Infections caused by OXA-48-producing Klebsiella pneumoniae in a tertiary hospital in Spain in the setting of a prolonged, hospital-wide outbreak

Infections caused by OXA-48-producing Klebsiella pneumoniae in a tertiary hospital in Spain in the setting of a prolonged, hospital-wide outbreak
复制标题

DOI:
10.1093/jac/dks364
复制
发表时间:
2013-01-01
影响因子:
5.2
通讯作者:
Mingorance, Jesus
Mingorance, Jesus
中科院分区:
医学2区
文献类型:
--
作者:
Ramon Pano-Pardo, Jose;Ruiz-Carrascoso, Guillermo;Mingorance, Jesus

文献摘要

被引文献

相似文献

我们描述了2011年1月在医院范围内发现的一次长时间爆发的产OXA-48肺炎克雷伯菌(O 48 KP)感染的临床和微生物学特征。收集了临床标本中O 48 KP生长的患者的临床、人口统计学和微生物学数据,直至2011年12月。采用PCR方法检测碳青霉烯酶和β-内酰胺酶基因。通过自动重复序列PCR确定遗传关系。确定了71例临床指导培养显示O 48 KP生长的患者。9个被认为是殖民,而不是造成感染。最常见的感染源是尿路(22/62),其次是手术部位感染(17/62)。62例患者中有23例血培养阳性。许多患者有明显的合并症和延长住院时间。O 48 KP感染患者的住院死亡率为43.5。厄他培南、亚胺培南和美罗培南的MIC(90)分别为32、16和16 mg/L。没有一种抗菌剂对所有分离株都有活性。对O 48 KP最敏感的抗生素是阿米卡星(97.2敏感)、粘菌素(90.1)、替加环素(73)和磷霉素(66.2)。虽然鉴定出8个克隆,但占优势的克隆引起73.2的感染。优势克隆的多位点序列分型(MLST)给出序列类型(ST)405和bla(TEM-1)、bla(SHV-76)、bla(CTX-M-15)和bla(OXA-1)基因以及Tn 1999转座子的插入序列IS 1999在该克隆中与bla(OXA-48)相关。这是在单中心爆发的情况下由O 48 KP引起的最大的感染报告系列,并提供了关于由O 48 KP引起的感染的临床相关性以及与其检测和控制相关的困难的进一步输入。
We describe clinical and microbiological features of infections caused by OXA-48-producing Klebsiella pneumoniae (O48KP) in the setting of a prolonged, hospital-wide outbreak detected in January 2011.Clinical, demographic and microbiological data of patients with growth of O48KP in clinical specimens were collected until December 2011. PCR was used to detect carbapenemase and -lactamase genes. The genetic relationships were determined by automated repetitive-sequence-based PCR.Seventy-one patients with clinically guided cultures showing growth of O48KP were identified. Nine were considered to be colonizing rather than causing infection. The most frequent source of infection was the urinary tract (22/62), followed by surgical site infections (17/62). Blood cultures were positive in 23/62 patients. Many patients had significant comorbidity and prolonged hospital stays. In-hospital mortality among patients with O48KP infections was 43.5. The MIC(90)s of ertapenem, imipenem and meropenem were 32, 16 and 16 mg/L, respectively. No single antimicrobial was active against all the isolates. The antibiotics most active against O48KP were amikacin (97.2 susceptible), colistin (90.1), tigecycline (73) and fosfomycin (66.2). Although eight clones were identified, a predominant clone caused 73.2 of the infections. Multilocus sequence typing (MLST) of the predominant clone gave sequence type (ST) 405 and bla(TEM-1), bla(SHV-76), bla(CTX-M-15) and bla(OXA-1) genes and the insertion sequence IS1999 of the Tn1999 transposon were associated with bla(OXA-48) in this clone.To our knowledge, this is the largest reported series of infections caused by O48KP in the setting of a single-centre outbreak and provides further input on the clinical relevance of infections caused by O48KP and the difficulties associated with its detection and control.