Duncan C J, Duncan S R, Scott S
School of Biological Sciences, University of Liverpool, Liverpool, L69 3BX, United Kingdom.
Theor Popul Biol. 1997 Oct;52(2):155-63. doi: 10.1006/tpbi.1997.1326.
The interepidemic interval (T) of measles in London from 1647 to 1837 evolved progressively from 5-yearly to 2-yearly by 1800. Measles mortality was significantly ( p<0.001) cross-correlated with the annual wheat prices, a good index of nutrition although at a 2-year lag. Epidemics correlated with low autumn temperatures (p<0. 001). A linearised model of the dynamics of epidemics shows that T is determined by the product of population (N) and susceptibility (beta) and that the system will settle at its steady state unless the epidemics are driven. It is suggested that (i) the progressive change in T was caused by a rise in population size (N) and an increased susceptibility (beta) related to malnutrition and (ii) epidemics were driven by oscillations in low autumn temperature (p<0. 001) and by cycles of susceptible young children produced by malnutrition during pregnancy.
1647年至1837年伦敦麻疹的流行间隔期(T)到1800年逐渐从每5年一次演变为每2年一次。麻疹死亡率与年度小麦价格显著(p<0.001)互相关联,小麦价格是营养状况的良好指标,不过存在2年的滞后。疫情与秋季低温相关(p<0.001)。疫情动态的线性化模型表明,T由人口数量(N)和易感性(β)的乘积决定,并且除非疫情受到驱动,该系统将处于稳定状态。有人提出:(i)T的逐渐变化是由人口规模(N)的增加以及与营养不良相关的易感性(β)增加所致;(ii)疫情是由秋季低温的波动(p<0.001)以及孕期营养不良导致的易感幼儿周期所驱动。