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Aims To assess the co-transmission risk of phenotypic and genetic resistance to cephalosporins, colistin, and fosfomycin in Salmonella strains collected along the whole pork production chain. Methods and Results From a total of 107 Salmonella isolates from samples collected in pig slaughterhouses and markets, 15 ESBL-producing Salmonella strains resistant to cefotaxime were identified by broth microdilution method and clavulanic acid inhibition test, including 14 monophasic Salmonella Typhimurium strains and one Salmonella Derby strain. Whole genome sequence analysis showed that nine monophasic S. Typhimurium strains coresistant to colistin and fosfomycin carried the resistance genes bla CTX-M-14, mcr-1 , and fosA3. Conjugational transfer tests demonstrated that the phenotypic and genetic resistance to cephalosporins, colistin, and fosfomycin could cotransfer back and forth between Salmonella and Escherichia coli via an IncHI2/pSH16G4928-like plasmid. Conclusions This study reports the cotransmission of phenotypic and genetic resistance to cephalosporins, colistin, and fosfomycin via an IncHI2/pSH16G4928-like plasmid in Salmonella strains of animal origin, giving an alarm for the prevention of the development and spread of bacterial multidrug resistance. [ABSTRACT FROM AUTHOR]

Development of cefotaxime-resistance and biofilm formation increase the difficulty to prevent and control the infection and contamination of Salmonella , one of the most important foodborne and zoonotic bacterial pathogen. Our previous study observed that 1/8 minimum inhibitory concentration (MIC) of cefotaxime induced the enhancement of biofilm formation and filamentous morphological change by a monophasic Salmonella Typhimurium strain SH16SP46. This study was designed to explore the role of three penicillin-binding proteins (PBPs) in mediating the induction effect of cefotaxime. Three deletion mutants of the genes mrc A, mrc B, and fts I, encoding the proteins PBP1a, PBP1b, and PBP3, respectively, were constructed using the parental Salmonella strain SH16SP46. Gram staining and scanning electron microscopy showed that these mutants showed normal morphology comparable to the parental strain without cefotaxime treatment. However, under the stress of 1/8 MIC of cefotaxime, the strains WT, Δmrc A, and Δfts I, rather than Δmrc B, exhibited filamentous morphological change. Moreover, cefotaxime treatment significantly enhanced biofilm formation by the strains WT, Δmrc A, and Δfts I, but not by the Δmrc B strain. The complement of mrc B gene in the Δmrc B strain recovered the enhanced biofilm formation and filamentous morphological change induced by cefotaxime. Our results suggest that PBP1b encoded by mrc B gene may be a binding target of cefotaxime for initiating the effect on Salmonella morphology and biofilm formation. The study will contribute to further understanding of the regulatory mechanism of cefotaxime on Salmonella biofilm formation. [ABSTRACT FROM AUTHOR]

Salmonella is one of the most important foodborne and zoonotic pathogens, and monophasic S. Typhimurium is ranked among the top-five Salmonella serovars causing animal and human infections worldwide. Resistance to the third- and higher-generation cephalosporins in Salmonella has attracted great attention. Bacteria are frequently exposed to sub-minimal inhibitory concentrations (sub-MICs) of antimicrobials that can trigger diverse adaptive responses such as biofilm formation. Biofilms can promote bacterial defense to external and internal harsh conditions. This study aimed to investigate the effect of sub-MICs of cefotaxime, one of the third-generation cephalosporins, on biofilm formation by non-clinical S. enterica strains. Crystal violet staining demonstrated that cefotaxime at 1/8 MIC enhanced biofilm formation by two monophasic S. Typhimurium strains. Confocal laser scanning microscopy and enzymatic treatment assay revealed that cellulose was the most dominant extracellular matrix component contributing to Salmonella biofilm formation. Scanning electron microscopy demonstrated that cefotaxime treatment led to bacterial incomplete cell division and filamentous morphology during the whole process of biofilm formation. Our study is the first to report the enhancement effect of cefotaxime on non-clinical, monophasic S. Typhimurium by affecting bacterial morphology. The results will contribute to conducting risk assessments of Salmonella in the pork production chain and guiding the rational use of antimicrobial agents to reduce the risk of biofilm formation. [ABSTRACT FROM AUTHOR]