Clostridium perfringens type B infections

Clostridium perfringens type B infections

Synonym: Lamb dysentery

Previous authors:
N P J KRIEK, M Q ODENDAAL AND P HUNTER

Current authors:
F A UZAL - Professor and Branch Chief, DVM, FRVC, MSc, PhD, Dipl. ACVP, California Animal Health and Food Safety Lab, University of California, Davis, San Bernardino, California, 92408, USA.
M NAVARRO - Assistant Professor of Veterinary Anatomic Pathology, DVM, MSc, PhD, Dipl. ACVP, Universidad Austral de Chile, Campus Isla Teja, Valdivia, Chile.
N P J KRIEK - Emeritus Professor, BVSc, MMed Vet (Path), Onderstepoort, Pretoria, Gauteng, 0110, South Africa.
P HUNTER-OBEREM - Self Employed, BVSc Hons, Mont Lorraine, Gauteng, South Africa.

Introduction

Infection by Clostridium perfringens type B causes a peracute, acute, subacute or chronic enterotoxaemia in lambs that is also occasionally encountered in goat kids and calves, and rarely in foals. The disease occurs mainly in countries in the Middle East and Europe.22 The infection has not been reported in the Americas, although anecdotal evidence suggests that cases may have occurred in this region.

In lambs, the disease is also known as lamb dysentery and it usually affects those that are younger than 14 days. It is characterized clinically by an acute, haemorrhagic to mucohaemorrhagic diarrhoea, and rarely, by neurologic signs. Lambs die after a few hours to two days in the peracute and acute cases, and after four or more days in the subacute and chronic cases.5, 12, 17, 21

Aetiology

The organism grows in the intestinal tract of affected animals where it produces the toxins responsible for the disease. Clostridium perfringens type B encodes alpha, beta and epsilon toxins, and a number of other, usually referred to as minor, toxins.3 The beta and epsilon toxins are metabolic products secreted during the exponential growth phase of C. perfringens type B in a suitable environment that contains the nutrients required for toxin production. Beta toxin is encoded in a plasmid14 and its concentration in the growth medium in vitro declines rapidly after prolonged incubation.3

For information on the cultural, morphological and biochemical characteristics of C. perfringens and its toxins, refer to the introductory chapter: Clostridium perfringens group infections.

Epidemiology

Although heavier breeds and crossbreeds are considered to be more resistant, lamb dysentery affects new-born lambs of all sheep breeds to the same extent. Goat kids are also affected, albeit less frequently, and information on the disease in this species is scant.4 In sheep, the disease seems to be more prevalent during cold weather, while it is rare in autumn, and it does not appear to occur in summer.4

Clostridium perfringens type B is excreted in the faeces of adult carrier animals and sick lambs, thereby contaminating soil and pastures. Although there is little scientific evidence to support this claim,15 it is thought that C. perfringens type B strains only survive for several months in soil and pastures, and they are also not considered to be part of the normal microbial flora of the soil. The teats of ewes become contaminated with faeces and soil, and their lambs acquire the infection per os while suckling.4 It has been suggested that lambs are more prone to develop the disease on certain parts of a farm, mainly those where ewes and lambs are confined to small areas. Close and prolonged confinement of sheep seem to increase the severity of the disease. The prevalence of the disease decreases when the ewes and lambs are removed from highly contaminated areas.

Pathogenesis

Clostridium perfringens type B organisms ingested within the first few hours after birth of the lambs, colonize the intestines, in all likelihood especially the small intestine, where they multiply and produce their toxins that act both locally and are absorbed into the general circulation.

The potent and lethal beta and epsilon toxins are the main virulence factors of C. perfringens type B,13 and they are, respectively, highly trypsin-sensitive, and fully dependent on trypsin for full activation. Although there is no evidence to substantiate it, it has been suggested that only one of the toxins is involved in the pathogenesis of C. perfringens type B disease at any given time.3 It is believed that the beta toxin is primarily responsible for the induction of the intestinal lesions characteristic of type B enterotoxaemia. The role of epsilon toxin in this condition is poorly understood but it is assumed to be responsible for the lesions (focal symmetrical encephalomalacia) in the central nervous system (CNS) in the a few cases of type B enterotoxaemia in which such lesions have been recorded.3

The toxins are produced in vitro during the exponential growth phase of C. perfringens, and it is assumed that the same pertains to their in vivo growth.3 Restriction of the occurrence of the disease to neonates is, as in the case of C. perfringens type C infections, thought to be due to the blocking effect of colostrum on trypsin and other proteases, as these enzymes are powerful beta-toxin inhibitors. The trypsin-blocking effect of colostrum is thought to be an evolutionary trait to protect colostral immunoglobulins from trypsin break-down.14, 22 In older animals these enzymes are not inhibited and remain in the intestinal lumen in sufficient quantities to inactivate beta toxin.18 In the portions of the small, and, to a lesser extent...

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