OBJECTIVES: To identify the mechanism(s) underlying cefotaxime resistance in 118 of 21,641 (0.55%) non-typhoidal Salmonella enterica isolates collected from humans throughout England and Wales from January 2010 to September 2012. METHODS: Non-duplicate isolates (n = 118) resistant to cefotaxime (MICs >1 mg/L) were screened by PCR for genes encoding CTX-M extended-spectrum β-lactamases (ESBLs) and associated ISEcp1-like elements, and for genes encoding acquired AmpC, SHV, TEM, VEB, PER and GES β-lactamases. Sequencing was used to identify specific alleles in selected isolates. Carbapenem resistance was sought by ertapenem disc screening. RESULTS: Seventy-nine isolates (0.37% of all referred S. enterica) produced ESBLs, 37 isolates (0.17%) produced CMY-type AmpC enzymes, and 1 isolate had both enzyme types; the mechanism of cefotaxime resistance in 3 isolates could not be identified. Group 1 CTX-M genes were identified in 57 isolates belonging to 22 serotypes, with CTX-M-1 (n = 11), -15 (n = 9) and -55/57 (n = 8) the most prevalent alleles among the 29 (51%) investigated. CTX-M-2 (n = 5), -14 (n = 5), -8 (n = 1) and -65 (n = 1) were also identified. TEM-52 was identified in two isolates and SHV-12 in seven isolates. There was no evidence of carbapenem resistance. ESBL and AmpC genes were detected in both domestically acquired and travel-associated salmonellae. Eighty-nine isolates (75%) were multidrug resistant (resistant to at least three antimicrobial classes) and 42 (36%) had decreased susceptibility to ciprofloxacin (MICs 0.25-1 mg/L), with a further 13 (11%) isolates resistant (MICs >1 mg/L). CONCLUSIONS: The prevalence of CTX-M and acquired AmpC genes in human non-typhoidal S. enterica from England and Wales is still low, but has increased from 0.03% in 2001-03 to 0.49% in 2010-12. Resistance to third-generation cephalosporins requires monitoring as it may reduce therapeutic options.
OBJECTIVES: To identify the mechanism(s) underlying cefotaxime resistance in 118 of 21,641 (0.55%) non-typhoidal Salmonella enterica isolates collected from humans throughout England and Wales from January 2010 to September 2012. METHODS: Non-duplicate isolates (n = 118) resistant to cefotaxime (MICs >1 mg/L) were screened by PCR for genes encoding CTX-M extended-spectrum β-lactamases (ESBLs) and associated ISEcp1-like elements, and for genes encoding acquired AmpC, SHV, TEM, VEB, PER and GES β-lactamases. Sequencing was used to identify specific alleles in selected isolates. Carbapenem resistance was sought by ertapenem disc screening. RESULTS: Seventy-nine isolates (0.37% of all referred S. enterica) produced ESBLs, 37 isolates (0.17%) produced CMY-type AmpC enzymes, and 1 isolate had both enzyme types; the mechanism of cefotaxime resistance in 3 isolates could not be identified. Group 1 CTX-M genes were identified in 57 isolates belonging to 22 serotypes, with CTX-M-1 (n = 11), -15 (n = 9) and -55/57 (n = 8) the most prevalent alleles among the 29 (51%) investigated. CTX-M-2 (n = 5), -14 (n = 5), -8 (n = 1) and -65 (n = 1) were also identified. TEM-52 was identified in two isolates and SHV-12 in seven isolates. There was no evidence of carbapenem resistance. ESBL and AmpC genes were detected in both domestically acquired and travel-associated salmonellae. Eighty-nine isolates (75%) were multidrug resistant (resistant to at least three antimicrobial classes) and 42 (36%) had decreased susceptibility to ciprofloxacin (MICs 0.25-1 mg/L), with a further 13 (11%) isolates resistant (MICs >1 mg/L). CONCLUSIONS: The prevalence of CTX-M and acquired AmpC genes in human non-typhoidal S. enterica from England and Wales is still low, but has increased from 0.03% in 2001-03 to 0.49% in 2010-12. Resistance to third-generation cephalosporins requires monitoring as it may reduce therapeutic options.
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