Pathogenesis of Staphylococcus aureus
المؤلف:
Cornelissen, C. N., Harvey, R. A., & Fisher, B. D
المصدر:
Lippincott Illustrated Reviews Microbiology
الجزء والصفحة:
3rd edition , p70-71
2025-07-01
448
Virulence factors are the genetic, biochemical, or structural features that enable an organism to produce disease. The clinical outcome of an infection depends on the virulence of the pathogen and the opposing effectiveness of the host defense mechanisms. S. aureus expresses many potential virulence factors (Figure 1). [Note: Coagulase activity results in localized clotting, which restricts access by polymorphonuclear neutrophils (PMNs) and other immune defenses. This would make coagulase a virulence factor, even though mutants lacking the ability to make this factor remain virulent in animal models]. For the majority of diseases caused by S. aureus, pathogenesis depends on the combined actions of several virulence factors, so it is difficult to determine precisely the role of any given factor.
Fig1. Virulence factors that may play a role in the pathogenesis of staphylococcal infections. MHC = major histocompatibility complex; IL = interleukin; IFN = interferon; TNF = tumor necrosis factor; IgG = immunoglobulin G.
1. Cell wall virulence factors:
a. Capsule: Most clinical isolates express a polysaccharide “microcapsule” of Types 5 or 8. The capsule layer is very thin but has been associated with increased resistance to phagocytosis. Clinical isolates produce capsule but expression is rapidly lost upon in vitro cultivation.
b. Protein A: Protein Ais a major component of the S. aureus cell wall. It binds to the Fc region of IgG, exerting an anti-opsonin (and therefore strongly antiphagocytic) effect.
c. Fibronectin-binding protein: Fibrinectin-binding protein (FnBP) and other staphylococcal surface proteins promote binding to mucosal cells and tissue matrices.
d. Clumping factor: This FnBP enhances clumping of the organ isms in the presence of plasma.
2. Cytolytic exotoxins: α, β, γ, and δ Toxins attack mammalian cell (including red blood cell) membranes, and are often referred to as hemolysins. α Toxin is the best studied, and is chromosomally encoded. It polymerizes into tubes that pierce membranes, resulting in the loss of important molecules and, eventually, in osmotic lysis.
3. Panton-Valentine leukocidin: This pore-forming toxin lyses PMNs. Production of this toxin makes strains more virulent. This toxin is produced predominantly by community-acquired methicillin-resistant S. aureus (MRSA) strains .
4. Superantigen exotoxins: These toxins have an affinity for the T cell receptor–major histocompatibility complex Class II antigen complex. They stimulate enhanced T-lymphocyte response (as many as 20 percent of T cells respond, compared with 0.01 per cent responding to the usual processed antigens). This difference is a result of their ability to recognize a relatively conserved region of the T-cell receptor. This major T-cell activation can cause toxic shock syndrome, primarily by release into the circulation of inordinately large amounts of T-cell cytokines, such as interleukin-2 (IL 2), interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α).
a. Enterotoxins: Enterotoxins (six major antigenic types: A, B, C, D, E, and G) are produced by approximately half of all S. aureus isolates. When these bacteria contaminate food and are allowed to grow, they secrete enterotoxin, ingestion of which can cause food poisoning. [Note: The toxin stimulates the vomiting center in the brain by binding to neural receptors in the upper gastrointestinal (GI) tract.] Enterotoxins are super antigens that are even more heat-stable than S. aureus. Therefore, organisms are not always recovered from incriminated food but the toxin may be recovered.
b. Toxic shock syndrome toxin (TSST –1): This is the classic cause of toxic shock syndrome (TSS). Because of similarities in molecular structure, it is sometimes referred to as staphylococcal enterotoxin F, although it does not cause food poisoning when ingested.
c. Exfoliatin (exfoliative toxin, ET) is also a superantigen. It causes scalded skin syndrome in children. The toxin cleaves desmoglein 1, which is a component of desmosomes (cell structures specialized for cell-to-cell adhesion). Cleavage results in loss of the superficial skin layer.
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