Section 14.2: Infectious Skin Conditions

Why This Matters for the PANCE

Infectious dermatopathology represents a significant portion of family medicine and emergency department visits. You must distinguish bacterial, viral, fungal, and parasitic skin infections, map them to their primary pathogens, and select first-line antimicrobial therapies.

Cellulitis and Erysipelas

Cellulitis and erysipelas are bacterial infections of the skin layers, but they differ in depth, margins, and typical pathogens.

• Pathophysiology and Pathogens:
  • Non-purulent Cellulitis: A deep infection of the dermis and subcutaneous tissues, most commonly caused by Streptococcus pyogenes (Group A beta-hemolytic Streptococcus), followed by S. aureus.
  • Purulent Cellulitis: Associated with purulent drainage, fluctuance, or an abscess. The primary pathogen is Staphylococcus aureus, including Methicillin-Resistant S. aureus (MRSA).
  • Erysipelas: A superficial infection of the upper dermis and lymphatic channels, almost exclusively caused by Streptococcus pyogenes (Group A Strep).
• Clinical Presentation:
  • Cellulitis: Localized erythema, warmth, edema, and tenderness. The borders are ill-defined and flat. Systemic symptoms are usually mild or absent.
  • Erysipelas: Bright red, warm, edematous plaque with sharply demarcated, raised, elevated borders. It classically affects the face or lower extremities, presenting with acute-onset high fever and chills.
• Clinical Management:
  • Non-purulent Cellulitis & Erysipelas: First-line oral therapy targets Streptococcus with cephalexin (500 mg four times daily) or dicloxacillin. Clindamycin is preferred for penicillin allergies.
  • Purulent Cellulitis: First-line oral therapy must cover MRSA with trimethoprim-sulfamethoxazole (TMP-SMX), doxycycline, or clindamycin.
  • Severe/Systemic: Requires IV antibiotics such as cefazolin, ceftriaxone, or vancomycin.

Herpes Zoster (Shingles)

Herpes zoster is the reactivation of latent Varicella-Zoster Virus (VZV) in the sensory dorsal root ganglia.

• Clinical Presentation: Typically begins with a prodrome of dermatomal pain, burning, or paresthesias, followed by clustered vesicles on an erythematous base in a unilateral, dermatomal distribution that does not cross the midline (most commonly thoracic or lumbar).
• High-Yield Clinical Syndromes and Red Flags:
  • Herpes Zoster Ophthalmicus: Reactivation in the ophthalmic division of the trigeminal nerve (CN V1). The presence of vesicles on the tip, side, or root of the nose (Hutchinson's sign) indicates nasociliary nerve involvement, which is an ophthalmic emergency requiring immediate referral to prevent permanent blindness.
  • Ramsay Hunt Syndrome: Reactivation in the geniculate ganglion of the facial nerve (CN VII). Presents with facial paralysis, ear pain, and vesicles in the external auditory canal.
• Diagnostic Workup: Primarily clinical. PCR of vesicle fluid is the most sensitive and specific confirmatory test.
• Clinical Management:
  • Antiviral Therapy: Oral valacyclovir (1000 mg three times daily) or acyclovir (800 mg five times daily) should be initiated within 72 hours of rash onset to accelerate healing and reduce the risk of post-herpetic neuralgia.
  • Post-Herpetic Neuralgia (PHN): Dermatomal pain persisting more than 90 days after rash onset. Managed with gabapentin, pregabalin, or tricyclic antidepressants (TCAs).

Scabies

Scabies is a highly contagious skin infestation caused by the mite Sarcoptes scabiei.

• Pathophysiology: The female mite burrows into the stratum corneum to lay eggs, triggering a delayed Type IV hypersensitivity reaction to the mite, eggs, and feces.
• Clinical Presentation: Intense pruritus, characteristically worse at night. Examination reveals excoriated papules and pathognomonic linear burrows, typically in the finger web spaces, wrists, elbows, axillae, beltline, and male genitalia.
• Diagnostic Workup: Skin scraping of a burrow suspended in mineral oil showing mites, eggs, or feces under light microscopy.
• Clinical Management:
  • First-line Therapy: Topical permethrin 5% cream applied thoroughly from the neck down, left on for 8-14 hours, then washed off. Treatment must be repeated in 7 days to kill newly hatched mites.
  • Alternative/Severe: Oral ivermectin is indicated for outbreaks or crusted (Norwegian) scabies.
  • Environmental Control: Treat all household contacts simultaneously. Wash all clothing and bedding in hot water and dry on high heat.

Dermatophytosis and Tinea Versicolor

• Tinea Corporis (Ringworm): Annular, erythematous plaque with a raised, scaly, active border and central clearing. KOH prep shows septate, branching hyphae. Treated with topical azoles.
• Tinea Capitis: Scalp hair follicle infection presenting with scaly patches, alopecia, and 'black dots' (broken hair shafts). Oral griseofulvin is first-line because topical agents cannot penetrate the hair follicle. Griseofulvin should be taken with a fatty meal to enhance absorption. Monitor CBC and LFTs for prolonged treatment.
• Tinea Versicolor: Overgrowth of the commensal yeast Malassezia furfur (not a dermatophyte). Presents as hypo- or hyperpigmented scaly macules on the chest and back that fail to tan. KOH prep shows the classic 'spaghetti and meatballs' pattern of short hyphae and round yeast spores. Treated with topical selenium sulfide 2.5% or topical ketoconazole.

Infectious Skin Conditions Comparison Table

Classic PANCE Traps and Clinical Pearls

• The Tinea Capitis Trap: Never treat tinea capitis with topical antifungals. Oral systemic therapy (griseofulvin or terbinafine) is mandatory.
• Hutchinson's Sign Priority: A vesicle on the tip of the nose during shingles requires an urgent ophthalmology referral, not just starting oral acyclovir.
• Cellulitis Demarcation: Always mark the borders of cellulitis. If the redness spreads rapidly or systemic symptoms worsen, suspect necrotizing fasciitis or treatment failure and escalate care.