The normal bacterial flora of the skin represents an important host defense mechanism against invasion by potentially pathogenic organisms. This flora is primarily composed of aerobic diphtheroids (Corynebacterium species), anaerobic diphtheroids (Propriono-bacterium acnes), and
coagulase-negative staphylococci. Gram-negative bacilli may be present in limited numbers in intertriginous areas. Localized cutaneous
infections occur in ostensibly normal hosts, often after trivial
trauma, examples being streptococcal or staphylococcal
impetigo, staphylococcal
furunculosis, or more unusual
infections due to agents such as Mycobacterium marinum. When the skin is injured more extensively by
trauma,
burns,
ischemia with ulceration, or iatrogenic manipulations, or when host immunologic defenses are suppressed, more severe
infections are likely to supervene, and the threat of systemic dissemination of infecting microorganisms increases. Cutaneous
infection in immunosuppressed hosts may involve the same pyogenic bacteria that affect normal subjects or it may involve a variety of opportunistic invaders, including herpes viruses, gram-negative bacilli, mycobacteria, and deep or superficial
mycoses. The skin may also be affected by
infections whose primary site lies elsewhere in the body. Cutaneous manifestations may be secondary to hematogenous seeding of the causative agent or to the effects of toxins or
immune complexes. Certain microbial agents may initiate a wide variety of cutaneous lesions, depending on route of
infection and the status of the host. Thus, cutaneous lesions attributable to Pseudomonas aeruginosa range from "green nail syndrome" and self-limited
folliculitis to
ecthyma gangrenosum. Similarly, group A streptococci may produce
pyoderma,
cellulitis,
lymphangitis,
erysipelas, or
scarlet fever. We recently described a syndrome of recurrent
cellulitis in the saphenous vein donor extremities of patients who have undergone
coronary artery bypass grafts. Most patients have associated
tinea pedis. The pathophysiologic aspects of this syndrome are probably multifactorial, involving compromise of lymphatic or venous drainage,
bacterial infection, elaboration of
bacterial toxins, and
hypersensitivity to bacterial or fungal products, or both.
Coagulase-negative staphylococci are exhibiting a more prominent pathogenic potential than heretofore. When they infect immunosuppressed hosts or patients with indwelling intravascular
catheters or cardiac
prostheses,
coagulase-negative staphylococci may cause life-threatening disease.(ABSTRACT TRUNCATED AT 400 WORDS)