PRJNA684578
Escherichia coli Genome sequencing and assembly
Salmonella enterica serovar Heidelberg (SH) is one of the prolific serovars causing poultry-associated food-borne illness in the world. Their promiscuity to plasmids that confer multidrug resistance to antibiotics of human health importance including plasmid-mediated AmpC (pAmpC) beta-lactamase makes them a public health threat . Although horizontal gene transfer (HGT) is the major mechanism responsible for an increase in antimicrobial resistance (AR) in Salmonella, the biology behind AR acquisition in SH is still unknown. We show that one day old broiler chicks challenged with an antibiotic susceptible SH strain and raised without antibiotics carried multidrug resistance SH strains 14 days after challenge. Horizontal acquisition of IncI1 plasmid multilocus sequence type 26 (pST26) from Escherichia coli strains was determined to be the source of the AR phenotype. The transfer rate of pST26 and the broiler chicken bacterial community was affected by SH route of inoculation. In vitro agar mating experiments between SH and E. coli strains isolated from 2-week-old broilers raised on fresh litter or reused litter confirmed that the transfer of pST26 was via conjugation. Conversely, pST12 carrying pAmpC was transferred through bacteriophage P22 transduction and evolved as a chimera of IncI1 and IncFIB/IncFII plasmids present in E. coli. Carriage of pST26 increased the fitness of SH under acidic selection pressure. Our results suggest that HGT shapes the evolution of AR in SH and that antibiotic use reduction alone is insufficient to limit AR plasmid transfer from commensal bacteria to Salmonella.