Department of Microbiology, Division of Laboratory Medicine, Oslo University Hospital, PB 4956 Nydalen, 0424 Oslo, Norway.
Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
J Med Microbiol. 2021 Dec;70(12). doi: 10.1099/jmm.0.001454.
Shiga toxin-producing (STEC) can cause severe to fatal disease in humans. Antimicrobial treatment is sometimes necessary, but contraindicated due to undesirable clinical outcome. However, recent studies have shown promising outcomes following antimicrobial treatment. Before the establishment of a possible antimicrobial treatment strategy for STEC infections, the prevalence of antimicrobial resistance in STEC needs to be determined. The resistance status of Norwegian clinical STEC is not known and should be assessed. We aim to characterize genotypic antimicrobial resistance determinants in clinical STEC in Norway, and determine the prevalence of genotypic resistance in order to inform possible antimicrobial treatment options for STEC infections. We included all clinical STEC submitted to the Norwegian Reference Laboratory from March 2018 to April 2020. All samples were whole-genome sequenced and screened for genotypic antimicrobial resistance,virulence determinants and plasmid incompatibility groups. We performed phylogenetic clustering of STEC by core-genome multi-locus sequence typing, and statistical association analyses between isolate characteristics and genotypic resistance. A total of 459 STEC were analysed. For 385 (83.9 %) STEC we did not identify any antimicrobial resistance determinants. Seventy-four STEC (16.1 %) harboured antimicrobial resistance determinants against one or more antimicrobial classes. The most frequent genotypic resistance was identified against aminoglycosides (10.5 %). Thirty-nine STEC (8.5 %) had a multi-drug resistance (MDR) genotype. Genotypic resistance was more prevalent in non-O157 than O157 STEC (=0.02). A positive association was seen between genotypic resistance and the low-virulent STEC O117:H7 phylogenetic cluster (no. 14) (<0.001). Genotypic resistance was not significantly associated to high-virulent STEC. STEC O146:H28 and isolates harbouring the plasmid replicon type IncQ1 were positively associated with MDR. The overall prevalence of genotypic resistance in clinical STEC in Norway is low (16.1 %). Genotypic resistance is more prevalent in non-O157 strains compared to O157 strains, and not significantly associated to high-virulent STEC. Resistance to antimicrobials suggested for treatment, especially azithromycin is low and may present an empiric treatment alternative for severe STEC infections.
产志贺毒素（STEC）可引起人类严重至致命疾病。有时需要进行抗菌治疗，但由于临床结果不理想而被禁忌。然而，最近的研究表明，在进行抗菌治疗后，效果令人鼓舞。在为 STEC 感染建立可能的抗菌治疗策略之前，需要确定 STEC 中的抗菌药物耐药性流行情况。挪威临床 STEC 的耐药现状尚不清楚，应进行评估。我们旨在确定挪威临床 STEC 中基因型抗菌药物耐药决定因素的特征，并确定基因型耐药的流行率，以便为 STEC 感染提供可能的抗菌治疗选择。我们纳入了 2018 年 3 月至 2020 年 4 月期间提交给挪威参考实验室的所有临床 STEC。所有样本均进行全基因组测序，并对基因型抗菌药物耐药性、毒力决定因素和质粒不相容群进行筛查。我们通过核心基因组多位点序列分型对 STEC 进行了系统发育聚类，并对分离株特征与基因型耐药性之间的统计学关联进行了分析。共分析了 459 株 STEC。385 株（83.9%）STEC 未鉴定出任何抗菌药物耐药决定因素。74 株（16.1%）STEC 对一种或多种抗菌药物类别具有抗菌药物耐药决定因素。最常见的基因型耐药是对氨基糖苷类耐药（10.5%）。39 株（8.5%）STEC 具有多药耐药（MDR）基因型。非 O157 型 STEC 比 O157 型 STEC 的基因型耐药更为常见（=0.02）。在低毒力 STEC O117:H7 系统发育群（第 14 群）中观察到基因型耐药与阳性关联（<0.001）。基因型耐药与高毒力 STEC 无显著相关性。STEC O146:H28 和携带质粒复制子类型 IncQ1 的分离株与 MDR 呈正相关。挪威临床 STEC 中基因型耐药的总体流行率较低（16.1%）。非 O157 型 STEC 比 O157 型 STEC 的基因型耐药更为常见，与高毒力 STEC 无显著相关性。对治疗用抗生素的耐药性较低，特别是阿奇霉素，可能为严重 STEC 感染提供经验性治疗选择。
