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Given the ability of S. There has been significant effort put forth in recent years to develop a vaccine designed to protect against S. Consistent with those findings, work in mouse infection models has demonstrated that antibodies directed against Hla, Coa, and vWbp protect against severe S. Collectively, these studies suggest that it should be possible to use a vaccine or similar eg, receptor blocking approach for treatment, moderation, or prevention of severe SSTIs. Although significant progress has been made eg, use of incision and drainage as a treatment approach , more work is needed in this general area to develop therapies that are not dependent on antibiotics.

This article is part of a review series on infectious disease. National Center for Biotechnology Information , U. Journal List Am J Pathol v. Kobayashi , Natalia Malachowa , and Frank R. Accepted Nov This article has been cited by other articles in PMC. Abstract Staphylococcus aureus causes many types of human infections and syndromes—most notably skin and soft tissue infections.

Open in a separate window. Innate Host Defense against S. Molecules Produced by S.


Coagulases Although the contribution of Hla to S. Treatment and Future Perspective Staphylococcus aureus is a human commensal microbe and has been a cause of infections throughout recorded history. Acknowledgments We thank Dr. Notes Infectious Disease Theme Issue. Changes in the prevalence of nasal colonization with Staphylococcus aureus in the United States, The role of nasal carriage in Staphylococcus aureus infections.

N Engl J Med. The changing epidemiology of bacteraemias in Europe: Laboratory-based surveillance of current antimicrobial resistance patterns and trends among Staphylococcus aureus: Ann Clin Microbiol Antimicrob. Community-associated meticillin-resistant Staphylococcus aureus. Epidemiology of Staphylococcus aureus blood and skin and soft tissue infections in the US military health system, Pulsed-field gel electrophoresis typing of oxacillin-resistant Staphylococcus aureus isolates from the United States: A clone of methicillin-resistant Staphylococcus aureus among professional football players.

Presence of genes encoding the panton-valentine leukocidin exotoxin is not the primary determinant of outcome in patients with complicated skin and skin structure infections due to methicillin-resistant Staphylococcus aureus: Classics in infectious diseases: Alexander Ogston Rev Infect Dis.

Microbiology of skin and soft tissue infections in the age of community-acquired methicillin-resistant Staphylococcus aureus. Diagn Microbiol Infect Dis. Comparative analysis of USA virulence determinants in a rabbit model of skin and soft tissue infection. Targeting of alpha-hemolysin by active or passive immunization decreases severity of USA skin infection in a mouse model. Genetic requirements for Staphylococcus aureus abscess formation and persistence in host tissues.

IL-1 and TNF-alpha play a pivotal role in the host immune response in a mouse model of Staphylococcus aureus-induced experimental brain abscess. J Neuropathol Exp Neurol. Innate and adaptive immune responses against Staphylococcus aureus skin infections. Keratinocyte production of cathelicidin provides direct activity against bacterial skin pathogens.

A peptide antibiotic from human skin. Robbins and Cotran Pathologic Basis of Disease. Neutrophil recruitment and function in health and inflammation. Immunity against Staphylococcus aureus cutaneous infections. Staphylococcus aureus stimulates neutrophil targeting chemokine expression in keratinocytes through an autocrine IL-1alpha signaling loop.

Neutrophil-derived IL-1beta is sufficient for abscess formation in immunity against Staphylococcus aureus in mice. Recurrent staphylococcal cellulitis and subcutaneous abscesses in a child with autoantibodies against IL Effects of Staphylococcus aureus leukocidins on inflammatory mediator release from human granulocytes.

IL is essential for host defense against cutaneous Staphylococcus aureus infection in mice. Epicutaneous model of community-acquired Staphylococcus aureus skin infections. Molecular explanation for the contradiction between systemic Th17 defect and localized bacterial infection in hyper-IgE syndrome. Perivascular macrophages mediate neutrophil recruitment during bacterial skin infection. Structure and regulation of the neutrophil respiratory burst oxidase: How human neutrophils kill and degrade microbes: Control of exocytosis in early neutrophil activation. NADPH oxidase activation and assembly during phagocytosis.

Neutrophils in innate host defense against Staphylococcus aureus infections. Neutrophil chemotaxis by pathogen-associated molecular patterns—formylated peptides are crucial but not the sole neutrophil attractants produced by Staphylococcus aureus. The crystal structure of staphylococcal superantigen-like protein 11 in complex with sialyl Lewis X reveals the mechanism for cell binding and immune inhibition.

Staphylococcus aureus extracellular adherence protein serves as anti-inflammatory factor by inhibiting the recruitment of host leukocytes. Immune evasion by a staphylococcal complement inhibitor that acts on C3 convertases.

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Chemotaxis inhibitory protein of Staphylococcus aureus, a bacterial antiinflammatory agent. A new staphylococcal anti-inflammatory protein that antagonizes the formyl peptide receptor-like 1. Antiphagocytic effects of staphylococcal protein A. Interactions with other bacteria. The majority of the interactions between S.

Cooperative interactions involving S.


Pathogenesis of Staphylococcus aureus Abscesses

Competitive interactions are observed between S. That the interactions are competitive does not mean that these organisms completely inhibit the colonization of S. Cooperative or competitive interactions lead to the development of more-persistent S. The interactions of S. The hemolysis of erythrocytes by S. However, Pettigrew et al. Both of those studies were designed to determine the microflora composition among children in the age group between 6 and 36 months.

The relation between S. They have common niches within the host, for example, the lungs of cystic fibrosis CF patients, peritoneum of dialysis patients, catheters, diabetic foot wounds, and other type of wounds caused by skin injury or skin burn 44 , Although coinfections of these pathogens are very common under in vivo conditions, several independent in vitro studies demonstrated that, when cocultured together, P.

The better survival of P. Despite its sensitivity to respiratory inhibitors, S. To counter the effect of the respiratory toxins produced by P. These SCVs are auxotrophic to hemin or menadione and are resistant to antibiotics, especially aminoglycosides, trimethoprim-sulfamethoxazol 60 , and the host antimicrobial peptide lactoferricin B 8. The resistance of SCVs is due in part to their severely decreased membrane potential as well as their reduced growth rate and metabolic processes.

These SCVs also persist better than their normal counterparts. LasA cleaves the glycyl-glycine and glycyl-alanine bonds of the pentaglycine interpeptide bridge in the S. Using the rat model of infection, Mashburn et al. However, this result is yet to be validated in clinical settings. Various studies have shown that colonization of the upper airway by S. This inverse relation suggests that one organism interferes with the colonization of the other. In vitro data demonstrate that hydrogen peroxide H 2 O 2 , a byproduct of aerobic metabolism produced by S. The SOS response induces the resident prophages, resulting in the lysis of lysogenic staphylococci.

Because the vast majority of S. H 2 O 2 , at concentrations typically produced by pneumococci, kills lysogenic but not nonlysogenic staphylococci It is interesting that S. A possible explanation could be that the amounts of free radical scavengers that S. However, other studies have offered hypotheses suggesting that the production of hydrogen peroxide may not be the main reason for the antagonistic relationship between these pathogens in vivo Although both pathogens colonize the upper respiratory tract, their microniches are different.

Therefore, direct antagonism mediated by H 2 O 2 is an unlikely reason for their antagonism. Rather, the antibody response generated during S. The lactic acid bacteria LAB consist of a group of heterogeneous bacterial species comprising nonsporulating, Gram-positive cocci and bacilli that are able to ferment sugars predominantly into lactic acid. This leads to acidification of the environment down to a pH of 3. LAB colonize the gut and urogenital tract and contribute to defense against S. The antistaphylococcal activity of LAB strains is attributed to the production of H 2 O 2 , organic acids, antimicrobial proteins, biosurfactants, surface proteins, and quorum-sensing inhibitors.

The most commonly studied members of intestinal and vaginal LAB include Lactobacillus acidophilus , L. In similarity to the results seen with S. Additionally, LAB secrete organic acids lactic, acetic, formic, caproic, propionic, butyric, and valeric acids that inhibit the growth of S. LAB-produced bacteriocins interfere with cell wall structure and biosynthesis and form pores in the S. Among the bacteriocins produced by LAB, the most important are nisin, produced by Lactococcus lactis ; pediocin, produced by Pediococcus acidilactici ; and lacticin , produced by Lactococcus lactis DPC 79 , Apart from inhibiting the growth of S.

Biosurfactants and surface proteins of LAB strains are involved in this competitive exclusion process. Some LAB strains were also shown to displace previously adhered S.

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In a recent study, it was also shown that the small signaling molecule cyclic dipeptides cyclo l -Tyr-LPro and cyclo l -Phe- l -Pro , produced by the human vaginal isolate L. To counter the detrimental effects of LAB species, S. Both organisms are associated with catheter-related infections. A lower incidence of S. No bacteriocin-like activity of Corynebacterium sp. However, a number of bacteriocins secreted by S.

These bacteriocins include Bac 17 , aureocin A70 29 , aureocin A53 82 and staphylococcin Besides these interactions, S. Several reports indicate antagonistic relationships between S.

The presence of S. The production of virulence factors and other extracellular proteins in staphylococci is globally regulated by the accessory gene regulatory system agr. The AIPs can activate the agr response in the other members of the same group but show mutually inhibitory effects between members of different groups. Based on the agr loci present, S. The anterior nares are generally considered to be the primary site of colonization of S.

Apart from the intestinal tract, E. The interaction between E. Many studies have focused on the mechanisms by which S. The transposon Tn harboring the vanA gene present on the pAM plasmid is related to the Inc18 family of broad-host-range conjugative plasmids and is responsive to the cAM pheromone secreted by the plasmid-free recipient strains of E. This conjugation results in the transfer of the vanA gene from E.

Genetic analysis of several vancomycin-resistant S. The acquisition of vanA by S. Interactions between these two bacteria have led to an increase in the numbers of multidrug-resistant staphylococci. Most infections are polymicrobial in nature and can be seen in almost every niche in the human body, particularly in mucosal surfaces, where different species of microorganisms such as bacteria, fungi, and viruses coexist as communities.

In polymicrobial infections, S. The altered immune response during polymicrobial infections could be beneficial or detrimental for S. For example, influenza virus infection inhibits Th 17 -mediated adaptive immune responses Activated Th17 cells are necessary for protection against S. Therefore, Th 17 cell-mediated immune activation is necessary to limit S.

By inhibiting the Th 17 cell-mediated immune response and subsequent neutrophil infiltration, influenza virus helps S.

In contrast to the immune suppression mediated by influenza virus that aids S. The antibody response generated during S. This bacterium forms electron transport-deficient small-colony variants during coinfection with P. These SCVs persist better than their normal counterparts and are resistant to aminoglycosides and trimethoprim-sulfamethoxazols A valent polysaccharide vaccine against S.

Therefore, prevention of one pathogenic infection provides opportunities to the competing pathogens to cause disease. These findings highlight the potential complications that could arise from conventional treatment and disease prevention strategies that target a single organism, thereby necessitating the need to introduce modified therapeutic approaches that take into account the coinfecting organisms. Several strategies could be used to address the difficulties in treatment of polymicrobial infections of S. One could be the use of combined vaccines against two or more coinfecting microbes; however, such vaccines are still in the experimental stages.

The next approach could be the judicious use of antimicrobial drugs. IS has only been found to influence teicoplanin resistance in S. It has also been shown that a mutation in the ica genes of a clinical S. The pathogenic mechanism of S. Because a considerable part of the toxin genes are located in SaPIs and prophages, phage dynamics are of apparent importance for the pathogenesis of S. Assays of consecutive isolates have revealed that commensal strains possess a very low transformation rate and evolved slowly over time; in contrast, phages are remarkably active within pathogenic strains and the genome plasticity of pathogenic strains is evidently elevated Goerke, Toxin genes do not accumulate within the chromosome without limit because MGEs can often exclude each other.

Although free transfer of MGEs is not allowed across lineages, it is allowed within the same sequence type. The TW strain has accumulated all detectable MGEs that were variably expressed by other epidemic ST strains in the United Kingdom, and developed an enhanced ability to cause bloodstream infection Edgeworth, The actual pathogenesis of phages in S.

Analysis of the sequence of the integrase gene demonstrated no difference between typical and atypical sak -encoding prophages. Thus, the integrase allows illegal integration, which contradicts the classical view that the integrase specifically recognizes the chromosome attB site. The knowledge of the type I RM system in S. The extent of how the type II RM systems restrict gene flow is also unclear. Phage K is a large, virulent bacteriophage that infects a broad range of staphylococci, including multiple-drug-resistant strains of S.

A remarkable paucity of the sau3A1 restriction site GATC is thought to be an efficient mechanism that phage K developed to avoid host restriction-modification systems O'Flaherty, In contrast, vanA -encoding Tn and the PVL locus have an abundance of sau3A1 restriction sites, which may be the basis for the two elements residing in only a small proportion of strains.

While these sequence properties support the role of the type II RM system in restricting gene flow, the contradicting phenomenon in Helicobacter pylori forces one to abandon the notion. A number of virulence genes have been identified in the S. Many of the previous epidemiologic studies have focused on the presence or absence of a given genetic determinant.

Regrettably, this type of research cannot explain the phenomenon that toxic shock syndrome cases are rare, while c. A direct comparison of S.

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  5. Thus, commensal and pathogenic strains are not two distinct types of organisms, but the same organism in different states. Thus, a global change of expression pattern is expected. Voyich found that under in vitro growth conditions, the highly expressed genes involved in transcription and protein biosynthesis, maturation, and folding typically dominate bacterial gene expression; when phagocytized by neutrophils, the overall functional profile of highly expressed genes would shift to pathogenicity-related genes, such as those involved in virulence, metabolism, capsule synthesis, and gene regulation.

    Phage dynamics also cause conversion between commensalism and pathogenicity, as discussed above. It should be noted that virulence factors in phages do not express their pathogenic roles independently. A recent study has shown that the expression of PVL leukotoxin induced global changes in transcriptional levels of genes encoding secreted- and cell wall-anchored staphylococcal proteins that are located in the core chromosome Labandeira-Rey, SarA also regulates several cell wall-associated proteins and exoproteins directly in an agr -independent way Chien, Most of these studies on agr regulation were performed under in vitro conditions.

    When it comes to in vivo conditions i. Furthermore, cell intensity may be an important source that gives S. When in the laboratory, S. Staphylococcus aureus more often grows in biofilm form during an infection because a biofilm can help it withstand stronger host defense responses and antibiotic stress.

    By microarray analysis, it is known that the processes involved in cell wall synthesis and other distinct physiologic activities of the cell play a crucial role in biofilm persistence Resch, What the exact role of agr in the actual pathogenic process is still unknown and there are many other phenomena that cannot be explained by the current knowledge. Given the enormous difficulty of deciphering the complicated network of virulence genes, a compromising approach would be to find an association between lineage and disease.

    Theoretically, strains from the same lineage have the same core variable genes and share the common pool of SaPIs and phages for genetic exchange. Therefore, they would potentially infect the same population of people and cause the same type of disease. However, it would be impertinent to conclude that all strains are equally virulent. Even though each lineage may have a specific set of core variable genes, especially adhesin genes, which could determine the power of adhering to epithelial cells of certain populations and decide the potential group of the host population, many other prerequisites, such as fast growth rate and strong survival ability, work together to determine whether a clone would develop into a successful pathogen.

    Indeed, some lineages deserve careful surveillance based on epidemiologic investigations. For example, CC1 has emerged as the leading lineage that has a strong association with community-acquired diseases. During the last two decades, staphylococci have shown a trend of increasing virulence. CoNS have generally been regarded as saprophytes or organisms with no or very low virulence. However, there has been an increase in the documentation of human infections due to CoNS, especially with S.

    With respect to S. This early MSSA clone waned in the s when methicillin was introduced into clinical use. However, it did not really disappear, but probably took refuge, in healthy people as a commensal strain. On the one hand, nosocomial colonization with MRSA usually goes undetected and may lead to infection many months after hospital discharge when the patient is in the community. A general definition now is that C-MRSA strains should be isolated in an outpatient setting or from patients within 48 h of hospital admission; such patients must have no history of MRSA infection and no history in the previous year of either admission to a nursing home, hospitalization, dialysis, or surgery.

    This high growth rate may be a prerequisite for C-MRSA to achieve successful colonization in humans by outcompeting the numerous bacterial species in the environment. Clinically, PVL is associated with skin abscesses and necrotizing pneumonitis Lina, ; Gillet, They both belong to CC30 and share very similar genetic backgrounds. USA strain was epidemic in community populations during — Binswanger, Although the short SCC mec and PVL locus are important for C-MRSA based on results of epidemiologic analyses, no studies have proven their exact biologic roles in the pathogenesis of community-acquired infections.

    Moreover, there has been research suggesting that the PVL locus is not the major determinant of C-MRSA because the PVL-negative and -positive strains performed similarly during neutrophil lysis Said-Salim, and were equally lethal in a sepsis model Voyich, Because the mechanism of C-MRSA infection is poorly understood, the genomics approach has been applied in some studies. Genetic exchanges inside S. A scarcity of recombination contributes to the highly clonal structure of S. A better understanding of the underlying mechanism of genetic exchange would help one to reconstruct the history of lineage formation and to make some interesting predictions, for example, whether those dangerous determinants, such as vanA and the PVL locus, would disseminate to a larger extent or whether the barriers to gene flow would make clonal complexes evolve to become a new biological species.

    Given the fact that C-MRSA and H-MRSA can be isolated within the same lineage, it is likely that the difference of virulence gene expression has differentiated the two types of organisms. Likewise, commensal and pathogenic strains are the same organism of two different states rather than two different types of organisms. Conversion from commensal to pathogen must also be achieved by a shift of the global expression profile. The suspicion therefore arises as to whether their roles in pathogenesis are overestimated.

    Thus, a future challenge for researchers is to investigate the interaction between regulators and the virulence genes in the pathogenesis of S. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.

    Sign In or Create an Account. Close mobile search navigation Article navigation. Evolution of the core genome. Evolution of the accessory genome. Evolution and pathogenesis of Staphylococcus aureus: Abstract Staphylococcus aureus is an opportunistic pathogen and the major causative agent of numerous hospital- and community-acquired infections. View large Download slide. Intercontinental spread of a multidrug-resistant methicillin-resistant Staphylococcus aureus clone. Carriage patterns of Staphylococcus aureus in a healthy non-hospital population of adults and children.

    The progressive intercontinental spread of methicillin-resistant Staphylococcus aureus. Genome and virulence determinants of high virulence community-acquired MRSA. Prophages of Staphylococcus aureus Newman and their contribution to virulence. Global gene expression in Staphylococcus aureus biofilms. High prevalence of abscesses and cellulitis among community-recruited injection drug users in San Francisco. Global analysis of community-associated methicillin-resistant Staphylococcus aureus exoproteins reveals molecules produced in vitro and during infection.

    The changing epidemiology of Staphylococcus aureus? Increased amounts of a novel penicillin-binding protein in a strain of methicillin-resistant Staphylococcus aureus exposed to nafcillin. Infection with vancomycin-resistant Staphylococcus aureus containing the vanA resistance gene. Molecular interactions between two global regulators, sar and agr , in Staphylococcus aureus. SarA, a global regulator of virulence determinants in Staphylococcus aureus , binds to a conserved motif essential for sar -dependent gene regulation.

    DNA microarray-based identification of genes associated with glycopeptide resistance in Staphylococcus aureus. An outbreak in an intensive care unit of a strain of methicillin-resistant Staphylococcus aureus sequence type associated with an increased rate of vascular access device-related bacteremia. Multilocus sequence typing for characterization of methicillin-resistant and methicillin-susceptible clones of Staphylococcus aureus.

    How clonal is Staphylococcus aureus? Evolutionary genomics of Staphylococcus aureus. Genome diversification in Staphylococcus aureus. Surface protein adhesins of Staphylococcus aureus.


    Association between Staphylococcus aureus strains carrying gene for Panton-Valentine leukocidin and highly lethal necrotising pneumonia in young immunocompetent patients. Direct quantitative transcript analysis of the agr regulon of Staphylococcus aureus during human infection in comparison to the expression profile in vitro.

    Impact of the regulatory loci agr , sarA and sae of Staphylococcus aureus on the induction of alpha-toxin during device-related infection resolved by direct quantitative transcript analysis. Increased frequency of genomic alterations in Staphylococcus aureus during chronic infection is in part due to phage mobilization. Extensive phage dynamics in Staphylococcus aureus contributes to adaptation to the human host during infection.

    Local variants of Staphylococcal cassette chromosome mec in sporadic methicillin-resistant Staphylococcus aureus and methicillin-resistant coagulase-negative Staphylococci. Staphylococcus aureus agr and sarA functions are required for invasive infection but not inflammatory responses in the lung. The emergence and evolution of methicillin-resistant Staphylococcus aureus. Complete genomes of two clinical Staphylococcus aureus strains.