13 Major Diseases Found in Animals

List of thirteen major diseases found in animals:- 1. Swine Erysipelas 2. Tuberculosis 3. Tubercular Mastitis 4. Gas Gangrene 5. Ranikhet Disease 6. Fowl Plague or Fowl Pest 7. Pseudorabies 8. Equine Piroplasmosis 9. Bovine Piroplasmosis 10. Canine Piroplasmosis 11. Bovine Theileriasis 12. Toxoplasmosis 13. Trichomoniasis.

Disease # 1. Swine Erysipelas:

Definition:

Swine erysipelas is an acute, subacute, chronic infectious disease of pigs and characterised by high fever, reddish spots on the skin, general debility, lameness and difficulty in breathing in chronic cases. Pathologically, it is characterised by gastroenteritis, swelling of the spleen, degeneration of liver and muscles and nephritis. There is usually cauliflower-like masses on the valves of the heart.

Bacteriology:

The bacillus of Swine erysipelas—Erysipelothrix rhusiopathiae – is a slender, fine straight or curved rod from 1^µ to 1.5^µ long. It is readily obtained from the spleen and kidneys of carcasses died of swine erysipelas. It stains easily with aniline dyes and is gram-posi­tive.

Animals susceptible:

The disease may oc­cur in man, also in chickens, turkeys, pheasants and pigeons.

Resistance:

Outside the body, the bacillus may remain alive on soil for at least one year and may multiply under favourable conditions. It-re­sists putrefaction, desiccation and sunlight. To destroy the bacillus by cooking, two and half hours of boiling is required for 6(15 cm -thick meat piece. Even the bacillus can survive and multiply in concentration of phenol which is bac­teriostatic and bacteriocidal to many other patho­genic bacteria.

Modes of Infection:

Infection enters the body through the digestive tract or the skin. It occurs chiefly from ingestion of food or water which have been contaminated by the faeces of the diseased animal. The disease may spread to healthy pigs from the convalescents or carriers.

Postmortem lesions:

The pathological changes of acute swine erysipelas are widely vari­able. The skin may be normal or extensively purple with Oedematous thickening; gastroen­teritis, swelling and congestion of mesenteric lymph glands and liver, enlarged spleen, haemorrhagic nephritis are seen. The liver is red­dish brown and the kidneys are swollen, soft and moist and petechial haemorrhages on the surface. The peritoneal and pleural cavities may contain some fluid. In the chronic form, the most charac­teristic lesion is verricose endocarditis with ob­struction of mitral valve.

Symptoms:

Symptoms of Swine erysipelas vary widely according to virulence of the bacillus and can be classified into two chief clinical forms — Acute septicaemic and chronic.

Acute erysipelas is the most important and common form in which most of the deaths occur. There is also a mild or subacute form. Acute erysipelas presents symptoms of septicaemia with chief localisation in the intestines and skin. The period of incubation is from 3 to 4 days, the onset is sudden and the temperature varies from 105° F —(40.6°C) to 108° F (42°C) and persists till death or recovery.

The animal is dull and do not eat and show weakness of hind quarters. There may be vomiting and initially there may be constipation followed by severe diarrhoea. On the 2nd or 3rd day, red patches may form on the ventral surface of the body, hind legs, throat, ears and they fuse to form large extensive dark red areas over a large part of the body.

The red colour of the skin is the prominent clinical characteristic. The usual course is from 2 to 4 days and in peracute cases, death may occur in 24 hours. Dyspnoea and cyanosis due to heart weakness are observed.

Mild or Sub-acute form:

There is fever, loss of appetite, dullness and a tendency to lie buried in litter, and when moved reluctantly, the skin over the chest, neck, back becomes flushed and soon changes to red or purple colour. The out­lines of the skin lesions are often square or shape of the playing card diamond and the areas are usually elevated above the level of surrounding skin. They are very painful to touch at first and the lesions last for 4 days and then disappear. Recovery may be followed by chronic form. Younger pigs between the ages 3 to 6 months are more susceptible.

Chronic form:

The chief symptoms are in the form of arthritis. It may be sequelae to acute form or may occur independently. The chief symptoms are swollen joints. Due to verricose endocarditis, there is difficulty in breathing and the animals are easily exhausted and they col­lapse when forced to move. The animals become stunted and emaciated. Stiffness and paralysis are sometimes noticed.

Treatment:

Penicillin and anti-erysipelas serum comprise the standard treatment and often administered together. Penicillin is very effective, when the bacillus is of mild virulence. Chronic cases do not respond well due to the damage to joints and endocardium cortisone given parenterally produces marked clinical improvement of the arthritis.

Immunisation:

The parenteral administra­tion of anti-erysipelas serum in the dose of 5 to 20 ml according to age will protect the in contact animals during an outbreak for 1 to 2 weeks.

Vaccination:

Simultaneous vaccination con­sists in the injection of immune serum and a boullion culture of the bacillus at the sometime. The injection is made at the base of the ear or into the axillary space, 5 ml of serum on one side and 0.5 ml of culture on the other side. Immunity lasts for 4 to 6 months. More lasting immunity may be conferred by giving a booster infection of the culture after two weeks.

Disease # 2. Tuberculosis:

Synonym:

Consumption, Phthisis, Grapes, Pearl disease.

Definition:

Tuberculosis is a chronic infec­tious disease of man, animals and birds caused by Mycobacterium (Bacillus) tuberculosis and characterised by specific cell proliferation and exudative processes and at a later stage caseation of the affected tissue.

Bacteriology:

Three types of T. B. bacilli are distinguished in warm blooded animals, hu­man, bovine and avian types. There is a fourth type which is nonpathogenic for mammals and birds — viz. that from fishes and other cold­blooded animals.

Bacilli of human type are usually longer and more slender than bovine type, while bacilli of avian type present marked polymorphism, some­times assuming a short, almost coccal form, some­times appearing as long and very slender rods.

The organism is slender, rod-shaped, straight or slightly curved, enclosed in a fine capsule consisting probably of a waxy substance, non- sporulating and non-motile, measuring 2^µ to 5 ^µ long by 0.5 ^µ occurring singly or in groups in a characteristic arrangement like a bundle of fag­gots or in pairs lying at an angle.

The three different types are not easily distin­guishable morphologically. Within recent years, evidence has been put forward in support of the view that a filtrable form of these organisms ex­ists which on inoculation into susceptible animals or appropriate culture media is supposed to de­velop into fine granules which later become coccoid, finally becoming very fine rods which then acquire acid-fast properties.

T. B. bacilli are stained by Ziehl-Neelsen method with warm carbol fuchsin in the same manner as Johne’s disease bacilli and are acid- fast.

Resistance:

Direct sunlight destroys cul­ture in 2 hours. In the pus and sputum, the organisms withstand diffused light for 30 to 40 days but becomes a virulent in 10 days. In faeces of cattle on pastures under ordinary conditions, f the organisms live about 2 months in summer and 5 months in winter. When light is excluded, the organisms remain active in dried sputum for 126 days. In putrid sputum, for 6 weeks, in buried cattle lungs for 167 days and in intestinal contents mixed with ingesta for 178 days.

Boiling and steaming of both dried and moist sputum will free it in 5 and 15 minutes respec­tively. But dried sputum exposed to dry heat at 212°F (100° C) will not sterilise it before an hour and moist one not always within this period. Milk containing the bacilli is sterilised in 25 minutes at (65°C) and in 5 minutes at 158°F (70°C) provided the milk is heated in a closed vessel, but in open vessel, they withstand heating for 6 minutes at (80° C).

The organisms are very resistant to chemical disinfectants and will stand exposure to 5% phe­nol for several hours. Glycerine has a preserva­tive action.

Animals susceptible:

All domestic ani­mals, man and birds. The cattle and man are most frequently affected and then in order comes the pig — dog — cat — horse — camel — sheep — goat. Donkeys and mules are reported to be immuned to T. B. infection.

Modes of Infection:

In animals, infection occurs chiefly by ingestion of infected or contaminated food and water or by inhalation of droplets of coughed up materials from animals with pul­monary T. B. or contaminated dust. Milk from cows with T. B. of the udder is another source of infection to suckling calves and others ingesting it.

Calves are sometimes known to suffer from T. B. contacted during their intrauterine life and that too, only when the uterus and placenta of the mother is affected (congenital infection); other­wise the disease does never occur in offsprings of tuberculous parents as a hereditary disease.

Pathogenesis:

In which tissue the T. B. bacilli settle, the commonest form of lesion they produce is that in which local cell proliferation predominates resulting in the formation of micro­scopic nodules at first and later due to the fusion and growth of neighbouring tubercles to the mi­croscopic or visible tuberculous nodules.

The second form of tuberculous inflamma­tion is the productive form in which there is diffuse proliferation of R. E. cells of a whole or part of an organ without distinct nodule forma­tion. A good example of this form is seen in tuberculous mastitis in cattle.

The third form in which there is an unusual amount of exudate formed. This is seen in some forms of tuberculous pleurisy in dogs and tuber­culous pericarditis in cattle.

Tissues affected with T. B. form a favourable soil for the growth of other bacteria. A purulent character in tubercular foci often indicates that pyogenic bacteria, chiefly consisting of Staphylo­cocci, specially albus and rarely coliform bacilli but Streptococci have taken part in the process of suppuration and the intermittent fever observed in many cases of tuberculosis is usually a sign of the presence of suppuration caused by pyogenic bacteria in tuberculous organs.

Incubation period:

In natural infection, it is months or years before the disease is mani­fested by clinical symptoms.

Symptoms:

In its early stages in cows as in the man, usually passes entirely unnoticed. The cough, fever, loss of flesh and other symptoms are not present for a considerable period until the disease has advanced to its later stage.

Pulmonary tuberculosis:

Which is the most common form in cattle—is first manifested by a short dry cough, followed usually after a few months, by symptoms indicating affections of the lungs, when the cough becomes more frequent and painful but usually remains dry and hoarse or it may become dull and toneless accompanied by muco-purulent yellowish grey expectoration, microscopic examination of which may reveal the presence of organisms. Respirations become rapid and laboured, which becomes more pronounced during exercise.

The appetite, which was undisturbed all along, gradually becomes variable and finally very poor and the animal may be further weakened by diarrhoea lasting for several days.

Towards the termination of the course, the respiratory troubles become very severe. The ani­mal stands with its elbows abducted, its head hanging down and tongue protruded, with rat­tling and groaning breathing which shakes the whole body. The cough which can be slight pres­sure on the back, is weak and very painful.

Puru­lent or sero-sanguinous discharge flows from the nose, which the animal is unable to lick from its muzzle. Eventually, the animal, being unable to remain standing, lies on the ground, diarrhoea supervenes and after prolonged suffering, death occurs unassociated with convulsions.

The super­ficial lymph glands may be enlarged and those at the back of the throat or at the corner of lower jaw or the glands of the neck, shoulder or stifle may be enlarged. The temperature usually remains undisturbed during the course of the disease.

In intestinal tuberculosis:

The most im­portant symptoms are periodical colicky pains and retention of faeces alternating with diarrhoea. The faeces are semifluid mixed with mucus and pus and sometimes with streaks of blood or larger blood clots. This is followed by progressive anaemia, rapid emaciation and death.

At an advanced stage of the disease, there is fever with evening rises and morning remissions. In very chronic cases, the febrile period lasts for a few days or weeks and alternate with longer a febrile interval. Towards the end of the disease, the temperature is usually high and continuous.

Miliary tuberculosis:

It is an acute form (which may follow the chronic) in which the bacilli invade the blood stream and form multiple tubercular abscesses in any or all the organs. This form of T. B. is rapidly fatal.

Disease # 3. Tubercular Mastitis:

It is much more com­mon than in other species. It usually occurs as a secondary development after the disease becomes generalised, but it may also occur as a primary affection by direct infection through the teats.

Frequently, there is only a painless, ill-de- fined thickening of one or both posterior quarters unaccompanied by any local heat. In other cases, several hard, painless nodes develop in the glan­dular tissue which later coalesce and form large indurated tumours with nodular surface, which compress the other parts of the udder and cause atrophy. At the same time, the directions of the teats are altered and they usually become conver­gent instead of divergent.

The supramammary and precrural lymph glands become greatly en­larged. The lactation remains unaltered in ap­pearance and quantity in the early stages. Gradu­ally, the milk becomes thinner containing fine greyish-white flakes and later greenish yellow and watery with numerous white flakes and debris, which sink to the bottom on standing and do not adhere to the floor or wall of the container. In a very advanced case, a small quantity of turbid watery fluid is obtained from the affected- quarter, which too gradually diminishes until it completely ceases.

N. B.:

T. B. bacilli are often revealed in the sediment of the milk by microscope.

In sheep and goat:

The disease is mani­fested by distressing cough which is always present and more noticeable upon exertion, loss of condition, progressive weakness. Sheep is not so susceptible as goats. In goats, anaemia, pneu­monia and sometimes diarrhoea are noticed.

In horse:

It is not very common. There is gradual emaciation in spite of good food and without any possible cause. Sometimes miliary tuberculosis develops, the animal-become fever­ish, refuses all food, distressed in breathing and dies in a few days.

In dogs and cats:

These pet animals are liable to become infected with tuberculosis either due to ingestion of infected milk or as a result of infection from sputum or discharges from a hu­man case. Not only these pet animals contact the disease from man but they may be dangerous sources of infection to human beings, specially to children.

The disease remain unnoticed till the disease is well-established. The first signs are capricious appetite, loss of condition, general weakness, the lungs, pleura or abdominal organs become affected, Pulmonary tuberculosis usually begins with a dry cough and vomiting follows in many cases. Later the cough becomes more frequent and there may be discharge from nostrils. Pulmo­nary tuberculosis is less common in these animals than the abdominal form.

Tuberculosis in abdominal organs is indi­cated by impaired nutrition and anaemia with attacks of diarrhoea and constipation alternately.

The mesenteric lymph glands are the seat of tu­bercular abscesses and the circulation to the intes­tines is hindered. Disturbance in the abdominal circulation results in congestion of the capillaries and the exudation of fluid serous material.

Owing to accumulator of fluid in the abdominal cavity, dropsy is noticed and this is a very common symptom of tuberculosis in cats. Emaciation is very rapid in these cases and death follows in a variable time. There is irregular rise and fall of temperature during the course of the disease. Subnormal temperature is usually noticed imme­diately before death. Joints and sinuses may be seats of infection in the cat.

Treatment:

The treatment of domesticated animals for tuberculosis is seldom attempted for the following reasons:

1. Because of the nature of the disease

2. Danger of affecting human beings

3. Cost of treatment

4. Humanitarian reasons.

Animals in Zoological gardens and pet ani­mals are sometimes treated with latest medicines.

Tuberculosis in human beings are now being treated with such drugs as Isoniazid, combina­tions of Streptomycin and para-aminosalicylic acid and other acids. Oral medication with isoniazid— both as treatment and as prophylaxis—has been claimed to have been efficient in case of animals. Rifampin is another good drug.

Course:

Variable:

This disease, as a rule, develops as a chronic disease and usually main­tains its chronic character until death.

Diagnosis:

(a) Microscopical

(b) Cultural

(c) Animal inoculation

(d) Allergic tests with tuberculin.

Allergic tests consists:

(i) S. I. D. test — 0.05 ml.

(ii) Subcutaneous test — 1 ml and

(iii) Ophthalmic test.

Dose table:

(i) S. I. D. test — 0.05 ml of tuberculin — This test is not very specific.

(ii) Subcutaneous test —

Average Cattle — 3 ml

Large bulls — 4 ml

Horse — 6ml

Dogs — 0.5 to 1 ml

(iii) Ophthalmic test:

One drop of Cone, tuberculin is dropped into the conjunctival sac, followed by 3 or 4 drops after 48 hours. The eye is examined 24 hours after the second instillation. If there is a purulent conjunctivitis, then the ani­mal is declared as tuberculous. A profuse watery or mucous exudate may occur in healthy animals and a reaction may be present 12 to 24 hours after the first instillation, which passes off.

N. B.:

This test is not reliable as the S. I. D. or Subcut tests. It is of value as a corroborative test.

Tuberculin:

It is a toxic product of Myco­bacterium tuberculosis grown on artificial cul­tures. In healthy animals, tuberculin—even in heavy—doses produce no reaction.

Immunity:

Immunisation of cattle may be brought about by inoculating them with the liv­ing human or avian types of culture, subcutaneously, but neither method has been put upon a practical basis because the organisms remain alive in the tissues for a long time and may establish themselves in certain tissues, e.g. udder, and may be excreted for years in the milk to the danger of man and animals.

The latest method of immunisation with liv­ing but avirulent organisms —

B. C. G. Vaccine (Bacillus Calmette Guerin)

This consists of bovine strain rendered aviru­lent by growth for many years upon glycerine- bile-potato, subsequently being maintained upon a medium without bile, though periodically retransferred to the bile medium.

By injecting large doses of culture suspension 50-100 ml intravenously or subcutaneously into the dewlap of calves as soon as after birth as possible (in any case within 15 days) and protect­ing them from natural infection till 6 weeks have elapsed after the injection, immunity is said to develop which will last more than a year. Injec­tion by intravenous route is attended by risk of severe systemic reactions.

The animals are re- inoculated annually as immunity lasts only so long as there are living B. C. G. present in the tissues. This is known as premonition, which means a form of immunity closely allied to the actual infection but with persistence of latent in­fection.

Eradication (Bang’s method):

The eradication of Bovine T. B. from a herd rests on repeated application of tuberculin test and retention of non-reactors in one herd and reactors in another herd (if it is not possible to dispose them) without intercommunication.

All clinical cases in the reacting herd should be destroyed.’ Calves from the reacting herd should be removed at birth, fed on a non-tuberculous milk, tested with tuberculin when they have weaned and then allowed to mix with the healthy herd if reaction is negative. The healthy herd is tested once a year and reactors, if any, removed to reacting herd. The reacting group may be permitted to breed for dairy purposes but the milk from them should be pasteurized.

Complete eradication of tuberculosis has not really been achieved in any country.

Disease # 4. Gas Gangrene:

Synonym:

Malignant Oedema.

Definition:

Gas gangrene is an acute wound infection caused by organisms of the genus Clostridium. There is acute inflammation at the site of infection and a systemic toxemia.

Etiology:

Clostridium septicum, CI. chauvei CI. perfringens, CI. sordellii and CI. novyi have all been isolated from lesions typical of Malignant oedema of animals. CI. sordellii has been associated chiefly with Malignant oedema of cattle but it has been found to be a cause of Malignant oedema and swelled head in sheep.

Mode of infection:

All ages and species of animals are affected. In most cases, a wound is the portal of entry and a dirty environment which permits contamination of wounds with soil, is the common predisposing cause.

The infection is usually soil-borne and the resistance of spores of the causative Clostridia to environmental influence leads to persistence of the infection for long periods in a local area. Deep punctured wounds accompanied by severe trauma provides the most favourable conditions for the growth of anerobes and Malignant oedema occurs most frequently under such conditions.

Infection may occur through surgical or acciden­tal wounds, following vaccination or Venepunc­ture or through unbilical cord in the newborn. An unusual method of infection occurs when crows have eaten infected carrion, carry the infection to live, weak sheep and to lambs when they attack their eyes. The disease is general in most parts of the world.

Pathogenesis:

Potent toxins are produced in the local lesion and cause death when absorbed in the blood stream. Locally, the exotoxins cause extensive oedema and necrosis followed by gan­grene.

Mortality:

Unless treatment is started in the early stages the death rate is extremely high.

Diagnosis and Clinical findings:

Clinical signs appear within 12-48 hours of infection. There is always a local lesion at the site of infection consisting of soft, doughy swelling with marked local erythema. At a later stage, the swelling becomes tense and the skin dark and taut. Em­physema may or may not be present depending on the type of infection and may be so marked as to cause extensive frothy exudation from the wound.

A high fever (41°-42°C, 106°-107°F) is always present and the affected animals are de­pressed, weak, show muscle tremor and usually stiffness or lameness. The illness is of short dura­tion and affected animals die within 24-48 hours of the first appearance of signs.

The association of profound toxemia with local inflammation and emphysema is characteristic. The disease is differ­entiated from-Black leg by the absence of typical muscle involvement and the presence of wound. A history of prior vaccination against Black leg and the age of animal may be of assistance in diagnosis.

Postmortem lesions:

Tissue changes occur rapidly after death, particularly in warm weather, and this must be kept in mind when evaluating post-mortem findings. There is usually gangrene of the skin with edema of the subcutaneous and inter-muscular connective tissue around the site of infection. The edema fluid varies from thin serum to a gelatinous deposit. It is usually blood stained and contains bubbles of gas except Cl. novyi infections when the deposit is gelatinous, clear and contains no gas. Subserous hemorrhages and accumulations of sero-sanguineous fluid in body cavities are usual.

Treatment:

Affected animals should be treated as emergency causes because of the acute nature of the disease. Specific treatment requires the administration of Penicillin or a broad-spectrum antibiotic. Antitoxin is effective in control­ling the toxemia but is usually too expensive for practical use and must be given very early in the course of the disease. Injection of Penicillin di­rectly into and around the periphery of the lesions may be of value in some cases. Local treatment consists of surgical incision to provide drainage, and irrigation with Hydrogen per­oxide.

Disease # 5. Ranikhet Disease:

Synonym:

Fowl pest, Doyle’s disease, New­castle disease and in America -— Avian pneumocephalitis.

Definition:

This is an acute, highly fatal, contagious, infective disease of fowls showing considerable resemblance to fowl plague, charac­terised by respiratory distress and caused by a separate and immunologically distinct virus. The size of the viruses has been determined to be 80 to 120m^µ.

Few species of birds can withstand a massive dose of virus, ducks and geese are comparatively resistant and the disease is usually mild. The domestic fowl is subject to peracute form. The pigeon, which is resistant to fowl plague, can be infected experimentally. The disease may be trans­mitted to man and gives rise to conjunctivitis.

Incubation period:

5 to 7 days according to Gaiger and Davis and 2 to 5 days according to G. Iyer.

Modes of infection:

By ingestion and ac­cording to G. Iyer, also by coition.

Symptoms:

Clinically, peracute, acute and chronic forms are seen —

In peracute cases, the birds die suddenly, usually without any visible signs of-illness.

In acute cases, there is loss of appetite, crouching as if trying to hide, sleepy appearance with eyes either partially or fully closed and rapid respiration. A watery, yellowish white diarrhoea with an offensive odour is present. The crop is usually distended with a sour smelling fluid which can be squeezed out by pressure.

The most characteristic sign is a long, gasp­ing inhalation through half open mouth and a discharge from the nostrils and mouth of a varying quantity of mucus which sometimes hangs in strings from the beak. Cyanosis of the comb and wattles is sometimes observed.

Rise of temperature at the onset of the dis­ease is fairly common, specially in disease caused by the Indian strain of the virus.

Majority of cases are of this acute type and the course is 3 to 4 days (G. Iyer) and 2 to 3 days (Gaiger and Davis).

In some cases, nervous symptoms in the form of blind, dashing, aimless flying and many other forms of peculiar movements are observed.

In chronic cases, as a result of injury to nerves, twitching of the head and neck and lameness or paralysis of the legs or wings may occur.

This form runs a prolonged course resulting in recovery. In some cases, if attention is paid to artificial feeding and watering, recovery rare but confers high degree of immunity in recovered birds.

Postmortem lesions:

There is no character­istic lesions of the disease. In peracute cases, there is practically no lesion discernible. In acute cases, there may be petechial on the mucosa of the duodenum, gizzard and also on the pericardium. In some cases, reddish ulcers with irregular mar­gin and coated with bran—like deposits are seen in the mucosa of the proventiculous and duode­num and occasionally along the entire length of the intestines.

Ileo caecal valve is also ulcerated and coated with necrotic tissue. The liver, spleen and kidneys may be congested and the trachea may show slight congestion coated with mucus.

N. B.:

The lungs show no change which is rather strange in view of the symptoms of respi­ratory distress shown by the birds during life.

Diagnosis:

This is based on the symptoms, post mortem lesions, negative bacterial findings and mainly on susceptibility of pigeons to inocu­lation. The H. I. (Haemagglutination Inhibition) Test is of great value.

Pigeons, specially young ones, are highly sus­ceptible to experimental infection with the virus of the disease. This fact is also invaluable in the differential diagnosis of this disease and fowl plague, in which the pigeons are not susceptible.

Treatment:

Medicinal treatment is of no value and, in naturally affected flocks, the mortal­ity may reach 100 per cent.

Immunity:

Inoculation of vaccines pre­pared by passage of virus serially through the developing chick embryos. It takes birds 10 to 14 days to acquire immunity following inoculation and at least 2 inoculations are needed. Inoculation must be carried out by expert technicians and proper hygienic measures must be taken by the persons handling the birds.

Disease # 6. Fowl Plague or Fowl Pest:

This is also a fatal infectious disease of fowls, turkeys and geese and many other birds except­ing pigeons caused by a virus.

Modes of infection:

By ingestion of con­taminated food and water and through cutaneous abrasions and conjunctiva are also possible.

Incubation period:

36 hours to 3 days.

Symptoms:

There is a rise of temperature of 112° F (44.5°C) or more, with severe systemic disturbances followed by somnolence, combs and wattles are dark red or blackish red, sometimes covered with gray scales. There may be swelling of the head from oedema of the eyelids, combs wattles and earlobes. Discharge of tenacious gray or reddish mucus through the nose and occa­sional diarrhoea with gray or greenish or reddish evacuation.

The sick birds isolate themselves from rest of the flock. The tail and wings droop and the eyes are kept closed. The bird may squat on its breast with its head tucked under a wing. Food is refused and thirst is often shown. Towards the end, the respirations become laboured and pa­ralysis sets in extending from the limbs to the head, followed by death. The illness seldom lasts more than 24 to 36 hours and in very rare cases up to 6 days.

Diagnosis and Post mortem lesions:

Diag­nosis is based on postmortem lesions (which con­sists of petechial haemorrhages on the heart, in­ternal fat, inner surface of the breast bone and particularly over the gizzard and proventiculous and reddish colouration of the skin and muscles, which are normally yellowish in fowls), negative bacterial findings and ability to reproduce the disease in fowls with filtrates of blood or tissue fluids — with negative results in case of pigeons.

Differential diagnosis:

The symptoms re­semble those shown in fowl cholera and peracute form of Ranikhet disease, and may lead to confu­sion.

Prevention:

Vermin should always be kept down in poultry-runs. Cages, crates etc. should be thoroughly disinfected before use.

Disease # 7. Pseudorabies:

Synonym:

Mad itch, Infec­tious Bulbar Paralysis.

Definition:

This disease was first described by Aujeszky in Hungary in 1902 and named after him. Pseudorabies is a noncontagious, fatal dis­ease caused by a filterable virus and characterised by intense itching, paralysis and death in from 12 to 18 hours. It also affects pigs, dogs, cats and rats but horse is immuned to this disease. But in case of pigs, it runs a mild course but highly conta­gious.

Incubation period:

Very short — 1 to 3 days.

Etiology:

It is caused by a filterable virus and is found in abundance at the seat of inocula­tion and also in blood and Central Nervous Sys­tem.

Symptoms (Cattle):

The first symptom ob­served is intense pruritus, rubbing or scratching of part of hind-quarters and sometimes on the face in an attempt to relieve itching. After some­time, the skin becomes denuded of hair. The animals rub violently against any hard object, such as posts, barbed wire and may bite themselves.

Bellowing, grinding of teeth, stamping with the hind feet and salivation may be ob­served. Within 24 hours, the animal is usually recumbent due to paralysis and death occurs within 36 to 48 hours. The pruritus may also occur on the head and neck. There is rarely any fever until shortly before death and is usually preceded by convulsions, bellowing and rapid breathing. In some cases, the pruritus is so severe that cattle become delirious attack attendants.

In pigs:

In these animals, the disease runs a milder course and mortality is less than 5 per cent. Symptoms include pruritus, loss of appetite, vomiting, diarrhoea, convulsions, salivation and paralysis of the throat. In case of pregnant sows, mummification of the foetus may occur.

Dogs and Cats:

Symptoms include loss of appetite, vomiting, salivation, restlessness, intense itching about the face or some other parts, groan­ing, moaning and screams are sometimes ob­served.

Postmortem lesions:

In cattle, persistent rubbing leaves the skin over the thighs arid but­tock to be denuded of hair, dark, leather-like and smeared with bloody serum, the subcutaneous tissue over the affected parts is thickened with a serious and gelatinous infiltration but the muscle is not involved. There are no changes in the abdominal and thoracic organs and the Central Nervous System.

Mode of infection:

This disease often oc­curs among rats and may be spread by rat bites. But recent researches have shown that the pigs may transmit the disease to cattle by transfer of virus on their snouts to the abraded skin of the cattle.

Immunity:

An attack confers immunity.

Treatment:

No treatment.

Disease # 8. Equine Piroplasmosis:

Synonym:

Biliary fever, Equine malaria.

Definition:

This disease in solipeds is caused by two distinct parasites — B. caballi and B. equi. The former is comparatively larger hav­ing a pear shape — 3 to 4^µ long, of which 1, 2 or 4 may be found in a single R. B. C. but they usually remain in pairs.

Babesia equi is smaller of the two and may have an oval, round and sometimes pear shape — 2^µ in diameter. It divides directly into 4, these 4 taking the form of a cross with their points to the centre. It has a wide distribution and, in India, infection by this organism is more common.

Mode of infection:

It is transmitted by ticks — Rhipicephalus and Dermacentor—but transmission by other biting insects is possible and suspected.

Pathogenesis:

The majority of Babesia ex­ert their pathogenic effect by penetrating and destroying R. B. C.s. This process gives rise to general febrile symptom, pronounced anaemia, and haemoglobinurea in a more or less degree.

When only a few R. B. C.s are destroyed, the free haemoglobin is transformed into bile pig­ments in the liver and is excreted; but when the destruction is heavy, part of the haemoglobin is excreted in the urine and icterus is manifested. In severe cases, the anaemia and nutritional distur­bance eventually lead to fatal termination.

Incubation period:

By natural infection, 6 to 21 days according to Marzinowsky and others and 6 to 11 days according to Pricolo. By inocula­tion — 5 to 6 days.

Postmortem lesions:

Pallor and yellow coloration of the tissues, thin and watery blood. Spleen and lymph glands acutely enlarged. The splenic pulp somewhat softened but not fluid and blackish red as in Red water of cattle. Liver may be enlarged. Intestinal mucosa swollen and in­flamed, sometimes with follicular ulcers in the large intestine.

Symptoms:

The disease commences with pronounced dullness and depression followed by reddish and yellow coloration of the visible mu­cosa (which is proportionate to the severity of the infection) and a rise of temperature of 104° F (40°C) or over, which in case of B. caballi infec­tion is almost continuous—usually lasting about 6 days; while in B. equi infection, it is either inter­mittent or recurrent. Petechial spots appear on the mucosa which deepens in colour and finally result in large purple blotches. Urticarial erup­tions occur in some cases.

At the onset, the appetite is diminished and thirst increased, the faeces scanty and in the form of small balls coated with mucus. In some cases, colicky symptoms are observed which later de­velop into diarrhoea.

The urine is usually passed in large quanti­ties. In B. equi infection, haemoglobinuria is often present, which however, cease in 1 to 2 days. The colour of urine is from reddish brown to choco­late colour (in severe cases). In B. caballi infection, the haemoglobinuria is also transient but may assume an intermittent form.

Severe heart weakness with a marked in­crease in the frequency of pulse and dyspnoea. In acute case, Babesia are found in 50 per cent of R. B. C.s and RBC. count may drop to 3 million/ m1³.

Diagnosis:

Detection of Protozoa under microscope.

Treatment:

Good diet, proper nursing and hygiene are essential. 2% solution of 200 ml intra­venously of Trypan blue is specific. Trypafiavine — 1 gm in 20 ml has also been known to produce good results when given intravenously. Many drugs—including Phenamidine, Diminazene, Pirevan, Berevil, Euflavine, Diampron and oxytetracycline—have been used. Imidocarb is the most favoured drug provided a strict treatment regimen is followed.

In B. equi infection, 4 intra­muscular injections of 10% solution at a dose of 4 mg/kg body weight at intervals of 72 hours. In B. caballi infection a regimen of 2 mg/kg body weight on two occasions at 24 hour – interval is sufficient. Ancillary treatment should include blood transfusion and haematinics during conva­lescence.

Disease # 9. Bovine Piroplasmosis:

Synonym:

Red water.

Definition:

Piroplasmosis of cattle is caused by Babesia bigemina and is indigenous in tropical and subtropical regions manifested by anaemia, icterus and haemoglobinuria.

B. bigemina is usually found in the RBCs in a characteristic double pear shaped form consist­ing of two large parasites with their pointed ends opposed to each other or in contact at an acute angle. Round or oval forms are rarely seen.

B. bovis or B. divergens is the causal organism of European Red water and is smaller than B. bigemina.

Modes of infection:

B. bigemina is trans­mitted by ticks of the genus Boophilus, the common species being Boophilus annulatus B. divergens or B. bovis is transmitted by tick — Ixodes ricinus.

Pathogenesis:

The majority of babesia ex­ert their pathogenic effect by penetrating and destroying RBCs. This process gives rise to gen­eral febrile symptom, pronounced anaemia and haemoglobinuria in a more or less degree.

When only a few RBCs are destroyed, the free haemoglobin is transformed into bile pig­ments in the liver and is excreted; but when the destruction is heavy, part of the haemoglobin is excreted in the urine and icterus is manifested. In severe cases, the anaemia and nutritional distur­bance eventually lead to a fatal termination.

Incubation period:

About 10 days to 28 days according to Gaiger and Davies and 14 to 18 days according to Theiler.

Postmortem lesions:

Besides pallor and yellow coloration of the tissues, the mucosa of the abomasum is swollen and catarrhal, sometimes showing small erosions in the pyloric end. Similar changes may be found in the intestines, specially in the rectum. The liver is flabby and lustreless and studded with yellowish streaks or spots. The gall bladder contains much thick mucoid clotted bile and its mucosa often sprinkled with small haemorrhagic spots.

The spleen is greatly enlarged—sometimes four times its normal size—with consistence usu­ally firm (but may be softened in some cases) and is blackish red in colour. The bladder usually contains bright red or dark red urine and its mucosa shows haemorrhages.

Symptoms:

In acute cases, the disease com­mences with the rapid rise of temperature 106° F (41 °C) to 107° F (41.6°C) accompanied by pro­nounced lassitude, acceleration of pulse and signs of other systemic disturbance. The temperature remains high for several days, when, in severe cases, it falls rapidly below normal, whereas, in mild cases, it comes down slowly to normal.

At first there is constipation, afterwards diar­rhoea with passage of mucus and blood clots. In lactating animals, there is decrease in milk secre­tion, pregnant cows often abort.

The mucosa are reddened first, but after­wards become pale and sometimes icteric.

Haemoglobin appears in urine in a day or two giving it a red colour. Later on, bile pigments are excreted in the urine giving it a greenish red or blackish red colour. In very severe cases, the urine may contain even R. B. C. and urination is usually accompanied with severe straining.

In unfavourable cases, the animals become so weak in 3 or 4 days that they continually lie on the ground, breathe with difficulty and some­times utter painful moans. At the same time, there is continuous lacrimation and salivation. Eventually, death takes place after a rapid fall of temperature.

In chronic cases, the symptoms described above are present in a milder degree, save and except haemoglobinuria which is seldom present. Besides, there is progressive emaciation and anaemia with relapsing fever lasting several days.

Treatment:

Trypan blue 1% solution — 50 ml for calves and 200 ml for large animals given intravenously in the early stages is quite effective. Acaprin and Trypaflavine are reported to be more effective than Trypan blue.

Quinuronium derivatives, such as Babesan, Pirevan, Piroparv and Piroplasmin can be given subcutaneously without causing sloughing but in case of alarming toxic reactions, adrenalin is the antidote. These drugs, specially Acaprin, is most widely used. The dose rate is 1 ml/50 kg body weight with a maximum dose of 6 ml.

Aromatic diamidines:

Stilbamidine, Propamidine, Phenamidine, Berenil are, in gen­eral, good drugs. The drugs are well tolerated and safe for intramuscular or subcutaneous injec­tion.

Disease # 10. Canine Piroplasmosis:

Synonym:

Tick fever, Malignant jaundice.

Definition:

Canine babesiosis is caused by two distinct species — Babesia canis and Babesia gibsoni. The disease is usually manifested by se­vere anaemia and, in acute cases, by icterus and haemoglobinuria.

B. canis is a large parasite almost resembling B. bigemina and is transmitted by Rhipicephalus sanguineus.

B. gibsoni is a very small parasite—usually of a ring or oval form with sometimes long forms— nearly the diameter of the R. B. C. The transmit­ting tick is Haemophysalis biponosa.

Pathogenesis:

The majority of Babesia ex­ert their pathogenic effect by penetrating and destroying R. B. Cs. This process gives rise to general febrile symptom, pronounced anaemia and haemoglobinuria in a more or less degree.

When only a few R. B. Cs. are destroyed, the free Hemoglobin is transformed into bile pig­ments in the liver and is excreted; but when the destruction is heavy, part of the haemoglobin is excreted in the urine and icterus is manifested. In severe cases, icterus and anaemia and nutritional disturbance eventually lead to fatal termination.

Incubation period:

7 to 10 days (Bromley).

Symptoms:

In B. canis infection:

In acute cases, the first symptom is a rise of temperature which in 2 to 3 days reaches 104° F (40°C) or over (and even up to 109° F) or 43°C which remains steady for 2 to 4 days when it drops suddenly and becomes subnormal. There is a marked lassitude, visible mucosa first pale and later cyanotic and in about 50 per cent cases also icteric.

There is loss of appetite but increase of thirst, often diarrhoea and, in some cases, Epistaxis. The animal walks with a staggering gait and finally it can scarcely remain standing. Paralysis of the posterior ex­tremities often takes place sometimes as early as 18 to 24 hours which rapidly ascends and be­comes generalised in 3 to 4 days.

The urine is albuminous from the very first and in some cases it contains a small amount of haemoglobin and sometimes bile when it presents a more or less red colour with a trace of green.

There is rapid emaciation, anaemia and ex­treme weakness ending in death within a week.

In chronic cases, which often result in recov­ery, fever is present only in the initial stages of the disease or it may be absent altogether. There is progressive anaemia and the mucosa are ex­tremely pale, sometimes of bluish colour but icterus is usually absent. In spite of maintained appetite, the animal becomes extremely emaci­ated and if it does not die from exhaustion, the anaemia gradually subsides after 3 to 4 weeks and recovery eventually takes place, but this ani­mal remains as a carrier (according to Robertson for 2 to 2¹/₂ years).

In B. gibsoni infection:

The disease usu­ally takes the chronic form with severe anaemia and emaciation and with icterus and haemoglo­binuria.

Postmortem lesions:

Hyperaemia of inter­nal organs, specially liver and spleen. Marked enlargement of the spleen, the pulp of which is dark bluish red and may be firm or somewhat softened. Mucosa of the gastro-intestinal canal either may be pale or slightly reddened, Oedematous in places and usually coated with tenacious mucus. Bladder contains pigmented urine and the gall bladder blackish-green bile.

N. B.:

Babesia are found in large numbers in the kidneys.

Treatment:

Trypan blue or Piroblue 1% solution—4 ml to 12 ml intravenously. This is effective against B. canis infection.

Acaprin 0.5% solution – 0.25 ml up to 5 kg body weight, 0.5 ml from 6 to 10 kg body weight and 1 ml from 11kg and upwards — may be given subcutaneously or intramuscularly. May be repeated after 24 hours if result is not obtained. This is suitable for both B. canis and B. gibsoni infection.

NAB:

0.01 gm per kg body weight dis­solved in 5 ml to 10 ml of distilled water intrave­nously repeated after an interval of 2 days. Excel­lent against B. gibsoni infection. Berenil is also another good drug.

Tryparsomide:

0.015 gm/500 gr of body weight made into 20% solution when given intra­muscularly or 10% solution when given subcutaneously or intravenously — repeated after an interval of 3 days. This drug is of good therapeu­tic value, has low toxicity and better tolerance than NAB.

Phenamidine:

5% solution — 0.30 ml/kg body weight given subcutaneously; one dose, as a rule, is completely effective. May be repeated if temperature does not come to normal on the day after the treatment.

Disease # 11. Bovine Theileriasis:

Synonym:

Coastal fever, Rhodesian Red water and Rhodesian Tick fever.

Definition:

This is a highly acute disease of cattle caused by Theileria parva which is usually transmitted by ticks of the genus Rhipicephalus excepting Rhipicephalus sanguineus.

Postmortem lesions:

Haemorrhagic swell­ing of all lymph glands, pure yellow coloration of all body fats, lungs infiltrated with straw coloured fluid which passes up the trachea and escapes by the nostrils as foam. Mucosa of the abomasum ulcerated, haemorrhagic spots throughout the in­testines, liver and kidneys studded with small white, yellow Or purplish infarcts, which are said to be diagnostic lesions.

Incubation period:

10 to 12 days on an average.

Symptoms:

Sudden and continued rise of temperature to 107° F (41-6 °C) or more, laboured respiration sometimes accompanied by short cough, salivation, conjunctivitis with lacrimation nasal catarrh with running from the nose, evacu­ation of very dry haemorrhagic or tarry faeces followed by diarrhoea, sometimes with blood in the faeces, marked swelling of the external lymph glands, emaciation and weakness of the hind quar­ters.

The blood:

Cells are not destroyed. The para­site multiplies in the lymphatic tissue and from there invades the blood in such large numbers that almost all R. B. Cs contains one or more parasites.

In contrast to Babesiosis, the appetite is well maintained in this disease, anaemia and icterus is rare and haemoglobinuria never observed. After the animals recover, the parasites disappear from the blood and such animal is longer a carrier or reservoir. Animals can only be infected by lym­phatic gland juice or by ticks.

Chronic form of the disease occurs, with en­larged glands, especially in calves from immune cows.

Course:

Death occurs sometimes suddenly and sometimes after a prolonged illness, average duration is 1 to 3 weeks.

Mortality:

In recently infected area, it may be 90% to 100%, but lower in area where the disease in enzootic.

Treatment:

Purely symptomatic as no spe­cific remedy has yet been discovered.

Prophylaxis:

Separate healthy animals from affected or suspected stock and detick them and keep them isolated.

Immunisation:

Theiler’s method of vacci­nation by intravenous injection of spleen or lymph gland pulp in peptone solution has been tried but has not prated very satisfactory.

Other Theileria:

Theileria dispar:

This produces a disease in cattle in Algeria similar to the infection, of T. parva but is somewhat milder and there may be anaemia, icterus and haemoglobinuria in a more or less degree as in Red water.

Treatment:

Acaprin – 5% solution – 2 ml/ 50 kg body weight, subcut, intravenous or intra­muscular.

Theileria annulate:

This is also responsible for a type of Theileriosis in cattle in Transcancasia, but is so mild that it is seldom recognised. Very rarely it may assume an acute course.

Treatment:

Same as suggested under T. dispar.

Theileria mutans:

This produces a very mild type of Theileriosis in cattle. Its distribution in South Europe, Australia and Asia (In India rarely). If there be any clinical symptom in this disease, these consist of a moderate variation of temperature and slight anaemia. Recovery is usual and fatal cases rare.

Disease # 12. Toxoplasmosis:

Definition:

This is a contagious disease of all species including man. It is manifested clini­cally by abortion and stillbirths in ewes and in all species by encephalitis, pneumonia and neonatal mortality. The causative agent is Toxoplasma gondi and occurs in all warm-blooded animals and man.

The principal hosts are feline species, the parasite undergoes a complicated life cycle in the intestinal epithelium of the cat. Sporulated oocysts are found in the faeces. They can survive in very large numbers and are infective when taken orally by any warm—blooded animal. The tissue cysts cause damage to nervous system, myocardium, lung tissue and placenta in the in­termediate host.

Toxpplasmosis is an true Zoonosis occurring naturally in man and in domesticated and wild animals and birds.

Modes of infection:

Infected carcasses, feed contaminated by saliva, nasal discharge or faeces or infected milk are the main sources of infection. Rodents and house pets may be a reservoir of infection in man.

Pathogenesis:

T. gondii is an intracellular parasite which attacks most organs with predilection for the Reticuloendothelial and central ner­vous system. After invasion of a cell, the parasite multiplies and eventually fills and destroys the cells. Liberated Toxoplasms reach other organs via the blood stream. The clinical character of the disease varies with the organs attached. The com­monest syndromes are encephalitis when infec­tion is congenital and febrile exanthema with pneumonitis and colitis when the disease is acquired postnatally. A powerful exotoxin is re­leased.

Symptoms:

In cattle:

The disease usually runs an acute course with fever, dyspnoea and nervous symp­toms including ataxia and hyper excitability. Con­genially affected calves show fever, dyspnoea, coughing, sneezing, nasal catarrh, grinding of the teeth and tremor of head and neck. Death occurs in 2 to 6 days.

In pigs:

Debility, weakness, cough, tremor and diarrhoea are observed in adult pigs but no fever. Piglets may be premature or still-born or may be ill from 1st day to 3 weeks of age with wasting and dyspnea being the major signs. Piglets may have high temperature — 104° F (40°C) to 107° F (41.6°C).

In sheep:

The common finding is of abor­tion and neonatal deaths. Fever, dyspnoea, tremor are also observed. Abortion occurs during the last 3 or 4 weeks of pregnancy.

In horses:

Neurological signs are observed in horses. Ataxia, circling, paresis and apparent blindness.

Postmortem lesions:

Multiple and prolif­erative granulomata are characteristic of Toxopl­asmosis. In cattle, the lesions may undergo calci­fication. Lesions may be seen in lungs and ner­vous system. Pneumonitis, hydrothorax, lympha­denitis, ascites, intestinal ulceration and necrotic foci in liver, spleen and kidneys are also ob­served.

Diagnosis:

The reciprocal dye test and complement-fixation tests are the only satisfac­tory method of diagnosing Toxoplasmosis in liv­ing animals.

Treatment:

The Sulphapyrimidine (Sulphadimidine, Sulphamerazine and Sulphadiazene) and Sulphapyrazine are the most effective drug. Best results are obtained when they are combined with pyrimethamine. These drugs are effective against the proliferating parasites and not against pseudocysts.

Control:

The carcasses of infected or sus­pect animals should be totally destroyed and must be made inaccessible to Carnivores. Limitation of cat numbers and avoidance of faecal contamina­tion by cats and also rodent population is neces­sary from public health point of view.

Disease # 13. Trichomoniasis:

Definition:

The flagellates of the germs Trichomonas are usually pear-shaped with 3 to 5 anterior flagella and one undulating membrane. Species of this genus very commonly occur in the intestinal canal of many mammals and birds. Only Trichomonas foetus is of importance as the cause of abortions, pyometra and sterility in cattle. The disease is rare in India. It is caused by a proto­zoan parasite.

Mode of infection:

It is a true venereal infection in cattle. The parasite is transmitted during coitus from an infected bull, or vice versa.

Symptoms:

After coitus with an infected bull, the cow may show a transient vaginitis. If conception has not occurred, a chronic form of endometritis is observed. In case of pregnant cows, the foetus dies and aborted 1 to 4 months later. It may also be retained in the uterus and pyometra develops.

Control:

It includes the disposal of infected bulls, breeding operations must be kept sus­pended for at least 3 months.