ABSTRACT
I. BACKGROUND Clostridium perfringens is ideally suited for its role as a major foodborne pathogen (1,2). The presence of this bacterium in soil and feces (both human and animal) provides ample opportunity to contaminate foods. Once established in foods, the rapid doubling time (<10 min) of C. perfringens allows quick attainment of pathogenic levels. The spores and vegetative cells of this bacterium are relatively heat-resistant, facilitating its survival in incompletely cooked foods (for further discussion see Secs. IV and VI). Finally, C. perfringens produces two toxins that are active in the human gastrointestinal (GI) tract and can thereby induce human foodborne illnesses. These two toxins are C. perfringens enterotoxin (CPE), the toxin responsible for the symptoms of C. perfringens type A food poisoning, and β-toxin, which is the toxin primarily responsible for the symptoms of necrotizing enteritis.
