Sheep cannot be safely dipped for scab during the cold weather. If thickened and scabby, the skin should be scrubbed with the dip, or the animal prepared for dipping or washing by first clipping the hair or wool and scrubbing the skin with water and a good soap. In order to prevent reinfection, it is necessary to remove the animal to new quarters, or thoroughly clean and disinfect the old. It is necessary to wash or spray the fences, floors, walls, brushes and curry-combs with a disinfecting solution. Manure and other litter should be removed to a place where there is no danger from its distributing the infection.
DISEASES OF POULTRY CAUSED BY MITES.—Mites or acarina that cause diseases of poultry may live on the feathers, beneath the skin, and within the body of the fowl.
The small, red mite (Dermanyssus gallinae)remains on the surface of the body only when feeding, and spends the rest of the time under collections of filth and in cracks in the roosts and walls of the house. This parasite causes the birds to become restless, emaciated and droopy.
A very small mite (Sarcoptes mutans)is the cause of scaly leg. It lives under the skin. The joints of the feet appear affected, and the foot and leg become enlarged, roughened and scaly.
Depluming scabiesis caused bySarcoptes laevis var. gallinae. This mite causes the feathers to break off at the surface of the skin. Masses of epidermic scales may form around the broken ends of the feathers. The diagnosis can be confirmed by examining the skin lesions and finding the mite.
The air sac mite(Cytodites nudus) may cause sufficient irritation to the mucous membrane lining the air sacs to seriously obstruct the air passages with mucus, or produce death from exhaustion. A post-mortem examination of a fowl that has died of this disease shows the mites on the surface of the lining membrane of the air-sacs. They appear as a white or yellow dust.
TREATMENT OF POULTRY DISEASES CAUSED BY MITES.—Diseases of poultry caused by mites may be prevented by quarantining all recently purchased birds for a period of from two to four weeks, and by keeping the poultry houses clean. Birds that are found infested with parasites should be destroyed or returned. In case the bird is valuable and suffering from external parasites only, it should be given the necessary treatment.
Red mites may be destroyedby thoroughly cleaning the poultry house, and spraying the roosts, nests, walls and floor with a three per cent water solution of liquor cresolis compositus. This should be repeated twice a week for two weeks.
Scaly-leg may be treatedby applying a penetrating oil to the feet and lower part of the leg. It is advisable to first remove the scales by scrubbing the part with soap and warm water. Dipping the feet in a mixture of kerosene one part and linseed oil two parts is recommended. This should be repeated as often as necessary.
1. Describe the different bot-flies.
2. Give the life history of the bot-fly of the horse; of the ox; of sheep.
3. Give the symptoms of bot-fly diseases.
4. Give the symptoms of lousiness.
5. Give treatment for lousiness of different farm animals.
6. What is the damage from the sheep-tick? Give treatment.
7. Describe the injury from scabies and mange.
8. Give treatments for these diseases.
9. Mention the several poultry mites and tell how to treat them.
The common parasitic diseases of domestic animals are caused by the following groups of worms:Flukesortrematoides;tapewormsorCestoides;thorn-headed wormsorAcanthocephales; andround-wormsorNematoids. Flat worms, such as tapeworms and flukes, require secondary hosts. The immature and mature forms of tapeworms are parasites of vertebrate animals, but an invertebrate host is necessary for the completion of the life cycle of the fluke. The hog is the only specie of domestic animals that becomes a host for the thorn-headed worm. The round-worm is a very common parasite. There are many species belonging to this class.
[Illustration: FIG. 70.—Liver flukes.]
DISTOMA HEPATICUM (COMMON LIVER FLUKE).—Sheep are the most common hosts for this parasite. It is present in the gall ducts and livers, and causes a disease of the liver known as liver rot. The liver fluke is flat or leaf-like and from thirteen to fifteen mm. long (Fig. 70). The head portion is conical. It has an oval and ventral sucker, and the body is covered with scaly spines. The eggs are oval and brownish in color.
The life history, in brief, is as follows: Each adult is capable of producing an immense number of eggs which are carried down the bile ducts with the bile to the intestine, and are passed off with the faeces. Under favorable conditions for incubation, such as warm, moist surroundings, the ova or eggs hatch and theciliated embryosbecome freed. The embryo next penetrates into the body of certain snails and encysts. Thesporocyst, as it is now called, develops into a third generation known asrediawhich escape from the cyst. Thedaughter rediaorcercaria, as they are now termed, leave the body of the snail and finally become encysted on the stems of grass, cresses and weeds. When taken into the digestive tract of the animal grazing over infested ground, the immature flukes are freed by the digestive juices. They then pass from the intestine into the bile ducts. The period of development varies from ten to twenty weeks; each sporocyst may give rise to from five to eightrediaand each redia to from twelve to twentycercaria.
Fluke diseases occur among animals pastured on low, wet, undrained land. Drying ponds and lakes are the homes of the fresh water snails, and in such places there are plenty of hosts for the immature flukes. Wet seasons favor the development of this parasite. Cattle and sheep that pasture on river bottom land in certain sections of the southern portion of the United States are frequently affected with fluke diseases.
The symptoms of liver rot of sheepmay be divided into two stages. The first stage is marked by increase in weight and improved condition. In the second stage of the disease, the animal shows a pale skin and mucous membrane, dropsical swellings, loss of flesh and weakness. The character of the symptoms of the disease depends on the age of the animals and the care that they receive. Young, poorly cared for animals suffer severely from the disease, and the death rate is usually heavy. The finding of fluke ova in the faeces is conclusive evidence of the nature of the disease. It may be advisable to kill one of the sick animals, and determine the nature of the disease by a post-mortem examination.
[Illustration: FIG. 71.—Tapeworm larvae in liver (Echinococcus polymorphus).]
[Illustration: FIG. 72.—Tapeworms.]
The treatment is preventive. Drainage water from a pasture infested with snails harboring immature flukes is a source of infection, and should not be used as a water supply for cattle and sheep. In sections where the disease is prevalent, sheep should not be pastured on low, poorly-drained land. Such land should be used for pasturing horses and cattle, but if possible, it should be first drained and cultivated. Careful feeding and good care may help the affected animals to recover.
[Illustration: FIG. 73.—Tapeworm larvae in the peritoneum (Cysticercus cellulosa).]
TAPEWORMS OR CESTOIDES.—Tapeworms are formed by a chain of segments, joined together at their ends, and are flat or ribbon-shaped (Fig. 71). The head segment is small, and possesses either hooks or suckers. It is by these that the worm attaches itself to the lining membrane of the intestine. The anterior segments are smaller and less mature than the posterior segments. Each segment is sexually complete, possessing both the male and female organs, and when mature, one or more of them break off and are passed out with the faeces. The mature or ripe segments are filled with ova. On reaching the digestive tract of a proper host, usually with the drinking water or fodder, the embryo is freed from the egg. Thearmed embryouses its hooklets in boring its way through the wall of the intestine. It then wanders through the tissues of its host until it finally reaches a suitable place for development (Figs. 71 and 73). On coming to rest, it develops into the larva or bladder-worm, which when eaten by a proper host gives rise to the mature tapeworm.
The following tables give the most important tapeworms:
Name Host Organ
Taenia expansa Sheep and ox IntestineTaenia fimbriata Sheep LiverTaenia denticulata Cattle IntestineTaenia alba Cattle IntestineTaenia perfoliata Solipeds IntestineTaenia mamillana Solipeds IntestineTaenia echinococcus Dog Intestine
Name Host
Cysticercus bovis CattleCysticercus cellulosa Swine and manCysticercus tennicollis Cattle, sheep and swineCoenurus cerebralis Cattle and sheepEchinococcus polymorphus Cattle, sheep, swine and man
The adult tapewormsTaeniae saginataandsoleum, of which theCysticerci bovisandcellulosaare the larvae forms, occur in man. The larvae are present in meat and pork, and this form of parasitism is termed beef measles in cattle and pork measles in hogs. Man becomes host for these two forms of tapeworms through eating measly pork or beef that is not properly cooked.
The dog is the host forTaeniae marginala,coenurusandechinococcus. The larvae forms of thesetaeniaeare theCysticercus tennicollis,Coenurus cerebralisandEchinococcus polymorphus.C. tennicollisis a parasite of the serous or lining membranes of the body cavities. It is not of great economic importance.C. cerebralisis a parasite of the brain of sheep, and may cause a heavy death rate in flocks that are infested with it.E. polymorphusis a parasite of the liver, but it may occur in other organs.
THE THORN-HEADED WORM OR ACANTHOCEPHALE.—This parasite requires a secondary host. In this case a particular species of the May-beetle larva or white grub that is commonly found about manure piles and in clover pastures is the host. The hog eats a white grub that is host for the larval form. The digestive juices free the larva, it then becomes attached to the intestinal mucous membrane and develops into the adult thorn-headed worm (Fig. 74). This parasite is characterized by a hooked proboscis or thorn at its anterior extremity, and the absence of a distinct digestive tract. The male is much smaller than the female. The eggs are passed out of the intestine with the faeces.
[Illustration: FIG. 74.—Thorn-headed worms.]
THE ROUND-WORMS OR NEMATOIDS.—Round-worms are very common parasites of domestic animals (Fig. 75). This group of worms is characterized by their cylindrical form, the presence of a true digestive canal and the separation into two sexes, male and female. The life history is more simple than in the flat worms. Intermediate hosts are not required for the development of the common forms. The eggs and embryos are deposited by the female in the intestinal tract, air passages, or excretory ducts of the kidneys of the host. Development may be completed here, or the eggs and embryos are passed off with the body excretions. They may live for a short time outside the animal body, or undergo certain development and again infest a host of the same species from which they came, through the water, grass and fodder that the animal may take into its digestive tract.
[Illustration: FIG. 75.—Large round-worm in intestine of hog.]
The following species of nematoids are common parasites of domestic animals:
Species OrganAscaris megalocephala IntestinesSclerostoma equinum Large intestine and blood-vesselsSclerostoma tetracanthum Large intestineOxyrus curvula Large intestineOxyrus mastigodes Large intestine
Species OrganStrongylus convolutus AbomasumAscaris vituli Small intestine (calves)Strongylus ventricosus Small intestineOesophagostomum inflatum Large intestineTrichocephalus affins Large intestineStrongylus micrurus BronchiStrongylus pulmonaris Bronchi
Species OrganHaemonchus contortus AbomasumAscaris ovis Small intestineStrongylus filicollis Small intestineOesophagostomum columbianum IntestinesUncinaria cernua Small intestineTrichocephalus affins Large intestineStrongylus filaria BronchiStrongylus rufescens Bronchi and air follicles
Species OrganAscaris suis IntestinesOesophagostomum dentatum Large intestineTrichocephalus crenatus Large intestineTrichina spiralis Muscles and intestinesStrongylus paradoxus Trachea and bronchiSclerostoma pingencola Renal fat and kidney
Species OrganAscaris inflexa IntestineSpiroptera hamulosa GizzardHeterakis papillosa CaecumSyngamus 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. TheA. megalocephalaor 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.
TheS. equinumandS. tetracanthumare 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 youngS. equinummay 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 treatmentis 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 theUncinaria radialus.
The treatmentis 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 wormsare 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.]
Thetreatmentis 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 theOEsopliagostomum 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 treatmentrecommended 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.—TheAscaris suisorcommon roundworm 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. TheA. suisis from 4 to 10 inches (10 to 26 cm.) long.
The Echinorhynchus gigasorthorn-headedworm 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.]
TheTrichocephalus crenatusorwhip 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.
TheOEsophagostomum dentatumorpin wormis from 0.3 to 0.6 inch (8 to 15 mm.) long. It is found in the large intestine (Fig. 78).
Thesymptomsof 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 treatmentof 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 micrurusandStrongylus 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. TheS. micrurusis from 1 to 3 inches (25 to 75 mm.) long. TheS. pulmonarisis 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 symptomsare 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 theStrongylus filariaand 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. TheS. filariais thread-like and theS. refuscenshair-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 bronchitisand 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 treatmentof 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 evidentin 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 pinguicolais 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 treatmentis 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 thatAcaris inflexaor large round-worm,Heterakis pipilosaor small round-worm, and theSpiroptera hamulosaor 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 treatmentof 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 symptomare 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 treatmentis 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.
1. Name the different groups of internal parasites; give examples of each.
2. What conditions favor liver rot? Give the life history of the liverfluke.
3. Name three common tapeworms; give the life history of the beef and porktapeworms.
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.
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 anultra-visible organismthat 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 virusis 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. Theexchange of helpat threshing and shredding time in neighborhoods where there is an outbreak of hog-cholera is the most common method of spreading the disease.Visiting farmswhere 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 hogsmay carry the disease directly to a healthy herd when allowed to run at large.Streamsthat are polluted with the drainage from cholera-infected yards are common sources of disease.
Pigeons, dogs, cowsandbuzzardsthat 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.
Ageis 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 symptomof disease is an elevation of body temperature.
At the beginning of any outbreak of hog-cholera thebody temperaturesof 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 appetiteis 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 rathercharacteristic 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.Diarrhoeaorconstipationmay 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 beatsare 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 thelungsare 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. Thepericardiummay be inflamed. In such cases the hog staggers and falls when forced to walk.
The central nervous systemmay 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 skinand 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 temperaturesof 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 wormsare 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.—Inacute hog-cholerathe inflammation is hemorrhagic in character. Small, red spots and blotches occur in different organs and tissues. In thechronic formof 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 skinover the under side of the neck, body and inside of the thighs may appear red or purplish-red in color. The different groups oflymphatic glandsare 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. Thekidneysare usually lighter colored than normal, and marked with red spots and blotches (Fig. 81). Thespleenmay show no evidence of disease. It may be large and soft, or even smaller than normal. Thelivermay be enlarged and dark, or mottled and light colored.
Thestomachandintestinesmay 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 thelungs(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 diseaseinto 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 thedouble methodconsists in injecting hypodermically or intramuscularly anti-hog-cholera serum and hog-cholera blood.
The vaccination or treatmentof 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 regioninto 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 hogsshould receive one-half cubic centimetre of serum for each pound of body weight, andcholera hogsshould 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 vaccinatingsmall pigsnot more than five, and in large hogs not more than twenty, cubic centimetres should be injected at any one point. Thebody temperatureof 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.
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.
[Illustration: FIG. 88.—Koch'sBacillus 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'sBacillus 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 infectionis 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 applyingthe 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 theintradermal 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.