Why Are Staph So Pathogenic (Able to Cause Diseases)?
Staphylococci have the ability to synthesize and secrete many factors that either allow the bacteria to survive in the host or cause damage to host tissues. The list below summarizes these substances and their effects on the host:
- Surface proteins (for example, capsular polysaccharide, protein A) -- enhance attachment to host cells; others reduce phagocytosis (host immune cell's ability to ingest and kill bacteria)
- Membrane-altering toxins (for example, alpha, beta toxins plus leukocidin) -- all damage host cells by making holes in their membranes
- Exfoliatin toxins (exotoxins ETA and ETB) -- cause scalded skin syndrome (exfoliation of skin after erythematous cellulitis) in infants and children
- Enterotoxins (exotoxins secreted into the gastrointestinal tract termed SE-A, B, C, D, E, and G) -- cause nausea and vomiting associated with food poisoning
- Toxic shock syndrome toxin (TSST-1 toxin) -- syndrome of rapidly onset of fever (102 F or higher), low blood pressure (hypotension), watery diarrhea, muscle aches, weakness, and a rash after about 24 hours associated with staph infections. This occurs usually in females with tampons in place but occasionally occur in males and females with other staph infections such as wound infections.
- Coagulase -- possibly protects staph bacteria from host immune cells by causing bacterial aggregation
- Slime (a biofilm secreted by S. epidermidis) -- Coats and protects bacteria from host's immune cells
- Antibiotic resistance -- Staph strains have developed remarkable resistance to a number of drugs which make antibiotic treatment frequently complex. Please see the methicillin-resistant Staphylococcus aureus (MRSA) infection article for a more complete discussion of this complicated topic.
Other factors produced by these bacteria that may play a role in causing disease are hyaluronidase, kinases, clotting factor, and others, but their disease-causing potentials are still being evaluated.
Medically Reviewed by a Doctor on 7/27/2015
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