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Infections of the Skin, Muscles, and Soft Tissues

Chapter 134 | Part 5: Infectious Diseases

KEY CLINICAL POINTS

  • Skin and soft tissue infections (SSTIs) are common globally, with rising incidence due to MRSA, natural disasters, and trauma.
  • Erysipelas and cellulitis are distinct infections: erysipelas is a superficial streptococcal infection with well-defined margins, while cellulitis is a diffuse bacterial infection.
  • Necrotizing fasciitis is a life-threatening infection requiring immediate surgical debridement and broad-spectrum antibiotics.
  • Viral infections like herpes simplex, varicella, and molluscum contagiosum present with vesicles, bullae, or crusted lesions.
  • Treatment varies by infection type, with MRSA requiring vancomycin or linezolid, and necrotizing fasciitis needing clindamycin + cephalosporin.

1. DEFINITION & OVERVIEW

Skin and soft tissue infections (SSTIs) encompass a wide range of bacterial, viral, fungal, and parasitic infections affecting the epidermis, dermis, subcutaneous tissues, muscles, and fascia. The epidermis acts as a mechanical barrier, but disruptions (e.g., abrasions, burns) allow pathogens to invade deeper structures. SSTIs range from mild (e.g., impetigo) to severe (e.g., necrotizing fasciitis).

Table 134-1 Skin and Soft Tissue Infections

LESION, CLINICAL SYNDROME INFECTIOUS AGENT(S) SEE ALSO CHAP(S)
Vesicles Smallpox S4
Vesicles Chickenpox 198
Vesicles Shingles (herpes zoster) 198
Vesicles Cold sores, herpetic whitlow, herpes gladiatorum Herpes simplex virus 197
Vesicles Hand-foot-and-mouth disease Coxsackievirus A16 210
Vesicles Orf Parapoxvirus 201
Vesicles Molluscum contagiosum Molluscum contagiosum poxvirus 201
Vesicles Rickettsialpox Rickettsia akari 192
LESION, CLINICAL SYNDROME INFECTIOUS AGENT(S) SEE ALSO CHAP(S)
Vesicles Blistering distal dactylitis Staphylococcus aureus or Streptococcus pyogenes 152, 153
Bullae Staphylococcal scalded-skin syndrome S. aureus 152
Bullae Necrotizing fasciitis S. pyogenes, Clostridium spp., mixed aerobes and anaerobes 153, 159, 182
Bullae Gas gangrene Clostridium spp. 159
Bullae Halophilic Vibrio Vibrio vulnificus 173
Crusted lesions Bullous impetigo/ecthyma S. aureus 152
Crusted lesions Impetigo contagiosa S. pyogenes 153
Crusted lesions Ringworm Superficial dermatophyte fungi 225
Crusted lesions Sporotrichosis Sporothrix schenckii 225
Crusted lesions Histoplasmosis Histoplasma capsulatum 218
Crusted lesions Coccidioidomycosis Coccidioides immitis 219
Crusted lesions Blastomycosis Blastomyces dermatitidis 220
Crusted lesions Cutaneous leishmaniasis Leishmania spp. 233
Crusted lesions Cutaneous tuberculosis Mycobacterium tuberculosis 183
Crusted lesions Nocardiosis Nocardia asteroides 179
Papular and nodular lesions Fish-tank or swimming-pool granuloma Mycobacterium marinum 185
Papular and nodular lesions Creeping eruption (cutaneous larva migrans) Ancylostoma braziliense 238
Papular and nodular lesions Dracunculiasis Dracunculus medinensis 240
Papular and nodular lesions Cercarial dermatitis Schistosoma mansoni 241
Papular and nodular lesions Verruca vulgaris Human papillomaviruses 1, 2, 4 203
Papular and nodular lesions Condylomata acuminata (anogenital warts) Human papillomaviruses 6, 11, 16, 18 203
Papular and nodular lesions Onchocerciasis nodule Onchocerca volvulus 240
Papular and nodular lesions Cutaneous myiasis Dermatobia hominis 472
Papular and nodular lesions Verruca peruana Bartonella bacilliformis 177
Papular and nodular lesions Cat-scratch disease Bartonella henselae 177
Papular and nodular lesions Lepromatous leprosy Mycobacterium leprae 184
LESION, CLINICAL SYNDROME INFECTIOUS AGENT(S) SEE ALSO CHAP(S)
Papular and nodular lesions Secondary syphilis Treponema pallidum 187
Papular and nodular lesions Tertiary syphilis T. pallidum 187
Ulcers with or without eschars Anthrax Bacillus anthracis S4
Ulcers with or without eschars Ulceroglandular tularemia Francisella tularensis 175, S4
Ulcers with or without eschars Bubonic plague Yersinia pestis 176, S4
Ulcers with or without eschars Buruli ulcer Mycobacterium ulcerans 185
Ulcers with or without eschars Leprosy M. leprae 184
Ulcers with or without eschars Cutaneous tuberculosis M. tuberculosis 183
Ulcers with or without eschars Chancroid Haemophilus ducreyi 162
Ulcers with or without eschars Primary syphilis T. pallidum 187
Ulcers with or without eschars Erysipelas S. pyogenes 153
Ulcers with or without eschars Cellulitis Staphylococcus spp., Streptococcus spp. various other bacteria
Ulcers with or without eschars Necrotizing fasciitis S. pyogenes, Clostridium spp., mixed aerobes and anaerobes 153, 159, 182
Ulcers with or without eschars Streptococcal gangrene S. pyogenes 153
Ulcers with or without eschars Fournier gangrene Mixed aerobic and anaerobic bacteria 182
Ulcers with or without eschars Staphylococcal necrotizing fasciitis Methicillin-resistant S. aureus 152

1.1 Anatomic Relationships

The dermal capillary plexus beneath the dermal papillae plays a key role in infection localization and immune response. Disruption of the stratum corneum allows bacterial translocation via lymphatics, leading to conditions like erysipelas. Postcapillary venules are sites of leukocyte sequestration and chemotaxis.

1.2 Classification

SSTIs are classified by lesion type (vesicles, bullae, crusted lesions) and depth (superficial vs. deep). Deep infections (e.g., necrotizing fasciitis) involve fascia and muscles, while superficial infections (e.g., cellulitis) affect the dermis and subcutaneous tissues.

2. EPIDEMIOLOGY

SSTIs are common globally, with rising incidence due to MRSA, natural disasters, and trauma. MRSA (USA300 clone) is a major cause of severe infections. Risk factors include immunocompromise, diabetes, and trauma. Necrotizing fasciitis and gas gangrene are often associated with penetrating injuries or underlying conditions like diabetes.

2.1 Demographics

Erysipelas and cellulitis are more common in elderly and immunocompromised patients. Necrotizing fasciitis is more severe in patients with comorbidities like diabetes or peripheral vascular disease.

3. ETIOLOGY & PATHOPHYSIOLOGY

SSTIs are caused by a wide range of pathogens, including bacteria (Staphylococcus, Streptococcus, Clostridium), viruses (HSV, VZV), fungi (dermatophytes), and parasites (Leishmania, Schistosoma). Pathogenesis involves disruption of the epidermal barrier, bacterial translocation via lymphatics, and immune-mediated inflammation.

3.1 Bacterial Pathogenesis

Staphylococcus aureus and Streptococcus pyogenes are common pathogens. Clostridium spp. cause gas gangrene. MRSA produces PVL toxin, contributing to necrotizing fasciitis. Vibrio vulnificus is associated with seawater exposure.

4. CLINICAL FEATURES

Clinical features vary by infection type. Vesicles (e.g., varicella), bullae (e.g., staphylococcal scalded-skin syndrome), and crusted lesions (e.g., impetigo) are common. Necrotizing fasciitis presents with severe pain, erythema, and systemic toxicity. Gas gangrene is characterized by gas formation and rapid progression.

5. DIFFERENTIAL DIAGNOSIS

Differential diagnoses include erysipelas vs. cellulitis, necrotizing fasciitis vs. cellulitis, and viral vs. bacterial infections. Key features include lesion morphology, progression, and systemic symptoms.

6. INVESTIGATIONS & DIAGNOSIS

Diagnosis involves clinical evaluation, imaging (CT/MRI), and laboratory tests (Gram stain, culture). Punch biopsy and frozen section analysis help differentiate conditions like SSSS vs. TEN. PCR and serology may be used for viral infections.

7. MANAGEMENT & TREATMENT

Management includes surgical debridement, antibiotics, and supportive care. MRSA requires vancomycin or linezolid. Necrotizing fasciitis needs clindamycin + cephalosporin. Antivirals (e.g., acyclovir) are used for HSV infections. Antifungals are required for fungal infections.

Table 134-2 Treatment of Common Infections of the Skin

DIAGNOSIS/CONDITION PRIMARY TREATMENT ALTERNATIVE TREATMENT SEE ALSO CHAP(S)
Animal bite (prophylaxis or early infection)a Amoxicillin–clavulanate (875/125 mg PO bid) Doxycycline (100 mg PO bid) 146
DIAGNOSIS/CONDITION PRIMARY TREATMENT ALTERNATIVE TREATMENT SEE ALSO CHAP(S)
Animal bitea (established infection) Ampicillin–sulbactam (1.5–3 g IV q6h) Clindamycin (600–900 mg IV q8h) 146
Animal bitea (established infection) plus Ciprofloxacin (400 mg IV q12h) or cefoxitin (2 g IV q6h)
Bacillary angiomatosis Erythromycin (500 mg PO qid) Doxycycline (100 mg PO bid) 177
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) 197
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) 198
Cellulitis (staphylococcal or streptococcalb,c) Nafcillin or oxacillin (2 g IV q4–6h) Erythromycin (0.5–1 g IV q6h) or clindamycin (600–900 mg IV q8h) 152, 153
MRSA skin infectiond Vancomycin (1 g IV q12h) Linezolid (600 mg IV q12h) 152
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) 153
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) 182
Gas gangrene Clindamycin (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) 159

7.1 Antibiotic Therapy

Empirical treatment for cellulitis includes penicillin or cephalosporin. Necrotizing fasciitis requires clindamycin + cephalobacillin. MRSA infections need vancomycin or linezolid. Anaerobic coverage is essential for mixed infections.

8. PROGNOSIS & COMPLICATIONS

Prognosis varies widely. Necrotizing fasciitis and gas gangrene have high mortality (20–50%) without prompt treatment. Complications include sepsis, multiorgan failure, and amputation. Chronic conditions like leprosy or tuberculosis may require long-term management.

9. SPECIAL CONSIDERATIONS

Pregnancy, pediatrics, and elderly patients require special attention. HIV-infected individuals are at higher risk for recurrent infections. Immunocompromised patients may present with atypical features (e.g., disseminated fungal infections).

10. KEY POINTS & CLINICAL PEARLS

  • Early surgical debridement is critical for necrotizing fasciitis.
  • MRSA is increasingly common and requires vancomycin or linezolid.
  • Viral infections (e.g., HSV, VZV) present with characteristic vesicles or bullae.
  • Imaging (CT/MRI) is essential for assessing depth and extent of infection.
  • IVIg may reduce mortality in severe group A streptococcal infections.