Opportunistic pathogen

form a fibrin barrier around localized infectious foci. This is mediated by production of one enzyme, coag-ulase, and by three specific surface-exposed proteins which bind fibrinogen, thereby inducing polymerization of fibrinogen to fibrin.


At least four different extracellular proteins have been described which lyse erythrocytes and are cytotoxic to a number of other cells. Human strains of S. aureus commonly produce a-lysin whereas strains isolated from bovine and other animals produce (3-lysin. The S-lysin has a broad cell specificity with amphipathic properties (detergent-like).


Although a-lysin is toxic to leukocytes, S. aureus strains also produce a separate toxin, the two Pan-ton-Valentine factors, exerting synergistic toxic activity to human leukocytes.


These belong to a family of proteins of which five immunologically distinct toxins, staphylococcal enterotoxins (SE) A-E, are recognized. They cause staphylococcal food poisoning, presenting with vomiting and diarrhea (Table 2). These toxins differ substantially from enterotoxins of gram-negative pathogens, such as Vibrio cholerae and Escherichia coli which bind to a specific receptor on intestinal cells. Instead, staphylococcal enterotoxins have been suggested to bind to neurons in the gastrointestinal tract, and may act as neurotoxins. They are also immuno-modulating toxins, like TSST (see below).

Toxic shock syndrome (TSS)

In the early 1980s this syndrome of fever, hypotension, a skin rash with subsequent desquamation, and symptoms from at least three organ systems was defined. It was initially related to tampon usage in young women, but since then TSS has been described in postoperative wounds and burns. One toxin, TSST-1 has been identified but also SEB and SEC can be involved (Table 2). TSST-1 has structural similarity with enterotoxins and with pyrogenic streptococcal toxins. It acts as a superantigen, like the enterotoxins, has mitogenic properties, and induces production of specific cytokines such as tumor necrosis factor.

Staphylococcal scalded skin syndrome (SSSS)

This syndrome is an uncommon cause of epidermolysis, painful desquamation of the skin surface, mainly in infants. It is caused by phage group II strains of S. aureus which produce toxin A and/ or B (synonyms: epidermolytic toxin, exfoliatin) (Table 2).

Extracellular enzymes

Staphylococcal strains can produce a range of enzymes, such as proteases, various nucleases and lipase which may act as spreading factors. One other enzyme, staphylokinase, activates plasminogen in a similar way to urokinase and a streptococcal kinase, forming plasmin, a potent proteolytic substance. Staphylokinase has a broad host specificity and acts also on plasmin from a number of animal species. It is produced only by S. aureus strains, and acts as a spreading factor by breaking down the fibrin barrier and blood clots.

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