Antimicrobial resistance and evolution of genomic epidemiology of multidrug- resistant Salmonella enterica serovar Enteritidis ST11 in China

Author:

Liu Jie1,Hou houyue2,Zhao Linna3,Chen Gang1,Chen Jialiang4,Zhao Qiang1,Ye Liyan1,Cui Shenghui3,Wang Chengbin1

Affiliation:

1. Chinese People's Liberation Army General Hospital

2. Beijing Chaoyang District Center for Disease Control and Prevention

3. The National Institutes for Food and Drug Control

4. National Institute for Communicable Disease Prevention and Control, Chinese Center for Disease Control and Prevention

Abstract

Abstract In recent years, with the change of multidrug resistant strains, the genetic characteristics of foodborne Salmonella enterica serovar Enteritidis and clinical isolates have changed, and ST11 is the most common genotype associated with the S. Enteritidis isolates from humans and food animals across the world. In this study, the phenotypes and genetic characteristics of antibiotic resistance in foodborne and clinical S. Enteritidis isolates were analyzed. The results showed that the antibiotic resistance of foodborne S. Enteritidis isolates from 2017 was more severe than that of clinical isolates from 2013 to 2017, with a wider antibiotic resistance spectrum and higher antibiotic resistance rate. The genetic characteristics of S. Enteritidis from different sources were also different. Compared with clinical isolates, food-borne S. Enteritidis carried more antibiotic resistance genes, and the context characteristics of antibiotic resistance genes were different. For example, blaCTX−M and dfrA17 were only present on the plasmid of clinical S. Enteritidis but existed in the plasmid and chromosome of foodborne S. Enteritidis, and the carrying rate of floR was higher than that of clinical isolates. Analysis of the reasons suggests that the isolation of foodborne S. Enteritidis is late, the gene evolution is faster, and some resistance genes can be integrated and stably exist on the chromosome, which speeds up the evolution of resistance genes and provides more mechanisms for resistance to antibiotics. Compared the virulence genes of S. Enteritidis from different sources, we found that except for the distribution of virulence plasmids, there was no difference in the distribution of other virulence genes, so we believe that foodborne S. Enteritidis has the potential to cause clinical infection, and once the evolution of these drug resistance genes starts to expand, it will cause a problem for clinical treatment. Therefore, we should always monitor the changes in drug resistance patterns of S. Enteritidis from different sources.

Publisher

Research Square Platform LLC

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