Abstract
In the present study, we have shown that virulence-resistance plasmids from emerging multidrug-resistant isolates of Salmonella enterica serovar Typhimurium were derived from a virulence-associated plasmid, essential for systematic invasiveness of S. Typhimurium in mice (pSLT), through acquisition of a large insert containing a resistance island flanked by IS1294 elements. A bla CMY-2-carrying plasmid from a cefotaxime-resistant isolate comprised a segment of Escherichia coli plasmid pAR060302 and the replication region (IncFIB) of a virulence-resistance plasmid. These results provide insights into the evolution of drug resistance in emerging clones of S. Typhimurium.
Highlights
Salmonella enterica serovar Typhimurium frequently causes salmonellosis in humans and animals
In 2002, we identified a non-definitive phage type 104 (DT104) multidrug-resistant clone with a pulsedfield gel electrophoresis (PFGE) pattern designated PFGE cluster VII and no recognized phage-type disseminating among cattle in Hokkaido [8]
Twenty-five of 165 PFGE cluster VII isolates exhibited blaCMY-2-mediated cefazolin resistance localized within the chromosomal genomic island GI-VII-6 [11]
Summary
Salmonella enterica serovar Typhimurium frequently causes salmonellosis in humans and animals. The left region in pYT2 includes genes encoding plasmid maintenance (vagC and vagD), the IncFIB replicon, and the iron acquisition-associated virulence gene (iutA) flanked by two copies of IS1 elements. The right region common to pYT1 (32,495 bp; position 3,129–35,623) and pYT2 (31,651 bp; positions 24,140–55,790) contains entire resistance genes (Figure 1).
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