Bacteriological characteristics of Staphylococcus aureus isolates from humans and bulk milk.

The aim of this study was to clarify the epidemiological association and bacteriological characteristics of human and animal Staphylococcus aureus isolates. Pulsed-field gel electrophoresis showed that pulsotypes (PT) of isolates from bulk milk differed from PT from human isolates, suggesting that there is no epidemiological association between isolates from these 2 sources. The absence of a common PT could result from the lack of contact between the sources. Methicillin-resistant S. aureus from human secretions and S. aureus from bulk milk in Japan consisted of 1 and 2 dominant clusters, respectively, whereas methicillin-susceptible S. aureus from humans consisted of assorted clusters. Isolates belonging to the dominant clusters showed the coagulase serotype, the capsule serotype, detection of exotoxin genes, and antimicrobial susceptibility. Isolates from bulk milk did not show the penicillin-binding protein 2a gene, and 252 of 275 isolates belonging to the 2 dominant clusters of bulk milk were susceptible to ampicillin, cefazolin, erythromycin, chloramphenicol, oxacillin, and vancomycin. Moreover, the LukM/LukF'-PV leukotoxin gene was detected in 233 of 275 isolates belonging to the dominant clusters in bulk milk isolates. These results support the hypothesis that a number of factors play a role in the adaptation of S. aureus isolates to specific hosts.

Overexpression of sigma factor, sigma(B), urges Staphylococcus aureus to thicken the cell wall and to resist beta-lactams.

Whole genome sequence analysis revealed that Staphylococcus aureus is provided with only a few sigma factors, including the alternative sigma factor, sigma(B), which is thought to regulate some stress responses. Since the sigB knock-out mutant did not show remarkable phenotypic difference, we constructed the over expressed mutant to examine the role of the sigB. Electron microscopic observation revealed that the mutant showed a variety of cell sizes compared with the parent strain which showed almost homogeneous cell sizes. The mutant delivered a thicker cell wall, about 20% thicker than the parent strain. It became resistant to the lytic activity of lysostaphin and also raised MICs to the cell-wall-affecting antibiotics. The yield of carotenoids and transcripts of pbps were also increased in the mutant. The result suggests that sigB plays some important roles in cell wall synthesis and in resistance to antibiotics that perturb the cell wall synthesis.