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Review
. 2010 Dec 1;172(11):1213-29.
doi: 10.1093/aje/kwq320. Epub 2010 Oct 26.

From emergence to eradication: the epidemiology of poliomyelitis deconstructed

Neal Nathanson  1 , Olen M Kew
Affiliations
Review

From emergence to eradication: the epidemiology of poliomyelitis deconstructed

Neal Nathanson et al. Am J Epidemiol. .

Abstract

Poliomyelitis has appeared in epidemic form, become endemic on a global scale, and been reduced to near-elimination, all within the span of documented medical history. Epidemics of the disease appeared in the late 19th century in many European countries and North America, following which polio became a global disease with annual epidemics. During the period of its epidemicity, 1900-1950, the age distribution of poliomyelitis cases increased gradually. Beginning in 1955, the creation of poliovirus vaccines led to a stepwise reduction in poliomyelitis, culminating in the unpredicted elimination of wild polioviruses in the United States by 1972. Global expansion of polio immunization resulted in a reduction of paralytic disease from an estimated annual prevaccine level of at least 600,000 cases to fewer than 1,000 cases in 2000. Indigenous wild type 2 poliovirus was eradicated in 1999, but unbroken localized circulation of poliovirus types 1 and 3 continues in 4 countries in Asia and Africa. Current challenges to the final eradication of paralytic poliomyelitis include the continued transmission of wild polioviruses in endemic reservoirs, reinfection of polio-free areas, outbreaks due to circulating vaccine-derived polioviruses, and persistent excretion of vaccine-derived poliovirus by a few vaccinees with B-cell immunodeficiencies. Beyond the current efforts to eradicate the last remaining wild polioviruses, global eradication efforts must safely navigate through an unprecedented series of endgame challenges to assure the permanent cessation of all human poliovirus infections.

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Figures

Figure 1.
Figure 1.
Reported numbers of paralytic cases in poliomyelitis epidemics occurring between 1880 and 1916, by country and year, including the countries where large outbreaks were first observed. Data were obtained from chart 1 in the article by Lavinder et al. (30).
Figure 2.
Figure 2.
Age distribution of patients with poliomyelitis (paralytic and nonparalytic) in Massachusetts, 1912–1952. Data were obtained from Dauer (35).
Figure 3.
Figure 3.
Annual poliomyelitis attack rates per 100,000 population in the United States (top) and New York City (bottom) during the first half of the 20th century. Upper panel: poliomyelitis incidence by 5-year period, United States, 1915–1954. Reports for 1915–1944 were almost entirely on cases of paralytic poliomyelitis, while reports for 1945–1954 comprised approximately equal numbers of paralytic and nonparalytic cases. Data were obtained from Serfling and Sherman (36) Sabin (37), and the Centers for Disease Control and Prevention (40). Lower panel: poliomyelitis incidence by 10-year period, New York City, 1910–1954. Data were obtained from Sabin (37), Greenberg et al. (38), and Siegel et al. (39).
Figure 4.
Figure 4.
Seasonal variation in reported poliovirus (striped bars) in New England during 1942–1951 and in isolation of rotavirus (dashed line) in the United States during 1991–1997. Data were obtained from Serfling and Sherman (36) and Török et al. (49).
Figure 5.
Figure 5.
Seasonal variation in poliomyelitis incidence (striped bars) and relative humidity (dashed line) in New England during 1942–1951 and in Hawaii during 1938–1952. Ratios show the degree of seasonal variation in poliomyelitis incidence. Data were obtained from Serfling and Sherman (36), Enright (50), and the National Oceanic and Atmospheric Administration (51).
Figure 6.
Figure 6.
Upper panel: annual numbers of reported cases of poliomyelitis in the United States, 1951–1982. For the years 1973–1982, cases were either imported cases or cases of vaccine-associated paralytic poliomyelitis, with the exception of an outbreak that occurred among the Amish population in 1979. Data were obtained from the Centers for Disease Control and Prevention (65). Lower panel: number of US states reporting indigenous poliomyelitis due to wild polioviruses, 1951–1982. Data were obtained from the Centers for Disease Control and Prevention (69).
Figure 7.
Figure 7.
Reported numbers of confirmed cases of paralytic poliomyelitis (solid line) in Latin America and the Caribbean region and percentages of children aged 12 months given at least 3 doses of oral poliovirus vaccine (OPV) (dashed line), 1969–1995. Data were obtained from de Quadros et al. (5).
Figure 8.
Figure 8.
Global incidence of poliomyelitis, reported as virologically confirmed cases of paralytic poliomyelitis, during the period 1980–2009. Cases for 2000–2009 have been replotted in the inset to demonstrate recent incidence. It is estimated that during the period from 1980 to the late 1990s, virologically confirmed cases represented only a modest proportion (15%–25%) of all cases of paralytic poliomyelitis. Data were obtained from the World Health Organization (100).
Figure 9.
Figure 9.
Transmission of wild polioviruses worldwide in 2009. Countries with wild polioviruses are classified into 3 categories: those with endemic polioviruses, those with imported viruses that have reestablished transmission, and those with recently imported viruses. Data were obtained from the World Health Organization (33).
Figure 10.
Figure 10.
Annual attack rate of type 1 paralytic poliomyelitis in Nigeria according to the percentage of children under age 5 years who were immunized with oral poliovirus vaccine (≥3 doses), 2001–2007. Data for 37 individual states for each of the 7 years were sorted according to attack rate and the proportion of children immunized. The data were then collated to construct each point on the graph. Shown next to each point is the number of instances with the parameters for that point. Data were obtained from Jenkins et al. (77).
Figure 11.
Figure 11.
Environmental surveillance for poliovirus excretion following the transition from oral poliovirus vaccine (OPV) to inactivated poliovirus vaccine (IPV) in New Zealand, 2001–2003. Sewage samples were collected weekly from 3 different sewage treatment plants before and after the termination of OPV utilization. Routine use of OPV ended on February 1, 2002, and the prevalence of OPV in sewage fell from approximately 90% to 0% by June 2002 (4 months later). During the following 10 months (July 2002–April 2003), there were 5 isolates of OPV; on the basis of sequence analysis, all of these isolates were determined to be from children recently immunized with OPV, suggesting that they represented imported OPV. Data were obtained from Huang et al. (108).
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