082098 Staphylococcus aureus Infections - Goodsamim.com

MEDICAL PROGRESS
Figure 1. Structure of S. aureus.
Panel A shows the surface and secreted proteins. The synthesis of many of these proteins is dependent on the growth phase, as
shown by the graph, and is controlled by regulatory genes such as agr. Panels B and C show cross sections of the cell envelope.
Many of the surface proteins have a structural organization similar to that of clumping factor, including repeated segments of amino
acids (Panel C). TSST-1 denotes toxic shock syndrome toxin 1.
that these proteins play an important part in the ability
of staphylococci to colonize host tissue. 11
Toxins
Staphylococci produce numerous toxins that are
grouped on the basis of their mechanisms of action.
Cytotoxins, such as the 33-kd protein-alpha toxin,
cause pore formation and induce proinflammatory
changes in mammalian cells. The consequent cellular
damage may contribute to manifestations of the
sepsis syndrome. 12,13 The pyrogenic-toxin superantigens
are structurally related, sharing various degrees
of amino acid sequence homology. They function as
superantigens by binding to major histocompatibility
complex (MHC) class II proteins, causing extensive
T-cell proliferation and cytokine release. 14 Different
domains of the enterotoxin molecule are responsible
for the two diseases caused by these proteins, the
toxic shock syndrome and food poisoning. 15 Despite
little amino acid sequence homology, toxic shock
syndrome toxin 1 is structurally similar to enterotoxins
B and C. The gene for toxic shock syndrome toxin
1 is found in 20 percent of S. aureus isolates. 14
The exfoliative toxins, including epidermolytic toxins
A and B, cause skin erythema and separation, as
seen in the staphylococcal scalded skin syndrome.
The mechanism of action of these toxins remains
controversial. Panton–Valentine leukocidin is a leukocytolytic
toxin that has been epidemiologically associated
with severe cutaneous infections. 16
Enzymes and Other Bacterial Components
Staphylococci produce various enzymes, such as
protease, lipase, and hyaluronidase, that destroy tissue.
These bacterial products may facilitate the spread
of infection to adjoining tissues, although their role
in the pathogenesis of disease is not well defined.
b-Lactamase is an enzyme that inactivates penicillin.
Penicillin-binding proteins are enzymes located
in the cytoplasmic membrane that are involved in
cell-wall assembly. 5 A novel penicillin-binding protein
is responsible for staphylococcal resistance to the
penicillinase-resistant penicillins and cephalosporins.
Coagulase, a prothrombin activator, converts fibrinogen
to fibrin. Its contribution to bacterial virulence
is uncertain.
Volume 339 Number 8 · 521
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