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New estimates of incidence of encephalitis in England.

ABSTRACT: Encephalitis causes high rates of illness and death, yet its epidemiology remains poorly understood. To improve incidence estimates in England and inform priority setting and treatment and prevention strategies, we used hospitalization data to estimate incidence of infectious and noninfectious encephalitis during 2005-2009. Hospitalization data were linked to a dataset of extensively investigated cases of encephalitis from a prospective study, and capture-recapture models were applied. Incidence was estimated from unlinked hospitalization data as 4.32 cases/100,000 population/year. Capture-recapture models gave a best estimate of encephalitis incidence of 5.23 cases/100,000/year, although the models' indicated incidence could be as high as 8.66 cases/100,000/year. This analysis indicates that the incidence of encephalitis in England is considerably higher than previously estimated. Therefore, encephalitis should be a greater priority for clinicians, researchers, and public health officials.

SUBMITTER: Granerod J

PROVIDER: S-EPMC3810913 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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New estimates of incidence of encephalitis in England.

Granerod Julia J Cousens Simon S Davies Nicholas W S NW Crowcroft Natasha S NS Thomas Sara L SL

Emerging infectious diseases 20130101 9

Encephalitis causes high rates of illness and death, yet its epidemiology remains poorly understood. To improve incidence estimates in England and inform priority setting and treatment and prevention strategies, we used hospitalization data to estimate incidence of infectious and noninfectious encephalitis during 2005-2009. Hospitalization data were linked to a dataset of extensively investigated cases of encephalitis from a prospective study, and capture-recapture models were applied. Incidence ...[more]

PMID: 23969035

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Project description:ImportanceThe SARS-CoV-2 Omicron subvariant, BA.2, may be less severe than previous variants; however, confounding factors make interpreting the intrinsic severity challenging.ObjectiveTo compare the adjusted risks of mortality, hospitalization, intensive care unit admission, and invasive ventilation between the BA.2 subvariant and the Omicron and Delta variants, after accounting for multiple confounders.Design, setting, and participantsThis was a retrospective cohort study that applied an entropy balancing approach. Patients in a multicenter inpatient and outpatient system in New England with COVID-19 between March 3, 2020, and June 20, 2022, were identified.ExposuresCases were assigned as being exposed to the Delta (B.1.617.2) variant, the Omicron (B.1.1.529) variant, or the Omicron BA.2 lineage subvariants.Main outcomes and measuresThe primary study outcome planned before analysis was risk of 30-day mortality. Secondary outcomes included the risks of hospitalization, invasive ventilation, and intensive care unit admissions.ResultsOf 102 315 confirmed COVID-19 cases (mean [SD] age, 44.2 [21.6] years; 63 482 women [62.0%]), 20 770 were labeled as Delta variants, 52 605 were labeled as the Omicron B.1.1.529 variant, and 28 940 were labeled as Omicron BA.2 subvariants. Patient cases were excluded if they occurred outside the prespecified temporal windows associated with the variants or had minimal longitudinal data in the Mass General Brigham system before COVID-19. Mortality rates were 0.7% for Delta (B.1.617.2), 0.4% for Omicron (B.1.1.529), and 0.3% for Omicron (BA.2). The adjusted odds ratio of mortality from the Delta variant compared with the Omicron BA.2 subvariants was 2.07 (95% CI, 1.04-4.10) and that of the original Omicron variant compared with the Omicron BA.2 subvariant was 2.20 (95% CI, 1.56-3.11). For all outcomes, the Omicron BA.2 subvariants were significantly less severe than that of the Omicron and Delta variants.Conclusions and relevanceIn this cohort study, after having accounted for a variety of confounding factors associated with SARS-CoV-2 outcomes, the Omicron BA.2 subvariant was found to be intrinsically less severe than both the Delta and Omicron variants. With respect to these variants, the severity profile of SARS-CoV-2 appears to be diminishing after taking into account various factors including therapeutics, vaccinations, and prior infections.

Project description:BackgroundEastern equine encephalomyelitis virus (EEEV) causes a highly pathogenic zoonosis that circulates in an enzootic cycle involving the ornithophagic mosquito, Culiseta melanura, and wild passerine birds in freshwater hardwood swamps in the northeastern U.S. Epidemic/epizootic transmission to humans/equines typically occurs towards the end of the transmission season and is generally assumed to be mediated by locally abundant and contiguous mammalophagic "bridge vector" mosquitoes.MethodsEngorged mosquitoes were collected using CDC light, resting box, and gravid traps during epidemic transmission of EEEV in 2012 in Addison and Rutland counties, Vermont. Mosquitoes were identified to species and blood meal analysis performed by sequencing mitochondrial cytochrome b gene polymerase chain reaction products. Infection status with EEEV in mosquitoes was determined using cell culture and RT-PCR assays, and all viral isolates were sequenced and compared to other EEEV strains by phylogenetic analysis.ResultsThe host choices of 574 engorged mosquitoes were as follows: Cs. melanura (n = 331, 94.3 % avian-derived, 5.7 % mammalian-derived); Anopheles quadrimaculatus (n = 164, 3.0 % avian, 97.0 % mammalian); An. punctipennis (n = 56, 7.2 % avian, 92.8 % mammalian), Aedes vexans (n = 9, 22.2 % avian, 77.8 % mammalian); Culex pipiens s.l. n = 6, 100 % avian); Coquillettidia perturbans (n = 4, 25.0 % avian, 75.0 % mammalian); and Cs. morsitans (n = 4, 100 % avian). A seasonal shift in blood feeding by Cs. melanura from Green Heron towards other avian species was observed. EEEV was successfully isolated from blood-fed Cs. melanura and analyzed by phylogenetic analysis. Vermont strains from 2012 clustered with viral strains previously isolated in Virginia yet were genetically distinct from an earlier EEEV isolate from Vermont during 2011.ConclusionsCuliseta melanura acquired blood meals primarily from birds and focused feeding activity on several competent species capable of supporting EEEV transmission. Culiseta melanura also occasionally obtained blood meals from mammalian hosts including humans. This mosquito species serves as the primary vector of EEEV among wild bird species, but also is capable of occasionally contributing to epidemic/epizootic transmission of EEEV to humans/equines. Other mosquito species including Cq. perturbans that feed more opportunistically on both avian and mammalian hosts may be important in epidemic/epizootic transmission under certain conditions. Phylogenetic analyses suggest that EEEV was independently introduced into Vermont on at least two separate occasions.

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New estimates of incidence of encephalitis in England.

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New estimates of incidence of encephalitis in England.

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