Outbreaks have occasionally occurred in subsets of unvaccinated susceptible individuals. Polio has been eliminated as an endemic disease in the United States and many developing countries. Public Health Service, 1962), but in 1964 the Committee on Infectious Diseases of the American Academy of Pediatrics recommended the use of OPV. Public Health Service, no preference for one or the other form of the vaccine was expressed (U.S. The trivalent OPV used today was licensed in 1963. Trials of OPV in the United States followed, and monovalent OPVs were quickly licensed. By then, over 100 million people in the former Soviet Union and Eastern Bloc countries-except Poland-had received the Sabin vaccine (LaForce, 1990).
Causality 7 trial#
The first OPV was licensed in 1960 after an extensive trial in the former Soviet Union (Benison, 1982). All of these problems have since been corrected. government's requirements for vaccine production were ambiguous. At that time the dynamics of the inactivation process were not fully understood, and the U.S.
The reason was traced to the method of inactivation. Shortly after the licensure of IPV in 1955, the vaccine manufactured by Cutter was found to cause paralytic disease. Currently, IPV and the Sabin strains of OPV are available for use in the United States however, OPV is the vaccine recommended for general use and is the most prevalent (American Academy of Pediatrics, Committee on Infectious Diseases, 1991). An enhanced-potency IPV was developed in the late 1970s and is used today. IPV was developed in 1953 by Jonas Salk (Salk, 1953 Salk et al., 1953) OPV was developed by Koprowski and colleagues (1952), who were the first to use it, and Albert Sabin (1956). Both were successful and today there are two forms of the vaccine: the inactivated polio vaccine (IPV), which is administered by the parenteral route, and the live attenuated vaccine, which is administered orally and hence is known as the oral polio vaccine (OPV). An alternative approach was to attenuate the wild-type virus and render it safe as a replicating antigen. This development was followed by efforts to generate sufficient quantities of the virus to inactivate it and use it as an inert antigen. Ment in 1949 of the tissue culture technique for supporting virus growth made development of a vaccine possible (Enders et al., 1949). Various attempts at developing a vaccine had been thwarted by the absence of an effective in vitro system of virus replication. (1953) demonstrated the effectiveness of passive immunization by injections of pooled gamma globulin. Nevertheless, the portent of these rare consequences is great, because they result in death or lifelong disability.Īlthough there are currently effective vaccines against poliovirus, even before they became available, Hammon et al. Only 1 to 2 percent of infected individuals develop disease in the central nervous system, and fewer still have residual paralysis. Antibodies appear within 1 week to 10 days after the initial infection, and viremia then ceases, probably as a consequence of neutralization by the antibodies. During the period of viremia, the virus can reach the central nervous system and initiate infection there. Within 24 hours it invades the regional lymph nodes, and after an additional 24 to 48 hours it enters the bloodstream, which carries it to the secondary sites of replication in many organs, and thus, viremia develops and is maintained and enhanced. The virus enters the body by the oral or respiratory route and multiplies in the pharynx and small intestine. Each type is capable of infecting humans there is no cross-immunity and only those individuals immune to each of the three types are protected against all three types. There are three types of this virus: types 1, 2, and 3. Poliomyelitis is an acute infectious disease caused by an enterovirus.