The Incidence and Clinical Characteristics of Herpes Zoster Among Children and Adolescents After Implementation of Varicella Vaccination
ABSTRACT The varicella-zoster virus (VZV) vaccine strain may reactivate to cause herpes zoster. Limited data suggest that the risk of herpes zoster in vaccinated children could be lower than in children with naturally acquired varicella. We examine incidence trends, risk and epidemiologic and clinical features of herpes zoster disease among children and adolescents by vaccination status.
Population-based active surveillance was conducted among <20 years old residents in Antelope Valley, California, from 2000 through 2006. Structured telephone interviews collected demographic, varicella vaccination and disease histories, and clinical information.
From 2000 to 2006, the incidence of herpes zoster among children<10 years of age declined by 55%, from 42 cases reported in 2000 (74.8/100,000 persons; 95% confidence interval [95% CI]: 55.3-101.2) to 18 reported in 2006 (33.3/100,000; 95% CI: 20.9-52.8; P<0.001). During the same period, the incidence of herpes zoster among 10- to 19-year-olds increased by 63%, from 35 cases reported in 2000 (59.5/100,000 persons; 95% CI: 42.7-82.9) to 64 reported in 2006 (96.7/100,000; 95% CI: 75.7-123.6; P<0.02). Among children aged<10 years, those with a history of varicella vaccination had a 4 to 12 times lower risk for developing herpes zoster compared with children with history of varicella disease.
Varicella vaccine substantially decreases the risk of herpes zoster among vaccinated children and its widespread use will likely reduce overall herpes zoster burden in the United States. The increase in herpes zoster incidence among 10- to 19-year-olds could not be confidently explained and needs to be confirmed from other data sources.
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ABSTRACT: Background. Herpes zoster infection is a painful worldwide disease. Inappropriate and delayed treatment causes prolongation of the disease with debilitating symptoms and postherpetic neuralgia. Method. A cross-sectional study evaluated shingles cases admitted in a teaching hospital with one-year followup in north of Iran from 2007 to 2013. Results. From 132 patients, 60.4% were male. Head and neck involvement occurred in 78 people (59.1%), thoracoabdominal region in 37 cases (28%), and extremities in 16 cases (12.1%), and one case (0.8%) got multisites involvement. 54 cases (40.9%) had predisposing factors including diabetes mellitus in 26 cases (19.7%), malignancy in 15 (11.4%), immunosuppressive medication in 7 (5.03%), HIV infection in 3 (2.3%), radiotherapy in 2 (1.5%), and tuberculosis in one patient (0.8%). The most common symptoms were pain (95.5%), weakness (56%), fever (31.1%), headache (30.3%), ocular complaints (27.3%), itching (24.2%), and dizziness (5.3%). 21 cases (15.9%) had bacterial superinfection on blistering areas and overall 18 cases (13.6%) had opium addiction. 4 cases (3.03%) died during admission because of comorbidities. Postherpetic neuralgia was reported in 56 patients (42.5%) after three months and seven cases (5%) in one-year followup. Conclusion. Shortening interval between skin lesion manifestation and starting medication can accelerate lesion improvement and decrease disease course, extension, and complication.03/2015; 2015. DOI:10.1155/2015/896098
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ABSTRACT: Immunization with the vOka vaccine prevents varicella (chickenpox) in children and susceptible adults. The vOka vaccine strain comprises a mixture of genotypes and, despite attenuation, causes rashes in small numbers of recipients. Like wild type virus, the vaccine establishes latency in neuronal tissue and can later reactivate to cause Herpes zoster (shingles). Using hybridization-based methodologies we have purified and sequenced vOka directly from skin lesions. We show that alleles present in the vaccine can be recovered from the lesions and demonstrate the presence of a severe bottleneck between inoculation and lesion formation. Genotypes in any one lesion appear to be descended from one to three vaccine-genotypes with a low frequency of novel mutations. No single vOka haplotype and no novel mutations are consistently present in rashes, indicating that neither new mutations nor recombination with wild type are critical to the evolution of vOka rashes. Instead, alleles arising from attenuation (i.e. not derived from free-living virus) are present at lower frequencies in rash genotypes. We identify eleven loci at which the ancestral allele is selected for in vOka rash formation and show genotypes in rashes that have reactivated from latency cannot be distinguished from rashes occurring immediately after inoculation. We conclude that the vOka vaccine, although heterogeneous, has not evolved to form rashes through positive selection in the mode of a quasispecies, but rather alleles which were essentially neutral during the vaccine production have been selected against in the human subjects, allowing us to identify key loci for rash formation.Molecular Biology and Evolution 10/2013; 31(2). DOI:10.1093/molbev/mst210 · 14.31 Impact Factor
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ABSTRACT: In a cooperative agreement starting January 1995, prior to the FDA's licensure of the varicella vaccine on March 17, the Centers for Disease Control and Prevention (CDC) funded the Los Angeles Department of Health Services' Antelope Valley Varicella Active Surveillance Project (AV-VASP). Since only varicella case reports were gathered, baseline incidence data for herpes zoster (HZ) or shingles was lacking. Varicella case reports decreased 72%, from 2834 in 1995 to 836 in 2000 at which time approximately 50% of children under 10years of age had been vaccinated. Starting in 2000, HZ surveillance was added to the project. By 2002, notable increases in HZ incidence rates were reported among both children and adults with a prior history of natural varicella. However, CDC authorities still claimed that no increase in HZ had occurred in any US surveillance site. The basic assumptions inherent to the varicella cost-benefit analysis ignored the significance of exogenous boosting caused by those shedding wild-type VZV. Also ignored was the morbidity associated with even rare serious events following varicella vaccination as well as the morbidity from increasing cases of HZ among adults. Vaccine efficacy declined below 80% in 2001. By 2006, because 20% of vaccinees were experiencing breakthrough varicella and vaccine-induced protection was waning, the CDC recommended a booster dose for children and, in 2007, a shingles vaccination was approved for adults aged 60years and older. In the prelicensure era, 95% of adults experienced natural chickenpox (usually as children)-these cases were usually benign and resulted in long-term immunity. Varicella vaccination is less effective than the natural immunity that existed in prevaccine communities. Universal varicella vaccination has not proven to be cost-effective as increased HZ morbidity has disproportionately offset cost savings associated with reductions in varicella disease. Universal varicella vaccination has failed to provide long-term protection from VZV disease.Vaccine 05/2012; 31(13). DOI:10.1016/j.vaccine.2012.05.050 · 3.49 Impact Factor