Poliomyelitis
Poliomyelitis is a crippling disease that results from infection with any one of the three related poliovirus types (referred to as types P1, P2, and P3), members of the enterovirus (picornavirus) family. Poliovirus is transmitted from one person to another by oral contact with secretions or faecal material from an infected person. Once viral reproduction is established in the mucosal surfaces of the nasopharynx, poliovirus can multiply in specialized cells in the intestines and enter the blood stream to invade the central nervous system, where it spreads along nerve fibres. When it multiplies in the nervous system, the virus can destroy nerve cells (motor neurons) which activate skeletal muscles.
These nerve cells cannot regenerate, and the affected muscles lose their function due to a lack of nervous enervation - a condition known as acute flaccid paralysis (AFP). Typically, in patients with poliomyelitis muscles of the legs are affected more often than the arm muscles. More extensive paralysis, involving the trunk and muscles of the thorax and abdomen, can result in quadriplegia. In the most severe cases (bulbar polio), poliovirus attacks the motor neurons of the brain stem - reducing breathing capacity and causing difficulty in swallowing and speaking. Without respiratory support, bulbar polio can result in death. It can strike at any age, but affects mainly children under three (over 50% of all cases).
In May 1988, at its annual meeting in Geneva, the World Health Assembly, the governing body of the World Health Organization (WHO), resolved to eradicate polio from the world. The global eradication initiative is concerned both with stopping new cases of poliomyelitis caused by poliovirus throughout the world as well as implementing mechanisms to prevent its reintroduction. In the ensuing years, the number of poliomyelitis cases have been reduced by over 99%, and as of the beginning of 2003, only 7 countries world wide had any detectable level of poliovirus transmission.
Related health topics
Production and control of polio vaccines
Poliovirus infection can provide lifelong immunity against the disease, but this protection is limited to the particular type of poliovirus involved (Type 1, 2, or 3). Infection with one type does not protect an individual against infection with the other two types. The development of effective vaccines to prevent paralytic polio was one of the major medical breakthroughs of the 20th century. Two different kinds of vaccine are available:
- An inactivated (killed) polio vaccine (IPV) developed by Dr. Jonas Salk and first used in 1955, and
- A live attenuated (weakened) oral polio vaccine (OPV) developed by Dr. Albert Sabin and first used in 1961.
Both vaccines are highly effective against all three types of poliovirus. There are, however, significant differences in the way each vaccine works as well as their safety and efficacy profiles.
Inactivated polio vaccine (IPV)
IPV is produced from wild-type poliovirus strains of each serotype that have been inactivated (killed) with formalin. As an injectable vaccine, it can be administered alone or in combination with other vaccines (e.g., diphtheria, tetanus, pertussis, hepatitis B, and haemophilus influenza). Generally three spaced doses are administered to generate adequate levels of seroconversion, and most countries, a booster dose is added during late childhood. IPV has been used successfully in the polio eradication programs in a few countries, notably in Scandinavia and the Netherlands, but until recently most countries have used the oral polio vaccine. IPV provides serum immunity to all three types of poliovirus, resulting in protection against paralytic poliomyelitis. Most studies indicate that the degree of mucosal immunity in the intestine is significantly less than that provided by OPV, although this difference may be less pronounced in the pharyngeal mucosal lining. Adverse events following administration of IPV are very mild and transient. Due to the risks associated with the large quantities of poliovirus needed for IPV production, following the global cessation of poliovirus transmission high level (BSL-3/polio) containment of all manufacturing and quality control areas where live virus is handled must be implemented.
Oral polio vaccine (OPV)
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.
Related documents
Technical report series
Including WHO guidelines and recommendations:
1 January 2002
Recommendations for the production and control of poliomyelitis vaccine (oral) (Addendum 2000) Annex 1
1 January 2002
Poliomyelitis vaccine, oral
1 January 2004
Guidelines for the safe production and quality control of inactivated poliomyelitis vaccine manufactured from wild polioviruses (Addendum, 2003, to the Recommendations for the Production and Quality Control of Poliomyelitis Vaccine (Inactivated)
1 January 2002
Recommendations for the production and control of poliomyelitis vaccine (inactivated)
22 October 1991
Anti-poliovirus serum (types 1,2,3)
27 October 1997
Poliovirus type 3 (Sabin) MAPREC analysis
15 November 2004
Poliomyelitis vaccine (live attenuated)
11 October 1994
Poliomyelitis vaccine (inactivated)
7 October 1996
Poliovirus type 3, MAPREC analysis
26 October 1997
Proposal to establish two new International reference reagents for the MAPREC assay of poliovirus type 3 (sabin)
Q&As on Poliomyelitis
Meeting reports
20 July 2010
WHO Working Group Meeting to discuss the Revision of the WHO Recommendations for OPV: TRS No. 904 and 910, Geneva, Switzerland, 20-22 July 2010
31 January 2005
IABS Scientific Workshop on Neurovirulence Tests for Live Virus Vaccines
29 July 2003
Polio vaccine containment meeting report
1 March 2002
Communication for polio eradication and routine immunization
1 May 2004
Global Polio Eradication Initiative Progress 2003
1 June 2000
Guidelines for implementing the pre-eradication phase of the global action lan for laboratory containment of wild pilioviruses
1 January 2004
Global Polio Eradication Initiative Strategic Plan 2004-2008
1 April 2000
Making use of vaccine vial monitors: Flexible vaccine management for polio supplementary immunization acitivities
19 January 2000
New polio vaccines for the post-eradication era
1 October 1998
Fourth informal consultation on the polio laboratory network
1 January 2004
WHO global action plan for laboratory containment of wild polioviruses
23 March 1998
Global eradication of polio: Report of the meeting on the scientific basis for stopping polio immunization
1 May 1997