Other clostridial infections

N P J KRIEK AND M W ODENDAAL

GENERAL INTRODUCTION: ENDOSPORE-FORMING GRAM-POSITIVE RODS AND COCCI Malignant oedema/gas gangrene group of Clostridium spp.

This chapter deals with a number of clostridia which are infrequently associated with disease. These include Clostridium sordellii, C. carnis, C. difficile and C. fallax. In general, they are associated with wound infections in which the clinical and pathologic features resemble those of malignant oedema or gas gangrene caused by the better-known histotoxic clostridia. In rare instances, as in the case of certain C. sordellii infections, they are also associated with sudden death in lambs or cattle, or with the occurrence of haemorrhagic enteritis in foals, sheep and feedlot cattle.

Clostridium sordellii infections

Introduction

Clostridium sordellii infection is associated sporadically with diarrhoea and haemorrhagic enteritis in cattle in feedlots, ¹ adult sheep² and foals,⁸ a sudden-death syndrome in lambs¹⁵ and feedlot cattle,^{6, 16} and malignant oedema which resembles that caused by C. novyi type A and C. septicum infections in cattle.²⁰

Clostridium sordellii was first described by Sordelli in 1922 as Bacillus oedematiens sporogenes. It is often isolated in association with other bacteria, including the well-known histotoxic clostridia, and may not be of primary importance as a cause of disease.¹⁶

Aetiology

Clostridium sordellii is an anaerobic, Gram-positive, rodshaped bacterium with rounded ends, 2 to 4 μm long and 0,5 to 1 μm wide, and occurs singly or in pairs. The cells are motile by virtue of their peritrichous flagella. Spores often form and are oval, situated centrally or subterminally and swell the cell slightly.¹⁷ Sporulation occurs readily in media such as chopped meat broth incubated for 24 hours or blood agar plates after 48 hours’ incubation. On rabbit blood agar the bacterium is slightly beta-haemolytic, and the surface colonies are 1 to 4mm in diameter, have a circular or irregular outline, are translucent to opaque or grey with a dull-white, shiny surface, and have a granular or mottled internal structure. The margin of the colonies is scalloped, lobate or entire.⁵

The optimum temperature for growth is 30 to 37 °C with only moderate growth taking place at 25 °C and 45 °C. Growth is inhibited by incorporating 6,5 per cent sodium chloride and 20 per cent bile in the medium. Phosholipase C is produced in small amounts in culture and its production is best demonstrated on egg yolk agar. No lipase is produced. Clostridium sordellii has saccharolytic and proteolytic characteristics. Glucose and maltose are fermented, while strains vary in their ability to ferment arabinose, fructose, glycerol, raffinose, ribose, and xylose. Adonitol, amygdalin, cellobiose, cellulose, dulcitol, erythritol, esculin, galactose, glycogen, inositol, sorbose, starch, sucrose and trehalose are not fermented. Fermentation in a peptoneyeast extract broth yields large amounts of acetic, isobutyric and isovaleric acids, as well as smaller amounts of propionic and isocaproic acids.^{5, 14}

Clostridium sordellii produces a variety of biological substances toxic to animals, though non-pathogenic strains do occur. The unnamed, major lethal exotoxin produces a severe, gelatinous oedema and is thermolabile and nonhaemolytic, while the lesser toxins include phospholipase C, an oxygen-labile haemolysin, a fibrinolysin, a collagenase, and those that are dermonecrotizing and haemorrhagic when injected into the skin of rats and guinea pigs.^{3, 17}

Epidemiology

Clostridium sordellii can be isolated from soil, which is its principal habitat, and from the intestinal content of humans and animals. Faecal dissemination assists in the spread of the organism in the environment. Infections occur either by ingestion or by contamination of wounds.¹⁷

The conditions under which the disease syndromes caused by C. sordellii occur in livestock, and their predisposing factors, have not been clearly defined.

Pathogenesis

The pathogenesis of the disease syndromes is essentially unknown. Anaerobic conditions, such as those that exist in necrotic tissues, are required for growth and toxin production by the organism.¹⁷

Clinical signs and pathology

In experimental cases of the sudden death syndrome in cattle, affected animals have a marked increase in their respiratory rate, suddenly go down, and then die quickly—animals may be found dead after having been seen to be healthy as little as three hours earlier.⁶ The lesions in cattle that have died of the sudden death syndrome and of malignant oedema (the two designations probably referring to the same syndrome) are characterized by the infiltration of a haemorrhagic, inflammatory oedema of the peritracheal and peripharyngeal areas, with a particularly foul odour.^{18, 20} This oedema may extend to involve the subcutaneous tissues of the neck, but the muscles in the region are unaffected. It may also occur in the subcutaneous tissues of the hind limbs.¹⁶ Severe haemolysis is also evident in some of the cases, as detected in blood specimens presented for chemical pathology.⁶

A sudden death syndrome¹⁵ has been reported in lambs. Animals that have died of this syndrome reveal generalized congestion, marked ascites and hydropericardium, and a markedly enlarged, degenerated liver at necropsy.

Adult sheep and cattle affected by the enteric syndrome may show diarrhoea for some time...