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Herpes Simplex Virus
Herpes Simplex Virus (HSV) infection is a common viral mucocutaneous disease affecting the lips, oral cavity, and perioral tissues. It typically presents as painful papulovesicular lesions that rupture and ulcerate before healing.
Following primary infection—usually acquired during childhood—the virus remains latent in sensory nerve ganglia, particularly the trigeminal ganglion, and may reactivate periodically, resulting in recurrent disease.
Two major types exist:
HSV-1 – predominantly oral and facial infections
HSV-2 – mainly genital infections (though overlap occurs)
Primary infection commonly involves the gingiva, palate, and oral mucosa, while recurrent infections usually affect the vermillion border of the lips (herpes labialis).
Pathophysiology
HSV infection occurs through:
Direct contact with infected saliva or lesions
Viral replication in epithelial cells
Local cell destruction leading to vesicle formation
After primary infection:
Virus migrates via sensory nerves
Establishes lifelong latency in trigeminal ganglion neurons
Reactivation occurs due to triggering factors
Common Reactivation Triggers
Fever (“fever blisters”)
Emotional stress
Sunlight exposure
Trauma or dental procedures
Immunosuppression
Hormonal changes
Fatigue or systemic illness
Reactivation results in viral replication and transport back to skin or mucosa causing recurrent lesions.
Risk Factors
Childhood exposure to HSV
Immunocompromised states (HIV, malignancy)
Malnutrition
Stress
Fever or systemic infections
Excess ultraviolet exposure
Local trauma
Poor oral hygiene
Signs and Symptoms
Primary Herpetic Gingivostomatitis
(Common in children)
Fever
Malaise
Painful oral ulcers
Gingival inflammation
Drooling
Difficulty eating or swallowing
Cervical lymphadenopathy
Recurrent Herpes Labialis
Burning or tingling sensation
Local pain
Clustered vesicles on erythematous base
Ulceration after vesicle rupture
Crusting and healing without scarring
Diagnostic Criteria
Diagnosis is mainly clinical.
Typical progression:
Prodrome:
Tingling
Warmth
Itching
Within ~12 hours:
Local erythema
Lesion evolution:
Papules → Vesicles → Ulcers → Crusting → Healing
Duration:
5–12 days (average 7 days)
Investigations
Usually not required in uncomplicated cases.
Indicated when:
Severe disease
Immunocompromised patient
Atypical presentation
Neonatal infection suspected
Possible tests:
Viral PCR (gold standard)
Viral culture
Tzanck smear
Serology (limited diagnostic value)
Management
HSV infection is generally self-limiting, but treatment reduces:
Pain
Viral shedding
Duration of symptoms
Recurrence severity
Non-Pharmacological Management
Maintain adequate hydration
Avoid salty, spicy, or acidic foods/drinks
Maintain oral hygiene
Avoid touching or picking lesions
Apply petroleum jelly to prevent cracking
Avoid kissing or sharing utensils during active lesions
Identify and control triggering factors
Pharmacological Management
1. Herpes Labialis
Acyclovir cream applied every 4 hours for 5 days
Best initiated during prodromal phase.
2. Herpetic Stomatitis
Acyclovir 200 mg orally every 6 hours for 5 days
AND
Topical acyclovir cream twice daily for 5 days
3. Immunocompromised Patients
Higher viral replication risk:
Acyclovir 400 mg orally five times daily for 5 days
Longer therapy may be required.
4. Oral–Facial Herpes Zoster (Differential Treatment)
Acyclovir 400–800 mg orally five times daily for 5 days
5. Pain Control
Paracetamol 1 g orally every 8 hours for 3 days
OR
Diclofenac 50 mg orally every 8 hours for 3 days
OR
Ibuprofen 400 mg orally every 8 hours for 3 days
Avoid NSAIDs in contraindicated patients.
Special Populations
Children
Risk of dehydration due to painful swallowing.
Encourage fluids and soft diet.
Immunocompromised Patients
Risk of:
Disseminated infection
Chronic ulcers
Systemic involvement
Require early antiviral therapy.
Pregnancy
Oral HSV generally low fetal risk.
Active genital HSV near delivery requires obstetric evaluation.
Complications
Secondary bacterial infection
Dehydration (children)
Herpetic whitlow
Herpetic keratitis (ocular emergency)
Eczema herpeticum
Disseminated HSV infection
Encephalitis (rare but life-threatening)
Differential Diagnosis
Aphthous ulcers
Angular cheilitis
Impetigo
Hand-foot-mouth disease
Varicella-zoster infection
Contact dermatitis
Prevention
Avoid direct contact with active lesions
Do not share utensils, towels, or cosmetics
Use lip sunscreen (UV protection)
Maintain immune health
Stress management
Early antiviral therapy during prodrome
Hand hygiene after touching lesions
For frequent recurrences:
Suppressive antiviral therapy may be considered under specialist care.
Prognosis
Lesions heal spontaneously within 7–10 days
Recurrences decrease with age
Lifelong latency persists
Early antiviral therapy improves outcomes
Patient Education
Patients should understand that:
HSV infection is lifelong but controllable.
Recurrences are common.
Early treatment during tingling phase shortens illness.
Lesions are contagious until crusted.
References
Whitley RJ, Roizman B. Herpes simplex viruses. Lancet. 2001;357:1513-1518.
Jameson JL, Fauci AS, Kasper DL, et al. Harrison’s Principles of Internal Medicine. 21st ed. McGraw-Hill; 2022.
Arduino PG, Porter SR. Herpes Simplex Virus Type 1 infection. Oral Dis. 2008;14(4):254-259.
World Health Organization. Herpes simplex virus infections guidelines. WHO; 2023.
Habif TP. Clinical Dermatology. 7th ed. Elsevier; 2021.
Centers for Disease Control and Prevention (CDC). Genital and Oral Herpes Guidelines. 2021.
Imeandikwa:
4 Novemba 2020, 08:59:15
