TITLE: COMMON SKIN INFECTIONS
AUTHORS: DIVYA SINGH-BEHL, MD -- Department of Dermatology
   KENNETH J. TOMECKI, MD -- Department of Dermatology
REVIEWED: AUGUST 4, 2004
    
Print Tables From This Chapter
BACTERIAL INFECTIONS
Humans are natural hosts for many bacterial species that colonize the skin as normal flora. Staphylococcus aureus and Streptococcus pyogenes are infrequent resident flora, but they account for a wide variety of bacterial pyodermas. Predisposing factors to infection include minor trauma, preexisting skin disease, poor hygiene, and, rarely, impaired host immunity.
IMPETIGO
DEFINITION AND PREVALENCE
Impetigo is a superficial skin infection usually caused by S aureus and occasionally by S pyogenes. Impetigo affects approximately 1% of children.
PATHOPHYSIOLOGY
S aureus produces a number of cellular and extracellular products, including exotoxins and coagulase, which contribute to the pathogenicity of impetigo, especially when coupled with preexisting tissue injury.
SIGNS, SYMPTOMS, AND DIAGNOSIS
Two clinical types of impetigo exist: nonbullous and bullous impetigo. The nonbullous type is more common and typically occurs on the face and extremities, initially with vesicles or pustules on reddened skin that eventually rupture to leave the characteristic "honey-colored" (yellow-brown) crust (Figure 1). Bullous impetigo, almost exclusively caused by S aureus, exhibits flaccid bullae with clear yellow fluid that rupture and leave a golden-yellow crust. Diagnosis depends on clinical presentation and confirmation by culture.1
MANAGEMENT
For most patients with impetigo, topical treatment is adequate, either with Polysporin bacitracin or mupirocin (Bactroban), applied three times a day for 7 to 10 days. Systemic therapy may be necessary for patients with extensive disease (Table 1).2
FOLLICULITIS, FURUNCULOSIS
(furuncles), and CARBUNCULOSIS
(carbuncles)
DEFINITION AND PREVALENCE
Folliculitis is a superficial infection of the hair follicles characterized by erythematous, follicular-based papules and pustules. Furuncles are deeper infections of the hair follicle characterized by inflammatory nodules with pustular drainage, which may coalesce to form larger draining nodules. The prevalence of folliculitis is unknown.
PATHOPHYSIOLOGY
S aureus is the usual pathogen, although exposure to Pseudomonas aeruginosa in hot tubs or swimming pools may lead to folliculitis.
SIGNS, SYMPTOMS, AND DIAGNOSIS
Folliculitis is generally asymptomatic, but may be pruritic or even painful. Commonly affected areas are the beard, posterior neck, occipital scalp, and axillae (Figure 2). Often a continuum of folliculitis, furunculosis (furuncles) arises in hair-bearing areas as tender, erythematous, fluctuant nodules that rupture with purulent discharge (Figure 3). Carbuncles are larger and deeper inflammatory nodules, often with purulent drainage (Figure 4), and commonly occur on the nape of the neck, back, or thighs. Carbuncles are often tender and painful and occasionally accompanied by fever and malaise.1,2,3
MANAGEMENT

Topical treatment with clindamycin 1% or erythromycin 2%, applied two to three times a day to affected areas, coupled with an antibacterial wash or soap, is adequate for most patients with folliculitis. Systemic antistaphylococcal antibiotics (Table 1) are usually necessary for furuncles and carbuncles, especially when cellulitis or constitutional symptoms are present.2 Additionally, small furuncles can be treated with warm compresses three to four times a day for 15-20 minutes, whereas larger furuncles and carbuncles often warrant incision and drainage.
ECTHYMA

DEFINITION AND PREVALENCE
Ecthyma is a deep infection of the skin that resembles impetigo. Ecthyma is somewhat common in patients with poor hygiene and/or malnutrition.

PATHOPHYSIOLOGY

S aureus or S pyogenes is the usual pathogen of ecthyma.
SIGNS, SYMPTOMS, AND DIAGNOSIS
Infection begins with vesicles and bullae that progress to punched-out ulcerations with an adherent crust, which heals with scarring. The most common site of infection is the legs. Diagnosis depends on clinical presentation with confirmation by culture.3,4
MANAGEMENT

Ecthyma requires treatment with an oral antistaphylococcal antibiotic (Table 1), coupled with warm compresses three to four times a day for 15-20 minutes.2

ERYSIPELAS AND CELLULITIS

DEFINITION AND PREVALENCE
Erysipelas is a superficial streptococcal infection of the skin. Cellulitis is a deeper process that extends to the subcutis. Erysipelas has a predilection for young children and the elderly.
PATHOPHYSIOLOGY
S aureus and S pyogenes are the most common pathogens responsible for erysipelas and cellulitis. S pyogenes produces enzymes that promote infection with systemic manifestations, such as fever/chills, tachycardia, and hypotension. Predisposing factors for erysipelas include venous stasis/insufficiency, diabetes mellitus, trauma, and alcoholism.3,4

SIGNS, SYMPTOMS, AND DIAGNOSIS
Classically, erysipelas is a tender, well-defined, erythematous, indurated plaque on the face or legs (Figure 5). Cellulitis is a warm, tender, erythematous, and edematous plaque with ill-defined borders that expands rapidly. Cellulitis is often accompanied by constitutional symptoms, regional lymphadenopathy, and, occasionally, bacteremia (Figure 6).3,4
MANAGEMENT
Penicillin (250 to 500 mg, four times daily for 7-10 days) is the treatment of choice for erysipelas; parenteral therapy may be necessary for extensive or facial disease. An oral antistaphylococcal antibiotic (Table 1) is the treatment of choice for cellulitis; parenteral therapy is warranted for patients with extensive disease or with systemic symptoms as well as for immunocompromised patients. Good hygiene, warm compresses three to four times a day for 15-20 minutes, and elevation of the affected limb help to expedite healing.
NECROTIZING FASCIITIS
DEFINITION AND PREVALENCE
Necrotizing fasciitis is a rare infection of the subcutaneous tissues and fascia that eventually leads to necrosis.

PATHOPHYSIOLOGY
S pyogenes may be the sole pathogen responsible for necrotizing fasciitis, but most patients have a mixed infection with other aerobes (group B and C streptococci) and anaerobes (Clostridium). Common predisposing factors are injury to soft tissues, eg, abdominal surgery, abrasions, surgical incisions, diabetes, and intravenous drug abuse.5,6

SIGNS, SYMPTOMS, AND DIAGNOSIS
Infection begins with warm, tender, reddened skin, and inflammation that rapidly extends horizontally and vertically. The most common site for infection is the legs, followed by the perineum (Figure 7). Within 48 to 72 hours, affected skin becomes dusky and bullae form, followed by necrosis and gangrene, often with crepitus. Without prompt treatment, fever, systemic toxicity, organ failure, and shock may occur, often followed by death.

Computed tomography or magnetic resonance imaging may help to delineate the extent of infection. Biopsy for histology, Gram stain, and tissue culture help to identify the causative organism(s).5,6

MANAGEMENT
Necrotizing fasciitis is a surgical emergency requiring prompt surgical debridement, fasciotomy, and, occasionally, amputation of the affected extremity to prevent progression to myonecrosis. Treatment with parenteral antibiotics (usually gentamicin and clindamycin) is mandatory. Even with treatment, mortality can approach 70%.

FUNGAL AND YEAST INFECTIONS
DERMATOPHYTE (Fungal Infections)
DEFINITION AND PREVALENCE
Dermatophytosis implies infection with fungi, organisms with high affinity for keratinized tissue, such as the skin, nails, and hair. Trichophyton rubrum is the most common dermatophyte worldwide.
PATHOPHYSIOLOGY
Three fungal genera—Trichophyton, Microsporum, and Epidermophyton—account for the vast majority of infections. Fungal reservoirs for these organisms include soil, animals, and infected humans.
SIGNS, SYMPTOMS, AND DIAGNOSIS
Tinea pedis (athlete's foot) is the most common fungal infection in humans in North America and Europe.4 Affected skin is usually pruritic, with scaling plaques on the soles, extending to the lateral aspect of the feet and interdigital spaces (Figure 8), often with maceration. Tinea cruris (jock itch) occurs in the groin and on the upper, inner thighs and buttocks as scaling annular plaques (Figure 9); disease is more common in men and typically spares the scrotum. Tinea capitis, or fungal infection of the scalp, is most common in children, characterized by scaly, erythematous skin, often with hair loss. Tinea capitis may resemble seborrheic dermatitis. Kerion etc is an inflammatory form of tinea capitis, characterized by boggy nodules, usually with hair loss and regional lymphadenopathy. Tinea corporis (body), faciei (face), and manuum (hands) represent infections of different sites, each invariably with annular scaly plaques. Tinea unguium (onychomycosis) is fungal nail disease, characterized by thickened yellow nails and subungual debris (Figure 10). Potassium hydroxide preparation and/or culture help to establish the diagnosis for all forms of fungal infection.2
MANAGEMENT
For most patients, topical treatment with terbinafine (Lamisil), clotrimazole (Lotrimin, Mycelex), or econazole (Spectazole) cream is adequate when applied twice daily for 6 to 8 weeks. For onychomycosis, tinea capitis, and extensive dermatophyte disease, systemic treatment is often necessary—itraconazole (Sporanox) or terbinafine (Lamisil) for nail disease, and griseofulvin for scalp or extensive dermatophyte disease.7,8,9
CANDIDIASIS
DEFINITION AND PREVALENCE
Cutaneous candidiasis is a yeast infection caused primarily by Candida albicans. Infection is common in immunocompromised patients, diabetics, the elderly, and patients receiving antibiotics.
PATHOPHYSIOLOGY
C albicans commonly resides on skin and mucosal surfaces. Alterations in the host environment may lead to its proliferation and subsequent skin disease.
SIGNS, SYMPTOMS, AND DIAGNOSIS
Candidal intertrigo is a specific infection of the skin folds (axillae, groin), characterized by reddened plaques, often with "satellite" pustules (Figure 11). Thrush is oropharyngeal candidiasis, characterized by white nonadherent plaques on the tongue and buccal mucosa. Paronychia is an acute or chronic infection of the nail characterized by tender, edematous, and erythematous nail folds, often with purulent discharge (Figure 12); disease is common in diabetics. Angular cheilitis is the presence of fissures and reddened scaly skin at the corner of the mouth, which often occurs in diabetics and in those who drool or chronically lick their lips (Figure 13). Candidal vulvovaginitis is an acute inflammation of the perineum characterized by itchy, reddish, scaly skin and mucosa; creamy discharge; and peripheral pustules. The counterpart in men is balanitis, characterized by shiny reddish plaques on the glans penis, which may affect the scrotum. Balanitis occurs almost exclusively in uncircumcised men.2
MANAGEMENT
For candidal intertrigo and balanitis, topical antifungal agents such as clotrimazole, terbinafine, or econazole cream, applied twice daily for 6 to 8 weeks is usually curative when coupled with aeration and compresses. For thrush, the treatment is nystatin suspension or clotrimazole troches four to six times daily until symptoms resolve. Systemic antifungal drugs such as fluconazole, 100 mg/day to 200 mg/day, or itraconazole, 100 mg/day to 200 mg/day, for 5 to 10 days may be necessary for severe or extensive disease. For paronychia, treatment consists of aeration and a topical antifungal agent such as terbinafine, clotrimazole, or clotrimazole for 2 to 3 months; occasionally, oral antistaphylococcal antibiotics (Table 1) are needed, coupled with incision and drainage for secondary bacterial infection. Cheilitis resolves with aeration, application of a topical antifungal agent, and discontinuation of any aggravating factors. A single 150-mg dose of fluconazole, coupled with aeration, is usually effective for vulvovaginitis.9
TINEA (Pityriasis) VERSICOLOR
DEFINITION AND PREVALENCE
Tinea versicolor is a common superficial infection of the skin caused by the ubiquitous yeast Pityrosporum ovale. Prevalence is high in hot, humid climates.
PATHOPHYSIOLOGY
P ovale produces phenolic compounds that inhibit tyrosinase, which may produce hypopigmentation in many patients.
SIGNS, SYMPTOMS, AND DIAGNOSIS
Infection produces discrete and confluent, finely scaly, well-demarcated, hypopigmented and/or hyperpigmented plaques on the chest, back, arms, and neck (Figure 14). Disease usually occurs in warmer months or in hot, humid climates. Potassium hydroxide (KoH) preparation exhibits short hyphae and spores with a spaghetti-and-meatball appearance.
MANAGEMENT
Selenium sulfide shampoo (2.5%) or ketoconazole shampoo is the mainstay of treatment, applied to the affected areas and the scalp daily for 3 to 5 days, then once a month thereafter. Alternatively, a variety of topical antifungal agents, including terbinafine, clotrimazole, or econazole cream, applied twice daily for 6 to 8 weeks, constitute adequate treatment, especially for limited disease.10
VIRAL INFECTIONS
HERPES SIMPLEX
DEFINITION AND PREVALENCE
Herpes simplex virus (HSV) infection is a painful, self-limited, often recurrent dermatitis, characterized by small grouped vesicles on an erythematous base. Eighty-five percent of the population has antibody evidence of HSV type 1 infection. Twenty to fifty percent of genital ulcerations are the result of HSV type 2 infection.
PATHOPHYSIOLOGY
Disease follows implantation of the virus via direct contact at mucosal surfaces or on sites of abraded skin. After primary infection, the virus travels to the adjacent dorsal ganglia where it remains dormant unless reactivated by psychological or physical stress, menses, or sunlight.
SIGNS, SYMPTOMS, AND DIAGNOSIS

Primary infection occurs most often in children, exhibiting vesicles and erosions on reddened buccal mucosa, palate, tongue and/or lips (acute herpetic gingivostomatitis) (Figure 15). Herpes labialis, (fever blisters or cold sores) appears as grouped vesicles on red denuded skin, usually the vermilion border of the lip; infection represents reactivated HSV. Primary genital infection is an erosive dermatitis on the external genitalia that occurs about 7 to 10 days after exposure; intact vesicles are rare. Recurrent genital disease is common (approximately 40% of affected patients).

Viral culture helps to confirm the diagnosis; direct fluorescent antibody (DFA) is a helpful but less specific test. Serology is helpful only for primary infection.

MANAGEMENT
Acyclovir remains the treatment of choice for HSV infection; newer antivirals, eg famciclovir and valacyclovir, are also effective (Table 2). For recurrent infection (more than six episodes per year), suppressive treatment (Table 2) is warranted. Primary infection in immunosuppressed patients requires treatment with acyclovir, 10 mg/kg, every 8 hours for 7 days.
HERPES ZOSTER
DEFINITION AND PREVALENCE

Herpes zoster (shingles) is an acute, painful dermatomal dermatitis that affects approximately 10 to 20% of adults, often in the presence of immunosuppression.
PATHOPHYSIOLOGY
Zoster represents reactivation of latent varicella-zoster virus within a single dermatome.
SIGNS, SYMPTOMS, AND DIAGNOSIS
Herpes zoster is primarily a disease of adults. It typically begins with pain in a dermatomal or band-like pattern followed by grouped vesicles within the dermatome (Figure 16), and occasionally accompanied by fever and malaise. Most patients with zoster do well with only symptomatic treatment, but postherpetic neuralgia (continued dysthesias and pain after resolution of skin disease) is common in the elderly. Disseminated zoster is uncommon and occurs primarily in immunocompromised patients. Diagnostic tests are the same as for HSV.2
MANAGEMENT
Zoster deserves treatment, if possible, with rest, analgesics, compresses applied to affected areas, and antiviral therapy, if possible, within 24-72 hours of disease onset. (Table 2). Disseminated and ophthalmic zoster warrants Rx with acyclovir 10 mg/kg intravenously every 8 hours for 7 days.
WARTS
DEFINITION AND PREVALENCE
Warts are common and benign epithelial growths caused by human papillomavirus (HPV). Warts affect approximately 5% of the population.
PATHOPHYSIOLOGY
HPV infection follows inoculation of the virus into the epidermis through direct contact, usually facilitated by a break in the skin.
SIGNS, SYMPTOMS, AND DIAGNOSIS
The common wart is the most common type-a, hyperkeratotic, flesh-colored papule and/or plaque studded with small black dots (thrombosed capillaries) (Figure 17). Other types of warts include flat warts (verruca plana), plantar warts, and condyloma acuminatum (venereal warts). Clinical appearance and location usually suggest the diagnosis.
MANAGEMENT
Therapy is variable and often challenging. Most modalities are destructive in nature, (eg, cryosurgery, electrodesiccation, curettage, and application of various topical products such as trichloroacetic acid, salicylic acid, podophyllin, and canthacur). For stubborn warts, laser therapy is often necessary. The immunomodulator, imiquimod cream (Aldara), is a novel topical agent recently approved for the treatment of condyloma acuminatum. Sexual partners of patients with condyloma warrant examination, and women require gynecologic examination.
MOLLUSCUM CONTAGIOSUM
DEFINITION AND PREVALENCE
Molluscum contagiosum is an infectious viral disease caused by the poxvirus. Infection is common in children, sexually active adults, and in patients with HIV infection.
PATHOPHYSIOLOGY
The disease follows direct contact with the virus, which replicates in the cytoplasm of the cells and induces hyperplasia.
SIGNS, SYMPTOMS, AND DIAGNOSIS
Molluscum are smooth flesh-colored, dome-shaped, umbilicated papules with a central keratotic plug (Figure 18), which usually resolve spontaneously, but often persist in immunocompromised patients.
MANAGEMENT
Treatment may not be necessary. If indicated, treatment is similar to the modalities outlined for warts.
REFERENCES
  1. Trent JT, Federman D, Kirsner RS. Common bacterial skin infections. Ostomy Wound Manage. 2001;47:30-34.

  2. Ko WT, Adal KA, Tomecki KJ. Infectious diseases. Med Clin North Am. 1998;82:1001-1031.

  3. O'Dell ML. Skin and wound infections: an overview. Am Fam Physician. 1998;57:2424-2432.

  4. Carroll JA. Common bacterial pyodermas. Taking aim against the most likely pathogens. Postgrad Med. 1996;100:311-322.

  5. Brook I, Frazier EH. Clinical and microbiological features of necrotizing fasciitis. J Clin Microbiol. 1995;33:2382-2387.

  6. Bisno AL, Stevens DL. Streptococcal infections of skin and soft tissues. N Engl J Med. 1996;334:240-245.

  7. Drake LA, Dinehart SM, Farmer ER, et al. Guidelines of care for superficial mycotic infections of the skin: onychomycosis. Guidelines/Outcomes Committee. American Academy of Dermatology. J Am Acad Dermatol. 1996;34:116-121.

  8. Drake LA, Dinehart SM, Farmer ER, et al. Guidelines of care for superficial mycotic infections of the skin: tinea capitis and tinea barbae. Guidelines/Outcomes Committee. American Academy of Dermatology. J Am Acad Dermatol. 1996;34:290-294.

  9. Drake LA, Dinehart SM, Farmer ER, et al. Guidelines of care for superficial mycotic infections of the skin: tinea corporis, tinea cruris, tinea faciei, tinea manuum, and tinea pedis. Guidelines/Outcomes Committee. American Academy of Dermatology. J Am Acad Dermatol. 1996;34:282-286.

  10. Hay RJ. The management of superficial candidiasis. J Am Acad Dermatol. 1999;40(6 Pt 2):S35-S42.

  11. Drake LA, Dinehart SM, Farmer ER, et al. Guidelines of care for superficial mycotic infections of the skin: Pityriasis (tinea) versicolor. Guidelines/Outcomes Committee. American Academy of Dermatology. J Am Acad Dermatol. 1996;34:287-289.
    12.

This information is provided for general medical education purposes only and is not meant to substitute for the independent medical judgment of a physician relative to diagnostic and treatment options of a specific patient's medical condition.

In no event will The Cleveland Clinic Foundation be liable for any decision made or action taken in reliance upon the information provided through this web site.
Copyright 2003 The Cleveland Clinic Foundation