Domenech A, Ardanuy C, Grau I, Calatayud L, Pallares R, Fenoll A, Brueggemann A B, Liñares J
Microbiology Department, Hospital Universitari de Bellvitge-IDIBELL-Barcelona University, Barcelona, Spain.
J Antimicrob Chemother. 2014 Apr;69(4):924-31. doi: 10.1093/jac/dkt473. Epub 2013 Dec 8.
We aimed to analyse the clinical epidemiology and genetic diversity of invasive pneumococcal disease (IPD) episodes attributed to the Spain(23F)-ST81 (PMEN1) clone.
Fifty-eight (2.7%) of 2117 invasive pneumococci isolated from adult patients during the 1990-2012 period shared a PFGE pattern related to the PMEN1 clone. The genotype was confirmed by multilocus sequence typing. The pbp2x, pbp1a, pbp2b and pspA genes were PCR-amplified and sequenced. Polymorphisms in the pspC gene were identified by PCR restriction fragment length polymorphism. The presence of transposons with erythromycin and tetracycline resistance determinants was detected by PCR.
The prevalence of the PMEN1 clone increased from 0.8% in 1991 to 6.2% in 2001, and decreased to 0% in 2010-12, concomitant with the introduction of the seven-valent pneumococcal conjugate vaccine for children. A total of 93.1% of patients had pneumonia, meningitis or peritonitis; 87.9% of patients had associated underlying diseases, mainly cancer, chronic obstructive pulmonary disease and diabetes. Two closely related sequence types (STs) (ST81, n = 52; ST85, n = 6) were detected, with different serotypes: 23F (n = 42), 19A (n = 9) and 19F (n = 6). All the isolates were resistant to penicillin, co-trimoxazole and chloramphenicol. All the isolates also shared the same pbp1a allele, whereas multiple alleles of pbp2b, pbp2x, pspA and pspC were detected. Of the isolates, 89.7% were tetracycline resistant and 60.3% (n = 35) were macrolide resistant, and resistance was associated with different Tn916-like transposons.
Adult IPD caused by this clone was mainly detected in patients with underlying conditions, and genetic variability was observed among PMEN1 isolates collected in our area over the past 20 years.
我们旨在分析由西班牙(23F)-ST81(PMEN1)克隆株引起的侵袭性肺炎球菌病(IPD)发作的临床流行病学和基因多样性。
在1990 - 2012年期间从成年患者中分离出的2117株侵袭性肺炎球菌中,有58株(2.7%)具有与PMEN1克隆株相关的脉冲场凝胶电泳(PFGE)图谱。通过多位点序列分型确认基因型。对pbp2x、pbp1a、pbp2b和pspA基因进行PCR扩增和测序。通过PCR限制性片段长度多态性鉴定pspC基因中的多态性。通过PCR检测带有红霉素和四环素抗性决定簇的转座子的存在。
PMEN1克隆株的流行率从1991年的0.8%上升至2001年的6.2%,并在2010 - 2012年降至0%,这与儿童七价肺炎球菌结合疫苗的引入同步。共有93.1%的患者患有肺炎、脑膜炎或腹膜炎;87.9%的患者有相关基础疾病,主要是癌症、慢性阻塞性肺疾病和糖尿病。检测到两种密切相关的序列类型(STs)(ST81,n = 52;ST85,n = 6),具有不同的血清型:23F(n = 42)、19A(n = 9)和19F(n = 6)。所有分离株对青霉素、复方新诺明和氯霉素耐药。所有分离株还共享相同的pbp1a等位基因,而检测到pbp2b、pbp2x、pspA和pspC的多个等位基因。在分离株中,89.7%对四环素耐药,60.3%(n = 35)对大环内酯类耐药,且耐药与不同的Tn916样转座子相关。
由该克隆株引起的成人IPD主要在有基础疾病的患者中检测到,并且在过去20年我们地区收集的PMEN1分离株中观察到基因变异性。