Greer Williams, Virus Hunters (1960)

No doubt many scenes which occurred in London during the great plague of 1665 were reenacted in our Long Island andWestchester towns. Under the sway of panic people looked with skepticism and suspicion on government health officers. The selectmen of many villages, whose doctors were struggling with the impossible and failing to stop the epidemic or save the individual case from paralysis, resorted to home-made martial law. Deputy sheriffs, hastily appointed and armed with shot-guns, patrolled the roads leading in and out of towns, grimly turning back all vehicles in which were found children under sixteen years of age. Railways refused tickets to these selected youngsters, the innocent victims of ignorance and despair. Indeed, the notion was firmly held that below the magic age, called sweet at other times, there lurked the dread disease, whereas above it no menace existed either for the individual or the community.

George Draper, Infantile Paralysis (1935)

The epidemic of 1916 will go down in history as the high-water mark in attempts at enforcement of isolation and quarantine measures.

John R. Paul, A History of Poliomyelitis (1971)

In the summer of 1916, while European armies battered each other senseless, New Yorkers were engaged in a very different kind of struggle. An invisible enemy was killing and crippling children, in particular, quite as effectively as bullets and shrapnel killed and maimed the infantrymen stumbling through the wire and mire of the Somme. On 1 July — day one of the Somme offensive — New York City's health commissioner, Dr Haven Emerson (a great-nephew of Ralph Waldo Emerson), was quoted in the New York Times as saying: `Our method of fighting the disease is this: whenever a case is reported in a block not previously affected, a house-to-house canvass of that block is made. In this way many unreported cases have been found. All cases are isolated at once ...'

    Since the outbreak started in the Italian community, immigrants became the scapegoats. According to the NY Times that same day, `There was a report yesterday that the disease had been brought to America by Italian immigrants,' though inquiries at the Quarantine Station at Ellis Island drew a blank: `no cases had been noticed among immigrants and ... Quarantine had no record of epidemics in any of the towns of Italy'. Yet the idea of a non-American source for such an unAmerican outbreak was too attractive for mere facts to be allowed to stand in its way. Haven Emerson himself favoured it. On 8 July, the NY Times reported him as saying that

since May 15 ... 90 immigrant Italians, including 24 children under the age of 10, had gone to live in Brooklyn, where the outbreak appeared, at about the date named. No symptoms of infantile paralysis were found among the Italians at Quarantine, but the Italian consul had been asked to ascertain whether the disease was present in any of the cities from which the immigrants came.

The next day, the health commissioner was again on the offensive. `Dr Emerson blamed the Brooklyn citizens themselves for whatever garbage there was in their streets. Brooklyn, he said, had not developed sufficient pride to keep its own streets clean.' Strict sanitary regulations were in force and reports of `violations of the Sanitary Code', leading to court cases and fines, appeared in the press with monotonous regularity. Yet the same report that spoke of Emerson's condemnation of Brooklyn's insanitary habits contained an unusually frank summary of the Department of Health's predicament:

In epidemics of typhoid fever and most other diseases the health authorities know exactly what to do. But fighting infantile paralysis consists largely in doing everything that seems effective in the hope that some of the measures taken will be effective?

This statement encapsulates Emerson and his colleagues' dilemma. The emphasis on hygiene was, in a sense, all that they knew: cleaning up New York could do no harm, and might well do good; whether it would radically alter the number of children, or indeed adults (since by no means all the victims were minors), stricken with poliomyelitis was a question to which they did not have the answer. But they could not afford to doubt; like the Scottish preacher who underlined a part of his sermon and wrote in the margin, `Weak point here, shout like hell', the authorities were relentless in enforcing sanitary measures.

    In response to a recommendation by an advisory committee of doctors, they ordered `the placarding of premises for poliomyelitis, a practice previously confined to smallpox, scarlet fever, diphtheria and measles'. And on 4 July the NY Times reported, `Commissioner Emerson and his lieutenants in the fight discussed yesterday a proposal for the police to compel every child in the city under 16 years of age to remain at home continuously for two weeks.' Fortunately for parents, this proposal was not adopted and playgrounds remained open, though an order to exclude children under sixteen from `moving picture shows' came into effect the next day.

    Even before the end of June, the Board of Health had passed resolutions increasing the period of isolation of patients from six to eight weeks, and demanding immediate hospitalisation of all those who could not satisfy stringent quarantine requirements in the home. This meant that the children of the comfortably-off could be nursed at home, while children from poor and overcrowded tenements had to be removed to hospital, despite the protests of their parents — not to mention their doctors. (The Department of Health recognised that `the administrative regulation of the disease implied not only interference with the personal liberty of the members of many households, but a sacrifice of important professional opportunities and income by the physicians to the poor, whose poliomyelitis patients were removed from insufficiently equipped homes to the hospitals'.) But keeping a child at home was not always an easy option, since quarantined premises were visited every other day by patrolmen of the so-called Sanitary, Squad, who ensured the regulations were upheld.

    Mrs Anna Henry, a nurse at a babies' clinic in Brooklyn, was so zealous in reporting cases of infantile paralysis and violations of the sanitary regulations in the Italian colony known as `Pigtown' that she received a `Black Hand' letter threatening her life and had to be escorted to and from work by police.

    Many mothers felt that sending their children to hospital was tantamount to condemning them to death or crippledom. They were hardly reassured by the information that suspected cases were kept separate from confirmed ones, and they protested against the forcible removal of their children. One woman in Brooklyn was reported in the New York Journal to be receiving medical attention as a direct result of a police raid on her house to remove her two-year-old nephew. Three policemen with drawn revolvers apparently burst into her room, tore the infant from her arms and passed him out of the window to a waiting surgeon.

    It was probably in response to such stories that Dr Emerson substituted nurses for policemen on ambulance duty. He told reporters that `trained women were more successful in persuading parents to let their children go to hospital'. But nothing could remove parents' fears. A social worker in a poor district reported to the social services committee of the Volunteer Hospital:

The mothers are so afraid that most of them will not even let the children enter the streets, and some will not even have a window open. In one house the only window was not only shut, but the cracks were stuffed with rags so that `the disease' could not come in. The babies had no clothes on, and were so wet and hot they looked as though they had been dipped in oil, and the flies were sticking all over them. I had to tell the mother I would get the Board of Health after her to make her open the window, and now if any of the children do get infantile paralysis, she will feel that I killed them. I do not wonder they are afraid. I went to see one family about 4 p.m. Friday. The baby was not well and the doctor was coming. When I returned Monday morning there were three little hearses before the door; all her children had been swept away in that short time. The mothers are hiding their children rather than give them up ...

One woman took the Department of Health to court for forcibly removing her child to hospital. The judge was sympathetic. In his summing-up, he said:

This good lady, the mother, tender, affectionate, cleaving to her child, wanting to have it at home was uncertain what she ought to do.... She was evidently confused by the conflicting opinions of the medical gentlemen with whom she ... came into contact ... The safeguards which are recognized as necessary to be thrown around a case of this particular disease, were taken down and removed by her, largely upon the opinion of ... Dr Smith and Dr Flynn, and naturally enough, too, because their opinions were in the line of her motherly affection and her motherly instinct, and in the line also of her personal desires as to herself, her children and others, that she should be free to receive anybody into the house and go into other houses and out upon the street, as though there were no communicable disease affecting the child.

Nevertheless, Mr Justice Garretson ruled in favour of the Board of Health, dismissing the suit.

    The sad story of `Paul Hughes, 5 years old, who lived with his parents at Great Kills, SI [Staten Island]', indicates the high level of collective hysteria engendered by the epidemic. Paul had fallen ill one night and his condition had so far deteriorated by dawn that his father sought medical attention:

Unable to obtain a physician, he put the boy into an automobile and drove to the Smith Infirmary at New Brighton, but the child died on the way and the doctors at the hospital would not receive the body, nor would they permit it to go in the hospital morgue for fear that infantile paralysis had caused death and might spread from the morgue to the hospital. Mr Hughes was unable to reach any Health Department official in the early morning, and he drove around Staten Island with the boy's body for hours looking for some one who would receive it. Thomas McGinley, an undertaker at Stapleton, finally communicated with the Department of Health in Manhattan and obtained permission for the father to leave the body at the department's disinfecting plant at Four Corners. Coroner Vail will hold an autopsy today to determine whether infantile paralysis caused death.

Another indication of the panic precipitated by this latter-day plague was the wholesale exodus from the city of the children of the well-to-do. On 5 July, the NY Times `conservatively' estimated that 50,000 of them had been sent out of New York `to places considered safe by their parents'; and on 7 July, `Reports of persons fleeing from town continue to come in.' Equally panicky was the response of several neighbouring states and communities, which took defensive action against the unwanted intruders. `Hoboken [New Jersey] led the way by isolating itself from the world, so far as new residents were concerned', the NY Times reported on 14 July.

Policemen were stationed at every entrance to the city—tube, train, ferry, road, and cowpath—with instructions to turn back every van, car, cart, and person laden with furniture and to instruct all comers that they would not be permitted under any circumstances to take up their residence in the city.

(Despite these precautions, the first case of infantile paralysis in Hoboken was recorded twelve days later.) On Tuesday 18 July, under the headline `QUARANTINE GUARDS ON ROAD', the NY Times informed its readers that `from noon Saturday until noon yesterday 150 families who attempted to enter Hastings-on-Hudson by train and automobile from New York were turned back by policemen stationed at every entrance to the village'.

    The Department of Health responded to pleas from the railroads and other transport organisations by issuing `health certificates, or more properly travellers' identification cards ... to those who presented themselves ... for medical inspection and could prove residence at an address from which no case of poliomyelitis had as yet been reported'. Dr Emerson attempted unsuccessfully to calm the public by repeating that there was `no cause for alarm' and that the epidemic appeared to be `on the wane'. (This was not true: the climax was not reached until the week beginning 5 August, during which 1,151 cases and 301 deaths from polio were recorded, though the worst single day was 3 August — the day on which Sir Roger Casement was executed for treason in England — with 217 new cases reported.) On Wednesday 19 July, 1,031 health certificates were issued to anxious parents and on the Thursday the number rose to 2,079. By then the US Public Health Service had taken over responsibility for the supervision of interstate travel, though the chaos continued. `Scenes in railroad and steamboat terminals of the city yesterday', the NY Times reported on Monday 24 July, `were indicative of the numbers going away and of the numbers returning against their will.' Emerson's policy of publishing in the newspapers' daily lists of the names and addresses of confirmed cases of polio can have done little to reassure an already jittery public.

    In the continuing search for scapegoats, black Americans were exonerated since `it has been found by the Department of Health that negro children are less susceptible to the disease than white children.' This was announced in early July. A week or so later it was reported that `Dr Ager [assistant health commissioner] has concluded that negro children are more or less immune and that the virus attaches itself more often to blondes than brunettes.' By 26 August, however, Haven Emerson was writing to the director of the Rockefeller Institute for Medical Research, Dr Simon Flexner:

Since the conference on Poliomyelitis on August 3rd and 4th, there has been such an increase in the number of cases of polio among colored people that the impression which I had at the time of our meeting and which I conveyed to you, I believe has been entirely dispelled, and it is apparent that the race incidence of the disease among colored people is not essentially different from its incidence among other racial groups in this city.

But the myth that black people did not get polio persisted.

    Cats and dogs were suspected of being carriers of the disease; strays were rounded up, and pets put down. In early July animals were being destroyed at a rate of `300 to 450 a day'. A headline in the NY Times for 26 July proclaimed `72,000 CATS KILLED IN PARALYSIS FEAR' and in Brooklyn, according to another account:

Much assistance was rendered the police by small boys, due to the circulation of a report that a bounty was to be paid on all the animals turned over to the authorities. Some stations were literally flooded with cats and small boys, the former demanding their liberty and the latter their money.

Unfortunately for the latter, the rumour of a payment of ten cents per head turned out to be false. (Perhaps it was put about by the police themselves to facilitate their task.)

    In any event, the wholesale slaughter of inoffensive animals was misguided. `The epidemiological evidence collected during the progress of this investigation', C.H. Lavinder, A.W. Freeman, and W.H. Frost of the US Public Health Service conclude, `lends no support to the idea of any relationship between paralytic disorders of animals and the occurrence of poliomyelitis in human beings.'

    Dr W.H. Frost's was one of the few voices of sanity to be heard during the epidemic. The NY Times reported him as saying that `the incidence of poliomyelitis is proportionately about the same among persons living under good conditions as among persons living under poor hygienic conditions'. He went on:

This practically eliminates from consideration as of great importance in the causation of the disease such factors as are intimately associated with poor hygienic conditions, insufficient and improper food, overcrowding, personal uncleanliness, and association with verminous insects."

Dr Charles Caverly, the health officer who had made a study of the first significant outbreak of infantile paralysis in America, which took place in Vermont in 1894, had made precisely the same observation in the Journal of the American Medical Association in 1896:

That the general sanitary surroundings and methods of living were in anywise responsible for the outbreak is ... more than doubtful, since the disease showed no partiality to that class of the population whose habits and surroundings are the most unsanitary. The so-called laboring classes were oftenest affected, but not out of proportion to their numbers ... general sanitary conditions did not seem to have any influence on the epidemic.

But three days after printing Dr Frost's words of wisdom, the NY Times reported, `"Clean-up" is being more persistently shouted at tenement house dwellers every day by public and private institutions.'

Two American doctors who wrote a textbook on `Infantile Paralysis' in the wake of the 1916 epidemic described it as `a disease of comparatively recent origin'. It was not the disease itself, but outbreaks of epidemic proportions that were of recent origin. An Egyptian stele, dating from the period 1580-1350 BC and depicting a young man with a withered leg leaning on a long staff, suggests that polio has been endemic since ancient times.

    The term poliomyelitis derives from the Greek words, polios, meaning `grey', and myelos, `matter', and refers to the grey matter of the spinal cord. The disease was called by many names in the nineteenth and early twentieth centuries, including: Dental Paralysis, Infantile Spinal Paralysis, Teething Paralysis, Essential Paralysis of Children, Regressive Paralysis, Myelitis of the Anterior Horns, Tephromyelitis (from the Greek tephros, meaning `ash-grey') and, most poetically, Paralysis of the Morning-after the way in which a child goes to bed apparently healthy, wakes feverish in the night and then is unable to get up in the morning. The number of names — and there were several others — reflects the confusion over the nature of the disease.

    Perhaps the earliest recorded case is that of Sir Walter Scott (born in Edinburgh in 1771), who was led to believe that he `showed every sign of health and strength' till he was about eighteen months old. Then:

One night, I have been told, I showed great reluctance to be caught and put to bed, and after being chased about the room, was apprehended and consigned to my dormitory with some difficulty. It was the last time I was to show much personal agility. In the morning I was discovered to be affected with the fever which often accompanies the cutting of large teeth. It held me three days. On the fourth, when they went to bathe me as usual, they discovered that I had lost the power of my right leg .... There appeared to be no dislocation or sprain; blisters and other topical remedies were applied in vain ...

The impatience of a child soon inclined me to struggle with my infirmity, and I began by degrees to stand, to walk, and to run. Although the limb affected was much shrunk and contracted, my general health, which was of more importance, was much strengthened by [my] being frequently in the open air, and, in a word, I who in a city had probably been condemned to helpless and hopeless decrepitude, was now a healthy, high-spirited, and, my lameness apart, a sturdy child ...

The first attempt at a clinical description of the disease was made by the English physician, Michael Underwood, in the second edition of his treatise on the Diseases of Children, published in 1789. He calls it `Debility of the Lower Extremities' and writes: `It is not a common disorder, I believe, and seems to occur seldomer in London than in some parts. Nor am I enough acquainted with it to be fully satisfied, either, in regard to the true cause or seat of the disease, either from my own observation, or that of others.' Nevertheless, he is inclined to attribute it to `teething and foul bowels'. Where both lower extremities `have been paralytic, nothing has seemed to do any good but irons to the legs, for the support of the limbs, and enabling the patient to walk'. (A later editor of Underwood's treatise, obviously unfamiliar with the flaccidity of the paralysis resulting from polio, comments parenthetically: `If the limbs are paralytic, how are irons to the legs to enable the patient to walk?')

The first account of an outbreak of the disease was written by a young doctor called John Badham, the son of a distinguished professor of medicine at the University of Glasgow. It took place in 1835 in Worksop, in north Nottinghamshire. There were four cases, described by Badham in meticulous detail. He comments on the `extraordinary youth' of all four patients; on the `cerebral symptoms', such as drowsiness or abnormality of the pupils of the eye; on the `remarkable [fact] that in no one instance has the health of the child been in any degree impaired'; and on the strabismus (squinting) apparent in one case, leading him `to suspect a cerebral complication, rather than a spinal one'. Unfortunately, the thirty-two-year-old John Badham died of consumption in 1840, the very year in which the first systematic investigation of poliomyelitis, written partly in response to his account of the Worksop outbreak, was published in Germany.

    Like Badham, Jacob von Heine draws attention both to the extreme youth of patients (six months to three years) and to their good general health (though he is referring to their health preceding the attack). But where Badham sees only `drowsiness', Heine recognises fever and pain in children during the pre-paralytic phase of the illness, which makes him think that the disease may be contagious, and far from suspecting `a cerebral complication, rather than a spinal one', he finds no cerebral involvement and concludes that all the symptoms `point to an affection of the central nervous system, namely the spinal cord'.

    In the matter of treatment (which had baffled Badham), Heine steered clear of fashionable nostrums such as purges, emetics, blisters and bleedings, and recommended `exercise, baths, and various simple surgical procedures, followed by the application of braces and apparatus'. As the historian of the disease and a leading participant in its `conquest', Dr John R. Paul of Yale University points out, `Considering the degree to which the handling of a given disease is wont to change over a period of 125 years, Heine's treatment of paralyzed limbs and the resulting deformities and disabilities of children has undergone remarkably little alteration.'

    In 1907 the Swedish paediatrician, Ivar Wickman, named the disease `Heine-Medin disease' after both the great German orthopaedist and the Swedish pioneer, Karl Oskar Medin, whose pupil Wickman was. Medin's involvement in an unprecedented outbreak of forty-four cases in Stockholm in 1887 led him to categorise various types of the disease — spinal, bulbar, ataxic, encephalitic and polyneuritic — as well as, crucially, to conclude that its acute phase consisted of two separate fevers, sometimes with a fever-free remission (what the American doctor George Draper mis-labelled the `dromedary form' — it is the Bactrian camel, not the dromedary, that has two humps). The initial fever was no more than a general malaise; it was the second attack that did the damage to the central nervous system.

    The significance of this finding was not lost on the young Ivar Wickman when he came to investigate the infinitely more serious Scandinavian epidemic of 1905, in which there were more than 1,000 cases. The questions that concerned him were: was the disease contagious and, if so, how was it spread — by direct contact with infected children, or by carriers of the virus who themselves showed no sign of infection? Others, including On Charles Caverly in his notes on the 1894 Vermont outbreak, had observed that there could be `abortive' or non-paralytic cases. Wickman's originality lay in suggesting that non-paralytic cases were both far more widespread than anyone had supposed and instrumental in spreading the disease. His experience of the 1905 epidemic convinced him that Heine-Medin disease was highly contagious, and that apparently healthy or only mildly affected persons played a key role in spreading it.

    Although he committed suicide at the age of forty-two, just two years before the New York epidemic, Wickman's historic monograph of 1907 earned him a place in the Polio Hall of Fame erected in 1958 at Warm Springs, Georgia, to celebrate the twentieth anniversary of the National Foundation for Infantile Paralysis (where fifteen doctors and scientists are honoured, along with the founders of the NFIP, Franklin D. Roosevelt and Basil O'Connor).

The end of the nineteenth and the beginning of the twentieth century was once considered a medical golden age, but has recently been dubbed `the Childhood of Scientific Medicine, a period of great stimulus and rapid growth, filled with the excitement of learning new things — and also filled with childish certainties'. Following Robert Koch's painstaking and brilliant work on anthrax, tuberculosis and cholera, and Pasteur's discovery of a rabies vaccine (a century after Jenner had started the whole business of vaccination by deliberately infecting people with cowpox as a preventive of smallpox), `Everybody, everywhere, tried to hunt microbes, see them, grow them, identify them, explain them, escape them. Their primary activity ... was finding and naming the causes of infectious diseases. It was the Day of Diagnosis.' The microbes being so assiduously hunted were largely bacteria, and the essential tackle needed for their capture included the microscope, dyes that highlighted the microorganisms, culture dishes, test tubes and some unfortunate laboratory animal to act as involuntary host. Bacteriology, or microbiology, was the name of this sport; virology had yet to be born.

    As far as microbe hunters were concerned, the only difference between bacteria and viruses was one of size. Bacteria were the organisms which would not pass through a porcelain filter; viruses the ones which would. If the filtration process succeeded in sterilising cultures of organisms, then they were bacteria; if not — and laboratory animals could be reinfected after filtration of the culture — it was called a virus. Bacteria became visible under the microscope if stained with certain types of dye; viruses, however, were too small to be seen, even through an optical microscope, and it was practically impossible to study them visually before the invention of the electron microscope in 1937.

    Despite the virtual invisibility of viruses, immunisation was first discovered in relation to a virus — smallpox — and the first two human vaccines (the second being rabies) were virus vaccines. But as John Rowan Wilson points out, `almost all the really productive developments in this field after the death of Pasteur until 1930 were in connection with bacteria. The reason for this lay in the technical difficulties of culturing the organisms'. In Vienna in 1908, Drs Karl Landsteiner and Erwin Popper discovered that the infectious agent for poliomyelitis was not a bacterium, but a `filterable virus' — as any micro-organism that passed through the porcelain filter came to be called. When Landsteiner and Popper injected filtered fluid taken from the spinal cord of a polio victim into the brains of two monkeys, both animals went down with the disease. Through their experiment, the two scientists not only established the cause of polio, but also set the pattern for future research, with monkeys as polio's primary `guinea pigs'.

    The importance of their discovery was widely recognised, not least by Simon Flexner in New York. Flexner had been appointed director of the newly established Rockefeller Institute for Medical Research in 1903 and had already successfully developed an antiserum (serum is the watery fluid left when blood coagulates and contains proteins called globulins which comprise antibodies) for cerebrospinal meningitis. In doing this, he had worked out one of `only about four big ideas [needed] in order to prevent human diseases via vaccination'.

The first big idea, at least two thousand years old, is that people who recover from certain infectious diseases are safe from a second attack. The second is that a scientist can find a suitable animal host, susceptible to the infection, that will manufacture virus for him in quantity. The third idea is that in such a host, or through some laboratory manoeuvre, the scientist can find a way of taming, stunning, or killing the virus so that it will still produce disease resistance but not the disease. The fourth idea is the use of antibodies in an immune serum — or antiserum, as it is also called — as a quantitative index for virus presence. This is called a virus-neutralization test.

The neutralisation test was originated by George M. Sternberg, a military doctor who was promoted to Surgeon General of the US army during Cleveland's presidency. It was already known that blood serum contained antitoxic properties in relation to bacteria, but Sternberg was the first to show that it was true for viruses, too. Following Sternberg's — and Landsteiner's — lead, Flexner `demonstrated in 1910 that the serum of monkeys convalescent from experimental [i.e. artificially induced] poliomyelitis contained antibodies, spoken of as "germicidal substances" — a finding that was made almost simultaneously by Landsteiner and others'.

Shortly after this, Netter and Levaditi [in Paris] and others also found these neutralizing substances in the blood of humans recovering from poliomyelitis. This demonstration of antibodies in convalescent patients was to prove another landmark in the therapeutic history of the disease. Its significance ranked almost on a par with the discovery of the virus, a fact unappreciated until some years later.

One of several sons of Jewish immigrant parents, Simon Flexner had had a distinctly unpromising childhood in Louisville, Kentucky. When he was ten, his father, Morris, had taken him along to the local jail as a tacit warning of what lay ahead of him if he did not mend his ways. But this visit filled the young Flexner with excitement rather than dread and he surprised his older brothers, who had gathered round to gloat over his humiliation, by saying that he had `had a swell time'. He left school at fourteen and was apprenticed to a plumber, according to one historian, who writes: `At the end of a week the plumber returned him to his father with the blunt evaluation that he was too dumb to be a plumber.' It is a good story, perhaps too good, since Flexner's son tells it rather differently:

Simon received a curt command to follow his father and was led into a plumber's shop. Morris pushed the boy forward and offered him to the plumber as an apprentice. The plumber said he did not need an apprentice. Morris went out and walked off, leaving the boy standing on the street.

Whichever version one accepts, there can be no doubt that during his adolescence Flexner was, in his own words, `in and out of wretched jobs leading nowhere'. It was not until he was apprenticed to a pharmacist that he found a sense of direction. After that, his rise was meteoric, through Johns Hopkins Medical School in its heyday and a professorship of pathology at the University of Pennsylvania to the Rockefeller Institute, whose first director he was — a post he held for more than thirty years. Considering the — perhaps disproportionate — influence he would have on medical research in the United States over three decades, it is worth noting that his initial medical education at the University of Louisville Medical School was a farce. Flexner recalls, `I did not learn to practice medicine, indeed, I cannot say that I was particularly helped by the school. What it did for me was give me the MD degree.' Appropriately enough, his own younger brother, Abraham, was to put an end to such anomalies by exposing them in his 1910 `Flexner Report' on Medical Education in the United States and Canada.

    Simon Flexner's lack of clinical competence and experience, combined with his belief that `medicine derived from such basic sciences as pathology, physiology, chemistry, and bacteriology', meant that his initial staff appointments to the Rockefeller Institute `were not of physicians interested in pursuing problems in clinical medicine, but rather of investigators skilled in the basic sciences who sought to cast light on medical problems through experimental research'. The success of the institute's experiments with monkeys in developing the antiserum for cerebrospinal meningitis, reducing the mortality rate from three in four to one in four, convinced Flexner of the validity of his methods and determined his approach to polio research, encouraging a degree of confidence which was scarcely justified by subsequent events.

    Initially, however, he succeeded in taking Landsteiner's work a crucial stage further by transferring poliovirus not just from humans to monkeys, but from monkey to monkey. (Others, including Landsteiner himself, also achieved this, but Flexner did it first.) When Flexner published his report, he omitted the word experimental from the title — a very significant omission, according to Dr John Paul:

Indeed this was a major mistake that was to dog Flexner's footsteps throughout his entire professional life — his failure to distinguish between certain aspects of experimental poliomyelitis in the monkey and the disease in man ... It was an error with unfortunate implications that were to influence thought at the Rockefeller Institute for a generation.

Paul compares Flexner's role as `laboratory doctor' unfavourably with the clinical investigations of a contemporary Swedish team headed by Carl Kling. Sweden had suffered another epidemic in 1911 (at nearly 4,000 cases the largest to date anywhere in the world), and Kling and his colleagues succeeded in isolating poliovirus from living patients — not just from those who had been paralysed, but from abortive cases as well, thus confirming Wickman's theories about the way the disease spread. From autopsies they also made important discoveries of the sites in the body favoured by the virus other than the central nervous system, where the damage was done; as they expected, they found it in the throat, but they were surprised to find it in the intestinal wall as well. This caused them to ponder such key questions as how the virus entered the body and how, once there, it penetrated the central nervous system. They did not come up with all the answers but, by combining clinical and laboratory techniques, at least they were asking the right questions.

    A news item in the New York Times of 9 March 1911 suggests that Simon Flexner was so confident of the rectitude of his approach that he was not looking to the Swedes or anyone else for help in solving the mysteries of polio:

The Rockefeller Institute in this city believes that its search for a cure for infantile paralysis is about to be rewarded. Within six months, according to Dr Simon Flexner, definite announcement of a specific remedy may be expected.

`We have already discovered how to prevent the disease,' says Dr Flexner in a statement published here today, `and the achievement of a cure, I may conservatively say, is not now far distant ...'

No cure for polio has ever been achieved and more than forty years would elapse before a safe and reliable method of prevention was developed.