What is Polio?
Polio, or more properly poliomyelitis, was one of the most feared and studied diseases of the first half of the 20th Century. Though the Salk and later the Sabin vaccines have essentially eliminated the disease in developed countries, many mysteries regarding polio remain. This is probably due to the fact that as polio epidemics ended in North America and Europe, research on the disease also came to an abrupt halt. Thus, as LaForce (1983) noted, knowledge about the epidemiology and pathology of polio is essentially frozen at a mid-1950s level.
In the paragraphs that follow, I will define the disease of polio and explore some of the mysteries that still surround it. Other sections of this site document polio's history, describe its late effects, and provide excerpts from narrative accounts of various aspects of the polio experience.
Poliomyelitis is an "inflammation of the gray matter of the spinal cord (Taber, 1970, p. P-77). Though the word "poliomyelitis" sounds complicated and impressive, it was formed by putting together the Greek words for the site of the disease - polios, meaning gray, myelos, meaning marrow, and adding the English suffix, itis, meaning inflammation. It has gone by many names including infantile paralysis, Heine-Medin's Disease, debility of the lower extremities, and spinal paralytic paralysis. In common usage, the term poliomyelitis is abbreviated to polio.
Polio is caused by a virus which results in an acute infection. However, contrary to what is commonly believed, the virus did not typically result in paralysis. Rather, the majority of infected individuals experienced only mild respiratory or gastrointestinal symptoms, often accompanied by fever, headache, and muscle stiffness. These symptoms lasted only a few days, and many had such mild cases that they did not even realize they were ill. Therefore, they often continued on with there daily routines, attending school or work, and exposing many others to the polio virus. This fact helps explain the reports of many polio survivors that they were the only ones in their family, neighborhood, or community to have had polio. In actuality, there could have been many individuals with whom they came into contact who had the minor illness, as non-paralytic polio was often called.
Only in a small number of cases did the virus penetrate the central nervous system, causing the major illness, or "true polio." In these cases, neurons (nerve cells) in the anterior horns of the spinal cord and the lower brain were affected, resulting in "tightness in the neck, back, and hamstring muscles as well as varying degrees of muscle weakness, as paralysis sets in" (Owen, 1990, p. 211). Though there was never a cure for polio, most who contracted it experienced improvement in muscle strength and control after the acute infection subsided. In some cases, however, motor neurons were left severely damaged or completely destroyed, resulting in permanent weakness or paralysis, most commonly to the lower extremities (Headley, 1995).
There are actually three separate strains or immunologic types of the disease: Type I (Brunhide), Type II (Lansing), and Type III (Leon). Most epidemics, at least in the United States, were the result of Type I virus (Nathanson and Martin, 1979).
The means by which the polio virus enters the central nervous system is still not definitely known. (Taber, 1970). However, it is interesting to note that relatively recent data from third-world nations suggests that when those experiencing acute polio are given injections such as DPT immunizations, antibiotics, antimalarials, or antipyretics, the injected limb develops paralysis within one week (LaForce, 1983).
Though this connection between injections and paralysis has repeatedly been demonstrated, "the mechanism by which this phenomenon occurs is not well understood. (However) the best evidence to date suggests the trauma initiates a reflex dilation of blood vessels at the corresponding spinal cord level and facilitates entry of the virus" (LaForce, 1983, p. 30).
Other factors thought to predispose individuals to the major disease were pregnancy and tonsillectomy, as well as other nose and throat procedures. Why these conditions were likely to increase the risk of the disease entering the central nervous system remains unknown.
There is also still some mystery surrounding the exact means by which the polio virus is transmitted. As Smith (1990) noted in her history of the development of the Salk vaccine, "Nobody has ever completely settled the question of how polio is spread, though the best evidence suggests the virus is excreted in the stool and passed through hand-to-hand contact . . ." (p. 36).
The belief that the polio virus is spread by contact with the feces of an already infected person has been offered as an explanation for the increased incidence of polio in developed countries such as the United States during the 20th Century. According to this theory, before the advent of modern sewage treatment plants and other improvements in public sanitation, virtually all individuals were exposed to the polio virus early in their lives when they were at least partially protected by maternal antibodies. Thus, they developed mild, non-paralytic infections, probably during infancy, which provided them with lifelong immunity. However, with better sanitation, both these early infections as well as the likelihood of receiving antibody protection decreased, resulting in greater susceptibility to paralytic polio. Thus, in the words of Smith:
Put simply, paralytic polio was an inadvertent by-product of modern sanitary conditions. When people were no longer in contact with the open sewers and privies that had once exposed them to the polio virus in very early infancy when paralysis rarely occurs, the disease changed from an endemic condition so mild that no one knew of its existence to a seemingly new epidemic threat of mysterious origins and terrifyingly unknown scope (p. 23).This central theory regarding the spread of polio is supported, at least to some extent, by experiences in third world countries. During World War II, for instance, U.S. and British troops stationed in undeveloped countries were much more likely to contract polio than native peoples, who apparently had already developed immunity (Paul, 1971). Even in the 1970's, when individuals from developed countries came into contact with those from a country without a modern sanitation system, the incidence of paralytic polio was about twenty times greater for those from the developed country (Nathanson and Martin, 1979).The above explanation for the transmission of polio is generally accepted and seems quite logical. However, the incidence of the disease in the United States during the epidemic years was very irregular, not only from year to year, but from area to area, apparently showing no relation to improvements in sewage treatment. The actual reason for this variation remains another of the polio mysteries. However, it has been suggested that this variability was possibly due to increased virulence of certain virus strains or the presence of environmental conditions that enhanced the disease's transmission (Nathanson and Martin, 1979).
Regarding the second factor of environmental conditions, it is well documented that polio was primarily a disease of the summer months. Readers old enough to recall the epidemic years of the 1940's and 50's probably have vivid recollections of community swimming pools and other public areas being closed during the "dog days" of July and August. Perhaps this was an appropriate precaution. The disease occurred thirty-five times more frequently in August than in April (the month of lowest incidence). Though no one really knows why this was the case, it does not appear that seasonal variation in interpersonal contacts is a sufficient explanation. Rather, it is more likely that warm, moist weather favored transmission of the disease, as Bradshaw (1989) and others have noted. This is, however, just a hypothesis. The actual reason for the seemingly random appearance of polio epidemics remains a mystery to this day.
Information on this page is from Chapter 1 of my book, Polio's Legacy: An Oral History (Sass, 1996).. This page was posted by Edmund Sass, Ed. D. and was last updated March 16, 2014. You may e-mail him at esass@csbsju.edu