Ascaris megalocephala Intestines
Sclerostoma equinum Large intestine and blood-vessels
Sclerostoma tetracanthum Large intestine
Oxyrus curvula Large intestine
Oxyrus mastigodes Large intestine
CATTLE
Species Organ
Strongylus convolutus Abomasum
Ascaris vituli Small intestine (calves)
Strongylus ventricosus Small intestine
Oesophagostomum inflatum Large intestine
Trichocephalus affins Large intestine
Strongylus micrurus Bronchi
Strongylus pulmonaris Bronchi
SHEEP
Species Organ
Haemonchus contortus Abomasum
Ascaris ovis Small intestine
Strongylus filicollis Small intestine
Oesophagostomum columbianum Intestines
Uncinaria cernua Small intestine
Trichocephalus affins Large intestine
Strongylus filaria Bronchi
Strongylus rufescens Bronchi and air follicles
SWINE
Species Organ
Ascaris suis Intestines
Oesophagostomum dentatum Large intestine
Trichocephalus crenatus Large intestine
Trichina spiralis Muscles and intestines
Strongylus paradoxus Trachea and bronchi
Sclerostoma pingencola Renal fat and kidney
POULTRY
Species Organ
Ascaris inflexa Intestine
Spiroptera hamulosa Gizzard
Heterakis papillosa Caecum
Syngamus trachealis Trachea and bronchi
INTESTINAL WORMS OF SOLIPEDS.--The large round-worms or ascarides and the
sclerostomes are the most injurious intestinal parasites of solipeds. The
_A. megalocephala_ or large round-worm is from 5 to 15 inches (12 to 35
cm.) long. It may be present in the double colon in such large numbers as
to form an entangled mass that completely fills a portion of the loop in
which it is lodged. It may interfere with digestion by obstructing the
passage of alimentary matter, and irritating the intestine.
The _S. equinum_ and _S. tetracanthum_ are small worms. The former
sclerostoma is from 0.6 to 1.5 inches (18 to 35 mm.) long, and the latter
is from 0.5 to 0.6 inch (8 to 17 mm.) long. Both sclerostomes attach
themselves to the lining membrane of the intestine by their mouth parts,
and suck blood. The young _S. equinum_ may live in tumor-like cysts that
they cause to form in the lining membrane of the intestine. The young worm
may penetrate the wall of a small blood-vessel as well, and drift into a
large vessel, where it may become lodged and undergo partial development.
The irritation to the blood-vessel results in an inflammation and dilation
of the vessel wall. This is termed verminous aneurism. A portion of the
fibrin-like lining of the aneurism may flake off and drift along in the
blood stream, until finally a vessel that is too small for the floating
particle or embolus to pass through is reached. The vessel is then plugged
or a thrombus is formed. If the vessel involved by the thrombus happens to
be a mesenteric vessel, then a loop of intestine has its blood supply cut
off, and colicky pains result. Such colics are dangerous, and may terminate
fatally. Intestinal obstruction, thrombo-embolic colics, unthriftiness and
a weakened, anaemic condition may be caused by intestinal worms.
_The treatment_ is both preventive and medicinal. The preventive treatment
consists in giving young, growing animals the best care possible.
Cleanliness about the stable, giving the colt plenty of range when running
in a pasture, and feeding a ration that is sufficient to keep the colt in
good physical condition are the important preventive measures. Tartar
emetic in one-half to one dram doses may be given with the feed daily until
five or six doses are given. Turpentine may be given in one to three ounce
doses in a pint of linseed oil. This may be repeated daily for two or three
days. Worms located in the posterior bowel may be removed by rectal
injections of a weak water infusion of quassia chips. The rectum should be
first emptied with the hand, and the nozzle of the syringe carried as far
forward with the hand as possible. The injections should be repeated daily
for several days.
INTESTINAL WORMS OF CATTLE.--Intestinal worms seldom cause serious losses
from unthriftiness or death in cattle. It is in calves only that we are
called on to treat this class of disease. The symptoms resulting from the
invasion of the intestinal tract by the different worms vary in severity
according to the number, habits of the parasite and care that the animal
receives. The usual symptoms are unthriftiness, indigestion, diarrhoea and
a stunted, anaemic condition. Stiles reported extreme anaemia,
unthriftiness and many deaths among cattle in a certain section of Texas,
due to extensive infection with the _Uncinaria radialus_.
_The treatment_ is largely preventive. Calves and yearlings should be
provided with plenty of feed at all seasons of the year. Good care and
careful feeding will keep them in a thrifty, healthy condition and enable
them to throw off invasions of intestinal worms. Turpentine is the
vermifuge usually administered to calves. The dose is from two to four
drams given in a milk or raw linseed oil emulsion.
STOMACH WORM OF SHEEP.--The twisted stomach worm, _Haemonchus contortus_,
is the most injurious internal parasite of sheep. It is a very small,
hair-like worm from 0.4 to 1 inch (9 to 25 mm.) in length. In the adult
form it attaches itself to the mucous membrane of the fourth stomach or
abomasum, and lives by sucking blood. The blood present in the digestive
tract of the worm gives it a brown color, and the white oviducts which are
wound around the digestive canal cause the body to appear twisted. When the
twisted stomach worm is present in large numbers, the worms become mixed
with the contents of the stomach and can be readily found on making a
post-mortem examination.
_Symptoms of stomach worms_ are first manifest in the lambs (Fig. 76). It
is not until early summer that the disease appears in the flock. The
symptoms are not characteristic unless we consider an unthrifty, anaemic,
weak, emaciated condition accompanied by diarrhoea, during the summer
months characteristic of stomach-worm disease. The sick animals are unable
to keep up with the flock, and they like to stand about in the shade. They
move slowly, the back is arched, the appetite poor, the mucous membranes
and skin are pale and the hind parts soiled by the diarrhoeal discharge.
More acute symptoms than the above sometimes occur. The disease may last
from a few days to several weeks. A large percentage of the affected
animals die.
[Illustration: FIG. 76.--Lamb affected with stomach worm disease.]
The _treatment_ is largely preventive. Frequent changing of pastures and
dry lot feeding are common preventive measures. Permanent sheep pastures
lead to heavy losses from stomach worm disease. A very effective preventive
measure, as we may term it, is the practice of administering a vermifuge to
the ewes in the late summer and again in early winter. This may be given in
a drench, or with the feed. This prevents the reinfection of the pastures
every spring, and the young lambs are not exposed to this form of
infection. The most effective treatment that the writer has ever used is
the following formula recommended by Dr. Law: Arsenous acid one dram,
sulfate of iron five drams, powdered areca nut two ounces, common salt four
ounces. This is sufficient for one dose for thirty sheep. It may be given
with the salt, or in ground feed. If the flock is apparently healthy, four
doses given at intervals of three days is sufficient. If symptoms of
stomach worms are manifested the animals should be dosed daily until they
have received from five to ten doses, depending on the condition of the
animal.
INTESTINAL WORMS OF SHEEP.--The most widely distributed and seemingly most
injurious intestinal worm of sheep is the _OEsopliagostomum columbianum_.
It is a small worm from 0.5 to 0.75 inch (12 to 18 mm.) long. It penetrates
the lining membrane of the intestines and encysts in the intestinal wall. A
tumor, varying in size from that of a millet seed to a hazelnut, then forms
in the wall of the intestine. These tumors undergo a cheesy degeneration,
and when mature, may appear as greenish, cheesy-like masses, covering a
large portion of the lining membrane of the intestine. Diarrhoea and
emaciation may result. These symptoms are most evident during the winter
months.
_The treatment_ recommended for ridding sheep of this intestinal worm is
largely preventive. Very little can be done with the medicinal treatment of
a sheep whose intestinal tract is badly infested with this parasite. Good
care and the feeding of a proper ration are the only curative measures that
are effective in such cases. The occasional administration of a vermifuge
for the purpose of ridding the digestive tract of worms, together with the
frequent changing of pastures during the spring and summer, are the most
effective preventive lines of treatment. The same treatment recommended for
stomach worms may be used for this disease.
INTESTINAL PARASITES OF HOGS.--The _Ascaris suis_ or _common round_ worm is
very commonly found in the small intestine. It is quite frequently found in
large numbers, almost filling the lumen of the intestine of an unthrifty
pig (Fig. 75). It may also work its way into the bile duct. Sometimes,
after a hog has died, this parasite migrates forward into the stomach and
gullet. The _A. suis_ is from 4 to 10 inches (10 to 26 cm.) long.
_The Echinorhynchus gigas_ or _thorn-headed_ worm is the most dangerous of
all intestinal worms (Fig. 74). It is usually found with its proboscis or
thorn imbedded in the wall of the small intestine. The Echinorhynchus is
not as common a parasite as the Ascaride, and it is not usually present in
large numbers. Usually, not more than a half-dozen of these worms are found
in the intestine of a hog, but in some localities and in hogs that are
allowed to root around manure piles and in clover pastures the herd may
become badly infected with them and serious losses occur. The average
length of the male is about 3 inches (8 cm.) and the female 10 inches (26
cm.).
[Illustration: FIG. 77.--Whip-worms attached to wall of intestine.]
[Illustration: FIG. 78.--Pin-worms in intestine.]
The _Trichocephalus crenatus_ or _whip worm_ (Fig. 77) is slender or
hair-like in its anterior two-thirds and thick posteriorly. It is from 1.5
to 2 inches (40 to 45 mm.) long. It is found in the caecum attached to the
wall by the hair-like portion.
The _OEsophagostomum dentatum_ or _pin worm_ is from 0.3 to 0.6 inch (8 to
15 mm.) long. It is found in the large intestine (Fig. 78).
The _symptoms_ of intestinal worms are not very evident in the average
drove of hogs. None of the other farm animals are such common hosts for
intestinal worms as hogs. But it is only in extreme cases of infection by
intestinal worms, and in stunted and poorly-cared-for hogs, that very
noticeable symptoms of disease are manifested. We must not take from the
above statement that it is unnecessary to resort to treatment unless in
exceptional cases. Intestinal worms interfere with the growth of young
hogs, and may irritate and inflame the intestine, causing chronic
indigestion, nervous symptoms, and in some cases death. This irritated and
inflamed condition of the intestine is best noted in the abattoir by the
ease with which the wall of the intestine that contains large numbers of
worms tears when handling it.
_The treatment_ of intestinal worms in hogs is both preventive and
medicinal. If the conditions in the pens and houses are such as to enable
the eggs and embryos to live for a long time, or the surroundings are
favorable for infection of the animals through their feed and water supply,
the herd may become badly infested with intestinal parasites. The
preventive treatment consists in keeping hogs in clean, well-drained yards
or pastures, and feeding them from clean troughs and concrete feeding
floors that can be washed, when necessary, in order to keep them clean.
Turpentine, given in a milk emulsion, is a common remedy for intestinal
worms in hogs. The dose is one teaspoonful for every eighty pounds weight.
This dose should be repeated daily for three days. The following vermifuge
can be recommended: Santonin three to five grains, calomel five to eight
grains. This is sufficient for one hundred pounds weight. If the pigs are
small and it requires two or three to weigh one hundred pounds, the large
dose should be given. If the hogs weigh one hundred pounds or more, they
should receive the small dose. The drove should be divided into lots of ten
or fifteen hogs each. The drugs should be mixed and divided into the same
number of powders as there are lots of hogs. Ground feed is placed in the
trough, dampened with milk, or water and the powder sprinkled evenly over
it. The hogs are then allowed to eat the feed. It is best to dose them in
the morning after they have been off feed for ten or twelve hours.
VERMINOUS BRONCHITIS IN CALVES.--The lung worms of cattle, _Strongylus
micrurus_ and _Strongylus pulmonaris_, may cause heavy losses in calves and
yearlings. Older cattle may harbor these parasites, but they do not seem to
be inconvenienced by them. The _S. micrurus_ is from 1 to 3 inches (25 to
75 mm.) long. The _S. pulmonaris_ is smaller. It is from 0.4 to 1.3 inches
(10 to 35 mm.) long. They are found in the trachea and small bronchial
tubes, where they are mixed with mucous secretions from the inflamed lining
membrane of the bronchial tubes.
Wet seasons and low, wet pastures are said to favor the development of lung
worms. Their life history is not fully understood. They do not persist
generation after generation in the air passages of an animal, but the eggs
and embryos are expelled and live for a time outside of the animal, when
they may again become parasites of another or the same host.
_The symptoms_ are the same as occur in bronchitis and pneumonia. Calves
and yearlings are the only animals in the herd that may show symptoms of
the disease. The air passages become irritated and inflamed, and the calf
shows a slight cough. As the inflammation increases and the worms and
mucous secretions plug up the small bronchial tubes, the coughing spells
become more severe and rattling, wheezing sounds may be heard on
auscultating the lungs. The calf finally loses its appetite, becomes
emaciated and weak, and wanders off alone. It is usually found lying down
and shows labored breathing that is occasionally interrupted by paroxysmal
coughing. The death rate in poorly-cared-for herds is heavy.
VERMINOUS BRONCHITIS AND PNEUMONIA OF SHEEP.--The two lung worms of sheep
are the _Strongylus filaria_ and Strongylus_ rufescens_. The former is from
1.3 to 3 inches (33 to 80 mm.) long, and the latter from 0.6 to 1 inch (16
to 25 mm.) long. The _S. filaria_ is thread-like and the _S. refuscens_
hair-like in appearance. For this reason they are termed thread and hair
lung-worms. The thread-worm is found in the trachea and the larger
bronchial tubes, and the hair-worm in the most minute as well as the larger
bronchioli.
This disease is most common in wet seasons. Undrained pastures and ponds
are said to favor the spread of the disease. Permanent pastures favor the
reinfection of the flock from year to year. The eggs and embryos are
expelled in coughing, and live for a time in the pastures, pens and houses.
The sheep become infected through the dust, drinking water or feed.
_The symptoms of verminous bronchitis_ and pneumonia are quite
characteristic. Lambs suffer most from these diseases. A number of animals
in the flock are affected. Coughing, rapid and labored breathing, loss of
appetite, emaciation and weakness are the usual symptoms noticed. When a
paroxysm of coughing occurs, considerable mucus is expelled. An examination
of the expectorations may result in finding a few lung worms. In
poorly-cared-for flocks, and when complicated by stomach and intestinal
worms, the death rate is usually heavy.
_The treatment_ of lung-worm diseases in lambs and calves is largely
preventive. We should use every possible precaution against introducing the
infection into the herd or flock. It is not advisable to bring animals from
an infected herd onto the premises, without subjecting them to a careful
examination and a long quarantine before allowing them to stable or pasture
with the other animals. Calves or lambs that show marked symptoms of
disease should be given comfortable quarters, and special care and feeding.
The entire herd or flock must be given the best care and ration possible.
This is the only satisfactory method of treatment. Changing the pasture or
lot frequently may help in ridding the premises of the infection.
VERMINOUS BRONCHITIS IN HOGS.--The lung worm, _Strongylus paradoxus_, is a
common parasite of young hogs. It is from 0.6 to 1.6 inches (16 to 40 mm.)
long. When the infection is light, the worms are found mostly in the
bronchial tubes of the margin and apex of the lung.
Infection with this parasite does not depend on the humidity of the soil,
or low, wet pastures containing ponds. Probably dusty quarters are
responsible in large degree for this disease.
_The symptoms are most evident_ in pigs weighing from forty to eighty
pounds. The first symptom is a cough, occurring on leaving the bed, after
exercise and after eating. In badly infected cases the paroxysm of coughing
is quite severe. The appetite usually remains good and the thriftiness of
the pig is not seriously interfered with. The feeding of a suitable ration,
and the good care that is usually given young hogs, are responsible for the
mildness of the disease.
The treatment that is of most importance is clean quarters, and the feeding
of a ration that will keep the pig growing and healthy. The sleeping
quarters should be kept free from dust. Disinfectants should be used freely
about the quarters.
THE KIDNEY WORM OF HOGS.--_Sclerostoma pinguicola_ is the kidney worm of
hogs. It is from 1 to 1.5 inches (25 to 27 mm.) long, and when seen against
the kidney fat it appears dark or mottled. It is usually found in the fat
in the region of the pelvis of the kidney. Although the kidney worm is
capable of causing inflammatory changes in the tissues surrounding the
kidney and the pelvis of this organ, the disease cannot be determined by
any noticeable symptom. Paralysis of the posterior portion of the body is
attributed to the presence of kidney worms by stockmen. There are no data
by which we may prove that the kidney worm is responsible for this
disorder.
_The treatment_ is preventive. Clean feed, pens, watering troughs and
feeding floors are the preventive measures indicated here. It is useless to
attempt treatment with drugs, as the worms are out of reach of any drug
that may be administered.
WORMS OF THE DIGESTIVE TRACT OF POULTRY.--Poultry are often seriously
infested with worms. A small number of the less injurious worms may not
cause any appreciable symptoms of disease; but the fowl that harbors them
is a source of infection to the other fowls. The infectious nature of
parasitic disease caused by worms should be recognized more fully than at
present by poultrymen.
The different species of poultry are hosts for many different species of
round-worms, thorn-headed worms and tapeworms. Dr. Kaupp states that
_Acaris inflexa_ or large round-worm, _Heterakis pipilosa_ or small
round-worm, and the _Spiroptera hamulosa_ or gizzard-worm are frequently
found in fowls. The common round-worm may be found in the first portion of
the intestine, and the small round-worm in the caecum. Neither of the
species are dangerous unless present in large numbers. They may then
obstruct the intestine, and irritate the intestinal mucous membrane. This
may cause constipation, catarrhal inflammation of the intestine and
diarrhoea. The gizzard-worm is the most dangerous of the parasites
mentioned. The gizzard has an important digestive function, and any
condition that may weaken its muscular walls may cause serious digestive
disorders. This parasite may encyst in the wall of the gizzard.
_The treatment_ of intestinal worms in poultry is both preventive and
curative. The preventive measures consist in keeping the houses and runs
clean. Air-slaked lime should be scattered over the runs every few weeks.
The drinking places should be cleaned and disinfected daily. All possible
precautions should be taken in order to prevent filth from getting into the
drinking water. Epsom salts, powdered areca nut and santonin are the
remedies commonly recommended for the treatment of intestinal worms. From
twenty to forty grains of Epsom salts may be given. Powdered areca nut is
recommended in from three to ten grain doses. Santonin may be given in from
one to two grain doses. Both the areca nut and santonin may be given with
the feed.
THE GAPES IN BIRDS.--The gape-worm, _Syngamus trachealis_, is from 0.2 to
0.8 inch (5 to 20 mm.) long. The male and female are permanently united.
The male is about one-third as long as the female, and when attached to the
anterior third of the female, gives the pair a forked appearance.
Fowls become infested with the gape-worm by eating the adult parasite that
has been expectorated, or an earth worm that is host for the immature
parasite. The embryo gape-worm is freed in the intestine, and from here
they are supposed to migrate into the abdominal air sacs and to the trachea
and bronchi.
_The symptom_ are most severe in very young fowls. The affected bird opens
its mouth and appears to gasp for breath, sneeze and attempt to swallow. In
the severe cases the appetite is interfered with, mucus accumulates in the
mouth and the bird is dull and listless. The death rate is quite high in
young-chickens and turkeys.
_The treatment_ is both preventive and curative. If the gape-worm is known
to be present in the runs, the ground should be covered with lime, and the
fowls moved to fresh runs if possible. The young birds should not be
exposed to the infection until they are well feathered out. Antiseptics may
be given with the drinking water. Disinfectants should be used freely about
the poultry houses, and the quarters kept clean. The worms may be snared by
inserting a stiff horse hair that has been twisted and forms a loop into
the trachea. This may be dipped into camphorated oil or turpentine. This
treatment should be repeated until the bird has been relieved.
QUESTIONS
1. Name the different groups of internal parasites; give examples of each.
2. What conditions favor liver rot? Give the life history of the liver
fluke.
3. Name three common tapeworms; give the life history of the beef and pork
tapeworms.
4. Name the common intestinal worms of horses and give the treatment.
5. Give the symptoms and treatment of stomach-worm disease of sheep.
6. Name the common intestinal worms of hogs and give treatment.
7. What species of domestic animals suffer most of verminous bronchitis?
Give the treatment.
8. Name the common internal parasites of poultry and give treatment.
PART VI.--INFECTIOUS DISEASES
CHAPTER XXVI
HOG-CHOLERA
HOG-CHOLERA is a highly infectious disease of swine. It is characterized by
an inflammation, of the lymphatic glands, kidneys, intestines, lungs and
skin. The inflammation is hemorrhagic in character, the inflamed organs
usually showing deep red spots or blotches.
Hog-cholera is especially prevalent in the corn-raising States which
possess a denser hog population than any other section of the United
States. In this country the loss from hog-cholera in 1913 amounted to more
than $60,000,000, and it may be considered of greater economic importance
than any of the other animal diseases.
SPECIFIC CAUSE.--The specific cause of hog-cholera is an _ultra-visible
organism_ that is present in the excretions, secretions and tissues of a
cholera hog. De Schweinitz and Dorset in 1903 produced typical hog-cholera
by inoculating hogs with cholera-blood filtrates that were free from any
organism that could be demonstrated by microscopical examination or any
cultural method. The term ultra-visible virus is applied to the virus of
hog-cholera.
_The ultra-visible virus_ is eliminated from the body of the cholera hog
with the body secretions and excretions. Healthy hogs contract the disease
by eating feed or drinking water that is infected with the virus. There are
other methods of infection, but field and experimental data show that
hog-cholera is commonly produced by taking the germs into the body with
food and drinking water.
ACCESSORY CAUSES.--The usual method of introducing hog-cholera into a
neighborhood is through the importation of feeding or breeding hogs that
were infected with the disease before they were purchased, or became
infected through exposure to the disease in the public stock-yards and
stock-cars. The shipping of feeding hogs from one section of the country to
another, and from public stock-yards, has always been productive of
hog-cholera. Dr. Dorset states that more than fifty-seven per cent of the
hog-cholera outbreaks are caused by visiting, exchanging work, exposure on
adjoining farms and harboring the infection from year to year (Fig. 79),
and more than twenty-three per cent to purchasing hogs and shipping in
infected cars, birds and contaminated streams.
[Illustration: FIG. 79.--A hog yard where the disease-producing germs may
be carried over from year to year.]
In neighborhoods where outbreaks of hog-cholera occur necessary precautions
against the spread of the disease are not taken. The _exchange of help_ at
threshing and shredding time in neighborhoods where there is an outbreak of
hog-cholera is the most common method of spreading the disease. _Visiting
farms_ where hogs are dying of cholera; walking or driving a team and wagon
through the cholera-infected yards; stock buyers, stock-food and
cholera-remedy venders that visit the different farms in a neighborhood may
distribute the hog-cholera virus through the infected filth that may adhere
to the shoes, horses' feet and wagon wheels. _Cholera hogs_ may carry the
disease directly to a healthy herd when allowed to run at large. _Streams_
that are polluted with the drainage from cholera-infected yards are common
sources of disease.
_Pigeons, dogs, cows_ and _buzzards_ that travel about the neighborhood and
feed in hog yards and on the carcasses of cholera hogs may distribute the
disease. Because of the active part that dogs, birds and surface drainage
take in the distribution of hog-cholera, the practice of allowing the
carcasses of dead hogs to lie on the ground and decompose is responsible
for a large percentage of the hog-cholera outbreaks.
_Age_ is an important predisposing factor. Young hogs are most susceptible
to cholera, and this susceptibility can be greatly increased by giving them
crowded, filthy quarters. Infection with lice, lung and intestinal worms,
the feeding of an improper ration and sudden changes in the ration lower
the natural resistance of a hog against disease. Pampered hogs usually
develop acute cholera when exposed to this disease.
Hog-cholera is more virulent or acute during the summer and fall months
than it is during the winter and spring months. After the disease sweeps
over a section of country, it becomes less virulent and takes on a subacute
or chronic form. Outbreaks of hog-cholera usually last two or three years
in a neighborhood. This depends largely on the number of susceptible hogs
that were not exposed to the infection the first season, and the preventive
precautions observed by the owners.
PERIOD OF INCUBATION.--The length of time elapsing between the exposure of
the hog to the cholera virus, and the development of noticeable symptoms of
hog-cholera, varies from a few days to two or three weeks. The length of
this incubation period depends on the susceptibility of the animal, the
virulence of the virus and the method of exposure. An acute form of
hog-cholera indicates a short period of incubation, and a chronic form, a
long period.
SYMPTOMS.--The symptoms of hog-cholera may differ widely in the different
outbreaks of the disease. The symptoms may be classified under the
following forms: Acute, subacute and chronic. The acute form of hog-cholera
is the most common. The early symptoms are tremors, fever, depressed
appearance, marked weakness, staggering gait, constipation and diarrhoea,
labored breathing and convulsions. Death may occur within a few hours or a
few days. Recovery seldom occurs. In the subacute form, the symptoms are
mild and develop slowly. Recovery may take place within a few days, or
after extending over a week or ten days it may assume the chronic form.
Very often in outbreaks of subacute cholera a large majority of the herd
does not show visible symptoms of the disease. In the chronic form, marked
symptoms of pleuropneumonia and chronic inflammation of the intestine are
common. Ulcers and sores form on the skin and the hair may come off. Large
portions of the skin may become gangrenous and slough. Young hogs are
usually stunted and emaciated.
_The first symptom_ of disease is an elevation of body temperature.
At the beginning of any outbreak of hog-cholera the _body temperatures_ of
the apparently healthy animals may vary from 105\260 to 108\260 F. After
a few days, animals that are fatally sick or recovering from the disease
may show normal or subnormal body temperature.
_Loss of appetite_ is the first symptom of disease usually noted by the
person in charge of the herd. The hog may show a disposition to eat dirt.
The sick hog is usually found lying in its bed, or off by itself in a quiet
place. It presents a rather _characteristic appearance_. The back is
arched, the hind feet are held close together, or crossed, the abdomen is
tucked up and the hog appears weak in its hind parts. _Diarrhoea_ or
_constipation_ may be present. The color of the diarrhoeal discharges
varies according to the character of the feed, and it may be more or less
tinged with blood and have a disagreeable odor. The urine is highly
colored.
_The respirations and pulse beats_ are quickened and abnormal in character.
Thumps sometimes occur. When the mucous membranes lining the throat and
anterior air passages are thickened, the respirations are noisy and
difficult. The animal may cough on getting up from its bed and moving
about. There is at times a noticeable discharge from the nostrils. When the
_lungs_ are inflamed the respirations are quickened and labored. In case
the pleural membrane is inflamed, the respiratory symptoms are more severe,
and the hog shows evidence of pain when the walls of the chest are pressed
on. The _pericardium_ may be inflamed. In such cases the hog staggers and
falls when forced to walk.
_The central nervous system_ may be involved by the inflammation. The usual
symptoms occurring in inflammation of the brain and its coverings are then
present. A sleepy, comatose condition may end in death, or the animal dies
in a convulsion.
_The secretions of the skin_ and mucous membranes are abnormal. The skin in
the regions of the ears, inside of the thighs and under surface of the body
is moist, dirty or discolored red. Just before death the skin over the
under surface of the body becomes a purplish red. In the chronic form, a
dirty, thickened, wrinkled skin is commonly observed. At first the
secretion from the eyes is thin and watery, but it becomes thick, heavy and
pus-like, causing the margins of the lids to adhere to each other.
The death rate in hog-cholera varies in the different forms of the disease.
The average death rate is about fifty per cent.
DIFFERENTIAL DIAGNOSIS.--The diagnosis of hog-cholera in the field must
depend on the clinical symptoms, post-mortem lesions and history of the
outbreak. The history should be that of a highly infectious disease.
[Illustration: FIG. 80.--Carcass of a cholera hog showing different groups
of lymphatic glands; kidneys; and ulcer on caecum.]
_Abnormal body temperatures_ of a large percentage of the herd indicate the
presence of an acute infectious disease. We should then destroy one of the
sick hogs and make a careful post-mortem examination (Fig. 80). An early
diagnosis of the disease is necessary, as this enables us to use curative
treatment when it will do some good, and take the necessary steps toward
preventing the spread of the disease to neighboring herds.
_Intestinal and lung worms_ are common in young hogs. The presence of these
worms does not always indicate that they are the cause of the sickness and
death of the animal. Such parasites are injurious and may cause disease,
but it is only in rare cases that they cause death.
"_Pig typhoid_" is sometimes spoken of as a highly infectious disease
involving the intestines. A disease of hogs that may be termed typhus-fever
sometimes affects a large number of the hogs in the herd. This disease
occurs among hogs kept in small yards and houses that are crowded,
unsanitary and in continuous use, or when the hogs drink from wallows,
ponds and creeks.
The term swine-plague should not be used in speaking of outbreaks of
hog-cholera, as it is now considered a form of hog-cholera involving
especially the lungs.
[Illustration: FIG. 81.--Kidneys from hog that died of acute hog-cholera.]
[Illustration: FIG. 82.--Lungs from hog that died of acute hog-cholera.]
LESIONS.--In _acute hog-cholera_ the inflammation is hemorrhagic in
character. Small, red spots and blotches occur in different organs and
tissues. In the _chronic form_ of the disease ulceration of the intestinal
and gastric mucous membrane, inflammation of the lungs and pleura and
sloughing of the skin are common lesions.
_The skin_ over the under side of the neck, body and inside of the thighs
may appear red or purplish-red in color. The different groups of _lymphatic
glands_ are enlarged and softened. They may vary in color from a
grayish-red to a deep red, depending on the degree of engorgement with
blood. The pleura and pericardium may show small red spots and blotches.
The _kidneys_ are usually lighter colored than normal, and marked with red
spots and blotches (Fig. 81). The _spleen_ may show no evidence of disease.
It may be large and soft, or even smaller than normal. The _liver_ may be
enlarged and dark, or mottled and light colored.
The _stomach_ and _intestines_ may show hemorrhagic spots and blotches.
Sometimes the gastric and intestinal mucous membrane is a brick red.
Ulceration of the mucous membrane is common (Fig. 83).
[Illustration: FIG. 83.--A piece of intestine from a hog that died of
chronic hog-cholera, showing appearance of intestinal ulcers.]
Small, red spots may be present on the surface of the _lungs_ (Fig. 82).
Scattered lung lobules or a large portion of the lungs may be inflamed. In
chronic hog-cholera, pleural exudation, adhesions and abscesses in the lung
tissue may occur. Inflammations of the pericardium and heart muscle are
less common lesions.
PREVENTIVE MEASURES.--Hog-cholera is the most widespread infectious disease
of hogs, and all possible precautions against its distribution to healthy
herds should be practised. Hogs coming from other herds and stock shows
should be excluded from the home herd until they are positively shown to be
free from disease. They should be quarantined in yards set off for this
purpose. The hogs should be cleaned by dipping or washing them with a
disinfectant. The quarantine period should be longer than the average
period of incubation. Three weeks is sufficient.
_The possible introduction of the disease_ into the pens by people, dogs,
birds and other carriers of the disease should be guarded against,
especially if cholera is present in the neighborhood. The exchange of help
at threshing and shredding time with a neighbor who has hog-cholera on his
farm is a common method of distributing the infection. It is not advisable
to allow a stranger to enter your hog-houses and yards, unless his shoes
are first disinfected. Whenever it is necessary for a person to enter yards
where the disease is present, the shoes should be cleaned and disinfected
on leaving. The wheels of wagons, and the feet of horses that are driven
through cholera yards, should be washed with a disinfectant. The feet of
feeding cattle that are shipped from stock-yards should be treated in the
same manner. Persons taking care of cholera hogs should observe the
necessary precautions against the distribution of the disease, and see that
others practise like precautions.
Hog-yards should be well drained and all wallow holes filled. Pens and
pastures through which the drainage from the swine enclosures higher up
flows should not be used for hogs.
CARE OF A DISEASED HERD.--When an outbreak of hog-cholera occurs on a farm
the farm should be quarantined. The herd should be moved away from running
streams, public roads and line fences, so that neighboring herds are not
unnecessarily exposed to the disease. During the hot weather shade and an
opportunity to range over a grass lot or pasture are highly necessary. A
recently mowed meadow, or a blue grass pasture and a low shed, open on all
sides and amply large for the herd to lie under, give the animals clean
range and comfortable, cool quarters. Roomy, dry, well-ventilated
sleeping-quarters that are free from drafts and can be cleaned and
disinfected are best when the weather is cold and wet.
In the subacute, and in the early part of an acute outbreak of hog-cholera,
it is advisable to separate the sick from the well hogs. The fatally sick
animals should be destroyed.
[Illustration: FIG. 84.--Cleaning up a hog lot.]
A very light ration should be fed and an intestinal antiseptic given with
the feed. A thin slop of shorts is usually preferred. Four ounces of
pulverized copper sulfate may be dissolved in one gallon of hot water, and
one quart of this solution may be added to every ten gallons of drinking
water and slop. Water and slop should not be left in the troughs for the
hogs to wallow in. The troughs should be disinfected and turned bottom side
up as soon as the hogs have finished feeding and drinking. Kitchen slop and
sour milk should not be fed. The care and treatment of the herd require
work and close attention on the part of the attendant. Indifferent,
careless treatment is of no use in this disease.
A disinfectant should be sprayed or sprinkled about the feed troughs,
floors, pens and sleeping quarters daily.
DISPOSING OF DEAD HOGS.--The carcasses of the dead hogs should be burned.
Before placing the carcass on the fire, it should be cut open and several
long incisions made through the skin. A crematory may be made by digging
two cross trenches that are about one foot deep at the point where they
cross, and shallow at the ends. Iron bars or pipe may be laid over the
trenches where they cross for the carcass to rest upon, or woven wire
fencing securely fastened with stakes may be used in the place of the iron
bars. If the carcass is disposed of by burying, it should be buried at
least four feet deep and covered with quicklime.
DISINFECTING THE YARDS AND HOUSES.--If the sick hogs are moved to new
quarters at the beginning of the outbreak, the hog houses and yards should
be cleaned and disinfected (Fig. 84). The manure and all other litter
should be hauled away to a field where there is no danger from this
infectious material becoming scattered about the premises, leaving a centre
of infection in the neighborhood and causing outbreaks of cholera among
neighboring herds. It may be advisable to burn the corn-cobs and other
litter that have accumulated about the yards. Loose board floors should be
torn up and the manure from beneath removed. Portable houses should be
removed. The floors, walls of the house and fences should be first cleaned
by scraping off the filth, and then sprayed with a three per cent water
solution of a cresol or coal tar disinfectant to which sufficient lime has
been added to make a thin whitewash. Three or four months of warm, sunny
weather are sufficient to destroy the cholera infection in well-cleaned
yards.
ANTI-HOG-CHOLERA SERUM.--The credit of developing the first and at present
the only reliable anti-hog-cholera serum and method of vaccination belongs
to Drs. Dorset and Niles. Anti-hog-cholera serum came into general use in
1908, and all of the swine-producing States have established State
laboratories for the production of this serum.
Anti-hog-cholera serum is produced by injecting directly, or indirectly,
into the blood-vessels of an immune hog a large quantity of cholera virus,
secured by bleeding a hog that is fatally sick with acute cholera, and
bleeding the injected animal after it has completely recovered from the
injection. The injection of the cholera blood is for the purpose of
stimulating the production of antibodies by the body tissues, and raising
the protective properties of the immune hog's blood. An animal so treated
is called a hyperimmune (Fig. 85). The blood from the hyperimmunes is
defibrinated and a preservative added, and after it has been tested for
potency and freedom from contaminating organisms, it is ready for use.
[Illustration: FIG. 85.--Hyperimmune hogs used for the production of
anti-hog-cholera serum.]
THE VACCINATION OF HOGS WITH ANTI-HOG-CHOLERA SERUM.--The vaccination of a
hog by the single method consists in injecting hypodermically or
intramuscularly anti-hog-cholera serum. The immunity conferred may not last
longer than three or four weeks.
The vaccination of a hog by the _double method_ consists in injecting
hypodermically or intramuscularly anti-hog-cholera serum and hog-cholera
blood.
_The vaccination or treatment_ of a cholera hog showing noticeable
symptoms, or a high body temperature, consists in injecting hypodermically
or intramuscularly anti-hog-cholera serum (Fig. 87).
[Illustration: FIG. 86.--Preparing the hog for vaccination by washing the
part where the serum is injected with a disinfectant.]
[Illustration: FIG. 87.--Vaccinating a hog.]
_The region_ into which the serum and cholera blood may be injected are the
inside of the thigh, within the arm, flank and side of the neck (Fig. 86).
Two hypodermic syringes, holding about twenty cubic centimetres and six
cubic centimetres, and having short, heavy, seventeen or eighteen-gauge
slip-on needles, should be used. The small syringe is used for injecting
the virulent or cholera blood which is injected into a different part than
the serum. The quantity of serum and virus injected varies with the size
and condition of the animal. _Young hogs_ should receive one-half cubic
centimetre of serum for each pound of body weight, and _cholera hogs_
should be given one-half more to twice the dose that is recommended for
healthy animals. The dose of virus recommended varies from one to two cubic
centimetres for each hog.
In vaccinating _small pigs_ not more than five, and in large hogs not more
than twenty, cubic centimetres should be injected at any one point. The
_body temperature_ of each animal should be taken. A body temperature of
103.5\260 F. in a mature hog and a body temperature of 104\260 F. in a
young hog may indicate hog-cholera. Exercise, feeding and close
confinement in a warm place may raise the body temperature above the
normal.
Hogs that are to be vaccinated or treated should not be given feed for at
least twelve hours before handling them. If possible they should be
confined in a roomy, clean, well-bedded pen. If this is practised, they are
cleaner and easier to handle and their body temperatures are less apt to
vary. After the treatment or vaccination the hogs should be fed a light
diet for a period of at least ten days, and the ration increased gradually
in order to avoid causing acute indigestion. This is necessary because of
the elevation in body temperature resulting from the inability of the
animal to digest heavy feeds, kitchen slops and sour milk. If poor judgment
is used in caring for the vaccinated hogs, and the person who vaccinates
them uses careless methods, heavy losses from acute indigestion, blood
poisoning, or hog-cholera may occur.
QUESTIONS
1. What is the specific cause of hog-cholera? Give and describe the
different methods of spreading the disease.
2. What are the symptoms of hog-cholera?
3. Give the preventive and curative treatment of hog-cholera.
4. What is anti-hog-cholera serum? Give the different methods of
vaccination and treatment.
CHAPTER XXVII
TUBERCULOSIS
[Illustration: FIG. 88.--Koch's _Bacillus tuberculosis._]
Tuberculosis is a contagious an and domestic animals, affecting any the
lymphatic glands and lungs, change in the tissues is the formation tubercle
or nodule.
HISTORY.--Tuberculosis is one of the oldest of known diseases of domestic
animals and man. Its contagious character was proven by Villemin in 1865,
who by experential infection transmitted tuberculosis from man to animals
and from animal to animal. It was in 1882 that Dr. Robert Koch discovered
and proved by inoculation experiments that the disease was caused by a
specific germ (Fig. 88). Prior to the experiments by Villemin and Koch, the
belief was that tuberculosis was due to heredity, unsanitary conditions and
inbreeding. Following discovery of the specific germ and conditions
favoring its development and spread, numerous scientifically conducted
experiments were made. These resulted in practical methods of control and
elimination of tuberculosis from herds having this disease. By carefully
conducted experiments and other forms of educational work the infectious
character of tuberculosis and the economic importance of preventative
measures have been demonstrated. The average stockman is well informed
regarding the character and economic importance of this disease, but there
is no general application of this knowledge, and tuberculosis is increasing
in dairy and breeding herds. The slow development of tuberculosis, and the
absence of visible symptoms during the early stage of the disease, are
responsible for this condition and the extensive infection of dairy and
breeding herds.
PREVALENCE OF THE DISEASE.--Tuberculosis is very prevalent among cattle and
swine in all countries where intensive agriculture is practised. It is a
rare disease among cattle of the steppes of eastern Europe and the cattle
ranges of the western portion of the United States. In countries where
dairying is an important industry, tuberculosis is a common disease of
cattle and hogs. The abattoir reports of Europe and the United States show
that tuberculosis is on the increase among domestic animals. The Bureau of
Animal Industry of the United States Department of Agriculture reports that
out of 400,008 cattle tested with tuberculin 9.25 per cent reacted. Melvin
states that the annual loss from tuberculosis in the United States is about
$23,000,000. In dairy herds in which the disease has existed for several
years, it is not uncommon to find from 25 to 75 per cent tubercular.
THE DIRECT CAUSE.--The direct cause of tuberculosis is Koch's _Bacillus
tuberculosis_. This is a slender, rod-shaped microorganisms (Fig. 88)
occurring in the diseased tissues, feces and milk of a tubercular animal.
It belongs to that small group known as acid-fast bacteria. The tubercle
bacillus is not really destroyed by external influences, and it may retain
its virulence for several months in dried sputum if protected from the
light. Its vitality enables it to resist high temperatures, changes in
temperature, drying and putrefaction to a, greater degree than most
non-spore-producing germs. Direct sunlight destroys the germ within a few
hours, but it may live in poorly lighted, filthy stables for months. A
temperature of 65\260 C. destroys it in a few minutes.
Animals that, have advanced or open tuberculosis may disseminate the germ
of the disease in the discharge from the mouth, nostrils, genital organs,
in the intestinal excreta and milk. The germs discharged from the mouth and
nostrils are coughed up from the lungs and may infect the feed. Milk is a
common source of infection for calves and hogs. Allowing hogs to run after
cattle is sure to result in infection of a large percentage of them, if
there are any open cases of tuberculosis in the herd.
PREDISPOSING CAUSES.--Any condition that may lessen the resistance of the
body or enable the tubercle bacillus to survive the exposure outside the
body favors the development of the disease and the infection of the healthy
animals. Crowded, poorly ventilated, filthy stables lower the
disease-resisting power of the animal, and favor the entrance of the germs
into the body. Under such unsanitary conditions, tuberculosis spreads
quickly among dairy cattle, and a large percentage of the animals develop
the generalized form of the disease. Sanitary stables and yards do not
prevent the spread of the disease among animals that live in close contact
with one another. Fresh air and sanitary surroundings only check the spread
and retard its progress.
INTRODUCTION OF TUBERCULOSIS INTO THE HERD.--The common method of
introducing tuberculosis into the herd is through the purchase of animals
having the disease. Such animals may be in apparent good health at the time
of purchase, and be affected with generalized or open tuberculosis.
_A source of infection_ is by unknowingly buying cows that have reacted to
the tuberculin test. The indiscriminate use and sale of tuberculin are
largely responsible for the large number of reacting animals that have been
placed on the open market. This dishonest practice has resulted in the
rapid spread of the disease in certain localities. For years a large
percentage of the breeding herds have been infected, and the writer has met
with several herds of dairy and beef cattle that became tubercular through
the purchase of tubercular breeding animals.
SYMPTOMS.--There is no one symptom by which we may recognize tuberculosis
in cattle and hogs. None of the symptoms shown by a tubercular animal are
characteristic, unless it is in the late stage of the disease. In a
well-cared-for animal, the lymphatic glands in the different regions of the
body, the lungs, liver and other organs, may be full of tubercles without
causing noticeable symptoms of disease (Fig. 89).
[Illustration: FIG. 89.--A tubercular cow. This cow was, to all
appearances, in good health, but showed generalized tuberculosis on
post-mortem examination.]
_Tuberculosis may attack any organ of the body_, and in the different cases
of the disease the symptoms may vary. Enlargement of the glands in the
region of the throat, and noisy, difficult breathing are sometimes present.
The udder frequently shows hard lumps scattered through the gland. Bloating
may occur if a diseased gland in the chest cavity presses on the oesophagus
and prevents the usual passage of gas from the paunch. Chronic diarrhoea
may occur. If the disease involves the digestive tract, the animal is
unthrifty and loses flesh rapidly. Coughing is not a characteristic
symptom, and we should not place too much emphasis on it. If the lungs
become tubercular the animal usually has a slight, harsh cough. The cough
is first noticed when the cattle get up after lying down, when the stable
is first opened in the morning and when the animals are driven. If the
chest walls are thin, soreness from pressure on the ribs may be noted. By
applying the ear to the chest wall and listening to the lung sounds,
absence of respiratory murmurs and abnormal sounds may be distinguished,
due to consolidation of the lung tissue, abscess cavities and pleural
adhesions. In a well-advanced case the hair is rough, the skin becomes
tight and the neck thin and lean. The animal may breathe through the mouth
when it is exercised. Weakness may be a prominent symptom.
[Illustration: FIG. 90.--Tubercular spleens.]
Breeding animals that are well fed and cared for may live for several years
before showing noticeable symptoms of tuberculosis. The disease progresses
more rapidly in milch cows, especially if given poor care. Calves allowed
to nurse a tubercular mother that is giving off tubercle bacilli frequently
develop enlarged throat glands and the intestinal form of the disease.
Hogs develop a generalized form of tuberculosis more quickly than cattle,
but an unthrifty, emaciated condition is seldom noted in hogs under ten
months old.
POST-MORTEM LESIONS.--The effect of the tubercle bacillus on the body is to
irritate and destroy the tissues. Lumps or tubercles form in the lymphatic
glands, liver, lungs, spleen (Fig. 90), serous membranes, kidneys and other
body organs (Figs. 91 and 92). The tubercles may be very small at first,
but as the disease progresses they continue to enlarge until finally a
tubercular mass the size of a base-ball, or larger, is formed (Figs. 93,
94, 95 and 96). Lymphatic glands may become several times larger than
normal and the liver and lungs greatly enlarged. The pleura and peritoneum
may be thickened and covered with tubercles about the size of a millet
seed, or larger. Pleural and peritoneal adhesions to the organs within the
body cavities are common.
[Illustration: FIG. 91.--The carcass of a tubercular cow. Note the
condition of the carcass, and the tubercular nodules on the chest wall,
showing that the disease was well advanced.]
[Illustration: FIG. 92.--A section of the chest wall of a tubercular cow
showing a better view of the diseased tissue.]
The tubercle usually undergoes a cheesy degeneration. Old tubercles may
become hard and calcareous. Sometimes the capsule of the tubercle is filled
with pus. A yellowish, cheesy material within the capsule of the tubercular
nodule or mass is typical of the disease.
THE TUBERCULIN TEST.--The only certain method of recognizing tuberculosis
is by this test. There is no other method of recognizing this disease that
is more accurate than the above test.
The substance used in testing animals for tuberculosis is a laboratory
product. It is a germ-free fluid prepared by growing the tubercle bacillus
in culture medium (bouillon) until charged with the toxic products of their
growth. The culture medium is then heated to a boiling temperature in order
to destroy the germs. It is then passed through a porcelain filter that
removes the dead germs. The remaining fluid is tuberculin.
[Illustration: FIG. 93.--A very large tubercular gland that had broken down
in the central portion.]
_There are two methods of applying_ the tuberculin test. The subcutaneous
test consists in injecting a certain quantity of tuberculin beneath the
skin, and keeping a record of the body temperature of the animal between
the eighth and eighteenth hours following the injection. Tubercular animals
show an elevation in temperature that comes on about the eighth or twelfth
hour of the test. In the _intradermal test_, a small quantity of a special
tuberculin is injected into the deeper layer of the skin. The seat of the
injection in cattle is a fold of the skin on the under side of the base of
the tail. In tubercular animals the injection is followed by a
characteristic local swelling.
[Illustration: FIG. 94.--A tubercular gland that is split open.]
[Illustration: FIG. 95.--Caul showing tuberculosis.]
[Illustration: FIG. 96.--Foot of hog showing tuberculosis of joint.]
The control of tuberculosis is largely in the hands of the breeder and
dairyman. This is a disease that requires the cooperation of stockmen and
sanitary officers in the application of control measures. If there are
several open cases of tuberculosis in a herd of cattle, the application of
the tuberculin test, removal of the reacting animals and disinfection of
the premises are not sufficient to eradicate the disease. It is necessary
to repeat the tuberculin test within six months, and later at twelve-months
intervals, until none of the animals that remain in the herd react.
The most practical method of disposing of dairy cows that react to the
tuberculin test is to slaughter them. Unless a large percentage of the herd
is tubercular, it is not advisable to practise segregation and quarantine.
This may be advisable if the reactor is a valuable breeding animal, unless
visible symptoms are shown. The milk from reacting cows may be used if it
is boiled or sterilized. Whenever a calf is born of a reactor, it should be
separated from the mother and fed milk from a healthy cow.
The separation of the tubercular from the healthy cows must be complete.
Separate buildings, yards and pastures that do not join the quarters where
the healthy animals are kept should be provided. The person attending the
reactors should not attend the healthy animals, and separate forks,
shovels, pails and other utensils should be provided for the two herds.
The best method of controlling tuberculosis in hogs is to slaughter all
reactors, disinfect yards and houses and move the herd. If the old quarters
are free from filth and carefully disinfected, the hogs may be returned
without danger of infection after six months. A retest of the herd should
be made before returning them to the permanent quarters and the reactors
slaughtered.
QUESTIONS
1. Give the history of the early experimental work in tuberculosis; give
the common methods of spreading the disease.
2. What are the symptoms and post-mortem lesions in tuberculosis?
3. Give the method of controlling tuberculosis.
CHAPTER XXVIII
INFECTIOUS DISEASES COMMON TO THE DIFFERENT SPECIES OF DOMESTIC ANIMALS
SEPTICAEMIA AND PYAEMIA.--The term commonly used in speaking of simple
septicaemia and pyaemia is blood poisoning.
These infectious diseases are _caused_ by several different species of
bacteria that gain entrance to the tissues by way of wounds. The bacteria
that cause pyaemia are transferred by the blood stream to different organs
and produce multiple abscesses. In septicaemia, the bacteria may occur in
immense numbers in the blood and produce a general infection of the
tissues, causing a parboiled appearance of the liver, heart, voluntary
muscles and kidneys, and enlargement of the spleen. The two forms of
infection are often present at the same time.
[Illustration: FIG. 97.--_Staphylococcus pyogenes_.]
[Illustration: FIG. 98.--_Streptococcus pyogenes_.]
_The forms of bacteria_ that may cause blood poisoning are the
_Staphylococcus pyogenes aureus_ and _albus_ (Fig. 97), _Streptococcus
pyogenes_ (Fig. 98), _Bacillus pyocyaneus_, _Bacillus coli communis_, and
the bacillus of malignant oedema (Figs. 99 and 100). The latter is included
with the bacteria that produce blood poisoning because it is a frequent
cause of wound septicaemia. Subcutaneous, punctured, lacerated, contused
and deep wounds without suitable drainage are the most suitable for the
development of and infection of the tissues with the above germs. Wound
infection is most common during hot weather.
_The symptoms are both general and local_. The tissues in the region of the
wound become swollen and painful. In malignant oedema the swelling pits on
pressure, and if the wound is open, the surface becomes soft and may
slough. The body temperature may be several degrees above the normal, the
appetite is impaired or the animal stops eating and acts sleepy. A small
amount of highly-colored urine may be passed. Nervous symptoms, such as
muscular twitching, excited condition, delirium and paralysis, may be
noted.
[Illustration: FIG. 99.--Bacillus of malignant oedema, showing spores.]
[Illustration: FIG. 100.--Bacillus of malignant oedema.]
_The prognosis is unfavorable_. In pyaemia the animal may live from a few
days to several months. Septicaemia usually terminates fatally in from two
to ten days.
_The treatment is largely preventive_. Wounds should be given prompt
attention. They should be freed from all foreign substances and washed with
a disinfecting solution. A contused-lacerated wound should not be sutured
if this interferes with the cleansing of it, and the escape of the wound
secretions. All punctured wounds should be enlarged so as to permit of
treatment and drainage.
HEMORRHAGIC SEPTICAEMIA.--An acute infectious disease of ruminants and
swine, characterized by hemorrhages in the different body tissues that
appear as small red spots or blotches.
_The specific cause of this disease_ is the _Bacillus bovisepticus_ (Fig.
101). This bacillus probably enters the body tissues by way of the lining
membrane of the intestinal and respiratory tracts. In the northern States,
cattle pasturing on marsh lands and swampy pastures are more often affected
with the disease in the late summer and fall than at other seasons of the
year.
The drinking of contaminated surface water that collects in muddy pools and
ponds may cause the disease. Cattle pasturing in stalk fields sometimes
become infected in this way. Dusty sleeping quarters and small, crowded,
muddy yards seem to favor the development of the disease in hogs. Exposure,
insufficient exercise and careless feeding are the predisposing factors.
[Illustration: FIG. 101.--_Bacillus bovisepticus_.]
_The symptoms_ vary according to the animal and organ, or organs of the
body affected and the violence of the attack. The disease may be acute or
subacute. The brain and its membranes, lungs and air-passages and
intestines may become affected. The symptoms may be classed under the head
of nervous, respiratory and intestinal (Fig. 102), and they may be very
unsatisfactory from the standpoint of diagnosis. The history and
post-mortem lesions are of most value in the recognition of this disease.
The local conditions, the loss of several animals in the herd and the
finding of hemorrhagic lesions in the different body tissues may enable
the examiner to correctly diagnose the disease. It is very advisable in
order to confirm the diagnosis to make a bacteriological examination of the
tissues.
The acute form of the disease is very fatal. Animals that have the subacute
form usually recover. The death-rate is between five and fifteen per cent
of the herd. The mortality is heavier than this unless prompt preventive
measures are taken.
_Preventive treatment_ is of the greatest importance. Cattle that become
affected when running on pasture should be moved, or in case a part of the
pasture is swampy, we may prevent further loss by fencing off this portion.
Drinking places that are convenient and free from filth should be provided.
Watering troughs and drinking fountains should be cleaned and disinfected
every few weeks. For this purpose, use a three per cent water solution of a
cresol disinfectant, or a ten per cent water solution of sulfate of iron.
Dusty quarters should be cleaned and disinfected. Dirt floors may be
sprinkled with crude oil.
[Illustration: FIG. 102.--A yearling steer affected with septicaemia
haemorrhagica, intestinal form.]
When an outbreak of septicaemia haemorrhagica occurs in a herd, both the
well and sick animals should be given a physic. Cattle may be given
one-half pound of Epsom salts, repeated in three or four days; sheep and
hogs from one to four ounces of raw linseed oil. Animals that have the
subacute form of the disease may be given stimulants, and iron and bitter
tonics.
ANTHRAX, CHARBON.--This is an acute infectious disease affecting many
different species of animals. Anthrax is one of the oldest animal diseases,
and early in the history of the race it existed as a plague in Egypt. It
most commonly affects cattle, sheep and horses. Man contracts the disease
by handling wool and hides from animals that have died of anthrax, and by
accidental inoculation in examining the carcass of animals that have died
of the disease.
_Cause_.--Anthrax is caused by a rod-shaped, spore-producing microorganism,
_Bacillus anthracis_ (Fig. 103). It gains entrance to the body by way of
the intestinal tract, lungs and air-passages and the skin. The bites of
insects play an important part in the distribution of the disease in some
localities, but the most common method of infection is by way of the
digestive tract, through eating and drinking food and water contaminated
with the anthrax germs. The spores of the _B. anthracis_ are very resistant
to changes in temperature and drying. They may live for years in rich,
moist inundated soils. River-bottom and swampy lands that have become
infected with discharges from the bodies of animals sick with anthrax, and
by burying the carcasses of animals that have died of this disease, retain
the infection for many years. Anthrax is very widely distributed. It is the
most prevalent in the southern portion of the United States, especially the
lower portion of the Mississippi Valley.
[Illustration: FIG. 103.--_Bacillus anthracis_.]
_The symptoms vary in different cases_, depending on the organs affected,
and the virulence and amount of virus introduced. The _apoplectic form_ is
very acute. The disease sets in suddenly; the animal trembles, staggers,
falls and dies in a convulsion. Blood may be discharged from the nose and
with the urine and faeces.
In the _abdominal form_, abdominal pain, diarrhoea, prolapse of the rectum,
bloating and doughy swellings in the region of the abdomen occur.
In the _thoracic form_, the symptoms are bloody discharge from the
nostrils, salivation, rapid, difficult breathing and swelling in the region
of the throat. Local or skin lesions may occur in conjunction with, or
independent of, the above forms of disease. These are carbuncles one or two
inches in diameter that are hot and tender at first, but later become
gangrenous, diffused swellings.
On post-mortem examination the blood is found tarry and dark, and bloody
exudates may be found in the abdominal and thoracic cavities. The spleen is
soft and two or three times larger than normal. The diagnosis should be
confirmed by finding the _B. anthracis_ in the blood and tissues. The
death-rate is very high, usually about seventy-five per cent.
_The treatment is preventive._ Animals should be kept away from lots and
pastures where deaths from anthrax have been known to occur, unless
immunized against the disease. Marshy, swampy land that is infected with
the germs of anthrax should be drained and cultivated.
When an outbreak of the disease occurs, all of the animals should be
vaccinated. The carcasses of the animals that die should be cremated at or
near the place where they die. If hauled or dragged, the necessary
precautions should be taken against scattering the infectious material from
the carcass, and plenty of disinfectants used. Persons attending the
animals should be warned against opening or handling the carcass without
protecting the hands with rubber gloves.
_Anthrax vaccine_ should not be used by incompetent persons.
ULCERATIVE STOMATITIS. (ULCERATIVE SORE MOUTH.)--This is an infectious
disease of young animals. Pigs from a few days to a few weeks of age are
the most commonly affected.
_The specific cause_ of ulcerative sore mouths is the _Bacillus
necrophorus_ (Fig. 104). The infectious agent is distributed by the udder
of the mother becoming soiled with filth from the stable floor and yards,
and by affected pigs nursing mothers of healthy litters. Filth, sharp teeth
and irritation to the gums from the eruption of the teeth are important
predisposing factors.
_The symptoms_ are, at first, an inflammation of the mucous membrane lining
the lips and cheeks and covering the gums. The inflamed parts are first
swollen and a deep red color; later, white patches form and the part
sloughs, leaving a deep ulcer. As ulceration progresses, difficulty in
nursing increases until finally the young animal is unable to suckle. If
ulceration of the mouth is extensive, the animal may be feverish, dull and
lose flesh rapidly. Portions of the lips, gums and snout may slough off.
The death-rate in pigs is very high.
[Illustration: FIG. 104.--_Bacillus necrophorus_.]
_The preventive treatment_ consists in keeping the quarters and yards in a
sanitary condition, and using all possible precautions against the
introduction of the disease into the herd. The diseased young and mother
should be separated from the herd and the quarters disinfected daily. The
mouths of all the young should be examined daily and the diseased animals
treated. The ulcers should be scraped or curetted and cauterized with lunar
caustic, and the mouth washed daily with a two per cent water solution of a
cresol disinfectant. Dipping pigs headforemost into a water solution of
permanganate of potassium (one-half teaspoonful dissolved in a gallon of
water), twice daily, may be practised if the herd is large.
It is usually most economical to kill the badly diseased animals, as they
usually die or become badly stunted.
RABIES, HYDROPHOBIA.--Rabies is an infectious disease affecting the nervous
system, that is transmitted by the bite of a rabid animal and the
inoculation of the wound with the virus present in the saliva. It is
commonly considered a disease of dogs, but because of the disposition of
rabid dogs to bite other animals, rabies is common in domestic animals and
man.
Rabies is widely distributed, being most prevalent in the temperate zone,
and where the population is most dense. It has been excluded from
Australia, Tasmania and New Zealand by a rigid inspection and quarantine of
all imported dogs.
_The specific cause of rabies_ is probably a protozoan parasite (the Negri
bodies present in nerve-cells, Fig. 105). The germ spreads from the wounds
through the nerves and central nervous system. The disease-producing
organisms are present in great numbers in the nerve-tissue and saliva.
_The period of incubation_ varies from a few days to several months. It is
usually from ten to seventy days.
_The symptoms_ differ in the different species. There are two forms of the
disease: the _furious_ and the _dumb_. The former is more common.
[Illustration: FIG. 105.--Negri bodies in nerve-tissue.]
_In the dog, the symptoms may be divided into three stages_. The first, or
_melancholy stage_, usually lasts from twelve to forty-eight hours. The
animal's behavior is altered and it becomes sullen, irritable and nervous.
Sometimes it is friendly and inclined to lick the hand of its master. An
inclination to gnaw or swallow indigestible objects is sometimes noted.
Frequently a certain part of the skin is rubbed or licked.
The second, or _furious stage_, may last several days. Violent nervous or
rabid symptoms are manifested, and the dog may leave home and travel long
distances. The animal usually shows a strong inclination to bite. It may
move about snapping at imaginary objects in its delirium, and may bite any
person or animal with which it comes in contact. The bark is peculiar, the
appetite is lost and the animal becomes weak and emaciated.
In the third, or _paralytic stage_, the dog may present an emaciated,
dirty, ragged appearance. The lower jaw may drop, the tongue hangs from the
lips and the eyes appear sunken and glassy. Paralysis of the hind parts may
be present.
_In the dumb form_, the paralytic symptoms predominate and the disease
pursues a short course. Rabies terminates in death in from four to ten
days.
_Furious rabies_ is more common in the _horse_. The animal is very nervous,
restless and alert. It may attack other animals in a vicious manner,
kicking and biting them. The animal does not seem to care to eat or drink,
and usually shows violent nervous symptoms, such as biting the manger,
rearing and kicking when confined in the stable.
_Cattle_ butt with the horns and show a tendency to lick other animals.
They bellow more than common and the sexual desire is increased. Paralytic
symptoms are manifested early in the disease, and the animal may fall when
moving about. They soon present a gaunt, emaciated appearance.
In dogs the diagnosis is confirmed by a _microscopical examination_ of the
vagus ganglia and that portion of the brain known as Amnion's horn, and the
finding of Negri bodies in the nerve-cells. In case a person is bitten by a
dog, the animal should be confined until the disease is well advanced and
killed or allowed to die. The head should then be removed and forwarded to
the State laboratory, or wherever such examinations are made.
_The treatment_ is preventive. Wherever an outbreak of rabies occurs all
dogs should be confined on the owner's premises or muzzled. All dogs
running at large without muzzles should be promptly killed. A heavy tax on
dogs, and the killing of all dogs not wearing a license tag, would prevent
the heavy financial loss resulting from rabies, and the ravages of
wandering dogs in the United States. In countries where the muzzling of
dogs is enforced during the entire year, rabies is a rare disease.
FOOT-AND-MOUTH DISEASE.--This is a highly contagious and infectious disease
of cattle, sheep, goats and swine. It is characterized by the eruption of
vesicles on the mucous membrane lining the mouth, the lips, between and
above the claws and in the region of the udder and perineum. Man may
contract the disease by caring for sick animals; or by drinking raw milk
from a sick cow. Babies are most susceptible to infection from milk.
Foot-and-mouth disease was introduced into eastern Europe from the steppes
of Prussia and Asia near the end of the eighteenth century. It was
introduced into England about 1839, and in 1870 into Canada through the
importation of cattle from England. From Canada the disease spread to the
United States. Very few animals were infected during the 1870 outbreak, and
the disease was quickly stamped out in both countries.
Europe has been unable to eradicate foot-and-mouth disease. The different
outbreaks that occur from time to time cause enormous financial loss. In
the United States outbreaks of the disease have occurred in the following
years: 1870, 1884, 1902-'03, 1908 and 1914-'15. In the first two outbreaks
very few cattle contracted the disease, and the infection was quickly
stamped out. The third and fourth outbreaks were more extensive, and it was
necessary to slaughter several thousand cattle and hogs in order to
eradicate the disease. The first four outbreaks occurred in the eastern
States, and the disease was prevented from spreading to the principal
live-stock centers of the country, and the leading stock-raising States by
slaughtering the diseased and exposed animals and by county and State
quarantines. Early in the 1914-'15 outbreak, the disease spread to the
Chicago Stock Yards, and from there, through shipments of cattle, to the
principal live-stock sections of the country. The financial loss resulting
from this outbreak has amounted to several million dollars. The Federal and
State authorities have always been successful in stamping out the disease
in the United States.
_The specific cause_ of foot-and-mouth disease is a filterable virus that
is present in the serum from the vesicles, the saliva, milk, and various
body secretions and excretions from the sick animal. In the early stage of
the disease it is present in the blood. None of the many investigators have
been able to discover the microorganism that produces the disease.
Two of the outbreaks of foot-and-mouth disease in the United States
originated from an infected vaccine used for the inoculation of vaccine
heifers. The origin of the 1914-'15 outbreak has not been discovered. When
introduced into a country, the disease spreads rapidly, through the
movement of live-stock affected by the disease. Animals recently recovered
may infect other animals. Dogs, birds, people, vehicles, milk, roughage,
grains and other material from an infected farm may spread the disease.
_The period of incubation is short_. Symptoms of disease may be manifested
in from one to six days following exposure.
[Illustration: FIG. 106.--A cow affected with foot-and-mouth disease. Note
the accumulation of saliva about the lips. (From report of the Bureau of
Animal Industry.)]
_The first symptoms_ are fever, dulness, trembling and loss of appetite.
This is followed by vesicles or blisters forming on the mucous membrane of
the mouth, lips, between and above the claws and the region of the udder.
The inflammation of the mouth and feet may be very painful. Long strings of
saliva may dribble from the mouth and collect about the lips (Fig. 106). A
smacking or "clucking" sound is produced when the animal moves its jaws and
lips. The severe pain resulting from the inflammation of the mouth and
feet, and the difficulty in moving about and eating and drinking, cause the
animal to lose flesh and become emaciated. Milk cows may go dry.
_The death-rate is not heavy_. Some writers place it as low as two or three
per cent. Because of the erosions and sloughing of the tissues of the
mouth, feet and udder it becomes necessary to kill many of the animals.
Young animals frequently die of inflammation of the digestive tract. The
immunity conferred by an attack of the disease is not permanent.
[Illustration: FIG. 107.--Slaughtering a herd of cattle affected with
foot-and-mouth disease. (Photographed by S. J. Craig, County Agricultural
Agent, Crown Point, Indiana.)]
The most economical measures of _prevention and control_ are to buy and
slaughter all diseased and exposed animals, bury the carcasses in
quicklime, disinfect the premises (Figs. 107, 108 and 109) and enforce a
district, county and State quarantine, until after the infection has died
out. This statement may not hold true of methods of control in countries
where foot-and-mouth disease is widely distributed.
TETANUS. LOCKJAW.--This is an acute infectious disease that is
characterized by spasmodic contractions of voluntary muscles. The specific
germ remains at the point of infection, and produces toxins that cause
tetanic contractions of the muscles. It commonly affects horses, mules,
cattle, sheep and swine. The disease is most common in warm, temperate
climates.
[Illustration: FIG. 108.--Disinfecting boots and coats before leaving a
farm where cattle have been inspected for foot-and-mouth disease.
(Photographed by S. J. Craig, County Agricultural Agent, Crown Point,
Indiana.)]
[Illustration: FIG. 109.--Cleaning up and disinfecting premises where an
outbreak of foot-and-mouth disease has occurred.]
The _specific cause_ is a pin-shaped germ, the _Bacillus tetani_ (Fig.
110), that is present in the soil, especially those that are rich and well
manured. The germ enters the body by way of a wound, especially punctured
wounds. Infection may take place through some wound in the mucous membrane
lining the mouth, or other parts of the digestive tract. Infection may
follow a surgical operation, such as castration. In any case, the germ
requires an absence of air (oxygen) for its development.
_The period of incubation_ varies from one to two weeks, the length of time
depending on the nearness of the wound to a large nerve trunk or brain.
[Illustration: FIG. 110.--_Bacillus tetani_.]
The first _symptom_ observed is a stiffness of the muscles, especially
those nearest the point of inoculation or wound. The muscles of the head,
neck, back and loins are often affected first, and when pressed upon with
the fingers feel hard and rigid. The disease rapidly extends, producing
spasms of other muscles of the body. In breathing, the ribs show less
movement than normal, the head is held in one position and higher than
usual, the ears are stiff or pricked, the nostrils dilated, the lips rigid
or drawn back and the eyes retracted, causing the "third eyelid" to
protrude over a portion of the eye (Fig. 111). In most cases the muscles of
mastication and swallowing are affected. The animal may be unable to open
its mouth and swallows with difficulty. When standing, the limbs are spread
out so as to increase the base of support, and in acute cases about to
terminate fatally, the pulse is quick and small and the respiration
shallow, rapid and labored. The animal sweats profusely, falls down and
struggles violently, but remains conscious to the end.
[Illustration: FIG. 111.--Head of horse affected with tetanus, showing
"third eyelid" protruding over the eye.]
In the _subacute form_ (Fig. 112) the symptoms are mild, and the animal may
be able to move about, eat and drink without very great effort.
[Illustration: FIG. 112.--A subacute case of tetanus.]
_Treatment_ is largely preventive. All wounds should be carefully
disinfected. This is especially advisable in punctured wounds of the foot.
In communities, or on premises where tetanus is a common disease, animals
that have punctured or open wounds should be given a protective dose of
tetanus antitoxin.
_The curative treatment_ is largely good care. If a wound is present, it
should be thoroughly disinfected. The animal may be supported by placing it
in a sling. A comfortable box-stall, where the animal is not annoyed by
noises or worried by other animals, is to be preferred. A fresh pail of
water should be given the animal several times daily.
_The course_ of the disease varies. Death may occur within a few days, or
the disease may last two or three weeks. Animals that recover from tetanus
may show symptoms of the disease for several weeks. The death-rate is
highest in hot climates and during the summer months.
If the animal can eat, it is not advisable to feed a heavy ration of
roughage or grain. A very light diet of soft food, such as chops and
bran-mash, prevents constipation and encourages recovery. Drugs that have a
relaxing effect on the muscles may be given. Tetanus antitoxin may be given
in large doses.
QUESTIONS
1. What is septicaemia and pyaemia?
2. What is haemorrhagic septicaemia? Give methods of spreading and
controlling this disease.
3. Give the cause of anthrax and symptoms.
4. What control measures are recommended in anthrax?
5. What is ulcerative sore mouth? Give the treatment.
6. Describe the symptoms occurring in rabies, and state the control
measures recommended.
7. Name the species of animals affected by foot-and-mouth disease, and the
countries where the disease is prevalent.
8. Give the methods of distribution and control of foot-and-mouth disease.
9. What is the specific cause and method of infection in tetanus? Give the
treatment.
CHAPTER XXIX
INFECTIOUS DISEASES OF THE HORSE
STRANGLES. DISTEMPER.--This is an acute infectious disease associated with
a catarrhal condition of the air-passages and suppuration of the lymphatic
glands in the region of the throat. Colts are the most susceptible to the
disease. One attack renders the animal immune against a second attack of
the disease, but the immunity is not always permanent.
_The specific cause_, _Streptococcus equi_ (Fig. 113), was discovered by
Schutz in 1888. Strangles is commonly spread by exposing susceptible
animals to diseased animals, either by direct contact, or by exposing them
to the infection in the stable and allowing them to drink or eat food from
watering and feeding troughs on premises where the disease exists. The
predisposing causes are cold and sudden changes in the weather. For this
reason the disease is most prevalent during the late winter and early
spring.
[Illustration: FIG. 113.--Streptococcus of strangles.]
_The period of incubation varies_, usually from four to eight days.
_The symptoms_ at the beginning of the attack are a feverish condition and
partial loss of appetite. The visible mucous membranes are red and dry.
This is followed by watery nasal secretions that become heavy and purulent
within a few days. The inflammation may extend to the larynx and pharynx.
The glands in the region of the jaw become hot, swollen and painful, and
the animal may be unable to eat or drink. The swelling and inflammation of
the throat, and the heavy, pus-like secretions that accumulate in the nasal
cavities, cause difficult respirations. After a few days the abscesses
usually break, and the symptoms are less severe. If the abscesses break on
the inside of the throat, the discharge from the nostrils is increased.
The disease may be accompanied by an eruption of nodules, or vesicles on
the skin, or nasal mucous membrane.
In severe and chronic cases multiple abscesses may form. This complication
is indicated by emaciation and weakness. Such cases usually terminate in
death. Severe inflammation and swelling in the region of the throat may
terminate in strangulation and death. The death-rate is from one to three
per cent.
_The preventive treatment_ consists in using all possible precautions to
prevent the exposure of susceptible animals and practising the immunization
of exposed animals. The curative treatment is principally careful nursing.
Rest, a comfortable stall, nourishing feed and good care constitute the
necessary treatment for the average case of distemper. When the abscesses
become mature, they should be opened and washed with a disinfectant.
Steaming the animal several times daily relieves difficult breathing and
the irritated condition of the mucous membranes. In case the abscesses do
not form promptly and the throat is badly swollen, a blistering ointment or
liniment may be applied. Bitter and saline tonics, the same as recommended
in the treatment of indigestion, may be given with the feed.
INFLUENZA (CATARRHAL OR SHIPPING FEVER).--This is a well-known acute
infectious disease of solipeds. It is characterized by depression, high
body temperature and catarrhal inflammation of the respiratory and other
mucous membranes.
Several epidemics of influenza have occurred in the United States. The most
serious epidemic occurred in the latter part of the '70's, and the last one
in 1900-'01. Influenza is present in the principal horse centers in a
somewhat attenuated form.
_The specific cause_ of the disease has never been determined. The virus is
present in the expired air, nasal secretions and excreta. Close proximity
to a diseased animal is not necessary in order to contract the disease.
Stables may harbor the infection, and it may be distributed by such disease
carriers as blankets, harness, clothing of the attendant and dust.
_The predisposing causes_ are cold, exposure and changes in climate. When
the disease appears in a country, it is first present in the large cities,
and from there it is scattered to the outlying districts. The _period of
incubation_ is usually from four to seven days.
_The early symptoms_ of the disease are a high fever, marked depression and
partial or entire loss of appetite. The horse usually stands in the stall
with the head down and appears sleepy. The visible and respiratory mucous
membranes are inflamed, the respirations are quickened and the animal may
cough. The eyes are frequently affected, the lids and cornea showing more
or less inflammation. The digestive tract may be affected. At the
beginning, colicky pains may be present and later constipation and
diarrhoea. Symptoms of a serious nervous disturbance are sometimes
manifested.
The limbs usually become swollen or filled. This disappears as the animal
begins to improve. Pregnant mares may abort. The death-rate is low.
_The treatment required for the sick animals_ is largely rest, a light diet
and a comfortable, clean, well-ventilated stall, free from draughts.
Windows in the stall should be darkened. If the stable is cold, the body of
the animal should be covered with a blanket and the limbs bandaged. Two
ounces of alcohol and one drachm of quinine may be given three or four
times daily. Small doses of raw linseed oil may be given if necessary.
Horses that are exposed to cold, wet weather or worked after becoming sick,
frequently suffer from pneumonia, pericarditis, gastro-enteritis and other
diseases. Such complications should be given prompt treatment.
It is very advisable to give a protective serum to horses that are shipped
or transported long distances, and exposed to the disease in sale or
transfer stables.
GLANDERS, FARCY.--This is a contagious and infectious disease of solipeds
that is characterized by the formation of nodules and ulcers on the skin,
nasal mucous membrane and lungs.
Although glanders is one of the oldest of animal diseases, it was not until
1868 that its contagious character was demonstrated. The disease is widely
distributed. It became more prevalent in the United States after the Civil
War. The vigorous control measures practised by the State and Federal
health officers have greatly decreased the percentage of animals affected
with glanders. At the present time the disease is more often met with in
the large cities than in the agricultural sections of the country.
[Illustration: FIG. 114.--_Bacillus mallei_.]
_The specific cause of glanders is the Bacillus mallei_ (Fig. 114). This
microorganism was discovered in 1882. It is present in the discharges from
the nasal mucous membrane and the ulcers. These discharges may become
deposited upon the feed troughs, mangers, stalls, harness, buckets,
watering troughs, drinking fountains and attendants' hands and clothing.
Healthy horses living in the same stable with the glandered animals may
escape infection for months. It is usually the diseased animal's mate, or
the one standing in an adjoining stall, that is first affected. Catarrhal
diseases predispose animals to glanders, as the normal resistance of the
mucous membranes is thereby reduced. The most common routes by which the
germ enters the body are by way of the digestive and respiratory tracts. It
may enter the body through the uninjured mucous membranes of the
respiratory tract and genital organs, or through wounds of the skin.
_The period of incubation_ may be from a few to many days.
_The symptoms_ may be _acute_ or _chronic_ in nature. The _acute form_
pursues a rapid course. It is frequently seen in mules and asses, and it
may develop from the subacute or chronic form in horses. When the disease
is acute, the animal has a fever, is stupid, does not eat, and may have a
diarrhoea. In this form the lymphatic glands suppurate, the animal loses
flesh rapidly and dies in from one to two weeks.
[Illustration: FIG. 115.--Nasal septum showing nodules and ulcers.]
The _chronic form_ is the most common. It develops slowly and lasts for
years. The early symptoms of the disease (chilling and fever) usually
escape notice. The first visible symptom is a nasal discharge of a dirty
white color from one or both nostrils. This is usually scanty at first, and
intermittent, but later becomes quite abundant. The discharge is very
sticky, and adheres to the hair and skin. The most frequent seat of the
disease is in the respiratory organs, lymph glands and skin. Nodules and
ulcers appear on the nasal mucous membrane (Fig. 115), but they may be so
high up as to escape notice. The ulcers are very characteristic of the
disease. They are angry looking, with ragged, raised margins, and when they
heal leave a puckered scar. The submaxillary glands may be enlarged, and at
first more or less hard and painful, but later they become nodular and
adhere to the jaw or skin. Nodules and ulcers may form on the skin over the
inferior wall of the abdomen and the inside of the hind limbs and are known
as "farcy buds." Lymphatic vessels near these buds become swollen and hard.
The animal loses flesh rapidly, does not withstand hard work, and the limbs
usually swell.
It is sometimes difficult to diagnose the disease. The ulcers on the nasal
mucous membranes and elsewhere are very characteristic, and when present
enable the examiner to form a diagnosis. In cases of doubt, a
bacteriological examination of the nasal discharge may be made, or we may
resort to one or several of the various diagnostic tests. The Mallein test
is quite commonly used. The sterilized products of a culture of the _B.
mallei_ are injected beneath the skin of the suspected animal. This causes
a rise in body temperature and a hot, characteristic swelling at the point
of injection in glandered animals.
[Illustration: FIG. 116.--_Streptococcus pyogenes equi_.]
_Treatment is not recommended_ at the present time. Nearly all of the
States have laws which aim to stamp out the disease wherever found by
killing all affected animals, and thoroughly disinfecting the stables,
harness and everything which has been near the animal. Diseased animals
should be carefully isolated until slaughtered, and all animals exposed to
them should be subsequently tested for glanders.
CONTAGIOUS PLEUROPNEUMONIA (STABLE PNEUMONIA).--This is an infectious
disease of solipeds that usually results in a fatal inflammation of the
lungs and pleural membrane.
Many writers have described this disease as associated with influenza, but
it is frequently seen as a separate disease, usually involving only the
lungs and pleurae. It is prevalent in several parts of the United States,
more particularly the horse centers or large markets, where it appears in
the form of epidemics. In several of these localities it is known as
western or stable fever.
_The specific cause is not definitely known_. The _Streptococcus pyogenes
equi_ (Fig. 116) is very commonly present. This germ grows in the diseased
tissues. The disease is spread by direct or indirect contact, as when well
or susceptible animals are placed in the same stable with an animal
affected with the disease, or in stalls which have recently held diseased
animals.
_The period of incubation_ is from four to ten days following exposure.
_The symptoms_ are those commonly seen at the beginning of an attack of
simple pneumonia and pleurisy. They consist of chills, high fever, cough,
depression, difficult and labored breathing and loss of appetite. The
disease usually runs a course of from one to three weeks. The death-rate is
thirty per cent or more.
_The treatment_ is mainly preventive. Stables where horses having
pleuropneumonia have been kept should be cleaned and disinfected by
spraying the floors, stalls and walls with a four per cent water solution
of a cresol disinfectant. It is advisable to subject all newly-purchased
animals to a short quarantine period before allowing them to mix with the
other animals in the stable. Exposed animals may be given a protective
serum.
_The curative treatment_ is the same as recommended for the treatment of
simple pneumonia and pleurisy.
QUESTIONS
1. What is the specific cause of distemper? Give the symptoms and
treatment.
2. What are the different methods of spreading influenza? Give the symptoms
and treatment.
3. Give the cause and methods of controlling glanders.
4. Give the cause and treatment of contagious pleuropneumonia.
CHAPTER XXX
INFECTIOUS DISEASES OF CATTLE
[Illustration: FIG. 117.--A case of "lumpy jaw."]
ACTINOMYCOSIS, "LUMPY JAW."--This is an infectious disease that is
characterized by the formation of tumors and abscesses (Fig. 117), and the
destruction of the infected tissues. The disease is common in cattle and
usually affects the bones and soft parts of the head. In the United States,
where the disease is known as "lumpy jaw" the jawbone is commonly affected.
In European countries the disease frequently involves the tongue, and the
term "wooden tongue" is applied to it. The disease may affect regions of
the body other than the head. Actinomycosis of the lungs sometimes occurs.
Swine and horses may be affected by this disease.
_The specific cause_ of actinomycosis is commonly known as the ray fungus
(Fig. 118). This fungus grows on certain plants, and the animal usually
contracts the disease by eating plants or roughage that have the fungus on
them. Grasses having awns that are capable of wounding the mucous membrane
of the mouth and penetrating the gums are most apt to produce the disease.
Young cattle that are replacing and erupting their teeth are most prone to
"lumpy jaw." Conditions that favor bruising of the jaw and external wounds
favor the development of actinomycosis.
The fungus grows in the tissues, causing an inflammatory reaction and
destruction of the tissue. The ray fungus can be seen in the diseased
tissue or the pus as yellowish, spherical bodies about the size of a grain
of sand. Each of these bodies is formed by a large number of club-like
bodies arranged about a central mass of filaments.
[Illustration: FIG. 118.--The ray fungus.]
_The local symptoms_ are characteristic (Fig. 117). The tumor may involve
the soft tissues of the head. If the jawbone is affected the tumor feels
hard and cannot be moved about. Sometimes it is soft and filled with pus.
Tumors of long standing may possess uneven, nodular surfaces and fistulous
openings. When the tongue is affected, it is swollen and painful, and
prehension and mastication of the food may be impossible. When the pharynx
is the seat of disease, breathing and swallowing are difficult and painful.
Actinomycosis of the lungs may present the appearance of a chronic
pulmonary affection. If the disease involves the head and lungs, the animal
may become unthrifty and emaciated. In doubtful cases a microscopic
examination of a piece of the tumor, or some of the pus, may be necessary.
_The treatment is surgical and medicinal_. Small, external tumors may be
removed by an operation. Sometimes an incision is made into the diseased
tissue and a caustic preparation introduced.
The most desirable method of treatment is the administration of large doses
of iodide of potassium in a drench, or in the drinking water. The dose is
from one to three drachms daily for a period of seven to fourteen days. The
size of the dose depends on the size of the animal and its susceptibility
to iodism. An animal weighing 1000 pounds may be given two drachms. The
treatment is kept up until the symptoms of iodism develop. The condition is
indicated by a loss of appetite and a catarrhal discharge from the eyes and
nostrils. When this occurs, the treatment should be stopped, and the animal
drenched with one-half pound of Epsom salts, and the dose repeated after
three or four days. After an interval of two weeks, the iodide of potassium
treatment should be repeated if the growth of the tumor is not checked.
EMPHYSEMATOUS ANTHRAX, "BLACK LEG."--"Black leg" is an acute infectious
disease of cattle that is characterized by lameness and superficial
swellings in the region of the shoulder, quarter or neck. The swellings are
hot and painful and usually contain gas.
_The specific cause_ of "black leg" is a rod-shaped, spore-producing germ,
the bacillus of emphysematous anthrax (Fig. 119). This germ possesses great
vitality, and may live indefinitely in the soil. It has been known to live
for years in clay and undrained soils. Young animals that are in high
condition are predisposed to the disease.
The germ enters the body through abrasions in the skin and mucous membrane
of the mouth and intestines.
"Black leg" is a common disease of young cattle in all sections of the
country where cattle-raising is engaged in extensively. Outbreaks of the
disease are most prevalent in the early spring after the snow has melted,
and in the late summer in localities where cattle graze over the dried-up
ponds and swampy places in the pasture. The germs of black leg may be
carried from a farm where the disease is prevalent to non-infected premises
by surface water. The opening up of drainage ditches through stock-raising
communities may be followed by outbreaks of the disease.
[Illustration: FIG. 119.--Bacillus of emphysematous anthrax.]
_The symptoms_ of black leg develop quickly and may terminate fatally in a
few hours. These are general dulness, stiffness, prostration and loss of
appetite. Lameness is a prominent symptom. The animal may show a swelling
in the regions of the shoulder and hindquarters or on other parts of the
body. The swelling is very hot and painful at first, but if the animal
lives for a time, it becomes less tender, crackles when pressed on and the
skin may feel cold and leathery. Fever is a constant symptom. In the highly
acute form of the disease nervous symptoms, such as convulsions and coma,
occur.
_The tissue changes_ in the region of the swelling are characteristic. An
incision into the swelling shows a bloody, dark exudate and the surface of
the muscular tissue is dark. Frothy, bloody liquid escapes from the mouth,
nose and anus.
_The preventive treatment_ consists in thoroughly draining pastures and
yards where cattle run. This measure does not insure cattle against the
disease. Cattle that die of "black leg" should be cremated. This should be
done at the spot where the animal dies. If the carcass is moved or opened,
the ground should be thoroughly wet with a four per cent water solution of
a cresol disinfectant and covered with lime.
_Vaccination_ of the exposed or susceptible animals should be practised. On
farms where the disease exists it may be necessary to vaccinate the young
animals (less than two years of age) once or twice every year in order to
prevent the disease. Medicinal treatment is unsatisfactory.
TEXAS OR TICK FEVER.--Tick fever is an infectious disease of cattle. It is
caused by an animal organism that is present in the blood, and is conveyed
from the animal that is host for the tick fever parasite to the
non-infected animal by a tick (Figs. 120 and 121).
[Illustration: FIG. 120.--Cattle tick (male).]
[Illustration: FIG. 121.--Cattle tick (female).]
Tick fever was introduced into the southern portion of the United States
through importation of cattle by the Spaniards. Previous to the
establishing of a definite quarantine line between the permanently infected
and the non-infected sections, heavy losses among northern cattle resulted
through driving and shipping southern cattle through the northern States.
The specific cause and the part taken by the tick in its distribution were
not discovered until 1889-'90. Smith recognized and discovered the specific
cause of the disease, and Kilborn and Salmon proved by a series of
experiments that the cattle tick was responsible for the transmission of
the disease from animal to animal.
_The specific cause_ of tick fever is a protozoan parasite, _Piroplasma
bigeminum_ (Fig. 122). It is present in the blood of cattle that are
affected with this disease. The natural method of entrance into the body is
through the bite of the cattle tick. The disease may be transmitted by
inoculating blood containing the parasite into a susceptible animal.
There are two forms of the disease, the _acute_ and _chronic_.
_The symptoms of the acute form_ of the disease are a high fever,
depression, loss of appetite, diarrhoea, dark or bloody urine, staggering
gait and delirium. Death may occur within a few days from the time the
first symptoms are manifested.
_The symptoms of the chronic form_ of the disease resemble the acute form,
but are more mild. The animal is unthrifty and loses flesh rapidly. The
bloodless condition of the body is manifested by the pale, visible mucous
membrane. Death seldom occurs.
[Illustration: FIG. 122.--Blood-cells with _Piroplasma bigeminum_ in them.]
The most characteristic _diseased changes_ found on post-mortem examination
occur in the liver and spleen. The liver is enlarged, and a yellowish,
mahogany-brown color. The gallbladder is filled with a very thick bile. The
spleen may be several times the normal size and dark colored. When it is
cut into, the pulpy tissue may resemble thick, dark blood. The kidneys are
pale and the bladder may contain dark or reddish-colored urine.
In the northern States and outside of the quarantined area, the direct or
indirect exposure of the affected cattle to southern cattle, and the
presence of the cattle tick, _Margarophus annulatus_, are sufficient
evidence to confirm the diagnosis of this disease.
_The prevention and control_ depend on destruction of the cattle tick. In
the early history of the disease, shipping and driving of southern cattle
into and through the northern States caused outbreaks of tick fever and
heavy losses among northern cattle. This finally resulted in the locating
of the infected district, and the establishment of the Texas-fever
quarantine line in 1891 by Dr. D. E. Salmon.
Previous to this time Kilborne and Salmon proved that the cattle tick was
essential to the spread and production of the disease. A further study of
the life history of the tick resulted in the discovery that it could not
mature unless it became a parasite of horses, mules, or cattle. This has
led to the eradication of the tick in certain sections of the South, by not
allowing cattle access to a pasture or lot for a certain period, and by
freeing the animals from ticks by hand-picking, dipping and smearing.
The immunization of cattle that are shipped into an infected district for
breeding purposes is often practised. Immunity is obtained by introducing
the P. bigeminun into the blood, either by placing a few virulent young
ticks upon the animal, or by repeated inoculation with a very small
quantity of virulent blood.
QUESTIONS
1. Give the cause and treatment of actinomycosis.
2. Give the cause and treatment of emphysematous anthrax.
3. Give the cause of tick fever; distribution of the disease and methods of
control.
CHAPTER XXXI
INFECTIOUS DISEASES OF POULTRY
FOWL CHOLERA.--This is a highly infectious disease of all species of
poultry, that is characterized by weakness, depression and yellowish
colored excrement.
The _specific cause_ of fowl cholera is the _Bacillus avisepticus_ (Fig.
123). This microorganism is transmitted to the healthy birds by the feed,
or water becoming contaminated with the discharges from the diseased birds.
According to Salmon, the period of incubating varies from four to twenty
days.
_The early symptoms_ are a falling off in appetite, high fever, dulness,
diarrhoea and weakness. The affected bird becomes drowsy, the head is drawn
toward the body, and it may remain asleep for long periods at a time.
Salmon states that the general outline of the sick bird becomes spherical
or ball-shaped.
[Illustration: FIG. 123.--_Bacillus avisepticus_.]
The disease is usually highly fatal. In the acute form the larger portion
of the flock may die off within a week. In the subacute and chronic forms,
the birds become greatly emaciated, and a few die off weekly through a
period of a month or longer.
_The tissue changes_ occurring in the disease are inflammation of all or a
few of the internal organs. Ward states that the most characteristic lesion
of fowl cholera is the severe inflammation of that portion of the small
intestine nearest to the gizzard. Small hemorrhagic spots may be found on
the heart and other organs.
_The treatment is both preventive and curative_. The preventive treatment
consists in quarantining newly purchased birds until we are satisfied that
they are free from disease. The occasional disinfection of the poultry
houses and runs is highly important. Cleaning the poultry house by removing
the floor, roosts, or any part of the house for the purpose of removing all
filth, and spraying the interior with a three per cent water solution of a
cresol disinfectant, should be practised. Lime should be scattered over the
runs, or the yards immediately about the house. The above preventive
measures form an important part of the care and management of the flock.
The carcasses of the dead birds should be burned. It is advisable to kill
all birds that are fatally sick.
All of the flock should be given antiseptics with the feed and water. Four
ounces of a water solution of copper sulfate, made by dissolving
one-quarter pound of this drug in one gallon of hot water, may be added to
each gallon of drinking water. Frequent disinfection of the drinking
fountains, feeding places and houses should be practised.
DISEASES RESEMBLING FOWL CHOLERA.--There are a few diseases, such as
septicaemia, limber neck and infectious enteritis, that are sometimes
mistaken for fowl cholera. These diseases are caused by different
microorganisms that may be found in the digestive tract and air-passages of
healthy birds, insanitary conditions and decomposed feed, especially meat.
It seems that under certain conditions, such as insanitary quarters and
birds that are low in constitutional vigor and weakened from other causes,
certain germs may become disease-producers. The death rate from mixed
infections is very heavy in poultry.
_The symptoms_ vary in the different cases. The disease may be highly
acute, as in limber neck, or chronic, extending over a period of a week or
more. Diarrhoea is not a prominent symptom in the majority of cases.
The post-mortem lesions vary from a hemorrhagic to a chronic inflammation
of the different body organs and serous membranes.
_The treatment_ is preventive. A frequent cleaning and disinfecting of the
poultry house and surroundings, avoiding the feeding of spoiled feed, or
allowing the drinking fountains and feeding places to become filthy, are
effective preventive measures. Sick birds should be either isolated and
quarantined, or destroyed. Antiseptics may be given with the feed and
drinking water.
AVIAN DIPHTHERIA (ROUP).--This infectious disease of poultry is especially
common in chickens. It is characterized by a catarrhal and diphtheritic
inflammation of the mucous membranes of the head.
_The specific cause of roup_ has not been determined. The disease-producing
germs are present in the discharges from the nostrils, eyes and mouth, and
the body excretions of sick birds. Birds having a mild form of roup, or
that have recently recovered from it, are common carriers of the disease.
The disease is usually introduced into the flock by allowing birds exposed
at poultry shows, or recently purchased breeding stock from an infected
flock, to mix with the healthy birds.
_The predisposing causes_ are very important factors in the development of
roup. Cold, damp, draughty, poorly ventilated poultry houses cause the
disease to spread rapidly and become highly acute.
_The symptoms_ differ in character in the different outbreaks of the
disease. Usually the first symptoms noticed are sneezing, dulness,
diminished appetite and a watery discharge from the nostrils and eyes.
Later the eyelids may become swollen and the nostrils plugged by the
discharge from the inflamed membranes. If the mouth is examined at this
time, an accumulation of mucus and patches of diphtheritic or false
membranes are found. In the acute form of roup the false membranes and
yellowish, cheesy-like material accumulate on the different mucous
membranes, and interfere with vision, breathing and digestion. The affected
bird becomes thin and weak. The death rate is very high in this form of the
disease.
_The preventive treatment_ consists in quarantining birds that have been
purchased from other flocks, and that have been exhibited, for a period of
three weeks. A careful examination of the mouth should be made. If a
catarrhal discharge from the nostrils and false membranes is present,
prompt treatment should be used. A sick bird should be held in quarantine
for several weeks after it has recovered, and receive a thorough washing in
a two per cent water solution of a cresol disinfectant before allowing it
to mix with the healthy birds.
The medicinal treatment consists in removing the discharges from the
nostrils and eyes with pledgets of absorbent cotton that are soaked with a
four per cent water solution of boric acid. Among the common treatments
mentioned are boric acid and calomel, equal parts by weight, blown into the
nostrils and eyes with a powder blower. Water solutions of boric acid,
potassium permanganate and hydrogen peroxide are recommended. Liquid
preparations are applied with pledgets of cotton, oil cans, or atomizers.
Many recoveries can be obtained with careful treatment. It is usually most
economical to kill the severely affected birds. Many poultrymen dispose of
the entire flock as soon as the disease makes its appearance, and clean and
disinfect the premises before restocking.
CHICKENPOX.--In some sections the disease appears in another form, known as
_chickenpox_ (contagious epithelioma), in which nodules form on the skin
along the base of the comb and other parts of the head, or both forms may
be met with in the same flock. The nodules should be treated with vaseline,
or glycerine ointments containing two per cent of any of the common
antiseptics or disinfectants.
ENTERO-HEPATITIS. "BLACKHEAD."--This is a very fatal disease of young
turkeys. Grown turkeys and other fowls are not so susceptible to the
disease. It is characterized by an inflammation of the liver and
intestines, especially the caeca.
_The specific cause_ is a protozoan microorganism, _Amoeba meleagridis_.
Adult fowls and turkeys may act as carriers of the germ, and the young
turkeys become infected at an early period.
_The symptoms_ are diminished or lost appetite, dulness, drooped wings,
diarrhoea, weakness and death. When the disease becomes well advanced, the
head and comb become dark.
_The course of the disease_ is from a few weeks to three months. Very few
of the young turkeys survive.
_The treatment_ is almost entirely preventive. The same precautionary
measures for the prevention of the introduction of disease into the flock,
recommended in other infectious diseases, should be practised. Turkeys that
survive should be disposed of. As chickens may harbor the disease-producing
germs, we should not attempt to raise turkeys in the same quarters with
them. Eggs should be obtained from disease-free flocks. Wiping the eggs
with a cloth wet with fifty per cent alcohol may be practised. The same
recommendations regarding the cleaning and disinfecting of the quarters
described in the treatment of fowl cholera should be practised.
If an outbreak of the disease occurs in the flock all of the sick birds
should be killed, and their carcasses cremated. Moving the flock to fresh
runs and the administration of intestinal antiseptics are the only
effective lines of treatment.
AVIAN TUBERCULOSIS.--Tuberculosis of poultry is a serious disease in some
countries. Poultry usually contract tuberculosis by contact with a
tubercular bird, and not from other domestic animals and man.
_The symptoms_ are of a general character, such as emaciation, weakness,
wasting of muscles and lameness. Tubercular growths may appear on the
surface of the body.
If we suspect the presence of the disease, it is advisable to kill one of
the sick birds and make a careful examination. The finding of yellowish,
white, cheesy nodules or masses in the liver, spleen, intestines and
mesenteries is strong evidence of tuberculosis. A bacteriological
examination of the tissues may be necessary in order to confirm the
diagnosis.
The same _methods of treatment_ as recommended in tuberculosis of other
domestic animals may be used in eliminating the disease from the premises
and flock. This consists in killing and cremating all birds showing visible
symptoms, moving the apparently healthy portion of the flock to new
quarters and wiping the eggs with alcohol. The old quarters should be
cleaned, disinfected, and then allowed to stand empty for several months,
when we should again spray with a disinfectant, and scatter lime over the
runs. If the cleaning and disinfecting have been thorough, we may safely
turn young or healthy birds into the old quarters. All possible precautions
against carrying the infection to the healthy flock must be observed.
QUESTIONS
1. Give the cause and treatment for fowl cholera.
2. What diseases resemble fowl cholera? Give the treatment.
3. Give the symptoms and treatment for roup.
4. Give the treatment for "blackhead."
5. Give the treatment for Avian tuberculosis.
REFERENCE BOOKS
Pathology and Therapeutics of the Diseases of Domestic Animals, Vol. I-II,
Hutyra and Marek.
Veterinary Medicine, Vol. I-V, Law.
General Therapeutics for Veterinarians, Frohner.
Prevention and Treatment of the Diseases of Domestic Animals, Winslow.
Age of the Domestic Animals, Huidekoper.
Veterinary Materia Medica and Therapeutics, Winslow.
Veterinary Anatomy, Sisson.
Chauveau's Comparative Anatomy of Domestic Animals.
Manual of Veterinary Physiology, Smith.
Annual Reports of Bureau of Animal Industry, from 1902 to 1911.
End of Project Gutenberg's Common Diseases of Farm Animals, by R. A. Craig