Skin and soft tissue infections are diagnosed principally by a careful history (e.g., temporal progression, travel, animal exposure, bites, trauma, underlying medical conditions) and physical examination (appearance of lesions and distribution). Treatment of common skin infections is summarized in Table 87-1 Treatment of Common Infections of the Skin ; parenteral treatment is usually given until systemic signs and symptoms have improved. Types of skin lesions include the following:
- Vesicles: due to proliferation of organisms, usually viruses, within the epidermis (e.g., VZV, HSV, coxsackievirus, poxviruses, Rickettsia akari)
- Bullae: caused by toxin-producing organisms. Different entities affect different skin levels. For example, staphylococcal scalded-skin syndrome and toxic epidermal necrolysis cause cleavage of the stratum corneum and the stratum germinativum, respectively. Bullae are also seen in necrotizing fasciitis, gas gangrene, and Vibrio vulnificus infections.
- Crusted lesions:Impetigo caused by either Streptococcus pyogenes (impetigo contagiosa) or Staphylococcus aureus (bullous impetigo) usually starts with a bullous phase before development of a golden-brown crust. Crusted lesions are also seen in some systemic fungal infections, dermatophytic infections, and cutaneous mycobacterial infections. It is important to recognize impetigo contagiosa because of its relation to poststreptococcal glomerulonephritis.
- Folliculitis: Localized infection of hair follicles is usually due to S. aureus. “Hot-tub folliculitis” is a diffuse condition caused by Pseudomonas aeruginosa. Freshwater avian schistosomes cause an allergic reaction after penetrating hair follicles, resulting in “swimmer's itch.”
- Papular and nodular lesions: Raised lesions of the skin occur in many different forms and can be caused by Bartonella henselae (cat-scratch disease and bacillary angiomatosis), Treponema pallidum, human papillomavirus, mycobacteria, and helminths.
- Ulcers, with or without eschars: can be caused by cutaneous anthrax, ulceroglandular tularemia, plague, and mycobacterial infection. Ulcerated lesions on the genitals can be caused by chancroid (painful) or syphilis (painless).
- Erysipelas: abrupt onset of fiery red swelling of the face or extremities, with well-defined indurated margins, intense pain, and rapid progression. S. pyogenes is the exclusive cause.
- Pathogenesis: Bacteria gain access to the epidermis through breaks in the skin, whether accidental (e.g., cuts, scratches, burns) or iatrogenic (e.g., surgical incisions, IV catheters). The expanding area of erythema may be due to extracellular toxins and/or the host immune response rather than to increasing bacterial numbers.
- Microbiology: Etiologic causes include commensal flora (e.g., S. aureus, S. pyogenes) or a wide variety of exogenous flora. With the latter, a thorough history and epidemiologic data may help identify the cause.
- Examples of exogenous bacteria causing cellulitis include the following: Pasteurella multocida after a cat or dog bite; Capnocytophaga canimorsus after a dog bite; Eikenella corrodens after a human bite; P. aeruginosa in association with ecthyma gangrenosum in neutropenic pts, a penetrating injury (stepping on a nail), or hot-tub folliculitis; Aeromonas hydrophila after a laceration sustained in fresh water; or Erysipelothrix rhusiopathiae after contact with domestic swine and fish.
- Clinical manifestations: This acute inflammatory condition of the skin is characterized by localized pain, erythema, swelling, and heat.
- Cellulitis due to S. aureus often spreads from a central site of localized infection, such as an abscess or an infected foreign body, and is referred to as purulent cellulitis.
- S. pyogenes can cause nonpurulent cellulitis, a rapidly spreading, diffuse process that often occurs with fever and lymphangitis.
- Diagnosis: If there is drainage, an open wound, or an obvious portal of entry, Gram's staining and culture may identify the etiology. Aspiration or biopsy of the leading edge of the cellulitic tissue yields a diagnosis in only 20% of cases.
- Treatment: See Table 87-1 Treatment of Common Infections of the Skin .
- Pathogenesis: Infection, either apparent or inapparent, results from a breach in integrity of the skin or mucous membrane barriers and can be associated with malignancy, a diverticulum, hemorrhoids, or an anal fissure.
- In the case of infections with no obvious portal of entry, transient bacteremia is thought to seed sites of nonpenetrating trauma (e.g., bruise, muscle strain).
- Infection spreads to the deep fascia and along fascial planes through venous channels and lymphatics.
- Microbiology: Necrotizing fasciitis is caused by S. pyogenes, mixed aerobic and anaerobic bacteria, or Clostridium perfringens; methicillin-resistant S. aureus (MRSA) strains that produce the Panton-Valentine leukocidin have also been reported as an occasional cause.
- Clinical manifestations: The timing of cutaneous manifestations (e.g., violaceous bullae; friable, necrotic skin; induration; brawny edema) depends on whether the infection began superficially (rapid onset) or in deeper structures (slower onset).
- Early in the disease course, severe pain and unexplained fever may be the only findings.
- Thrombosis of blood vessels in dermal papillae leads to ischemia of peripheral nerves and anesthesia of the affected area.
- In later stages, pts appear toxic and often develop shock and multiorgan failure.
- Diagnosis: Diagnosis is based on clinical presentation. Other findings may include gas detected in deep tissues by imaging studies (particularly with clostridial species but rarely with S. pyogenes) and markedly elevated serum CPK levels (in the case of concomitant myositis).
- Treatment: Emergent surgical exploration to deep fascia and muscle, with removal of necrotic tissue, is essential. Table 87-1 Treatment of Common Infections of the Skin provides recommendations for adjunctive antibiotic therapy.
- Clinical manifestations and microbiology: Infections involving the muscle have differing manifestations, depending on the etiology.
- - Myositis: can be caused by bacteria (clostridia, streptococci), viruses (influenza virus, dengue virus, coxsackievirus), or parasites (Trichinella, Taenia solium, Toxoplasma). This condition usually manifests with myalgias, but pain can be severe in coxsackievirus, Trichinella, and bacterial infections.
- - Pyomyositis: a localized muscle infection usually due to S. aureus, common in tropical areas, and typically with no known portal of entry.
- - Myonecrosis: can be caused by clostridial species (C. perfringens, C. septicum, C. histolyticum, C. sordellii) or by mixed aerobic and anaerobic bacteria. Myonecrosis is usually related to trauma; however, spontaneous gangrene-usually due to C. septicum-can occur in pts with neutropenia, GI malignancy, or diverticulosis. Myonecrosis of the uterus, typically due to C. sordellii, occurs in women after spontaneous or medically induced abortion and in healthy postpartum women; infection is rapidly and almost uniformly fatal as there are few or no localizing clinical findings.
- Diagnosis and treatment
- Emergent surgical intervention to visualize deep structures, obtain materials for culture and sensitivity testing, remove necrotic tissue, and reduce compartment pressure is both diagnostic and therapeutic.
- Empirical antibiotic treatment should target likely etiologies-e.g., vancomycin (1 g IV q12h) for pyomyositis and ampicillin/sulbactam (2-3 g IV q6h) for mixed aerobic-anaerobic infections.
- For treatment of clostridial myonecrosis (gas gangrene), see Table 87-1 Treatment of Common Infections of the Skin .