■ Leukocidin damages microphages and macrophages by degranulation.
■ Exfoliatins are responsible for a form of epidermolysis.
■ Food poisoning symptoms can be caused by eight serologically differentiated enterotoxins (A-E, H, G, and I). These proteins (MW: 35 kDa) are not inactivated by heating to 100 °C for 15-30 minutes. Staphylococcus enterotoxins are superantigens (see p. 72).
■ Toxic shock syndrome toxin-1 (TSST-1) is produced by about 1% of Staphylococcus strains. TSST-1 is a superantigen that induces clonal expansion of many T lymphocyte types (about 10%), leading to massive production of cytokines, which then give rise to the clinical symptoms of toxic shock.
Pathogenesis and clinical pictures. The pathogenesis and symptoms of S. aureus infections take one of three distinct courses:
■ Invasive infections. In this type of infection, the pathogens tend to remain in situ after penetrating through the derma or mucosa and to cause local infections characterized by purulence. Examples include furuncles (Fig. 4.2), carbuncles, wound infections, sinusitis, otitis media, and mastitis puerperalis.
Other kinds of invasive infection include postoperative or posttraumatic os-titis/osteomyelitis, endocarditis following heart surgery (especially valve replacement), postinfluenza pneumonia, and sepsis in immunocompromised patients. S. aureus and E. coli are responsible for approximately equal shares of nearly half of all cases of inpatient sepsis.
Inert foreign bodies (see p. 158 for examples) can be colonized by S. aureus. Colonization begins with specific binding of the staphylococci, by means of cell wall-associated adhesion proteins, to fibrinogen or fibronectin covering the foreign body, resulting in a biofilm that may function as a focus of infection.
— Multiple Furuncles -
— Multiple Furuncles -
■ Toxicoses. Food poisoning results from ingestion of food contaminated with enterotoxins. The onset a few hours after ingestion takes the form of nausea, vomiting, and massive diarrhea.
■ Mixed forms. Dermatitis exfoliativa (staphylococcal scalded skin syndrome, Ritter disease), pemphigus neonatorum, and bullous impetigo are caused by exfoliatin-producing strains that infect the skin surface. Toxic shock syndrome (TSS) is caused by strains that produce TSST-1. These strains can cause invasive infections, but may also only colonize mucosa. The main symptoms are hypotension, fever, and a scarlatiniform rash.
Diagnosis. This requires microscopic and culture-based pathogen identification. Differentiating S. aureus from the coagulase-negative species is achieved by detection of the plasma coagulase and/or the clumping factor. The enterotoxins and TSST-1 can be detected by means of immunological and molecular biological methods (special laboratories).
■ To detect plasma coagulase, suspend several colonies in 0.5 ml of rabbit plasma, incubate the inoculated plasma for one, four, and 24 hours and record the levels of coagulation.
■ For the clumping factor test, suspend colony material in a drop of rabbit plasma on a slide. Macroscopically visible clumping confirms the presence of the factor.
Therapy. Aside from surgical measures, therapy is based on administration of antibiotics. The agents of choice for severe infections are penicillinase-resistant penicillins, since 70-80% of all strains produce penicillinase. These penicillins are, however, ineffective against methicillin-resistant strains, and this resistance applies to all betalactams.
Epidemiology and prevention. S. aureus is a frequent colonizer of skin and mucosa. High carrier rates (up to 80%) are the rules among hospital patients and staff. The principle localization of colonization in these persons is the anterior nasal mucosa area, from where the bacteria can spread to hands or with dust into the air and be transmitted to susceptible persons.
S. aureus is frequently the causal pathogen in nosocomial infections (see p. 343f.). Certain strains are known to cause hospital epidemics. Identification of the epidemic strain requires differentiation of relevant infection isolates from other ubiquitous strains. Lysotyping (see p. 186) can be used for this purpose, although use of molecular methods to identify genomic DNA "fingerprints" is now becoming more common.
The most important preventive measure in hospitals is washing the hands thoroughly before medical and nursing procedures. Intranasal application of antibiotics (mupirocin) is a method of reducing bacterial counts in carriers.
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