Mani N, Baddour L M, Offutt D Q, Vijaranakul U, Nadakavukaren M J, Jayaswal R K
Department of Biological Sciences, Illinois State University, Normal 61790-4120.
Infect Immun. 1994 Apr;62(4):1406-9. doi: 10.1128/iai.62.4.1406-1409.1994.
In an earlier report, we had described the isolation and characterization of autolysis-defective mutants of Staphylococcus aureus (N. Mani, P. Tobin, and R.K. Jayaswal, J. Bacteriol. 175:1493-1499, 1993). In the study reported here, an autolysis-defective mutant showed attenuated virulence in a rat model of experimental endocarditis, supporting the role of autolysins in pathogenicity. Transmission electron micrographs of the mutant cells revealed a rough outermost surface as compared with the parent strain, ISP2018. Treatment of mutant cells with lysozyme, proteases, and lipase failed to alter this rough appearance. Physical and genetic data locate the site of mutation between the omega 1100 and ilv loci on the S. aureus chromosome.
在一份较早的报告中,我们描述了金黄色葡萄球菌自溶缺陷型突变体的分离与特性鉴定(N. 马尼、P. 托宾和R.K. 贾亚斯瓦尔,《细菌学杂志》175:1493 - 1499,1993年)。在此报道的研究中,一个自溶缺陷型突变体在实验性心内膜炎大鼠模型中显示出毒力减弱,这支持了自溶素在致病性中的作用。与亲本菌株ISP2018相比,突变体细胞的透射电子显微镜图像显示其最外层表面粗糙。用溶菌酶、蛋白酶和脂肪酶处理突变体细胞未能改变这种粗糙外观。物理和遗传数据将突变位点定位在金黄色葡萄球菌染色体上的ω1100和ilv基因座之间。