"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.



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).



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.



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.



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).



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 103.5260 F. in a mature hog and a body temperature of 104260 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



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 65260 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).



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.



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.



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.



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.



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.



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.



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.



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.



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.



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.



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.



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.



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.



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.



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.



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.



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.



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.



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.



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.



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.



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



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.



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.



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).



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.



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.



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.

THE END