Age affected: Newborn, piglets pre-weaning.
Causes: Bacteria – Clostridium perfringens types A, B or C.
Effects: Diarrhoea, dysentery, death.
Clostridium perfringens types A and C cause diarrhoea, dysentery and death in pigs. C. perfringens is a large bacterium which grows in the absence of oxygen (anaerobic) and uses starch and lactose. It can produce spores and persist indefinitely outside the pig. C. perfringens type A produces two toxins, alpha toxin and enterotoxin which contribute to diarrhoea and C. perfringens type C produces beta toxin which causes intestinal haemorrhage and death. Infection is oral and occurs at birth and the organisms rapidly reach very high numbers within the last part of the small intestine and the large intestine. The beta toxin of C. perfringens type C rapidly destroys the cells lining the small intestine, so that blood is lost into the intestine resulting in death. From 2 days of age onward the toxin is destroyed by the digestive enzyme trypsin and disease is restricted to the first 48-72 hours of life. The toxins of C. perfringens type A cause secretion of fluid in the small intestine, and some inflammation and diarrhoea. It may also reach high numbers and cause diarrhoea in the weaned pig. Disease in piglets is prevented by passive immunity from the colostrum of an immune mother.
C. perfringens is spread between pigs by the ingestion of the bacterial cells or spores present in material contaminated with infected faeces. Infection takes place from birth from other pigs, including the sow, and from spores which persist in the environment, even after superficial cleaning. Within houses, poor hygiene, rodents, contaminated equipment and clothing may spread the organisms. Transmission between farms is by means of carrier pigs, contaminated vehicles and clothing and equipment. There is little clear documentary evidence for any role of rodents and birds in spread between farms.
Piglets affect by C. perfringens type C are born to sows without immunity, are normal at birth, sicken on the first or second day of life and usually die within 12-24 hours of the onset of clinical signs. A dramatic, profuse diarrhoea occurs and rapidly become claret-coloured. The hindquarters may be soiled with bloody faeces. Affected piglets become weak, collapse and die. Some may be found dead. In more chronic cases, shreds of necrotic (dead) material may appear in the reddish-brown watery faeces. Affected animals become very thin and pale before death. Depression of growth rate may be a feature in chronically infected piglets. Piglets with abdominal discolouration, subnormal temperatures or severe blood-stained diarrhoea do not recover. C. perfringens type A causes a milder disease in piglets. Affected diarrhoeic sucking piglets appear dull with sunken flanks and lose condition. The perineal area is heavily pasted with yellowish faeces. Faeces present on the pen floor frequently contains mucus but is often creamy or pasty and is pinkish in colour. C. perfringens type A can cause a greyish, sometimes mucoid diarrhoea lasting 3-7 days in weaned pigs. Inappetence, loss of condition and faecal staining of the perineum and coat are common.
Fatal bloodstained diarrhoea in piglets of 36-48 hours of age strongly suggests C. perfringens type C infection. In some cases, animals may die before the diarrhoea is obvious. C. perfringens type A diarrhoea in piglets is suggested by the clinical signs of pasty pink diarrhoea at 48 hours of age, and loss of condition. Greyish diarrhoea or soft motions and loss of condition in pigs aged from 56 weeks onwards suggests a diagnosis of C. perfringens type A disease in weaned pigs which can be confirmed by detecting enterotoxin in faecal filtrates.
The pathology of C. perfringens Type C disease is unmistakable. The carcase is often in good condition. The small intestine is red in colour and the contents are blood stained. In mild or chronic cases, the lining may be covered in necrotic material. Diagnosis is confirmed by the demonstration of the beta toxin in the intestinal contents in the laboratory by ELISA (serological test) using a specific monoclonal antibody to the toxin. The organism may be isolated in anaerobic culture or the toxin gene demonstrated.
The lesions on C. perfringens Type A infection are less obvious. The thickened small intestines has an inflamed or necrotic lining and C. perfringens type A may be demonstrated by direct culture or immunofluorescence and the elimination of similar diseases of piglets such as type C disease.
Affected piglets usually die from C. perfringens type C infection. Oral ampicillin can be used to treat the survivors of an affected litter and, given soon after birth, may prevent the occurrence of the disease completely. Injection of newborn piglets with 2 ml hyperimmune antiserum to type C toxin gives complete protection, and usually protects animals which have not yet developed clinical signs. These measures, coupled with improved hygiene, may stop an outbreak but more permanent control is obtained by vaccination. Vaccines containing the toxoid of C. perfringens type C, or killed cultures of the organism, may be used alone or in combination with other vaccines such as E. coli. Sows should be vaccinated 6 and 2 weeks prior to farrowing and piglets will be protected provided they ingest colostrum. Levels of antibody in colostrum may vary considerably. Very low levels of protection may allow the development of chronic disease. The milder C. perfringens type A diarrhoea in piglets responds well to oral treatment or injection with penicillin, ampicillin or antibiotics other than neomycin or other aminoglycosides. A vaccine has been produced for sows which protects against the disease in piglets. Disease in weaned pits can be treated with oral penicillin or ampicillin.