Chickenpox

Abstract: Dr Hope-Simpson presents a study of all cases of herpes zoster occurring in his general practice during a sixteen-year period. The rate was 3.4 per thousand per annum, rising with age, and the distribution of lesions reflected that of the varicella rash.It was found that severity increased with age, but that the condition did not occur in epidemics, and that there was no characteristic seasonal variation. A low prevalence of varicella was usually associated with a high incidence of zoster.Dr Hope-Simpson suggests that herpes zoster is a spontaneous manifestation of varicella infection. Following the primary infection (chickenpox), virus becomes latent in the sensory ganglia, where it can be reactivated from time to time (herpes zoster). Herpes zoster then represents an adaptation enabling varicella virus to survive for long periods, even without a continuous supply of persons susceptible to chickenpox.

Abstract: Varicella-zoster virus (VZV) is a ubiquitous human alphaherpesvirus that causes varicella (chicken pox) and herpes zoster (shingles). Varicella is a common childhood illness, characterized by fever, viremia, and scattered vesicular lesions of the skin. As is characteristic of the alphaherpesviruses, VZV establishes latency in cells of the dorsal root ganglia. Herpes zoster, caused by VZV reactivation, is a localized, painful, vesicular rash involving one or adjacent dermatomes. The incidence of herpes zoster increases with age or immunosuppression. The VZV virion consists of a nucleocapsid surrounding a core that contains the linear, double-stranded DNA genome; a protein tegument separates the capsid from the lipid envelope, which incorporates the major viral glycoproteins. VZV is found in a worldwide geographic distribution but is more prevalent in temperate climates. Primary VZV infection elicits immunoglobulin G (IgG), IgM, and IgA antibodies, which bind to many classes of viral proteins. Virus-specific cellular immunity is critical for controlling viral replication in healthy and immunocompromised patients with primary or recurrent VZV infections. Rapid laboratory confirmation of the diagnosis of varicella or herpes zoster, which can be accomplished by detecting viral proteins or DNA, is important to determine the need for antiviral therapy. Acyclovir is licensed for treatment of varicella and herpes zoster, and acyclovir, valacyclovir, and famciclovir are approved for herpes zoster. Passive antibody prophylaxis with varicella-zoster immune globulin is indicated for susceptible high-risk patients exposed to varicella. A live attenuated varicella vaccine (Oka/Merck strain) is now recommended for routine childhood immunization.

Abstract: These recommendations represent the first statement by the Advisory Committee on Immunization Practices (ACIP) on the use of a live attenuated vaccine for the prevention of herpes zoster (zoster) (i.e., shingles) and its sequelae, which was licensed by the U.S. Food and Drug Administration (FDA) on May 25, 2006. This report summarizes the epidemiology of zoster and its sequelae, describes the zoster vaccine, and provides recommendations for its use among adults aged > or =60 years in the United States. Zoster is a localized, generally painful cutaneous eruption that occurs most frequently among older adults and immunocompromised persons. It is caused by reactivation of latent varicella zoster virus (VZV) decades after initial VZV infection is established. Approximately one in three persons will develop zoster during their lifetime, resulting in an estimated 1 million episodes in the United States annually. A common complication of zoster is postherpetic neuralgia (PHN), a chronic, often debilitating pain condition that can last months or even years. The risk for PHN in patients with zoster is 10%-18%. Another complication of zoster is eye involvement, which occurs in 10%-25% of zoster episodes and can result in prolonged or permanent pain, facial scarring, and loss of vision. Approximately 3% of patients with zoster are hospitalized; many of these episodes involved persons with one or more immunocompromising conditions. Deaths attributable to zoster are uncommon among persons who are not immunocompromised. Prompt treatment with the oral antiviral agents acyclovir, valacyclovir, and famciclovir decreases the severity and duration of acute pain from zoster. Additional pain control can be achieved in certain patients by supplementing antiviral agents with corticosteroids and with analgesics. Established PHN can be managed in certain patients with analgesics, tricyclic antidepressants, and other agents. Licensed zoster vaccine is a lyophilized preparation of a live, attenuated strain of VZV, the same strain used in the varicella vaccines. However, its minimum potency is at least 14-times the potency of single-antigen varicella vaccine. In a large clinical trial, zoster vaccine was partially efficacious at preventing zoster. It also was partially efficacious at reducing the severity and duration of pain and at preventing PHN among those developing zoster. Zoster vaccine is recommended for all persons aged > or =60 years who have no contraindications, including persons who report a previous episode of zoster or who have chronic medical conditions. The vaccine should be offered at the patient's first clinical encounter with his or her health-care provider. It is administered as a single 0.65 mL dose subcutaneously in the deltoid region of the arm. A booster dose is not licensed for the vaccine. Zoster vaccination is not indicated to treat acute zoster, to prevent persons with acute zoster from developing PHN, or to treat ongoing PHN. Before administration of zoster vaccine, patients do not need to be asked about their history of varicella (chickenpox) or to have serologic testing conducted to determine varicella immunity.

Abstract: Varicella–zoster virus is an exclusively human herpesvirus that causes chickenpox (varicella), becomes latent in cranial-nerve and dorsal-root ganglia, and frequently reactivates decades later to produce shingles (zoster) and postherpetic neuralgia. In immunocompetent elderly persons or immunocompromised patients, varicella–zoster virus may produce disease of the central nervous system. Since the last major review of varicella–zoster virus in the Journal, 1,2 advances in molecular biology have provided important new insights into the pathogenesis of infection with varicella–zoster virus. The detection of varicella–zoster virus in blood vessels and other tissues by methods based on the polymerase chain reaction (PCR) has widened the recognized . . .