Emergence of extended-spectrum β-lactam resistance among Escherichia coli at a US academic children's hospital is clonal at the sequence type level for CTX-M-15, but not for CMY-2.
Emergence of extended-spectrum β-lactam resistance among Escherichia coli at a US academic children's hospital is clonal at the sequence type level for CTX-M-15, but not for CMY-2.
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DOI：
10.1016/j.ijantimicag.2013.01.006
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发表时间：
2013-05
影响因子：
10.8
通讯作者：
Zerr DM
中科院分区：
文献类型：
--
作者：
Weissman SJ;Adler A;Qin X;Zerr DM
在世界范围内，大肠杆菌对广谱β-内酰胺的耐药性正在增加，并与社区和医院环境中从肠外感染中恢复的少数新出现的克隆（例如ST38、ST131和ST405）有关。然而，关于细菌菌株、质粒和β-内酰胺酶基因对儿科感染中β-内酰胺广谱耐药的相对贡献的数据有限。我们对1999-2007年在西雅图儿童医院（Seattle， WA）回收的49株先前报道的系列大肠杆菌分离株的系统发育、毒力和抗生素耐药性相关特性进行了广泛的分子分析。C类酶CMY-2和A类酶CTX-M-15是收集中最突出的扩展谱β-内酰胺耐药酶，分别于2001年和2003年首次出现在该患者群体中，然后在研究期间的其余时间内频率稳步增加。在19株CMY-2阳性分离株中，检测到16株不同的STs (D = 98.25%, 95% CI 96 ~ 100.25%)，表明CMY在宿主株水平上的传播是非克隆性的。相比之下，在10株ctx - m -15阳性分离株中，检测到3株STs (D = 37.78%, 95% CI 2.36-73.20%)，其中8株代表全球传播的ST131谱系，与ctx - m -15相关耐药的克隆传播一致。对10个ST131分离株（包括2个ctx - m阴性分离株）的fimHTR亚型分型显示，在ST131中，携带fimHTR30等位基因与CTX-M-15阳性相关，而携带非fimHTR30等位基因与携带非ctx - m酶相关。因此，CMY-2在ST水平上的传播是非克隆的，但CTX-M-15的克隆传播可能与特定的fimhtr定义的ST131亚谱系有关。
Resistance to extended-spectrum β-lactams is increasing worldwide among Escherichia coli and has been linked to a small number of emergent clones (e.g. ST38, ST131 and ST405) recovered from extraintestinal infections in community and hospital settings. There are, however, limited data about the relative contributions of bacterial strains, plasmids and β-lactamase genes to extended-spectrum β-lactam resistance in paediatric infections. We performed an extensive molecular analysis of phylogenetic, virulence and antibiotic resistance-related properties of 49 previously reported serial E. coli isolates recovered during 1999–2007 at Seattle Children’s Hospital (Seattle, WA). Class C enzyme CMY-2 and class A enzyme CTX-M-15 were the most prominent extended-spectrum β-lactam resistance enzymes in the collection, first appearing in this patient population in 2001 and 2003, respectively, and then steadily increasing in frequency over the remainder of the study period. Among 19 CMY-2-positive isolates, 16 distinct STs were detected (D = 98.25%, 95% CI 96–100.25%), indicating that CMY spread is non-clonal at the host strain level. In contrast, among ten CTX-M-15-positive isolates, three STs were detected (D = 37.78%, 95% CI 2.36–73.20%), of which eight represented the worldwide-disseminated ST131 lineage, consistent with clonal spread of CTX-M-15-associated resistance. fimHTR subtyping of ten ST131 isolates (including two CTX-M-negative isolates) revealed that, within ST131, carriage of allele fimHTR30 correlated with CTX-M-15 positivity, whilst carriage of non-fimHTR30 alleles correlated with carriage of non-CTX-M enzymes. Thus, spread of CMY-2 is non-clonal at the ST level, but clonal spread of CTX-M-15 may be associated with a specific fimHTR-defined sublineage of ST131.
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