通过在 235 型铜绿假单胞菌的 OXA-2 型β-内酰胺酶（OXA-539）中复制氨基酸 D149，产生对新型头孢菌素-β-内酰胺酶抑制剂组合的耐药性。
Emergence of Resistance to Novel Cephalosporin-β-Lactamase Inhibitor Combinations through the Duplication of Amino Acid D149 from OXA-2 β-Lactamase (OXA-539) in Sequence Type 235 Pseudomonas aeruginosa.
机构信息
Servicio de Microbiología and Unidad de Investigación, Hospital Universitario Son Espases, Instituto de Investigación Sanitaria Illes Balears (IdISBa), Palma de Mallorca, Spain.
Servicio de Microbiología and Unidad de Investigación, Hospital Universitario Son Espases, Instituto de Investigación Sanitaria Illes Balears (IdISBa), Palma de Mallorca, Spain
出版信息
Antimicrob Agents Chemother. 2017 Aug 24;61(9). doi: 10.1128/AAC.01117-17. Print 2017 Sep.
Abstract
Resistance development to novel cephalosporin-β-lactamase inhibitor combinations during ceftazidime treatment of a surgical infection by was investigated. Both initial (97C2) and final (98G1) isolates belonged to the high-risk clone sequence type (ST) 235 and were resistant to carbapenems (), fluoroquinolones (GyrA-T83I, ParC-S87L), and aminoglycosides (). 98G1 also showed resistance to ceftazidime, ceftazidime-avibactam, and ceftolozane-tazobactam. Sequencing identified in 97C2, but 98G1 contained a 3-bp insertion leading to the duplication of the key residue D149 (designated OXA-539). Evaluation of PAO1 transformants producing cloned OXA-2 or OXA-539 confirmed that D149 duplication was the cause of resistance. Active surveillance of the emergence of resistance to these new valuable agents is warranted.
摘要
研究了在手术感染患者使用头孢他啶治疗期间，新型头孢菌素-β-内酰胺酶抑制剂组合的耐药性发展情况。初始（97C2）和最终（98G1）分离株均属于高风险克隆序列型（ST）235，对碳青霉烯类（）、氟喹诺酮类（GyrA-T83I、ParC-S87L）和氨基糖苷类（）耐药。98G1 也对头孢他啶、头孢他啶-阿维巴坦和头孢洛扎-他唑巴坦耐药。测序发现 97C2 中有，但 98G1 含有导致关键残基 D149 重复（命名为 OXA-539）的 3 个碱基插入。对产生克隆 OXA-2 或 OXA-539 的 PAO1 转化子的评估证实，D149 重复是耐药的原因。有必要对这些新的有价值药物的耐药性出现进行主动监测。
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