zwitterionic capsule (both positively and negatively charged)
can also induce abscess formation [17, 18]. The MSCRAMM
protein A binds the Fc portion of immunoglobulin [31] and,
as a result, may prevent opsonization. S. aureus may also secrete
chemotaxis inhibitory protein of staphylococci or the extracellular
adherence protein, which interfere with neutrophil extravasation
and chemotaxis to the site of infection (reviewed
by Foster [16]). In addition, S. aureus produces leukocidins
that cause leukocyte destruction by the formation of pores in
the cell membrane [19].
During infection, S. aureus produces numerous enzymes, such
as proteases, lipases, and elastases, that enable it to invade and
destroy host tissues and metastasize to other sites. S. aureus is
also capable of producing septic shock. It does this by interacting
with and activating the host immune system and coagulation
pathways. Peptidoglycan, lipoteichoic acid, and a-toxin may all
play a role [22–24] (reviewed by Lowy [32]). In addition to
causing septic shock, some S. aureus strains produce superantigens,
resulting in various toxinoses, such as food poisoning and
toxic shock syndrome [25, 33]. Unlike the structural components
noted earlier, these superantigens can produce a sepsis-like syndrome
by initiating a “cytokine storm.” Some strains also produce
epidermolysins or exfoliative toxins capable of causing
scalded skin syndrome or bullous impetigo [26].
Regulation of expression of staphylococcal virulence factors
plays a central role in pathogenesis. To reduce undue metabolic
demands, expression occurs in a coordinated fashion—only
when required by the bacterium. Expression of MSCRAMMs
generally occurs during logarithmic growth (replication)