The prevalence of plasmid-coded cpe enterotoxin, β2 toxin, tpeL toxin, and tetracycline resistance in Clostridium perfringens strains isolated from different sources

Abstract

Clostridium perfringens, an anaerobic, spore-forming bacterium, causes infections in humans and animals by producing several toxins encoded by genes found either on the chromosomes or on diverse plasmids. The plasmids may code for more than one toxin gene or antimicrobial-resistance gene. In this study, the prevalence of the β2, cpe and tpeL toxin genes and the tetA(P), tetB(P) and tetM tetracycline-resistance genes, in 56 strains of C. perfringens type A isolated from diseased domestic animals and 15 strains isolated from chickens, was compared with that in 74 strains isolated from other sources. The frequency of chromosome-associated cpe enterotoxin genes was higher in strains not isolated from diseased domestic animals; however, plasmid-associated cpe genes were found in strains from some animal sources more than others. Enterotoxin production was detected in some strains that had chromosomal or plasmid cpe genes, but not in all. The percentages of strains carrying β2 toxin genes among chicken, swine, human patient and soil isolates were higher than those among bovine, canine and food isolates. The incidence of the tpeL toxin gene was lower than that of the β2 gene. Phenotypic resistance to tetracycline was found in more than 50% of the porcine, bovine, and canine isolates, which carried a wide range of plasmids of 2–100 kb size, most of which had the tcpH clostridial transfer gene. PCR amplified tetA(P) and tetB(P) genes from most isolates from diseased animals. Some strains that carried <40 kb plasmids and had the tcpH gene also had one or more toxin genes or tetracycline-resistance gene. This study shows that the prevalence of plasmid-borne toxins and antimicrobial resistance genes varied among C. perfringens strains isolated from different sources. Plasmids of smaller size than those previously reported in strains of C. perfringens type A may also harbor toxin genes and antimicrobial-resistance genes.