The 1918–1919 influenza pandemic in England and Wales: spatial patterns in transmissibility and mortality impact

Abstract

Spatial variations in disease patterns of the 1918-1919 influenza pandemic remain poorly studied. We explored the association between influenza death rates, transmissibility and several geographical and demographic indicators for the autumn and winter waves of the 1918-1919 pandemic in cities, towns and rural areas of England and Wales. Average measures of transmissibility, estimated by the reproduction number, ranged between 1.3 and 1.9, depending on model assumptions and pandemic wave and showed little spatial variation. Death rates varied markedly with urbanization, with 30-40% higher rates in cities and towns compared with rural areas. In addition, death rates varied with population size across rural settings, where low population areas fared worse. By contrast, we found no association between transmissibility, death rates and indicators of population density and residential crowding. Further studies of the geographical mortality patterns associated with the 1918-1919 influenza pandemic may be useful for pandemic planning.

Disparities in influenza mortality and transmission related to sociodemographic factors within Chicago in the pandemic of 1918

“…Some studies have argued that, because the 1918 H1N1 influenza virus was highly virulent, it indiscriminately killed, regardless of social class (30,31), whereas some studies have proposed that sociodemographic differences affected mortality during this pandemic at the scale of countries, provinces, and counties (2,7,32,33). This study found that, despite the highly virulent nature of the virus, influenza did not behave in a wholly democratizing fashion at the within-city scale.…”

“…The lower estimates found in this study could be the result of population immunity after a spring outbreak of this pandemic virus in Chicago or the impact of control measures (24, 34). This study observed a significant association between transmissibility and population density at the census tract level, which has not been observed at greater spatial scales (4,7). The association between R and population density may be a result of an increased number of effective contacts between individuals in denser population tracts, but the relationship is confounded by the strong associations between population density and other sociodemographic factors and the largely nonsignificant association between population density and weekly R estimates (Tables S7 and S8).…”

Inferring the causes of the three waves of the 1918 influenza pandemic in England and Wales

“…Several statistical analyses of data from past pandemics have identified potential causes of mortality patterns. For example, Chowell et al [14] found that death rates during the 1918 pandemic in the UK were 30-40% higher in cities and towns when compared with rural areas; and Pearce et al [15] found that the occurrence of epidemic waves in the UK in 1918 was associated with patterns of socioeconomic status and age, potentially as a result of prior immunity within some age groups. An analysis by Andreasen et al [3] suggests that immunological history might play a role.…”

Transmissibility of the highly pathogenic avian influenza virus, subtype H5N1 in domestic poultry: a spatio-temporal estimation at the global scale

“…The assumption of the stR 0 method was that the Euclidean distance-based nearest neighbouring sub-district within the infectious duration window was the infection source for each following outbreak of interest, which assumed that proximity in both time and space is the strongest factor driving the spread of the HPAIV H5N1 virus (Ward et al, 2009). The infectious duration is an important parameter for estimating tR 0 and stR 0 Chowell et al, 2007Chowell et al, , 2008Andreasen et al, 2008;, but accurate estimates of the duration of infectiousness at the sub-district level are unavailable (Garske et al, 2007) so different researchers have assumed different values (Mannelli et al, 2007;Tiensin et al, 2007). In this study, we assumed that sub-district-based infectious duration was 7 days, which remained constant during the whole epidemic similar to the village-based study conducted by Ward et al (2009).…”

“…For the 1918-1919 influenza A (H1N1) pandemic, the R 0 estimates were between 1.3 and 3.0, depending on different models and model assumptions (Mills et al, 2004;Germann et al, 2006;Massad et al, 2007;Chowell et al, 2008;; R 0 was estimated to be 1.68 for the 1957-1958 influenza (H2N2) pandemic (Longini et al, 2004) and 1.89 for that of 1968-1969 (H3N2) (Rvachev and Longini, 1985). The fact that the R 0 estimates for HPAIV H5N1 in poultry, including our current estimates, were located in the same range as those of previous influenza pandemics suggests that HPAIV H5N1 constitutes a risk for a potentially pandemic influenza in humans based on transmissibility.…”