Department of Infectious Diseases, King's College London School of Medicine, United Kingdom.
Clin Infect Dis. 2012 Mar 1;54(5):591-600. doi: 10.1093/cid/cir858. Epub 2011 Dec 20.
Antimicrobial resistance and bacterial virulence factors may increase the risk of hematogenous complications during methicillin-resistant Staphylococcus aureus (MRSA) bloodstream infection (BSI). This study reports on the impact of increasing vancomycin minimum inhibitory concentrations (V-MICs) and MRSA clone type on risk of hematogenous complications from MRSA BSI during implementation of an effective MRSA control program.
In sum, spa typing, staphylococcal cassette chromosome mec allotyping, and vancomycin and teicoplanin MICs were performed on 821 consecutive MRSA bloodstream isolates from 1999 to 2009. Prospectively collected data, including focus of infection, were available for 695 clinically significant cases. Logistic and multinomial logistic regression was used to determine the association between clone type, vancomycin MIC (V-MIC), and focus of infection.
MRSA BSIs decreased by ∼90% during the 11 years. Typing placed isolates into 3 clonal complex (CC) groups that had different population median V-MICs (CC30, 0.5 μg/mL [n = 349]; CC22, 0.75 μg/mL [n = 272]; non-CC22/30, 1.5 μg/mL [n = 199]). There was a progressive increase in the proportion of isolates with a V-MIC above baseline median in each clonal group and a disproportionate fall in the clone group with lowest median V-MIC (CC30). In contrast, there were no increases in teicoplanin MICs. High V-MIC CC22 isolates (1.5-2 μg/mL) were strongly associated with endocarditis (odds ratio, 12; 95% confidence interval, 3.72-38.9) and with a septic metastasis after catheter-related BSI (odds ratio, 106; 95% confidence interval, 12.6-883) compared with other clone type/V-MIC combinations.
An interaction between clone type and V-MIC can influence the risk of endocarditis associated with MRSA BSI, implying involvement of both therapeutic and host-pathogen factors.
耐甲氧西林金黄色葡萄球菌（MRSA）血流感染（BSI）期间，抗菌药物耐药性和细菌毒力因子可能会增加血液并发症的风险。本研究报告了在实施有效的 MRSA 控制计划期间，万古霉素最低抑菌浓度（V-MIC）增加和 MRSA 克隆型对 MRSA BSI 血液并发症风险的影响。
对 1999 年至 2009 年连续 821 株 MRSA 血流分离株进行 spa 分型、葡萄球菌盒染色体 mec 基因分型以及万古霉素和替考拉宁 MIC 检测。对 695 例临床显著病例前瞻性收集感染部位等数据。采用逻辑回归和多项逻辑回归分析确定克隆型、万古霉素 MIC（V-MIC）和感染部位之间的关联。
11 年间，MRSA BSI 下降了约 90%。分型将分离株分为 3 个克隆复合体（CC）组，其人群中位 V-MIC 不同（CC30，0.5μg/ml [n=349]；CC22，0.75μg/ml [n=272]；非 CC22/30，1.5μg/ml [n=199]）。每个克隆组中 V-MIC 高于基线中位数的分离株比例逐渐增加，而中位 V-MIC 最低的克隆组（CC30）则明显减少。相反，替考拉宁 MIC 没有增加。高 V-MIC CC22 分离株（1.5-2μg/ml）与心内膜炎（比值比，12；95%置信区间，3.72-38.9）和导管相关 BSI 后败血症转移（比值比，106；95%置信区间，12.6-883）强烈相关，与其他克隆型/V-MIC 组合相比。
克隆型和 V-MIC 之间的相互作用可能会影响 MRSA BSI 相关心内膜炎的风险，这意味着治疗和宿主-病原体因素都有参与。
