Cutaneous infections: Microbiologic and epidemiologic considerations

Abstract

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 (Proprionobacterium 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. A newly recognized, probable virulence factor in these bacteria is the elaboration of surface slime, a substance that facilitates adherence of the staphylococci to artificial surfaces. Slime production is present much more frequently in strains recovered from clinically significant bloodstream infections than in strains recovered from other sources. The clinical significance of surface slime is currently under intense investigation. Normal human skin plays an indispensable role in the protection of the host against a wide range of pathogenic microorganisms. The mechanics of this host defense system are incompletely understood, but they appear to depend, at least in part, on the barrier imposed by the intact keratin layer of the epidermis, the relative dryness of the skin surface, and the presence of normal, nonpathogenic cutaneous bacterial flora. Thus, patients at risk include those in whom (1) the surface integrity of the skin has been breached by trauma, surgical incision, or insertion of medical devices; (2) the skin has become moistened and macerated by constant contact with bodily secretions or by application of occlusive dressings; and (3) the usual bacterial flora has been ablated by antimicrobial therapy or other mechanisms. Moreover, processes that impede local arterial, venous, or lymphatic flow, or processes that suppress generalized host immunologic competence allow opportunistic pathogens to initiate significant local cutaneous infections. Finally, infected skin may be a source of systemic dissemination, and conversely, systemic infections may express themselves in a variety of cutaneous manifestations.