A doença meningocócica em São Paulo, Brasil, no século XX: características epidemiológicas Meningococcal disease in São Paulo, Brazil, in the 20th century: epidemiological characteristics

Este estudo analisa o comportamento epidemiológico da doença meningocócica na cidade de São Paulo, Brasil, ao longo do século XX. Utilizando dados de prontuários, atestados de óbito e do sistema de vigilância epidemiológica os autores descrevem a tendência secular da doença, sua variação sazonal, a distribuição espacial e por idade e sexo. A tendência secular mostra incidência constante nos períodos endêmicos, interrompida pela presença de epidemias. As quatro epidemias registradas durante o século XX ocorreram em momentos de graves perturbações sociais e foram produzidas pelos sorogrupos A, A e C, e B e C. A variação sazonal com exacerbação no outono/inverno mantém-se constante durante todo o século. A distribuição espacial acompanha os deslocamentos da população pobre no espaço urbano. A distribuição por idade e sexo mantém-se inalterada em todos os períodos endêmicos, mostrando maior risco entre os menores de um ano e decréscimos acentuados à proporção que aumenta a idade. Os períodos epidêmicos, com exceção do último, mostram alteração significante na distribuição etária, com aumento do risco entre jovens e adultos jovens, e ocorrência de casos em todas as faixas etárias.<br>This study analyzes the epidemiological behavior of meningococcal disease in the city of São Paulo, Brazil, over the course of the 20th century. Applying data from patient records, death certificates, and epidemiological surveillance, the authors describe trends in the disease throughout the century, seasonal variations, and incidence distribution by area, age, and gender. The temporal trends show constant incidence during endemic periods, interrupted by epidemic events. Four epidemic events during the last century occurred in circumstances of serious social disturbances and were caused by serogroups A (the first two), A and C, and B and C, respectively. Seasonal variations involved aggravation during autumn and winter throughout the entire century. Geographic distribution followed the displacement of the poor population in the urban territory. Age and gender distribution remained unaltered during all the endemic periods, showing an increased risk associated with younger age. The epidemic periods (except for the last) showed major alterations in age and gender distribution, with an increased risk among young people and youth adults and occurrence in all age brackets

Has Rift Valley fever virus evolved with increasing severity in human populations in East Africa?

Rift Valley fever (RVF) outbreaks have occurred across eastern Africa from 1912 to 2010 approximately every 4–15 years, most of which have not been accompanied by significant epidemics in human populations. However, human epidemics during RVF outbreaks in eastern Africa have involved 478 deaths in 1998, 1107 reported cases with 350 deaths from 2006 to 2007 and 1174 cases with 241 deaths in 2008. We review the history of RVF outbreaks in eastern Africa to identify the epidemiological factors that could have influenced its increasing severity in humans. Diverse ecological factors influence outbreak frequency, whereas virus evolution has a greater impact on its virulence in hosts. Several factors could have influenced the lack of information on RVF in humans during earlier outbreaks, but the explosive nature of human RVF epidemics in recent years mirrors the evolutionary trend of the virus. Comparisons between isolates from different outbreaks have revealed an accumulation of genetic mutations and genomic reassortments that have diversified RVF virus genomes over several decades. The threat to humans posed by the diversified RVF virus strains increases the potential public health and socioeconomic impacts of future outbreaks. Understanding the shifting RVF epidemiology as determined by its evolution is key to developing new strategies for outbreak mitigation and prevention of future human RVF casualties

The origin and application of experimental autoimmune encephalomyelitis

Experimental autoimmune encephalomyelitis (EAE) is a model of the neuroimmune system responding to priming with central nervous system (CNS)-restricted antigens. It is an excellent model of post-vaccinal encephalitis and a useful model of many aspects of multiple sclerosis. EAE has been established in numerous species and is induced by priming with a large number of CNS-derived antigens. As a consequence, the pathogenesis, pathology and clinical signs vary significantly between experimental protocols. As I describe in this Timeline article, the reductionist approach taken in some lines of investigation of EAE resulted in a reliance on results obtained under a narrow range of conditions. Although such studies made important contributions to our molecular understanding of inflammation, T-cell activation, and MHC restriction, they did not advance as effectively our knowledge of the polyantigenic responses that usually occur in CNS immunopathology and autoimmunity