Eradication of poliomyelitis: when can one be sure that polio virus transmission has been terminated?

Most polio virus infections are silent. Vaccination reduces the incidence of infection, and the period between clinical cases of poliomyelitis becomes longer. As the point of eradication is approached, it becomes increasingly difficult to use the case-free period to determine whether silent infections have ceased. In this paper, the authors use stochastic computer simulations to relate case-free periods to the presence or absence of silent infections. After 2 years without paralytic cases in a population of 200,000 inhabitants, the probability for the presence of silent infections can still be as high as 38%. The case-free period must exceed 3 years before one can be 95% certain that there has been local extinction of the wild polio virus infection. Even after 5 years without cases, the probability of silent polio virus transmission can still be in the range of 0.1-1.0%.

[1]  K. Dietz.  The estimation of the basic reproduction number for infectious diseases , 1993, Statistical methods in medical research.

[2]  D. Gillespie.  A General Method for Numerically Simulating the Stochastic Time Evolution of Coupled Chemical Reactions , 1976 .

[3]  R. Henderson.  The World Health Organization's Plan of Action for Global Eradication of Poliomyelitis by the Year 2000 a , 1989, Annals of the New York Academy of Sciences.

[4]  R. Warren,et al.  Effect of Sabin Type 1 poliomyelitis vaccine administered by mouth to newborn infants. , 1961, The New England journal of medicine.

[5]  D. Horstmann.  POLIOMYELITIS: SEVERITY AND TYPE OF DISEASE IN DIFFERENT AGE GROUPS , 1955, Annals of the New York Academy of Sciences.

[6]  K. Hadeler,et al.  Deterministic models for the eradication of poliomyelitis: vaccination with the inactivated (IPV) and attenuated (OPV) polio virus vaccine. , 1995, Mathematical biosciences.

[7]  M. Miller,et al.  Poliomyelitis in Liberia; prevalence of the disease, sero-immunity resulting from subclinical infection, and indications for prophylactic vaccination. , 1956, The American journal of tropical medicine and hygiene.

[8]  J. Melnick,et al.  A survey of neutralizing antibodies to poliomyelitis virus in Cairo, Egypt. , 1952, American journal of hygiene.

[9]  Y. Ghendon,et al.  Comparison of the Resistance of the Intestinal Tract to Poliomyelitis virus (Sabin's Strains) in Persons after Naturally and Experimentally Acquired Immunity. , 1961 .

[10]  J. Fox,et al.  Studies on the development of natural immunity to poliomyelitis in Louisiana. I. Over-all plan, methods and observations as to patterns of seroimmunity in the study group. , 1957, American journal of hygiene.

[11]  Herbert W. Hethcote,et al.  Asymptotic Behavior and Stability in Epidemic Models , 1974 .

[12]  J. Fox,et al.  Studies on the development of natural immunity to poliomyelitis in Louisiana. II. Description and analysis of episodes of infection observed in study group households. , 1957, American journal of hygiene.

[13]  T. Chin,et al.  Limitation of fecal and pharyngeal poliovirus excretion in Salk-vaccinated children. A family study during a type 1 poliomyelitis epidemic. , 1962, American journal of hygiene.

[14]  A. Beale,et al.  A study of polio vaccination in infancy: excretion following challenge with live virus by children given killed or living poliovaccine , 1966, Journal of Hygiene.

[15]  F. Fenner.  Smallpox and its eradication , 1988 .