Cherazard Regine, Epstein Marcia, Doan Thien-Ly, Salim Tanzila, Bharti Sheena, Smith Miriam A
1Department of Medicine, Long Island Jewish Hospital Forest Hills, Northwell Health, Forest Hills, NY; 2Department of Medicine, Division of Infectious Disease, North Shore University Hospital, Northwell Health, Manhasset, NY; and 3Department of Pharmacy, Long Island Jewish Medical Center, Northwell Health, New Hyde Park, NY.
Am J Ther. 2017 May;24(3):e361-e369. doi: 10.1097/MJT.0000000000000551.
Streptococcus pneumoniae is a major cause of pneumonia, meningitis, sepsis, bacteremia, and otitis media. S. pneumoniae has developed increased resistance to multiple classes of antibiotics.
Systematic literature review of prevalence, mechanisms, and clinical implications in S. pneumoniae resistance.
Since S. pneumoniae resistance to penicillin was first reported with subsequent development of resistance to other classes of drugs, selection of appropriate antibiotic treatment is challenging.
We searched PubMed (English language) for citations to antibiotic resistance in S. pneumoniae published before March 1, 2016.
We present a review of S. pneumoniae resistance to beta-lactams, macrolides, lincosamides, fluoroquinolones, tetracyclines, and trimethoprim-sulfamethoxazole (TMP-SMX). There has been a steady decline in susceptibility of S. pneumoniae to commonly used beta-lactams. Phenotypic expression of penicillin resistance occurs as a result of a genetic structural modification in penicillin-binding proteins. Between 20% and 40% of S. pneumoniae isolates are resistant to macrolides. Macrolide resistance mechanisms include ribosomal target site alteration, alteration in antibiotic transport, and modification of the antibiotic. Approximately 22% of S. pneumoniae isolates are resistant to clindamycin. Similar to macrolide resistance, clindamycin involves a target site alteration. The prevalence of fluoroquinolone resistance is low, although increasing. S. pneumoniae resistance to fluoroquinolones occurs by accumulated mutations within the bacterial genome, increased efflux, or acquisition of plasmid-encoded genes. S. pneumoniae resistance has also increased for the tetracyclines. The primary mechanism is mediated by 2 genes that confer ribosomal protection. The prevalence of TMP-SMX resistance is around 35%. As with fluoroquinolones, resistance to TMP-SMX is secondary to mutations in the bacterial genome.
Effective treatment of resistant S. pneumoniae is a growing concern. New classes of drugs, newer formulations of older drugs, combination antibiotic therapy, nonantibiotic modalities, better oversight of antibiotic usage, and enhanced preventive measures hold promise.
肺炎链球菌是肺炎、脑膜炎、败血症、菌血症和中耳炎的主要病因。肺炎链球菌对多种类抗生素的耐药性有所增加。
对肺炎链球菌耐药性的患病率、机制及临床意义进行系统的文献综述。
自从首次报道肺炎链球菌对青霉素耐药，随后又出现对其他类药物的耐药性以来，选择合适的抗生素治疗具有挑战性。
我们在PubMed（英文）中检索了2016年3月1日前发表的有关肺炎链球菌抗生素耐药性的文献。
我们综述了肺炎链球菌对β-内酰胺类、大环内酯类、林可酰胺类、氟喹诺酮类、四环素类和甲氧苄啶-磺胺甲恶唑（TMP-SMX）的耐药性。肺炎链球菌对常用β-内酰胺类药物的敏感性一直在稳步下降。青霉素耐药性的表型表达是由于青霉素结合蛋白的基因结构改变所致。20%至40%的肺炎链球菌分离株对大环内酯类耐药。大环内酯类耐药机制包括核糖体靶位点改变、抗生素转运改变和抗生素修饰。约22%的肺炎链球菌分离株对克林霉素耐药。与大环内酯类耐药相似，克林霉素耐药涉及靶位点改变。氟喹诺酮类耐药的患病率较低，但呈上升趋势。肺炎链球菌对氟喹诺酮类的耐药性是由细菌基因组内的累积突变、外排增加或获得质粒编码基因引起的。肺炎链球菌对四环素类的耐药性也有所增加。主要机制由两个赋予核糖体保护作用的基因介导。TMP-SMX耐药的患病率约为35%。与氟喹诺酮类一样，对TMP-SMX的耐药性继发于细菌基因组的突变。
有效治疗耐药肺炎链球菌日益受到关注。新型药物、旧药的新剂型、联合抗生素治疗、非抗生素治疗方式、更好地监督抗生素使用以及加强预防措施都有前景。
