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Biological and Epidemiological Features of Antibiotic-Resistant Streptococcus pneumoniae in Pre- and Post-Conjugate Vaccine Eras: a United States Perspective.
Clinical Microbiology Reviews ( IF 19.0 ) Pub Date : 2016-07-01 , DOI: 10.1128/cmr.00058-15
Lindsay Kim 1 , Lesley McGee 2 , Sara Tomczyk 1 , Bernard Beall 3
Affiliation  

Streptococcus pneumoniae inflicts a huge disease burden as the leading cause of community-acquired pneumonia and meningitis. Soon after mainstream antibiotic usage, multiresistant pneumococcal clones emerged and disseminated worldwide. Resistant clones are generated through adaptation to antibiotic pressures imposed while naturally residing within the human upper respiratory tract. Here, a huge array of related commensal streptococcal strains transfers core genomic and accessory resistance determinants to the highly transformable pneumococcus. β-Lactam resistance is the hallmark of pneumococcal adaptability, requiring multiple independent recombination events that are traceable to nonpneumococcal origins and stably perpetuated in multiresistant clonal complexes. Pneumococcal strains with elevated MICs of β-lactams are most often resistant to additional antibiotics. Basic underlying mechanisms of most pneumococcal resistances have been identified, although new insights that increase our understanding are continually provided. Although all pneumococcal infections can be successfully treated with antibiotics, the available choices are limited for some strains. Invasive pneumococcal disease data compiled during 1998 to 2013 through the population-based Active Bacterial Core surveillance program (U.S. population base of 30,600,000) demonstrate that targeting prevalent capsular serotypes with conjugate vaccines (7-valent and 13-valent vaccines implemented in 2000 and 2010, respectively) is extremely effective in reducing resistant infections. Nonetheless, resistant non-vaccine-serotype clones continue to emerge and expand.

中文翻译:

结合疫苗时代前后抗生素耐药肺炎链球菌的生物学和流行病学特征:美国的观点。

肺炎链球菌作为社区获得性肺炎和脑膜炎的主要原因,造成了巨大的疾病负担。在主流抗生素使用后不久,多重耐药肺炎球菌克隆出现并在世界范围内传播。抗性克隆是通过适应自然存在于人类上呼吸道内时施加的抗生素压力而产生的。在这里,大量相关的共生链球菌菌株将核心基因组和辅助耐药决定簇转移到高度可转化的肺炎球菌中。β-内酰胺耐药性是肺炎球菌适应性的标志,需要多个独立的重组事件,这些重组事件可追溯到非肺炎球菌起源并在多重耐药克隆复合物中稳定地延续。β-内酰胺 MIC 升高的肺炎球菌菌株通常对其他抗生素具有耐药性。尽管不断提供增加我们理解的新见解,但大多数肺炎球菌耐药性的基本机制已被确定。尽管所有肺炎球菌感染都可以用抗生素成功治疗,但某些菌株的可用选择有限。1998 年至 2013 年期间通过基于人群的活性细菌核心监测计划(美国人口基数为 30,600,000)汇编的侵袭性肺炎球菌疾病数据表明,针对流行的荚膜血清型使用结合疫苗(2000 年和 2010 年实施的 7 价和 13 价疫苗,分别)在减少耐药感染方面非常有效。尽管如此,抗性非疫苗血清型克隆继续出现并扩大。
更新日期:2019-11-01
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