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Molecular Pathogenesis of Staphylococcus Aureus Infection

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Molecular Pathogenesis of Staphylococcus Aureus Infection 0031-3998/09/6505-0071R Vol. 65, No. 5, Pt 2, 2009 PEDIATRIC RESEARCH Printed in U.S.A. Copyright © 2009 International Pediatric Research Foundation, Inc. Molecular Pathogenesis of Staphylococcus aureus Infection GEORGE Y. LIU Division of Pediatric Infectious Diseases and the Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048; Department of Pediatrics, University of California, Los Angeles, California 90025 ABSTRACT: S. aureus has evolved a comprehensive strategy to open wound. More commonly, the human host is infected by address the challenges posed by the human immune system. The bacteria that colonize her or his skin or mucosal surface (7,8). emergence of community-associated methicillin-resistant S. aureus The mucosal surfaces that harbor S. aureus include the nose, (CA-MRSA) infections in individuals with no predisposing condi- throat, vaginal wall, and GI tract. Nasal carriage is probably tions suggests an increased pathogenicity of the bacterium, which most important because nose-picking could effectively dis- may be related to acquisition of novel genetic elements. Remarkably, seminate the bacterium to other body surfaces and other hosts despite an abundance of research, the underlying cause of the epi- demic is not known. Here, the various strategies used by S. aureus to (9). Remarkably, 20% of individuals are persistently colo- evade obstacles laid out by the human host during colonization and nized in the nose and 30% are transiently colonized. The infection were reviewed. The controversies surrounding MRSA re- definition of persistent and transient carriage varies according search were described, and how acquisition of the novel genes could to the study, but generally is described as a single positive explain the increased incidence and severity of CA-MRSA diseases culture on a nasal swab (transient) versus at least two consec- was described. (Pediatr Res 65: 71R–77R, 2009) utive positive cultures 1 wk apart (persistent). Colonization is also more frequent among younger children and patients with aureus has an extraordinary repertoire of virulence factors HIV and diabetes (4). S that allows it to survive extreme conditions within the Although colonization predisposes an individual to S. au- human host. Such an elaborate armamentarium might prompt reus infection, one study shows that after nosocomial infec- one to speculate that human kind would be no match for this tion, colonized individuals have less severe S. aureus disease pathogen and could be highly vulnerable to severe S. aureus compared with noncolonized individuals (7). This begs the infection. Surprisingly, S. aureus maintains fine control of question whether colonization could induce low-level adap- virulence expression, and for the most part, it rarely causes tive immunity so that subsequent infections become milder. In severe infection in previously healthy individuals. support of this view, a study showed that carriage of S. aureus The past 10 y however have witnessed the emergence of harboring the Toxic Shock Syndrome Toxin (TSST) is asso- new clones of MRSA that have rapidly spread across conti- ciated with production and maintenance of antibody to the nents, causing rampant skin and soft tissue infections and toxin (10). Conversely, most individuals who acquire Staph- some unusually severe diseases. Unlike traditional MRSA ylococcus toxic shock syndrome do not have antibody to clones which are largely confined to healthcare settings and TSST. prey on immunocompromised hosts or hosts with predispos- For S. aureus, colonization of the human nose presents a ing factors, these community-associated methicillin-resistant significant challenge that requires not only adherence to nasal S. aureus (CA-MRSA) clones infect previously healthy hosts, epithelial cells, but also an ability to cope with host defense particularly children, young and middle-aged adults. and competing resident microorganisms. S. aureus adheres This review is written with clinician scientists as the target and invades host epithelial cells using a variety of molecules audience. To impart a better appreciation of MRSA pathogen- that are collectively termed microbial surface components esis, I will first describe the obstacles that S. aureus needs to recognizing adhesive matrix molecules (MSCRAMM). A overcome to establish an infection and then highlight the number of bacterial products (including MSCRAMM) have aspects of pathogenesis that are unique to healthcare- been suggested to be important for adhesion and attachment to associated MRSA (HA-MRSA) and CA-MRSA. Readers are nasal epithelial cells, but two factors (clumping factor B and referred to many excellent reviews of S. aureus colonization wall-associated teichoic acid) have so far proven roles in nasal and pathogenesis (1–6) that describe more fully the mecha- colonization of humans and rats (11,12). nisms of virulence. Host immune deterrents for bacterial nasal colonization Colonization. S. aureus acquired from an external source include antimicrobial peptides, lysozyme, lactoferrin, and IgA could be the cause of an infection when inoculated into an Abbreviations: agr, accessory gene regulator; ACME, arginine catabolic Received November 4, 2008; accepted January 13, 2009. mobile element; CA-MRSA, community-associated methicillin-resistant S. Correspondence: George Y. Liu, M.D., Ph.D, Division of Pediatric Infectious Dis- aureus; HA-MRSA, healthcare-associated methicillin-resistant S. aureus; eases, Cedars-Sinai Medical Center, 8700 Beverly Blvd. NT4221, Los Angeles, CA MSSA, methicillin-sensitive S. aureus; PSM, phenol soluble modulin; PVL, 90048; e-mail: [email protected] G. Y. Liu is the recipient of a Burroughs-Wellcome Career Award and a National Panton-Valentine Leukocidin; ROS, reactive oxygen species; SCCmec, Institutes of Health grant AI074832. Staphylococcal cassette chromosome mec 71R 72R LIU (4). However, little is known of the critical host defenses on its surface a capsule, clumping factor A, protein A, and a against S. aureus colonization. A study in mice has identified number of complement inhibitors, all of which inactivate or the cystic fibrosis transmembrane conductance regulator and prevent host opsonins from binding or targeting the bacterium toll-like receptor 2, but not toll-like receptor 4 as important for destruction (3,6) (Fig. 1). factors controlling S. aureus carriage (13). S. aureus can shelter within epithelial cells, endothelial Resident nasal flora present an equally formidable chal- cells, and even macrophages (25). By contrast, neutrophils lenge for S. aureus. Studies of S. aureus carriers and noncar- present a more formidable challenge to S. aureus,asis riers have shown that presence of certain bacteria, such as evidenced by increased incidence of invasive S. aureus infec- corynebacterium, S.epidermidis,orS. pneumoniae, could pre- tions in patients with neutrophil dysfunctions (e.g., chronic clude carriage of S. aureus (14). Introduction of the S. pneu- granulomatous disease and leukocyte adhesion deficiency). S. moniae vaccine, for example, has been shown in some studies aureus deploys a number of strategies to resist neutrophil (15), but not others (16), to lead to a significant increase in S. killing. First, it secretes two molecules, chemotaxis inhibitory aureus colonization leading some to speculate that S. pneu- protein (CHIP) and extracellular adherence protein (Eap), moniae and S. aureus could compete for the same niche. The which respectively block neutrophil recognition of chemotac- general mechanism of niche competition is proposed to be a tic factors (26) and neutrophil binding to endothelial adhesion bacterial competition for adhesion to the same host receptor. molecule ICAM-1 (27). Inhibition of ICAM-1 binding pre- In addition, certain competitors such as S. pneumoniae secrete vents leukocyte adhesion, diapadesis, and extravasation from hydrogen peroxide, which at high concentration suppresses S. the bloodstream to the site of infection. aureus growth (17). S. aureus could counter by secreting Upon arriving at the infection site, neutrophils unleash a catalase and likely other antioxidants which neutralize hydro- battery of antimicrobial substances, including antimicrobial gen peroxide (18). peptides, reactive oxygen species (ROS), reactive nitrogen Once colonization is established, S. aureus is positioned in species, proteases, and lysozyme. Defense against ROS is close proximity to the throat, ears, mouth, and sinus; yet, mediated in S. aureus by deployment of a large number of surprisingly nasal carriage rarely leads to overt infection of antioxidant enzymes (e.g., catalase, pigment, superoxide dis- these sites. Studies of S. aureus regulation suggest that during mutase) that neutralize ROS and reactive nitrogen species (3). colonization, many S. aureus virulence genes may be down- Antimicrobial peptides which rely partly on targeting of neg- regulated (19). Among the genes that control S. aureus colo- atively charged bacteria are repelled by S. aureus strategies nization and virulence, the best known global regulator is the that alter its surface charges (28,29). Additionally, antimicro- accessory gene regulator agr, which has been described in bial peptides are degraded (aureolysin) (30) and neutralized details in many excellent reviews (19). Briefly, agr is a (staphylokinase) (31). quorum sensing locus, which directly controls expression of a As a preemptive measure, S. aureus counters by secreting number of virulence and colonizing factors.
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