The general epidemiology of polioviruses is similar to that of other enteroviruses and is discussed more fully in Chapter 194, Nonpolio Enteroviruses and Parechoviruses. The spread of polioviruses and the clinical manifestations of infection are affected markedly by the degree of vaccine use and the socioeconomic conditions of the population. The epidemiology of poliomyelitis was a mystery until researchers discovered that unrecognized infections were the main source of the spread of the virus. Historically, in populations with poor sanitation and hygiene, epidemics of poliomyelitis did not occur, but widespread dissemination of polioviruses occurred continually. In such populations, immunizing infections with all three poliovirus types occurred in infants who usually were protected from significant clinical disease by transplacentally acquired antibodies. In populations with improved standards of hygiene, immunizing infections in infants no longer occur regularly, so pools of susceptible children form in the population. When poliovirus is introduced into such a population, infection occurs in these older children, and poliomyelitis not infrequently occurs. The age spread of cases of poliomyelitis in a population depends on the overall hygienic standards of the population, as well as such factors as family size and crowding.

The evolution of poliomyelitis from an endemic to epidemic situation followed a characteristic pattern. Initially, only isolated cases occurred. Over the course of years, the endemic rate gradually increased, followed by periodic, then yearly, severe epidemics with high attack rates. Once a community reached a socioeconomic situation in which epidemic poliomyelitis occurred regularly, a gradual shift occurred in the incidence according to age. Relatively few cases occurred in infants, the peak occurred in the 5- to 14-year-old age group, and an increasing proportion of cases occurred in young adults.

The universal use of oral polio vaccines, beginning in the early 1960s, resulted in the elimination of infection with wild polioviruses in the Western Hemisphere and much of the developed world. In 1988, the World Health Assembly established the objective of global polio eradication. By the close of the year 2001, the area of endemic poliomyelitis had been reduced to 10 countries and a reporting of fewer than 1,000 cases.

The general pathophysiology of enteroviral infections is presented in Chapter 194, Nonpolio Enteroviruses and Parechoviruses.

The virus can be recovered from the blood, throat, and feces of the infected person 3 to 5 days after exposure. At this time, minor illness may occur, or the infection may be unrecognized. Major illness, with involvement of the central nervous system (CNS), has its onset approximately 10 days after infection. Most likely, the blood is the main pathway for viral invasion of the CNS in natural disease. Experimental infections in monkeys, however, have demonstrated that the virus can reach the CNS by traveling along axons of peripheral nerves.

The neuropathology of poliomyelitis usually is pathopneumonic. Neuronal damage is caused directly by multiplication of the virus in the cells; little evidence exists of infection in surrounding tissues except for slight histologic evidence of meningitis and perivascular cuffing. Neuronal lesions are found most commonly in the anterior horn cells of the spinal cord.

In susceptible persons, 90% to 95% of infections are inapparent and approximately 4% to 8% are classified as minor illness (abortive poliomyelitis); rarely does nonparalytic poliomyelitis (aseptic meningitis) or paralytic poliomyelitis develop. In general, older persons are more likely to have severe paralytic disease and higher mortality rates. Bulbar poliomyelitis may be precipitated by tonsillectomy at the time of inapparent infection; a history of tonsillectomy also is related to a higher rate of bulbar disease.

Abortive poliomyelitis (minor illness) is similar to many other enteroviral infections and frequently is unrecognized as a significant infection. The illness is mild and nonspecific, with low-grade fever, malaise, anorexia, and sore throat. On physical examination, no significant abnormalities are noted.