The Prevalence of Inducible and Constitutive Macrolide-lincosamide-streptogramin B-Resistant (iMLSB and cMLSB) Phenotypes among Clinical Isolates of Staphylococcus aureus at a Tertiary Care Hospital in South Mumbai

A. Sakle, S. Swaminathan
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Abstract

Staphylococcus aureus is one of the most common causative organisms of health care as well as community-acquired infections in every region of the world. Moreover, increase in the prevalence of methicillin resistance among Staphylococci is a matter of concern.[1] Due to this, there has been a renewed interest in the usage of macrolide-lincosamide-streptogramin B (MLSB) antibiotics for the treatment of S. aureus infections. Moreover, clindamycin is the preferred agent because of its exceptional pharmacokinetic properties.[2] Clindamycin can be used as an alternative antibiotic in penicillin-allergic patients for the treatment of skin and soft-tissue infections caused by S. aureus. It achieves high intracellular levels in phagocytic cells, high levels in bone, and appears to be able to reduce toxin production in toxin-producing strains of staphylococci. Except central nervous system, it has very good tissue penetration.[3] It is a good option for outpatient prescription or as a follow-up drug after intravenous therapy because of its good oral absorption.[4] However, a possibility of inducible clindamycin resistance among Staphylococcal isolates is a major concern in use of clindamycin.[5] There are three mechanisms of resistance to the MLSB class of antibiotics: Modification of target site, enzymatic inactivation, and impermeability or macrolide efflux pumps.[6] Resistance due to modification of ribosomal target is mediated by erythromycin ribosomal methylases encoded by ermA/ ermC genes and it affects the activities of macrolides as well as clindamycin. This type of resistance may be inducible or constitutive.[7,8] The constitutive resistance MLSB (cMLSB) strains can easily be detected by standard susceptibility testing methods because they are resistant to both macrolides and lincosamides alike. However, the inducible resistant MLSB (iMLSB) strains appear erythromycin resistant and clindamycin sensitive in routine laboratory tests, unless the tests include measures that result in induction of clindamycin resistance.[4] In such cases, therapy with clindamycin may ABSTRACT
南孟买一家三级医院金黄色葡萄球菌临床分离株中诱导型和组成型大环内酯-利可沙胺-链霉素b耐药(iMLSB和cMLSB)表型的流行
金黄色葡萄球菌是世界上每个地区卫生保健和社区获得性感染中最常见的病原生物之一。此外,葡萄球菌中甲氧西林耐药性的增加也是一个值得关注的问题正因为如此,人们对使用大环内酯-利可沙胺-链状gramin B (MLSB)抗生素治疗金黄色葡萄球菌感染重新产生了兴趣。此外,克林霉素因其独特的药代动力学特性而成为首选药物克林霉素可作为青霉素过敏患者的替代抗生素,用于治疗金黄色葡萄球菌引起的皮肤和软组织感染。它在吞噬细胞内达到高水平,在骨骼中达到高水平,并且似乎能够减少葡萄球菌产毒素菌株的毒素产生。除中枢神经系统外,有很好的组织穿透性由于其良好的口服吸收,它是门诊处方的一个很好的选择,或作为静脉治疗后的随访药物然而,葡萄球菌分离株中诱导克林霉素耐药的可能性是克林霉素使用中的一个主要问题对MLSB类抗生素的耐药机制有三种:靶点修饰、酶失活和不渗透或大环内酯外排泵核糖体靶点修饰引起的耐药是由ermA/ ermC基因编码的红霉素核糖体甲基化酶介导的,它影响大环内酯类药物和克林霉素的活性。这种类型的电阻可以是诱导性的,也可以是本构性的。[7,8]本构耐药型MLSB (cMLSB)菌株对大环内酯类和林肯胺类均有耐药性,因此可以通过标准药敏试验方法很容易检测到。然而,诱导耐药MLSB (iMLSB)菌株在常规实验室试验中表现出红霉素耐药和克林霉素敏感,除非试验包括导致克林霉素耐药的措施在这种情况下,用克林霉素治疗可能是抽象的
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