Abstract
The spread of antibiotic resistant bacteria worldwide presents a major health threat to human health care that results in therapy failure and increasing costs. The transfer of resistance conferring plasmids by conjugation is a major route by which resistance genes disseminate at the intra- and interspecies level. High similarities between resistance genes identified in foodborne and hospital-acquired pathogens suggest transmission of resistance conferring and transferrable mobile elements through the food chain, either as part of intact strains, or through transfer of plasmids from foodborne to human strains. To study the factors that affect the rate of plasmid transfer, the transmission of an extended-spectrum β-lactamase (ESBL) plasmid from a foodborne Escherichia coli strain to the β-lactam sensitive E. coli MG1655 strain was documented as a function of simulated environmental factors. The foodborne E. coli isolate used as donor carried a CTX-M-1 harboring IncI1 plasmid that confers resistance to β-lactam antibiotics. Cell density, energy availability and growth rate were identified as factors that affect plasmid transfer efficiency. Transfer rates were highest in the absence of the antibiotic, with almost every acceptor cell picking up the plasmid. Raising the antibiotic concentrations above the minimum inhibitory concentration (MIC) resulted in reduced transfer rates, but also selected for the plasmid carrying donor and recombinant strains. Based on the mutational pattern of transconjugant cells, a common mechanism is proposed which compensates for fitness costs due to plasmid carriage by reducing other cell functions. Reducing potential fitness costs due to maintenance and expression of the plasmid could contribute to persistence of resistance genes in the environment even without antibiotic pressure. Taken together, the results identify factors that drive the spread and persistence of resistance conferring plasmids in natural isolates and shows how these can contribute to transmission of resistance genes through the food chain.
Highlights
Bacteria can become resistant against antibiotics by phenotypic adaptation, genetic changes or uptake and incorporation of resistance genes
This strain was resistant against penicillin-like antibiotics as demonstrated by high minimum inhibitory concentration (MIC) for ampicillin and amoxicillin 1024 μg/ml (Table 1), but not against cephalosporins (MIC for cefazidime 16 μg/ml)
The rapid transfer of resistance genes in the absence of antibiotic pressure reported in this study partly explains the global spread of resistance conferring plasmids seen in the agricultural and medical sector [33,34]
Summary
Bacteria can become resistant against antibiotics by phenotypic adaptation, genetic changes or uptake and incorporation of resistance genes. Transfer of R-plasmids through conjugation dramatically enhances the spread of antibiotic resistance. This in turn causes a range of problems, such as increased treatment costs and a lack of effective components against multidrug resistant pathogenic bacteria [2]. Transfer of resistance genes from farms to humans is believed to be a result of direct contacts with animals or the consumption of affected food [5]. Livestock-associated methicillin-resistant Staphylococcus aureus was shown to be transferred directly from animals to farm workers or close relatives [6,7]. Transfer of R-plasmids from agricultural bacteria to human pathogens creates a potential link between selection for resistance at farms and clinical cases involving resistant strains
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