National Antimicrobial Resistance Monitoring System, Centers for Disease Control and Prevention, Atlanta, Georgia 30329, USA.
Foodborne Pathog Dis. 2010 Dec;7(12):1503-9. doi: 10.1089/fpd.2010.0607. Epub 2010 Aug 12.
We describe the antimicrobial susceptibility to extended-spectrum cephalosporins in non-Typhi Salmonella (NTS) isolated from humans in the United States and explore resistance mechanisms for isolates displaying decreased susceptibility to ceftriaxone or ceftiofur. We further explore the concordance between the newly revised Clinical and Laboratory Standards Institute (CLSI) breakpoints for ceftriaxone and the presence of a β-lactamase.
In 2005 and 2006, public health laboratories in all U.S. state health departments forwarded every 20th NTS isolate from humans to Centers for Disease Control and Prevention as part of the National Antimicrobial Resistance Monitoring System (NARMS) for enteric bacteria. Minimum inhibitory concentrations (MICs) were determined by broth microdilution. Isolates displaying decreased susceptibility (MIC ≥ 2 mg/L) to ceftriaxone or ceftiofur were included in the study. The presence of β-lactamase genes was investigated by polymerase chain reaction amplification and sequencing, targeting six different genes (bla(TEM), bla(OXA), bla(SHV), bla(CTX-M), bla(PSE), and bla(CMY)). Plasmid location of bla(CMY) was confirmed by transforming plasmids into Escherichia coli.
Among the 4236 isolates of NTS submitted to NARMS in 2005 and 2006, 175 (4.1%) displayed decreased susceptibility to either ceftriaxone or ceftiofur. By polymerase chain reaction screening, one or more β-lactamase genes could be detected in 139 (80.8%) isolates. The most prevalent resistance mechanism detected was the AmpC β-lactamase gene bla(CMY.) Other β-lactamase genes detected included 11 bla(TEM-1), 3 bla(PSE-1), 2 bla(OXA-1), and 1 bla(CTX-M-15). The ceftriaxone MIC values for the bla(CMY)-containing isolates ranged from 4 to 64 mg/L; all bla(CMY)-bearing isolates were classified as ceftriaxone resistant according to current CLSI guidelines.
Among NTS isolates submitted to NARMS in 2005 and 2006, cephamycinase β-lactamases are the predominant cause of decreased susceptibility to ceftriaxone. The fact that all bla(CMY)-containing isolates were classified as resistant to ceftriaxone (MIC ≥ 4 mg/L) supports the newly revised CLSI breakpoints for cephalosporins and Enterobacteriaceae.
描述美国人类分离的非伤寒沙门氏菌(NTS)对扩展谱头孢菌素的药敏情况,并探讨对头孢曲松或头孢噻肟敏感性降低的分离株的耐药机制。我们还进一步探讨了新修订的临床和实验室标准协会(CLSI)头孢曲松折点与β-内酰胺酶存在之间的一致性。
2005 年和 2006 年,美国各州卫生部门的公共卫生实验室将每 20 个从人类分离的 NTS 分离株作为国家食源性细菌抗药性监测系统(NARMS)的一部分转发给疾病控制和预防中心。通过肉汤微量稀释法测定最小抑菌浓度(MIC)。对头孢曲松或头孢噻肟敏感性降低(MIC≥2mg/L)的分离株纳入研究。通过聚合酶链反应扩增和测序,针对 6 种不同基因(bla(TEM)、bla(OXA)、bla(SHV)、bla(CTX-M)、bla(PSE)和 bla(CMY))检测β-内酰胺酶基因的存在。通过将质粒转化为大肠杆菌,确认 bla(CMY)的质粒位置。
2005 年和 2006 年 NARMS 提交的 4236 株 NTS 中,175 株(4.1%)对头孢曲松或头孢噻肟的敏感性降低。通过聚合酶链反应筛选,在 139 株(80.8%)分离株中可检测到一种或多种β-内酰胺酶基因。检测到的最常见的耐药机制是 AmpCβ-内酰胺酶基因 bla(CMY)。其他检测到的β-内酰胺酶基因包括 11 个 bla(TEM-1)、3 个 bla(PSE-1)、2 个 bla(OXA-1)和 1 个 bla(CTX-M-15)。bla(CMY)携带株的头孢曲松 MIC 值为 4-64mg/L;根据现行 CLSI 指南,所有 bla(CMY)携带株均被归类为头孢曲松耐药。
2005 年和 2006 年 NARMS 提交的 NTS 分离株中,头孢菌素酶β-内酰胺酶是导致头孢曲松敏感性降低的主要原因。所有 bla(CMY)携带株均被归类为头孢曲松耐药(MIC≥4mg/L),这支持了新修订的头孢菌素和肠杆菌科的 CLSI 折点。