Herpes zoster, commonly known as shingles, is an acute viral disease that primarily affects the nervous system, the skin, and sometimes the mucous membranes. It is characterized by severe localized pain, a distinctive vesicular skin rash, and the potential for long-term neurological complications, such as postherpetic neuralgia. The condition occurs most frequently in adults and older individuals but can affect anyone who has previously had chickenpox (varicella).
The disease is considered a reactivation of latent varicella-zoster virus (VZV), the same virus responsible for chickenpox. After the initial infection, the virus remains dormant in the nerve ganglia, often for decades. Under certain conditions—such as immunosuppression, aging, stress, trauma, or systemic illness—the virus reactivates, traveling along sensory nerves and producing the characteristic shingles rash in the affected dermatome.
Herpes zoster is caused by the varicella-zoster virus (VZV), a member of the herpesvirus family (Herpesviridae). Following a primary infection (usually in childhood as chickenpox), the virus enters a latent phase in the sensory nerve ganglia. The endogenous reactivation of this latent virus triggers shingles.
Risk factors that contribute to VZV reactivation include:
VZV reactivation is not typically spread to others as shingles per se. However, direct contact with fluid from shingles blisters can transmit the virus to a non-immune individual, resulting in chickenpox, not shingles.
The hallmark symptom of herpes zoster is a localized, painful vesicular rash that typically appears on one side of the body, following the distribution of a single dermatome—the area of skin supplied by one sensory nerve. This dermatomal pattern of the rash is due to the virus traveling from the dorsal root ganglion along the peripheral nerve to the skin.
The most commonly affected areas include:
The disease usually progresses through the following stages:
The pain associated with herpes zoster can be intense and persistent, described as burning, stabbing, or electric shock-like sensations. In severe cases, paresthesia (abnormal skin sensation) and hyperesthesia (increased sensitivity to touch) are reported. Pain often precedes the rash and can continue after lesion resolution, evolving into postherpetic neuralgia.
The diagnosis of herpes zoster is primarily clinical and is based on the characteristic dermatomal distribution of vesicular lesions combined with unilateral pain. The presence of lesions at varying stages—papules, vesicles, pustules, crusts—on a red, edematous base along a single nerve route strongly suggests herpes zoster.
Additional diagnostic tools may be used in the following scenarios:
Confirmatory laboratory methods include:
The main goals of treatment are to shorten the duration of symptoms, accelerate lesion healing, reduce viral replication, and prevent complications such as postherpetic neuralgia.
Antiviral drugs are most effective when started within 72 hours of rash onset. Common agents include:
Because pain is often the most debilitating symptom, the following medications may be used:
While most cases of herpes zoster resolve within 2–4 weeks, serious complications can occur, especially in older adults and immunosuppressed individuals:
Prevention of shingles is focused primarily on vaccination and immune system support:
Vaccination is the most effective method to reduce both the incidence and severity of herpes zoster and postherpetic neuralgia. There are two main vaccine options:
Herpes zoster is a potentially debilitating disease that goes beyond skin manifestations, often involving significant nerve pain and long-term complications. Early recognition, timely antiviral therapy, and adequate pain management are key to minimizing morbidity. Vaccination offers powerful protection, especially in older adults who are at the greatest risk.
Through proper education, proactive health management, and access to medical care, individuals can significantly reduce the impact of shingles and maintain better quality of life—even in the face of this challenging reactivation disease.
