Black Quarter in Animals

Black Quarter in animals also known as Symptomatic anthrax or Quarter ill. It is an acute, infectious, and fatal disease of cattle, sheep and goats.

Black Quarter affected animals develop skeletal muscle damage, severe gangrenous, necrotising, emphysematous myositis and a fatal systemic toxaemia.

Etiology

• Black Quarter (BQ) is caused by Clostridium chauvoei.
• It is a gram positive, spore forming, rod shaped bacteria measuring 0.6µ in dia and 3-8µ in length.
• It is a toxin producing anaerobic bacterium.
• The name C. chauvoei came after the Professor J.A.B. Chauveau, a french bacteriologist.
• There are 23 strains of C. chauvoei identified so far around the world.
• Spores produced by this organism persists in soil for many years and is highly resistant to disinfectants, dryness and hot.
• Both natural and accidental hosts are supposed to be affected by these strains.
• In India, Strain 49 is used in BQ vaccine production.

Epidemiology

Prevalence of infection

Disease is endemic in both developed and developing countries.In India, the disease occurs sporadically, however, in some region, the disease is endemic.

Economic impact

It causes major financial losses to cattle and sheep industry but the major outbreaks can be prevented by vaccination.

Predisposing factors

Occasional outbreak: Damage to tissues caused by administration of formalised vaccines, accidental injury of muscle and injury made by chemical agents. Cattle: Digging of soil spreads the infection. Alternate hot and dry seasons followed by heavy rainfall favors the dispersion of spores for long distance. Turning up of soil expose the spores to the top surface.

Sources of infection

Organism present in decomposed carcass of black leg affected animals and persists in soil for long period.

Sheep: Infection mostly spreads via wound developing during shearing, docking and navel infection etc., hence, it is called as traumatic BQ.

Inhabitation: Organism exists as normal inhabitant in spleen, liver and alimentary tract of healthy animals.

Transmission

It is transmitted by ingestion,  inhalation of spores and  absorption of toxins through wound. Wound contamination by spores especially in sheep and goats is possible.

Host Affected

The disease is highly fatal in cattle. Cattle, 6 months to 2 years and well nourished are mostly affected. In sheep all age groups are susceptible. It is reported also in deer, elephant and horses.

Both, C. chauvoei and C. septicum influence the development of gas gangrene in pigs. Organism has also been isolated from wounds of dogs and cats.

Pathogenesis

Black quarter is a soil borne infection.Spores ingested would be taken via alimentary mucosa and then distributed to tissues and skeletal muscles via the circulation. Injured muscles favors spores germination in the wound that provides anaerobic condition.Mostly, the organism affects muscles of loin, shoulder and gluteal muscle. In addition, muscles of diaphargm may be affected.

If animals consume the preformed toxins while grazing, ingested toxins is directly absorbed and spread along the systemic circulation which leads to fatal toxaemia.

Some spores are directly phagocytosed by the immune cells, the remaining assumes latency in the muscle, followed by transformation as vegetative form once the muscle is injured.

Injured muscle: The oxidation reduction potential (creates anaerobiosis) and reduced hydrogen ion concentration (pH) provides a condusive atmosphere for germination of spores and causes true black leg following the release of exotoxin. C.septicum is a potent exotoxin producer as compared to C.chauvoei because virulent form of C.chauvoei only able to produce exotoxin. These exotoxin is responsible for the development of edema and pulmonary congestion.C.chauvoei produce neuraminidase at optimum pH 4.5 and at 40° C. At low pH neuraminidase promotes anaerobiosis, muscle damage and leads to gas accumulation. At optimum pH and temperature neuraminidase desialate haemoglobin free RBC membrane of cattle, sheep, goats, and horses at a significant level. High neuraminidase activity is found in edema fluid. Cleaving of sialic acid from blood vessels by neuraminidase causes vascular permeability and inflammation of muscles. During pyrexia, the removal of sialic acid is at the peak.Toxins develops hyperplasia and congestion in spleen, haemorrhages and degenerative foci in liver and kidney. Toxins causes damage to leucocytes, platelets which leads to leucopenia and thrombocytopenia. Toxins released by the organism produces a severe necrotizing myositis in skeletal muscles and a systemic toxaemia followed by death.In cattle and sheep during atypical outbreak, sudden death follows attributable to clostridial cardiac myositis.

Clinical Signs

Cattle

Peracute form

Affected animals with peracute form of BQ show sudden death.

Acute form

Incubation period is 2 to 5 days. Disease follows a rapid and fatal course of infection following ingestion of preformed toxins. Fever (41°C) not common, marked depression, anorexia and ruminal tympany. Prominent swelling on the upper part of the affected limbs leads to marked lameness.

Swelling of throat, tongue and protrusion of the tongue. Edema, emphysema, crepitation of affected heavy muscles on thigh with muscle stiffness.

Discoloured, gangrenous to black, dry and cracked skin. Increased pulse rate 100 to 120 per minute. Death follows in 12 to 36 hours of infection. Cattle with cardiac myositis are found dead. A thin sanguineous fluid containing bubbles of gas from affected sites.

Sheep

No palpable crepitation swelling as in cattle. Stiff gait, disinclined to move, severe lameness either unilateral or bilateral.Painful walking, discoloration of skin with no necrosis and gangrene.

Extensive local lesion in vulva and vagina occurs through skin wounds. Head swelling leads to haemoptysis, high fever, anorexia, depression and quick death. Short course of the disease, dyspnoea and recumbancy in 3 to 4 days occurs.

Horses

Pectoral edema, stiff gait and incoordination is recorded.

Necropsy Findings

Cattle

Bloat and putrefaction occurs quickly and blood stained fluid oozes out from the external orifices such as nostrils, anus and oral with rapid clotting of blood. Freshly cut surfaces of muscles are often dry and may have a metallic sheen. Affected muscles become dark red to black, swollen and emanates a rancid odour.The thoracic cavity and pericardial sac may contain excess blood fluid with fibrin. Serositis is often get confused with pleuropneumonia. Lungs are usually congested and is atelectatic.

Sheep

In sheep, Muscle lesions are more localised and deeper. Mild subcutaneous edema is found around the neck. No gaseous crepitations and subcutaneous edema seen before death.

Diagnosis

• Based on clinical signs and necropsy findings.
• Isolation of organism by culture of heart blood, peritoneal fluid, muscles and liver is important for both Cl. chauvoei and Cl. septicum.
• Muscle bundle separation by gas.

Tube agglutination test, counter immuno electrophoresis, double immuno diffusion test used to detect humoral antibody, Immunofluorescence, Fluorescent antibody test to detect antigen.

Biological inoculation: Filtrate containing spores obtained from infected animals heated at 60°C for 30 minutes and injected one ml into glutial muscle of guinea pig leads to death in 48 hours.

Sample Collection

Muscle samples should be collected in a air tight container. Air dried impression smears obtained from surface of freshly cut lesion for bacteriology, 10% formalin fixed samples from suspected muscles for histopathology.

Impression smears of heart blood and liver examination shows numerous gram positive sub terminal spores.

Differential Diagnosis

• Malignant edema
• Anthrax
• Lightening stroke
• Bacillary haemoglobinuria

Treatment

Penicillin 10,000 IU/kg IM is a drug of choice for 5-6 days, (Large dose of 40,000 IU/kg body weight) can be given following administration of Crystalline Penicillin via IV. Oxytetracycline in high doses i.e. 5-10 mg/Kg body weight IM or IV. Tease the swelling.

Prevention

Maternal immunity persists for atleast 3 months, so until this time calves should not be vaccinated and this may interfere with the development of vaccine immunity.

In enzootic areas, annual vaccination of all cattle between 3-6 months must be done with 2 vaccinations at 4 weeks interval followed by annual booster vaccination.

Best time is earlier than monsoon. In an outbreak area, all cattle should be vaccinated immediately and treated with penicillin at 10, 000 IU/kg body weight IM or in combination with penicillin and benzathine penicillin.

Sheep

In enzootic areas, ewes should be vaccinated twice. Vaccination should be given one month before lambing and subsequently yearly booster before lambing to prevent infection of lambs and ewes and umbilical infection at birth.

In Oubreak

Prophylactic injections of penicillin and antiserum may be effective. Vaccination of lambs before they go into pasture is recommended. Clostridial vaccines have poorer antigenicity in sheep and goats than in cattle, so, combined vaccine which contain antigen of C. chauvoei, C. septicum, C. novyi is essential.

Vaccines

The vaccine is prepared from highly antigenic strain of C. chauvoei by anaculture method, inactivated by formalin and precipitated by addition of alum.

Active immunization of cattle, buffaloes, sheep and goats against black quarter:

• Cattle and buffaloes 3 ml SC
• Sheep and goats 1-2 ml SC
• Immunity last for 6 months

Control

• Control Isolation of affected cattle
• Constant surveillance and early treatment is necessary
• Destruction of carcasses