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Skin infections with the Gram-positive bacteria Staphylococcus aureus and group A streptococcus (Streptococcus pyogenes) are an important source of morbidity and even mortality. These bacteria produce toxins that can induce characteristic syndromes, including staphylococcal scalded-skin syndrome (SSSS) and toxic shock syndrome (TSS). Moreover, the production of these toxins is thought to underlie the ability of infection with these bacteria to initiate and/or to propagate inflammatory skin diseases.
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All conditions discussed here are relatively rare but have high morbidity, and some have considerable mortality.
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Staphylococcal and streptococcal pathogenicity is due to the production of a range of immunomodulatory proteins including toxins, exoenzymes, and adhesins.1 Among the best characterized are the toxins (Table 177-1).
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Many risk factors play a role in the ability of a toxin-forming Staphylococcus or Streptococcus to produce disease. The development of disease is related to the resistance of the host to infection and to the virulence of the organism. Host resistance depends, among other factors, on intact skin and mucous membranes functioning as barriers to invasion and the host's ability to mount an immune response (e.g., neutralizing antibodies) against such toxins. Colonization by virulent Staphylococcus or Streptococcus toxin-producing organisms exposed to optimal, focal conditions for growth and toxin production (e.g., menstruation + tampon use or abscess) allows these bacteria to initiate and/or propagate infection.
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Minor defects in these barriers such as those produced by superficial excoriations, toe web fungal infections or alternatively, major defects produced by surgery, trauma, burns, or foreign substances (packing, sutures, intravascular catheters, shunts) increase the risk of infection. The role of host response cannot be overstated. For example, if a patient has an underlying immunodeficiency and cannot produce adequate neutralizing antibodies; or, as in chronic granulomatous disease where neutrophils lack the oxidative burst to destroy catalase-positive bacteria (e.g., S. aureus...