Clostridium perfringens type D infections

Clostridium perfringens type D infections

N P J KRIEK, M W ODENDAAL AND P HUNTER

Introduction

Pulpy kidney disease is a peracute, acute or occasionally chronic infectious enterotoxaemic disease that is common in sheep, uncommon in goats, and virtually unknown in cattle in South Africa. It is caused by the systemic effects of Clostridium perfringens type D epsilon toxin which is absorbed into the general circulation from the intestinal tract where it is elaborated by the rapidly multiplying organisms. Pulpy kidney disease in sheep affects animals of any age, but young animals in good condition are particularly susceptible. Predisposing factors, such as sudden changes in diet from poor to good quality, precipitate the occurrence of the disease. Peracute and acute cases are characterized by sudden death, and chronic cases by the development of a neurological syndrome that results from focal symmetrical encephalomalacia (FSE). In goats, the disease may be peracute, as in sheep, or it may manifest as an acute or chronic diarrhoea due to enterocolitis2 terminating in death, or as a chronic, lingering and debilitating condition.4 The differences between the disease in sheep and in goats, in general, relate to clinical signs and responses to treatment and vaccination. 4

Pulpy kidney disease occurs all over the world wherever small ruminants are maintained. It was first described by Gilruth in New Zealand in 1903 and thereafter in Australia, the UK, the USA and South Africa. The association of an unknown potent toxin with the pathogenesis of this disease was first demonstrated by Montgomerie and Rowlands and then by other workers in 1931, 1933 and 1934. The organism, then referred to as Bacillus ovitoxicus, was isolated in 1932.25 The bacterium, now known as C. perfringens type D, occurs in large numbers in the intestinal tract of normal sheep without causing any clinical signs and can be regarded as an obligate parasite.6, 55

In South Africa it is believed that many of the cases diagnosed as ‘geilsiekte’ (prussic acid poisoning) in the past were, in fact, pulpy kidney disease.53 That the disease remains one of the most important diseases of sheep in South Africa today is confirmed by the annual vaccine sales which exceed 50 million doses.

Aetiology

Clostridium perfringens type D has the same morphological and biochemical characteristics as the other members of the perfringens group and produces two major lethal toxins, alpha and epsilon, and a number of minor toxins, which may be either lethal or non-lethal (Clostridium perfringens group).

Epsilon toxin, the significant major toxin and cause of pulpy kidney disease, is produced as a prototoxin.32, 39, 40, 51, 69, 71, 72 Its in vitro production is dependent on the presence of suitable conditions which must include optimal pH and the availability of an appropriate carbohydrate source.23, 24

Epidemiology

Pulpy kidney disease is one of the most important diseases of sheep in southern Africa, as it is in many other parts of the world. It occurs in sheep of all ages, but most commonly in lambs of two age groups; from three weeks to three months, and from 6 to 12 months of age. Cases of C. perfringens type D enterotoxaemia have been reported in seven- to ten-week- old calves,21 in young cattle in good condition up to two years old,30 as well as in adult animals.37 Though cattle of all ages are affected, it is mainly a disease of calves and young cattle up to two years of age in feedlots. In the USA, C. perfringens type D is associated with overeating disease or sudden death of feedlot cattle. As opposed to the disease in sheep, it only affects individual animals over a period.30 In goats, most outbreaks have been reported in dairy animals3although it has also been described in Angora goats under extensive conditions in South Africa.73 The condition in goats appears to be poorly understood and has not been properly defined. Significant differences occur between pulpy kidney disease in goats and sheep.63

In endemic areas, C. perfringens type D is harboured in the alimentary tract of animals as an obligate parasite and its presence in this situation provides the focus for a potentially fatal infection. Small numbers occur in the forestomachs, but not in the abomasum. The numbers increase towards the ileum where most C. perfringens organisms are found. Conditions here are ideal for the organisms to multiply under normal conditions. The numbers become less in the large intestine, but sufficient numbers of the organism are excreted in the faeces to allow its bacteriological isolation. As is the case with type B, type D isolates are not considered part of the microbial soil flora, as they cannot compete with type A isolates in this habitat. Clostridium perfringens type D is, however, able to survive for a number of months in soil before dying.55, 57

There appears to be a number of predisposing factors which precipitate the occurrence of the disease. These include stasis of the intestinal tract; sudden changes in the feeding regimen; sudden changes from poor to lush pastures; grazing on fodder crops, such as green oats, green wheat and green lucerne (alfalfa); very high protein diets; overeating on concentrates and lush pastures;26 deworming; and coccidiosis.41 Sudden changes in the weather and wilting of pasture...

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