Staphylococci are gram-positive cocci that form grapelike clusters on Gram’s stain; they are catalase positive (unlike streptococci), nonmotile, aerobic, and facultatively anaerobic. Staphylococcus aureus, which is distinguished from other staphylococci by its production of coagulase, is the most virulent species.
S. aureus is an important cause of community-acquired infections and a leading cause of nosocomial infections.
S. aureus is a component of the normal human flora, most frequently colonizing the anterior nares and oropharynx but also colonizing the skin (particularly damaged skin), vagina, axilla, and perineum. These sites of colonization are reservoirs for future infection.
Of healthy persons, 20–40% are transiently colonized with S. aureus, while ∼10% are persistently colonized. The rate is elevated among insulin-dependent diabetic pts, HIV-infected persons, injection drug users, hemodialysis pts, and pts with skin damage.
Transmission of S. aureus most frequently results from direct personal contact, although spread via respiratory secretions has been reported. Most S. aureus infections are caused by a strain that is already a component of the pt’s own microbiota.
Methicillin-resistant S. aureus (MRSA) is common in hospitals, and its prevalence is increasing dramatically in community settings among individuals without prior medical exposure.
S. aureus is a pyogenic pathogen known for its capacity to induce abscess formation.
Invasive disease: For invasive S. aureus infection to occur, some or all of the following steps are necessary:
– Colonization/inoculation: Bacteria colonize tissue surfaces, particularly the anterior nares, or are inoculated directly into tissue—e.g., as a result of minor abrasions or via IV access catheters.
– Invasion: Bacteria replicate at the site of infection and elaborate enzymes that facilitate survival and local spread. CA-MRSA isolates that produce the Panton-Valentine leukocidin toxin have been linked to more serious infections.
– Evasion of host defense mechanisms: S. aureus possesses an antiphagocytic polysaccharide microcapsule that facilitates evasion of host defenses and plays a role in abscess formation. Organisms can survive intracellularly and then cause recrudescent infections when conditions are suitable.
– Metastatic spread: S. aureus can survive in PMNs and may use these cells to spread to and seed other tissue sites.
Toxin-mediated disease: S. aureus produces three types of toxin: cytotoxins, pyrogenic toxin superantigens, and exfoliative toxins.
– Antitoxin antibodies are protective against toxin-mediated staphylococcal illness.
– Enterotoxins and toxic shock syndrome toxin 1 (TSST-1) act as “superantigens” or T-cell mitogens and cause the release of large amounts of inflammatory mediators, producing multisystem disease that includes fever, rash, and hypotension.
S. aureus infections are readily diagnosed by Gram’s stain and microscopic examination of infected tissue.