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Fifty years ago this year, following the largest public health trial in American history, a killed-virus polio vaccine developed by Jonas Salk, M. The news set off a national celebration. But as the years passed, the essential contributions of other researchers to this lifesaving vaccine were lost to history. What follows is the story of Dorothy Millicent Horstmann, M.

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NCBI Bookshelf. Poliomyelitis is an acute infectious disease caused by an enterovirus. There are three types of this virus: types 1, 2, and 3. 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.

The virus enters the body by the oral or respiratory route and multiplies in the pharynx and small intestine. 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. During the period of viremia, the virus can reach the central nervous system and initiate infection there. 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.

What is post-polio syndrome?

Only 1 to 2 percent of infected individuals develop disease in the central nervous system, and fewer still have residual paralysis. Nevertheless, the portent of these rare consequences is great, because they result in death or lifelong disability. Although there are currently effective vaccines against poliovirus, even before they became available, Hammon et al. Various attempts at developing a vaccine had been thwarted by the absence of an effective in vitro system of virus replication.

The establishment in of the tissue culture technique for supporting virus growth made development of a vaccine possible Enders et al.

Adverse events associated with childhood vaccines: evidence bearing on causality.

It was for these findings that J. Enders, F. Robbins, and T. Weller received the Nobel Prize in This development was followed by efforts to generate sufficient quantities of the virus to inactivate it and use it as an inert antigen. An alternative approach was to attenuate the wild-type virus and render it safe as a replicating antigen.

Both were successful and today there are two forms of the vaccine: the inactivated polio vaccine IPVwhich 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 enhanced-potency IPV was developed in the late s and is used today. Shortly after the licensure of IPV inthe vaccine manufactured by Cutter was found to cause paralytic disease.

What causes post-polio syndrome?

It contained residual infectious virus. The reason was traced to the method of inactivation. At that time the dynamics of the inactivation process were not fully understood, and the U. All of these problems have since been corrected. The trivalent OPV used today was d in In the recommendations of the U. Public Health Service, no preference for one or the other form of the vaccine was expressed U. Polio has been eliminated as an endemic disease in the United States and many developing countries.

Outbreaks have occasionally occurred in subsets of unvaccinated susceptible individuals. A persistent concern has been the possibility of the Polio short leg women complication of paralytic poliomyelitis in vaccinees and their contacts, particularly those with impaired immunity. This is discussed in detail later in this chapter. Each of the three immunologically distinct types of poliovirus—types 1, 2, and 3—can cause paralytic disease.

The mechanism of attenuation of the neurovirulence and that of occasional reversion to neurovirulence have been described in detail in a recent review Racaniello, Recipients of OPV shed the virus in their feces, and contacts exposed to the virus can become infected. Infection with poliovirus can take several forms: inapparent infection, mild illness, aseptic meningitis nonparalytic poliomyelitisand paralytic poliomyelitis.

Approximately 4 to 8 percent of all wild-type poliovirus infections result in nonparalytic polio disease. This manifests as fever, malaise, headache, nausea, stiffness of the neck and back, and meningeal s. Approximately 1 percent of infections in paralytic disease. In paralytic poliomyelitis, the virus invades the central nervous system, replicating in motor neurons within the anterior horn of the spinal cord, in the brainstem, and in the motor cortex. When viral replication destroys sufficient s of neurons, paralysis occurs Racaniello, The Polio short leg women begins with a headache, fever, and stiff neck; this is followed by paralysis of the voluntary muscles ly controlled by the destroyed neurons of either the spinal cord or the brainstem.

The muscle paralysis is usually asymmetrical. The spinal fluid contains an increased of lymphocytes, the protein concentration is elevated, and the glucose concentration is normal. The association between live attenuated polio vaccine and cases of paralytic poliomyelitis dates back to the time of administration of the first live attenuated polio vaccine tried by Kolmer in the s Kolmer, Leake described nine cases of poliomyelitis that occurred following vaccination with the Kolmer vaccine and that seemed to be caused by the vaccine.

The concept that live attenuated polio vaccine causes a small of poliomyelitis cases thus has a history of at least six decades.

Henderson et al. They evaluated cases of paralytic polio that had occurred within 30 days of OPV administration and decided that 57 cases were compatible with vaccine-induced disease. Fifteen of the cases occurred after receiving the type 1 vaccine, with an estimated incidence of 0.

Thirty-six cases occurred following vaccination with the type 3 vaccine, with an incidence of 0. Two cases occurred following vaccination with the type 2 vaccine, and four cases occurred following vaccination with the trivalent vaccine. The authors also described three cases of poliomyelitis that occurred in contacts of a recipient of the type 3 vaccine, but it is not clear whether the contact cases were included in the overall counts of vaccine-associated cases.

Following publication of the paper by Henderson et al. Table summarizes the early case reports that described vaccine-associated poliomyelitis. ByChang et al. InMorse et al. This was similar to the case of polio in an unimmunized father of a recently vaccinated infant reported by Swanson et al.

Two reports provided evidence that contacts other than the parents or household members were also at risk of contracting polio. Balduzzi and Glasgow and Stolley et al. OPV consists of live attenuated viruses that multiply in the intestinal tract and that can revert to a more virulent form, causing disease. A vaccine recipient excretes live virus for several Polio short leg women, and recipients or contacts may become infected with the virus.

Since the s there have been about studies reporting individual cases, case series, and national surveillances of vaccine-associated cases of paralytic poliomyelitis.

Case definitions have been well developed by the CDC and the World Health Organization WHO ; a case of vaccine-associated paralytic poliomyelitis is said to occur in recipients if the onset of the disease begins days postvaccination and is said to occur in contacts of vaccine recipients if the onset of the disease begins days after a recipient's vaccination.

Laboratory tests can identify the strain of the infecting virus as a wild-type or vaccine strain of poliovirus. The cases described above in the section History of Suspected Association are typical of those that followed in the s and s. WHO and CDC have used standard definitions of cases of paralytic poliomyelitis for almost 30 years, and many nations have implemented polio surveillance systems to monitor their polio immunization programs.

Despite differences in the ways that data are categorized and reported Polio short leg women the changes in the incidence of polio from to the present, all the national data show a low incidence of vaccine-associated paralytic polio, on the order of a few cases per 1 million doses given or a few cases per 1 million vaccine recipients.

The CDC data for the years to show an incidence of 1 case of vaccine-associated paralytic polio per 3. When cases among immunodeficient recipients and contacts and patients with vaccine-like virus are included, the incidence is 1 case per 2.

The incidence is greater with the first dose of vaccine. The CDC has estimated that the overall dose-related incidence is 1 case perfirst doses distributed versus 1 case per The Monitoring System for Adverse Effects Following Immunization MSAEFI does not list poliomyelitis as a separate adverse event, although it may be included under such as "other neurologic symptoms," "other reactions," and "serious events.

Of the eight VAERS reports suggestive of vaccine-associated poliomyelitis, six provided insufficient information, one provided enough information to rule out vaccine-associated poliomyelitis the time interval exceeded WHO guidelinesand one report provided information sufficient to be a well-documented case of vaccine-associated poliomyelitis. The report, which was filled out by a physician, stated, "Vaccine associated paralytic poliomyelitis confirmed by box 12 oligonucleotide sequencing of type III viral isolate.

Occurred in an unvaccinated contact of a recently vaccinated eight-month old. The data regarding OPV-related nonparalytic polio are more scarce than those for paralytic disease. A Polio short leg women of poliomyelitis surveillance in England and Wales from to documented 44 cases of nonparalytic poliomyelitis Smith and Wherry, Included in this definition were patients with a clinical diagnosis of nonparalytic poliomyelitis, as well as those with encephalitis or aseptic meningitis who also had cultural or serologic evidence of poliovirus infection.

Twelve of those cases were believed to have been associated with administration of OPV 11 in recipients, 1 in a contact. Poliovirus was isolated from 8 of the 11 recipient cases. All of the viruses were typed as the vaccine strain on the basis of reproductive capacity temperature RCT tests.

Virus isolated from the one contact case was also typed as the vaccine strain.

What causes post-polio syndrome?

The authors calculated incidence rates of 0. The authors noted that the definition of nonparalytic disease was, perhaps, broad, and thus, this represents an estimate of the highest possible of nonparalytic cases. Poliovirus was isolated from recently vaccinated patients in the former West Germany between and Thraenhart and Kuwert, Of the 34 patients with aseptic meningitis, virus isolated from 17 patients was typed by the RCT test as vaccine strain, from 13 patients as wild-type, and from 4 patients as intermediate. A study of the incidence of aseptic meningitis in Olmsted County, Minnesota, from to reported that 2 of the patients with aseptic meningitis had received polio vaccine within 4 weeks prior to the onset of symptoms Beghi et al.

However, no mention of virus isolation was made, and the disease cannot be ascribed to the vaccine. Vaccination with live virus mimics a natural process of exposure to virus that in immunity to the disease. Although the vaccine virus is attenuated, approximately 1 in 1 million vaccinations with attenuated virus le to paralytic disease. Infection in the intestinal tract with the vaccine strain of poliovirus in virus shedding in the feces and the risk that the contacts of a recipient might become infected.

The vaccine virus can revert to a virulent form, and this lends demonstrated biologic plausibility to the finding that occasional contacts of vaccine recipients contract polio. The presence of vaccine virus in patients suspected of having vaccine-associated polio is often confirmed by laboratory tests that permit specific identification of the virus as the vaccine or wild-type virus. In countries where wild-type poliovirus has almost been eradicated, there is usually no other means of exposure to poliovirus that could explain a case of polio. The confirmation by laboratory tests, the absence of circulating wild-type virus, and the temporal association of paralytic polio with receipt of OPV onset of illness within 30 days postvaccination in recipients and 60 days in contacts of vaccine recipientsall of which have been seen in the well-documented cases of vaccine-associated polio, fulfill the criteria of infectious disease causality.

Surveillance of nonparalytic polio following Polio short leg women administration has been much less rigorous and thus, less well-documented in the literature. The arguments in support of accepting a causal relation between OPV and paralytic poliomyelitis apply, most certainly, to the relation between OPV and nonparalytic polio.