Distribution of Neuraminidase among Food-poisoning Strains of Clostridium perfringens

A survey was made to determine the distribution of the enzyme neuraminidase among 76 strains of Clostridium perfringens. Representative strains from each toxigenic type (A to F) and atypical C. perfringens type A food-poisoning strains of both American and English (Hobbs types) origin were tested. Both the American food-poisoning and nonfood-poisoning associated cultures consisted of both neuraminidase-positive and -negative strains. Furthermore, American strains which could not be differentiated from the original Hobbs cultures consisted of both neuraminidase-positive and -negative representatives. In contrast, the English (Hobbs) strains uniformly failed to produce an active intracellular or extracellular neuraminidase. No enzyme activity was detected in these strains when cultures were grown in different growth media, when grown in the presence of substrate (neuraminlactose), or upon extended incubation of enzyme preparations with substrate. With the exception of a type F strain, representative strains of the other toxigenic types (A to F) produced neuraminidase; 85% of the typical type A strains contained the enzyme.     

Detection of Enterotoxin in Faeces and Anti-enterotoxin in Serum after Clostridium perfringens Food-poisoning

Two outbreaks of Clostridium perfringens food-poisoning involving the same person were investigated. In the first, typical symptoms with diarrhoea and abdominal pain were observed. In the second, there were no classical signs of food-poisoning; the victim felt some flatulence and the faeces had a pasty appearance and an unpleasant smell. Counterimmunoelectrophoresis and the reversed passive haemagglutination test were rapid and reliable assay methods for enterotoxin in faeces. In the first outbreak, 13–16 μg enterotoxin/g faeces were detected, and 3–4 μg/g in the second. The detection of enterotoxin in faeces indicates the potential use of enterotoxin tests on diarrhoeal samples for diagnosing C. perfringens food-poisoning. No enterotoxin was detected in serum during the acute stage of the illness, but the antibody titre showed a considerable rise in the first two months after the food-poisoning outbreak.