Pathogenesis and connection with primary infection
Following typical or atypical chickenpox, the infectious process does not end with the complete elimination of the pathogen. The virus enters a latent form and is capable of persisting in the host organism for decades. The primary reservoir consists of the neurons of sensory nerve ganglia.
The disease manifests as Herpes zoster upon exposure to triggering factors. A key condition for virus reactivation is immunosuppression of any origin (including in risk groups, debilitated patients, individuals with severe comorbidities, or those receiving corticosteroids). Epidemiologically, it is important to remember that contact between a non-immune person (without a history of the infection or vaccination) and a patient suffering from shingles during the incubation period can lead to the development of classic chickenpox.
Clinical presentation
The manifestation of Herpes zoster is characterized by an acute onset. The disease proceeds with pronounced neurological and cutaneous manifestations.
- Prodromal period: lasts from 1 to 2 days. It is accompanied by the development of intoxication syndrome and specific preherpetic neuralgia. Patients report radicular pain, as well as severe pain along the affected nerve trunks.
- Rash period: skin elements appear against the background of a low-grade fever. The formation of clustered vesicular rash foci is characteristic. The exanthem forms on a hyperemic background, with elements arranged in groups.
Laboratory diagnostics
The diagnosis is often based on clinical and epidemiological data, although specific laboratory methods are used in atypical cases. The material used for testing includes rash elements (papule scrapings, vesicle fluid, crusts), and cerebrospinal fluid in neurological complications.
- Virus-scopical methods: characterized by speed (2–6 hours). Light microscopy with silver staining reveals intranuclear inclusions in the vesicle contents. The direct immunofluorescence assay (DFA) allows the detection of viral antigens in imprint smears.
- Molecular-biological methods (PCR): used in diagnostic difficulties (material — blood, vesicle contents, cerebrospinal fluid).
- Serological diagnostics: ELISA, CFtest, HI test have retrospective significance. Antibodies are detected starting from the 2nd week, peaking at the 3rd week. A reliable criterion is a 4-fold increase in the titer of specific antibodies.
- Virological method: isolation of the virus in tissue culture. A lengthy (3–14 days) and laborious process that is practically unused in modern practice.
Differential diagnosis of vesicular rashes
When performing a differential diagnosis of vesicular skin lesions, other infections accompanied by exanthem should be excluded:
- Impetigo (strepto-staphyloderma): develops after microtraumas, fever is not typical. The rash is localized on exposed areas. Red spots and bumps turn into flaccid blisters that rupture, forming weeping ulcers and thick "honey-colored" crusts.
- Vesicular rickettsiosis: transmitted through the bites of gamasid mites. 7 days before the rash, a primary affect forms at the bite site (papule $\rightarrow$ vesicle $\rightarrow$ ulcer with a dark crust). The exanthem is abundant, with denser vesicles appearing in the center of the papules.
- Smallpox (Variola): characterized by a monomorphic rash with umbilication. The vesicles are multilocular (do not collapse when punctured), located on a firm base, and spread from the face to the trunk and extremities. Accompanied by severe intoxication syndrome and fever up to 40°C.
Briefly: answers to topical questions
What drugs are used for etiotropic therapy of shingles?
For the etiotropic therapy of shingles, antiviral drugs from the nucleoside analogue group are used; the standard course is 7–10 days.
- Acyclovir — for uncomplicated forms, it is prescribed orally 800 mg 5 times a day; for disseminated forms, it is administered intravenously 10 mg/kg 3 times a day.
- Famciclovir — used orally at 500 mg 3 times a day for uncomplicated and disseminated forms.
- Foscarnet — a reserve drug when first-line therapy is ineffective or not tolerated; administered strictly intravenously.
What neurological complications develop after having shingles?
After suffering from shingles, a neurological complication can develop — postherpetic neuralgia.
- Postherpetic neuralgia — develops frequently in immunosuppressed patients; accompanied by severe pain syndrome. Clinically, it may manifest as agonizing burning pain, itching, or soft tissue edema in the area of one half of the face.
Class and exam questions
Why does shingles occur?
It occurs as a reactivation of a latent viral infection that persists in sensory nerve ganglia following a prior primary infection. Immunosuppression acts as the main trigger.
Is a patient with shingles contagious?
Yes, contact with such a patient during the incubation period can cause a primary infection with characteristic exanthem in individuals without immunity (those who have neither had the disease nor been vaccinated).
What is preherpetic neuralgia?
This is a pain syndrome occurring in the prodromal period (1–2 days before the rash). It manifests as radicular pain and pronounced soreness along the nerve trunks.
What else to study on this topic
- Severe forms of primary infection (hemorrhagic, gangrenous, visceral)
- Specific nervous system complications (encephalitis, myelitis, polyradiculoneuritis)
- Internal organ involvement (viral pneumonia, hepatitis, nephritis)
- Purulent complications secondary to secondary bacterial microflora
- Features of cerebrospinal fluid examination in meningeal syndrome
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