Viral, Fungal, Bacterial and Parasitic Skin Infections

Connect the organism, tissue involved, characteristic lesion, diagnostic clue and antimicrobial approach for rapid KMU revision.

1. THE TOPIC IN ONE CONNECTED FLOW

Skin infections become easier to distinguish when the organism is linked to the tissue it prefers. The site and mechanism of infection determine whether the patient develops vesicles, scaling, crusting, diffuse inflammation, an abscess, tissue necrosis or a chronic ulcer. Diagnosis and treatment then follow from this same relationship.

Causative Agent

Virus, fungus, bacterium or Leishmania

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Preferred Site

Epithelium, keratin, follicle, dermis, deep tissue or macrophage

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Pathological Change

Replication, inflammation, pus formation or tissue destruction

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Clinical Pattern

Vesicle, scale, crust, pustule, erythema, abscess, necrosis or ulcer

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Diagnostic Clue

Distribution, depth, lesion morphology and exposure

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Treatment Logic

Antibacterial, antifungal, antiviral or appropriate referral

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Outcome

Resolution, recurrence, scarring or serious tissue damage

2. KEY CLINICAL CONNECTIONS

Vesicles: HSV versus Herpes Zoster

HSV latency in sensory ganglia → reactivation toward local epithelium → recurrent grouped vesicles.

VZV reactivation in a sensory ganglion → spread along one sensory nerve → painful unilateral dermatomal eruption.

Superficial Fungal Pattern

Dermatophyte keratin utilization → growth in skin, hair or nails → scaling and advancing lesion margin.

Candida + warm moist environment → superficial overgrowth → macerated erythema with peripheral satellite lesions.

Depth Determines Bacterial Presentation

Epidermis → impetigo; follicle → folliculitis/furuncle; upper dermis and lymphatics → erysipelas; deeper dermis/subcutis → cellulitis.

Deep rapidly spreading infection → vascular thrombosis → ischemia and necrosis → urgent concern for necrotizing infection.

Drug and Parasite Connection

Azoles → reduced ergosterol synthesis; terbinafine → squalene epoxidase inhibition; acyclovir → reduced viral DNA synthesis.

Sandfly inoculation → Leishmania uptake by macrophages → chronic papule or nodule → ulcer → confirmation and appropriate referral.

3. AIM HIGH-YIELD INTEGRATION REVIEW

⭐ HSV: sensory ganglion latency → reactivation → recurrent localized vesicles; herpes zoster: sensory nerve involvement → unilateral dermatomal vesicles with pain.

Dermatophytes: keratin utilization → infection of stratum corneum, hair or nails → scaly superficial lesions; nail involvement may require systemic therapy.

Candida: moisture and host susceptibility → opportunistic overgrowth → macerated erythema with satellite lesions.

⭐ Bacterial infection depth predicts appearance: superficial epidermis → impetigo; follicular infection → folliculitis/furuncle; superficial lymphatics → erysipelas; deeper tissue → cellulitis.

⭐ Necrotizing infection: rapid deep spread → vascular thrombosis → ischemia → tissue necrosis; severe pain with rapid progression requires urgent assessment.

Antifungal therapy: azoles reduce ergosterol synthesis, while terbinafine inhibits squalene epoxidase → disruption of fungal membrane function and growth.

Antiviral therapy: acyclovir activation in infected cells → inhibition of viral DNA polymerase → reduced herpesvirus replication.

⭐ Cutaneous leishmaniasis: sandfly transmission → macrophage infection → slowly progressive papule or nodule → chronic ulcer; lesion site and extent guide confirmation and referral.

AIM Exam Trap: Erysipelas is the more superficial infection and therefore has a raised, relatively sharply defined margin; cellulitis extends into deeper dermis and subcutaneous tissue and is more poorly demarcated.

Viral, Fungal, Bacterial and Parasitic Skin Infections

1. THE TOPIC IN ONE CONNECTED FLOW

2. KEY CLINICAL CONNECTIONS

3. AIM HIGH-YIELD INTEGRATION REVIEW

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