Infections of the skin can result from microbial invasion from an external source or from organisms reaching the skin through the bloodstream as part of a systemic disease. Blood-borne involvement is evidenced by rashes in many viral and bacterial infections, such as measles and secondary syphilis, or may yield more chronic granulomatous skin lesions in blastomycosis, tuberculosis, and syphilis. Skin lesions remote from sites of in-fection can be produced by some bacterial toxins, such as the pyrogenic exotoxins of group A streptococci and Staphylococcus aureus. They can also result from immunologic responses to microbial antigens that have reached the skin. Thus, there are manifold skin manifestations of infections;.
The skin is an organ system with multiple functions, including protection of the tis-sues from external microbial invasion. Its keratinized stratified epithelium prevents direct microbial invasion under normal conditions of surface temperature and humidity, and its normal flora, pH, and chemical defenses tend to inhibit colonization by many pathogens. However, the skin is subject to repeated minor traumas that are often unnoticed but that destroy its integrity and allow organisms to gain access to its deeper layers from the external environment. The surface is also penetrated by ducts of pilosebaceous units and sweat glands, and microbial invasion can occur along these routes, particularly if the ducts are obstructed.
Folliculitis is a minor infection of the hair follicles and is usually caused by S. aureus. It is often associated with areas of friction and of sweat gland activity and is thus seen most frequently on the neck, face, axillae, and buttocks. Blockage of ducts with inspissated se-bum, as in acne vulgaris, predisposes to the condition. Folliculitis can also be caused by Pseudomonas aeruginosa, and this form of the disease has become more common in re-cent years, with the popularity of hot tubs and whirlpool baths. Unless these facilities are thoroughly cleansed and adequately chlorinated, they can grow large numbers of pseudomonads at their normal operating temperatures, causing extensive folliculitis on areas of the body that have been immersed. The lesions subside rapidly when the insult is discontinued. Occasionally, folliculitis may be caused by infection with Candidaalbicans. Such cases are particularly common in immunocompromised hosts.
Acne vulgaris also involves inflammation of hair follicles and associated sebaceousglands. The comedo of acne results from multiplication of Propionibacterium acnes,the predominant anaerobe of the normal skin, behind and within inspissated sebum. Organic acids produced by the organism are believed to stimulate an inflammatory response and thus contribute to the disease process. However, the primary cause of the disease is hor-monal influences on sebum secretion that occur at puberty, and the disease usually re-solves in early adult life.
The furuncle is a small staphylococcal abscess that develops in the region of a hair folli-cle. Furuncles may be solitary or multiple and may constitute a troublesome recurrent dis-ease. Spread of infection to the dermis and subcutaneous tissues can result in a more extensive multiloculated abscess, the carbuncle.
Folliculitis and individual furuncles are normally treated locally by measures designed to establish drainage without the use of antibiotics. Chronic furunculosis may require at-tempts to eliminate nasal carriage of S. aureus, which is sometimes the source of the in-fection. Antimicrobics are not usually required unless surrounding cellulitis or carbuncles develops. Severe acne can often be treated effectively with topical drying agents. Pro-longed administration of low oral doses of a tetracycline or macrolide is often effective, although the reason for the therapeutic response is uncertain.
Minor or inapparent skin lesions serve as the route of infection in many localized skin infections and in some systemic diseases, such as syphilis and leptospirosis.
The only organisms that can use the keratin on cells, hairs, and nails are the dermatophyte fungi. The dermatophytes are particularly well adapted to these sites, cannot grow at 37°C, and fail to invade deeper layers. The clinical manifestations of these infections re-sult from the inflammatory and delayed hypersensitivity responses of the host, and the desquamation induced by these processes is a major factor in the ultimate control of the infection by removing infected skin. In candidiasis, control involves cell-mediated im-mune mechanisms, and chronic Candida skin and nail infections are often associated with defects in cellular immunity.
Pyoderma, also termed impetigo, is a common, sometimes epidemic skin lesion. This disease is caused primarily by group A streptococci. The initial lesion is often a small vesicle that develops at the site of invasion and ruptures with superficial spread char-acterized by skin erosion and a serous exudate, which dries to produce a honey-colored crust. The exudate and crust contain numerous infecting streptococci. S. aureus may occasionally produce pustular impetigo or contaminate the lesions caused by streptococci. Epidemic impetigo is most common in childhood and under conditions of heat, humidity, poor hygiene, and overcrowding. The infection may be spread by fomites such as shared clothing and towels. It is sometimes caused by nephritogenic strains of S. pyogenes, particularly in the tropics, and acute glomerulonephritis may result. Rheumatic fever is not associated with streptococcal lesions of the skin.
Treatment is usually with penicillin or erythromycin and topical antimicrobics or skin antiseptics to limit spread.
Bullous impetigo is a distinct disease caused by strains of S. aureus that produce ex-foliation. It is most common in small children, but may occur at any age. The infection is characterized by large serum-filled bullae (blisters) within the skin layers at the site of in-fection. Minor infections are treated topically; however, bullous impetigo in infants is a serious disease that usually requires systemic antimicrobic treatment. Epidemic spread may occur under conditions similar to those described for streptococcal impetigo.
Erysipelas is a rapidly spreading infection of the deeper layers of the dermis that is al-most always caused by group A streptococci. It is associated with edema of the skin; marked erythema; pain; and systemic manifestations of infection, including fever and lymphadenopathy. Because the infection is intradermal, the streptococci cannot usually be isolated from the skin surfaces. The disease can progress to septicemia or local necro-sis of skin. It is serious and requires immediate treatment with penicillin or erythromycin.
Cellulitis is not a skin infection as such, but it can develop by extension from skin or wound infections. It usually presents as an acute inflammation of subcutaneous connective tissue with swelling and pain and often with marked constitutional signs and symptoms. It can be caused by many pathogenic bacteria, but S. aureus and group A streptococci are most common. Haemophilus influenzae type b is a cause in infants and children. Enteric Gram-negative rods, clostridia, and other anaerobes may also cause cellulitis as a compli-cation of wound infections, particularly in immunocompromised hosts and individuals with uncontrolled diabetes.
Many acute and subacute skin infections are characterized by ulceration or a granuloma-tous response. Some are sexually transmitted. Others de-rive from systemic infection and are not direct infections of skin. A few examples of di-rect infections, which pose special diagnostic problems, are considered below. Herpes simplex virus can invade through the skin to produce a local vesicular lesion followed by ulceration. The lesion may then recur in the infected area. Primary herpetic lesions of the finger can mimic staphylococcal paronychia very closely, as well as produce lymphangitis and local lymph node enlargement with pain and fever.
Skin diphtheria, which remains common in some tropical areas, also occurred endem-ically among the transient population of the West Coast of the United States during the 1970s and early 1980s. The organism gains access through a wound or insect bite and causes chronic erosion and ulceration of the skin, sometimes with evidence of the sys-temic effects of diphtheria toxin.
Mycobacterium marinum produces a self-limiting granuloma, usually of the forearmsand knees. The organism usually enters through superficial abrasions from rocks or swim-ming pool walls. Infections with M. ulcerans are more serious and produce progressive ulceration, but are limited to tropical areas and do not occur in the United States or Europe. Several rare forms of necrotic spreading skin ulceration tend to develop in immunosuppressed hosts, in diabetics, and as complications of abdominal surgery. These lesions include bacterial synergistic gangrene, caused by mixtures of peptostreptococcus, S. aureus, and group A streptococci. Variants of these conditions produce extensive andspreading necrotic cellulitis. The major form of treatment is to excise the infected tissues widely and supplement such surgery with massive chemotherapy.
Several primary fungal diseases are associated with cutaneous ulceration or cellulitis, including mycetoma and chromoblastomycosis, which involve the feet, and sporotri-chosis, in which ulceration often develops from infected subcutaneous lymph nodes and vessels. Likewise, some parasites directly infect and ulcerate the skin, as in cutaneous leishmaniasis and cutaneous amebiasis. These latter two diseases are not contracted in the United States.