Hagiwara Eri, Baba Tomohisa, Shinohara Takeshi, Kitamura Hideya, Sekine Akimasa, Komatsu Shigeru, Ogura Takashi
Department of Respiratory Medicine, Kanagawa Cardiovascular and Respiratory Center, Yokohama, Japan.
Chemotherapy. 2017;62(4):256-261. doi: 10.1159/000470828. Epub 2017 May 5.
Antimicrobial resistance of Streptococcus pneumoniae, especially against β-lactam antibiotics, is a global concern. We aimed to analyze a 10-year trend in the antimicrobial resistance genotype of respiratory isolates of S. pneumoniae and to clarify whether resistance genotypes were correlated with phenotypic drug susceptibility, pathogenicity, and host clinical background.
Respiratory isolates of S. pneumoniae from 2003 to 2012 were analyzed with polymerase chain reaction for the presence of β-lactam resistance gene mutations on pbp1a, pbp2x, and pbp2b. Sixty-eight strains isolated from different patients in 2012 were particularly analyzed for the association between genotypes and clinical data.
The 10-year trend analysis showed a recent increase in gPRSP (genotypic penicillin-resistant S. pneumoniae) with all 3 β-lactam resistance genes (from 21.7 to 35.3% in 3 years) and a steady level of gPSSP (genotypic penicillin-susceptible S. pneumoniae) without any β-lactam resistance genes (13.2% in 2012). This resistance trend in genotypes was more prominent than resistance phenotypes determined with a drug susceptibility test. The probability of being a causative pathogen did not differ in gPSSP (55.6%), gPISP (genotypic penicillin-intermediate resistant S. pneumoniae; 54.3%), and gPRSP (54.2%). There was no significant difference in the ratio of patients who presented with respiratory failure in respiratory infection caused by gPSSP, gPISP, or gPRSP. Host clinical characteristics including age and gender were not different among resistance genotypes.
There was no difference in pathogenicity or clinical background between gPSSP, gPISP, and gPRSP. Antimicrobial resistance in respiratory isolates of S. pneumoniae was more prevalent in genotypes than in phenotypes.
肺炎链球菌的抗菌耐药性,尤其是对β-内酰胺类抗生素的耐药性,是一个全球关注的问题。我们旨在分析肺炎链球菌呼吸道分离株抗菌耐药基因型的10年趋势,并阐明耐药基因型是否与表型药物敏感性、致病性和宿主临床背景相关。
采用聚合酶链反应分析2003年至2012年肺炎链球菌呼吸道分离株中pbp1a、pbp2x和pbp2b上β-内酰胺耐药基因突变的情况。特别分析了2012年从不同患者分离出的68株菌株,以研究基因型与临床数据之间的关联。
10年趋势分析显示,最近具有所有3种β-内酰胺耐药基因的基因型青霉素耐药肺炎链球菌(gPRSP)有所增加(3年内从21.7%增至35.3%),而没有任何β-内酰胺耐药基因的基因型青霉素敏感肺炎链球菌(gPSSP)保持稳定水平(2012年为13.2%)。这种基因型的耐药趋势比药敏试验确定的耐药表型更为突出。gPSSP(55.6%)、基因型青霉素中介耐药肺炎链球菌(gPISP;54.3%)和gPRSP(54.2%)作为致病病原体的可能性没有差异。由gPSSP、gPISP或gPRSP引起的呼吸道感染中出现呼吸衰竭的患者比例没有显著差异。包括年龄和性别在内的宿主临床特征在耐药基因型之间没有差异。
gPSSP、gPISP和gPRSP在致病性或临床背景方面没有差异。肺炎链球菌呼吸道分离株的抗菌耐药性在基因型中比在表型中更为普遍。