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DOI 10.1016/j.diagmicrobio.2012.04.005

Медицинская библиотека · Diagnostic microbiology and infectious disease · 2012

High prevalence of acquired quinolone-resistance genes among Enterobacteriaceae from Saudi Arabia with CTX-M-15 β-lactamase.

Shibl Atef M, Al-Agamy Mohamed H, Khubnani Harish, Senok Abiola C, Tawfik Abdulkader F, Livermore David M

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

We examined the prevalence of acquired quinolone resistance determinants among Enterobacteriaceae with extended-spectrum β-lactamases (ESBLs) in Riyadh, Saudi Arabia. qnrA, qnrB, qnrS, aac(6')-Ib-cr, and qepA genes were sought by polymerase chain reaction (PCR) in 160 nonduplicate, clinical Enterobacteriaceae with ESBLs from Prince Salman Hospital in Riyadh during 2009. MICs were determined for qnr- and aac(6')-Ib-cr-positive isolates. Mutations in gyrA and parC were determined for isolates with qnr. ESBL genes were characterized by PCR and sequencing. Among 99 ESBL-producing Escherichia coli, 73% were ciprofloxacin resistant, as were 74% of 61 ESBL-positive Klebsiella pneumoniae. The aac(6')-1b-cr gene was present in 76 ESBL producers, comprising 34 K. pneumoniae and 42 E. coli, whereas qnrA or qnrB genes were found in 21 isolates, all of them also harbouring aac(6')-1b-cr and bla(CTX-M-15), with the latter encoding what was considerably the dominant ESBL in the collection. The qnr-positive isolates harboured a variety of mutation in gyrA and parC but, even with aac(6')-1b-cr also present, high-level ciprofloxacin resistance (MIC >32 μg/mL) was invariably associated with double mutations in gyrA, affecting both Ser83 and Asp87 along with >1 substitution in parC, affecting Ser80 or Glu84.

Для цитирования: Shibl Atef M, Al-Agamy Mohamed H, Khubnani Harish, Senok Abiola C, Tawfik Abdulkader F, Livermore David M. High prevalence of acquired quinolone-resistance genes among Enterobacteriaceae from Saudi Arabia with CTX-M-15 β-lactamase.. Diagnostic microbiology and infectious disease. 2012. DOI: 10.1016/j.diagmicrobio.2012.04.005.

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