Virological characteristics and epidemiology
The causative agent of shingles is human herpesvirus type 3 — Varicella-zoster virus (VZV). Among all members of the herpesvirus family, it has the smallest genome, although it bears significant structural similarity to them. In laboratory conditions, the virus is cultured in human diploid fibroblasts, where it forms characteristic intranuclear inclusions. Its cytopathic effect manifests as the formation of syncytia — giant multinucleated cells. An important feature of VZV kinetics is that its replication cycle proceeds much slower compared to the herpes simplex virus.
The infection is a strict anthroponosis and is characterized by extremely high contagiosity. The vast majority of the world's population suffers from the primary form — chickenpox. The main transmission route of the virus is airborne, but infection is also possible via contact (through direct contact with the contents of skin vesicles) and via transplantation. After primary infection, the pathogen does not leave the body, but enters a state of prolonged persistence. It is this latent infection that creates the risk of developing shingles in the future. The incidence ranges from 3 to 5 cases per 1,000 population per year, with the frequency of the pathology steadily increasing with age. In HIV-infected patients, shingles occurs in 5–10% of cases and is caused by damage to spinal roots and ganglia.
Clinical picture and stages of development
Shingles is not a primary infection — it is the result of reactivation of a latent virus. The disease manifests with a specific vesicular rash that characteristically "crawls" along the nerve trunks.
In some cases, the disease is preceded by a prodromal period accompanied by mild general infectious manifestations: fever, general fatigue, and malaise. The onset of the pathology begins with the appearance of unilateral pain, a burning sensation, or pronounced hyperesthesia in the innervation zone of several dermatomes. A few days later, a skin rash forms in the pain area.
Stages of skin manifestations:
- Appearance of erythematous macules and papules.
- Transformation of elements into specific vesicles.
In an atypical course of infection, in addition to classical segmental rashes, the patient may develop additional scattered vesicles.
Typical localization of lesions:
- Thoracic segments (occurs in more than 50% of cases).
- Ophthalmic branch of the trigeminal nerve (ramus ophthalmicus nervi trigemini) — about 20% of cases.
- Lumbosacral segments — about 20% of cases.
In an uncomplicated course, the disease resolves within a few weeks: the pain syndrome stops, and the rash disappears completely. Skin dispigmentation or scars often remain at the site of the former rash.
Complications and diagnostic workup
The most frequent and severe complication of shingles is postherpetic neuralgia. It develops in almost a third of patients (up to 30% of cases), with elderly individuals being at the greatest risk.
Clinically, postherpetic neuralgia manifests as severe pain that does not go away even after the complete regression of all skin rashes. The nature of the pain syndrome in the area of former skin manifestations can be of two types:
- Paroxysmal pain: sharp, cutting, or stabbing.
- Constant pain: exhausting, boring, or burning.
Diagnosis of the disease most often does not cause any difficulties for clinicians. It is based exclusively on the evaluation of clinical data: the presence of a characteristic pain syndrome combined with specific vesicular rashes strictly localized along the dermatomes.
Therapeutic approaches
Treatment of uncomplicated forms of shingles with sparse rashes and moderate pain is based on symptomatic therapy. The main areas of treatment include:
- Prescription of analgesics for effective relief of the pain syndrome.
- Use of local antiseptics, which is necessary for the prevention of secondary purulent bacterial complications at the sites of ruptured vesicles.
- Application of local anesthetics for local reduction of sensitivity and relief of the patient's condition.
The "TTP" rule will help remember the typical localization of rashes: Thoracic segments (50%), Trigeminal nerve ophthalmic branch (20%), Pelvic/lumbosacral segments (20%).
Class and exam questions
Is shingles a primary infection?
No, this is always a secondary manifestation. The disease occurs due to the reactivation of the Varicella-zoster virus, which persisted in a latent state for a long time after chickenpox suffered in childhood.
What cytopathic effect does the virus have on cells?
The virus multiplies in human diploid fibroblasts, forming intranuclear inclusions and causing the formation of syncytia — giant multinucleated cells.
What is the peculiarity of the pain syndrome in postherpetic neuralgia?
Pain persists even after complete resolution of the skin rash. It can be of a constant burning, boring nature or manifest as acute cutting, stabbing attacks in the area of former rashes.
How often does shingles occur in HIV-infected individuals?
In HIV patients, this pathology is diagnosed in 5–10% of cases. Its development is associated with damage to spinal roots and ganglia against the background of immunodeficiency.
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