. If this can not be done, place a layer of cement under the
stable floor to prevent water from entering from below. The stable should
be well ventilated and the soil in the pastures thoroughly drained. If this
is carefully carried out, the contagion should be destroyed and the danger
of the reappearance of the disease in a great measure lessened.
MALIGNANT EDEMA.