Epidemiology

In most years it is very difficult to assess epidemics because there may be several polioviruses of different virulence and types circulating. Thus the extent of the circulation of the virulent viruses will not be known and the cases will not necessarily correspond to the geographic boundaries used for reporting. Moreover, because viruses change their virulence, the number of nonimmunes will be unknown. Surveys of immune status and examination of feces for virus are expensive and time-consuming, and sam-

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A6E IN YEARS

Figure VIII. 110.2. Case-fatality rates for poliomyelitis based on records from (X) England and Wales, 1947-50 (average of male and female rates; 28 notified cases); (O) Denmark, 1947-50 (28 paralytic cases); (•) France, 1952 (average of male and female rates; 28 notified cases); (■) Sweden, 1935-44 (28 confirmed paralytic cases); (+) Eskimos, Chesterfield Inlet (14 cases); (□) Cutter vaccinees (27 cases); (A) West Virginia (18 cases); (A) Malta, 1942-3 (service cases, 20-30 years of age, no. of cases not specified); (V) Sweden, 1911-13 (5 cases). [From Harold V. Wyatt. 1975. Medical Hypotheses 1 (1): 35-42, by permission of Churchill-Livingstone, publishers.]

pie only a tiny fraction of a given population. Thus our epidemiological knowledge of the disease is very dependent on virgin soil epidemics in islands and isolated communities with definite boundaries that contain many nonimmunes.

After an epidemic in 1919, polio was made a notifiable disease in Malta. About three cases were reported each year (Figure VIII.110.1) until 1942, when almost 3 percent of children under 3 years of age were stricken. Other epidemics followed at intervals of 2 or 3 years. Some of these epidemics were probably caused by the importation of virulent viruses from Egypt by returning Maltese in 1919, 1945, and 1947 and by the arrival by overnight flight of about 250 RAF men in 1942. Nearly all the Maltese cases were children under 5 years of age.

Prior to the 1930s, most polio cases occurred in young children, except in small isolated communities where older children, adolescents, and even adults were sometimes affected. Beginning in the 1930s, however, there was a shift to older children and adolescents, first in Scandinavia and the United States, and then in Europe. The older children suffered less paralysis, and, as Figure VIII.110.2 shows,

the case-fatality rate was low. By contrast, young adults had paralysis and case-fatality rates like those of small children. In many severe epidemics, the case-rate for 2-year-olds has been about 2 percent with increasing rates up to about 10 years of age, when the rate stabilizes at 25 percent. In a virgin soil epidemic among an Eskimo population in 1948, 2 out of 53 children and 25 percent of adolescents and adults were paralyzed.

Incidence in monozygotic and dizygotic twins suggests genetic susceptibility, and there are families who have had many cases over several generations. Yet, the overall level of familial incidence is low, and genetic susceptibility has been largely discounted. On the other hand, the changes in paralysis and case-fatality rates at about 3 years of age can be explained if two groups are genetically susceptible -the 2 percent of the population who are homozygotes and the 24 percent who are heterozygotes. This model suggests that genetic susceptibility is a maturation process, with about half the homozygotes becoming phenotypically susceptible at 1 year of age and all at 2 years. Heterozygotes would mature more slowly, reaching 24 percent at about 10 years.

Early epidemiological surveys often included all cases whether there was residual paralysis or not, and cases of abortive polio were also frequently included, although diagnosis in these cases is difficult and uncertain. From the late 1930s, it became increasingly common to restrict inclusion in the statistics to those with paralysis, and later only to those with residual paralysis. In countries where there is universal immunization and very few cases, each suspected case is investigated. A positive virus isolation or a rise in antibody titer between acute and convalescent sera is evidence of poliovirus involvement. Polioviruses are tested for affinity to vaccine and wild strains.

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