【摘 要】
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If the acquisition of virulence genes (VGs) for pathogenicity were not solely acquired through horizontal gene transfers of pathogenicity islands,transposons and phages,then clonal clusters of enterot
【机 构】
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暨南大学理工学院食品科学与工程系 广州 510632;Immunology and Molecular Diagnostic Research Unit, Elizabeth Macarthur Ag
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If the acquisition of virulence genes (VGs) for pathogenicity were not solely acquired through horizontal gene transfers of pathogenicity islands,transposons and phages,then clonal clusters of enterotoxigenic E.coli (ETEC) would contain few or even none of the VGs found in strains responsible for extraintestinal infections.To evaluate this possibility,47 post-weaning diarrhea (PWD) ETEC strains from different geographical origins and 158 commensal E.coli isolated from the gastrointestinal tracts of 8 group-housed healthy pigs were screened for 36 extraintestinal and 18 enteric VGs using multiplex PCR assays.Of 36 extraintestinal VGs,only 8 were detected (fimH,traT,fyuA,hlyA,kpsMtlI,k5,iha and ompT)in the ETEC collection.Among these,hlyA (α-hemolysin) and iha (nonhemagglutinating adhesin) occurred significantly more frequently amongst the ETEC isolates,in comparison to the commensal isolates.Clustering analysis based on the VG profiles separated commensal and ETEC isolates and even differentiated serogroup O141 from O149.On the other hand,pulsedfield gel electrophoresis (PFGE) successfully clustered ETEC isolates according to both serotype and geographical origin.In contrast,the commensal isolates were heterogeneous with respect to both serotype and DNA fingerprint.This study has validated the use of VG profiling to examine pathogenic relationships between porcine ETEC isolates.The clonal relationships of these isolates can be further clarified by PFGE fingerprinting.The presence of extraintestinal VGs in porcine ETEC confirmed the hypothesis that individual virulence gene acquisitions can occur concurrently against a background of horizontal gene transfers of pathogenicity islands.Over time,this could enable specific clonotypes to respond to host selection pressure and to evolve into new strains with increased virulence.
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