BLACK QUARTER

BLACK QUARTER

Synonyms : Symptomatic Anthrax, Quarter ill, Black leg, Emphysematous gangrene.

Introduction

• It is an acute ,infectious, and fatal disease of cattle, sheep and goats. It spreads rapidly following heavy rainfall.

• Affected animals develop skeletal muscle damage, severe gangrenous, necrotizing, 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.
• Spores produced by this organism persists in soil for many years and is highly resistant to disinfectants, dryness and hot.
• Spores can withstand 120 degree Celsius for 10 minutes.
• 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.
• Both natural and accidental hosts are supposed to be affected by these strains.
• In India - Strain 49 - used in BQ vaccine production .

Predisposing factors

• Occasional outbreak: Damage to tissues caused by administration of formalized 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, lambing, castration, 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 and thus the animals may excrete the organisms through their feces.

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.

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.
• Some of the spores in the muscles are destroyed by phagocytosis and others remain latent for at least several weeks.
• Mostly, the organism affects muscles of loin, shoulder and gluteal muscle.
• There is necrosis of the muscles and blood capillaries. Gases used to accumulate within the muscle fibres due to fermentation.
• If animals consume the preformed toxins while grazing, ingested toxins is directly absorbed and spread along the systemic circulation which leads to fatal toxaemia.
• 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.
• 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.

Clinical Findings

Cattle

(1)Peracute form

• Affected animals show sudden death. 

(2)Acute form

• Incubation period is 2 to 5 days.
• Disease follows a rapid and fatal course of infection following ingestion of preformed toxins.
• Fever may be as high as 106 or 108°F (41°C) but 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
• Swellings are hot and painful in the early stage and become cold and painless later..
• Edema, emphysema, crepitation of affected heavy muscles on thigh with muscle stiffness.
• Discolored, gangrenous to black, dry and cracked skin.
• Increased pulse rate 100 to 120 per minute with labored breathing.
• 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 hemoptysis, high fever, anorexia, loss of appetite, depression and quick death.
• Short course of the disease, dyspnea and recumbancy in 3 to 4 days occurs.

Horses

Pectoral edema, stiff gait and incoordination is recorded (ataxia).

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 48hrs.

Sample collection

• Muscle samples should be collected in an 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.