31.3 Viral Oral Infections

Viral Oral Infections

Viruses affecting the oral cavity are predominantly DNA viruses of the Herpesviridae family, alongside enteroviruses of the Picornaviridae family.

                                   Viral Infections of the Oral Cavity
                                                   │
         ┌────────────────────────┬────────────────┴────────────────┬────────────────────────┐
         ▼                        ▼                                 ▼                        ▼
Herpes Simplex (HSV-1)   Varicella Zoster (VZV)           Epstein-Barr (EBV)          Enteroviruses
• Primary: Acute         • Primary: Varicella (Chickenpox)• Mononucleosis             • Coxsackie A
  gingivostomatitis      • Reactivation: Shingles         • Oral Hairy Leukoplakia    • Herpangina
• Secondary: Cold sore     - Unilateral dermatomal          - Lateral tongue            (soft palate)
  (herpes labialis)        - Respects midline               - Corrugated white        • Hand-foot-and-mouth
• Fiery red gingiva        - Prodromal severe neuralgia     - HIV indicator             (hands/feet/mouth)

Herpes Simplex Virus 1 (HSV-1)

HSV-1 is transmitted via infected saliva or active perioral lesions. It establishes lifelong latency within the sensory trigeminal ganglion (Gasserian ganglion).

1. Primary Herpetic Gingivostomatitis:

   • Epidemiology: Typically affects young children (aged 6 months to 5 years) following the loss of maternal antibodies, or increasingly, young adults.
   • Systemic Signs: Sudden onset of high pyrexia (>38.5°C), irritability, headache, marked submandibular and cervical lymphadenopathy, and general malaise.
   • Oral Manifestations: Generalized acute marginal gingivitis; the attached and marginal gingiva becomes fiery red, edematous, and boggy. Within 24–48 hours, crops of fragile, pinhead-sized vesicles erupt across both keratinised and non-keratinised oral mucosa (gingiva, tongue, hard palate, buccal mucosa, lips). These vesicles rapidly rupture, coalescing into painful, shallow, yellowish-grey ulcers with distinct red halos.
   • Course: Self-limiting within 10 to 14 days. Management is supportive: adequate hydration (prevent dehydration in toddlers), paracetamol or ibuprofen for pain/pyrexia, and soft diet. In severe cases presenting within the first 72 hours of vesicle onset, systemic Aciclovir (200 mg 5 times daily; adjusted for pediatric weight) accelerates resolution.

2. Recurrent Herpes Labialis ("Cold Sores"):

   • Occurs upon reactivation of latent HSV-1 within the sensory trigeminal ganglion. Virions travel down the sensory axon to the mucocutaneous junction of the vermilion border of the lip.
   • Triggers: Ultraviolet sunlight exposure, febrile illness, physical trauma, immunosuppression, menstruation, and psychological stress.
   • Clinical Stages:
     1. Prodrome: Tingling, burning, itching, or paresthesia at the site lasting 6–24 hours.
     2. Vesicular Stage: Cluster of tense, fluid-filled micro-vesicles on an erythematous base.
     3. Ulcer / Crusting Stage: Vesicles rupture within 24–48 hours, exuding infectious clear fluid, followed by golden-brown crusting.
     4. Resolution: Re-epithelialisation without scarring within 7–10 days.
   • Management: Topical Aciclovir 5% cream applied 5 times daily, initiated during the prodromal phase to abort or reduce lesion duration.

Varicella Zoster Virus (VZV / HHV-3)

1. Primary Infection (Chickenpox / Varicella):

   • Highly contagious childhood exanthem presenting with pyrexia and a centripetal, itchy, vesicular rash progressing from macules to papules, vesicles, and crusts ("dewdrops on a rose petal"). Intraoral vesicles on the palate and fauces may precede the skin eruption.

2. Reactivation (Herpes Zoster / Shingles):

   • Reactivation of dormant VZV from dorsal root ganglia or cranial nerve sensory ganglia (most commonly the ophthalmic V1 or maxillary V2 / mandibular V3 divisions of the trigeminal nerve).
   • Clinical Picture: Characterized by a strict unilateral dermatomal distribution respecting the anatomical midline.
   • Prodrome: 2 to 4 days of intense, severe, burning or lancinating neuropathic pain localized to the dermatome. Intraoral prodromal pain in V2/V3 can mimic severe irreversible pulpitis, frequently prompting misdiagnosis and inappropriate root canal therapy or extraction of vital teeth.
   • Eruption: Unilateral crops of vesicles erupting on the skin and/or corresponding intraoral mucosa (e.g., strictly unilateral hard palate in V2; mandibular gingiva and tongue half in V3). Vesicles rupture to form coalescent, deeply painful ulcers that heal over 2–4 weeks.
   • Complications:
     • Post-Herpetic Neuralgia (PHN): Persistent, intractable, burning neuropathic pain persisting for >3 months after the rash has completely healed. Occurs in up to 50% of patients over age 60; managed with gabapentin, pregabalin, or amitriptyline.
     • Hutchinson's Sign: Vesicles on the tip and side of the nose, indicating involvement of the external nasal branch of the nasociliary nerve (CN V1). Heralds severe, sight-threatening ocular complications (corneal ulceration, uveitis) and requires immediate emergency ophthalmology referral.
     • Ramsay Hunt Syndrome (Herpes Zoster Oticus): Reactivation within the geniculate ganglion of the facial nerve (CN VII); presents with the classic triad of ipsilateral lower motor neuron facial palsy, severe ear pain (otalgia), and vesicular eruptions in the external acoustic meatus, tympanic membrane, and anterior two-thirds of the tongue.
   • Management: High-dose systemic antiviral therapy initiated within 72 hours of rash onset: Aciclovir 800 mg orally 5 times daily for 7 days, or Valaciclovir 1 g orally 3 times daily for 7 days.

Epstein-Barr Virus (EBV / HHV-4)

1. Infectious Mononucleosis (Glandular Fever):

   • Primary EBV infection in adolescents and young adults. Triad of high pyrexia, severe exudative pharyngotonsillitis, and prominent cervical lymphadenopathy. Diagnostic oral sign: multiple petechiae at the junction of the hard and soft palate appearing early in the disease course.

2. Oral Hairy Leukoplakia (OHL):

   • Pathophysiology: Opportunistic productive EBV replication within the spinous keratinocytes of the lingual epithelium, occurring almost exclusively in individuals with significant cell-mediated immunosuppression (classic hallmark of HIV infection with CD4 count <200 cells/μL, or solid organ transplant recipients on immunosuppressants).
   • Clinical Appearance: Asymptomatic, white, vertically corrugated, non-wipeable, "hair-like" or folded hyperkeratotic patches along the lateral borders of the tongue (frequently bilateral).
   • Clinical Significance: OHL is benign and has zero premalignant potential. However, it is an invaluable surrogate marker of advanced systemic cellular immunosuppression. Identification in an apparently healthy individual warrants urgent HIV and immunological testing.
   • Histology: Marked hyperparakeratosis, epithelial acanthosis, "ballooning" pale degeneration of upper stratum spinosum cells with nuclear pyknosis, and ground-glass intranuclear viral inclusions (nuclear beading).

Enteroviruses (Coxsackievirus A)

1. Herpangina:

   • Caused by Coxsackievirus A strains (A1–A6, A8, A10, A22). Sudden onset of high fever, sore throat, and dysphagia in children.
   • Oral Lesions: Small (1–2 mm) vesicles that rupture into punched-out ulcers surrounded by red haloes, confined strictly to the posterior oral cavity: soft palate, uvula, anterior tonsillar pillars, and posterior pharyngeal wall. The anterior mouth (gingiva, buccal mucosa, hard palate) is characteristically spared.

2. Hand, Foot, and Mouth Disease (HFMD):

   • Caused predominantly by Coxsackievirus A16 and Enterovirus 71. Common in preschool children.
   • Presentation: Low-grade fever accompanied by painful, shallow, oval oral vesicles on the buccal mucosa, tongue, and hard palate, concurrent with non-pruritic maculopapular and grey-white vesicular eruptions on the palms of the hands, soles of the feet, and buttocks.