Autolysis-defective mutant of Staphylococcus aureus: pathological considerations, genetic mapping, and electron microscopic studies

Abstract

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.

Evidence for autolysin‐mediated primary attachment of Staphylococcus epidermidis to a polystyrene surface

“…Therefore, some peptidoglycan hydrolases have been called autolysins. Autolysins have also been suggested to contribute to virulence of bacteria (Berry et al, 1989;Wuenscher et al, 1993;Mani et al, 1994). The P60 protein produced by Listeria monocytogenes, for instance, has bacteriolytic activity and is suggested to play an essential role in cell division (Wuenscher et al, 1993).…”

The autolysin Ami contributes to the adhesion of Listeria monocytogenes to eukaryotic cells via its cell wall anchor

“…This might result in the killing of inflammatory cells and major tissue damage. Autolysis-defective mutants of Staphylococcus aureus have attenuated virulence in models of endocarditis (Mani et al, 1994). The staphylococcal glucosaminidase alters the host immune response by inhibiting the response of human lymphocytes to mitogens and by interfering with the production of antibodies in mice (Valisena et al, 1991).…”

Identification of novel staphylococcal virulence genes by in vivo expression technology

“…S. aureus contains at least three autolytic enzymes, the biological roles of which are unclear. Mani et al (1994) showed that an S. aureus strain defective in autolysis is attenuated in an endocarditis model but conceded that the attenuation may be caused by compromised cellular integrity rather than by a specific virulence defect. If, like LytR in bacillus, the ivi102 gene product does repress transcription of the S. aureus atl gene, it would suggest that atl is downregulated in vivo and would argue against Mani et al's conclusion that autolysin impacts virulence.…”