Our research on the natural history of autism convinced us that while there may have been a few scattered cases throughout history, the disorder first occurred in appreciable numbers – as clusters and ultimately as an epidemic -- only after 1930. Observations at that time about the rarity and novelty of the disorder are far more persuasive than retrospective efforts to claim significant numbers of cases before then.
The same holds true for poliovirus. Nowhere is that clearer than in the 1917 book “Poliomyelitis In All Its Aspects,”[i] by John Ruhrah and Erwin E. Mayer. “It seems to be a disease of comparatively recent origin,” they wrote. “In the history of most diseases there is a gradual shading off into the older writers until the disease is lost in confusion of inaccurate descriptions. Not so with polio.”
They continued: “The disease is so striking in its symptomatology, so devastating in its results, and produces such a deep impression on the popular mind that it does not seem possible that any very considerable epidemics could have happened in the countries in which there were physicians making records of what occurred.”
The same point is driven home by John R. Paul in his standard 1971 text on the disease, A History of Poliomyelitis [ii]. “There was no idea in the eighteenth and early nineteenth centuries that poliomyelitis was contagious,” wrote Paul, a professor of preventive medicine and epidemiology at Yale who conducted important polio research himself. A half a dozen cases within a half-mile of each other might have escaped notice, but “had there been larger outbreaks in the early or mid-19th century it seems highly unlikely that they would have gone unnoticed.”
But just as arsenic and lead caused instances of paralysis before the invention of lead arsenate, there was also an emerging medical literature of poliomyelitis before recurring outbreaks began in 1893. Beginning just before 1800, there’s a history of doctors who took a reasonable cut at identifying the disease. These include, in 1789, Michael Underwood, who used the term “debility of the lower extremities”[iii]; and in 1840, Jacob Heine, who is sometimes credited as the first to diagnose poliomyelitis.
Several doctors later used the word “paralysis” in describing a similar condition in infants: West in 1843; Rillet in 1851; Duchesne in 1864. By 1860, Heine had pinpointed the spinal cord as the source of the paralysis, and in 1872, the great French neurologist Jean-Martin Charcot called it “tephromyelitis anterior acuta parenchymatose.” This was a pretty modern description, but his precise nomenclature didn’t quite catch hold. In 1874, German doctor Adolph Kussmaul coined the term “poliomyelitis anterior acuta,” later shortened to poliomyelitis.
Going further back, plausible descriptions grow sparse but include the crippled Egyptian priest in a stele dated from 1580-1350 B.C. In 460 B.C., Hippocrates wrote about clubfoot, which may have included some cases of infantile paralysis. And in 200, Galen also discussed clubfoot.
But those were vanishingly rare, and when Underwood described “debility of the lower extremities” in 1789, he clearly thought he was reporting a new phenomenon, just as Ruhrah and Paul asserted with the benefit of much greater epidemiological sophistication. “This disorder either is not noticed by any medical writer within the compass of my reading, or is not so described as to ascertain the disease here intended,” Underwood wrote. “It is not a common disorder anywhere, I believe.”
Outbreaks of more than one case, then, were a distinctly 19th-century phenomenon, and until the 1890s worldwide episodes can be counted on two hands[iv]:
-- In 1835, John Badham’s description of 4 cases in Worksop, England.
-- In 1830-36, Charles Bell’s discussion of multiple cases in St. Helena.
-- In 1841, George Colmer’s discussion of 8-10 cases in Feliciana, Louisiana.
-- In 1868, Bull’s discussion of 14 cases in Odalen, Norway (cited by Leegard, 1914).
-- In 1881, Bergenholtz’s description of 13 cases in Umea, Sweden.
--In 1883, a report of 5 cases in Arenzano, Italy (cited by Hull, 1917).
--In 1885, another report of 13 cases in Sainte-Foy L’Argentiere, France (cited by Hull, 1917).
--In 1886, 9 cases in Mondel, Norway (cited by Hull, 1917).
-- In 1887, Oskar Medin’s discussion of 44 cases in and around Stockholm. This description uses the term “poliomyelitis anterior acuta,” argues that it is likely to be infectious and gives a pretty clear description of the modern disorder. His piece is considered a classic and polio used to be called “Heine-Medin disease” in honor of his very contemporary description.
Obviously, all these cases were described before the invention of lead arsenate in 1893. So there were undoubtedly other ways to make this pattern occur; a prime suspect would be arsenic in other forms, as well as other toxic metals, since they are well known to cause paralysis in workers and others exposed to them. Interestingly, both Badham and Colmer mention teething, and the latter said it was a likely cause. In fact, “teething paralysis” was sometimes used as a term for infantile paralysis.[v]
Teething powders containing calomel – mercurous chloride – were used beginning around then, and mercury is well-known to cause paralysis. Mercury in medicine was so widespread that it doubtless caused numerous disorders identified as something else, especially by the doctors who prescribed it. (Badham even prescribed calomel in “repeated doses” for his paralyzed patients.)
Teething powders also caused pink disease, a feature of which was sometimes paralysis. In “Pink Disease,” Charles Rocaz reports that “Karl Petren of Lund (Sweden) has suggested that pink disease is due to chronic arsenical intoxication. … Nervous manifestations occur in the form of paresis [paralysis] of the lower limbs with pain, tingling and burning of the hands and feet.”[vi]
So a number of outbreaks might be explained by exposures to metals, including earlier pesticides and other products and medicines containing arsenic. The arsenic-containing Paris Green was originally a pigment and was used in wallpaper as early as 1814.
As for the larger Scandinavian clusters in the later 1880s, northern climes – think Campobello Island, Canada – are hospitable to berries. Also, apples are grown there and are part of the traditional cuisine. Keeping “worms” (actually codling moths, not gypsy moths) out of apples was something people were obviously concerned about for a long time before the war on gypsy moths provided the tools to fight codling moths.
But none of these reached the scale, or occurred with the frequency, of poliomyelitis outbreaks after 1893 and the invention of lead arsenate. This leads to the second test of our theory – once lead arsenate and DDT disappeared from the scene, why did poliomyelitis outbreaks continue, albeit in diminished fashion?
(Next: After -- The Persistence of Polio)
[i] John Ruhrah and Erwin E. Mayer, Poliomyelitis in all its aspects, New York: Lea and Febiger, 1917.
[ii] J.R. Paul. A History of Poliomyelitis. Yale studies in the history of science and medicine. New Haven, Conn: Yale University Press, 1970.
[iii][iii] Michael Underwood, “Debility of the lower extremities,” A treatise on the diseases of children, with general direction for the management of infants from birth, 1789.
[iv] T.G. Hull, “A Graphical Study of the Epidemiology of Poliomyelitis.” The American Journal of Public Health. xx[v] Walter Scott, for example, was described as suffering from "a severe fever which deprived him of the power of his right leg."teething
[vi] Charles Rocaz, Pink Disease (Infantile Acrodynia) (London: Martin Hopkinson Ltd., 1933).