The enterotoxin-producing Clostridium perfringens type A isolates are responsible for the third most common foodborne illness in the United States and can also cause non-foodborne human gastrointestinal (GI) diseases such as antibioticassociated and sporadic diarrheas. Three important factors contribute to the ability of C. perfringens to cause GI diseases, including its extremely rapid growth rate, its ubiquitous distribution in foods and environments, and its capability to form highly resistant endospores. In the first study, the antimicrobial peptide nisin was evaluated for its antimicrobial effect against enterotoxigenic C. perfringens food poisoning (FP) and non-foodborne (NFB) GI disease isolates. Nisin did not affect spore germination, whereas germinated spores were very susceptible to low concentration of nisin and thus spores outgrowth were arrested. Nisin also exerted its inhibitory effect against vegetative growth of C. perfringens FP and NFB isolates in rich medium; however, FP cells were less resistant to nisin than NFB cells. Nevertheless, nisin was not effective in controlling germination and outgrowth of C. perfringens spores in cooked meat products during storage at abusive temperature, even at ~ 4 times elevated concentration than the regulatory approved level. Strikingly, spores of NFB isolates also exhibited higher resistance to nisin than that of FP isolates in both laboratory medium as well as in meat systems. Collectively, despite its effectiveness in controlling spore outgrowth and vegetative cell growth in laboratory conditions, nisin showed no antimicrobial activity against C. perfringens spores inoculated into meat model systems.
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