Avian pathogenic Escherichia coli (APEC) and uropathogenic E. coli (UPEC) establish infections in extraintestinal habitats of different hosts. As the diversity, epidemiological sources and evolutionary origins of extraintestinal pathogenic E. coli (ExPEC) are so far only partially defined, in the present study,100 APEC isolates and 202 UPEC isolates were compared by their content of virulence genes and phylogenetic groups. The two groups showed substantial overlap in terms of their serogroups, phylogenetic groups and virulence genotypes, including their possession of certain genes associated with large transmissible plasmids of APEC. In a chicken challenge model, both UPEC U17 and APEC E058 had similar LD 50 , demonstrating that UPEC U17 had the potential to cause significant disease in poultry. To gain further information about the similarities between UPEC and APEC, the in vivo expression of 152 specific genes of UPEC U17 and APEC E058 in both a murine urinary tract infection (UTI) model and a chicken challenge model was compared with that of these strains grown statically to exponential phase in rich medium. It was found that in the same model (murine UTI or chicken challenge), various genes of UPEC U17 and APEC E058 showed a similar tendency of expression. Several iron-related genes were upregulated in the UTI model and/or chicken challenge model, indicating that iron acquisition is important for E. coli to survive in blood or the urinary tract. Based on these results, the potential for APEC to act as human UPEC or as a reservoir of virulence genes for UPEC should be considered. Further, this study compared the transcriptional profile of virulence genes among APEC and UPEC in vivo.

bExtraintestinal pathogenic Escherichia coli (ExPEC) is capable of colonizing outside of the intestinal tract and evolving into a systemic infection. Avian pathogenic E. coli (APEC) is a member of the ExPEC group and causes avian colibacillosis. TransfermRNA-small protein B (tmRNA-SmpB)-mediated trans-translation is a bacterial translational control system that directs the modification and degradation of proteins, the biosynthesis of which has stalled or has been interrupted, facilitating the rescue of ribosomes stalled at the 3= ends of defective mRNAs that lack a stop codon. We found that disruption of one, or both, of the smpB or ssrA genes significantly decreased the virulence of the APEC strain E058, as assessed by chicken infection assays. Furthermore, the mutants were obviously attenuated in colonization and persistence assays. The results of quantitative real-time reverse transcription-PCR analysis indicated that the transcription levels of the transcriptional regulation gene rfaH and the virulence genes kpsM, chuA, and iss were significantly decreased compared to those of the wild-type strain. Macrophage infection assays showed that the mutant strains reduced the replication and/or survival ability in the macrophage HD11 cell line compared to that of the parent strain, E058. However, no significant differences were observed in ingestion by macrophages and in chicken serum resistance between the mutant and the wild-type strains. These data indicate that the tmRNA-SmpB system is important in the pathogenesis of APEC O2 strain E058.

Aims The aim of this study is to investigate Streptococcus suis strains present in Jiangsu province, China. Methods and Results In all, 1650 nasal and anal swab samples and 100 tonsils were collected from clinically healthy swine. Culture characteristics, colony morphology and PCR‐based analysis of the glutamate dehydrogenase (gdh) gene were performed for S. suis identification, and eight isolates were confirmed to be S. suis. The isolates serogroups were identified by agglutinating test, including 4, 7, 3, 5 and 8. Gene profiling by PCR showed that the manN, purD, orf2, gdh genes were conserved among the isolates and that 50% of the isolates carried dltA, pgdA, srtA and sspA. Antimicrobial susceptibility test showed the isolates displayed resistance to clindamycin, erythromycin, tetracycline, penicillin G, vancomycin and linezolid; while none was resistant to chloramphenicol, multi‐drug resistance was seen in most of the isolates. Finally, the LD50 (assessed by zebrafish) of isolates RD105 was 2·6431 × 105 and HA24 was 7·1198 × 106, which showed RD105 more virulent and was consistent with the results of virulence factor identification. Conclusions There is a very low proportion of S. suis in the healthy pigs. The virulence factors were related to pathogenicity. Bacteria in Nantong possess greater virulence potential than those in Huaian. Significance and Impact of the Study Systematic investigation of S. suis provided the most basic theoretical support for the prevention and control of swine streptococcosis.

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