烧伤患者耐甲氧西林和广谱β-内酰胺酶金黄色葡萄球菌的分子特征

Shawnm Ahmed Aziz
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引用次数: 0

摘要

抗生素耐药性已成为一个主要的世界卫生挑战,并限制了医生的治疗能力。金黄色葡萄球菌是最臭名昭著的病原体,尤其在烧伤患者中引起发病率和死亡率。然而,金黄色葡萄球菌迅速获得对多种抗生素的耐药性。万古霉素是一种糖肽抗生素,仍然是治疗严重耐甲氧西林金黄色葡萄球菌感染的首选药物。本研究旨在检测β -内酰胺和糖肽抗性基因的出现。从苏莱曼尼-伊拉克市烧伤和整形外科医院烧伤患者中采集了50份金黄色葡萄球菌临床标本。所有标本均证实金黄色葡萄球菌阳性。采用NCCL标准对各菌株进行药敏试验,并采用双盘扩散协同试验进行扩展谱β -内酰胺酶检测。采用几种常规方法和聚合酶链反应对分离菌株的β-内酰胺酶产量进行了评价。其中耐甲氧西林菌94%,扩展谱β内酰胺酶产生菌34.28%。利用特异引物对β-内酰胺酶相关的bla基因及对万古霉素降低敏感性相关基因进行PCR分子检测。结果表明,除vraR基因外,所有分离到的PBP1、PBP2、PBP3、PBP4、trfA和trfB、graSR、vraS基因均与耐甲氧西林感染的替柯planin治疗时间延长有关,替柯planin耐药的增加可能是万古霉素耐药的前奏。总之,过量服用β -内酰胺可增加万古霉素-中间金黄色葡萄球菌菌株,导致万古霉素耐药的出现,尽管治疗万古霉素耐药感染具有挑战性。
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Molecular Characterization of Methicillin Resistant and Extended Spectrum β-Lactamase Staphylococcus aureus Isolated from Burn Patients
Antibiotic resistance has become a major world health challenge and has limited the ability of physician's treatment. Staphylococcus aureus the most notorious pathogens causes morbidity and mortality especially in burn patients. However, Staphylococcus aureus rapidly acquired resistance to multiple antibiotics. Vancomycin, a glycopeptide antibiotic remains a drug of choice for treatment of severe Methicillin Resistance S. aureus infections. This study aimed to detect the emergence of beta-lactam and glycopeptide resistance genes. 50 clinical specimens of S. aureus collected from burn patients in burn and plastic surgery units in Sulaimani-Iraq city. All specimens were confirmed to be positive for S. aureus. All the isolates were assessed for their susceptibility to different antibiotics depending on NCCL standards, followed by Extended Spectrum Beta Lactamase detection by double disk diffusion synergy test. The production of β- lactamases was evaluated in the isolated strains by several routine methods and polymerase chain reaction. Among the isolates 94% were Methicillin resistance and 34.28% were Extended Spectrum Beta Lactamase producer. PCR based molecular technique was done for the bla genes related to β- lactamase enzymes by the specific primers, as well as genes which related to reduced sensitivity to Vancomycin were detected. The results indicated that all isolated showed the PBP1, PBP2, PBP3, PBP4, trfA and trfB, graSR, vraS except the vraR gene and the prolonged therapy of Methicillin resistance infection with teicoplanin have been associated with progress of resistance and the rise of tecoplanin resistance may be a prologue to evolving Vancomycin resistance. In conclusion, beta-lactam over taking can rise Vancomycin- Intermediate S. aureus strains leading to appearance of Vancomycin resistance although the treatment of Vancomycin resistant infections is challenging.
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