Towards an Understanding of the Role of Clostridium Perfringens Toxins in Human and Animal Disease

ABSTRACT:

Clostridium perfringens uses its arsenal of >16 toxins to cause histotoxic and intestinal infections in humans and animals. It has been unclear why this bacterium produces so many different toxins, especially since many target the plasma membrane of host cells. However, it is now established that C. perfringens uses chromosomally encoded alpha toxin (a phospholipase C) and perfringolysin O (a pore-forming toxin) during histotoxic infections. In contrast, this bacterium causes intestinal disease by employing toxins encoded by mobile genetic elements, including C. perfringens enterotoxin, necrotic enteritis toxin B-like, epsilon toxin and beta toxin. Like perfringolysin O, the toxins with established roles in intestinal disease form membrane pores. However, the intestinal disease-associated toxins vary in their target specificity, when they are produced (sporulation vs vegetative growth), and in their sensitivity to intestinal proteases. Producing many toxins with diverse characteristics likely imparts virulence flexibility to C. perfringens so it can cause an array of diseases.

KEYWORDS:

• animal disease
• avian necrotic enteritis
• Clostridium perfringens
• enterocolitis
• enterotoxemia
• food poisoning
• gas gangrene
• human disease
• toxins

Authors’ note

For our colleagues, please note that this review cites many reviews from older work due to reference limitations.

Financial & competing interests disclosure

The National Institute of Allergy and Infectious Diseases grants AI056177 and AI19488 supported this work. The authors also acknowledge the support of grants from the Australian National Health and Research Council, the Australian Research Council and the Poultry Cooperative Research Centre. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

The National Institute of Allergy and Infectious Diseases grants AI056177 and AI19488 supported this work. The authors also acknowledge the support of grants from the Australian National Health and Research Council, the Australian Research Council and the Poultry Cooperative Research Centre. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.