Black Quarter: Cause, Transmission, Symptoms, Diagnosis

Black quarter

Synonyms: Symptomatic Anthrax, Quarter ill.

Introduction

1. It is an acute, infectious, and fatal disease of cattle, sheep, and goats.
2. Affected animals develop skeletal muscle damage, severe gangrenous, necrotizing, emphysematous myositis, and fatal systemic toxemia.

Etiology

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

Prevalence of infection

1. The disease is endemic in both developed and developing countries.
2. In India, the disease occurs sporadically, however, in some regions, the disease is endemic.

Economic impact

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

Predisposing factors

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

Sources of infection

1. Organism present in the decomposed carcass of blackleg affected animals and persists in soil for long period.
2. Sheep: Infection mostly spreads via wound developing during shearing, docking, and navel infection, etc., hence, it is called traumatic BQ.
3. Inhabitation: Organism exists as a normal inhabitant in the spleen, liver and alimentary tract of healthy animals.

Transmission

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

Host affected

1. The disease is highly fatal in cattle.

i) Cattle, 6 months to 2 years and well-nourished are mostly affected.

ii) In sheep all age groups are susceptible.

iii) It is reported also in deer, elephants, and horses.

iv) Both, C. chauvoei and C. septicum influence the development of gas gangrene in pigs.

v) The organism has also been isolated from the wounds of dogs and cats.

Pathogenesis:

The black quarter is a soil-borne infection.

1. Spores ingested would be taken via alimentary mucosa and then distributed to tissues and skeletal muscles via the circulation.
2. Injured muscles favor spores germination in the wound that provides anaerobic condition.
3. Mostly, the organism affects muscles of the loin, shoulder, and gluteal muscle.
4. In addition, muscles of the diaphragm may be affected.
5. If animals consume the preformed toxins while grazing, ingested toxins are directly absorbed and spread along with the systemic circulation which leads to fatal toxemia.
6. 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.
7. Injured muscle: The oxidation-reduction potential (creates anaerobiosis) and reduced hydrogen ion concentration (pH) provides a conducive atmosphere for germination of spores and causes true black leg following the release of exotoxin.
8. C.septicum is a potent exotoxin producer as compared to C.chauvoei because the virulent form of C.chauvoei is only able to produce exotoxin. This exotoxin is responsible for the development of edema and pulmonary congestion.
9. C.chauvoei produces neuraminidase at optimum pH 4.5 and 40° C. At low pH, neuraminidase promotes anaerobiosis, muscle damage and leads to gas accumulation.
10. At optimum pH and temperature neuraminidase desolate hemoglobin-free RBC membrane of cattle, sheep, goats, and horses at a significant level. High neuraminidase activity is found in edema fluid.
11. Cleaving of sialic acid from blood vessels by neuraminidase causes vascular permeability and inflammation of muscles.
12. During pyrexia, the removal of sialic acid is at its peak.
13. Toxins develop hyperplasia and congestion in the spleen, hemorrhages, and degenerative foci in the liver and kidney.
14. Toxins cause damage to leucocytes, platelets which leads to leucopenia and thrombocytopenia.
15. Toxins released by the organism produce severe necrotizing myositis in skeletal muscles and systemic toxemia followed by death.
16. In cattle and sheep during atypical outbreaks, sudden death follows attributable to clostridial cardiac myositis.

Clinical Findings

Cattle

Peracute form

1. Affected animals show sudden death.

Acute form

The incubation period is 2 to 5 days.

1. The disease follows a rapid and fatal course of infection following ingestion of preformed toxins.
2. Fever (41°C) is not common, marked depression, anorexia, and ruminal tympany.
3. Prominent swelling on the upper part of the affected limbs leads to marked lameness.
4. Swelling of throat, tongue, and protrusion of the tongue.
5. Edema, emphysema, crepitation of affected heavy muscles on the thigh with muscle stiffness.
6. Discolored, gangrenous to black, dry, and cracked skin.
7. Increased pulse rate from 100 to 120 per minute.
8. Death follows in 12 to 36 hours of infection.
9. Cattle with cardiac myositis are found dead.
10. A thin sanguineous fluid containing bubbles of gas from affected sites.

Sheep

1. No palpable crepitation swelling as in cattle.
2. Stiff gait, disinclined to move, severe lameness either unilateral or bilateral.
3. Painful walking, discoloration of the skin with no necrosis and gangrene.
4. The extensive local lesion in the vulva and vagina occurs through skin wounds.
5. Head swelling leads to hemoptysis, high fever, anorexia, depression, and quick death.
6. A short course of the disease, dyspnoea, and recumbency in 3 to 4 days occurs.

Horses

1. Pectoral edema, stiff gait, and incoordination are recorded.

Necropsy findings

Cattle

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

Sheep

1. Muscle lesions are more localized and deeper.
2. Mild subcutaneous edema is found around the neck.
3. No gaseous crepitations and subcutaneous edema is seen before death.
4. Sheep with cardiac myositis are usually found dead.
5. More obvious superficial, subcutaneous edema, and swelling of deep musculature were observed.
6. Invasion in the genital tract develops typical lesions in perineal tissues, walls of the vagina, occasionally in the uterus and testes.

Diagnosis

1. Based on clinical signs and necropsy findings.
2. Isolation of organisms by the culture of heart blood, peritoneal fluid, muscles, and liver is important for both Cl. chauvoei and Cl. septicum.
3. Muscle bundle separation by gas.
4. Tube agglutination test, counter immunoelectrophoresis, double immunodiffusion test used to detect humoral antibody, Immunofluorescence, Fluorescent antibody test to detect antigen.
5. Biological inoculation: Filtrate-containing spores obtained from infected animals heated at 60C for 30 minutes and injected one ml into the gluteal muscle of guinea pig leads to death in 48hrs.

Sample collection

1. Muscle samples should be collected in an airtight container.
2. Air-dried impression smears obtained from the surface of the freshly cut lesion for bacteriology, 10% formalin-fixed samples from suspected muscles for histopathology.
3. Impression smears of heart blood and liver examination show numerous gram-positive subterminal spores.

Differential diagnosis

1. Malignant edema.
2. Anthrax.
3. Lightning stroke.
4. Bacillary hemoglobinuria.

Treatment of black quarter

1. Penicillin 10,000 IU/kg IM is a drug of choice for 5-6days, (A large dose of 40,000IU/kg BW) can be given following administration of Crystalline Penicillin via IV.
2. Oxytetracycline in high doses i.e. 5-10 mg/Kg body weight IM or IV.
3. Tease the swelling and drain off.
4. B.Q. antiserum in large doses, if available.
5. Injection of antihistamines can be given.
6. It can also be sprayed directly on affected tissues.

In outbreak

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

Vaccines

1. The vaccine is prepared from a highly antigenic strain of C. chauvoei by and culture method, inactivated by formalin and precipitated by the addition of alum. It is used for active immunization of cattle, buffaloes, sheep, and goats against black quarter. Cattle and buffaloes 3 ml, s/c, sheep and goats 1-2 ml, s/c. Immunity lasts for 6 months.

Control

1. Isolation of affected cattle.
2. Constant surveillance and early treatment are necessary.
3. Destruction of carcasses by burning or deep burial to limit soil contamination is essential.
4. The organism can be destroyed by 3% formalin in 15 minutes is advisable.