Sporulation and Enterotoxin Production by Mutants of Clostridium perfringens

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Abstract
The ability of Clostridium perfringens type A to produce an enterotoxin active in human food poisoning has been shown to be directly related to the ability of the organism to sporulate. Enterotoxin was produced only in a sporulation medium and not in a growth medium in which sporulation was repressed. Mutants with an altered ability to sporulate were isolated from an sp + ent + strain either as spontaneous mutants or after mutagenesis with acridine orange or nitrosoguanidine. All sp 0 − mutants were ent − . Except for one isolate, these mutants were not disturbed in other toxic functions characteristic of the wild type and unrelated to sporulation. A total of four of seven osp 0 mutants retained the ability to produce detectable levels of enterotoxin. None of the ent − mutants produced gene products serologically homologous to enterotoxin. A total of three sp − mutants, blocked at intermediate stages of sporulation, produced enterotoxin. Of these mutants, one was blocked at stage III, one probably at late stage IV, and one probably at stage V. A total of three sp + revertants isolated from an sp − ent − mutant regained not only the ability to sporulate but also the ability to produce enterotoxin. The enterotoxin appears to be a sporulation-specific gene product; however, the function of the enterotoxin in sporulation is unknown.