OP 1.1

Vesiculobullous Diseases

Viral Diseases

Overview of Viral Diseases
  • Herpes Simplex Infections
  • Varicella-Zoster Infections
  • Hand-Foot-and-Mouth Disease
  • Herpangina
  • Measles (Rubeola)

Immunologic Diseases

  • Pemphigus Vulgaris
  • Mucous Membrane Pemphigoid
  • Bullous Pemphigoid
  • Dermatitis Herpetiformis
  • Linear Immunoglobulin A Disease

Hereditary Diseases

  • Epidermolysis Bullosa

Viral Diseases Detailed

Introduction to Viral Diseases

  • Oral mucous membranes can be affected by various viruses, each causing distinct clinical and pathological presentations.
  • Herpesviruses: This extensive family contains viruses with a DNA core, surrounded by a capsid and an envelope. Seven types are pathogenic in humans, with six affecting the head and neck area.

Herpes Simplex Infections

General Information
  • Herpes Simplex Virus (HSV) infections result in widespread vesicular eruptions on the skin and mucosa, existing in two forms:
    • Systemic or Primary
    • Localized or Secondary
  • Both forms typically resolve without treatment, though recurrent outbreaks of the secondary form are common due to latent virus sequestering in ganglionic tissue.
  • Treatment usually focuses on control rather than cure.
Pathogenesis
  • Transmission: Infection in seronegative individuals typically occurs through physical contact with an infected individual.
  • The virus binds to the cell epithelium via heparan sulfate, activating specific genes (immediate early, early, and late genes) involved in viral replication and structural protein formation.
  • Infection Spread: Lacks significant evidence for transmission via airborne droplets or contaminated surfaces.
  • Clinical manifestations vary: Many individuals experience subclinical infection, identifiable only by the presence of antibodies to HSV in the blood.
  • Incubation: Ranges from several days to 2 weeks.
Primary Herpetic Gingivostomatitis
  • Symptoms: Vesicular lesions appear in the oral and perioral area (primarily gingiva and palate), often accompanied by systemic symptoms: fever, malaise, cervical lymphadenopathy.
  • The primary infection may resolve in 7-10 days, potentially leading to virus latency in the trigeminal ganglion.
Latency and Reactivation
  • Virulence factors during Latency: During latency, no free virus or major histocompatibility (MHC) antigens are present, resulting in no T-cell response.
  • Reactivation Triggers: Factors such as sunlight, cold, trauma, stress, and immunosuppression may reactivate the virus, leading to secondary infections characterized by similar vesiculoulcerative lesions.
Clinical Features
Primary Infection
  • Occurs mainly in children, with adults susceptible if naive to the virus.
  • By age 15, about half of the population is infected.
  • Primary Herpetic Symptoms:
    • Vesicular eruptions that rupture to form ulcers.
    • Systemic reactions include fever and malaise, followed by resolution without scarring.
Secondary Infection
  • Represents reactivation of latent HSV.
  • Most common in individuals who have previously infected, with prodromal symptoms often presenting as tingling before lesions develop.
  • Lesion Characteristics:
    • Typically appear on vermilion, lips, and gingiva, healing within 1-2 weeks.
    • The recurrence rate may vary greatly and decreases as individuals age.
Immunocompromised Host
  • Secondary herpes can result in severe manifestations in immunocompromised individuals, featuring chronic and destructive lesions.
  • Co-infection with cytomegalovirus (CMV) may occur in HIV patients, but its pathogenesis remains unclear.
Differential Diagnosis
  • Many differential diagnoses exist including:
    • Streptococcal Pharyngitis: No vesicular stage, lesions localized.
    • Erythema Multiforme: Larger ulcers, less likely to affect gingiva.
    • Acute Necrotizing Ulcerative Gingivitis (ANUG): Mainly affects young adults with significant oral malodor.
    • Aphthous Stomatitis: Non-keratinized mucosa and lesions differ clinically.
Treatment Options
  • Timing: The effectiveness of treatment relies on prompt initiation (within 48 hours).
  • Acyclovir and Analogs:
    • Acyclovir is converted by viral enzymes to inhibit viral DNA polymerase, sparing host cellular processes.
    • Dosage: Systemic acyclovir can be administered in doses of 200-400 mg five times daily.
    • Topical Treatment: A 5% acyclovir ointment has limited efficacy.
  • Supportive Measures: Fluids, rest, analgesics, and antipyretics are integral parts of the treatment regimen for herpes simplex infections, particularly for systemic primary infections.
Clinical Observations
  • Asymptomatic shedding of virus can occur in healthy adults. The risk of transmission from shedding has not been definitively established, though it is presumed low.
  • Previous associations with HSV and carcinoma have largely been refuted, attributing little or no etiological significance to HSV in oral cancers.
Summary
  • The vast majority of HSV infections are manageable with early intervention and support, especially in immunocompromised populations who may endure more severe consequences.