Data concerning numerous severe epidemics of poliomyelitis were surveyed for information useful in estimating the size of the immune component of the population by age groups of 1 year. The New York epidemic of 1916 and the Mauritius epidemic of 1945 were chosen as the most suitable for this purpose. It is shown that there was a regularly progressive decline in attack rates for successively older age groups from 2 to 8 years in New York. The attack rate in 8-year-olds was less than 10 % as large as that in 2-year-olds. It is noted that a difference of this magnitude could be accounted for by immunizing infections amounting to 30 % per year for 6 years.
A similar analysis of age specific attack rates during the Mauritius epidemic shows progressive declines of 28, 60, 50 and 53 % for the successive age groups 5–9. An average annual infection rate of 45 % over a 4 year period could account for the ten-fold difference in infection rates between 5-year-olds and 9-year-olds.
An immunizing infection rate of 30 % a year would lead to a pattern of immunity in which the seven youngest age groups had a total susceptible component of 30 % at the beginning of a ‘ poliomyelitis season’. Twenty per cent would remain susceptible at the end of the season when spread of virus terminated.
An annual immunizing infection rate of 45 % would bring about a situation in which 21 % of the five youngest age groups were susceptible at the start of a period of viral prevalence and 12 % at the end. Alternatively, one could consider that on Mauritius there may have been a continuous prevalence of virus in a population in which approximately 15 % of the five youngest age groups were susceptible at any time.
It is suggested that the essentially similar attack rates among children 3–5 years old on Mauritius may have reflected a 3-year period during which homotypic virus was not prevalent, in contrast to its great prevalence during the years prior to that time.
A more detailed discussion and analysis of additional data concerning age-specific attack rates in poliomyelitis will be found in the thesis submitted by Dr Sample to the University of Washington School of Medicine entitled, ‘Some observations on statistical and theoretical epidemiology of infectious diseases, principally poliomyelitis’, in 1955. This is obtainable by Inter-library Loan from the Health Sciences Library, University of Washington, Seattle.
We wish to express our sincere thanks to Dr Blair M. Bennett and Dr William E. Reynolds of the University of Washington for their advice on the statistical and epidemiologic aspects of this study.