Viral Skin Infections — Molluscum Contagiosum, Warts (HPV), Herpes Simplex and Herpes Zoster: Features, Tzanck Smear and Treatment

All four are diagnosed mainly clinically. Immunosuppression (HIV, transplant, chemotherapy) makes every one of them more extensive, atypical and persistent, and is a favourite cue in exam vignettes.

Molluscum contagiosum (MC) is a benign epidermal eruption caused by a double-stranded DNA virus of the Poxviridae family. Humans are the only known host, and the virus infects only epidermal keratinocytes; it replicates in the cytoplasm and cannot be cultured in standard cell lines. Lesions stay in the skin — there is no viraemia or systemic illness.

• Spread by skin-to-skin contact, autoinoculation (scratching) and fomites — towels, gym equipment, pool surfaces; in adolescents and adults also sexual contact.
• Incubation about 2–6 weeks (range from 1 week to 6 months); lesions usually resolve within a year.
• MCV-1 causes most paediatric cases; MCV-2 is commoner in sexually transmitted infection and in severe disease in the immunocompromised.
• Sites — trunk, limbs and face in children; genital, perineal and lower abdominal areas in sexually active adults. The oral mucosa is rarely involved.
• Children typically have 10–20 lesions; children with atopic dermatitis are at particular risk of extensive disease.
• Molluscum dermatitis (red scaly eczema around lesions) is an immune reaction and often a sign that lesions are about to resolve — not a bacterial infection.
• HIV / advanced immunodeficiency — numerous lesions, 'giant' molluscum (10–15 mm or more), atypical sites such as face and eyelids, and resistance to treatment.

Observation ('benign neglect') is first-line in immunocompetent patients because most lesions clear spontaneously and no treatment is consistently superior. Treat when lesions are persistent, symptomatic, cosmetically distressing, or to reduce spread.

Warts are benign proliferations caused by HPV, a double-stranded DNA virus; over 150 HPV types are known, and only some infect skin. Infection begins in the basal layer of the epidermis, causing keratinocyte proliferation and hyperkeratosis. Spread is by skin contact or autoinoculation — scratching can produce a line of warts (pseudo-Koebner phenomenon). The incubation period can reach 12 months. Children, people with dermatitis (damaged barrier) and the immunosuppressed are most often affected.

Most cutaneous warts resolve spontaneously: in children about 50% clear within six months and 90% within two years. Treat for immunosuppression, complications (nail damage, painful plantar warts) or patient preference. Treatments remove virus-containing skin; they do not kill the virus, so recurrence is common.

• Genital warts (condylomata acuminata) — HPV 6 and 11 cause about 90%. Only 14 of the 200-plus HPV types are considered high-risk for malignant change (for example types 16 and 18), and they are different from the types in genital warts.
• Genital wart therapy includes imiquimod 5% cream three times weekly, trichloroacetic acid (clinic use) and physical removal.
• HPV vaccines prevent anogenital warts; see cervical cancer screening for the vaccine and screening context.
• Recurrence is commoner in smokers and the immunosuppressed; immunity is likely type-specific.

HSV is a double-stranded DNA herpesvirus. HSV-1 mainly causes oral and facial disease, HSV-2 mainly genital and rectal disease, though either can infect any skin or mucosa. After the primary episode the virus remains latent in the dorsal root ganglia and travels along the nerve to the skin during recurrence. A lesion is infectious for about 7–12 days, and the incubation period is 2–12 days.

• Complications — dendritic corneal ulcer, erythema multiforme (target lesions), facial nerve palsy, rarely meningitis; disseminated disease in immunocompromised patients.
• Diagnosis — clinical; confirm doubtful cases by PCR or culture of a swab from a fresh vesicle. Serology is of little use because most adults are positive.
• Treatment — mild disease needs none. Antivirals shorten attacks but cannot clear latent virus: aciclovir 200 mg five times daily for 5 days, valaciclovir 500 mg twice daily for 5 days, or famciclovir; longer or higher doses for immunocompromised patients or eczema herpeticum.

Herpes zoster (shingles) is reactivation of latent varicella-zoster virus from cranial nerve or dorsal root ganglia, driven by loss of cell-mediated immunity. Triggers include emotional stress, immunosuppressive drugs, illness and malignancy. Incidence is about 1.2–3.4 per 1000 person-years in healthy younger adults and 3.9–11.8 per 1000 in those over 65.

• Prodrome — burning pain, malaise, fever, 48 hours or more before the rash.
• Eruption — grouped vesicles on an erythematous base, in 1–3 crops over 3–5 days, unilateral and limited to one dermatome (thoracic about 53%, cervical 20%, trigeminal 15%, lumbosacral 11%). Patients are infectious until lesions crust.
• Herpes zoster ophthalmicus — ophthalmic division of the trigeminal nerve, in roughly 10–25% of cases; Hutchinson sign (vesicles on the nasal tip) points to nasociliary involvement and a high risk of ocular disease.
• Ramsay Hunt syndrome — zoster of the facial and vestibulocochlear nerves causing ear vesicles, hearing loss and vertigo.
• Postherpetic neuralgia — pain lasting beyond about 4 weeks, sometimes 12 months or more; the principal morbidity.

A Tzanck smear is a stained scraping from the base of a fresh vesicle. In varicella-zoster infection it shows multinucleated giant cells. It is quick but has lower sensitivity and specificity than direct fluorescent antibody testing or PCR, which are preferred when confirmation is needed.