140 –1,519

lornajarrettblanchard January 1, 1925

–1,519 Census Bureau. Mortality Statistics 1925, Part I. 1927, Table 6, p. 88, Table 8, p. 137.[1]

— 25 Alabama Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 140.

— ? Alaska (not listed)

— ? Arizona (not listed)

— ? Arkansas (not listed)

–149 California Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 145.[2]

— 8 Colorado Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 148.

— 19 Connecticut Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 151.

— 1 Delaware Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 154.

— 7 District of Co. Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 157.

— 18 Florida Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 161

— ? Georgia (not listed)

— 1 Hawaii Census. Mortality Statistics 1925…Part I, 1927, Table 5, p. 380.

— 42 Idaho Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 166.

— 44 Illinois Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 168.

— 29 Indiana Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 171.

— 48 Iowa Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 175.

— 35 Kansas Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 178.

— 45 Kentucky Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 181.

— 18 Louisiana Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 186.

— 10 Maine Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 190.

— 17 Maryland Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 193.

— 45 Massachusetts Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 198.

— 28 Michigan Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 202.

–140 Minnesota Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 204.

— 25 Mississippi Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 208.

— 55 Missouri Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 212.

— 6 Montana Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 215.

— 40 Nebraska Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 218.

— ? Nevada (not listed)

— 5 New Hampshire Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 221.

— 33 New Jersey Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 224.

— ? New Mexico (not listed)

–208 New York Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 227.

— 25 North Carolina Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 230.

— 42 North Dakota Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 235.

— 68 Ohio Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 238.

— ? Oklahoma (not listed)

— 2 Oregon Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 241.

— 67 Pennsylvania Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 244.

— 10 Rhode Island Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 247.

— 38 South Carolina Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 250.

— ? South Dakota (not listed)

— 35 Tennessee Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 254.

— ? Texas (not listed)

— 0 Utah Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 259.

— 13 Vermont Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 262.

— 29 Virginia Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 264.

— 34 Washington Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 269.

— 14 West Virginia Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 272.

— 62 Wisconsin Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 275.

— 0 Wyoming Census Bureau. Mortality Statistics 1925…Part I, 1927, p. 278.

Narrative Information

Draper: The polio virus “…can be pressed through the interstices of a porcelain filter which holds back germs of ordinary size such as those which cause pneumonia or meningitis. The virus of poliomyelitis though small, has certain remarkable survival powers. Thus Flexner, Clark and Amoss showed that when they put it away in the icebox submerged in 50 per cent glycerin, it remained in full activity for over a year. Later experiments with glycerin ran to even greater lengths of time until finally Rhoades showed that the virus was potent after eight years of immersion in glycerin.

“But while these observations indicate that the virus has great survival powers such artificial conditions are not comparable to those found in nature. However, when the virus is surrounded by moist albuminous substances, as for example nasal secretions, it withstands drying for several weeks. Furthermore, it resists freezing at 2 to 4 degrees centigrade for forty days. But it is more easily destroyed by heat, for it has been found that temperatures of 45 to 50 degrees centigrade [104-122 Fahrenheit] are too much for it.

“To chemical agents it displays variable reactions. Thus a 2 per cent solution of hydrogen peroxide easily destroys it as do menthol and mercury bichloride. Strangely enough, however, the poliomyelitis virus shows a remarkable resistance to carbolic acid which it withstands in solutions of 0.5 per cent strength….Probably one reason why even such potent substances as hydrogen peroxide are ineffective in preventing the disease is simply because we cannot bring it in contact with the invading virus at the appropriate time.” (Draper 1935, pp. 78-79.)

“Probably no other infecting agent, whether bacterium or virus, has ever been subjected to such painstaking, ingenious and persistent investigation under the auspices of the best laboratories throughout the world.” (Draper 1935, p. 80.)

“…perhaps the three outstanding characteristics of the poliomyelitis virus are first, its extremely small size; second, its capacity to remain alive and virulent for long periods provided it is prevented from drying by a moist, preferably albuminous coating, and third, its swings of virulence. Another remarkable point about the virus is that it has never been found in nature outside the human body. This at once brings up the question: ‘Where does it come from, and how does it get into the bodies of human beings?’….The answer to the first question is the simple and unsatisfactory one, ‘We do not know.’….we are led at present to accept the thesis that the poliomyelitic virus is as old as man, has dwelt always in the mucous passages of his nose and throat, and from time to time has displayed surges of increased virulence.” (Draper 1935, 82.)

“….poliomyelitis is actually rather a rare and mild disease…even the great epidemic of 1916 in New York, not quite three individuals for every thousand of population were stricken. In most average epidemics of poliomyelitis not more than one individual in a thousand of population, or two in four thousand are attacked….” (Draper 1935, 87.)

“Another especially interesting feature of epidemic poliomyelitis is its geographical distribution. While the disease has now made its appearance in almost every part of the world, there is more of it, no doubt, in some places than in others. It may be properly said that in all countries where it has appeared at all extensively it attacks the population dwelling in northern temperate zones. Small epidemic outbreaks have been reported in tropical regions, it is true, but their numbers and extent are limited. There have also been a few outbreaks far north of the Arctic circle in which the temperature was either below freezing every day, or in some instances registered 29 degrees Fahrenheit below zero.” (Draper 1935, 96.)

“…the belief that there is a relationship between epidemic wave and temperature (or season) is given most suggestive support by the uncanny repetition in point of time, at which the wave rises, reaches its peak and declines. [shows a chart from the NYC Dept. of Health which plots the rise and fall of the 1916 and 1931 epidemics there, in which the plots are very similar – to the point that the peak day is August 1 in both epidemics]. (Draper 1935, 97.)

“How does the virus leave the body and, once escaped, how is it conveyed to the next susceptible individual? Many experiments have been done which seem conclusively to exclude the mechanism of an intermediary host like the mosquito for malaria, or rat-ticks for plague. Water and milk have been duly suspected of playing a part and a fairly strong case for the latter was at one time made out…But the search for active virus in all the body excretions failed to show it in any of the eliminated substances or fluids except in the secretions of nose and pharynx. Thus it would seem that the virus emerges ‘by that same door wherein it went.’

“Because of inability to find active virus anywhere in nature outside the human host and because it is found in the nasal secretions almost exclusively, the notion now prevails that the virus is transmitted directly from person to person.” (Draper 1935, 102.)

“…it is apparent that to fix accurately the length of time which intervenes between the moment at which the virus passes into a new subject (contact) and the onset of symptoms is not easy. Consequently, the estimated number of days varies through a considerable range. Some observers place it as low as two, others as high as twenty days. In the experimental disease in monkeys, when the exact time at which the virus enters is known, the duration of the incubation period is easier to establish. Yet even in this case there is considerable variation. Flexner and Lewis[3] for example found the average to be 9.8 days, Levaditi 5.8, Aycock and Luther 5.8. When all the evidence, collected from the observation of human cases and from the experimental disease, is put together the best estimate which can be arrived at is from six to twenty days.” (pp. 106-107.) Draper, George, M.D. Infantile Paralysis. NY and London: D. Appleton-Century Co., Inc., 1935.

Google Health: “Poliomyelitis is a viral disease that can affect nerves and can lead to partial or full paralysis…. Poliomyelitis is a disease caused by infection with the poliovirus. The virus spreads by direct person-to-person contact, by contact with infected mucus or phlegm from the nose or mouth, or by contact with infected feces.

“The virus enters through the mouth and nose, multiplies in the throat and intestinal tract, and then is absorbed and spread through the blood and lymph system. The time from being infected with the virus to developing symptoms of disease (incubation) ranges from 5 – 35 days (average 7 – 14 days). Risks include:

Lack of immunization against polio and then exposure to polio.

Travel to an area that has experienced a polio outbreak.

“In areas where there is an outbreak, those most likely to get the disease include children, pregnant women, and the elderly. The disease is more common in the summer and fall.

“Between 1840 and the 1950s, polio was a worldwide epidemic. Since the development of polio vaccines, the incidence of the disease has been greatly reduced. Polio has been wiped out in a number of countries. There have been very few cases of polio in the Western hemisphere since the late 1970s. Children in the United States are now routinely vaccinated against the disease.

“Outbreaks still occur in the developed world, usually in groups of people who have not been vaccinated. Polio often occurs after someone travels to a region where the disease is common. Thanks to a massive, global, vaccination campaign over the past 20 years, polio exists only in a few countries in Africa and Asia.” (Google Health. “Poliomyelitis.”)

Paul on Seasonality: “…although seasonal trends occur in a number of diseases spread by human contact, no satisfactory reason has as yet been proposed to explain why the effect of season in poliomyelitis is so sharp and dramatic; and why epidemics of poliomyelitis occur at such a higher rate in the summer and early autumn than in the winter. There are several possible explanations: something happens during summer weather which either introduces virus into a community, or enormously facilitates the dissemination of virus throughout a community, or makes certain people, the non-immune, far more susceptible. In any event it does seem that man can contaminate not only his fellow associates, but his immediate environment, and it is possible that an analogy can be drawn in this respect between poliomyelitis and salmonellosis.

“As an example of contamination of the environment, poliomyelitis virus has been found not only in human faeces, but under natural circumstances in urban sewage; and in faecal material collected in open privies.” (p. 19) (Paul, John R., M.D. “Epidemiology of Poliomyelitis,” pp. 9-29 in Poliomyelitis, World Health Organization (Geneva), 1955. Accessed at: http://whqlibdoc.who.int/monograph/WHO_MONO_26.pdf )

Smallman-Raynor: “Closed. A familiar sign outside swimming pools, cinemas, and other places of public entertainment that was, until the middle of the twentieth century, the signal in the developed world that another summer poliomyelitis epidemic was under way. Few diseases scored higher on the ‘dread’ factor for parents as epidemic poliomyelitis became, from the early years of the twentieth century, systematically more severe and regular in its visitations, initially in the developed nations and then across the developing world. Each successive wave left in its wake thousands of crippled and dead children. But, from the mid-1950s, this picture changed abruptly when first Salk and then Sabin developed suitable vaccines that prevented the disease….

“…at the beginning of a new millennium, poliomyelitis…stands on the edge of eradication with under 1,300 wild-virus poliomyelitis cases confirmed globally in 2004. Eleven years after the close of its successful smallpox campaign, the Forty-First World Health Assembly, meeting in Geneva in 1988, committed WHO to the global eradication of poliomyelitis. Like smallpox, this target involves not only eliminating the disease, but eradicating the causative wild virus. The goal has been made possible by half a century of research and vaccine development since the breakthroughs of Salk and Sabin.

“Second, with the passing of poliomyelitis, one of the great episodic diseases of the twentieth century will have gone. The disease itself may be as old as humankind. An Egyptian stele from about 1400 BC shows a young priest with a shortened deformed foot typical of poliomyelitis. But, despite its antiquity, in so far as records allow reconstruction, it remained epidemiologically minor compared with many other infectious diseases until the twentieth century. However, from the first decade, poliomyelitis surged in importance across the globe. Its rapid evolution to significance marks it out as one of the world’s major emergent infections…” (Preface, p. ix.)

“As we show in Appendix I, around 600 of the papers in the poliomyelitis literature have a strong locational focus in the sense of reporting an epidemic or an outbreak in a particular country or region of the world. We have woven these studies into our own original research to create an account of the historical geography of poliomyelitis in three principal phases. The first [endemic phase] begins in antiquity. Like other primarily childhood infections such as diphtheria, whooping cough, and measles, poliomyelitis is probably one of the ‘crowd’ diseases associated with humans since they first began to live together in large urban agglomerations in the ancient riverine civilizations of the Tigris-Euphrates basin 5,000 years ago. It remained a little noted and recorded infection until the late nineteenth century which saw the beginning of the second phase of poliomyelitis activity – its emergence from obscurity into an epidemic disease of global significance [epidemic phase]. The third and concluding phase [vaccine phase][4] began from the mid-1950s when vaccine developments, linked to worldwide vaccination programmes, forced the retreat of the disease into ever smaller geographical pockets and from which it will eventually be eradicated.” (p. x.)

“Derived from the Greek polios (meaning grey), muelos (marrow), and itis (inflammation), poliomyelitis is the name given to the response made by human or animal tissues to invasion by poliovirus.” (pp. 1 and 3)

“In his classic book, A History of Poliomyelitis, John R. Paul follows Cecil and Loeb[5] in describing poliomyelitis as a ‘common, acute viral disease characterized clinically by a brief febrile illness with sore throat, headache and vomiting, and often with stiffness of the neck and back. In many cases a lower neuron paralysis develops in the early days of illness’ (Cecil and Loeb, 1959, cited in Paul, 1971: 1).” (p. 3)

“…the infectious agent of poliomyelitis is the poliovirus types 1, 2, and 3 – type species of the entero-virus genus of the Picornaviridae family of viruses. All three virus types can cause paralysis, but type 1 is most often isolated from paralytic cases, and it is the same strain which is generally implicated in epidemics. The reservoir for the virus is humans. These are usually people with inapparent infections, especially children. Long-term carriers are rarely found. The primary mode of transmission is person-to-person spread, principally through the faecal-oral route. A secondary route is via the respiratory tract. The infection cycle is therefore HUMAN → HUMAN. The incubation period is normally 7-14 days. The period of communicability for poliomyelitis is not precisely defined, but transmission is possible for as long as the virus is excreted. Susceptibility to infection is common. Immunity, apparently life-long, follows from infection, but it is restricted to the particular poliovirus type. Second attacks are rare but they can be caused by a different poliovirus type….” (p. 4)

“Poliomyelitis rarely causes symptoms in those infected; indeed, some 85-90 per cent of children have no symptoms at all. In the remainder, there is a brief illness (slight fever, sore throat, headache, vomiting) after three to five days. Most children recover rapidly. Bu, in a small minority of cases, there is major illness with symptoms caused by inflammation of the meninges (the membrane covering the brain and spinal chord). In about 1 per cent of cases, this cause flaccid paralysis within three to four days, and this may led on to permanent muscle paralysis. Where poliomyelitis is highly endemic, typical cases can be recognized on clinical grounds, but , in countries where the disease is absent or occasional, laboratory confirmation may be needed.” (p. 4)

“Attempts to trace the history of poliomyelitis are hindered by the overwhelming variety of names that the disease has been given over time. Following Paul (1971: 5), a list of various names involved in the nomenclature of poliomyelitis includes:

Debility of the lower extremities (Underwood: 1789)….
Morning paralysis (West: 1843)
Parakysie essentielle chez les enfants (Rilliet: 1851)….
Spinale Kinderlahmung (Von Heine: 1860)….
Poliomyelitis anterior acuta (Kussmaul, quoted by Frey: 1874)
Heine-Medin disease (Wickman: 1907)
Infantile paralysis
Poliomyelitis
Polio

“While additional names are given in Table 1.1 [not included here], it is interesting to note from the foregoing list that Underwood, who coined the phrase, ‘debility of the lower extremities,’ was a pediatrician and so we may reasonably assume that the malady he was characterizing was primarily of infants and children. Although it was a very vague description, it lasted for 50 years (Paul, 1971: 4).

“In the nineteenth century, a variety of terms were introduced from many different languages. This may have contributed to the confusion surrounding the disease….” (pp. 4-5)

“The primary mode of communication of poliovirus to a susceptible individual is through close association with an infected person. Two main routes of person-to-person transmission are generally recognized: (1) excretion of virus in the faeces, with entry via the mouth into the alimentary tract – a method of propagation poliomyelitis shares with diseases like cholera and typhoid; and (2) droplet spread from the pharynx, a corridor of spread used by other childhood diseases like chickenpox, measles, and rubella. As with other members of the human enterovirus group, faecal contamination (of fingers, eating utensils, milk, or foodstuffs) is generally considered to be the more common means of transmission. Laboratory studies have identified the presence of large amounts of poliovirus in the faeces of infected persons, with virus excreted for upwards of three weeks after infection (Christie, 1987). In contrast, virus has been found to be present in the throat of infected individuals for only about a week after the start of the major illness, and in relatively low quantities (Horstmann et al., 1959, Bodian and Horstmann, 1965).” (p. 38-39)

“Changing Age Patterns. Although characteristically a disease of children, the first half of the twentieth century was associated with steady rise in the age of poliomyelitis cases (Dauer, 1955b). Immediately prior to the licensing of inactivated poliovirus vaccine in the mid-1950s, the peak age incidence of notified cases in the United States had risen to 6 years, with a substantial proportion of cases occurring among teenagers and young adults (Hall et al., 1957)….” (p. 43)

“Case Control and Disease Prevention in Epidemic Periods. There is little that can be done to prevent the spread of poliomyelitis through non-specific methods. While the isolation of patients and their contacts was invoked as a means of poliomyelitis control in some early epidemics, the method was rendered ineffective by the sub-clinical nature of large numbers of infections.” (p. 49) “Rather, Melnick (1997: 647) recommends the adoption of the following measures of case control and prevention in epidemic periods:

Bed rest for febrile children, with the avoidance of undue exercise or fatigue (especially in those cases for which there is a suspicion of nervous system involvement;
Avoidance of elective nose and throat operations and dental extractions;
Avoidance of the unnecessary movement of children to or from epidemic areas; protection of food and human excrement from flies;
Adherence to hospital regulations for poliomyelitis admissions, with all pharyngeal and bowel discharges to be considered infectious;
The mass administration of the appropriate type-specific monovalent OPV to susceptible persons.” (pp. 49, 52)

“The Hygiene Model of Poliomyelitis Emergence… it seems likely that poliovirus was a long-standing member of the pool of infectious agents in the urban centres of earlier times, existing in equilibrium with its host population and with a continuous supply of susceptible infants in which endemic infection could be maintained. According to the hygiene model of poliomyelitis emergence, the development of epidemic potential was contingent upon a reduction in the level of fecal exposure to poliovirus in early infancy and hence the level of latent immunization in the population. The former Yale and Baylor virologist, Joseph L. Melnick…succinctly summarizes the model in the following terms:

The shift from the endemic to the epidemic phase of poliomyelitis was first seen in societies that had advanced systems of hygiene and sanitation and were located in cooler climates. In the latter part of the 19^th century and early in the 20^th, the urban, industrialized parts of northern Europe and he United States began to suffer from epidemics of paralytic polio that became larger, more frequent, and more severe in an increasing number of localities. The generally accepted explanation, borne out by numerous studies, is that with increased economic development and correspondingly improved resources for community and household hygiene, and with the additional advantage of a temperate-zone climate, the opportunities for immunizing infections among infants and young children were reduced. Therefore, more persons encountered poliovirus for the first time in later childhood or in adult life, at ages when poliovirus infections are more likely to take the paralytic form. Furthermore, the delay in exposure increased the pool of susceptibles, opening the way for rapid and explosive spread of the viruses once they did enter the population, in contrast to the steady endemic transmission of the preceding phrase. In some instances this transition from the endemic phase to the epidemic phase took place in a abrupt shift, but in other areas it was characterized by gradual increases in the annual case rates of ‘sporadic’ poliomyelitis. (Melnick, 1997): 611)[6] [Smallman-Raynor, p. 88]

….

“The Scandinavian Focus: Scandinavia holds a special place in the epidemic history of poliomyelitis. Beginning with the localized outbreaks in Modums (Norway) in 1868 and Västerbotten (Sweden) in 1881, the countries of the Scandinavian Peninsula were among the first to record ‘undoubted’ epidemics of poliomyelitis (Wernstedt, 1912: 235). From that time on, poliomyelitis ‘appeared more frequently and relatively more severely in Scandinavia than in any other part of the world’ (Low, 1917: 18), eventually to manifest itself in the great Norwegian and Swedish epidemics of 1905 – the largest epidemics of poliomyelitis then recorded.” (p. 89) ….

“After Scandinavia, poliomyelitis began to emerge as a significant epidemic disease in several European countries – Austria, Belgium, England and Wales, France, Germany, Holland, Hungary, Italy, Poland, and Switzerland….the role of communal activities – schools, fairs, shows, galas, weddings, funerals – in fuelling major epidemics was increasingly recognized…” (p. 127) ….

“…the story told…of the emergence of epidemic poliomyelitis across Europe from the latter years of the nineteenth century was repeated again and again between 1900 and 1920, first in North America, then in Latin America, and finally in Oceania.” (p. 129) ….

“The New England outbreaks of 1893-4 [Boston (1893), Rutland Co., VT (1894)] were the first of several to strike the United States in the late nineteenth and early twentieth centuries….a series of generally small and geographically localized outbreaks – centered largely on New York and the proximal states of New England – were a precursor to the first major epidemic event in the country: the New York City epidemic of 1907. From thereon, epidemics of increased incidence and geographical extent began to sweep the Northeast and Midwest, to manifest in state-wide outbreaks in 1907 (Massachusetts), 1908 (Florida, Iowa, Massachusetts, Minnesota, and Wisconsin), and 1909 (Massachusetts and Nebraska.” (p. 133)

Smallman-Raynor on Polio Seasonality: “The seasonal proclivity of poliomyelitis is one of the outstanding epidemiological features of the disease (Freyche and Nielsen, 1955;[7] Spicer, 1959;[8] Melnick, 1997).[9] Historically, seasonal swings in poliomyelitis morbidity and mortality have been especially prominent in temperate latitudes where during the inter- and early post-war years, the summer/autumn months of July-October (northern hemisphere and January-April (southern hemisphere) marked the usual period of peak disease activity (van Rooyen and Rhodes, 1948).[10]” (p. 207)

“Seasonal patterns of disease activity are commonly a response to environmental controls (Cliff et al., 1998: 208-13). As regards poliomyelitis, studies have correlated the seasonal distribution of the disease in mid-latitude environments with a range of meteorological variables, including temperature (Lawrence, 1956; Spicer, 1959), humidity (Armstrong, 1950); Spicer, 1959); Hemmes et al., 1962) and solar radiation (Petersen, 1941). More generally, Spicer (1959) speculates on the importance of meteorological conditions that promote rapid outdoor drying, thereby favouring the survival of poliovirus in faeces, as critical controls in the seasonal occurrence of the disease.” (p. 213)

[Polio] “Global Retreat, 1955-1988….we turn our attention to the dramatic achievements in global poliomyelitis control which accompanied the introduction and mass administration of safe and effective poliovirus vaccines. Our examination spans the 33-year interval from the licensing of the first poliovirus vaccine in the United States (Apr. 1955) to the historic resolution of the Forty-First World Health Assembly which committed the World Health Organization (WHO) to the global eradication of the disease (May 1988). As Melnick (1997: 613)[11] wrote of the period under review:

Rarely has a serious disease been controlled so quickly and dramatically as was poliomyelitis…In 1955, the Soviet Union, 23 other European countries, the United States, Canada, Australia, and New Zealand experienced a total of more than 76,000 reported cases of poliomyelitis. Only 12 years later, in 1967, 1,013 cases were recorded in these same countries, a reduction of almost 99%.

Even further reductions followed. In 22 industrialized European countries, the total average annual number of poliomyelitis cases in…1971-1975…was 357; in 1976, there were 151 cases, and in 1977, 145. Adding the data for the same periods from Australia, Canada, Japan, New Zealand and the United States, these 27 industrialized countries around the world (containing a total of approximately 680 million persons) had total annual case rates of…377 in 1971-1975, 165 in 1976, and 169 in 1977.

“The virtual elimination of disease associated with indigenous wild poliovirus in Cuba, Chile, and the United States – among other locations – by the early 1980s clearly demonstrated the potential for the interruption of poliovirus transmission in several countries of the Western Hemisphere. Such were the developments that, at the International Symposium on Poliomyelitis Control (Washington, 1983), Michael B. Gregg of the Epidemiology Program Office, Centers for Disease Control, could argue for the scientific basis of global poliomyelitis eradication. ‘In a variety of dissimilar settings,’ Gregg (1984:S577)[12] observed, ‘paralytic poliomyelitis has been controlled, eliminated or eradicated’. ‘The control worldwide and the ultimate elimination of poliomyelitis,’ he added, ‘are really then not scientific issues but, as in the smallpox campaign, are issues of commitment, execution and evaluation’.” (pp. 429, 431)

“Vaccination: The United States Campaigns….the licensing of Salk’s inactivated poliovirus vaccine (IPV) in the United States in April 1955 was accompanied by a dramatic reduction in disease incidence. But it was the introduction and mass administration of Sabin’s live attenuated oral poliovirus vaccine (OPV) in the early 1960s that finally broke the chain of wild poliovirus transmission. Following a large-scale trial of OPV in Cincinnati in 1960, with further testing and licensing of the vaccine in 1961, the first mass vaccination programmes with monovalent OPV were implemented in the counties of Maricopa and Pima, Arizona, in January 1962 (Johns et al., 1963). As Sabin (1985) notes, such was the appeal of the Arizona plan to county medical societies across the United States that, between 1962 and 1964, some 100 million US citizens were vaccinated with OPV. From 1965, a newly developed trivalent OPV was administered as part of the routine US childhood immunization schedule. By the mid-1970s, the average annual number of poliomyelitis notifications had reduced to less than 25, with the last recorded outbreak of indigenously acquired wild poliovirus –centered on a population that had refused vaccination on religious grounds – occurring in 1979 (Centers for Disease Control and Prevention, 1997b).”[13] (pp. 433-434)

Smallman-Raynor on CDC and Polio: “According to Alexander D. Langmuir, former Chief Epidemiologist of the US Communicable Disease Center (CDC), poliomyelitis was the ‘dominant problem’ for the agency in the early 1950s, and ‘continued through the 1950s and well into the 1960s as probably the leading concern’ (Langmuir, 1980: 473[14]). As Langmuir explains:

We embarked on a national evaluation of gamma globulin in 1953, participated heavily in the Francis field trial of inactivated polio vaccine (Salk) in 1954-55, and played a crucial role in the resolution of the Cutter incident and the practical field evaluation of polio vaccine beginning in April 1955. The experience led to the establishment of the poliomyelitis surveillance program that continued through the problems of the introduction and safety of the oral attenuated polio vaccine from 1961 to 1964 and that has continued to operate at reduced levels to the present time.

“Among the varied operations of CDC, the work of the Epidemic Intelligence Service (established July 1951) and the National Poliomyelitis Surveillance Program (established Apr. 1955) is especially valuable in providing perspectives upon the sub-national pattern of poliomyelitis outbreaks in the continental United States and elsewhere.” (p. 456)

Smallman-Raynor on Last US Polio Outbreaks: “Only two outbreaks of poliomyelitis were recorded in the United States between 1972 and 1988. Both outbreaks were centered on the spread of wild type 1 poliovirus in minority religious communities, and both were the consequence of residual pockets of susceptibility in an otherwise heavily vaccinated population…

“Poliomyelitis in a Christian Science Community: Connecticut, 1972.

“Foote et al. (1973) describe a small outbreak of poliomyelitis in Daycroft School – a private boarding school in Greenwich, Connecticut, whose faculty and students were Christian Scientists. The first recognized case of the disease in the school’s 128-strong student body was admitted to hospital with paraplegia in mid-October 1972, having returned home to New York on account of illness. Subsequent investigations revealed a total of 11 cases (including eight cases of paralysis) among the Daycroft students, with the earliest onset in a patient with paralytic disease dating to late September… As a remedial response to the demonstrably low vaccination coverage (46%) of the student population, vaccination of students, along with faculty members and all other school employees, was undertaken on 26-7 October. Other Christian Science families living in Greenwich, and whose children did not attend Daycroft School, were also contacted and administered trivalent OPV as required. Investigations failed to identify a source of poliovirus in the school.

“The Amish Outbreak of 1979.

“Almost seven years were to elapse before poliomyelitis reappeared in epidemic form – an event which, in retrospect, was to mark the last recorded outbreak of wild poliovirus in the United States (Centers for Disease Control and Prevention, 1997b). The epidemic which occurred in the months of January-June 1979 was focused on members of a US Mennonite sect (Amish) that traces its origins to the Anabaptist movement of sixteenth-century Switzerland. The Amish migrated to the United States in 1709 to escape religious persecution, with the first settlements founded in Pennsylvania. By the late 1970s, Amish communities were located in more than 20 states of the Union…with the total population numbering some 75,000. As Cliff et al. (1993: 239) observe, several characteristics of the Amish predispose them to epidemics of common infectious diseases, of which the rejection of immunization by some sect members is pertinent to the events to be described. When coupled with the high level of national and international socialization of the Amish and related sects, the epidemic of 1979 provides an illustration of how spatially separated pockets of susceptibility may sustain a chain of wild poliovirus transmission over extended periods of time.

“Source of Poliovirus.

“All available evidence – virological and epidemiological – indicates that the Amish outbreak resulted from the importation of a wild strain of type 1 poliovirus (Centers for Disease Control, 1981; Hatch et al., 1981)…. The ultimate source of the epidemic can be traced to the spring of 1978 and a large epidemic of poliomyelitis, associated with more than 100 documented cases, among unvaccinated members of a Protestant sect of fundamentalist reformed churches (Netherlands Reformed Congregation) in the Netherlands… Coincidentally, members of the afflicted sect travelled to Canada, where cases of the disease appeared among their hosts and fellow sect members in Ontario (six cases), British Columbia (two cases) and Alberta (1 case) in the summer of 1978 (World Health Organization, 1978a; Furesz, 1979). As for the appearance of the disease in the United States, an epidemiological link with the Canadian outbreak was forged by an Amish family which, in the late summer of 1978, relocated from the environs of an infected locality in Ontario to Pennsylvania (Centers for Disease Control, 1981: 14).

“Course of the Outbreak.

“The first case of poliomyelitis in a US citizen presented in January 1979 in an unvaccinated resident of the same community in Pennsylvania to which the Amish family had moved in the previous year. The main phase of the outbreak awaited the months of April, May, and June, when a further 14 cases of poliomyelitis were recorded among US nationals in such disparate locations of Pennsylvania (seven cases), Iowa (three cases), Wisconsin (three cases), and Missouri (one case… All 15 cases were Amish (13 patients) or members of the Mennonite church in frequent contact with Amish persons (two patients) and all were unvaccinated (Centers for Disease Control, 1981).

“Outbreak control. Given the frequent contact between Amish communities nation-wide, and the potential for inapparent transmission during the summer, CDC recommended that the entire Amish population of 75,000 should be vaccinated. Beginning with Pennsylvania in mid-February, and extending to 20 other states in the weeks and months that followed, at least 70 percent of the nation’s Amish had received at least one dose of OPV by 1 July 1979. By mid-August, five states had achieved immunization levels of 90 percent or more, while vaccination coverage in the three states with the largest Amish populations (Indiana, Ohio, and Pennsylvania, with a combined Amish population of 56,000) had reached 46060 percent (World Health Organization, 1979b; Centers for Disease Control, 1981). The last documented case of poliomyelitis associated with the outbreak occurred on 3 June….

“The demonstration that the virus responsible for the 1979 outbreak in the United States was identical to the virus that had caused the 1978 outbreaks in the Netherlands and Canada represented ne of the first instances of the use of molecular epidemiology by CDC – a collaboration between epidemiologists and virologists that has subsequently formed a central plank of the global poliomyelitis eradication programme (Centers for Disease Control and Prevention, 1997b: 1197).” (pp. 462-466)

Last US Wild Polio cases: “During the period 1980-8, a total of five imported cases of wild-virus poliomyelitis were recorded in the United States – a rate of somewhat less than one case per year. Of the five cases, Mexico (two cases), Haiti (one case), Nepal/Burma (one case), and Zaire (one case) were the presumed sources of infection, with the disease occurring in three travelers and two recent immigrants. No secondary cases of disease were attributed to the imported cases. The fifth and final case in the series, detected in 1986, was the last confirmed case of wild-virus poliomyelitis in the United States (Strebel et al., 1992; Centers for Disease Control and Prevention, 1995).” P. 467.

Polio Eradication? “While vaccines introduced from the mid-1950s virtually eliminated the disease in western countries over the next quarter of a century, it remained a major threat elsewhere. As we have seen…11 years after the close of its successful smallpox campaign, the World Health Assembly, meeting in Geneva in 1988, committed the World Health Organization to the global eradication of the disease. By 1993, no countries in the Americas reported cases, while much of Europe and the Western Pacific was also free of poliomyelitis. The success was made possible by the widespread use of vaccination. Overall, the level of vaccination worldwide rose from less than 5 percent of children in 1974 to over 80 percent at the beginning of the new millennium. Between 1974 and 1994, the number of polio cases reported globally fell from some 50,000 to 9,000. The decline has continued so that the World Health Organization hopes that the global interruption of wild poliovirus transmission will be achieved during 2005, with certification of the worldwide eradication of poliomyelitis by 2008,.” (p. 628.) (Smallman-Raynor, R. R., A. D. Cliff, B. Trevelyan, C. Nettleton, S. Sneddon. Poliomyelitis: Emergency to Eradication – A World Geography. Oxford: Oxford University Press, 2006.)

Sources

Bureau of the Census, U.S. Department of Commerce. Mortality Statistics 1925 – Twenty-Sixth Annual Report: Part I, Summary and Rate Tables and General Tables for the Death Registration Area in Continental United States, with Supplemental Statistics for Hawaii and the Virgin Islands. Washington: GPO, 1927. Accessed 11-18-2013 at: http://www.cdc.gov/nchs/data/vsushistorical/mortstatsh_1925.pdf

Centers for Disease Control and Prevention. “Epidemiologic Notes and Reports: Follow-up on poliomyelitis–United States, Canada, Netherlands.” MMWR Weekly (Morbidity and Mortality Weekly Report), Vol. 46, 7-27-997, pp. 1195-1199.

Dickie, Walter M. (M.D.). “A Review of Communicable Disease Control in 1924-1925.” Weekly Bulletin, CA State Board of Health. Vol. IV, No. 34, 10-3-1925, p. 134. Google digitized. Accessed 9-15-2016 at: https://books.google.com/books?id=7ow9AQAAIAAJ&printsec=frontcover#v=onepage&q&f=true

Draper, George, M.D. Infantile Paralysis. NY and London: D. Appleton-Century Co., Inc., 1935.

Google Health. “Poliomyelitis.” Accessed 8/23/2010 at: https://health.google.com/health/ref/Poliomyelitis

Langmuir, A. D. “The Epidemic Intelligence Service of the Centers for Disease Control,” Public Health Reports, Vol. 95, 1980, pp. 470-477.

Paul, John R., M.D. “Epidemiology of Poliomyelitis,” pp. 9-29 in Poliomyelitis, World Health Organization (Geneva), 1955. Accessed at: http://whqlibdoc.who.int/monograph/WHO_MONO_26.pdf

Smallman-Raynor, R. R., A. D. Cliff, B. Trevelyan, C. Nettleton, S. Sneddon. Poliomyelitis: Emergency to Eradication – A World Geography. Oxford: Oxford University Press, 2006.

United States Bureau of the Census, Department of Commerce. Mortality Statistics 1931 (Thirty-Second Annual Report). Washington: GPO, 1935. Accessed 10-24-2013 at: http://www.cdc.gov/nchs/data/vsushistorical/mortstatsh_1931.pdf

United States Census Bureau. Historical National Population Estimates: July 1, 1900 to July 1, 1999. Internet release date: 4-11-2000. Accessed 10-29-2013 at:

http://www.census.gov/population/estimates/nation/popclockest.txt

[1] Within Table 6 it is noted that within the “Registration States” (40 plus DC), there were 1,492 polio deaths. The polis list number is 22, and entitled “Acute anterior poliomyelitis.”

[2] Dickie (Sec. and Exec. Officer, CA State Health Board) notes 70 polio deaths (700 cases) in CA Jan-July.

[3] No citation, but the only Flexner and Lewis in the bibliography is: Flexner, S., and Lewis, P. A. The Transmission of Acute Poliomyelitis to Monkeys; First Note. J. Am. M. Ass., 1909, 53:1639.”

[4] The names of the phases are given on page 6.

[5] R. I. Cecil and R. F. Loeb (eds.) A Textbook of Medicine (10^th ed.). Philadelphia: Saunders, 1959.

[6] Melnick, J. L. “Poliovirus and other enteroviruses.” In A. S. Evans and R. A. Kaslow (eds.), Viral Infections of Humans: Epidemiology and Control (4^th ed.). London: Plenum Medical Book Co., 1997, pp. 583-663.

[7] M. J. Freyche and J. Nielsen. “Incidence of poliomyelitis since 1920,” in Poliomyelitis (Geneva: World Health Organization, 1955).

[8] C. C. Spicer. “Influence of some meteorological factors in the incidence of poliomyelitis,” British Journal of Preventive and Social Medicine, Vol. 13, 1959, pp. 139-144.

[9] J. L. Melnick. “Poliovirus and other enteroviruses,” in A. S. Evans and R. A. Kaslow (eds.), Viral Infections of Humans: Epidemiology and Control (4^th edn.). London: Plenum Medical Book Co., 1997.

[10] C. E. van Rooyen and A. J. Rhodes. Virus Diseases of Man. NY: Thomas Nelson and Sons, 1948.

[11] Ibid.

[12] Michael B. Gregg. “Paralytic poliomyelitis can be eliminated.” Reviews of Infectious Diseases, Vol. 6 (suppl. 2), 1984, pp. S577-580.

[13] U.S. CDC. “Epidemiologic Notes and Reports: Follow-up on poliomyelitis–United States, Canada, Netherlands.” MMWR Weekly, Vol. 46, 7-27-997, pp. 1195-1199.

[14] A. D. Langmuir. “The Epidemic Intelligence Service of the Centers for Disease Control,” Public Health Reports, Vol. 95, 1980, pp. 470-477.