Is poliomyelitis a genetically-determined disease? II. A critical examination of the epidemiological data

Abstract

The genetic model proposed in a previous paper has been applied to a number of epidemics believed to represent virgin-soil epidemics among the age-groups used. Twelve different kinds of predictions are made concerning the number of expected cases in populations, institutions and hypogammaglobulinaemics, the proportion of families with cases, the incidence of cases in families with cases, the incidence of multiple cases in families, the incidence in twins and various combinations of these predictions. For the Chesterfield Inlet outbreak, the numbers of families with cases, the number of cases in families and the total number of cases are predicted by the model. For New York, 1916, it is shown that the prediction of the number of families with multiple cases is close to that recorded. A further 30 epidemics are shown to have age-specific age rates similar to those postulated. It is suggested that a few small outbreaks with higher age-specific attack rates have occurred where chance matings have resulted in a high number of susceptibles. The waterborne epidemic at Huskerville, 1952, is not explained by the model. The incidence in twins is recalculated and shown to be consistent with the model. The number of expected second attacks is discussed. A number of corrections are made to the literature of some virgin soil epidemics. The significance of the prediction that about one quarter of all adults might be susceptible to paralytic poliomyelitis, with a very high death rate, if they were not already immune, is briefly discussed.