Polio prevention
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Two polio vaccines are used throughout the world to combat polio. Both vaccines induce immunity to polio, efficiently blocking person-to-person transmission of wild poliovirus, thereby protecting both individual vaccine recipients and the wider community (so-called herd immunity).
Prevention
Vaccination
Click here to read more about the polio vaccine.
As a result of the introduction of inactivated poliovirus vaccine (IPV) in the 1950s, followed by oral poliovirus vaccine (OPV) in the 1960s, poliomyelitis control has been achieved in numerous countries worldwide, including the entire Western Hemisphere.[1][2][3] Two forms of the vaccine are available, the Inactivated Poliovirus Vaccine (IPV) and the Live-Attenuated Poliovirus Vaccine (OPV). In 1955 the Salk IPV was introduced, leading to an important reduction of endemic and epidemic poliomyelitis. However, this form of the vaccine showed low potency, since 17% of the infants who had received the vaccine, developed paralytic poliomyelitis.[4] The OPV vaccine was introduced in 1962, as a monovalent vaccine, and the trivalent form was made available in 1964. This form of the vaccine was rapidly accepted in developing countries, due to:[5]
- Better immunogenicity
- Lower cost
- Easily administrated
- Vaccine virus is able to induce immunity in susceptible persons
- Induction of gastrointestinal immunity
Because of the risk of developing paralytic poliomyelitis with the OPV, developed countries use only the IPV form of the vaccine.[1]
Inactivated Poliovirus Vaccine
Vaccine containing the inactivated and more potent forms of the virus. IPV vaccine contains all 3 serotypes of the polivirus, and be administered concomitantly with other routine vaccines or simply as trivalent IPV. IPV should be administered in 4 doses, at the 2nd, 4th, and between the 6th and the 18th month of life, and then between the 4th and 6th year of life.[1][6]
The vaccine leads to the formation antibodies for the 3 serotypes of virus, after the 2nd dose in 99% of cases, and after the 3rd dose in 100% of cases.[7][8] After the 3rd dose of the vaccine, antibody titers for serotypes 1 and 3 are higher in IPV, when compared to OPV, and similar for serotype 2.[9] Antibody titers may persist in circulation in some cases during 5 years.[10] However the efficacy of the first two doses of IPV is thought to be inferior to the same two doses of OPV.[11]
Children immunized with the IPV, when exposed to the live poliovirus, were more prone to shed greater amount of the virus in feces, and for a more extended period, when compared to children immunized with OPV. This indicated a greater tendency to asymptomatic poliomyelitis and to transmission of the virus in these individuals.[12][13]
Oral Poliovirus Vaccine
Live-Attenuated Poliovirus Vaccine
The live-attenuated poliovirus vaccine (OPV) is not available in the United States, however it is still used in other countries. Commonly, after the first dose of OPV, children show the following seroconversion rates:[14]
- Serotype 1 - 50%
- Serotype 2 - 85%
- Serotype 3 - 30%
On the second month after the third dose of OPV, the antibody prevalence to serotypes 1, 2 and 3 is > 96%.[8][15]
Monovalent
The first polio vaccine was developed in 1952 by Jonas Salk at the University of Pittsburgh, and announced to the world on April 12, 1955. The Salk vaccine, or inactivated poliovirus vaccine (IPV), is based on poliovirus grown in a type of monkey kidney tissue culture (Vero cell line), which is chemically-inactivated with formalin. After two doses of IPV, ninety percent or more of individuals develop protective antibody to all three serotypes of poliovirus, and at least 99% are immune to poliovirus following three doses. IPV is currently the vaccine of choice in most countries.
Oral Poliovirus Vaccine
Eight years after Salk's success, Albert Sabin developed an oral polio vaccine (OPV) using live but weakened (attenuated) virus, produced by the repeated passage of the virus through non-human cells at sub-physiological temperatures. Human trials of Sabin's vaccine began in 1957 and it was licensed in 1962. The attenuated poliovirus in the Sabin vaccine replicates very efficiently in the gut, the primary site of wild poliovirus infection and replication, but the vaccine strain is unable to replicate efficiently within nervous system tissue. OPV produces excellent immunity in the intestine, which helps prevent infection with wild virus in areas where the virus is endemic. A single dose of oral polio vaccine produces immunity to all three poliovirus serotypes in approximately 50% of recipients. Three doses of live-attenuated OPV produce protective antibody to all three poliovirus types in more than 95% of recipients.
OPV consists of a mixture of live attenuated poliovirus strains of each of the three serotypes, selected by their ability to mimic the immune response following infection with wild polioviruses, but with a significantly reduced incidence of spreading to the central nervous system. Three or more spaced doses of OPV are required to generate adequate levels of seroconversion. The action of oral polio vaccine (OPV) is two-pronged. OPV produces antibodies in the blood ('humoral' or serum immunity) to all three types of poliovirus, and in the event of infection, this protects the individual against polio paralysis by preventing the spread of poliovirus to the nervous system. OPV strains also produce a local immune response in the lining ('mucous membrane') of the intestines - the primary site for poliovirus multiplication. The antibodies produced there inhibit the multiplication of subsequent infections of 'wild' (naturally occurring) virus. This intestinal immune response to OPV is probably a reason why mass campaigns with OPV have been shown to stop person-to-person transmission of wild poliovirus. In very rare cases, the administration of OPV results in vaccine-associated paralysis associated with a reversion of the vaccine strains to the more neurovirulent profile of wild poliovirus. In a few instances, such vaccine strains have become both neurovirulent and transmissible and have resulted in infectious poliomyelitis.
Passive Immunization
In 1950, William Hammon at the University of Pittsburgh purified the gamma globulin component of the blood plasma of polio survivors.[16] Hammon proposed that the gamma globulin, which contained antibodies to poliovirus, could be used to halt poliovirus infection, prevent disease, and reduce the severity of disease in other patients who had contracted polio. The results of a large clinical trial were promising; the gamma globulin was shown to be about 80% effective in preventing the development of paralytic poliomyelitis.[17] It was also shown to reduce the severity of the disease in patients that developed polio.[16] The gamma globulin approach was later deemed impractical for widespread use, however, due in large part to the limited supply of blood plasma, and the medical community turned its focus to the development of a polio vaccine.[18]
References
- ↑ 1.0 1.1 1.2 "Poliomyelitis Prevention in the United States".
- ↑ Kim-Farley RJ, Bart KJ, Schonberger LB, Orenstein WA, Nkowane BM, Hinman AR; et al. (1984). "Poliomyelitis in the USA: virtual elimination of disease caused by wild virus". Lancet. 2 (8415): 1315–7. PMID 6150330.
- ↑ Nathanson N, Martin JR (1979). "The epidemiology of poliomyelitis: enigmas surrounding its appearance, epidemicity, and disappearance". Am J Epidemiol. 110 (6): 672–92. PMID 400274.
- ↑ Melnick JL (1978). "Advantages and disadvantages of killed and live poliomyelitis vaccines". Bull World Health Organ. 56 (1): 21–38. PMC 2395534. PMID 307445.
- ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
- ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
- ↑ Simoes EA, John TJ (1986). "The antibody response of seronegative infants to inactivated poliovirus vaccine of enhanced potency". J Biol Stand. 14 (2): 127–31. PMID 3020057.
- ↑ 8.0 8.1 McBean AM, Thoms ML, Albrecht P, Cuthie JC, Bernier R (1988). "Serologic response to oral polio vaccine and enhanced-potency inactivated polio vaccines". Am J Epidemiol. 128 (3): 615–28. PMID 2843039.
- ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
- ↑ Swartz TA, Roumiantzeff M, Peyron L, Stopler T, Drucker J, Epstein I; et al. (1986). "Use of a combined DTP-polio vaccine in a reduced schedule". Dev Biol Stand. 65: 159–66. PMID 2881820.
- ↑ Robertson SE, Traverso HP, Drucker JA, Rovira EZ, Fabre-Teste B, Sow A; et al. (1988). "Clinical efficacy of a new, enhanced-potency, inactivated poliovirus vaccine". Lancet. 1 (8591): 897–9. PMID 2895828.
- ↑ Onorato IM, Modlin JF, McBean AM, Thoms ML, Losonsky GA, Bernier RH (1991). "Mucosal immunity induced by enhance-potency inactivated and oral polio vaccines". J Infect Dis. 163 (1): 1–6. PMID 1845806.
- ↑ Modlin JF, Halsey NA, Thoms ML, Meschievitz CK, Patriarca PA (1997). "Humoral and mucosal immunity in infants induced by three sequential inactivated poliovirus vaccine-live attenuated oral poliovirus vaccine immunization schedules. Baltimore Area Polio Vaccine Study Group". J Infect Dis. 175 Suppl 1: S228–34. PMID 9203721.
- ↑ Cohen-Abbo A, Culley BS, Reed GW, Sannella EC, Mace RL, Robertson SE; et al. (1995). "Seroresponse to trivalent oral poliovirus vaccine as a function of dosage interval". Pediatr Infect Dis J. 14 (2): 100–6. PMID 7746690.
- ↑ Hardy GE, Hopkins CC, Linnemann CC, Hatch MH, Witte JJ, Chambers JC (1970). "Trivalent oral poliovirus vaccine: a comparison of two infant immunization schedules". Pediatrics. 45 (3): 444–8. PMID 5442915.
- ↑ 16.0 16.1 Hammon W (1955). "Passive immunization against poliomyelitis". Monogr Ser World Health Organ. 26: 357–70. PMID 14374581.
- ↑ Hammon W, Coriell L, Ludwig E; et al. (1954). "Evaluation of Red Cross gamma globulin as a prophylactic agent for poliomyelitis. 5. Reanalysis of results based on laboratory-confirmed cases". J Am Med Assoc. 156 (1): 21–7. PMID 13183798.
- ↑ Rinaldo C (2005). "Passive immunization against poliomyelitis: the Hammon gamma globulin field trials, 1951–1953". Am J Public Health. 95 (5): 790–9. PMID 15855454.