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; parenteral treatment is usually given until systemic signs and symptoms have improved. Types of skin lesions include the following:

  1. Vesicles: due to proliferation of organisms, usually viruses, within the epidermis (e.g., VZV, HSV, coxsackievirus, poxviruses, Rickettsia akari)
  2. 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.
  3. 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.
  4. 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.”
  5. 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.
  6. 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).
  7. 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.
TABLE 87-1: Treatment of Common Infections of the Skin
Animal bite (prophylaxis or early infection)aAmoxicillin–clavulanate (875/125 mg PO bid)Doxycycline (100 mg PO bid)29
Animal bitea (established infection)Ampicillin–sulbactam (1.5–3 g IV q6h)Clindamycin (600–900 mg IV q8h) plus Ciprofloxacin (400 mg IV q12h) or cefoxitin (2 g IV q6h)29
Bacillary angiomatosisErythromycin (500 mg PO qid)Doxycycline (100 mg PO bid)94
Herpes simplex (primary genital)Acyclovir (400 mg PO tid for 10 days)Famciclovir (250 mg PO tid for 5–10 days) or valacyclovir (1000 mg PO bid for 10 days)102
Herpes zoster (immunocompetent host >50 years of age)Acyclovir (800 mg PO 5 times daily for 7–10 days)Famciclovir (500 mg PO tid for 7–10 days) or valacyclovir (1000 mg PO tid for 7 days)102
Cellulitis (staphylococcal or streptococcalb,c)Nafcillin or oxacillin (2 g IV q4–6h)Cefazolin (1–2 g q8h) or ampicillin/sulbactam (1.5–3 g IV q6h) or erythromycin (0.5–1 g IV q6h) or clindamycin (600–900 mg IV q8h)89, 90
MRSA skin infectiondVancomycin (1 g IV q12h)Linezolid (600 mg IV q12h)89
Necrotizing fasciitis (group A streptococcalb)Clindamycin (600–900 mg IV q6–8h) plus penicillin G (4 million units IV q4h)Clindamycin (600–900 mg IV q6–8h) plus a cephalosporin (first- or second-generation)90
Necrotizing fasciitis (mixed aerobes and anaerobes)Ampicillin (2 g IV q4h) plus clindamycin (600–900 mg IV q6–8h) plus ciprofloxacin (400 mg IV q6–8h)Vancomycin (1 g IV q6h) plus metronidazole (500 mg IV q6h) plus ciprofloxacin (400 mg IV q6–8h)95
Gas gangreneClindamycin (600–900 mg IV q6–8h) plus penicillin G (4 million units IV q4–6h)Clindamycin (600–900 mg IV q6–8h) plus cefoxitin (2 g IV q6h)95
aPasteurella multocida, a species commonly associated with both dog and cat bites, is resistant to cephalexin, dicloxacillin, clindamycin, and erythromycin. Eikenella corrodens, a bacterium commonly associated with human bites, is resistant to clindamycin, penicillinase-resistant penicillins, and metronidazole but is sensitive to trimethoprim-sulfamethoxazole and fluoroquinolones.
bThe frequency of erythromycin resistance in group A Streptococcus is currently ∼5% in the United States but has reached 70–100% in some other countries. Most, but not all, erythromycin-resistant group A streptococci are susceptible to clindamycin. Approximately 90% of Staphylococcus aureus strains are sensitive to clindamycin, but resistance—both intrinsic and inducible—is increasing.
cSevere hospital-acquired S. aureus infections or community-acquired S. aureus infections that are not responding to the β-lactam antibiotics recommended in this table may be caused by methicillin-resistant strains, requiring a switch to vancomycin, daptomycin, or linezolid.
dSome strains of methicillin-resistant S. aureus (MRSA) remain sensitive to tetracycline and trimethoprim-sulfamethoxazole. Daptomycin (4 mg/kg IV q24h) or tigecycline (100-mg loading dose followed by 50 mg IV q12h) is an alternative treatment for MRSA.

There's more to see -- the rest of this topic is available only to subscribers.