Department of Veterinary Medicine, College of Veterinary Medicine, National Chung-Hsing University, No. 250, Guoguang Road, Taichung 402, Taiwan, Republic of China.
Eur J Clin Microbiol Infect Dis. 2010 Jun;29(6):689-98. doi: 10.1007/s10096-010-0915-1. Epub 2010 Apr 11.
Klebsiella pneumoniae-caused liver abscess (KLA) is an emerging infectious disease. However, factors other than K1-specific loci that contribute to the pathogenesis of this disease have not been identified. pLVPK is a 219,385-bp plasmid of K. pneumoniae CG43, an invasive K2 strain associated with KLA. We aimed in this study to evaluate the involvement of pLVPK in K. pneumoniae virulence and its clinical significance in abscess formation. A pLVPK-cured CG43 was isolated and its virulence was examined in a mouse model. The prevalence of pLVPK-derived loci terW, iutA, rmpA, silS, and repA was investigated in 207 clinical isolates by screening with specific primers. Loss of pLVPK abolished the ability of K. pneumoniae to disseminate into extraintestinal sites and, consequently, attenuated abscess formation in mice. Primary K. pneumoniae abscess isolates (n = 94) were more likely to be terW (+)-iutA (+)-rmpA (+)-silS (+) than those related to non-abscess infections (n = 113) (62% vs. 27%; p < 0.0001). Logistic regression analysis indicated that the presence of the terW-rmpA-iutA-silS loci was a significant risk factor (odds ratio, 4.12; 95% confidence interval, 2.02-8.4; p < 0.0001) for abscess formation. pLVPK is a determinant for K. pneumoniae virulence and infection with strains carrying the pLVPK-derived terW-rmpA-iutA-silS loci may predispose patients to abscess formation.
肺炎克雷伯菌肝脓肿（KLA）是一种新兴的传染病。然而，除了 K1 特异性基因座以外，导致这种疾病的其他因素尚未确定。pLVPK 是肺炎克雷伯菌 CG43 的一个 219385bp 的质粒，CG43 是一种侵袭性 K2 株，与 KLA 有关。本研究旨在评估 pLVPK 在肺炎克雷伯菌毒力中的作用及其在脓肿形成中的临床意义。从 CG43 中分离出 pLVPK 缺失株，并在小鼠模型中检测其毒力。通过使用特异性引物筛选，研究了 207 株临床分离株中 pLVPK 衍生基因座 terW、iutA、rmpA、silS 和 repA 的流行情况。pLVPK 的缺失消除了肺炎克雷伯菌向肠道外部位传播的能力，从而减弱了小鼠脓肿的形成。原发性肺炎克雷伯菌脓肿分离株（n=94）比非脓肿感染相关分离株（n=113）更有可能为 terW（+）-iutA（+）-rmpA（+）-silS（+）（62% vs. 27%；p<0.0001）。logistic 回归分析表明，terW-rmpA-iutA-silS 基因座的存在是脓肿形成的一个显著危险因素（比值比，4.12；95%置信区间，2.02-8.4；p<0.0001）。pLVPK 是肺炎克雷伯菌毒力的决定因素，携带 pLVPK 衍生的 terW-rmpA-iutA-silS 基因座的菌株感染可能使患者易患脓肿形成。
