The Journal of infectious diseases · 2008
Epidemiologic characterization of the 1918 influenza pandemic summer wave in Copenhagen: implications for pandemic control strategies.
Историческая статьяСтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Andreasen Viggo, Viboud Cécile, Simonsen Lone
Аннотация
BACKGROUND: The 1918-1919 A/H1N1 influenza pandemic killed approximately 50 million people worldwide. Historical records suggest that an early pandemic wave struck Europe during the summer of 1918.
METHODS: We obtained surveillance data that were compiled weekly, during 1910-1919, in Copenhagen, Denmark; the records included medically treated influenza-like illnesses (ILIs), hospitalizations, and deaths by age. We used a Serfling seasonal regression model to quantify excess morbidity and mortality, and we estimated the reproductive number (R) for the summer, fall, and winter pandemic waves.
RESULTS: A large epidemic occurred in Copenhagen during the summer of 1918; the age distribution of deaths was characteristic of the 1918-1919 A/H1N1 pandemic overall. That summer wave accounted for 29%-34% of all excess ILIs and hospitalizations during 1918, whereas the case-fatality rate (0.3%) was many-fold lower than that of the fall wave (2.3%). Similar patterns were observed in 3 other Scandinavian cities. R was substantially higher in summer (2.0-5.4) than in fall (1.2-1.6) in all cities.
CONCLUSIONS: The Copenhagen summer wave may have been caused by a precursor A/H1N1 pandemic virus that transmitted efficiently but lacked extreme virulence. The R measured in the summer wave is likely a better approximation of transmissibility in a fully susceptible population and is substantially higher than that found in previous US studies. The summer wave may have provided partial protection against the lethal fall wave.
METHODS: We obtained surveillance data that were compiled weekly, during 1910-1919, in Copenhagen, Denmark; the records included medically treated influenza-like illnesses (ILIs), hospitalizations, and deaths by age. We used a Serfling seasonal regression model to quantify excess morbidity and mortality, and we estimated the reproductive number (R) for the summer, fall, and winter pandemic waves.
RESULTS: A large epidemic occurred in Copenhagen during the summer of 1918; the age distribution of deaths was characteristic of the 1918-1919 A/H1N1 pandemic overall. That summer wave accounted for 29%-34% of all excess ILIs and hospitalizations during 1918, whereas the case-fatality rate (0.3%) was many-fold lower than that of the fall wave (2.3%). Similar patterns were observed in 3 other Scandinavian cities. R was substantially higher in summer (2.0-5.4) than in fall (1.2-1.6) in all cities.
CONCLUSIONS: The Copenhagen summer wave may have been caused by a precursor A/H1N1 pandemic virus that transmitted efficiently but lacked extreme virulence. The R measured in the summer wave is likely a better approximation of transmissibility in a fully susceptible population and is substantially higher than that found in previous US studies. The summer wave may have provided partial protection against the lethal fall wave.