Abstract

Clostridium perfringens, capable of causing intestinal infections in both animals and humans, represents a significant public health concern. This study aimed to assess the occurrence of the beta2 toxin-coding gene cpb2 in C. perfringens from various host species and to explore the genetic contexts of this gene. The results showed an enrichment of cpb2 in pig-derived C. perfringens. A comparative analysis of the detection rates of cpb2 and pCP13-like plasmids revealed that the cpb2 gene itself, rather than the pCP13-like plasmids, caused the enrichment. Sequence comparison of cpb2-positive pCP13-like plasmids showed that cpb2 was located on the cpb2-hp-transcriptional regulator (PadR family) segment. Despite the diverse plasmid structures of pCP13-like plasmids, the cpb2-hp-transcriptional regulator (PadR family) segment was consistently observed in all cpb2-positive C. perfringens strains, suggesting the potential transmission of the cpb2 gene on this specific genetic segment. Additionally, phylogenetic analysis of the C. perfringens strains harboring pCP13-like plasmids, as well as 31 pCP13-like plasmids, indicated that cpb2 did not affect the evolutionary relationship of either pCP13-like plasmids or C. perfringens. Genetic markers, particularly those located on mobile genetic elements (MGEs), that can help bacteria survive in external environments are more readily enriched in the population. The high prevalence of cpb2 in pig-derived strains indicated that it might confer a selective advantage, enhancing the survival and persistence of C. perfringens in the pig intestine. In conclusion, our study elucidated the genetic context, host tropism and potential biological functions of cpb2, which can provide references for further research.

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