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The condition known as shingles is due to a reactivation of the varicella zoster virus.
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More than 90% of cases occur in immunocompetent individuals; however, immunosuppression increases the risk by 20- to 100-fold.
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The prodrome of shingles may last up to several weeks before the development of a vesicular rash.
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The zoster vaccine reduces the incidence of herpes zoster by approximately 50% and the occurrence of post-herpetic neuralgia by two-thirds, with vaccinated individuals experiencing
Herpes Zoster
Section snippets
Key points
Epidemiology
Varicella zoster virus (VZV) causes 2 distinct clinical entities. Primary infection with the varicella virus results in a diffuse vesicular rash commonly called chicken pox. The reactivation of latent varicella infection manifests as a painful blistering rash called herpes zoster or shingles, and tends to present in adulthood as cellular immunity declines. Ninety percent of the United States population has serologic evidence of varicella infection and is at risk for the development of herpes
Pathogenesis
VZV is a DNA herpesvirus, which infects susceptible individuals through airborne transmission. The virus enters the body through contact with mucous membranes, where it replicates and disseminates via the blood and lymphatics. The virus incubates and replicates for approximately 2 weeks, at which time it overwhelms the host immune response, and the disseminated vesicular rash of chicken pox develops.8 During the course of varicella, the VZV infects the sensory nerve endings and travels along
Presentation
The rash of herpes zoster starts with erythematous macules or papules developing into grouped vesicular lesions or bullae in a dermatomal distribution. Over the course of 7 to 10 days, the lesions develop into pustules and eventually crust over. If a patient continues to develop new lesions after about 1 week, the possibility of immunodeficiency should be explored.17 Zoster involving mucous membranes is often overlooked because the fragile epidermis in these areas may not allow for the
What are the most important complications of herpes zoster?
PHN is the most common complication of herpes zoster. Risk factors for PHN include advanced age, and severity of rash and pain at the time of initial infection.27, 28 There is no consensus on the actual definition of PHN.26 Definitions range from pain persisting beyond 30 days from the initial onset of rash to pain persisting beyond 3 months from initial rash. The actual prevalence of PHN varies greatly depending on the definition used. In one study, PHN incidence was as high as 30% in people
What is the differential diagnosis for herpes zoster?
There are numerous conditions that mimic the presentation of disseminated zoster. The focus here is on the more common causes of localized rashes in adults that may present similarly to dermatomal zoster. Herpes simplex virus generally affects the lips, genitalia, and buttocks. The initial infection is often severe with associated lymphadenopathy, fever, and flu-like symptoms. Recurrence is common and usually occurs in the same location. When herpes simplex virus presents in less typical
How is herpes zoster diagnosed?
Most often the diagnosis of herpes zoster is made clinically. However, on occasion confirmation of infection may be necessary; this becomes more important in patients with atypical rash, especially in an immunocompromised host or if there is concern for disseminated disease with or without skin lesions. Key elements of the history used to diagnose herpes zoster clinically include: (1) painful or abnormal sensory prodrome (not always present); (2) dermatomal distribution; (3) grouped vesicles or
How contagious are patients with herpes zoster?
Although less contagious than primary varicella, it is important to counsel patients with herpes zoster about the risk of transmitting the infection to others. Susceptible individuals such as those without a history of varicella infection or varicella vaccination are at risk of developing primary varicella infection. Contagiousness begins when the rash develops, and lasts until the lesions crust over.19 Transmission can occur either by direct contact or via airborne spread from respiratory
Does Treatment with Antivirals Shorten Infection and Change Clinical Course in Immunocompetent Patients?
The goal of treatment for herpes zoster is to shorten and lessen the clinical course and possibly decrease complications from the disease. There is evidence that treatment with the antiretrovirals acyclovir, famciclovir, and valacyclovir lessens acute neuritis and hastens healing of the rash.38, 39, 40, 41 Optimal duration of treatment is 7 days; there appears to be no benefit for prolonged courses of treatment.42 One head-to-head trial of valacyclovir and acyclovir showed quicker healing in
How effective is zoster vaccine and who should receive it?
More than 95% of adults aged 50 years and older have had chicken pox, putting them at risk for developing shingles. The risk of developing shingles increases significantly after age 50 as cell-mediated immunity wanes. A boost in VZV-specific T-cell immune response likely explains the mechanism behind zoster vaccine efficacy in preventing and attenuating disease.74 In 2006, the Food and Drug Administration (FDA) approved a zoster vaccine for the prevention of shingles in individuals aged 60 and
Summary
Herpes zoster is a common condition that significantly affects health-related quality of life. The majority of cases occur in immunocompetent individuals older than 60 years; however, immunosuppressed patients are at particularly high risk. Diagnosis is most often made clinically. If the diagnosis is unclear, the results of a DFA test can be obtained within a few hours, allowing for early initiation of treatment. PHN is the most common complication of herpes zoster, and can be debilitating. The
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Herpes zóster en la infancia
2022, PielS100A9 plays a pivotal role in a mouse model of herpetic neuralgia via TLR4/TNF pathway
2020, Brain, Behavior, and ImmunityCitation Excerpt :Furthermore, no alteration in mechanical pain hypersensitivity was observed after inoculation with inactive HSV-1, excluding the possibility that hyperalgesia was due to an inflammatory response to virus proteins. These results suggest that pain development was restricted to the infected dermatome, as described for rodents and humans (O’Connor and Paauw, 2013; Silva et al., 2017). Post peripheral HSV-1 infection, the virus promotes a progressive infiltration of leukocytes into the DRGs (Silva et al., 2017).
Conflict of Interest: None.