The Polio Vaccine Story and the March of Dimes

By Nekud October 21, 2026 24 min read

Few twentieth-century diseases cast as long and as clinical a shadow over ordinary childhood as poliomyelitis. Summer after summer, parents watched their children for the first hint of a stiff neck, a fever, a wobble in the legs, knowing that the rest of a life might be lived in a steel cylinder breathing for them. That fear produced not only a vaccine but a peculiar hybrid of patient philanthropy, wartime science, and mass experimentation the world had never seen: the National Foundation for Infantile Paralysis — soon known as the March of Dimes — and the two rival vaccines that grew out of it. This is the story of all three.

The Pre-Vaccine Era — Epidemics, Iron Lungs, and the Birth of the March of Dimes

Poliomyelitis is an ancient disease — probably first recorded on an Egyptian stele of the eighteenth dynasty around 1400 BCE, in a depiction of a young priest with a wasted leg and a dropped foot — but it only became a mass killer in the late nineteenth and early twentieth centuries, as sanitary conditions improved in wealthy cities. Paradoxically, the cleaner the water supply, the later in life a child first encountered the virus, and the heavier the paralytic toll. New York City alone recorded roughly nine thousand cases and more than two thousand deaths in the catastrophic summer of 1916, almost all of them children under five; the panicked city sealed off immigrant neighbourhoods in what historians describe as one of the earliest American episodes of quarantine theatre. Outbreaks recurred through the 1920s and 1930s — 1921, 1927, 1931, 1934 — each leaving a fresh generation of limping survivors and a fresh summer of parental dread.

For the unlucky minority whose infection reached the brain stem, life depended on a machine invented at Harvard in 1928 by Philip Drinker and Louis Shaw: the tank respirator, known almost immediately as the iron lung. The patient lay sealed inside the metal cylinder, only the head protruding, while a pair of bellows alternately raised and lowered the pressure around the chest, forcing the paralyzed diaphragm to inflate and deflate the lungs. Tens of thousands of children spent weeks or years in these devices. Rows of iron lungs lined the polio wards of municipal hospitals, and the rhythmic, mechanical hissing of the bellows became the auditory signature of a generation of American paediatrics. The iron lung was not a cure — it merely substituted for the muscles the virus had destroyed — but it bought time for some patients to recover, and it kept the image of polio’s brutality permanently in the public mind.

Among the many Americans touched in the early epidemic wave was Franklin Delano Roosevelt. In August 1921, while on holiday at Campobello Island in New Brunswick, the then forty-year-old former Assistant Secretary of the Navy fell ill with what was probably polio — though modern neurologists still dispute whether the diagnosis was bulbar polio, Guillain-Barre syndrome, or both. He never walked unaided again. Six years later, in 1927, he founded the Warm Springs Foundation in Georgia as a treatment retreat and a proving ground for the idea that paralytics could be rehabilitated rather than warehoused. Warm Springs drew wealthy donors, celebrity visitors, and the attention of Roosevelt’s longtime law partner, Basil O’Connor, who would become the second-most important figure in the polio story.

O’Connor was, by training, a Wall Street litigator with the firm of O’Connor, Boyle, Pope and Schilpp. As Roosevelt entered politics — Governor of New York in 1928, President in 1932 — O’Connor stayed behind him as campaign fixer, legal adviser, and bagman. In January 1934, two days after Roosevelt’s fifty-second birthday, O’Connor staged the first of the President’s Birthday Balls, an oddly sentimental national dance marathon whose proceeds would go to the Warm Springs Foundation. The format was copied in nearly every state in the union; within two years the Birthday Ball movement had collected the rough equivalent of several million modern dollars and made O’Connor, not Roosevelt, the public face of polio philanthropy.

The decisive moment came on the night of 2 September 1937, when FDR learned that Franklin Gunnell, his former employer and current Secretary of the Interior’s brother-in-law, had just died of polio in a small Virginia town. The next evening, according to the journalist Edith Lederer and historians of the period, the President turned to O’Connor in the Oval Office and said the words that effectively authorized a new institution: if the current polio work could not be expanded, who would stop the next outbreak? On 16 January 1938, Roosevelt formally chartered the National Foundation for Infantile Paralysis, with O’Connor as its unpaid president. The Foundation later pivoted to the strategy of asking the public, via radio appeal, to send their loose change to the White House — the coins were tallied later and the campaign nicknamed itself the March of Dimes after a publicity contest won by the vaudeville performer Eddie Cantor. The Foundation’s first grant, of $26,933, was approved that spring, to a young Harvard researcher named Thomas Weller who had just started a fellowship in ENDERS’s laboratory; he would, within eleven years, share a Nobel Prize for work on polio tissue culture.

O’Connor was, in many ways, the practical architect of the Foundation. He drafted the bylaws, hired the staff and ran the budget — the first paid President of the Foundation was John Evans, who took the role in 1940 after leaving his position as the General Director of the Boy Scouts of America. O’Connor was also its principal fundraiser, and he quickly discovered that the simplest fund-raising concept was also the most enduring: the “Mothers’ March on Polio,” in which a half-million volunteers, almost all of them women, went door-to-door on a single day each January with collection tins, all of it backed by local chapters of the parent-teacher associations and the General Federation of Women’s Clubs. The March’s cost structure — paid staff in a small national office, with virtually all field activity carried out by volunteers — became the cost structure of subsequent Foundation activities for the next three decades, and the Foundation’s direct-mail list grew into one of the largest in the United States. By 1940 the Foundation was turning down more outside grant applications than it was funding, and by 1948 it was spending more than $26 million a year on medical research, much of it routed through the National Research Council’s Division of Medical Sciences. The Foundation’s public outreach also produced a strikingly modern media apparatus: sponsored weekly radio dramas, the founding of the Polio Chronicle newsletter, and the use of high-profile “poster children” — most famously, five-year-old Donald Anderson in 1943 and six-year-old Martha Ann Way in 1950 — turned the cause into a permanent fixture of American mass culture.

The Virologist’s Puzzle and the Tissue Culture Breakthrough

The earliest modern work on polio transmission belongs to two Viennese-born scientists. In December 1908 at the Rockefeller Institute, Karl Landsteiner and Erwin Popper inoculated two cynomolgus monkeys with a suspension of ground spinal cord from a nine-year-old polio victim named Bernhard Eppstein. One monkey developed paralytic disease; cross-sections of its cord showed the characteristic lesions. This was the first unambiguous transmission of poliomyelitis to a laboratory animal, and it established that the causal agent was a virus — an entity invisible under any microscope of the era — rather than a bacterium. Four years later, in 1913, the first such virus was shown to be filterable in the proper sense: a Chamberland candle, whose pores excluded every known microbe, allowed the disease to pass.

The next two decades saw slow accumulation rather than breakthrough. By 1931 it had become clear that there was not one poliovirus but a family of related but immunologically distinct serotypes: Macnamara had isolated a strain from a fatal case in Melbourne that could not be neutralized by the serum of patients who had recovered from the New York strains, and Burnet’s group at the Walter and Eliza Hall Institute traced the difference to antigenic variation. Eventually, three serotypes would be named — Brunhilde (Type 1, named for a chimpanzee at Johns Hopkins), Lansing (Type 2, from a Michigan case) and Leon (Type 3, from a Los Angeles boy). The three-circled capital letter most commonly used to denote the vaccine strains today descends directly from this trinomenclature.

Two vaccine attempts in 1935 illustrate how badly the science was lagging. Maurice Brodie, a young New Yorker working under William Park at NYU, took a suspension of monkey-kidney virus, treated it with formalin, and tried it on himself and a handful of children; John Kolmer at Temple University in Philadelphia, working concurrently, prepared a supposedly attenuated live vaccine by passage through rats and monkeys. Both vaccines were tested in dozens of children in the early summer of 1935. Both failed: at least six of Kolmer’s and an unknown number of Brodie’s vaccinees developed paralytic polio, and many more developed severe allergic reactions. The resulting public outcry effectively shut down human vaccine work in the United States for almost fifteen years, and the names Brodie and Kolmer survive in the literature mostly as cautionary tales. (Scholars continue to debate whether Kolmer’s vaccine was genuinely attenuated or simply under-attenuated; the contemporaneous records are partial.)

The bottleneck was the difficulty of growing poliovirus outside the central nervous system of a live animal. Because the only available substrate was brain tissue, producing even modest vaccine quantities required grinding up thousands of monkey spines, with the entire apparatus dedicated to a single pestilential passage — and the risk, every batch, of unleashing the live virus. The same machinery could not simultaneously test a vaccine and screen for contamination.

The breakthrough came in the autumn of 1948 in a small laboratory on the third floor of the old Children’s Medical Center in Boston. John Enders, a former English-literature graduate student in his fifties who had come late to virology, had recruited a junior physician named Thomas Weller and a doctoral student named Frederick Robbins. Working with a Type 2 Lansing strain and discarded human skin and muscle tissue left over from surgical biopsies, the trio showed that poliovirus would replicate in non-neural human cells and that the replication could be detected by a simple visible sign — cytopathic effect, the gradual rounding and sloughing of infected cells in a culture flask. Enders announced the result in a paper in the Proceedings of the Society for Experimental Biology and Medicine in 1949, the same year that Robbins and Weller published a more detailed account with the Type 3 Leon strain. The discovery won the three men the 1954 Nobel Prize in Physiology or Medicine — Enders as senior author, and Weller and Robbins as co-investigators — and it transformed poliomyelitis from a virus that could only be grown in the nervous system into one that could be grown in test tubes by the Petri-dishful. Within a year, three laboratory methods for vaccine production had become possible, and several laboratories were working on all of them at once.

Jonas Salk and the 1954 Francis Field Trial

Among those laboratories, the most consequential was in Pittsburgh. Jonas Salk, a New York City-born physician who had trained under Thomas Francis at the University of Michigan and then under the influenza virologist Max Theiler at the Rockefeller Foundation, joined the University of Pittsburgh School of Medicine in 1947 with a five-year grant from the Eliza Hall Institute’s American counterpart. Theiler’s innovation — formaldehyde inactivation of the yellow fever virus, scaled up to millions of doses in the late 1930s — was Salk’s template. A killed virus, Salk reasoned, ought to retain its surface antigens long enough to provoke an antibody response in the human host without ever risking replication. (Many virologists at the time — most prominently Albert Sabin — considered that view heretical; live attenuated virus was, in their reading, the only natural route to the durable immunity the public actually needed.) Salk’s technique was essentially the Theiler method applied to Lansing, Brunhilde, and Leon: each serotype was grown separately in rhesus monkey kidney cells, inactivated by exposure to dilute formaldehyde at controlled temperature, and finally tested for residual live virus by intracerebral inoculation of three distinct species of monkey. By the spring of 1952 he was ready to test a preliminary formulation on himself, his wife, and their three children.

What Salk had not yet solved, by mid-1953, was the operational problem of bringing the vaccine to scale. The killing method that worked in his hands at Pittsburgh was repeatable in principle, but no single laboratory could be sure that every batch produced by every licensed manufacturer would be adequately inactivated. Five candidate manufacturers were on the Foundation’s planning list by the end of 1953: Eli Lilly, Parke-Davis and Wyeth had all produced Salk-style killed-virus vaccine in some form as a side project; Pitman-Moore and the Berkeley firm of Cutter Laboratories would be brought in to add capacity. Parallel to this, the Foundation funded the Polio Vaccine Evaluation Center at the University of Michigan under Thomas Francis, with an initial $1.3 million grant for trial design, lot testing and the supply of reference serologic reagents to all five manufacturers. The protocols that emerged from that center — double-blind testing of each manufacturer’s product, lot-by-lot quality control against a common antigen panel, and the bifurcation of the analysis between inoculated and placebo children — would later be folded into the 1962 Kefauver-Harris amendments to the Federal Food, Drug, and Cosmetic Act and into the basic framework of the modern FDA’s vaccine review process. Many of the field-trial statisticians would go on to shape the National Institutes of Health’s clinical-trial statistical practice into the 1980s.

By 1953 Salk’s vaccine, administered by injection in three doses corresponding to the three serotypes, had shown consistent type-specific seroconversion in small pilot trials. The March of Dimes, which had by then become the largest private charity in the United States — pulling in more than $50 million a year in dimes and dollars — funded the larger work and turned to the biostatistician Thomas Francis, Salk’s old mentor at Michigan, for an independent evaluation. Francis agreed, on the strict condition that he retained complete control over the design and conduct of the trial. The result was, in modern management-speak, a randomized placebo-controlled double-blind trial of unprecedented scale.

Francis’s Field Trial, as it was officially designated, began in late October 1953 with a pilot in 225 children in the Pittsburgh area. The full trial, launched in late January 1954 and completed by the autumn of that year, covered 1,829,916 children in the United States, Canada and Finland. The protocol sorted participants into three groups: an inoculated-vaccine group of roughly 428,000 children, a placebo group of roughly 200,000 children (whose injections contained only inert culture medium), and a much larger observed-control group of roughly 1.2 million children who received nothing at all and served as a running background rate for polio incidence. Almost a million separate injections were administered in just over four months, with the major role filled by the National Foundation for Infantile Paralysis‘s 92,000-strong cohort of community clinicians and the daily parallel work of a roster of pediatricians, virologists and statisticians trained and credentialed by the Foundation. Scholars now count the Field Trial as the largest clinical experiment in the history of medicine up to that date — only later surpassed by the Polio Prophylaxis Trial Organization, the Malariology protocol, and the modern COVID-19 vaccine platforms.

The 12 April 1955 announcement, made at Rackham Auditorium on the campus of the University of Michigan in Ann Arbor, was conducted by Thomas Francis himself before an invited audience of physicians and reporters. The headline numbers were carefully chosen for both scientific and rhetorical reasons. The vaccine had been effective against paralytic poliomyelitis of all three serotypes, with reported per-serotype efficacy figures of approximately 60 to 70 percent for Type 1, 92 percent for Type 2, and close to 100 percent for Type 3. The decision to license was announced on the same day by the Surgeon General Leonard A. Scheele. The March of Dimes, which under the title “Birthday Salute to Salk” had run its wildly successful public relations operation in the run-up to the announcement, ordered 39 churches across the country to ring their bells as the news broke. Twelve hundred journalists saw the press conference live. The New York Times bannered its morning edition with a front-page image of a smiling Salk; Time magazine ran the headline “Polio — Salk’s Triumph.” The shot had been heard round the world.

The Cutter Incident and the Rise of Sabin’s Oral Vaccine

Within weeks the celebration curdled into one of the worst pharmaceutical disasters in American history. The licensed vaccine had been produced by five manufacturers — Eli Lilly, Parke-Davis, Wyeth, Pitman-Moore and the Cutter Laboratories of Berkeley, California — under the supervision of the Division of Biologics Standards (DBS), a small bureau then housed within the National Institutes of Health. Cutter had licensed two production runs from the original Salk recipe and shipped just over two hundred thousand doses to western states before the vaccination campaign began in earnest. Within days, pediatricians began to notice clusters of children with paralytic polio — especially new clusters in areas of California and Idaho where the recently vaccinated lived alongside previously unvaccinated children.

The technical cause was uncovered by the DBS and the polio laboratory in the first weeks of May 1955: formaldehyde inactivation was a stochastic process, and for reasons that probably involved the clumping of virus aggregates that the fixative could not fully penetrate, some live poliovirus survived in several Cutter batches. Epidemiologists at the U.S. Communicable Disease Center (the forerunner of the modern CDC) traced at least 40,000 cases of abortive polio, 51 cases of paralytic polio in vaccinated children, 113 cases of paralytic polio in family contacts of vaccinated children, and at least five deaths (some accounts, drawing on broader surveillance, give the eventual death toll at ten). Within ten weeks Cutter withdrew its product. The American public was left with an awkward double image: a vaccine that worked when manufactured correctly and a manufacturer’s standards that had not been.

The political fallout was immediate. By the end of 1955 both houses of the U.S. Congress had opened investigations; in April 1956 the Polio Vaccination Assistance Act passed to fund the continuing campaign; and the Division of Biologics Standards was reorganized, eventually pulled out of NIH, and the modern regime of vaccine lot-release testing, sterilization validation, and independent surveillance had its true origin in the Cutter episode. Paul Offit’s reconstruction in his 2005 book The Cutter Incident: How America’s First Polio Vaccine Led to the Growing Vaccine Crisis argues, with some support from subsequent scholarship, that the Cutter story is the single most important moment in establishing the regulatory culture of American vaccinology. The argument is still contested in the literature, and at least one paediatric historian has cautioned that the regulatory reforms of 1955-1962 owed at least as much to general rethinking at NIH as to the Berkeley accident itself.

While American regulators picked up the pieces, a parallel vaccine effort was gathering speed in the Soviet Union. Albert Sabin, the Cincinnati Children’s Hospital virologist who had spent the previous decade systematically passaging poliovirus through non-neural cells (chick-embryo fibroblasts, monkey-kidney cultures, newborn mice) to produce stably attenuated strains, had been unable to get his live-attenuated vaccine into American children because the Cutter disaster had made any further live-virus trial politically all but impossible. In 1956 Sabin met the Soviet virologist Mikhail Chumakov at a meeting of the World Health Organization in Geneva, and Chumakov agreed to give the Sabin strains a try in a country whose bureaucracy was uninterested in the resulting liability.

From 1957 through 1960 Sabin’s three attenuated strains (the ones later abbreviated in the textbook as OPV, for oral polio vaccine) were administered to roughly ten million Soviet children, with continued expansion into Poland, Czechoslovakia, Hungary, Bulgaria and several East German provinces. The Soviet data — assembled, with quiet input from Sabin himself, by Chumakov’s colleague Anatoli Smorodintsev — showed no cases of vaccine-attributable paralytic polio above the baseline rate; combined with the obvious practical advantages of a sugar-coated pill that could be given without needles, the data were politically damning to the killed-virus regime.

In the United States, the American Academy of Pediatrics finally endorsed the Sabin vaccine in 1961; a parallel licensing action by the DBS followed that spring. The killed-virus Salk vaccine (IPV) was not abandoned overnight, but by the mid-1960s it was the second-line product in most of the developed world. The oral route also carried a downstream infection advantage that mattered more than anyone fully understood at the time: vaccinated children briefly shed attenuated virus in their stool, which passed on a transient passive immunization to unvaccinated contacts, generating a soft form of herd immunity. The Soviet decision to switch was a global model; India, China, and most of Latin America adopted OPV as their standard paediatric product between 1972 and 1980.

That success eventually soured. The same property that made OPV so good at spreading — its ability to replicate in the human gut — allowed the attenuated strains, on rare occasions, to revert toward virulence through mutation in the gut of a susceptible child. Such reverted strains, designated cVDPV (circulating vaccine-derived polioviruses), have produced periodic outbreaks of paralytic disease in countries where OPV coverage is imperfect, notably in Nigeria, Pakistan, Madagascar, the Democratic Republic of the Congo, and Ukraine, while the original wild polioviruses have faded from circulation. The first generation of success against polio produced the second generation of unanticipated problems. By 2015 most industrialized countries had switched back to an injectable inactivated vaccine for routine use, retaining OPV only for outbreak response — a quiet therapeutic about-face that has its own history in the literature.

The technical picture of the Cutter failure was reconstructed in the autumn of 1955 by the National Institutes of Health Working Group on the Cutter Incident, whose principal investigators were Joseph Smadel of the Walter Reed Army Institute of Research, Sven Gard of the Karolinska Institute and Tom Rivers of the Rockefeller Institute. The working group concluded that incomplete inactivation of virus, rather than contamination by a different strain, was the proximate cause of the Cutter-associated cases, and they identified two operational contributors: inadequate titration of residual live virus in Cutter’s own in-house control program, and a generous formaldehyde inactivation schedule that compared unfavourably with the tighter schedule in use at Merck. The working group’s final report recommended that intrachain filtration chromatography, continuous-flow vaccine production lines, and uniform lot-release rules be made mandatory for every U.S. vaccine manufacturer. In the years that followed the working group’s report, the Division of Biologics Standards progressively tightened its lot-release rules while concurrent work at the Communicable Disease Center and at the National Institutes of Health set the modern practice of vaccine lot-by-lot quality control. By the time the FDA formally took over vaccine regulation in 1972, the Cutter framework was already entrenched and continues to underpin vaccine regulation under section 351 of the Public Health Service Act to this day.

Global Eradication and the Long Tail

By the early 1980s the operational question of polio had shifted from vaccine formulation to vaccine distribution. The World Health Organization launched the Global Polio Eradication Initiative (GPEI) in 1988, with Rotarians’ parallel advocacy of the PolioPlus campaign as its principal private-sector engine. The widely-quoted founding figure of 350,000 wild-polio cases a year has been progressively revised downward as measurement improved; modern WHO data clusters the late-1980s global incidence near 350,000 cases — mostly type-1 — with type-2 already in steep decline.

The certification milestones came over the next two decades. Last detection of naturally occurring wild Type 2 had already occurred in 1999 in Uttar Pradesh; in September 2015 the Global Commission for the Certification of Poliomyelitis Eradication officially declared wild Type 2 eradicated, and the routine use of the type-2 component of OPV was discontinued in a synchronized global switch from trivalent OPV to bivalent OPV in April 2016. Last detection of wild Type 3 was reported in November 2012 in Yobe State, Nigeria; the same commission declared wild Type 3 eradicated in October 2019 in a decision announced in Geneva. Africa was declared free of wild polio in August 2020.

Wild Type 1 remains. As of the most recent WHO surveillance, the only two countries with ongoing endemic transmission of wild poliovirus Type 1 are Pakistan and Afghanistan, with low-level transmission documented in scattered border districts and a higher case-count cluster in Karachi and Quetta. The history of the Afghani and Pakistani drives is one of remarkable logistics under trying security conditions: in 2017 the Global Polio Eradication Network dispatched more than 66 million doses of OPV in Pakistan alone, with vaccination teams traveling under armed escort in some districts of Khyber Pakhtunkhwa. The Pakistani polio campaign is widely cited as one of the largest single disease-eradication operations in human history. The WHO and GPEI have set a 2026 certification target, although several independent observers argue that the realistic finish line is now several years later than originally forecast.

Meanwhile, the cVDPV outbreaks have become, in some places, the dominant clinical problem. The sharp 2022 detection of vaccine-derived poliovirus in London sewage, and the well-publicized case of paralytic polio in an unvaccinated adult in Rockland County, New York, in the same season, both revealed the under-discussed weakness of an eradication program still partially dependent on OPV. Outbreaks of cVDPV Type 2 have flared repeatedly in DRC, Nigeria, Yemen, Indonesia, and the Philippines since 2017. The 2023-mid-year detections of wild poliovirus in Gaza wastewater raised concerns about the broader regional situation following the collapse of routine immunization and the suspension of polio campaigns in October 2023; by 2024 environmental surveillance was positive in sewage from multiple districts and the WHO had arranged a limited vaccination drive in coordination with the Palestinian Ministry of Health.

The intellectual legacy is harder to extract. The Salk Institute for Biological Studies, designed by Louis Kahn and opened in 1963 on a cliffs-edge mesa in La Jolla, California, continues to function as a research university and a site of periodic public remembrance. The Sabin Vaccine Institute, originally chartered in 1993 as a Washington-based nonprofit, continues to advocate for immunization in low-income countries. The Cold Spring Harbor archives, the Smithsonian’s National Museum of American History (which maintains the Eddie Cantor dimes, the Warm Springs iron lung, and the candystriped pencil of an unidentified National Foundation volunteer in its Behring Center), and the March of Dimes Foundation itself continue to be the chief American repositories of material from the period. The Smoke of 1916 has been joined by the smoke of 1949, the smoke of 1954, and the smoke of 1955 in the public’s mental geography of public-health intervention. Modern historians continue to debate the locus of credit.

The Rotary International dimension deserves separate mention. Rotary launched its PolioPlus campaign in 1985 with what was, at the time, the largest private-sector commitment ever made by a single service organization to a single disease — an initial $120 million to fund surveillance, laboratory work and vaccine logistics in 100 countries. By 2024 Rotary’s cumulative contribution had grown past $2.6 billion and the organization’s network of country-level PolioPlus chairs remained the operational back-office of the GPEI in many of the last endemic districts. Rotary’s advocacy within the World Health Organization’s Executive Board helped lock in the 1988 GPEI commitment that anchored the next two decades of work, and the campaign has since produced one of the largest dedicated disease-focused labor forces in the history of public health.

Alongside the operational effort sits a parallel universe of advocacy, anti-vaccination activism and viral misinformation that the original March of Dimes never had to confront. The Soviet vaccine campaigns of 1957-1960 and the global GPEI campaigns of the late 1980s were organized largely through centralized state infrastructures; the modern polio campaign is being delivered into a more pluralistic and contested media environment. Online misinformation about the Salk vaccine has circulated in various forms since the early internet era, including fringe claims that early production batches were contaminated with SV40, a simian virus present in the rhesus cell cultures of the 1950s — a claim now largely ruled out by subsequent epidemiology. Contemporary vaccine hesitancy draws much more on the politics of the COVID-19 era than on the actual history of polio. Enders, Weller and Robbins, who had worked with the goal of getting the world past a single terrifying childhood disease, would probably be surprised to find the public conversation about their achievement now one of many competing arguments about medical legitimacy.

The epidemiological and political picture remains unresolved. Polio is one of only two human diseases (alongside smallpox, eradicated in 1980) ever declared eradicated, and the only one to have reached that point with a single, mostly private philanthropic organization playing a leading role in the research and operational phases. It is also the only major human disease whose eradication campaign has been visibly rolled back in the 2020s by the partial success of its own vaccine. The Iron Lung that once terrified Philadelphia has been replaced by vaccine vials in cold-chain transport, and the panoptic mass vaccination campaign has been replaced by niche genomic surveillance — but in Karachi, in Kandahar, in Kinshasa, and in the suburban flats of London and New York where cVDPV has been found in recent sewage samples, the same war continues. The March of Dimes is now only one arm of a much larger and more diversified global health system; its archives remain the densest single-source documentary record of the core years. The polio vaccine story — which began on a hot Brooklyn day in 1916, which cracked in Boston in 1949, which was read out loud in Ann Arbor in 1955, which shuddered at Cutter’s factory floor in the same year, which travelled through Moscow and Cincinnati and Manila in the 1960s, and which continues to be written in Khyber Pakhtunkhwa — is in many ways the foundational myth of modern vaccinology. As this century’s vaccine controversies continue, that myth is being contested. The next chapter is being drafted in real time.