Agata Pruss, Magdalena Wrona, P. Kwiatkowski, H. Masiuk, Marta Cettler, Stefania Giedrys-Kalemba, E. Dudzińska, B. Dołęgowska
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The aim of the study was to detect selected virulence genes among clinical multidrug-resistant strains of K. pneumoniae. Materials and methods: We determined the drug susceptibility of strains and confirmed the presence of antibiotic resistance mechanisms using phenotypic methods. Additionally, we assessed the presence of genes encoding selected resistance mechanisms and genes determining selected virulence factors. A total of 134 strains from various hospital units were used for the study. Results: The highest percentage of strains was isolated from urine (46%). Among the isolates, 72% were from male patients. Fifty-seven percent of K. pneumoniae produced ESBL (KpESBL), while the remaining 43% carried the New Delhi metallo-β- lactamase (NDM) mechanism. The drug susceptibility of the KpESBL varied, with full sensitivity observed only in the case of antibiotics from the carbapenem group. New Delhi metallo- β-lactamase-producing K. pneumoniae showed sensitivity only to amikacin and gentamicin. In KpESBL strains, genes from the TEM family were most observed (74/76). Most of the strains had all 4 β-lactamase-encoding genes (61/76). In the group of strains producing carbapenemases, only the bla NDM gene was detected. Regardless of the resistance mechanisms, the tested strains most often had virulence genes related to the adhesion ability (fimH) and the structure of LPS (wabG).","PeriodicalId":91594,"journal":{"name":"Pomeranian journal of life sciences","volume":"267 1","pages":"1 - 9"},"PeriodicalIF":0.0000,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Virulence genes and antibiotic resistance among clinical Klebsiella pneumoniae strains\",\"authors\":\"Agata Pruss, Magdalena Wrona, P. Kwiatkowski, H. 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The aim of the study was to detect selected virulence genes among clinical multidrug-resistant strains of K. pneumoniae. Materials and methods: We determined the drug susceptibility of strains and confirmed the presence of antibiotic resistance mechanisms using phenotypic methods. Additionally, we assessed the presence of genes encoding selected resistance mechanisms and genes determining selected virulence factors. A total of 134 strains from various hospital units were used for the study. Results: The highest percentage of strains was isolated from urine (46%). Among the isolates, 72% were from male patients. Fifty-seven percent of K. pneumoniae produced ESBL (KpESBL), while the remaining 43% carried the New Delhi metallo-β- lactamase (NDM) mechanism. The drug susceptibility of the KpESBL varied, with full sensitivity observed only in the case of antibiotics from the carbapenem group. New Delhi metallo- β-lactamase-producing K. pneumoniae showed sensitivity only to amikacin and gentamicin. In KpESBL strains, genes from the TEM family were most observed (74/76). Most of the strains had all 4 β-lactamase-encoding genes (61/76). In the group of strains producing carbapenemases, only the bla NDM gene was detected. 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引用次数: 0
摘要
摘要 引言:肺炎克雷伯氏菌是引起医院内感染的病原体之一。近来,由于对多种抗生素产生耐药性,这些细菌引起的感染变得更加危险,严重限制了治疗选择。肺炎链球菌最常见的耐药机制是产生广谱β-内酰胺酶(ESBL)。然而,更危险的机制是产生碳青霉烯酶。感染过程还受到各种毒力特征的影响,主要是使其能够粘附和帮助避免宿主免疫反应。大多数编码抗性和毒力机制的基因都位于质粒上,这为它们的传播提供了便利。本研究旨在检测临床耐多药肺炎克氏菌菌株中的部分毒力基因。材料和方法我们测定了菌株对药物的敏感性,并使用表型方法确认了抗生素耐药机制的存在。此外,我们还评估了编码特定耐药机制的基因和决定特定毒力因子的基因的存在情况。研究共使用了来自不同医院单位的 134 株菌株。研究结果从尿液中分离出的菌株比例最高(46%)。在分离出的菌株中,72%来自男性患者。57%的肺炎克雷伯菌可产生 ESBL(KpESBL),其余 43% 的肺炎克雷伯菌则具有新德里金属-β-内酰胺酶(NDM)机制。KpESBL 对药物的敏感性各不相同,只有对碳青霉烯类抗生素才完全敏感。新德里产金属β-内酰胺酶肺炎克氏菌只对阿米卡星和庆大霉素敏感。在 KpESBL 菌株中,来自 TEM 家族的基因最多(74/76)。大多数菌株都有全部 4 个 β-内酰胺酶编码基因(61/76)。在产生碳青霉烯酶的菌株中,只检测到 bla NDM 基因。无论抗药性机制如何,被检测菌株最常见的毒力基因与粘附能力(fimH)和 LPS 结构(wabG)有关。
Virulence genes and antibiotic resistance among clinical Klebsiella pneumoniae strains
Abstract Introduction: Klebsiella pneumoniae is one of the etiological factors of nosocomial infections. Recently, infections caused by these bacteria have become more dangerous due to the acquired resistance to many antibiotics, severely limiting therapeutic options. The most common mechanism of resistance in K. pneumoniae rods is the production of extended-spectrum β-lactamases (ESBL). However, a more perilous mechanism is the production of carbapenemases. The course of the infection process is also influenced by various virulence characteristics, primarily enabling adhesion and aiding in avoiding host immune responses. Most genes encoding mechanisms of resistance and virulence are located on plasmids, facilitating their spread. The aim of the study was to detect selected virulence genes among clinical multidrug-resistant strains of K. pneumoniae. Materials and methods: We determined the drug susceptibility of strains and confirmed the presence of antibiotic resistance mechanisms using phenotypic methods. Additionally, we assessed the presence of genes encoding selected resistance mechanisms and genes determining selected virulence factors. A total of 134 strains from various hospital units were used for the study. Results: The highest percentage of strains was isolated from urine (46%). Among the isolates, 72% were from male patients. Fifty-seven percent of K. pneumoniae produced ESBL (KpESBL), while the remaining 43% carried the New Delhi metallo-β- lactamase (NDM) mechanism. The drug susceptibility of the KpESBL varied, with full sensitivity observed only in the case of antibiotics from the carbapenem group. New Delhi metallo- β-lactamase-producing K. pneumoniae showed sensitivity only to amikacin and gentamicin. In KpESBL strains, genes from the TEM family were most observed (74/76). Most of the strains had all 4 β-lactamase-encoding genes (61/76). In the group of strains producing carbapenemases, only the bla NDM gene was detected. Regardless of the resistance mechanisms, the tested strains most often had virulence genes related to the adhesion ability (fimH) and the structure of LPS (wabG).