by Maysy Noori

Polio, also known as poliomyelitis, is caused by the poliovirus. The name poliomyelitis is derived from the joining of two Greek words, polio (gray) and myelon (marrow, denoting the spinal cord). The Greek name is logical since it is the effects of the poliomyelitus virus on the spinal cord that causes the characteristic paralysis of this disease (1). Poliomyelitus is caused by three strains of poliovirus. The three antigenically different strains of poliomyelitus (serotype 1,2, and 3) are classified in the genus Enterovirus within the family Picornaviridae (10). Picornaviruses are viruses with an RNA genome, and enteroviruses are inhabitants of the gastrointestinal tract. The poliovirus is a rough, spherical, virus with an icosahedral protein capsid that consists of 60 identical subunits, or protomers (5). The virus is close to 270 nm in diameter (small virus), contains a single-stranded RNA core, and lacks a lipid envelope (4). The poliovirus is transmitted via the fecal-oral route (very rarely the oral-oral route) from person to person and sometimes by a fomite. The virus is mainly found in human feces, contaminated water, and sewage (2). Humans are the only known reservoir of poliovirus, and people with no apparent signs of infection most often transmit the virus (1).

Polio is contracted when the poliovirus enters the body, primarily through the mouth. The incubation period is usually 6 to 20 days, but it has a range of 3 to 35 days (1). There are many different responses to the poliovirus, and these responses differ based on the level of severity of the disease. The mildest result of infection is called inapparent or asymptomatic. About 95% of polio cases are asymptomatic (no symptoms); however, the virus can still be detected in stool samples and the person can still transmit the disease (1). The next level of severity is called minor, nonspecific illness. This occurs in 4%-5% of the people infected by the poliovirus, and is characterized by sore throat, fever, upper respiratory tract infection, nausea, vomiting, abdominal pain, constipation, and influenza-like symptoms. There is no central nervous system invasion in this type, and recovery occurs in less than a week (1). The third type of infection is called nonparalyti! c aseptic meningitis. This occurs in 1%-2% of polio infections, and recovery occurs after 2-10 days of symptoms. The first few days of this infection have the same symptoms as minor, nonspecific illness. After this prodromal period, there are symptoms of stiffness in the neck, back, and legs, as well as abnormal sensations throughout the body (1). The final type of polio accounts for 1% of polio infections and it results in flaccid paralysis. The beginning symptoms are similar to nonparalytic aseptic meningitis, and after about 10 days, the paralytic symptoms begin to occur, and last for 2-3 days. Diminished deep tendon reflexes and severe muscle aches in the legs and back characterizes the paralysis. The paralysis is usually asymmetrical and lasts from days to weeks (1). Many people with paralytic polio recover and retain some motor functions in their infected muscles. However, if the paralysis lasts for more than one year, then it is probably going to be permanent. Paralytic polio is divided into three categories, according to the level of severity. The first type is called spinal polio. About 79% of paralytic cases are from spinal polio, and it is characterized by asymmetrical paralysis of the legs. The second type is called bulbar polio and it accounts for 2% of polio infections. It is characterized by weakness of muscles due to damaged cranial nerves. The third type is called bulbospinal polio. It is a combination of symptoms from bulbar polio and spinal polio, and it accounts for 19% of the paralytic polio cases (1). The death rate for polio varies from children to adults. In children, 2%-5% of all cases result in death, and in adults, 15%-30% of all cases result in death. The death rate increases to 25%-75%, when there is bulbar involvement (1).

When the poliovirus enters the body it begins replicating in the pharynx and the gastrointestinal tract. Before any symptoms appear, the virus is present in the throat and intestines of the host. One week after onset of the disease, there are fewer viruses in the throat and an increase of the number of viruses in the intestines (1). At this point, the virus begins to attack the cells of the intestinal mucosa, and then spread to the lymphatic system and nervous system (4). How the virus travels throughout the body is not exactly known yet, but there are a couple theories. One theory states that the virus attaches itself to clusters of cells in the intestines called Peyer’s Patches, which are closely associated with the immune system. From here, it is believed that the virus enters the blood stream, and travels to the spinal cord (2). A second theory states that the virus travels directly to the spinal cord through the nerves, and doesn’t enter the blood at all! (2). Nevertheless, once the virus reaches the spinal cord, it begins to attack the motor neurons of the anterior horn and the lower brain stem. When the disease begins attacking these cells, the usual result is paralysis. Very rarely, the virus can spread to specific motor nerves and damage them resulting in a wide range of paralysis. These include the facial muscles, and the pharyngeal and laryngeal muscles, and the result is severe difficulties in breathing and swallowing (4).

There are many virulent factors that aid the poliovirus in its effectiveness. One factor is that the poliovirus lacks a lipid coat, and therefore it is resistant to lipid solvents. Also, since the virus is surrounded by a protein capsid, it is stable at low pH, and is able to survive the rough environment in the stomach and intestines. It is also capable of retaining its ability to infect even after several days at room temperature, without a host. The poliovirus also undergoes many mutations while in the intestines, that aid it in dodging antibodies produced by the body (4). The two main factor that aid the virus are its ability to cause cytolysis (lyse the sell it infects) and its immunoglobin-like binding sites. These sites allow the virus to bind to a specific protien on the surface of the immunoglobin and gain access into the cell to reproduce (2).

Currently, there is no medication to directly treat a person once they have been infected by the poliovirus. However, while ill, supportive care can help reduce suffering and maintain vital functions. Also, sanitation is very important in preventing the spread of the disease to others. The best preventitive measure is to be vaccinated against polio either by the killed Salk vaccine, or by the live Sabin vaccine. The Salk vaccine is grown in monkey kidney cultures and after three doses; the recipient has immunity to all three serotypes of the poliovirus. However, the Sabin vaccine seems to offer more immunity against the virus in the intestines, than the Salk vaccine. The Sabin vaccine is ingested orally and it is also grown in monkey kidney cultures. After three doses of this vaccine, the patient also attains immunity to all three serotypes of the poliovirus (1). The success of these vaccines are about 95%-99% effective (1). However, in the early days of the ! vaccine, not all the cases were successful. In the late 1950s and early 1960s, small outbreaks occurred due to small amounts of the live viral parts present in the doses of the Salk vaccine. This problem was fixed through better filtering methods in the laboratory (3). The two vaccines can also be given in combination, but the success rate against full (against all of the serotypes) immunity is a little less. In the United States, the choice vaccine is the live, oral, Sabin vaccine (1).

The poliovirus can be detected in sewage and drinking water through laboratory testing. Once the virus infects a person, it can be detected in several ways. One way is to test the stool of an infected person for the presence of the virus. A second way is to test the blood for the poliovirus, or for the presence of anti-polio antigens (4). A final way is to test the cerebrospinal fluid for an elevated number of white blood cells and a slight increase in the number of proteins (1).

People who have suffered from paralytic polio as a child, can develop a disorder, as adults, called post-polio syndrome. The symptoms usually appear 30-40 years after the initial illness, and they include progressive muscle weakness, debilitating fatigue, and loss of function and pain in joints. The syndrome is due to neurological damage to the cells in the anterior horn and to motor neurons. There is no cure for this disorder, but doctors are capable of providing medicine that can ease the pain and improve muscle function (7).

The first signs of poliomyelitis appeared over 3000 years ago in an Egyptian stone engraving of an adult man with a crippled leg. The man is depicted with a crunch under one arm and a shrunken leg, which is a characteristic of adults who have suffered from polio as a child (3). Polio was also described in the writings of the Greek and Roman physicians such as Hippocrates and Galen, who both wrote about an acquired clubfoot (3). Polio continued to be a problem throughout history and it wasn’t until 1813 when Giovanni Battista, an Italian surgeon, published the first medical description of polio (3). In Battista’s time polio was an endemic infection that occurred frequently in childhood and rarely resulted in paralysis. However, in the nineteenth century many small outbreaks of paralytic polio were occurring, and an increase in the number of adults affected also began to occur. Around 1887, Karl Oskar Medin, a scientist investigating an outbreak in Germany, con! cluded that people with mild cases, instead of those with the paralytic cases caused the outbreaks of polio. During this time, Andre Cornil and Jean Martin Charcot, both French pathologists, performed the first autopsy of the brain and spinal cord of a person who had suffered from paralytic polio (3). They concluded that the poliovirus destroyed the tissue in the anterior horn of the spinal cord, which produces the nerve cells that are in charge of muscle control (3). Outbreaks of polio continued to occur throughout the world, with peaks occurring in the summer months. An increase in the number of infected adults and paralysis caused by polio also occurred. It wasn’t until 1908, when Karl Landsteiner and Erwin Popper first identified the causative agent of polio to be the poliomyelitis virus (3). Nearly 50 years later, in 1955, the first vaccine against polio was licensed for general use. The vaccine was prepared from killed polioviruses and developed by Jonas Salk (3). In t! he early 1960s, Albert Sabine developed three live monovalent oral virus vaccines for each of the three serotypes of the poliovirus. In 1963, a trivalent oral poliovirus was developed to provide immunity against all the serotypes of the poliovirus (1).

Even though the western hemisphere has eradicated polio, it is still prevalent in the eastern hemisphere of the world. There are currently six countries that are polio-endemic- Nigeria, India, Niger, Pakistan, and Afghanistan. With the help of the World Health Organization, these countries are planning to eradicate poliomyelitus. Immunizations are under way in these countries, and also preventative measures that will stop the spread of the disease (6). The most recent polio outbreak occurred in Nigeria, and it is now spreading to Niger. The rapid growing number of people infected in this outbreak, is due to poor sanitary conditions and a lack of immunizations among the country’s inhabitants (8). The World Health Organization is currently doing all that they are capable of doing, but there is decent among the leaders of these countries about vaccinations, due to fear and misunderstandings that the vaccine will spread the disease (6). Nevertheless, polio remain! s a crippling and debilitating disease that will hopefully be eradicated soon.


 1. Centers foe Disease Control and Prevention. "Poliomyelitus" 4/19/04    URL http://www.cdc.gov/nip/publications/pink/polio.pd

 2. The Polio Information Center Online. 4/19/04    URL http://cumicro2.cpmc.columbia.edu/PICO/Chapters/History.html  URL http://cumicro2.cpmc.columbia.edu/PICO/Chapters/Pathogenesis.html  URL http://cumicro2.cpmc.columbia.edu/PICO/Chapters/Epidemiology.htm

  3. Daniel, Thomas M. and Robbins, Frederick C. Polio  1997, University of Rochester Press. Rochester, New York.

  4. Bennet, Clause J. M.D., Smith, Lloyd H. Jr. M.D., Wyngaarden, James B. M.D. Cecil Textbook of Medicine, 19th Edition, 1992, W.B. Saunders  Company, Philadelphia, PA.

 5. Kokko, Gill, Smith, Lloyd H. Jr. M.D., Bennet, Clause J. M.D., Plum, Mandell. Cecil Textbook of Medicine, 20th Edition, 1996, W.B. Saunders Company, Philadelphia, PA.

 6. World Health Organization. "Polio Eradication" 4/19/04  URL http://www.who.int/features/2004/polio/en/

 7. Halstead, Lauro S. "Post-Polio Syndrome" Scientific American, April  1998, volume 278, issue4, p.42-47.

 8. Pan American Health Organization. "Polio" 4/19/04  URL http://www.paho.org/English/DD/PIN/pr030513.htm

 9. Merck &Co., Inc. Home Page. "Polio"    URL http://www.merck.com/mrkshared/mmanual_home2/sec23/ch273/ch273h.jsp

10. Bug's Index- Organisms "Polio" 4/19/04  URL http://www.medinfo.ufl.edu/year2/mmid/bms5300/bugs/index.html