How Shingles Develops
Shingles (herpes zoster) is caused by the reactivation of varicella zoster virus (VZV) that has remained dormant in sensory nerve ganglia after a primary varicella (chickenpox) infection. 1
Pathophysiology of Shingles
- After primary varicella infection (chickenpox), the virus establishes latency in neuronal ganglia throughout the body 1
- The virus can remain dormant in the dorsal root ganglia or sensory ganglia of the cranial nerve for decades 1
- Reactivation of latent VZV causes herpes zoster (shingles) when the cellular immune response fails to control the latent replication of the virus 1
- Approximately 20-30% of people will develop herpes zoster over their lifetime 1
Risk Factors for VZV Reactivation
- Age: Disease incidence increases markedly beginning at approximately 50 years of age 1
- Declining immunity: The increase in herpes zoster incidence is associated with a relative loss of cell-mediated immunity to VZV that occurs naturally with aging 1
- Immunocompromised status: Herpes zoster occurs more frequently in immunocompromised patients 1
- Early chickenpox: Children who acquire chickenpox during the first year of life have an increased risk of developing shingles later 1
- Other health conditions: Increased risk is observed in those with comorbidities such as:
- Diabetes mellitus
- Rheumatoid arthritis
- Cardiovascular diseases
- Renal disease
- Systemic lupus erythematosus
- Inflammatory bowel disease 1
Clinical Manifestations of Shingles
- Herpes zoster manifests as a painful vesicular cutaneous eruption in a dermatomal distribution 1
- The rash is often preceded by prodromal pain in the affected dermatome 1
- Common sites for herpes zoster include:
- Thoracic dermatomes (40-50% of cases)
- Cranial nerve (20-25%)
- Cervical (15-20%)
- Lumbar (15%)
- Sacral (5%) dermatomes 1
- Skin changes begin with an erythematous maculopapular rash, followed by clear vesicles accompanied by pain 1
- New vesicle formation typically continues for 3-5 days, followed by pustulation and scabbing 1
Complications of Shingles
- Postherpetic neuralgia (PHN): Persistent pain after the rash has healed, occurring in approximately 10-15% of patients 1
- Ocular complications: Including keratitis, iridocyclitis, secondary glaucoma, and vision loss 2
- Neurological complications: Various motor neuropathies, encephalitis, Guillain-Barré syndrome 2
- Secondary bacterial infection of vesicles 2
- More severe disease in immunocompromised patients, including potential for cutaneous dissemination and visceral involvement 2
Prevention
- Vaccination is the most effective strategy to prevent both varicella and herpes zoster 1
- Two types of zoster vaccines are available:
- Zoster vaccine live (ZVL): A live, attenuated vaccine for adults 50-79 years of age 1
- Recombinant zoster vaccine (RZV): An inactivated, recombinant, subunit vaccine recommended for adults aged 50 years and older or adults aged at least 18 years who are at increased risk of herpes zoster due to immunodeficiency or immunosuppression 1
- The risk of herpes zoster after immunization appears to be lower than the risk after wild-type varicella infection 1
Understanding the mechanism of viral latency and reactivation is crucial for developing effective prevention and treatment strategies for this painful condition that significantly impacts quality of life, particularly in older adults.