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Prevalence of Aminoglycoside-Modifying Enzymes in Escherichia coli and Klebsiella pneumoniae Producing Extended Spectrum β-Lactamases Collected in Two Multicenter Studies in Spain

机译:在西班牙的两项多中心研究中收集的大肠埃希菌和肺炎克雷伯菌产生扩大谱β-内酰胺酶的氨基糖苷修饰酶的流行

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摘要

The in vitro activity of amikacin, gentamicin, kanamycin, tobramycin, neomycin, and netilmicin against 420 Escherichia coli producing extended spectrum β-lactamases (Ec-ESBLs) and 139 Klebsiella pneumoniae producing extended spectrum β-lactamase (Kp-ESBL) collected in two multicenter studies performed in Spain in 2000 and 2006 was determined. The presence of genes encoding aminoglycoside-modifying enzymes (AMEs) and 16S ribosomal RNA (rRNA) methylases [aac(3)-Ia, aac(3)-IIa, aac(3)-IVa, aac(6′)-Ib, ant(2")-Ia, ant(4′)-IIa, aph(3′)-Ia, aph(3′)-IIa, armA, rmtB, and rmtC] was also investigated. The resistance to (one or more) aminoglycosides was significantly higher in Kp-ESBL (104/139, 74.8%) than in Ec-ESBL (171/420, 40.7%; p < 0.0001). The lowest resistance rates for both species in the two studies were observed for amikacin. The prevalence of AME genes was significantly different in Ec-ESBL (161/420, 38.3%) than in Kp-ESBL (115/139, 82.7%; p < 0.0001). The most prevalent AME genes in Ec-ESBL and Kp-ESBL were aac(6′)-Ib (16.2% and 44.6%) and aac(3)-IIa (14.7% and 43.1%), respectively. The expected phenotypic profile correlated with the found AMEs encoding genes in 59.6% Ec-ESBL and 26.1% Kp-ESBL. In Ec-ESBL, aac(6′)-Ib was usually associated in 2000 with blaSHV (26.6%), but with blaCTX-M-1 group (34.8%) in 2006, while aac(3)-IIa was coincident in 2000 with blaTEM (14.6%) and with blaCTX-M-1 group (16.3%) in 2006. Among Kp-ESBL, the aac(6′)-Ib and aac(3)-IIa genes were more frequent in strains with blaTEM (22.0% and 44.0%) in 2000 and with blaCTX-M-1 group (46.4% and 34.0%) in 2006. Resistance to aminoglycosides in Ec-ESBL and Kp-ESBL is frequent and related to production of AMEs; this limits the clinical use of aminoglycosides against these organisms.
机译:阿米卡星,庆大霉素,卡那霉素,妥布霉素,新霉素和奈替米星对420种产生超广谱β-内酰胺酶(Ec-ESBLs)和139个肺炎克雷伯菌产生超广谱β-内酰胺酶(Kp-ESBL)的体外活性确定了2000年和2006年在西班牙进行的多中心研究。存在编码氨基糖苷修饰酶(AMEs)和16S核糖体RNA(rRNA)甲基化酶[aac(3)-Ia,aac(3)-IIa,aac(3)-IVa,aac(6')-Ib,还研究了ant(2“)-Ia,ant(4')-IIa,aph(3')-Ia,aph(3')-IIa,armA,rmtB和rmtC]。对(一种或多种)的抗性)氨基糖苷在Kp-ESBL(104/139,74.8%)中显着高于Ec-ESBL(171/420,40.7%; p <0.0001)。在两项研究中,两种抗阿米卡星的耐药率最低。Ec-ESBL中AME基因的患病率(161/420,38.3%)与Kp-ESBL中的AME基因患病率(115/139,82.7%; p <0.0001)有显着差异。 -ESBL分别为 aac(6')-Ib (16.2%和44.6%)和 aac(3)-IIa (14.7%和43.1%)。表型谱与59.6%的Ec-ESBL和26.1%的Kp-ESBL中发现的AMEs编码基因相关。在Ec-ESBL中, aac(6')-Ib 通常在2000年与相关bla SHV(26.6%),但带有 bla CTX-M-1组(34.8%),而 aac(3)-IIa 在2000年与 bla TEM(14.6%)和< 2006年,em> bla CTX-M-1组(16.3%)。在Kp-ESBL中, aac(6')-Ib aac(3)-IIa 基因在2000年的 bla TEM菌株(22.0%和44.0%)和 bla CTX-M-1组的菌株(46.4%和34.0)中更为常见在2006年。)Ec-ESBL和Kp-ESBL中对氨基糖苷类药物的耐药性很常见,并且与AMEs的产生有关。这限制了氨基糖苷类抗这些生物的临床用途。

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