Article

Immune evasion by staphylococci.

Microbiology Department, Moyne Institute of Preventive Medicine, Trinity College, Dublin 2, Ireland.
Nature Reviews Microbiology (Impact Factor: 23.32). 01/2006; 3(12):948-58. DOI: 10.1038/nrmicro1289
Source: PubMed

ABSTRACT Staphylococcus aureus can cause superficial skin infections and, occasionally, deep-seated infections that entail spread through the blood stream. The organism expresses several factors that compromise the effectiveness of neutrophils and macrophages, the first line of defence against infection. S. aureus secretes proteins that inhibit complement activation and neutrophil chemotaxis or that lyse neutrophils, neutralizes antimicrobial defensin peptides, and its cell surface is modified to reduce their effectiveness. The organism can survive in phagosomes, express polysaccharides and proteins that inhibit opsonization by antibody and complement, and its cell wall is resistant to lysozyme. Furthermore, S. aureus expresses several types of superantigen that corrupt the normal humoral immune response, resulting in anergy and immunosuppression. In contrast, Staphylococcus epidermidis must rely primarily on cell-surface polymers and the ability to form a biolfilm to survive in the host.

3 Followers
 · 
131 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Microorganisms of different species interact in several ecological niches, even causing infection. During the infectious process, a biofilm of single or multispecies can develop. Aspergillus fumigatus and Staphyloccocus aureus are etiologic agents that can cause infectious keratitis. We analyzed in vitro single A. fumigatus and S. aureus, and mixed A. fumigatus-S. aureus biofilms. Both isolates were from patients with infectious keratitis. Structure of the biofilms was analyzed through microscopic techniques including scanning electron microscopy (SEM), transmission electron microscopy (TEM), confocal, and fluorescence microscopy (CLSM) in mixed biofilm as compared with the single A. fumigatus biofilm. To our knowledge, this is the first time that the structural characteristics of the mixed biofilm A. fumigatus-A. fumigatus were described and shown. S. aureus sharply inhibited the development of biofilm formed by A. fumigatus, regardless of the stage of biofilm formation and bacterial inoculum. Antibiosis effect of bacterium on fungus was as follows: scarce production of A. fumigatus biofilm; disorganized fungal structures; abortive hyphae; and limited hyphal growth; while conidia also were scarce, have modifications in their surface and presented lyses. Antagonist effect did not depend on bacterial concentration, which could probably be due to cell-cell contact interactions and release of bacterial products. In addition, we present images about the co-localization of polysaccharides (glucans, mannans, and chitin), and DNA that form the extracellular matrix (ECM). In contrast, single biofilms showed extremely organized structures: A. fumigatus showed abundant hyphal growth, hyphal anastomosis, and channels, as well as some conidia, and ECM. S. aureus showed microcolonies and cell-to-cell bridges and ECM. Herein we described the antibiosis relationship of S. aureus against A. fumigatus during in vitro biofilm formation, and report the composition of the ECM formed.
    BMC Microbiology 12/2015; 15(1). DOI:10.1186/s12866-015-0363-2 · 2.98 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Community-Acquired Methicillin-resistant S. aureus infections, generally occurring in previously healthy persons without recognizable risk factors for health care setting-related MRSA, are emerging as serious clinical and public health concerns. Community-Acquired Methicillin-resistant S. aureus, like all strains of S. aureus, is transmitted by direct contact with the organism. An overabundance of surface proteins and secreted virulence factors provide S. aureus with great potential to cause disease. Methicillin resistance is conferred by expression of the mecA gene, which encodes a modified penicillin-binding protein (PBP2a´hat has low affinity for β-lactam antibiotics and facilitates cell-wall synthesis in the presence of methicillin and other β-lactams. Geographically, there are two types of Community-Acquired Methicillin-resistant S. aureus: one (sequence type ST30) that is worldwide (pandemic) and the other (sequence types, ST1, ST8 or ST80) that is continent-specific. Panton-Valentine leukocidin (PVL) toxin, which is postulated to be at least partly responsible for the increased virulence of Community-Acquired Methicillin-resistant S. aureus compared to Health care Acquired Methicillin-resistant S. aureus. A latex agglutination test and nucleic acid amplification methods can be used to detect PBP2a and mecA gene. Incision and drainage continue to be the mainstay therapy for abscesses and furuncles. Patients with severe CA-MRSA infections require hospital admission and Vancomycin is still considered the first line treatment for severe infections. Standard infection control precautions should be used for all patients in outpatient and inpatient healthcare settings.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Complement is recognized as a key player in a wide range of normal as well as disease-related immune, developmental and homeostatic processes. Knowledge of complement components, structures, interactions, and cross-talk with other biological systems continues to grow and this leads to novel treatments for cancer, infectious, autoimmune- or age-related diseases as well as for preventing transplantation rejection. Antibodies are superbly suited to be developed into therapeutics with appropriate complement stimulatory or inhibitory activity. Here we review the design, development and future of antibody-based drugs that enhance or dampen the complement system. Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.

Preview

Download
1 Download
Available from