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Possible healthcare-associated transmission as a cause of secondary infection and population structure of Staphylococcus aureus isolates from two wound treatment centres in Ghana

机译:来自加纳两个伤口治疗中心的可能与卫生保健有关的传播是继发感染和金黄色葡萄球菌分离株种群结构的原因

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We have previously shown that secondary infections of Buruli ulcer wounds were frequently caused by Staphylococcus aureus. To gain understanding into possible routes of secondary infection, we characterized S. aureus isolates from patient lesions and surrounding environments across two Ghanaian health centres. One hundred and one S. aureus isolates were isolated from wounds (n=93, 92.1%) and the hospital environment (n=8, 7.9%) and characterized by the spa gene, mecA and the Panton-Valentine leucocidin toxin followed by spa sequencing and whole genome sequencing of a subset of 49 isolates. Spa typing and sequencing of the spa gene from 91 isolates identified 29 different spa types with t355 (ST152), t186 (ST88), and t346 dominating. Although many distinct strains were isolated from both health centres, genotype clustering was identified within centres. In addition, we identified a cluster consisting of isolates from a healthcare worker, patients dressed that same day and forceps used for dressing, pointing to possible healthcare-associated transmission. These clusters were confirmed by phylogenomic analysis. Twenty-four (22.8%) isolates were identified as methicillin-resistant S. aureus and lukFS genes encoding Panton-Valentine leucocidin were identified in 67 (63.8%) of the isolates. Phenotype screening showed widespread resistance to tetracycline, erythromycin, rifampicin, amikacin and streptomycin. Genomics confirmed the widespread presence of antibiotic resistance genes to @b-lactams, chloramphenicol, trimethoprim, quinolone, streptomycin and tetracycline. Our findings indicate that the healthcare environment probably contributes to the superinfection of Buruli ulcer wounds and calls for improved training in wound management and infection control techniques.
机译:以前我们已经表明,布鲁氏溃疡伤口的继发感染通常是由金黄色葡萄球菌引起的。为了加深对继发感染的可能途径的了解,我们对加纳两个卫生中心的患者病变和周围环境中的金黄色葡萄球菌进行了分离。从伤口(n = 93,92.1%)和医院环境(n = 8,7.9%)中分离出一百零一金黄色葡萄球菌,其特征在于spa基因,mecA和潘顿-华伦丁白花青素毒素,然后是spa测序和49个分离株的子集的全基因组测序。来自91个分离株的spa基因的spa分型和测序确定了以t355(ST152),t186(ST88)和t346为主的29种不同的spa类型。尽管从两个卫生中心都分离出许多不同的菌株,但在两个卫生中心内均发现了基因型聚类。此外,我们确定了一个集群,其中包括来自医护人员的分离株,当天换药的患者以及用于换药的钳子,指出可能与医疗相关的传播。这些簇通过系统植物学分析证实。鉴定出二十四株(22.8%)的菌株为耐甲氧西林的金黄色葡萄球菌,在其中67株(63.8%)的菌株中鉴定出编码Panton-Valentine leucocidin的lukFS基因。表型筛选显示对四环素,红霉素,利福平,丁胺卡那霉素和链霉素普遍耐药。基因组学证实了对β-内酰胺类,氯霉素,甲氧苄啶,喹诺酮,链霉素和四环素的抗生素抗性基因的广泛存在。我们的发现表明,医疗环境可能会导致Buruli溃疡伤口的过度感染,并要求在伤口处理和感染控制技术方面进行更好的培训。

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