Abstract
Staphylococcus aureus colonizes the nose, throat, skin, and gastrointestinal (GI) tract of humans. GI carriage of S. aureus is difficult to eradicate and has been shown to facilitate the transmission of the bacterium among individuals. Although staphylococcal colonization of the GI tract is asymptomatic, it increases the likelihood of infection, particularly skin and soft tissue infections caused by USA300 isolates. We established a mouse model of persistent S. aureus GI colonization and characterized the impact of selected surface antigens on colonization. In competition experiments, an acapsular mutant colonized better than the parental strain Newman, whereas mutants defective in sortase A and clumping factor A showed impaired ability to colonize the GI tract. Mutants lacking protein A, clumping factor B, poly-N-acetyl glucosamine, or SdrCDE showed no defect in colonization. An S. aureus wall teichoic acid (WTA) mutant (ΔtagO) failed to colonize the mouse nose or GI tract, and the tagO and clfA mutants showed reduced adherence in vitro to intestinal epithelial cells. The tagO mutant was recovered in lower numbers than the wild type strain in the murine stomach and duodenum 1 h after inoculation. This reduced fitness correlated with the in vitro susceptibility of the tagO mutant to bile salts, proteases, and a gut-associated defensin. Newman ΔtagO showed enhanced susceptibility to autolysis, and an autolysin (atl) tagO double mutant abrogated this phenotype. However, the atl tagO mutant did not survive better in the mouse GI tract than the tagO mutant. Our results indicate that the failure of the tagO mutant to colonize the GI tract correlates with its poor adherence and susceptibility to bactericidal factors within the mouse gut, but not to enhanced activity of its major autolysin.
Highlights
Staphylococcus aureus is a bacterial pathogen that commonly colonizes the nose, skin, and mucosal surfaces of healthy individuals
We developed a murine model of S. aureus GI colonization to investigate bacterial factors that promote staphylococcal colonization of the gut
We identified several surface-associated S. aureus antigens that modulate colonization of the GI tract and identified a surface glycopolymer as critical for the early steps in colonization
Summary
Staphylococcus aureus is a bacterial pathogen that commonly colonizes the nose, skin, and mucosal surfaces of healthy individuals. S. aureus may cause a variety of superficial and invasive infections in hospitalized patients, as well as in individuals within the community who lack the risk factors commonly associated with nosocomial infections [1,2]. The anterior nares are the most common anatomic site of S. aureus carriage, ~20% of adults are positive for intestinal carriage of S. aureus [3]. Nasal carriage apparently predisposes the host to intestinal carriage, ~37% of intestinal carriers are not positive for S. aureus nasal colonization [3]. Compared to nasal colonization only, simultaneous nasal and intestinal colonization was associated with a significant increase in the frequency of positive skin cultures [7]. Squier et al [8] observed that critically ill patients who had both rectal and nasal carriage were significantly more likely to develop staphylococcal infection (40% infection rate) than those with nasal carriage only (18% infection rate)
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