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.