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2017 年,澳大利亚新南威尔士州,耐阿奇霉素淋病奈瑟菌在男男性行为者(MSM)和异性恋者中传播。

Azithromycin-resistant Neisseria gonorrhoeae spreading amongst men who have sex with men (MSM) and heterosexuals in New South Wales, Australia, 2017.

机构信息

Faculty of Medicine, Centre for Clinical Research, The University of Queensland, Herston, Queensland 4029, Australia.

Pathology Queensland Central Laboratory, Brisbane, Queensland 4029, Australia.

出版信息

J Antimicrob Chemother. 2018 May 1;73(5):1242-1246. doi: 10.1093/jac/dky017.

Abstract

OBJECTIVES

To identify the genetic basis of resistance as well as to better understand the epidemiology of a recent surge in azithromycin-resistant Neisseria gonorrhoeae in New South Wales, Australia.

METHODS

Azithromycin-resistant N. gonorrhoeae isolates (n = 118) collected from 107 males, 10 females and 1 transsexual between January and July 2017 were genotyped using a previously described iPLEX method. The results were compared with phenotypic resistance profiles and available patient data.

RESULTS

The iPLEX results revealed 10 different N. gonorrhoeae genotypes (designated AZI-G1 to AZI-G10) of which three were responsible for the majority of infections; AZI-G10 (74.6%, 88 isolates; 87 males and 1 transsexual), AZI-G4 (11.0%, 13 isolates; 7 males and 6 females) and AZI-G7 (6.8%, 8 isolates; 7 males and 1 female). The observed resistance was attributable to one of two different azithromycin resistance mechanisms; the 23S rRNA C2611T mutation was identified in 24% of isolates, whereas the majority of resistance (76%) was associated with a meningococcal-type mtrR variant. Additionally, one isolate was found to harbour both the 23S rRNA C2611T mutation and a type XXXIV mosaic penA sequence associated with cephalosporin resistance.

CONCLUSIONS

These data indicate outbreaks of azithromycin-resistant gonococci amongst networks of MSM and heterosexuals in New South Wales. The results also provide further evidence that azithromycin may soon be an ineffective treatment option for gonococcal infection and highlight the urgent need to explore alternative therapies.

摘要

目的

确定耐药的遗传基础,并更好地了解澳大利亚新南威尔士州近期耐阿奇霉素淋病奈瑟菌激增的流行病学情况。

方法

使用先前描述的 iPLEX 方法对 2017 年 1 月至 7 月期间采集的 107 名男性、10 名女性和 1 名变性人共 118 例耐阿奇霉素淋病奈瑟菌分离株进行基因分型。将结果与表型耐药谱和可用的患者数据进行比较。

结果

iPLEX 结果显示 10 种不同的淋病奈瑟菌基因型(命名为 AZI-G1 至 AZI-G10),其中三种基因型导致了大多数感染;AZI-G10(74.6%,88 株;87 名男性和 1 名变性人)、AZI-G4(11.0%,13 株;7 名男性和 6 名女性)和 AZI-G7(6.8%,8 株;7 名男性和 1 名女性)。观察到的耐药性归因于两种不同的阿奇霉素耐药机制之一;23S rRNA C2611T 突变在 24%的分离株中被发现,而大多数耐药性(76%)与脑膜炎球菌型 mtrR 变体有关。此外,还发现一株同时携带 23S rRNA C2611T 突变和与头孢菌素耐药相关的 XXXIV 型嵌合 penA 序列。

结论

这些数据表明,新南威尔士州的男男性行为者和异性恋者网络中存在耐阿奇霉素淋病奈瑟菌的爆发。结果还进一步证明,阿奇霉素可能很快成为治疗淋病奈瑟菌感染的无效选择,并强调迫切需要探索替代疗法。

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