Staphylococcus aureus is responsible for a wide range of infections, including soft tissue infections and potentially fatal bacteremias. The primary niche for S. aureus in humans is the nares, and nasal carriage is a documented risk factor for staphylococcal infection. Previous studies with rodent models of nasal colonization have implicated capsule and teichoic acid as staphylococcal surface factors that promote colonization. In this study, a mouse model of nasal colonization was utilized to demonstrate that S. aureus mutants that lack clumping factor A, collagen binding protein, Staphylococcus aureus causes a diverse spectrum of severe infections in humans, including bacteremia, endocarditis, and osteomyelitis, as well as skin and soft tissue infections. Notorious for decades as a major source of nosocomial infections, S. aureus has recently taken on a new role in causing an escalating number of community-acquired infections. To offset the problems of antibiotic-resistant S. aureus strains, preventive measures (e.g., immunization) should be explored as a complement to existing therapeutic approaches aimed at controlling this bacterial pathogen.Humans are a reservoir for S. aureus, and the nose is the principal site of staphylococcal colonization. Approximately 20% of people persistently carry S. aureus in the anterior nares, ϳ60% are intermittent carriers, and ϳ20% are noncarriers (19). Nasal carriage is a known risk factor for staphylococcal infection in a number of clinical settings (51). Certain patient populations that show higher rates of S. aureus nasal colonization have an increased risk of staphylococcal infection. These populations include patients with diabetes, eczema, and human immunodeficiency virus infection, individuals receiving continuous ambulatory peritoneal dialysis or hemodialysis, and injection drug users (19). Moreover, patients in hospitals or individuals living in crowded conditions often show higherthan-normal rates of S. aureus nasal colonization. The source of ϳ80% of S. aureus bacteremias is endogenous since infecting bacteria have been shown by genotypic analysis to be identical to organisms recovered from the nasal mucosa (48, 53). These observations support an approach in which systemic S. aureus infections are prevented by eliminating or reducing nasal carriage.One approach commonly used to reduce S. aureus carriage in individuals at risk for staphylococcal infection involves topical treatment with a nasal ointment containing the antibiotic mupirocin. Eradication of nasal carriage with topical mupirocin has been correlated with a reduction in the incidence of S. aureus infection in some patient populations (20, 45), but not in others (40,54). Whereas mupirocin is effective in decolonizing nasal carriers, recolonization often occurs from extranasal carriage sites (52). Of further concern is the emergence of mupirocin resistance in S. aureus (31, 46). The utility of
؉ , and a reducing agent. Enzymatic activity was quantitated indirectly by measuring the increase in absorbance at 340 nm resulting from NADH formation. The product of the reaction was confirmed as UDP-ManNAcA by gas chromatography-mass spectroscopy. A cap5O mutation, created by deletion of 727 bp in the 5 end of the gene, was introduced by allelic replacement into S. aureus Reynolds, rendering it CP5 negative. Mice inoculated intravenously or subcutaneously with the wild-type strain Reynolds had greater numbers of S. aureus recovered from their kidneys (P ؍ 0.019) or their subcutaneous abscesses (P ؍ 0.0018), respectively, than did animals inoculated with the cap5O mutant. The results of this study indicate that S. aureus cap5O is essential for capsule production and that capsule promotes staphylococcal virulence in mouse models of abscess formation.
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