Clostridium perfringens infections

Cl. perfringens is a rod-shaped, spore-bearing anaerobic organism. It is capsulated and non-motile. A characteristic feature of the organism is high rate of growth and production of large quantities of gas. Cl. perfringens (C1. welchii) is a common cause of gas gangrene in human beings and enterotoxaemia infections in sheep, and less frequently in other animal species. The organism is present in the soil and in the intestines of healthy animals and man. When the organism multiplies unusually rapidly and produces toxin the disease is produced. On the basis of toxin production, the organisms have been classified as types A, B, C, D and E. Cl. perfringens produces a variety of toxic and enzymic substances, which are important in identification of strains and pathogenesis of disease.

Cl. perfringens type A: The organisms are widely distributed in air, soil, water,sewage and manure. Type A infections are associated with gas gangrene and food poisoning in man. An atypical blackleg due to this organism has been reported in cattle in Manipur. In horses watery diarrhoea and death with colitis has been seen.Similar condition has been reported in lambs, pigs, calves and man. Lambs may suffer with severe haemolytic anaemia. The animal dies within 8-12 hr. A toxin is mainly responsible for the disease condition. No vaccine is available in India against this disease.

Cl. perfringens type B: Type B affects young lambs 2-5 days of age causing acute enterotoxaemia known as lamb dysentery. The organism is present in soil and is ingested by lambs by suckling. It becomes a normal inhabitant of intestines of healthy animals. There are certain predisposing factors responsible for rapid and unusual high rate of growth of the organism in intestines with the consequent production and absorption of toxin. The exact predisposing factors are not known but lambs which ingest large quantities of milk are reported to be more susceptible.Symptoms: The acute form of the disease occurs in strong and healthy lambs of 2-4 days of age. The animals show signs of abdominal pain, bloat, collapse and die within a few hours. The animals may also have blood-stained diarrhoea.

Lesions: The lesions seen are haemorrhagic ulcers in the intestine and large quantity of milk in stomach. The intestinal mucosa is red. Subendocardial and subepicardial haemorrhages are often present.

Diagnosis: The symptoms, lesions and age provide a strong presumptive diagnosis.Confirmation is obtained by identifying the presence of toxins.
Control: Before lambing season, the ewes are vaccinated with formalinised whole culture alum-precipitated vaccine. The lambs derive passive immunity by suckling of colostrums. The immunity lasts for about 3 weeks. Alternatively the lambs may be protected by inoculating hyperimmune serum immediately after birth. A few cases of enterotoxaemia with type B have also been recorded in calves, goats and sheep.

Cl. perfringens type C: The disease due to type C is known as struck. It affects adult sheep causing enterotoxaemia due to high rate of multiplication of type C organism and consequent absorption of toxin from intestines. The organism is present in the soil but the disease occurs during winter and spring when the grazing is scanty. The predisposing factors of the disease are little known.

Symptoms: The disease occurs mainly among adult sheep during early spring. Inmany cases fatal toxaemia develops before the obvious lesions of ulceration occur in the intestines. Death suddenly takes place soon after the animal develops symptoms of rigidity. There are signs of abdominal pain but seldom diarrhoea is seen. There is acute inflammation of abomasum, ulceration of small intestine and excessive fluid in abdominal cavity. Degenerative changes develop in the kidneys particularly in the carcass which are not examined soon after death.

Diagnosis: The disease history, symptoms and lesions are strongly suggestive of the disease. The confirmation can be obtained by identifying the toxin present in the abdominal and intestinal contents.

Prophylaxis: Vaccination with formalinised whole culture vaccine is done.

Cl. perfringens type D: toxin of this organism causes enterotoxaemia in sheep. It develops as a result of rapid multiplication of Cl. pefringens type D among sheep of different ages. In lambs aged 3-8 weeks , the disease is known as pulpy kidney while  in lambs 6-12 months old or in adult sheep, the disease is called enterotoxaemia. It also occurs in goats. The organism is a normal inhabitant of soil and intestines of healthy animals. It is only under particular circumstances that organism multiplies at a high rate and produces toxin which is subsequently absorbed and produces disease. The predisposing causes are not known. It is observed that feeding of concentrated protein (grains) favours multiplication and absorption of toxin. It is also believed that when fresh pastures are available, sheep graze beyond their capacity resulting in ruminal statis which helps the organisms to grow rapidly and produce the toxin which causes enterotoxaemia. The disease due to type D has also been reported among calves and young cattle. The disease is similar to sheep but some infected cattle show nervous symptoms.

Symptoms: The death may be sudden without any symptoms. The animals become dull, weak and collapse within 2 to 12 hrs. The characteristic lesion noticed in lambs on post-mortem examination is degeneration of kidney cortex which will be more advanced in carcasses opened several hours after death. The kidney becomes soft and pulpy. Areas of congestion in abomasums, small intestine, and endocardial haemorrhages can be observed. Excessive quantities of straw-coloured fluid is present in pericardium.

Diagnosis: Diagnosis can be arrived by examining lesions in the carcases, but confirmed diagnosis can only be made by demonstrating a specific toxin, known as epsilon toxin. Intravenous inoculation in suckling mouse is the test for demonstration of this toxin. Mouse protection assay using specific antiserum confirms the identification of the toxin.

Prophylaxis: The disease can be controlled by inoculating alum-precipitated formalin-killed anaculture vaccine (vaccine containing toxoid and killed bacteria). The vaccination is done in pregnant ewes or in young lambs. The first injection is given at 72 hours of age and the second at 4 weeks of age. Local reactions may appear after the booster vaccination.

Cl. perfringens type E: Enterotoxaemia in calves and lambs due to type E has also been noticed but infections are not of major economic importance.