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Logo of procrsmedFormerly medchtJournal of the Royal Society of MedicineProceedings of the Royal Society of Medicine
Proc R Soc Med. 1929 March; 22(5): 569–592.
PMCID: PMC2102678

Human Adaptation to the Parasitic Environment


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.

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