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The morbidity and mortality of Staphylococcus aureus infections remain high despite antibiotic therapy. To investigate further the observation that penicillins increase the hemolytic activity of staphylococcal cultures, 37 strains were grown in broth with and without subinhibitory nafcillin. Nafcillin stimulated hemolytic activity in nafcillin-susceptible and -resistant isolates. Sterile broth filtrates of nafcillin-associated cultures injected intraperitoneally in mice were more rapidly lethal than filtrates of the same strain grown without nafcillin. Lethality was neutralized by anti-α-toxin antisera. DNA-RNA hybridization revealed a nafcillin-associated increase in α-toxin mRNA during the postexponential growth phase after the activation of agr. Isolates grown in slightly inhibitory nafcillin concentrations had more α-toxin mRNA than did nafcillin-free cultures, whereas agr RNAIII levels were comparable. This suggests that nafcillin-induced α-toxin production is not entirely attributable to agr. A supplemental regulatory mechanism may be involved. [ABSTRACT FROM PUBLISHER]

The increasing prevalence of methicillin-resistant Staphylococcus aureus as a wound pathogen in some institutions has prompted the use of vancomycin for surgical prophylaxis, although clinical data comparing vancomycin and cephalosporins are not available. A guinea pig model was used to compare the efficacy of vancomycin and cefazolin in preventing intermuscular abscess formation by 7 S. aureus strains. Both antibiotics were administered to achieve peak serum levels at the time of bacterial inoculation, and each remained > 1 micrograms/mL for a comparable duration. Vancomycin provided equivalent protection from infection by 1 methicillin-susceptible strain and significantly better protection against 4 methicillin-susceptible and both methicillin-resistant S. aureus strains. For most strains, the bacterial inoculum with a 50% probability of causing an abscess was 2 to 4 log10-fold higher with vancomycin than cefazolin prophylaxis. Prophylaxis with vancomycin is superior to cefazolin in preventing intermuscular infection by methicillin-susceptible and -resistant S. aureus. [ABSTRACT FROM AUTHOR]

Thirty Staphylococcus aureus isolates from five hospitals were determined to exhibit borderline susceptibility to the antistaphylococcal penicillins. Of the isolates submitted for phage typing, 9696 belonged to phage group 94/96, and 9696 possessed a common plasmid, pBW15. Also, four reference borderline-susceptible isolates from the Centers for Disease Control belonged to phage group 94/96 and possessed pBW15. Screening of 43 other phage group 94/96 isolates demonstrated that 36 (8496) contained pBW15 and exhibited the borderline phenotype. In contrast, pBW15 was not identified among 10 penicillin-susceptible, 10 methicillin-resistant, and 40 penicillin-resistantbut non-borderline-susceptible S. aureus. These datashow a close association between pBW15, phage group 94/96, and the borderline-susceptible phenotype. Furthermore, these isolates were associated with infections in multiple institutions, suggesting the widespread dissemination of a clinically important and pathogenic strain of S. aureus. [ABSTRACT FROM PUBLISHER]

Clinical trials in surgery suggest that some failures of antibiotic prophylaxis are related to the in vivo degradation of β-lactams by Staphylococcus aureus β-lactamase. To explore this issue further, isogeneic isolates of S. aureus differing only in whether they contained the structural gene for type A staphylococcal β-lactamase were constructed and compared for their ability to establish an abscess in a guinea pig model. With ampicillin prophylaxis, the ID50 was 870 cfu for the β-lactamase-negative isolate VK7114 and 240 cfu for the β-lactamase-producing isolate VK7115 (P < .001). Similarly, the ID50 was greater for the β-lactamase-negative isolate when cefazolin prophylaxis was administered (599 vs. 128 cfu, VK7114 and VK7115; P < .001). In the setting of prophylaxis with β-lactamase-susceptible antibiotics, β-lactamase contributes to the pathogenesis of S. aureus wound infections. [ABSTRACT FROM PUBLISHER]

The author reflects on a study related to macaque model to determine the role of SigH in controlling lung infections by the Mycobacterium tuberculosis (M. tuberculosis). He states that nonhuman primates have higher potential to show the host responses that prevent the Mycobacterium infections. An overview regarding the growing evidence of mycobacterium antioxidants in controlling lung immunopathology is discussed. The author suggests for tuberculosis vaccine construction based on this finding.