An Overview on Viral Folliculitis

Introduction: Folliculitis – the inflammation of hair follicles – most commonly arises from bacterial invasion, notably Staphylococcus aureus. However, a spectrum of viral agents can likewise infect the follicular unit, giving rise to viral folliculitis, a comparatively rare but clinically significant entity. Unlike classical bacterial or fungal forms, viral folliculitis involves direct infection of the follicle by viruses such as herpes simplex virus (HSV), varicella-zoster virus (VZV), and molluscum contagiosum virus (MCV). These infections may occur in healthy people via direct skin-to-skin contact or fomite transmission, or they may herald systemic viral spread in immunocompromised individuals. This article provides an in-depth exploration of viral folliculitis, covering its anatomy, epidemiology, pathogenesis, clinical features, diagnostic strategies, management, prognosis, and preventive measures.

Anatomy of the Pilosebaceous Unit: Understanding viral folliculitis begins with the pilosebaceous unit, which comprises:

1. Infundibulum: The superficial segment from the follicular orifice to the sebaceous duct opening.
2. Isthmus: The midportion between the sebaceous duct and arrector pili muscle insertion, rich in progenitor cells.
3. Inferior segment: Encompasses the hair bulb and dermal papilla, the site of active hair growth.

Viral infection is usually confined to the infundibulum, manifesting as folliculitis, though deeper inoculation can produce more extensive cutaneous involvement.

Epidemiology and Risk Factors: Viral folliculitis is uncommon, and precise incidence data are sparse. Reported cases cluster in the following contexts:

• Immunocompromised hosts: HIV/AIDS, organ transplantation, chemotherapy. MCV folliculitis in particular may signal underlying immunosuppression.
• Intravenous drug users (IVDU): Share of contaminated equipment can introduce HSV or VZV into follicular structures.
• Close-contact settings: HSV transmission during shaving or close skin contact; MCV in swimming pools, gyms or among children attending school together.
• History of recurrent herpes outbreaks: Individuals with frequent orolabial or genital HSV episodes may develop herpetic folliculitis in adjacent skin.

Though most viral folliculitis arises in those with predisposing factors, sporadic cases in healthy individuals have been documented.

Causative Viruses and Pathogenesis: The principal viruses implicated in folliculitis include:

1. Herpes Simplex Virus (HSV-1 and HSV-2): Pathogenesis: HSV gains entry through microtrauma (e.g., shaving nicks) to infect the infundibular keratinocytes, replicates locally, and spreads cell-to-cell. Host response: Initial neutrophilic infiltration, followed by lymphocytic perivascular cuffing and T-cell–mediated cytotoxicity.
2. Varicella-Zoster Virus (VZV): Pathogenesis: Reactivation of latent VZV in dorsal root ganglia leads to cutaneous eruption along a dermatome; follicular infection occurs as vesicles overlie follicular ostia. Host response: Similar to HSV but often more pronounced neuralgia due to neurotropic reactivation.
3. Molluscum Contagiosum Virus (MCV): Pathogenesis: A poxvirus that infects epidermal keratinocytes, inducing localized hyperplasia and molluscum bodies. Follicular involvement may occur when lesions develop over follicles or in cases of widespread disease. Host response: Eosinophil-poor, mixed inflammatory infiltrate; lesions often persist longer in immunosuppressed hosts.

Other rare viral causes reported in isolated cases include Vaccinia virus (post-smallpox vaccination folliculitis) and Orf virus (in zoonotic exposures).

Clinical Presentation: The manifestations of viral folliculitis vary by pathogen:

• Herpetic Folliculitis: Begins as clusters of small vesicles on an erythematous base, often around the beard, mustache, or shaved areas. Vesicles evolve into pustules or ulcerations, later crusting over. Lesions are typically painful, burning or pruritic. May be preceded or accompanied by prodromal tingling or paresthesia. Often occurs in patients with prior facial or genital HSV outbreaks.
• Zoster-Associated Folliculitis: Linear distribution of grouped vesiculopapular lesions following a dermatome. Intense neuralgic pain, even before rash onset. Vesicles may overlie hair follicles, with secondary folliculitis in some lesions.
• Molluscum Contagiosum Folliculitis: Smooth, dome-shaped, umbilicated papules clustered in hair-bearing areas such as the axillae, groin or trunk. Lesions are usually asymptomatic but may become inflamed when secondary bacterial or viral infection occurs. In immunosuppressed individuals, lesions can be larger, more numerous, and resistant to resolution.

Differential Diagnosis: Viral folliculitis must be distinguished from:

• Bacterial folliculitis (S. aureus, Pseudomonas).
• Fungal folliculitis (Malassezia, Candida, dermatophytes).
• Acneiform eruptions (acne vulgaris, rosacea).
• Eosinophilic pustular folliculitis (Ofuji disease).
• Demodex folliculitis (mite overgrowth).

Key clues favoring viral etiology include clustered vesicles, dermatomal distribution (area of skin that receives sensory input from a single spinal nerve), umbilicated papules (having a small depression that resembles a navel), poor response to antibiotics, and relevant exposure history.

Diagnostic Modalities: Accurate diagnosis combines clinical assessment with laboratory techniques:

1. Tzanck Smear: Scrapings from base of vesicles examined for multinucleated giant keratinocytes, suggestive of HSV/VZV.
2. Viral Culture and PCR: Swabs of vesicular fluid sent for viral culture or PCR to determine HSV type or confirm VZV. PCR offers higher sensitivity and faster turnaround than culture.
3. Histopathology: Biopsy may demonstrate ballooning degeneration of keratinocytes, acantholysis and intranuclear inclusion bodies (Cowdry type A) in HSV/VZV; Henderson-Patterson bodies in molluscum.
4. Dermoscopy: Useful noninvasive tool: HSV lesions show clustered “targetoid” structures, while molluscum reveals central umbilication with polylobular crypts.
5. Serology: Limited utility for acute diagnosis but may support a history of past exposure.

Management: Approaches differ by virus, infection severity, and host immunity:

• Herpes Simplex Virus Folliculitis: First-line: Oral acyclovir, or valacyclovir daily for 5 days. Alternative: Famciclovir daily for 5 days. Adjunctive: Oral antihistamines for pruritus; topical zinc oxide or low-potency steroids to soothe inflammation.
• Varicella-Zoster Virus Folliculitis: First-line: Acyclovir up to five times daily for 7–10 days, or valacyclovir three times daily; initiated within 72 hours of rash onset for maximal benefit. Pain control: Gabapentin or tricyclic antidepressants for post-herpetic neuralgia prophylaxis.
• Molluscum Contagiosum Folliculitis: Localized disease: Physical removal (curettage), cryotherapy, or application of keratolytics (e.g., salicylic acid). Extensive or recalcitrant: Topical imiquimod, cantharidin, or in immunosuppressed patients, off-label use of oral cimetidine. Emerging therapies: Photodynamic therapy and intralesional bleomycin have shown promise.

In immunocompromised hosts, combination antiviral therapy and immune reconstitution – where feasible – are critical. Hospitalization may be necessary for disseminated or severe cases.

Prognosis: HSV/VZV Folliculitis: Lesions typically heal within 1–2 weeks with antiviral therapy; prompt treatment reduces risk of secondary bacterial infection and scarring.

• Molluscum Contagiosum: In immunocompetent individuals, lesions often resolve spontaneously over 6–12 months; in immunosuppressed, persistence and recurrence are common until immune function improves.

Overall, viral folliculitis carries a favorable prognosis when diagnosed early and managed appropriately; delayed or inadequate treatment may lead to complications such as secondary bacterial superinfection, scarring alopecia, or chronicity.

Prevention: Strategies to reduce transmission and recurrence include:

1. Hygiene and Barrier Measures: Avoiding sharing razors, towels or personal care items. Using separate washcloths and launder frequently in hot water. Applying barrier creams or emollients after shaving.
2. Vaccination: VZV: Varicella vaccine in children reduces primary infection; zoster vaccine in adults ≥50 years lowers reactivation risk. HSV: No approved vaccine; investigational vaccines are in clinical trials.
3. Behavioral Modifications: Instructing patients to avoid shaving over active lesions; using electric clippers or let hair grow until lesions have resolved. Encouraging safe practices among IVDU.
4. Immune Optimization: For HIV-positive patients, maintaining antiretroviral therapy adherence to preserve CD4 counts. Minimizing systemic corticosteroids and other immunosuppressants when possible.

Conclusion: Although rare, viral folliculitis demands clinical vigilance, particularly in patients with risk factors such as immunosuppression, recurrent herpes infections or close communal living environments. Distinguishing viral from bacterial or fungal etiologies is essential to avoid misdirected antibiotic therapy and to initiate pathogen-specific antiviral or lesion-directed treatments. A combination of careful history, clinical examination, laboratory diagnostics and appropriate antiviral or procedural interventions ensures favorable outcomes. Preventive measures, ranging from vaccination to personal hygiene, play a pivotal role in reducing both initial infections and recurrences, thereby safeguarding cutaneous health and patient quality of life.

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