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The immune status of a population at the termination of a severe epidemic of poliomyelitis

Published online by Cambridge University Press:  15 May 2009

C. A. Evans
Affiliation:
Department of Microbiology, University of Washington, Seattle, and the Washington State Department of Health
Velma C. Chambers
Affiliation:
Department of Microbiology, University of Washington, Seattle, and the Washington State Department of Health
W. R. Giedt
Affiliation:
Department of Microbiology, University of Washington, Seattle, and the Washington State Department of Health
A. N. Wilson
Affiliation:
Department of Microbiology, University of Washington, Seattle, and the Washington State Department of Health
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Summary and conclusions

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In October, November and early December 1952, an epidemic of poliomyelitis, with an attack rate exceeding 1 %, occurred in Ketchikan, Alaska, a community of approximately 6000 persons. Approximately half of the cases were paralytic.

Type 1 virus was regarded as the principal cause of the epidemic because Type 1 virus was isolated from one patient, and sera from eleven of twelve paralytic patients tested were positive for neutralizing antibodies to Type 1 virus. Three patients had antibodies to Type 2 virus and eight to Type 3.

Serological tests were made to determine the immune status of the general population at the time the epidemic terminated. Approximately one-third of twenty-five children from 6 months to 4 years of age had antibodies to Type 1 virus. Of the 105 children aged 5 to 9 years, approximately three-quarters were positive for antibodies to this virus. All but two of the twenty-six persons more than 9 years of age who were tested were similarly positive.

Spread of Type 2 and Type 3 viruses was more limited in Ketchikan than spread of Type 1 virus. Serological evidence is presented to show that Type 3 poliomyelitis virus was present in Ketchikan some time within the 3-year-period prior to the collection of serum in December 1952. Since the proportion of children showing antibodies to Type 3 virus did not increase with age from 3 to 9 years, it is surmised that virus of this type was not prevalent for a number of years prior to its last occurrence. It is further concluded that spread of Type 3 virus must have terminated when 40 % or less of the children of pre-school age and early school age had been infected and developed antibodies.

Type 2 virus apparently had not been prevalent for several years prior to December 1952. Only one of twenty-one specimens of serum from children under age 5 showed definite evidence of neutralizing antibodies and this child had resided elsewhere during the first 3 months of its life. The proportion of positive results in all ages to 9 years inclusive was well below that obtained in tests with Type 1 virus.

From a review of published data concerning the age distribution of cases in the 1916 epidemic in New York, it is concluded that termination of the spread of Type 1 virus in Ketchikan occurred when the proportion of susceptibles in the general population was comparable to that in New York in each of several non-epidemic years preceding 1916. It is further evident that spread of Type 2 virus in Baltimore during a period of low prevalence of poliomyelitic disease was comparable to that of Type 1 virus in Ketchikan in 1952, in that the proportion of susceptibles in the population at the end of the period of spread of virus was similar.

Serological studies of residents of Metlakatla, an Indian community near Ketchikan, showed evidence of essentially uniform infection with Type 1 virus, a very high incidence of antibodies to Type 3 virus, and a much lower incidence of antibodies to Type 2 virus.

The epidemiological aspects of poliomyelitis in Ketchikan cannot be reasonably attributed to susceptibility resulting from isolation of the community, since travel to and from Ketchikan was considerable and a relatively large proportion of persons with paralytic disease were adults who had travelled extensively, and resided for periods of years in various parts of the United States. It is noted that the municipal water supply showed frequent evidence of faecal pollution.

The willing co-operation and valuable assistance of the following persons is gratefully acknowledged: Mr Alfred Baker, Mrs Dixie M. Baade, Miss Geneva Hubbard and Miss Lorraine Singer of the Ketchikan office of the Alaska Territorial Health Department; and Dr C. Earl Albrecht, Director and Dr Charles R. Hayman, Chief of Section of Preventive Medical Services, of the Alaska Territorial Department of Health.

The National Foundation for Infantile Paralysis financed the initial visits to Ketchikan. Testing of specimens was accomplished through the support of the University of Washington Fund for Biological and Medical Research and the Office of Naval Research.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1957

References

REFERENCES

Frost, W. H. (1913). Epidemiologic studies of acute anterior poliomyelitis. Bull. Hyg. Lab. U.S. Publ. Hlth Serv., Wash., no. 90.Google Scholar
Mainland, D. (1952). Elementary Medical Statistics, the Principles of Quantitative Medicine. Philadelphia and London: W. B. Saunders Co.Google Scholar
Melnick, J. L. & Ledinko, N. (1953). Development of neutralizing antibodies against the three types of poliomyelitis virus during an epidemic period. The ratio of inapparent infection to clinical poliomyelitis. Amer. J. Hyg. 58, 207.Google ScholarPubMed
Miller, C. A. & Wenner, H. A. (1954). Antibody responses to naturally occurring poliomyelitis infections in children. I. Neutralizing antibodies against the prototype and patient's own viruses. Pediatrics, Springfield, 14, 573.CrossRefGoogle ScholarPubMed
Paul, J. R. (1955). Epidemiology of poliomyelitis. Poliomyelitis, World Health Organization Monograph Series, no. 26. Geneva, 9.Google Scholar
Sabin, A. B. (1952). Transitory appearance of Type 2 neutralizing antibody in patients infected with Type 1 poliomyelitis virus. J. exp. Med. 96, 99.CrossRefGoogle ScholarPubMed
Salk, J. E., Youngner, J. S. & Ward, E. N. (1954). Use of color change of phenol red as the indicator in titrating poliomyelitis virus or its antibody in a tissue-culture system. Amer. J. Hyg. 60, 214.Google ScholarPubMed
Sample, D. W. & Evans, C. A. (1957). Estimates of the infection rates for poliomyelitis virus in the years preceding the poliomyelitis epidemics of 1916 in New York and 1945 on Mauritius. J. Hyg., Camb., 55, 254.CrossRefGoogle ScholarPubMed
Turner, T. B., Hollander, D. H., Buckley, S., Kokko, U. P. & Winsor, C. P. (1950). Age incidence and seasonal development of neutralizing antibodies to Lansing poliomyelitis virus. Amer. J. Hyg. 52, 323.Google ScholarPubMed