Lincolnshire Post-Polio Library - A Service of The Lincolnshire Post-Polio Network
The late effects of Polio Information for Health Care Providers
Charlotte Leboeuf

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Polio is caused by an enterovirus. There are three distinct strains, none of which provides cross-immunity to the others (1). Infection occurs through the faecal-oral route, through direct or indirect contact. The polio virus survives outside the intestinal environment for a long time and has also been found to be more difficult to remove from the skin with soap and water than other viruses (2). It is contagious during the incubation period as well as during the acute stages.


The infection rate is high in areas with poor hygiene. Exposure to the virus at an early age is thought to be less likely to result in paralytic disease. The disease:infection ratio is therefore low. Paradoxically, in areas of improved hygiene where the infection rate decreases, the disease:infection ratio increases, probably because exposure to the virus will occur later in life, when the development of clinical symptoms is more likely (3). This probably explains the high rate of paralytic polio which was observed during the epidemics of the 1930s, 1940s and 1950s in countries such as Australia, turning polio into a "modern" disease.

Today most of acute cases of paralytic polio in the developed world are vaccine-related (4). Individuals most at risk are non-immune vaccine contacts and older vaccine recipients. Another common source of infection is through direct or indirect contact with infected individuals in the developing world (5). There is concern that if herd immunity falls in Australia the acute disease can reappear.

The World Health Organization has set as a goal the immunisation of all children by 1990 and the eradication of the disease by year 2000 (6). Although considerable success has been noted in areas where widespread and efficient mass immunisation programs have been conducted, the reality is that paralytic polio is still very much a continuing issue in the developing world, where the yearly incidence is thought to be about 10 cases per 100,000 inhabitants, increasing considerably during major epidemics. In Australia we are likely to see sequelae of previous polio in new migrants from developing countries.


  1. Krupp MA, Chatton MJ. Current diagnosis and treatment. Lange Medical Publications, Los Altos CA; 1973:746-7.
  2. Eggers HJ. Handwashing and horizontal spread of viruses (letter to the Editor). Lancet 1989; June 24, 1452. [PubMed Abstract]
  3. Martyn CN, Baker DJP, Osmond C. Motoneuron disease and past poliomyelitis in England and Wales. Lancet 1988; June 11:1(8598):1319-22. [PubMed Abstract]
  4. Sutter RW, Brink EW, Cochi SL et al. A new epidemiologic and laboratory classification system for paralytic poliomyelitis cases. Am J Public Health 1989;79:495-8. [PubMed Abstract]
  5. Assaad F, Ljungars-Esteves K. World overview of poliomyelitis: regional patterns and trends. Rev Infect Dis 1984;6 Suppl 2:S302-7 (abstract).
  6. Keja K, Chan C, Hayden G, Henderson RH. Expanded programme on immunization. World Health Stat Q 1988;41:59-63 (abstract). [PubMed Abstract]

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Copyright The Lincolnshire Post-Polio Network 1997 - 2010.

This document comprises an index, foreword, introduction and seventeen other sections or subdocuments. Permission for printing copies is granted only on the basis that ALL sections are printed in their entirety and kept together as a single document.

Document preparation: Chris Salter, Original Think-tank, Cornwall, United Kingdom.
Created: 7th July 1997
Last modification: 20th January 2010.
Last information content change: 6th June 2000

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