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Polio is a viral disease that has caused considerable suffering for much of human history. The oldest clearly identifiable reference to paralytic poliomyelitis is an Egyptian stone engraving from 14th century BCE. Prior to the introduction of effective vaccines in the 1950s, polio was a common infection of childhood, with a small proportion of infections resulting in death or lifelong paralysis. Control began in 1955 after the first inactivated poliovirus vaccine (IPV) and subsequently several years later an oral polio vaccine (OPV) was also introduced. In most developed countries, a good level of control was achieved by the mid 1960s. In 1985, the Pan American Health Organization (PAHO) launched an initiative to eradicate polio in the Americas by 1990. Based on the success of the PAHO program, in May 1988, the 41st World Health Assembly committed the Member States of the World Health Organization (WHO) to the global eradication of poliomyelitis by the year 2000 (resolution WHA41.28). Despite great progress, by the end of 2006, there were still four countries in which polio was endemic (Nigeria, India, Pakistan, and Afghanistan), with another eight countries experiencing importations (Angola, Cameroon, Ethiopia, Indonesia, Nepal, Niger, Somalia, and Yemen).

Infectious Agent and Transmission

The poliovirus is an enterovirus with man as the only reservoir. There are three antigenic types: 1, 2, and 3. Type 1 most commonly causes paralysis, Type 3 less frequently, and Type 2 uncommonly. Most epidemics historically are due to Type 1. The risk of vaccineassociated poliomyelitis per million persons vaccinated ranged from .05 to .99 (Type 1), 0 to .65 (Type 2), and 1.18 to 8.91 (Type 3).

Infection is spread from person-to-person with fecaloral transmission most common in developing countries where sanitation is poor, while oral-pharyngeal transmission is more common in industrialized countries and during outbreaks. The mouth is the usual site of entry, and the virus first multiplies at the site of implantation in the lymph nodes in the pharynx and gastrointestinal tract. Incubation is usually from 7 to 10 days and may range from 4 to 40 days. The virus is usually present in the pharynx and in the stool before the onset of paralytic illness. One week after onset, there is low virus concentration in the throat, but the virus continues to be excreted in the stool for several weeks. Cases are most infectious during the first few days before and after onset of symptoms. For poliomyelitis, the ratio of inapparent (either subclinical or mild) infections to paralytic cases is very high, somewhere between 100 and 1,000 to 1. Long-term carriers are not known to occur.

Immunity

Susceptibility to poliomyelitis is universal. Epidemiologic evidence indicates that infants born to mothers with antibodies are naturally protected against paralytic disease for a few weeks. Immunity is obtained from infection with the wild virus or from immunization. Immunity following natural (including inapparent and mild) infections, or a completed series of immunizations with live OPV, results in both humoral (related to antibody production) and local intestinal cellular responses (a more localized response). Such immunity is thought to be lifelong and can serve as a block to infection with subsequent wild viruses and, therefore, helps in breaking chains of transmission. Vaccination with the IPV confers humoral immunity, but relatively less intestinal immunity; thus, vaccination with IPV does not provide resistance to carriage and spread of wild virus in the community. There is thought to be little, if any, cross-immunity between poliovirus types.

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