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Antimicrobial resistant zoonotic pathogens present on food constitute a direct risk to public health. Antimicrobial resistance genes in commensal or pathogenic strains form an indirect risk to public health, as they increase the gene pool from which pathogenic bacteria can pick up resistance traits. Food can be contaminated with antimicrobial resistant bacteria and/or antimicrobial resistance genes in several ways. A first way is the presence of antibiotic resistant bacteria on food selected by the use of antibiotics during agricultural production. A second route is the possible presence of resistance genes in bacteria that are intentionally added during the processing of food (starter cultures, probiotics, bioconserving microorganisms and bacteriophages). A last way is through cross-contamination with antimicrobial resistant bacteria during food processing. Raw food products can be consumed without having undergone prior processing or preservation and therefore hold a substantial risk for transfer of antimicrobial resistance to humans, as the eventually present resistant bacteria are not killed. As a consequence, transfer of antimicrobial resistance genes between bacteria after ingestion by humans may occur. Under minimal processing or preservation treatment conditions, sublethally damaged or stressed cells can be maintained in the food, inducing antimicrobial resistance build-up and enhancing the risk of resistance transfer. Food processes that kill bacteria in food products, decrease the risk of transmission of antimicrobial resistance.

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Salmonella enterica serovar Typhimurium phage type DT204 strains isolated from cattle and animal feed in Belgium were characterized for high-level fluoroquinolone resistance mechanisms [MICs to enrofloxacin (Enr) and ciprofloxacin (Cip), 64 and 32 microg/ml, respectively]. These strains isolated during the periods 1991-1994, and in 2000 were clonally related as shown by pulsed-field gel electrophoresis (PFGE). Selected strains studied carried several mutations in the quinolone target genes, i.e., a double mutation in the quinolone resistance-determining region (QRDR) of gyrA leading to amino acid changes Ser83Ala and Asp87Asn, a single mutation in the QRDR of gyrB leading to amino acid change Ser464Phe, and a single mutation in the QRDR of parC leading to amino acid change Ser80Ile. Moreover, Western blot analysis showed overproduction of the AcrA periplasmic protein belonging to the AcrAB-ToIC efflux system. This suggested active efflux as additional resistance mechanism resulting in a multiple antibiotic resistance (MAR) phenotype, which was measurable by an increased level of resistance to the structurally unrelated antibiotic florfenicol in the absence of the specific floR resistance gene. The importance of the AcrAB-TolC efflux system in high-level fluoroquinolone resistance was further confirmed by inactivating the acrB gene coding for the multidrug transporter. This resulted in a 32-fold reduction of resistance level to Enr (MIC = 2 microg/ml) and actually in a susceptible phenotype according to clinical breakpoints. Thus, AcrB plays a major role in high-level fluoroquinolone resistance, even when multiple target gene mutations are present. The same effect was obtained using the recently identified efflux pump inhibitor (EPI) Phe-Arg-naphthylamide also termed MC207,110. Among several fluoroquinolones tested in combination with EPI, the MIC of Enr was reduced most significantly. Thus, using EPI together with fluoroquinolones such as Enr may be promising in combination therapy against high-level fluoroquinolone-resistant S. enterica serovar Typhimurium.