Clostridium perfringens type B infections

Clostridium perfringens type B infections



Lamb dysentery is a peracute to chronic enterotoxaemia caused primarily by the action of the beta toxin and, to a lesser extent, the epsilon toxin, produced by Clostridium perfringens type B in the intestines. It usually affects lambs and goat kids less than 14 days old. It is characterized clinically by an acute haemorrhagic to mucohaemorrhagic enteritis, resulting in death after a few hours to one or two days in the peracute and acute cases, and after four or more days in chronic cases. This type of enterotoxaemia has also been described in foals and calves.5, 11, 17, 19, 20, 28

The disease in lambs has been well known in the UK, western Europe and in the USA for many years. It is probable that the condition described in 1811 as ‘milk-ill’ was lamb dysentery. In Europe it was reported in 1871,2 while in 1927 Jungherr and Welch first described a disease in the USA that resembles lamb dysentery.10

Lamb dysentery was prevalent and fairly well known to sheep farmers in certain parts of the present Western and Eastern Cape provinces of South Africa during the latter part of the nineteenth century and its occurrence in this province was recorded in the Colesberg Advertiser in 1888.10 Walker, in 1923,29 referred to a similar disease in Kenya.

Dalling, in 1926, was the first to identify the cause of lamb dysentery as C. perfringens but noticed that it differed from the classical C. perfringens. He therefore named it the lamb dysentery bacillus, Bacillus agni. It was later renamed C. perfringens type B.

Lamb dysentery currently occurs in the UK, Europe, South Africa and the Middle East, but not in North America or New Zealand. The disease occurs endemically, although rarely, in all the sheep farming areas of South Africa, including the Karoo, the Eastern Cape and Free State provinces, and the Highveld of the northern provinces. 22


Clostridium perfringens type B produces the alpha, beta and epsilon toxins, as well as a number of minor toxins. For information on the cultural, morphological and biochemical characteristics of C. perfringens as well as its toxins, see the introduction, Clostridium perfringens group: Table 1.

There are strong indications that the production of beta toxin is coded for by a plasmid.3 The beta and epsilon toxins are metabolic products secreted during active exponential growth of C. perfringens type B in a suitable medium and in the presence of the necessary nutriments required for toxin production. The beta toxin concentration in the medium declines rapidly after prolonged incubation.22 The organism grows in vivo in the intestinal tract of the affected animal where it produces the toxins responsible for its pathogenic effect.


In South Africa, lamb dysentery affects new-born lambs of all sheep breeds to the same extent, although the heavier breeds and cross-breds are considered more resistant; goat kids are also affected.9 During winter and spring, its presence is favoured by the extremely cold weather in certain parts of South Africa; it is rare in autumn and does not seem to affect summer lambs.10

Clostridium perfringens type B would seem to be an obligate parasite, as is the case with types C, D and E.25 Organisms are excreted in the faeces of adult carrier animals and sick lambs, and contaminate soil and pastures. In contrast to C. perfringens type A, which survives indefinitely in soil, type B strains only survive for several months in soil and pastures and are not considered to be part of the normal microbial flora of the soil.25

Lambs are more prone to develop the disease on certain parts of a farm. The infection is favoured when the ewes and lambs are confined to small camps, lambing pens, small fenced-off grazing areas, or sheds and kraals during the day or night as a precaution against theft or predation. Close and prolonged confinement of the animals seems to increase the severity of the disease. The teats of the ewes become contaminated with faeces and soil and lambs acquire the infection per os during suckling.10 The prevalence of the disease decreases when the ewes and lambs are removed from highly contaminated areas.


Clostridium perfringens type B organisms ingested within the first few hours after birth of the lambs colonize the small intestines, especially the ileum, where they multiply and produce their toxins. It is generally believed that the beta toxin is primarily responsible for the induction of the lesions of lamb dysentery while the role of epsilon toxin is unknown. 18 In vitro these toxins are produced during the exponential growth phase and it is assumed that the same pertains to the in vivo situation. Restriction of the occurrence of the disease to neonates is associated with the susceptibility of the beta toxin to the effect of trypsin in the intestinal tract, which is secreted by animals in this age group in insufficient amounts to inactivate the toxin.28 In older animals these enzymes are produced in sufficient quantities to inactivate the beta toxin. In addition, the presence of trypsin inhibitors in the colostrum aggravates the situation for neonates.19 In the portions of the small, and to a lesser extent the large, intestine where the toxins are produced, an...

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