Dudley S F
Proc R Soc Med. 1929 Mar;22(5):569-92. doi: 10.1177/003591572902200501.
Man, in contact with the pathogens in his environment, responds by developing immunity with or without symptomatic illness. The incidence of infectious disease in a community depends on the parasitic factor or "infection pressure," and the host factor, "herd immunity," i.e., the resistance of the community as a whole to the infection. Environment is only a secondary factor which alters the relative values of the two primary factors. Morbidity varies directly as the "infection pressure," and inversely as the "herd immunity." The great difficulty heretofore has been to separate the two factors expressing morbidity. In diphtheria, to some extent, this is now possible by means of the Schick test. By using clues gained from the study of diphtheria, and examining the age-incidence, severity, and fatality, of other infections under various environmental conditions, the hypothesis is reached that herd-immunity increases with the herd's past experience of the bacterial causes of most, if not all, infectious diseases. This immunity may be acquired latently, without illness, and, even if not always enough to prevent symptomatic infection, may be such that severity and fatality are decreased. The process is an example of the general biological mechanism by which the members of a species acquire adaptative variations more suitable to the environment. Of recent years air-borne droplet infections have caused less fatality and trouble to the English herd than a century ago. The manifold increase of the density and of the motion in the English herd must have greatly raised the average infection-pressure, but since severity of clinical disease has diminished and incidence has not increased in proportion, the herd-immunity of the English must have outstripped the increase of infection-pressure, i.e., the herd has become more closely adapted to its bacterial environment. It must not, however, be forgotten that adaptive fluctuations in parasitic characters must also play some part in all the phenomena of infectious disease.
人类在接触其环境中的病原体时,无论有无症状性疾病,都会通过产生免疫力来做出反应。社区中传染病的发病率取决于寄生因素或“感染压力”以及宿主因素“群体免疫”,即整个社区对感染的抵抗力。环境只是一个次要因素,它会改变这两个主要因素的相对值。发病率与“感染压力”成正比,与“群体免疫”成反比。迄今为止,最大的困难在于区分表示发病率的两个因素。在某种程度上,通过锡克试验现在可以在白喉中做到这一点。通过利用从对白喉的研究中获得的线索,并检查其他感染在各种环境条件下的年龄发病率、严重程度和死亡率,得出这样的假设:群体免疫随着群体过去对大多数(如果不是全部)传染病的细菌病因的经验而增加。这种免疫力可能是潜在获得的,没有疾病,即使不一定足以预防症状性感染,也可能使严重程度和死亡率降低。这个过程是一个普遍生物学机制的例子,通过这个机制,一个物种的成员获得更适合环境的适应性变异。近年来,空气传播的飞沫感染给英国人群体造成的死亡和麻烦比一个世纪前少。英国人群体密度和流动性的大量增加一定大大提高了平均感染压力,但由于临床疾病的严重程度有所降低,发病率没有成比例增加,英国人的群体免疫一定超过了感染压力的增加,即群体已经更紧密地适应了其细菌环境。然而,绝不能忘记,寄生特征的适应性波动在所有传染病现象中也一定起到了一定作用。