Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, and Bethesda, Maryland, USA.
J Infect Dis. 2011 Sep 15;204(6):937-41. doi: 10.1093/infdis/jir441.
Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) infections are frequently associated with strains harboring genes encoding Panton-Valentine leukocidin (PVL). The role of PVL in the success of the epidemic CA-MRSA strain USA300 remains unknown. Here we developed a skin and soft tissue infection model in rabbits to test the hypothesis that PVL contributes to USA300 pathogenesis and compare it with well-established virulence determinants: alpha-hemolysin (Hla), phenol-soluble modulin-alpha peptides (PSMα), and accessory gene regulator (Agr). The data indicate that Hla, PSMα, and Agr contribute to the pathogenesis of USA300 skin infections in rabbits, whereas a role for PVL could not be detected.
社区获得性耐甲氧西林金黄色葡萄球菌（CA-MRSA）感染通常与携带编码杀白细胞素（PVL）的基因的菌株有关。PVL 在流行的 CA-MRSA 菌株 USA300 成功中的作用尚不清楚。在这里，我们开发了一种兔皮肤和软组织感染模型，以测试 PVL 是否有助于 USA300 发病机制的假设，并将其与既定的毒力决定因素进行比较：α-溶血素（Hla）、酚可溶性调节素-α 肽（PSMα）和辅助基因调节剂（Agr）。数据表明，Hla、PSMα 和 Agr 有助于兔 USA300 皮肤感染的发病机制，而 PVL 的作用则无法检测到。
