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INTRODUCTION

Poliomyelitis, or infantile paralysis, is an acute contagious disease characterized by fever, flaccid paralysis, and muscle atrophy as a result of the destruction of motor neurons in the spinal cord and less commonly the brain stem. Three serotypes of poliovirus cause infections that result in severity ranging from inapparent illness to acute flaccid paralysis (AFP) and death. Paralysis may resolve or lead to permanent disability and deformity. Decades after the acute episode, new paralysis or progressive weakness may appear.1 This clinical entity is referred to as postpolio syndrome. Poliomyelitis probably has afflicted mankind for thousands of years, as manifested by an Egyptian stele originating from the eighteenth dynasty (dating from 1403 to 1365 BC) that depicts a priest with a typical leg deformity. However, only in 1789 was the disease first described. Epidemic poliomyelitis emerged as a public health problem in the United States and Northern Europe in the late nineteenth and early twentieth centuries, with tens of thousands of cases reported annually. Improved hygiene and sanitation delayed poliovirus exposure to older children and young adults that were at higher risk for severe paralytic disease (“central polio dogma”). Effective vaccines, developed in the 1950s and 1960s, rapidly eliminated poliomyelitis in industrialized countries as a public health problem, but not in the developing world.2 To remedy this, the World Health Assembly, the governing body of the World Health Organization, resolved in 1988 to eradicate poliomyelitis globally by the year 2000.3 Although this target has not yet been reached, substantial progress has been made, and achievement of eradication remains feasible. The last wild poliovirus type 2 was detected in 1999, the last wild poliovirus type 3 in 2012, and wild poliovirus 1 circulation appears to be restricted to parts of Afghanistan and Pakistan with 22–33 paralytic cases per year during 2017–18. However, a resurgence of cases in 2019 led to major increases in case count, with over 176 paralytic cases (data as of June 2, 2019).

ETIOLOGY

In 1908, Landsteiner and Popper demonstrated that poliomyelitis was caused by a virus (“filterable agent”). Polioviruses caused paralytic disease in monkeys by intraperitoneal inoculation of spinal cord materials from a patient with fatal poliomyelitis. In 1931, Burnet and Macnamara established that more than one virus strain can cause poliomyelitis, and that immunity to one strain was not protective against the other strain (i.e., no heterotypic immunity). A typing effort by the Committee on Typing of the National Infantile Paralysis Society in 1951 determined that there were only three serotypes of polioviruses, designated as poliovirus types 1, 2, and 3.4 The closely related but antigenically distinct viruses are part of the Enterovirus genus and belong to the family Picornaviruses.5 In the early 1940s, it was shown that the infectious agent was present usually in the stools of patients with symptomatic disease and their symptom-free contacts. In 1949, Enders, Weller, and Robbins successfully propagated poliovirus ...

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