Skin Infections

Skin Infections: Clinical Importance and Exam Focus

Skin infections are among the most common presenting complaints in primary care, accounting for a substantial portion of ambulatory visits. For the Family Nurse Practitioner (FNP), rapid and accurate diagnosis is essential to initiate appropriate therapy, prevent complications, and reduce antibiotic resistance. This guide covers the high-yield bacterial, viral, and fungal skin infections seen on the AANP and ANCC certification exams and in everyday clinical practice.

Diagnostic Terms for Common Skin Infections

  • Cellulitis – Acute bacterial infection of the dermis and subcutaneous tissue, most commonly caused by Streptococcus pyogenes or Staphylococcus aureus[1].
  • Erysipelas – A superficial form of cellulitis with well-demarcated, raised borders; almost always caused by group A Streptococcus[1].
  • Impetigo – Highly contagious superficial infection seen primarily in children; presents as honey-colored crusted lesions (nonbullous) or fragile bullae (bullous)[2].
  • Folliculitis – Inflammation of the hair follicle, often due to S. aureus; may progress to furuncles (abscesses) or carbuncles (deeper, coalescing abscesses)[3].
  • Tinea infections – Dermatophyte fungal infections of the skin (tinea corporis, tinea pedis, tinea cruris, tinea capitis)[4].
  • Herpes simplex virus (HSV) – HSV-1 (often orolabial) and HSV-2 (often genital) cause recurrent vesicular eruptions[5].
  • Herpes zoster – Reactivation of varicella-zoster virus (VZV) presenting as a painful, unilateral vesicular rash in a dermatomal distribution[5].

Pathophysiology and Diagnostic Reasoning Framework

Pathophysiology Overview

Bacterial skin infections usually arise from breaks in the skin barrier (trauma, insect bites, eczema). Host defenses are overwhelmed by bacterial proliferation, leading to inflammation, pus formation, and systemic signs. Viral infections (HSV, VZV) involve latency in sensory ganglia and reactivation triggered by stress, immunosuppression, or trauma. Fungal infections are typically superficial; dermatophytes invade keratinized tissue (stratum corneum, hair, nails) without deeper penetration[4].

Key Diagnostic Approach for the FNP

  1. Identify the morphology (erythematous plaque, vesicle, pustule, crust, scaling patch).
  2. Determine distribution (dermatomal, intertriginous, hair-bearing areas, exposed skin).
  3. Assess for systemic symptoms (fever, malaise) and risk factors (diabetes, immunosuppression, IV drug use).
  4. Use point-of-care testing when appropriate (KOH prep for fungi, Tzanck smear for HSV/VZV, wound culture for MRSA).

Recognizing Distinctive Presentations of Skin Infections

Bacterial Skin Infections

Infection Key Clinical Findings
Cellulitis Erythema, warmth, edema, tenderness; poorly marginated borders; lymphangitis possible
Erysipelas Well-demarcated, raised, “butterfly” rash often on face or lower extremities; fiery red
Impetigo (nonbullous) Honey-colored crusts around nose and mouth; contagious
Furuncle/Carbuncle Tender, erythematous, fluctuant nodule; multiple drainage points in carbuncle

Viral Skin Infections

  • Herpes simplex (orolabial/genital): grouped vesicles on an erythematous base; prodromal tingling or burning[5].
  • Herpes zoster: unilateral, painful vesicular eruption confined to a single dermatome; post-herpetic neuralgia common in older adults[5].

Fungal Skin Infections

  • Tinea corporis (ringworm): annular, erythematous plaque with central clearing and raised, scaly border.
  • Tinea cruris (jock itch): erythematous, pruritic rash in groin folds; spares the scrotum.
  • Tinea pedis (athlete's foot): interdigital maceration, scaling, and pruritus.
  • Tinea capitis: scaling patches of alopecia with broken hairs (“black dot” tinea); common in children[4].

Clinical Workup and Differential Diagnosis Strategies

  • History: Onset, prior antibiotics, animal contact, travel, insect bites, immunocompromised status, fever.
  • Physical exam: Document borders (well- vs. poorly marginated), presence of fluctuance, lymphadenopathy, systemic toxicity.
  • Diagnostic tests:
    • WBC, ESR, CRP – may be elevated in cellulitis but not routinely needed for mild cases[1].
    • Wound culture and sensitivity – for purulent infections, suspect MRSA[3].
    • KOH preparation – confirm dermatophyte infections (hyphae visible).
    • Tzanck smear – for HSV/VZV (multinucleated giant cells).
    • Wood's lamp – tinea capitis (Microsporum canis fluoresces green).
  • Differential diagnoses: Contact dermatitis, insect bite reaction, gout flare, deep vein thrombosis (DVT) – always rule out DVT using Wells criteria when a lower extremity is involved.

Therapeutic Regimens for Bacterial, Viral, and Fungal Infections

Bacterial Skin Infections

  • Mild cellulitis (no systemic signs): cephalexin (500 mg PO QID) or dicloxacillin (500 mg PO QID) for 5–7 days[1].
  • Purulent infections (MRSA suspected): trimethoprim-sulfamethoxazole (1–2 DS tablets PO BID) or doxycycline (100 mg PO BID) for 7–10 days[3].
  • Impetigo: mupirocin 2% ointment TID x 5–7 days (limited disease); if widespread, oral cephalexin[2].
  • Furuncles/carbuncles: incision and drainage (I&D) is the cornerstone; antibiotics if surrounding cellulitis or immunocompromised[3].
  • Imaging: Consider ultrasound if abscess suspected; MRI for deep infection or necrotizing fasciitis (emergency).

Viral Skin Infections

  • Herpes simplex (first episode): acyclovir (400 mg PO TID) or valacyclovir (1 g PO BID) x 7–10 days[5].
  • Herpes zoster: acyclovir (800 mg PO 5x/day) or valacyclovir (1 g PO TID) x 7 days; start within 72 hours of rash[5].
  • Pain management: NSAIDs, gabapentin, or tricyclic antidepressants for post-herpetic neuralgia; adding a short course of corticosteroids may reduce acute pain but does not prevent neuralgia[5].

Fungal Skin Infections

  • Tinea corporis/cruris/pedis: topical terbinafine 1% cream, clotrimazole 1% cream, or ketoconazole 2% cream once daily for 2–4 weeks[4].
  • Tinea capitis: oral griseofulvin (20–25 mg/kg/day microsize) or terbinafine (3–6 mg/kg/day) for 4–6 weeks; topical therapy alone is ineffective[4].
  • Patient education: Keep skin clean and dry; avoid sharing towels, linens; treat pets if suspected zoophilic infection (e.g., tinea capitis from cats).

Managing Risks and Preventing Severe Outcomes

  • Necrotizing fasciitis: severe pain out of proportion, rapid spread, bullae, gas on imaging, systemic toxicity – emergent surgical consult[1].
  • Sepsis: Fever, tachycardia, hypotension require immediate hospitalization and IV antibiotics.
  • Antibiotic resistance: Avoid fluoroquinolones as first-line for uncomplicated cellulitis; consider MRSA risk factors (prior MRSA, IV drug use, recurrent boils).
  • Post-herpetic neuralgia: Greatest risk in patients > 60 years old; prevention with VZV vaccine (Shingrix) recommended for adults ≥ 50 years[5].
  • Immunocompromised patients: May present atypically; skin infections can be fungal or viral (e.g., disseminated HSV, candidiasis); check CD4 count if HIV suspected.

Critical Distinctions for Certification Success

  • Differentiate cellulitis vs. erysipelas: Cellulitis has poorly defined borders; erysipelas has well-defined, raised borders. Both treated similarly.
  • Impetigo hallmark: Honey-colored crusts (nonbullous). Bullous impetigo (staphylococcal) has fragile blisters that rupture leaving a thin varnish.
  • Suspect MRSA if abscess fails to respond to beta-lactam antibiotics, or if risk factors present: recent hospitalization, IV drug use, crowded living.
  • Tinea corporis shows central clearing – this is the classic “ringworm” appearance.
  • Tinea capitis requires oral therapy; topical antifungals do NOT penetrate the hair follicle deep enough.
  • Herpes zoster is typically unilateral and does NOT cross the midline. If bilateral or extensive, investigate for immunosuppression.
  • Vaccination reduces incidence and severity of herpes zoster; Shingrix is preferred over Zostavax (live attenuated).
  • First-line treatment for mild cellulitis is a beta-lactam (cephalexin or dicloxacillin). For penicillin allergy: clindamycin (300 mg PO QID) or doxycycline.
  • I&D alone is sufficient for a simple abscess in immunocompetent patients without significant surrounding cellulitis; antibiotics are added if cellulitis extends > 2 cm from the edge or if the patient is immunocompromised[3].

References and Sources

  1. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft-tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):e10-e52. https://doi.org/10.1093/cid/ciu444
  2. Bowen AC, Mahé A, Hay RJ, et al. Impetigo: diagnosis, treatment, and prevention. Lancet Infect Dis. 2015;15(10):1253-1265. https://doi.org/10.1016/S1473-3099(15)00132-X
  3. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the Infectious Diseases Society of America for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis. 2011;52(3):e18-e55. https://doi.org/10.1093/cid/ciq146
  4. Weitzman I, Summerbell RC. The dermatophytes. Clin Microbiol Rev. 1995;8(2):240-259. https://doi.org/10.1128/CMR.8.2.240
  5. Whitley RJ, Gnann JW. Herpes zoster in the older adult. Infect Dis Clin North Am. 2017;31(4):789-803. https://doi.org/10.1016/j.idc.2017.07.011

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