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The study of the disease poliomyelitis, and the development of treatments for the disease, is often held up by the pro-vivisection lobby as an example of the "triumph" of animal research. For example, the Research Defense Society's Scientific Officer has stated that "Animal experiments...were critical in the elucidation of the nature of polio and...in the formation of a vaccine." However, a careful study of medical history demonstrates that researchers were misled by animal experiments, resulting in decades of delays in progress.

The first major breakthrough in the study of polio was the discovery of its infectious nature through epidemiological studies conducted in Sweden by Strumpell, Seigmuller and Marie in 1884, and the investigation of an epidemic in Sweden in 1887 by Medin.  Epidemiology is the study of diseases in human populations.  One of Medin's pupils, Wickman, went further. He demonstrated that not only was polio infectious, but that less severe cases of polio, such as those that did not cause paralysis, acted as important carriers of the disease. Wickman also identified the incubation period in humans.  Other researchers went on to inject infected tissues from human cadavers into monkeys.  But, as Dr Paul wrote in his major historical overview, History of Poliomyelitis, in the end no amount of experimentation on the monkey  could upset the fundamental clinical epidemiological truth that Wickman had discovered." In other words, the study of humans produced reliable information that no animal experimentation could ever hope to provide.

Acceptance that polio was an infectious disease led to the search for its causes. For almost 25 years animal researchers searched for a bacterial cause, but their experiments were in vain (Polio is caused by a virus.).  Several sets of subsequent animal experiments gave conflicting results. One of the leading researchers, Landsteiner, eventually abandoned the study of polio because of the unfortunate reliance on a monkey model of the disease, which was proving to be inadequate. A blizzard of inconsistent information was continually generated from experiments using different species and different strains of virus, with no indication as to which experiments were of any relevance to the human situation.

Back in 1909, Wickman had concluded that infection was via the intestinal route. This was followed by the autopsy studies of Kling and his colleagues from 1911-1913. But despite this clinical evidence, another researcher, Flexner, suggested in 1910 that the polio virus entered the central nervous system via the nasal mucosa instead. He "confirmed" this by his animal experiments, which gave rise to the theory of a NASAL PORT OF ENTRY.  In 1917, a respected scientists at Yale called Draper converted to Flexner theory in spite of his own contrary clinical observations. This was a momentous decision because, as Paul recounts, "The clock had been set back about 25 years in poliomyelitis research."

Paul continues: "So the theoretical experimentalists, like so many who have immured themselves in their laboratories before and since, drifted further and further away from the human disease in their attempts to use experiments in the monkey for interpretation of the disease in Man." It was not until the late thirties that the failure of the nasal portal of entry theory became so obvious as to necessitate a re-evaluation. Finally, the so-called "oral alimentary tract portal of entry theory" gained acceptance, where the virus entered through the mouth and then via the intestine.

The next question to be answered was how the virus reached the spinal cord from the intestines. Once again, animal experimentation misled researchers.  Initially, Wickman's human-based studies had suggested that the virus travelled in the blood stream via the veins. However, various animal experiments undermined this correct observation.

Further confusion in the study of polio originated from the use of
monkey-adapted strains of the virus - this led researchers further away from an understanding of the human disease and how it spread through the human body. Differences in the incubation period of monkey polio and human polio exacerbated the uncertainty and created further false trails.

The study of poliomyelitis demonstrates clearly the inherent limitations of animal-based research as a means to investigate human disease. Subtle yet crucial differences in the biology of the disease in human and non-human primates meant researchers were misled for decades.