Livestock Diseases
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Livestock Diseases
Foot and Mouth Disease
HEMORRHAGIC SEPTICEMIA
ANTHRAX
Rinderpest
INFECTIOUS BOVINE RHINOTRACHEITIS
Para tuberculosis
PROPHYLAXIS
Tuberculosis
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Foot and Mouth Disease


ETIOLOGY  Classification of the causative agent


Virus family
Picornaviridae
GenusAphthovirus.
Seven immunologically distinct serotypesA, O, C, SAT1, SAT2, SAT3, Asia1
Temperature 
Resistance to physical and chemical action
 Preserved by refrigeration and freezing and progressively inactivated by temperatures above 50°C
pHInactivated by pH 9.0
Disinfectants
Inactivated by sodium hydroxide (2%), sodium carbonate (4%), and citric acid (0.2%). Resistant to iodophores, quaternary ammonium compounds, hypoclorite and phenol, especially in the presence of organic matter
  

EPIDEMIOLOGY
  1. One of the most contagious animal diseases, with important economic losses
  2. Low mortality rate in adult animals, but often high mortality in young due to myocarditis
Hosts  
 Bovidae (cattle, zebus, domestic buffaloes, yaks), sheep, goats, swine, all wild ruminants and suidae. Camelidae (camels, dromedaries, llamas, vicunas) have low susceptibility
Transmission    1. Direct or indirect contact (droplets)
   2. Animate vectors (humans, etc.)
   3. Inanimate vectors (vehicles, implements)
   4. Airborne, especially temperate zones (up to 60 km overland and 300 km by sea)
 
Sources of virus
 
  1. Incubating and clinically affected animals
  2. Breath, saliva, faeces, and urine; milk and semen (up to 4 days before clinical signs)
  3. Meat and by-products in which pH has remained above 6.0
  4. Carriers: particularly cattle and water buffalo; convalescent animals and exposed vaccinates (virus persists in the oropharynx for up to 30 months in cattle or longer in buffalo, 9 months in sheep). African Cape buffalo are the major maintenance host of SAT serotypes
Occurrence FMD is endemic in parts of Asia, Africa, the Middle East and South America (sporadic outbreaks in free areas) For detailed information on occurrence, see recent issues of World Animal Healt


DIAGNOSIS

Incubation period is 2-14 days

Clinical diagnosis

Cattle

  • Pyrexia, anorexia, shivering, reduction in milk production for 2-3 days, then
  • smacking of the lips, grinding of the teeth, drooling, lameness, stamping or kicking of the feet: caused by vesicles (aphthae) on buccal and nasal mucous membranes and/or between the claws and coronary band
  • after 24 hours: rupture of vesicles leaving erosions
  • vesicles can also occur on the mammary glands
  • Recovery generally occurs within 8-15 days
  • Complications: tongue erosions, superinfection of lesions, hoof deformation, mastitis and permanent impairment of milk production, myocarditis, abortion, death of young animals, permanent loss of weight, loss of heat control (‘panters’)

Sheep and goats

  1. Lesions are less pronounced. Foot lesions may go cularsis. Lesions in dental pad of sheep. Agalactia in milking sheep and goats is a feature. Death of young stock

Pigs

  1. May develop severe foot lesions particularly when housed on concrete. High mortality in piglets a frequent occurrence

Lesions

  1. Vesicles or blisters on the tongue, dental pad, gums, cheek, hard and soft palate, lips, nostrils, muzzle, coronary bands, teats, udder, snout of pigs, corium of dewclaws and interdigital spaces
  2. Post-mortem lesions on rumen pillars, in the myocardium, particularly of young animals (tiger heart)

Differential diagnosis

Clinically indistinguishable:

  • Vesicular stomatitis
  • Swine vesicular disease
  • Vesicular exanthema of swine

Other differential diagnosis:

  1. Rinderpest
  2. Mucosal disease
  3. Infectious bovine rhinotracheitis
  4. Bluetongue
  5. Bovine mammillitis
  6. Bovine cular stomatitis
  7. Bovine viral culars

Laboratory diagnosis

Procedures

Identification of the agent

  1. ELISA
  2. Complement fixation test
  3. Virus isolation: inoculation of primary bovine thyroid cells and primary pig, calf and lamb kidney cells; inoculation of BHK-21 and IB-RS-2 cell lines; inoculation of mice


Serological tests

   1. ELISA     (prescribed tests in the Manual)
   2. Virus cularsisd test

Samples

  1. 1 g of tissue from an unruptured or recently ruptured vesicle. Epithelial samples should be placed in a transport medium which maintains a pH of 7.2-7.4 and kept cool
  2. Oesophageal-pharyngeal fluid collected by means of a cular cup Probang samples should be frozen to below -40°C immediately after collection
Special precautions are required when sending perishable suspect FMD material within and between countries.

PREVENTION AND CONTROL

Sanitary prophylaxis

   1. Protection of free zones by border animal movement control and surveillance
   2. Slaughter of infected, recovered, and FMD-susceptible contact animals
   3. Disinfection of premises and all infected material (implements, cars, clothes, etc.)
   4. Destruction of cadavers, litter, and susceptible animal products in the infected area
   5. Quarantine measures (Code Chapter 2.1.1.)

Medical prophylaxis

Inactivated virus vaccine containing an adjuvant. Immunity: 6 months after two initial vaccinations, 1-month apart, depending on the antigenic relationship between vaccine and outbreak strains


HEMORRHAGIC SEPTICEMIA


 DefinitionClassical hemorrhagic septicemia is a particular form of pasteurellosis caused by Pasteurella multocida and manifested by an acute and highly fatal septicemia mainly in susceptible cattle and water buffaloes.

The name hemorrhagic septicemia is used rather loosely in some countries to include pneumonic pasteurellosis (shipping or transport fever), a disease caused mainly by P. haemolytica, although various serotypes of P. multocida are occasionally involved. Although the morbidity of pneumonic pasteurellosis of cattle can be high, the mortality rate is much less than that of hemorrhagic septicemia.
 Etiology Hemorrhagic septicemia is caused by two serotypes of P. multocida; namely, B:2 and E:2. The letter denotes the capsular antigen as determined originally by the indirect hemagglutination test of Carter (5), and the numeral 2 stands for the somatic or O antigen as determined by the agar gel diffusion precipitin test developed by Heddelston and associates (17). This somatic antigen 2 is the equivalent to the 6 in the classification of Namioka and associates. In a new classification, Pasteurella multocida strains causing most pasteurella infections, including hemorrhagic septicemia, are called P. multocida subspecies multocida.
 Host Range Cattle and water buffaloes are the principal hosts of hemorrhagic septicemia, and it is widely considered that buffaloes are the more susceptible. The disease is thought to be endemic in one large herd of North American range bison; however, epidemics appear to be rare. In the United States, the disease has been confirmed only in American bison in 1912, 1922, and 1965. The P. multocida isolant from the 1922 outbreak, a serotype B:2, is maintained in the USDA culture collection as a reference strain. Although outbreaks of hemorrhagic septicemia have been reported in sheep and swine, it is not a frequent or significant disease. Cases have been reported in deer, elephants and yaks. There is as yet no evidence of a reservoir of infection outside the principal hosts: cattle, water buffaloes, and bison.
 Geographic DistributionHemorrhagic septicemia in epidemic form is a disease mainly of cattle and water buffaloes either maintained separately or together. Radical changes in weather, including the advent of monsoons, debility caused by seasonal levels of low nutrition, and the pressure of work (draft animals) are related to the explosive occurrences of the disease in certain parts of the world. Southeast Asia, where such conditions often coincide, is the area of highest incidence. The disease occurs in the Middle East and Africa where the environmental circumstances and predisposing conditions are not as clearly defined as in Southeast Asia. As in Asia, the disease is frequently associated with the rainy season and poor physical condition.

Hemorrhagic septicemia was recognized in Japan as a specific disease of cattle caused by particular strains of Pasteurelia as early as 1923. Since 1926, the disease has been controlled, and the last recorded case in cattle in Japan occurred in 1952.

The B:2 serotype has been recovered from hemorrhagic septicemia in countries of Southern Europe, the Middle East, and Southeast Asia, including China. This same serotype has been reported from Egypt and the Sudan. The E:2 serotype has been recovered from hemorrhagic septicemia occurring in Egypt, the Sudan, the Republic of South Africa, and several other African countries. There is no report of either serotype being recovered from Australia, New Zealand, and countries of South and Central America.

There is no evidence that the disease has spread from carrier bison in the Western United States to neighboring cattle. Given the conditions in which hemorrhagic septicemia occurs in endemic areas (e.g., primitive husbandry practices, low country plains, and well-defined dry and wet seasons), it seems unlikely that the disease will reach epidemic proportions in the United States.
TransmissionThe disease is spread by direct and indirect contact (fomites). The source of the infection is infected animals or carriers. The carrier state may be greater than 20 percent shortly after an outbreak, but within 6 weeks the rate is usually less than 5 percent. The causal agent does not survive for more than 2 to 3 weeks in the soil or on pastures. Close herding and wetness, as occurs during the rainy season, appear to contribute to spread. There is no evidence that biting arthropods are significant vectors.
Incubation Period The influence of extrinsic factors in the development of the clinical pasteurelloses, and particularly in hemorrhagic septicemia, has been noted by many workers. When favorable circumstances for the growth and multiplication of P. multocida in the animal body occur, severe septicemia develops within a few hours. However, the organisms may be harbored for varying periods in a small percentage of carrier animals without any clinical sign. The perpetuation of the disease from year to year or season to season is generally attributed to the carrier state. The immune status of the animal is thought to influence the severity of the disease.

Cattle or buffalo artificially inoculated subcutaneously with lethal doses (approximately 20,000 bacilli) show clinical signs within a few hours and succumb within 18 to 30 hours.
Clinical Signs 
The majority of cases in cattle and buffalo are acute or peracute with death occurring from 6 to 24 hours after the first recognized signs. In a few outbreaks, animals may survive as long as 72 hours. Dullness, reluctance to move, and elevated temperature are the first signs. Following these signs, salivation and nasal discharge appear, and edematous swellings are seen in the pharyngeal region and then spread to the ventral cervical region and brisket. Visible mucous membranes are congested, and respiratory distress is soon followed by collapse and death. Recovery, particularly in buffaloes, is rare. Chronic manifestations of hemorrhagic septicemia do not appear to occur.
Gross LesionsWidely distributed hemorrhages, edema, and general hyperemia are the most obvious tissue changes observed in infected animals. In almost all cases there is an edematous swelling of the head, neck, and brisket region (Fig. 63). Incision of the edematous swellings reveals a coagulated serofibrinous mass with straw-colored or blood-stained fluid. This edema, which distends tissue spaces, is also found in the musculature (Fig. 64). There are subserosal petechial hemorrhages throughout the animal, and blood-tinged fluid is frequently found in the thoracic and abdominal cavities. Petechiae may be found scattered throughout some tissues and lymph nodes, particularly the pharyngeal and cervical nodes, which are also swollen and often hemorrhagic. Pneumonia is not usually extensive nor is gastroenteritis. Cases that are atypical in regard to throat swelling (absent) and pneumonia (extensive) are occasionally seen.
Morbidity and MortalityHusbandry, weather and immunity affect morbidity. In endemic areas, from 10 to 50 percent of the cattle or buffalo populations acquire solid immunity through exposure or subclinical infection. Close herding and wetness predispose to an increased morbidity. Most animals that develop clinical signs die.


Diagnosis

Field Diagnosis

In countries where hemorrhagic septicemia is endemic, it is usually readily diagnosed — particularly if there is a history of previous outbreaks and a failure to vaccinate. When a small number of animals are affected, diagnosis may be more difficult. This could be the case if hemorrhagic septicemia were to occur in the United States. In endemic areas, the rapid course, usual high herd incidence, and the appearance of edematous swellings in the throat, cervical, and parotid regions is highly suggestive.

Specimen for Laboratory

From an animal with typical signs, the organism can be isolated from heparinized blood, affected tissue, liver, lung, kidney, and spleen. All samples should be collected aseptically. Samples should be kept cool and shipped on wet ice as soon as possible. Swabs in transport media, ribs, and tips of ears are sometimes submitted from remote areas in developing countries.

Laboratory Diagnosis

Isolation of a small gram-negative rod or coccobacillus in pure or nearly pure culture with the general colonial appearance of a Pasteurella species from an animal with typical signs is grounds to suspect hemorrhagic septicemia. If there has been postmortem decomposition with the presence of extraneous bacteria, the inoculation of mice and rabbits with blood or suspensions of tissues will facilitate recovery of the pasteurellae of hemorrhagic septicemia in pure or nearly pure culture. Both mice and rabbits are highly susceptible to the two serotypes B:2 and E:2. Definitive diagnosis depends upon the identification of the cultures as P. multocida and the subsequent identification of serotype B:2 or E:2. Because several different serotypes of P. multocida that do not produce classical hemorrhagic septicemia occur in cattle, it is necessary to serotype the isolate. The National Veterinary Services Laboratories, Ames, IA should be contacted regarding the serotyping of suspected hemorrhagic septicemia strains of P. multocida.

Serologic procedures for the detection of specific antibody are not used in diagnosis.

Differential Diagnosis

The sudden death seen with peracute and acute hemorrhagic septicemia must be differentiated from that due to lightning, snakebites, blackleg, rinderpest, and anthrax.

Treatment

The onset and course of the disease are generally rapid and leave little time for antimicrobial therapy. However, several of the sulfonamides and antibiotics such as penicillin and the tetracyclines can be used successfully in the early stages. In some outbreaks in Southeast Asia, animals with elevated temperatures are isolated and treated intravenously with a soluble sulfonamide.

Vaccination

The most efficacious immunizing agent has been the oil-adjuvant vaccine prepared from the appropriate serotype. Vaccine of this type is more slowly absorbed and produces a longer-lasting immunity than do regular and alum-precipitated-type bacterins. The oil-adjuvant bacterin has the advantage of requiring only one dose annually, but it has the disadvantages of being difficult to syringe and occasionally produces a marked local reaction. A live vaccine prepared from a fallow deer strain of P. multocida has shown considerable promise with protection for as long as a year. This strain, serotype B:3,4, is closely related immunologically to serotype B:2 but is less virulent.

Control and Eradication

In endemic areas the only practical ways to protect animals are by an organized program of vaccination and maintenance of animals in as good a condition as possible. When favorable conditions for outbreaks are known to recur periodically, such preventive measures can be carried out in advance, and the potential consequences of the disease will thus be lessened.

Public Health

There is as yet no authenticated report of human infections due to serotypes B:2 and E:2. However, because other serotypes of P. multocida can cause a variety of human infections, precautions should be taken to minimize exposure to the hemorrhagic septicemia varieties of P. multocida.
 

ANTHRAX

 
Synonyms : Splenic fever,  Milzbrand  ,   Charbon,Wool sorter’s disease,Tarka.

It is an acute widespread infectious disease of livestock that occurs throughout the globe. It is considered to be a very serious infectious disease of herbivorous animals. Other animals like goats, horse, pig may get the infection. This is a zoonotic disease and therefore man can contact the infection through infected cattle. The disease has occasionally been recorded in dogs The disease is also known as splenic fever due to the fact that there is extensive enlargement of the spleen (splenomegaly) due to this infection.

Distribution

The disease is in existence in all parts of the world. In India, the disease is enzootic in nature and occur in almost all the districts of different States. Some districts are considered as anthrax districts (anthrax belts) due to enzootic nature of the disease in those pockets.

Etiology

Bacillus anthracis. The bacilli are straight, very large rod shaped non- motile, capsulated, aerobic, spore bearing, gram + ve organisms. The organisms remain in chains The capsules are formed in the body of an infected animal. The spores are never formed so long the organisms remain in the circulation. But, when the organisms come out of the body, the spores are formed. The spores may remain viable in the soil for a considerable period of time and for ten years in the infected tissues and cultures. The soil can maintain the organisms in spore stage for years together without endangering the life of animals.

The organisms can be grown on blood agar under aerobic conditions

The Vegetative form of the bacteria can be killed at 60°C for 30 minute\

the spore form cannot be killed with ease. The spore remains resistant 10 100°C for 5 minutes. But, it will be destroyed at 100°C for 10 minutes. In autoclave at 120°C for 15 minutes all the vegetative forms can be kille_ Commonly available chemicals cannot kill the spores. 5% NaOH can effectively destroy the spore contaminated objects

Bacillus anthracis produces three types of toxins. The toxins are. Extracellular in nature.   The toxins are:

  • Factor-I – Denotes oedema toxin
  • Factor-II – Denotes protecting antigen
  • Factor-III – Denotes lethal factor.

Susceptible hosts

Most of the food animals are affected with anthrax. No mammals have got absolute natural immunity against anthrax. The most susceptible animals are cattle and sheep. Next in order is horse and pig. Anthrax has been recorded in dogs, though dog is thought to be resistant to anthrax Birds are refractory to natural infection but outbreaks have been reported in chicken. The disease is not uncommon in camels. Anthrax has been reported amongst elephants of India, Siam, Burma and Tanzania Anthrax has been reported in tigers of zoo.

Anthrax is a zoonotic disease. Man occupies an intermediate position between the susceptible group of animals and the relatively resistant group of animals.

Mode of transmission

The anthrax spores have got the ability to remain viable in the soil for a considerable period of time and thus remain as a continuous source of spread to the susceptible animals. Soil borne outbreaks of anthrax occur in a definite season of year in definite pocket. The pH and humidity of the soil have got some clinical bearing on the spread of the disease. It has been pointed out that alkaline soil is a factor for soil borne outbreaks. It is suggested that degeneration of grasses and plants and accumulation of alluvial soil following significant rainfalls and thereafter draught are contributory factors for the propagation of aerobic spore forming organisms. The stream, rivers- and flood may carry the spores from one place to other and thus may spread the disease to the-virgin soil. Carnivore animals may carry the infection to the distant places. Carnivores may contact the infection through ingestion of contaminated carcases. Various flies have been implicated as carrier of infection during the fly breeding seasons. Animals while grazing in the infected pasture pick up the infection through ingestion or through breach in the oral mucosa or skin. The injury of the oral mucosa may help in the entrance of the infection. In a nutshell, the spores are carried from one place to the other by :  WATER – AIR CURRENT – VECTOR.On gaining access in the animal’s body, the spores turn into vegetative form and set up the disease process.

Pathogenesis

Anthrax organism has got three factors viz, oedema factor, protein antigen and lethal factor with  which they exert their virulent effect on the-host. None of the factors can act individually. Protein antigen transport oedema factor and lethal factor to the target cells. Protein antigen and oedema factor combination produce oedema and protein antigen and lethal factor combination lead to fatal termination of hosts. The foregoing factors decrease the resistance of the hosts and inhibit the phagocytic activities in them. The poly-D-glutamate capsule of anthrax bacilli is responsible for the interference in opsonization and thus enhances the function of oedema and lethal factors.

On gaining entry the spores are transformed into vegetative form and tend to move towards lymph nodes. From the lymph nodes following multiplication the bacilli enter the blood by way of lymphatic channel. Thus a septicaemic condition of the hosts develop .Bacilli then invade all the body tissues and organs. The bacilli at this stage elaborate toxins and thus produce damaging effect and oedema of tissues. Animal may die at this stage due to shock and acute renal failure. Due to changes in blood components and damage of central nervous tissues, severe anoxia may ensue and this may lead to death .

The presence of antibodies in the host can neutralize the toxin and therefore help the animal to recover from the attack of anthrax.

Clinical findings

 The clinical findings differ in different species of animals. The incubation  period ranges from 2 to 10 days. The disease may appear as per-acute, acute and sub-acute form.

Acute form is predominantly noticed in cattle where the disease occurs in an outbreak, proportion. There is elevation of body temperature (104 to 1O8°e). Animal refuses to eat and there is development of bloat. Animal is extremely depressed. Pulse and respiratory rates are accelerated to a great extent. With the advancement of disease process there is development of muscular tremor. Some animals may show extreme aggressiveness following depression stage. At ‘the end, animal shows distressed breathing. Extreme dyspnoea leads to mouth breathing due to oxygen, hunger. Following death there is oozing of blood from all the natural orifices. The blood used to contain significant number of anthrax bacilli. Death usually takes place within 48 hours.

In per-acute form animals may be found dead without any premonitory signs.

Sub-acute form is characterized by oedema. Oedema is predominantly noticed under the neck, brisket region, thorax, abdomen and flank. The oedema of the thorax and brisket region produces respiratory distress. Jugular pulse is noticed at the terminal stage of the disease. Pregnant cattle may abort. Some may survive for 2 to 3 months.

Man: Anthrax is considered as a zoonotic disease (Tweihons, 1970). Food animals and their products constitute potential danger to those persons whose occupation necessitates handling of animal products or contact with animals. Usually, butchers, skinners, meat retailers, meat inspectors, tanners and veterinarians are the worst victim. The main symptoms in man are the formation of malignant carbuncles and pneumonia due to involvement of skin and lungs.

Lesions

In anthrax, carcase decomposes rapidly with formation of gas and distension of abdomen. Rigor mortis is absent. Blood and blood stained fluid usually escape from the natural orifices and the visible mucous membranes remain purple in colour. The blood is dark red or black in appearance and does not clot rapidly. Due to lack of oxygen the blood is dark in colour. Yellow gelatinous fluid is found in every part of subcutaneous tissues. Subserous, subepicardial and subendocardial haemorrhages are commonly found. Sero sanguinous fluids may accumulate in the body cavities. The spleen is very much enlarged and soft. In some cases, the spleen is so much enlarged that its capsule gets ruptured. The liver and kidneys are congested. The mucous membrane of the intestine is intensely red in some parts. There is prolapse of rectum. The lungs are congested, swollen and oedematous. In pigs, the changes are mostly confined to pharyngeal region. The connective tissues and lymphatic glands of this region are swollen, oedematous with jelly like appearance.

Diagnosis

Animal that dies suddenly with bloody discharges from mouth, nostrils, anus must be suspected to have died of anthrax. The anthrax infected carcase should not be opened. It is generally difficult to demonstrate the anthrax bacilli in the blood during the early stages of the disease. The organisms are present in sufficient numbers in the blood towards the terminal stages of the disease.

Laboratory examination

Microscopic examination of blood films

Thick blood films of blood sample are to be made on clean glass slide dried in air, fixed slightly with heat and stained with polychrome methylene blue or Giemsa’s stain. Wash in water, dry; examine under oil immersion. Positive blood films stained with Polychrome methylene blue will show the presence of large square ended blue rods in short chains. The Giemsa stained smear will show reddish discolouration of capsules.

Cultural examination

A loop full of suspected blood sample is to be streaked on 5% blood agar and nutrient agar plates and the plates are to be incubated aerobically for 18-24 hours at 37°C. Following incubation the plates are to be examined for cultural characteristics compatible with B. anthracis. Positive diagnosis can be arrived based on microscopical and cultural characteristics. In solid media positive cases will show cultural characteristic compatible to B. anthracis viz. absence of motility, very little or no haemolysis medusa head appearance and inverted fir tree appearance on gelatine stab culture

Animal Inoculation

For biological tests, suspension is to be made with small quantity of sterile normal saline from materials like blood from the ear or swab of blood stained discharges. The materials are to be heated at 60°C for 30 minutes in order to kill all the vegetative bacteria. Then 0.5 ml of the suspension is to be injected into the thigh of guineapig subcutaneously. The animal will die in 36-40 hours in positive cases of anthrax. Gelatinous exudates will be found at the site of inoculation. Blood smear of guinea pig will reveal large number of anthrax bacilli.

Vesicular fluid from human lesion

Samples of fluid are to be obtained from cutaneous lesions of the hand, having malignant vesicles with the aid of sterile cular pipettes. Some of the 1 fluid samples may be streaked upon 5% sheep blood and nutrient agar.

Serological test: Ascoli’s test

This is a thermoprecipitation test; this test is employed for the detection of anthrax in hide or tissues. A piece of hide or tissue is boiled in water and extract is obtained. The clear fluid thus obtained is layered on a very narrow precipitating serum. In a positive cases whitish ring appear at the junction of the two fluids.

Fluorescent staining

A fluorescent anti phage staining system for Bacillus anthracis can be performed for its diagnosis.


Differential diagnosis

Anthrax must be differentiated from

  • lighting stroke
  • black quarter
  • haemorrhagic septicaemia
  • babesiosis
  • acute lead poisoning
  • snake bite
  • Electric injury
  • Acute tympany
  • Acute lead poisoning
  • Prussic acid (HCN) poisoning
  • Acute leptospirosis
  • Acute infectious anaemia
Treatment

Per-acute cases of anthrax may not allow any opportunity for rendering treatment due to the obvious reason that the animals die after a very short clinical course. Treatment is always effective provided the cases are attended at the initial stage of the disease. Anthrax bacilli are sensitive to penicillin and other broad spectrum antibiotics. Penicillin 10,000 units per kg body weight twice daily through parenteral route has been proved to be effective against anthrax. Miller (1946) recommended the use of streptomycin @8 to 10 gm in divided doses through intra muscular injection in cattle. Apart from the above, Oxytetracycline, erythromycin, chloramphenicol or sulphonamide have been advocated against anthrax.

Anti anthrax serum @ 100-200 C.c. through intravenous route along with a course of penicillin may be given.

In all cases treatment has to be continued at least for 5-7 days. As a routine measure, a case of anthrax may be brought under the regimen of aqueous penicillin through intravenous route followed by use of procaine penicillin through intramuscular route.

Control  
  • Control of anthrax in areas free from the disease should be achieved at by preventing the introduction of infected animals.
  • The fodder from infected pasture should be destroyed and not to be given to the susceptible animals.
  • The disease should be brought under the notice of the regulatory officials in case of an outbreak.
  • The strict quarantine arrangement should be made in the anthrax prone areas.
  • Care should be taken to destroy the dead body by deep burial with quick lime.
  • The adjacent areas of the dead and infected animals should be thoroughly disinfected by applying 3% per acetic acid or 10% caustic soda or 10% formaline. 3% per acetic acid is considered as an efficient sporicide and thus may be applied to the soil for effective sterilization with a dose of 8 lit res per square metre
  • Hides, wools, bone meals etc. should be sterilized by gamma irradiation and get certified from competent authority as free from anthrax spores.
  • Carcasses should not be opened as it may contaminate the pasture.
  • Persons handling the anthrax infected animals should adopt adequate sanitary measures for their own safety.
  • Animal clinicians should take care while making blood smear from dead animals

Immunization

In countries where the anthrax is enzootic in nature there is a  need of a continual vaccination programme. Anthrax vaccine should be done annually one to two months prior to anthrax season. In heavily contaminated surroundings two doses of vaccines may be given at 15 to 30 days interval.

Vaccine used : Sterne vaccine



Rinderpest

ETIOLOGY

Classification of the causative agent

Virus family Paramyxoviridae, genus Morbillivirus

Resistance to physical and chemical action

Temperature: Small amounts of virus resist 56°C/60 min or 60°C/30 min
pH: Stable between pH 4.0 and 10.0

Chemicals: Susceptible to lipid solvents

Disinfectants:      Susceptible to most common disinfectants (phenol, cresol, sodium hydroxide 2%/24 hours used at a rate of 1 litre/m2)

Survival:      Remains viable for long periods in chilled or frozen tissues

EPIDEMIOLOGY
  1. High morbidity rate, mortality rate is high with virulent strains but variable with mild strains

Hosts

  1. Cattle, zebus, water buffaloes and many species of wild animals: African buffaloes, eland, kudu, wilde-beest, various antelopes, bushpigs, warthog, giraffes, etc.
  2. Sheep, goats are susceptible
  3. Asian pigs seem more susceptible than African and European pigs
  4. Rinderpest is rare among camelidae
No age- or sex-linked predisposition


Transmission


   1. By direct or close indirect contacts

Sources of virus

   1. Shedding of virus begins 1-2 days before pyrexia in tears, nasal secretions, saliva, urine and faeces
   2. Blood and all tissues are infectious before the appearance of clinical signs
   3. Infection is via the epithelium of the upper or lower respiratory tract
   4. No carrier state

Occurrence

The virus has never established itself in the Americas or Australia/New Zealand. Its distribution in other parts of the world is restricted. In Africa it has been eradicated from several countries and sub-regions, and is normally absent from the northern and southern parts of the continent. Rinderpest occurs in the Middle East and in southwestern and central Asia For detailed information on occurrence, see recent issues of World Animal Health and the OIE Bulletin


DIAGNOSIS

Incubation period is 3-15 days

Clinical diagnosis

Classic form: four stages

  • Incubation period
  • Febrile period (40-42°C) with depression, anorexia, reduction of rumination, increase of respiratory and cardiac rate
  • Mucous membrane congestion (oral, nasal, ocular and genital tract mucosae)
  • intense mucopurulent lachrymation and abundant salivation
  • anorexia – necrosis and erosion of the oral mucosae
  • this phase lasts 2-3 days
  • Gastrointestinal signs appear when the fever drops: profuse haemorrhagic culars containing mucus and necrotic debris. Severe tenesmus. Dehydration, abdominal pain, abdominal respiration, weakness, recumbency and death within 8-12 days. In rare cases, clinical signs regress by day 10 and recovery occurs by day 20-25

Peracute form

No prodromal signs, high fever (>40-42°C), sometimes congested mucous membranes, and death. This form occurs in highly susceptible young and newborn animals

Subacute form

Clinical signs limited to one or more of the classic signs. Low mortality rate

Atypical form

Irregular pyrexia and mild or no diarrheoa. The lymphotropic nature of rinderpest virus favours recrudescence of latent infections and/or increased susceptibility to other infectious agents

Sheep, goats and pigs

  • Variable pyrexia and anorexia
  • Inconsistent culars

Pigs

Pyrexia, prostration, conjunctivitis, erosions of buccal mucosa, death

Lesions

  • Either areas of necrosis and erosions, or congestion and haemorrhage in the mouth, intestines and upper respiratory tracts
  • Enlarged and oedematous lymph nodes
  • White necrotic foci in Pepyer’s patches
  • Zebra striping’ in the large intestine
  • Carcass emaciation and dehydration


Differential diagnosis

Cattle

  •  Foot and mouth disease
  •  Bovine viral culars/mucosal disease
  • Infectious bovine rhinotracheitis
  • Malignant catarrhal fever
  • Vesicular stomatitis
  • Salmonellosis
  • Necrobacillosis
  • Paratuberculosis
  • Arsenic poisoning

Small ruminants

Peste des petits ruminants

Laboratory diagnosis

Procedures

Identification of the agent

Antigen detection

  • Agar gel immunodiffusion test
  • Direct and indirect immunoperoxidase tests
  • Counter immunoelectrophoresis
  •  Immunohistopathology


Virus isolation and identification

  • Virus isolation
  • Virus cularsisd  in VERO or bovine kidney cell cultures
  • Immunoperoxidase staining


Virus RNA detection

  • Rinderpest-specific cDNA probes
  • Amplification by polymerase chain reaction (PCR

Serological tests

  •  ELISA
  • Virus cularsisd

Samples

  • Sterile whole blood preserved in heparin (10 IU/ml) or EDTA (0.5 mg/ml) and transferred to laboratory on ice (but not frozen)
  • Spleen, prescapular or mesenteric lymph nodes of dead animals chilled to sub-zero temperatures
  • Ocular and nasal secretions of infected animals during either the prodromal or the erosive phase


PREVENTION AND CONTROL

No treatment

Sanitary prophylaxis

  • Isolation or slaughtering of sick and in-contact animals
  • Destruction of cadavers
  • Disinfection
  • Protection of free zones

Medical prophylaxis

  • Cell-culture attenuated virus vaccines are highly effective
  • The commonly used vaccine is an attenuated strain of rinderpest virus. In some countries a mixed rinderpest/contagious bovine pleuropneumonia vaccine is used
  • Immunity lasts at least 5 years and is probably life-long. Annual revaccination is recommended in order to obtain a high percentage of culars animals in an area
  • Genetically engineered thermostable recombinant vaccines are currently undergoing limited field trials

INFECTIOUS BOVINE RHINOTRACHEITIS



Synonyms.      Viral bovine rhinotracheitis, I.B.R,

Red nose; Necrotic rhinitis

 It is an acute highly contagious viral disease of cattle characterized by high temperature, rhinitis, dyspnoea, abortion, meningo encephalitis, kerato conjunctivitis and pustular vulvovaginitis.

ETIOLOGY

Classification of the causative agent

The disease is caused by bovine herpes virus. The virus is morphologically indistinguishable from other herpes virus group.

Resistance to physical and chemical action

The virus is stable at pH 6.9 and can remain alive for a long-period but is susceptible to lower pH, ether, acetone and alcohol.

Susceptible hosts

  • Cattle of all ages are affected.
  • Besides, cattle, the disease have been traced in goat, swine and water buffalo.
  • The disease has also been identified in wild ruminants. Wild animals remain as reservoir of infection.

Mode of transmission

  • The virus is usually transmitted through infected feed and water.
  • The virus can be spread through ocular, nasal and reproductive secretion and excretion of the infected cattle ( droplet infection)
  • Venereal transmission and transmission through semen via artificial insemination is possible.

Sources of virus

Tears, nasal discharge, coughed secretions, and all secretions and excretions of incubating and sick animals. Bulls may transmit the infection-especially when the bull is in carrier stage.

Predisposing Factors

  • Anti body deficient cularsi fed calves.
  • Treatment with drugs that contribute to immuno-deficiency.
  • Transportation stress
  • Stress during parturition.
  • Parasitic infestations. Eg. Dictyocaulus cularsi
  • Nutritional defiency. Eg. Selenium, Zinc

The disease is widely prevalent in all parts of the cattle in the world .In India, the disease has been recorded from Uttar Pradesh , Kerala,, Gujrat Tamilnadu;, Orissa, AndhraPradesh  and Karnataka.

Pathogenesis

The virus multiplies in the upper respiratory tract and causes inflammatory changes like rhinitis, laryngitis, and tracheitis. Tracheal damage leads to marked depletion of tracheal microvilli  The virus may produce pneumonic changes which may lead to fatality. Lesions may extend to eyes from nasal tract through nasolacrymal duct and may give rise to conjunctivitis and vascularization of the cornea. The virus may enter the brain tissues from nasal mucosa via trigeminal nerves and produce meningo encephalitis. The virus may produce changes in the placenta and foetus and cause abortion. On certain occasions the virus may cause systemic form of the disease with high mortality rate in young calves.


Clinical findings

The clinical signs may vary widely. The clinical signs have been grouped as:

  • Respiratory from
  • Vulvo-vaginal form
  • Occular form
  • Encephalomyelitic form affecting the central nervous system. .
  • Abortive form

Respiratory form.

This form is characterized by mild to severe rise of temperature, depression of appetite, acceleration of respiration and dyspnoea. The nasal discharges are initially serous which later on turn to mucopurulent. Whole of the upper respiratory tract mucosa like pharynx, larynx may show hyperaemia, oedema along with mucopurlent exudation causing dyspnoea. Necrotic plaque may appear on the nasal bones. Animal may exhibit open mouth breathing in severe cases. The mortality rate is comparatively less unless there is super imposed bacterial or viral infection. Animal may show signs of bronchitis and pneumonitis. The disease is more prevalent in feed lot cattle. Due to red appearance of the nasal mucosa, the disease is termed as red nose. The recovered animal may remain as carrier and thus shed the virus for a considerable period. .

Vulvo-vaginal form.

This form is characterized by sharp fall in milkyield and appearance of erythematous and pustular lesions on the vulvar and vaginal mucosa. Vulva may remain swollen and animal may urinate at frequent intervals. There may be muco-purulent discharge from vulva and vagina. Animal is unable to put its tail in normal position following urination due to pain. The virus may produce pustular balanoposthitis in bull. The semen of the affected bull become contaminated and thus pose problem in natural or artificial breeding.

Occular form.

This form may appear along with respiratory form. There is inflammation of the conjunctiva in addition to respiratory changes. But, in some occasions severe conjunctivitis and cular discharge may be noted without respiratory involvement. The cular discharge vary from serous to purulent. Petechial haemorrhage may be noted on the conjunctiva and sometime corneal opacity may appear as main attribute of the disease

Encephalomyelitic form.

The   virus   may   produce   severe encephalomyelitis syndrome in calf terminating in death. The signs of encephalomyelitis comprise of high rise of temperature, incoordination, tremor, circling, falling, coma and death. Death ensues within 4 days following appearance of neurological disorders.

Abortive form.

The pregnant cattle may abort following infection. The abortion may supervene as “abortion storm.” Foetus die at about 4 months of gestation and the foetus is expelled in 1-7 day. Foetus is autolysed in most cases

Lesions

Respiratory system.

White necrotic lesions are noted on the nostrils and muzzle. Due to considerable erosion of the nasal mucosa, the name red nose has been given Degenerative and necrotic changes are noted on the nasal passage, paranasal sinuses, pharynx, larynx and trachea. Lungs show the signs of emphysema and pneumonia.

Reproductive system.

Pustular lesions are noted on the mucosa of vulva and vagina. Foetus may undergo mummification, necrosis and autolysis. Necrotic lesions may appear in the liver and spleen of the foetus


Central nervous system.

Lesions are noted on the cerebral cortex.

Diagnosis

Differential Diagnosis

Pasteurellosis

  • Rinderpest
  • Malignant catarrah
  • Bovine viral culars
  • Rabies
  • Pseudo rabies
  • Parainfluenza
  • Verminous pneumonia
  •  CBPP

Lab: diagnosis.

  • ELISA TEST
  • Serum neutralization test
  • Fluorescent antibody technique using liver and spleen of the foetus
  • Virus isolation

Treatment.

There is no fruitful treatment. Superimposed bacterial infection can be checked by broad spectrum antibiotic or sulphonamide. Ancillary treatment includes restoration of fluid and electrolyte balance and provision of adequate ration and shelter. Hyper immune serum may be tried.

Control

Strict isolation of the affected animals

Vaccinations available.


Para tuberculosis


Synonyms: Johne’s disease ,Chronic specific enteritis of cattle, Chronic bacterial enteritis of cattle

Chronic bacillary dysentery.

Paratuberculosis is a chronic infectious disease of cattle, sheep, and occasionally other animals caused by Mycobacterium paratuberc’Ulosis and characterized by re­current diarrhea, progressive emaciation and thickening and corrugation of the intestinal mucosa.

ETIOLOGY

M. paratuberculosis – small, short, thick rod, 0.5 by 1-2J.L, stains with usual acid-fast stains, considered Gram-positive, aerobic.

Difficult to culture; requires a growth factor as:

  1. Tuberculin.
  2. Extracts of saprophytic acid-fast bacteria.
  3. Extracts from lymph nodes of calf.
  • Habitat outside body is unknown but it is believed that it will live in pastures and premises contaminated with faeces for months.
  • Killed by pasteurization temperatures.
  • Susceptible to common disinfectants as:
  • Sodium orthophenylphenate, 1/200 for 15 min.
  • 3% liquor cresolis cularsi.


Antigenic relationship to:

  • Avian tubercle bacillus.
  • Some rare cases, mammalian tubercle bacillus.

EPIZOOTIOLOGY

Distribution:

  • Widely prevalent in Europe, including England and the Channel Islands.

Transmission:

  • Direct contact with faecal material.
  • Contaminated food and water with faecal matter.

Susceptible hosts:

  • Cattle, sheep primarily.
  • Reported in deer, horse, mule, swine, monkey.

Factors affecting susceptibility:

A. Age.

  • Not necessarily a disease of adults.
  • Lesions and symptoms most often occur from 2-6 years of age.
  • Calfhood is the period of greatest susceptibility to infection - difficult to infect calv–s over 4 months of age.

B. Sex - no relationship.

C.  Con–ition - no relationship.

D. Feed–ng - fecal contamination of f–ed, water, and pastures increases infection hazard. e. Housing - premises contaminated wi–h feces are an important source of infection.

SYMPTOMATOLOGY

  1. Incubation period at least two years in natural infection.
  2. Three- types of infections.'
  3. 10-20% animals in her’ showing symptoms of profuse, diarrhea and emaciation.
  4. Occasional animal showing symptoms.
  5. Those reacting to johnin test but showing no lesions on postmortem.
  6. First distinctive symptom is chronic fetid diarrhoea without strainincularsetite is usually good and attitude lively.
  7. Milk flow decreases.
  8. Temperature is normal.
  9. Progressive diarrhoea.
  10. Diarrhoea macularsodic and is aggravated by a ration of green feed.
  11. No apparent disturbance of respiratory, urinary, or circulatory systems.
  12. Finally emaciation becomes extreme, eyes sunken, and recumbency constant. 11. Almost always fatal in a month to 2 years.
  13. Disease often becomes active after parturition.

PATHOLOGY

Pathogenesis:

  1. Organism ingested and passes through epithelium of intestine.
  2. Packets of organisms appear in mucosa and act as foreign body producing specific in­flammatory reaction.
  3. Organisms carried to mesenteric lymph nodes by lymphatic system, acting as fore.ign bodies.


Postmortem lesions:

  1. Diarrhea in early stages caused by inflammatory reaction with resulting oedema.
  2. Diarrhea in later stages caused by developing fibrosis of intestine preventing reabsorp­tion of water.
  3. Thickening and corrugation of intestinal mucosa due to fibrosis.
  4. Emaciation due to loss of intestinal functions.
  5. Chronic serous lymphadenitis of mesenteric lymph nodes – enlarged and soft.
  6. Thickened and corrugated intestinal mucosa.
  7. Occurs most frequently in first 20-30 feet of intestinal tract posterior to duodenum.
  8. Cecum frequently involved.


Microscopic lesions:

  1. Infiltration of monocytes into intestinal mucosa, submucosa, and villi.
  2. Lymphocytes and eosinophils collect around foci of large mononuclear phagocytes.
  3. Giant cells are formed.
  4. Infiltration of connective tissue in latter stages.
  5. No caseation necrosis or calcification in cattle; may be present in sheep.
  6. Microscopic appearance of mesenteric lymph nodes.
  7. Infiltration of monocytes cause lymph nodes to be enlarged and soft.
  8. Packets of acid-fast organism very evident.


DIAGNOSIS

Field:

History of Johne’s disease in herd or community.

Symptoms.

  1. Chronic recurrent culars.
  2. Progressive cachexia.

Postmortem.

  1. Thickened and corrugated intestinal mucosa.

Diagnostic tests.

Intradermal johnin.

  1. Inject 0.2 mI. intradermal johnin in caudal fold, vulva or skin side of neck.
  2. Read in 48 hrs.


Positive reaction is diffuse swelling 3 mm. or more in thickness.

Intradermal avian tuberculin used but not as satisfactory as intradermal johnin.

Temperature test using avian tuberculin.

  1. 3 pre-injection temperatures taken at 2-hour intervals.
  2. Omit animals with temperature at 103°F. or higher.

Inject 10 mI. tuberculin intravenously.

  1. Take temperature one hour after injection; then every hour for 12 hrs.
  2. Majority reactions occur 3-8 hrs. after injection.
  3. Positive reaction is rise of 1.5 degrees over pre-injection temperature.
  4. Physical reaction often present – diarrhea, chills, and dyspnea.

Close antigenic relationship of bacillus of Johne’s disease, bovine tuberculosis, and avian tuberculosis causes difficulties in accurate test results.

Laboratory:

  1. Microscopic examination of piece of rectal mucosa for acid-fast organisms.
  2.  Microscopic examination of section of affected intestinal tract and lymph nodes.

PROGNOSIS

  1. Animals showing clinical symptoms rarely recover.
  2. Chronic progressive emaciation and death.

TREATMENT

  1. Case – various antibiotic agents have been tried, resulting in improvement but not total recovery.
  2. Herd – none.

PROPHYLAXIS
  1. Immunization – some value in sheep; produced tuberculin sensitivity in cattle.
  2. Sanitation and control:
  3. Test all animals regardless of age and remove reactors from herd.
  4. Inspect, clean, and disinfect buildings and rest pastures containing fecal material. C. Isolate calves from mature animals from birth until 1 year old.
  5.  Add only disease-free animals to herd, thus test all new additions.
  6. Thoroughly discuss control measures with owner when Johne’s disease suspected or diagnosed.

Tuberculosis


Synonyms:
Pearly disease,Consumption Scrofula,Phthisis.

Tuberculosis is a chronic, infectious disease of mammals caused by Mycobac­terium tuberculosis and characterized by the development of tubercles and by abscess formation, with resulting caseation and calcification.

ETIOLOGY

Mycobacterium tuberculosis:

Types:

  1. Avian.
  2. Mammalian.
  3. Var. bovis.
  4. Var. hominis.

Morphological characteristic:

  1. Slender rod – 0.2 to 0.6p: x 1.5 to 4JJ.
  2. Coccoid and filamentous shapes are frequently seen.
  3. Acid-fast organism and usually Gram-positive.

Growth characteristics:

Grows slowly, reaching maximum in 8 wks.

  1. Human type – thick, wrinkled.
  2.  Bovine type – sparse, rough, and dry.


Avian type – heavy, smooth, and moist.

  1. Crumbly dry mass on surface of media.
  2. Aerobic.
  3. Bovine strains grow best in acid medium, human strains in alkaline medium.
  4. Slightly acidified, glycerin bouillon is rendered more acid in reaction by the growth of human strains while growth is inhibited in bovine strains.


Pathogenicity:

 

Human

Bovine

Avian

Man

+++

+

-/+

Bovine

+

+++

+

Chicken

-

-

+++

Pig

+

++

++

Rabbit

+

++

+++

Guinea pig

++

+

+

Sheep

+

+

+

Goat

+

+

+

Horse

+/-

+

+

Dog

+

+

+

Cat

+/-

+

-

Parrot

+

+

+

Resistance to physical and chemical agents:

  1. Killed by light in 3-10 days.
  2. Resists drying -150 days in dry cattle feces.
  3. Putrefaction not effective in causing death of organism, survives in cattle lung 167 days.
  4. Pasteurization, 143°F for 30 min kills organism.
  5. Phenolic compounds 2-3%, sodium orthophenyl-phenate 1% - kills organisms
  6. Not sensitive to penicillin but is to streptomycin.


EPIZOOTIOLOGY

Distribution;

Disease present in man and animals in all areas of the world, especially the old world, and thickly populated areas.

Tends to be more prevalent in temperature of cold climates because housing of animals during unfavorable weather is necessary.

Transmission:

Bovine:

  • Contamination of feed and water which is ingested. Contamination is from the faeces to the ground and feed. Water is contaminated by the organisms being washed from infected animal’s mouth in the process of drinking.
  • Aerosol and dust.

Swine:

  • Ingestion of contaminated feed and water when running with the infected bovines.
  • Aerosol and dust.
  • Ingestion of diseased chickens or contaminated droppings.

Avian:

  • Ingestion of contaminated feed and water.
  • Aerosol and dust.

Susceptible hosts:

Bovine strain
  • Cattle, primarily.
  • Man.
  • Swine.
  • Horses, sheep, goats, and parrots, rarely.
  • Experimental animals.

Rabbit – very susceptible.

Guinea pig – not as much as rabbit.

Chicken – not susceptible.

Avian strain

 

  • Domestic fowl and pheasant.
  • Ducks, geese, and pigeons are relatively resistant.
  • Swine.
  • Cattle and sheep, rarely.
  • Experimental animals.
  • Rabbit – very susceptible.
  • Guinea pig resistant.
  • Chicken – kills.

Human strain:

  • Man.
  • Anthropoid apes and monkeys.
  • Parrots.
  • Cattle, swine, cats and dogs, rarely.
  • Experimental animals.
  • Guinea pigs are highly susceptible.
  • Rabbits are susceptible but rarely succumb.
  • Chickens  not susceptible.

Factors influencing susceptibility:

Age:   

  • Little influence except that the aged have had more opportunity to come in contact with infection.
  • Younger ages of people more susceptible. Effects noted later in life. This is par­ticularly true in relation to the bovine strain.

Sex:

No differences.

Condition:

Little influence, but poor condition increases an existing infection.

Feeding:

  • Lack of cleanliness from poor feeding and drinking facilities is dangerous from the standpoint of spreading the disease.
  • Milk and dairy by-products are a source of infection for calves.

Housing:

  • Crowded facilities are conducive to the spread of the disease.
  • Poorly lighted and poorly arranged stables promote spread of tuberculosis.
  • Common drinking troughs are dangerous.

SYMPTOMATOLOGY

On account of the insidious nature of the disease and the variability of the lesions produced, the observable symptoms are variable, not only in the different species of animals, but also in the different individuals of the same species. In the majority of cases of tuberculosis in cattle and swine, symptoms are either entirely lacking or so vague and obscure as to be of no material assistance in the recognition of the disease. Small lesions in lymph nodes may produce no symptoms, and even extensive lesions, particularly of the abdominal viscera, may be charac­terized by a complete lack of clinical symptoms. General symptoms of weakness, anorexia, emaciation, and a low grade fever may occur if the disease is progressive.


Bovine tuberculosis:

With few exceptions the course is chronic.

Poor condition.

When disease is extensive, or

  1. If respiratory, digestive, or circulatory systems are involved.
  2. Temperature is usually normal.
  3. Respiratory system is usually the seat of clinical tuberculosis

(a) Dyspnea.-  Increased frequency of breathing. Inspiratory interference from stenosis due to swollen lymph nodes.  Cough from pulmonary lesions- Harsh and dry, becoming soft, moist, and low- Occurs at irregular intervals.- May be easily and repeatedly produced-by pinching the trachea.

(b) Auscultation may reveal louder vesicular sounds in one lung.-  Rales occur frequently.

I Percussion – Areas of dullness – Pain occurs -    Induces cough.

Udder

     (a) Swelling of supramammary lymph nodes

     (b) Nodular, circumscribed, or diffuse swellings.    

     I Milk secretion may cease.

(5) Palpable lymph nodes show enlargement.

     (a) Retropharyngeal.

     (b) Submaxillary.

      I Precrural.

     (d) Supramammary.

     (e) Mediastinal nodes when enlarged cause tympany of the rumen.

(6) Genital involvement.

     (a) Rarely occurs, but when present any part of the genital tract may be involved, causing sterility.

     (b) Avian type may cause abortion.

(7) Central nervous system involvement.

     (a) Paresis.

     (b) Hyperesthesia.

     I Motor irritation.

     (d) Maniacal symptoms, rarely.

(8) Intestinal symptoms.

     (a) Diarrhea.

     (b) Emaciation.   

     I Chronic bloat after feeding following enlarged mediastinal lymph nodes.

     (d) Rectal examination may reveal roughened peritoneum and enlarged mesenteric lymph nodes.   

(9) Liver abscesses.

     (a) Pain on percussion.

Porcine tuberculosis:

The great majority of cases remain unrecognized until discovered at time of slaughter.

The chronic course of the disease and the relatively short life of swine account for lack of observable symptoms.

Unthriftiness, nodular swelling of the neck region, digestive disturbance, enlargements of bones and joints, and pulmonary symptoms have been observed.

Poultry:

  1. Ravenous appetite and general emaciation – feel breastbone (going light),
  2. Pale wattles and comb, swollen joints and culars.
  3. Eyes usually bright.
  4. Lameness in one or both legs.
  5. Birds extensively infected usually more than one year old.
  6. Birds seldom suffer from tuberculosis of the lung.
  7. Avian-type tubercle bacilli viable in soil for as long as 4 years and in buried fowl car­cula more than 2 years.

Canine and feline:

  1. May be infected by human or bovine types.
  2. Lesions resemble neoplasms; often grayish-white and are circumscribed.
  3. Rarely observed due to the gradual eradication of the disease in cattle.

PATHOLOGY

Pathogenesis:

Organisms enter on feed, water, dust.

  1. Digestive tract.
  2. Respiratory tract.
  3. Wound infection.
  4. Congenital.

Organisms are ingested by leucocytes.

Multiplication occurs in leucocytes.

Leucocytes with the organism localize in the lymph nodes.

  1. Submaxillary lymph nodes.
  2. Mesenteric lymph nodes.
  3. Pulmonary lymph nodes.
  4. May localize primarily in tissue other than lymph nodes.

Formation of tubercles.

  1. Started by the leucocyte reaction and reticulo-endothelial cell reaction. Lymphocytes appear “giant cell” forms.
  2. Encapsulated by fibrous connective tissue which is produced by fibroblasts.
  3. Reticulo-endothelial granulation tissue occurs.

Necrosis.

  1. Caseation to liquefaction.
  2. From center to periphery.
  3. Causes extension of tubercles.
  4. Necrosis through a blood vessel may result in generalized tuberculosis.
Progressive tuberculosis.
  1. Multiplication.
  2. At old lesion.
  3. At new site.

Calcification of tubercle.

Death of animal.

Cause of symptoms.

(1) Destruction of tissue.

(2) Absorption of products of necrosis.

         (a) A tissue toxemia.

(3) A part becomes dysfunctional.

(4) Secondary complications cause death.

(5) Hemorrhage as from pulmonary tuberculosis causes death.

Postmortem lesions:

a. The tubercle.

(I) At first, barely visible, gray, translucent nodule.

(2) When plain, visible to naked eye:

            (a) Yellow in cattle, sheep, goats, and swine.

            (b) White in horses and carnivores.

(3) Tubercles fuse to form tuberculous masses.

            (a) Dry and cheesy – caseous lesions.

            (b) Gritty if calcification is present – (caseocalcareous lesions).

            I Pearly disease.

(4) Generally considered impossible to differentiate from other granulomatous neo­plasms by gross pathology.

b. Location of lesions.

(I) Cattle:

          (a) Lungs and pleura.

          (b) Liver, spleen, and peritoneum.

          I Regional lymph nodes.

          (d) Skin and bones, occasionally.

(2) Swine:

         (a) Cervical lymph nodes.

         (b) Bronchial lymph nodes.

         I Portal and mesenteric lymph nodes.

        (d) Liver, lungs, and spleen.

(3) Fowls:

        (a) Liver, spleen, intestines. Lungs, bones, joints,peritoneum, kidneys, and ovaries.

Differential diagnosis

  • Parasitic nodules
  • neoplastic masses
  • fat necrosis
  • coccidioidomycosis
  • histoplasmosis
  • actinobacillosis


DIAGNOSIS

Intradermal test:

Intradermal tuberculin 0.1 mI. is injected into dermis of animal.

     (a) Cattle:

  1) Thin skin of the’caudal fold Md/or vulva.

  2) Cervical region

     (b) Swine:

1) Ear skin and/or vulva.

I Chicken:

  1) Wattle.

Positive reaction in 48-72 hrs. (72 official), small firm swelling at the point of in­jection.

Ophthalmic test:

(1) Concentrated tuberculin is placed into the conjunctival sac of the eye with a camel’s­

     hair brush or with a medicine dropper.

  (a) Ophthalmic-tuberculin discs may be used.

  (b) Two applications of tuberculin are required.

1) First application is for purpose of sensitization.

2) Second application is given 2 to 3 days later for purpose of diagnosis. Close observation required for 8 hrs. following last application.

(2) Positive reaction.

(a) Marked inflammation of the conjunctiva.

(b) Profuse lacrimation.

I Mucopurulent culars.

(3) Rarely used except for retest.

Stormont test:

(1) 0.1 mI. of P.P.D. is injected into the skin of the cervical region.

(2) On 7th day original site is reinjected.

(3) Increase in skin thickness of 5 mm. or more 24 hrs. after 2nd injection is a positive      result.

PROGNOSIS

1. If tuberculous rate of a herd or area is high, the mortality may be as high as 15% in areas of world where disease is uncontrolled.

TREATMENT

     1. Of no consequence

PROPHYLAXIS

1. Immunity:

a. Little development of immunity from having the disease.

b. Immunizing agents have been sought with little success; current ones are:

(1) B.C.G. (Bacillus of Calmette and Guerin).

(a) A dissociated strain which is relatively avirulent. It does not produce lesions. (b) It is used as pre-immunization in early life.

 (2) Vole Tubercle Bacillus.

(a) Isolated from the vole in Great Britain.

(b) Considered to be as satisfactory as B.C.G.

2. Sanitation:

a. Addition of diseased animal into a herd is hazardous.

b. The ARS requires a thorough cleanup with the use of disinfectants after an infected animal is discovered in a cattle herd.

PUBLIC HEALTH RELATIONSHIPS

1. Bovine tubercle bacillus.

a. A public health problem in man.

(1) Transmitted through contaminated milk and milk products.

(2) Children under 16 years of age are most susceptible

Contagious bovine pleuropneumonia

ETIOLOGY


Classification of the causative agent

Mycoplasma mycoides subsp. Mycoides SC (bovine biotype)

Mycoplasmas are microorganisms deprived of cell walls and are, therefore, a) pleomorphic and b) resistant to antibiotics of the beta-lactamine group, such as penicillin

Growth of the mycoplasma is relatively fastidious and requires special media rich in cholesterol (addition of serum).

There is only one antigenic type

Resistance in the environment and to chemicals

Mycoplasma mycoides subsp. Mycoides (SC) is not resistant in the environment and transmission requires close contact

Temperature:     In saline solution -      susceptible to 45°C/120 min and/or 47°C/2 min

In lymph – susceptible to 45°C/240 min and/or 60°C/2 min

It is: Inactivated by acid and alkaline pH

Susceptible: to ether, mercuric chloride (0.01%), calciumhydroxide, phenol (1%/3min),and

formaldehyde solution (0.5%/30 seconds)

Survival:  Survives well in frozen tissues

EPIDEMIOLOGY

Hosts

Cattle (Bos cular), zebu (Bos indicus) and water buffalo (Bubalus bubalis).

Wild bovids and camels are resistant

Transmission

  1.  Aerial, mostly by direct contact: droplets emitted by coughing animals, saliva, and urine. Transmission up to several cularsi has been suspected under favourable climatic conditions
  2. Transplacental infection can occur
  3. Inapparent carriers are a major source of infection
  4. Cattle movement is important in the spread of the disease

Virulent material

Lungs, pleuropneumonia lymph and possibly brain, liver, kidneys, lymph nodes, uterus, fetus and fetal membranes, and urine

Occurrence

CBPP is widespread in Africa and it is also present in other regions of the world, including southern Europe, the Middle East and parts of Asia. In Africa, its economic importance is particularly high in Sahelian and Sahelo-Sudanese countries


For detailed information on occurrence, see recent issues of World Animal Health and the OIE Bulletin

DIAGNOSIS

Incubation period is 1-3 months (sometimes longer)

During an outbreak of natural disease, only 33% of animals present symptoms (hyperacute or acute forms), 46% are infected but have no symptoms (subclinical forms) and 21% seem to be resistant

Clinical diagnosis

In adults

  1. Moderate fever with respiratory, pulmonary and pleuretic symptoms: polypnoea, characteristic attitude (elbows turned out, arched back, head extended), cough (at first dry, slight, and not fitful, becoming moist)
  2. When the animal gets up or after exercise, breathing becomes laboured and grunting can be heard
  3. At percussion, dull sounds can be noticed in the low areas of the thorax

In calves

  1. Pulmonary tropism is not the general rule, and infected calves present arthritis with swelling of the joints
  2. Co-existence of pulmonary symptoms in adults and arthritis in young animals should alert the clinician to a diagnosis of CBPP

Lesions

  1. Important amount of yellow or turbid culars in the pleural cavity (up to 30 litres) that coagulates to form large fibrinous clots
  2. Fibrinous pleurisy: thickening and inflammation of the pleura with fibrous deposits
  3.  Interlobular oedema, marbled appearance due to hepatisation and consolidation at different stages of evolution usually confined to one lung
  4.  Sequestrae with fibrous capsule surrounding grey necrotic tissue in recovered animals


Differential diagnosis

Acute form

   1. East Coast fever
   2. Acute bovine pasteurellosis
   3. Bronchopneumonia and pleuropneumonia resulting from mixed infections

Chronic form

   1. Hydatid cyst
   2. Actinobacillosis and tuberculosis, bovine farcy

Laboratory diagnosis

Procedures

Identification of the agent

   1. Isolation of pathogen and identification by metabolic and growth inhibition tests
   2. MF-dot
   3. Polymerase chain reaction

Serological tests

  1. Complement fixation (prescribed test in the Manual). This test should be used only at herd level and never for individual diagnosis
  2. Competitive ELISA (under validation by International Atomic Energy Agency and several reference laboratories), and haemagglutination
  3. Agglutination test can be used as penside test in active outbreaks at the herd level

Samples

  1. Lung lesions, pleural fluids, lymph nodes, lung tissue culars – frozen for isolation of the organism
  2. Acute and convalescent sera

PREVENTION AND CONTROL

No efficient treatment. Antibiotic treatment should be prohibited

Sanitary prophylaxis

  1. In disease-free areas: quarantine, serological tests (complement fixation) and slaughtering of all animals of the herd in which positive animals have been found
  2. Control of cattle movements is the most efficient way of limiting the spread of CBPP

Medical prophylaxis

   1. In infected areas: a CBPP vaccine containing T1 strain is widely used
   2. A CBPP-rinderpest combined vaccine is sometimes used

Surveillance

Recommended Standards for Epidemiological Surveillance for Contagious Bovine Pleuropneumonia were drawn up by an OIE Ad hoc Group on 7-9 June 1993. After revision, these standards were approved by the International Committee during the 63rd General Session

Peste des petits ruminants (PPR)

ETIOLOGY

Classification of the causative agent

Virus family   Paramyxoviridae,

Genus   Morbillivirus.

Antigenically close to rinderpest virus

Resistance to physical and chemical action

Temperature: Some virus may resist 60°C/60 min

pH: Stable between pH 4.0 and 10.0

Chemicals: Susceptible to alcohol, ether, detergents

Disinfectants:  Susceptible to most disinfectants, e.g. phenol, sodium hydroxide 2%/24 hours

Survival:Survives for long periods in chilled   and frozen tissues

EPIDEMIOLOGY

   1. Morbidity rate 90% (susceptible population)
   2. Mortality rate 50-80% (susceptible population)

Hosts

  1. Sheep and especially goats. To date diagnosed only in captive wild ungulates from families of Gazellinae (dorcas gazelle), Caprinae (Nubian ibex and Laristan sheep) and Hippotraginae (gemsbok)
  2. Experimentally the American white-tailed deer (Odocoileus virginianus) is fully susceptible
  3. Cattle and pigs develop inapparent infections
  4. Breed-linked predisposition in goats


Transmission

   1. Direct contact between animals
   2. No carrier state
   3. Seasonal variations: more frequent outbreaks during the rainy season or the dry cold season

Sources of virus

Tears, nasal discharge, coughed secretions, and all secretions and excretions of incubating and sick animals

Occurrence

PPR occurs in Africa, the Arabian Peninsula, the Middle East and India

DIAGNOSIS

Incubation period is 3-10 days.

Clinical diagnosis

Acute form

  1. Sudden rise in body temperature (40-41°C) with effects on the general state: restlessness, dull coat, dry muzzle, depression of appetite
  2. Serous nasal discharge becoming mucopurulent and resulting, at times, in a profuse catarrhal culars which crusts over and occludes the nostrils. Respiratory distress
  3. Small areas of necrosis on the visible nasal mucous membrane
  4. Congestion of conjunctiva, crusting on the medial canthus and sometimes profuse catarrhal conjunctivitis
  5. Necrotic stomatitis with halitosis is common
  6. Severe non-haemorrhagic culars
  7.  Bronchopneumonia evidenced by coughing is a common feature
  8. Abortion
  9. Dehydration, emaciation, dyspnoea, hypothermia and death within 5-10 days


Per acute form

   1. Frequent in goats

Sub acute and chronic forms

   1. Frequent in some areas because of local breed susceptibility
   2. 10-15 days development with inconsistent symptoms
   3. Pneumopathy

Lesions

  • Emaciation, conjunctivitis, erosive stomatitis involving the inside of the lower lips and adjacent gum near the commisures and the free portion of the tongue
  • Lesions on the hard palate, pharynx and upper third of the oesophagus in severe cases
  • Rumen, reticulum and omasum rarely have lesions
  • Small streaks of haemorrhages and sometimes erosions: in the first portion of the duodenum and the terminal ileum
  • Extensive necrosis and sometimes severe ulceration of Peyer’s patches
  • Congestion around the ileo-caecal valve, at the caeco-colic junction and in the rectum. ‘Zebra stripes’ of congestion in the posterior part of the colon
  • Small erosions and petechiae on the nasal mucosa, turbinates, larynx and trachea
  • Bronchopneumonia is a constant lesion
  • Possibility of pleuritis and hydrothorax
  • Congestion and enlargement of spleen
  • Congestion, enlargement and oedema of most of the lymph nodes
  • Erosive vulvovaginitis may exist

Differential diagnosis

  • Rinderpest
  • Contagious caprine pleuropneumonia
  • Bluetongue
  • Pasteurellosis
  • Contagious ecthyma
  • Foot and mouth disease
  • Heartwater
  • Coccidiosis
  • Mineral poisoning


Laboratory diagnosis


Procedures

Identification of the agent

  • Antigen detection
  • Agar gel immunodiffusion
  • Counter immunoelectrophoresis
  • Indirect fluorescent antibody test
  • ELISA
  • Immunohistopathology
  • Virus isolation and identification
  • In primary lamb kidney cells or VERO cell line
  • Virus cularsisd
  • Electron microscopy
  • Virus RNA detection
  • PPR-specific cDNA probes
  • Amplification by polymerase chain reaction (PCR)


Serological tests

Virus cularsisd OIE approved

  • Competitive ELISA
  • Counter immunoelectrophoresis
  • Agar gel immunodiffusion
  •  Immunodiffusion inhibition test

Samples

  • Swabs of the conjunctival discharges and from the nasal, buccal and rectal mucosae
  • Whole blood collected on heparin (blood and anticoagulant should be mixed gently)
  • Lymph nodes, especially the mesenteric and bronchial nodes
  • Spleen
  • Large intestine and lungs

Samples should be transported under refrigeration

PREVENTION AND CONTROL

  • No specific treatment
  • Antibiotics may prevent secondary pulmonary infections (oxytetracycline, chlortetracycline)


Sanitary prophylaxis

Recommended when the disease appears in previously PPR-free countries.

Medical prophylaxis

  • Rinderpest vaccine is commonly used
  • A homologous PPR vaccine is also available and is preferable, to avoid confusion when retrospective serological surveys are done
  • Both vaccines give strong immunity
  • Genetically engineered recombinant vaccines are currently undergoing limited field trials


Sheep pox and goat pox

ETIOLOGY

Classification of the causative agent

Virus family  Poxviridae

 Genus   Capripoxvirus

Resistance to physical and chemical action

Temperature:   Susceptible to 56°C/2 hours; 65°C/30 min

pH:        Susceptible to highly alkaline or acid pH

Chemicals: Sensitive to ether (20%), chloroform, and formalin (1%)

Disinfectants:   Inactivated by phenol (2%) in 15 min. Sensitive to detergents, e.g. sodium dodecyl sulphate

Survival:   Can survive for many years in dried scabs at ambient temperatures. Virus remains viable in wool for 2 months and in premises for as long as  6  months

EPIDEMIOLOGY

  • Morbidity rate: Endemic areas 70-90%
  • Mortality rate: Endemic areas 5-10%, although can approach 100% in imported animals

Hosts

Sheep and goats (breed-linked predisposition and dependent on strain of capripoxvirus)

Transmission

  • Direct contact
  • Indirect transmission by contaminated implements vehicles or products (litter, fodder)
  • Indirect transmission by insects (mechanical vectors) has been established (minor role)
  • Contamination by inhalation, intradermal or subcutaneous inoculation, or by respiratory, transcutaneous and transmucosal routes

Sources of virus

  • Cutaneous lesions (crusts, nodules) resulting in aerosols
  • Saliva
  •  Nasal secretions
  •  Faeces


Occurrence


Sheep pox and goat pox are endemic in most of Africa, the Middle East and Asia

DIAGNOSIS

Incubation period is up to 21 days. Following contact, incubation period is approximately 12 days, but is shorter than this following intradermal inoculation by insects

Clinical diagnosis

  • Subclinical cases
  • Clinical cases vary from mild to severe:
  • fever, depression, polypnoea
  • conjunctivitis, lacrimation, rhinitis, oedema of eyelids, photophobia
  • cutaneous eruption beginning with erythematous areas especially noticeable in hair or wool-free parts of the body, such as the perineum, inguinal area, scrotum, udder, muzzle, eyelids and axillae
  • olesions evolve into papules
  • Papulo-vesicular form
  • Papules become a white-grey colour, desiccate and form crusts that are easy to remove
  • Rarely, papules may transform into vesicles. After rupture of vesicles, a thick crust covers the lesions
  • Nodular form (‘stone pox’)
  • Papules give rise to nodules involving all the layers of the skin and the subcutaneous tissue
  • Necrosis and sloughing of the nodules leaves a hairless scar
  • In both forms, nodules develop in the lungs causing bronchopneumonia with cough, abundant nasal discharge, depression, anorexia and emaciation
  • Animals may recover within 20-30 days
  • Death is frequent when complications occur (abortion, which is rare, secondary infections, fly strike, septicaemia, digestive cularsis)


Lesions

  • Skin lesions: congestion, haemorrhage, oedema, vasculitis and necrosis. All the layers of epidermis, dermis and sometimes musculature are involved
  • Lymph nodes draining infected areas: enlargement (up to eight times normal size), lymphoid proliferation, oedema, congestion, haemorrhage
  • Pox lesions: on mucous membranes of the eyes, mouth, nose, pharynx, epiglottis, trachea, on the rumenal and abomasal mucosae, and on the muzzle, nares, in the vulva, prepuce, testicles, udder, and teats. Lesions may coalesce in severe cases
  • Lung lesions: severe and extensive pox lesions, focal and uniformly distributed throughout the lungs; congestion, oedema, focal areas of proliferation with necrosis, lobular atelectasis. Enlargement, congestion, oedema and haemorrhages of mediastinal lymph nodes


Differential diagnosis

  • Bluetongue
  • Peste des petits ruminants
  •  Contagious ecthyma
  • Photosensitisation
  •  Dermatophilosis
  •  Insect bites
  • Parasitic pneumonia
  • Caseous lymphadenitis
  • Mange (scrabies)


Laboratory diagnosis

Procedures

Identification of the agent

  • Cell inoculation and identification by immunofluorescence staining of intracytoplasmic inclusion bodies
  • Inhibition of cytopathic effect using positive serum
  • Antigen detection ELISA


Serological tests

  • Virus cularsisd
  •  Indirect fluorescent antibody test
  • Agar gel immunodiffusion
  • ELISA


Samples

  • Full skin thickness biopsies taken within 1 week of the first appearance of the lesions
  • Lesions in the lungs
  • Paired sera


PREVENTION AND CONTROL


No treatment

Sanitary prophylaxis

  • Isolation of infected herds and sick animals for at least 45 days after recovery
  • Slaughtering of infected herd (as far as possible)
  • Proper disposal of cadavers and products
  • Stringent disinfection
  • Quarantine before introduction into herds
  • Animal and vehicle movement controls within infected areas


Medical prophylaxis

  • There are numerous attenuated virus vaccines delivered by subcutaneous or intradermal route
  • The conferred immunity lasts up to 2 years

 

 

 

 

 
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