Polio – A Shot in the Dark

RTB presents a reprint of Janine Robert’s ground-breaking presentation of the story and data of the first great success of the modern pharmaceutical era: The Polio Vaccine. What is revealed beneath the gloss of press releases and public hagiography is story that leaves you wondering if anything the public health authorities tell us is actually, factually true – or if it is all in service of a kind of modern church of scientism.

You can read Janine Robert’s work at Fear of the Invisible.com and the Polio Myth. In her work, Roberts followed the trail blazed by researcher Jim West, who is a pioneer in detailing the hidden history of the US polio era and medical-scientific response. His website is Here.

Polio: The Virus and The Vaccine – Part 1
The Ecologist
Date:01/05/2004
Author:Janine Roberts

There is a rarely mentioned epidemic raging in the world today, one that is crippling children in more than 100 countries. In extreme cases the disease starts with a fever, which is followed by vomiting, delirium and spreading pain. Within days of being infected, the motor-neurone cells in victims’ spines cease to function properly. Pain intensifies as victims’ limbs are paralysed.

In the very worst cases, their chests are also paralysed, which prevents them from breathing. Even when the children recover, the illness often returns in later life. Health authorities say it has no cure. The number of cases increased by over 250 per cent worldwide between 1996 and 2003. It is a disease with a long history and many names. The condition’s official name now is ‘Acute Flaccid Paralysis’ but it was once known as ‘infantile paralysis’/ ‘poliomyelitis’ (polio for short). Some people called it ‘the crippler’.

A shot in the dark

Polio is a devastating disease; the preferred method for fighting it is vaccination. Yet there is a mass of historic evidence that suggests it is not caused by a virus but by industrial and agricultural pollution.

During the first half of the 20th century infantile paralysis surged like a bush fire, moving from place to place, afflicting large numbers of children, but only in the industrialised West. Prior to these outbreaks it affected very few and was often called ‘palsy’. In the 19th century scientists gave it the name ‘poliomyelitis’, referring to the inflammation of the grey nerves of the spinal column in cases of paralysis. Poisonous metals were suspected of causing this disease, particularly lead, arsenic and mercury. In 1824 the English scientist John Cooke stated: ‘The fumes of these metals, or the receptance of them in solution into the stomach, often cause paralysis.’

In 1878 the link between palsy and toxins was strengthened when Alfred Vulpian found that dogs dosed with lead suffered the same damage in their motor-neurone cells as found in the human victims of infantile paralysis. The Russian Popow discovered in 1883 that the same damage could be done with arsenic. This should have sent shockwaves through the medical establishment as the arsenic-based pesticide Paris Green had been widely used since 1870 to stop Codling moth caterpillars ruining apple crops. But strangely it didn’t.

In 1892 Paris Green was replaced in Massachusetts by the more toxic pesticide lead arsenate. Two years later the first recorded epidemic of infantile paralysis struck in Massachusetts’ neighbouring state of Vermont. The outbreak was investigated by Dr Charles Caverly, who reported that it was probably caused by a toxin rather than a micro-organism. Caverly said: ‘It usually occurred in families of more than one child, and as no efforts were made at isolation it was very certain it was non-contagious.’

Lead arsenate rapidly became the principal pesticide used on fruit and berries throughout the industrial world. In 1907 calcium arsenate was introduced for use primarily on cotton crops and in cotton mills. A year later 69 healthy children suddenly fell paralytically ill in Massachusetts. They lived in a town with three cotton mills, and in settlements downstream from those mills. Nearby there were also orchards on which lead arsenates were almost certainly in use. They were also living only a short distance downstream from the location of the Vermont outbreak.

A further epidemic in Massachusetts in 1908 caused enormous public concern, but, despite the evidence that exposure to toxins might have been responsible, the investigating health officials overlooked the newly introduced pesticides; they thought them essential to their war against viruses and bacteria – and to the financial health of the agricultural industry. Thus, the children paralysed in Massachusetts were not treated with toxin antidotes to see if these would benefit them. Instead, parents were advised to keep their children clean while the scientists, distracted by the then brand new theory that all epidemics had to be caused by infectious germs, looked for the virus ‘responsible’.

In 1908 two scientists working in Austria, Karl Landsteiner and Erwin Popper, reported that they might have found an ‘invisible virus’ that had caused these epidemics. They had made their discovery, they claimed, after making a suspension in water of minced diseased spinal cord from a nine-year-old victim of infantile paralysis. They had tested this noxious suspension by injecting one or two cups of it directly into the brains of two monkeys. The monkeys fell severely ill (as might have been predicted). One died and the other had its legs paralysed. The scientists then dissected the monkeys and found damage in their central nervous tissues similar to that found in human cases of infantile paralysis.

Today the World Health Organisation (WHO) still credits Landsteiner and Popper as having found the poliovirus with this experiment. Why it does so is inexplicable. The fluid they injected must have contained much human cellular debris, any toxins involved in the child’s illness, and probably several kinds of viruses. So, it was no wonder the monkeys fell so desperately ill. Such a soup could in no way be considered an ‘isolate’ of the tiny organism we now call a virus. It was also strangely non-infectious for a so-called virus, for the monkeys were not paralysed when made to drink it or when one of their limbs was injected with it, nor did they pass it on to other monkeys. The experiment, in fact, shed no light on what had paralysed the monkeys, and for that matter, the children.

Nevertheless, the following year Simon Flexner and Paul Lewis of the illustrious Rockefeller Institute for Medical Research in the US ‘proved’ a similarly made noxious soup was ‘infectious’ by injecting it into the brain of one monkey. They then extracted some fluid from its brain, injected this into another monkey, and so on through a series of monkeys, paralysing all of them in the process. Flexner and Lewis reported: ‘We failed utterly to discover bacteria… that could account for the disease [paralysis]… The infecting agent of epidemic poliomyelitis [probably] belongs to the class of the minute and filterable viruses that have not thus far been demonstrated with certainty under the microscope.’

In other words, we’ve injected a cocktail of viruses, cellular debris and DNA into a series of monkeys, and we believe that a virus, not yet identified within this noxious cocktail, is responsible! The procedure of Flexner and Lewis was just as dubious as their conclusion: they took no account of the contaminants in their mashed-up soup; they presumed what happened in monkeys would be replicated in humans; and surprisingly, given the evidence around at the time, they didn’t inject samples of cyanide or lead into the brains of monkeys to see if they also caused paralysis. In 1910 neonatologist L Emmett Holt reported: ‘Even five years ago if anyone had suggested that the disease under discussion was an infectious or contagious one, it would have been looked upon as a joke.’

Nevertheless, this crude science inspired a 40-year hunt for the infantile paralysis virus. All kinds of biological materials – spinal cord, brain, faecal matter, even flies – were ground up and injected into monkeys’ brains to try to induce paralysis.

Meanwhile, US president Franklin D Roosevelt, himself a victim of infantile paralysis, set up in 1938 the National Foundation for Infantile Paralysis (NFIP). The NFIP promptly decided that there was no cure for those already suffering from the disease. It would also refuse to examine reports of successful treatment involving antidotes against toxins. It instead focused on raising money for vaccine research by releasing stories about the horrors of infantile paralysis. The worst cases were indeed frightening: some victims had to be placed in ‘iron lungs’ to help them breathe.

This advertising drive was sensationally successful, effective both in raising money and in spreading fear of the poliovirus, especially among parents. But the authorities had little immediate help for them. They simply advised them to keep their children clean, away from places where infections could be passed on, such as public swimming pools, and to kill flies. The zeal of the parents was encouraged by advertisements showing giant flies attacking children.

While the poorer families responded by swatting flies and using more soap and water, the more affluent tried to turn their homes into sterile zones by constantly spraying them with insecticides. But these sprays proved useless. And what was even more peculiar was that doctors reported the disease was affecting mostly the children from better-off families – especially those who ate the most fresh fruit. People thus started to call the disease ‘the middle-class plague’. All this was so utterly inexplicable that parents were left feeling helpless and despairing.

By the end of the 1930s the vaccine scientists had tested various ‘viral isolates’ from infected monkey brains, but when these isolates were fed orally to monkeys the animals did not fall ill. This was most puzzling. The monkeys produced antibodies afterwards, so some virus must have harmlessly infected them. The only way the scientists found they could create a version of infantile paralysis in the monkeys was by injecting large quantities of the ‘virus’ suspensions directly into their brains.

In 1941 the work of the virus hunters received a potentially fatal setback. Dr John Toomey reported in The Journal of Pediatrics that it was not passed between individuals ‘no matter how intimately exposed.’ If the disease was non-infective, then it could not be caused by a virus and thus a vaccine would not work.

Other holes started to appear in the virus theory. During WWII army doctors found widespread immunity to the suspected poliovirus, and no evidence of infantile paralysis epidemics, in the Middle East, Asia and Africa. In Turkey they found people who called infantile paralysis ‘the American disease’. The doctors were surprised: immunity to the virus presumably meant that it had infected the population. So, how come it caused no epidemics in these countries?

However, the scientists racing to find a vaccine were so convinced that a virus was to blame that they effectively disregarded any evidence to the contrary. Among these it seems was Jonas Salk. In 1947 he found among the debris and toxins of ‘viral isolates’ from monkey brain experiments what he believed to be the poliovirus. Although he had not proved that this could cause polio in humans, he hoped he could use it to make a vaccine. But the highly respected bacteriologist Claus Jungeblut thought otherwise. He observed that such ‘viral isolates’ did not create in monkeys the same disease as found in human cases of infantile paralysis.

He concluded: ‘The highly specialised … virus which has been maintained in the past by intra-cerebral passage in rhesus monkeys is more likely a laboratory artefact than the agent which causes the natural disease in man’. In other words, the ‘virus’ found by the vaccine scientists probably did not exist in the wild but was a product of their experiments.14 If he were right, the consequences were vast. It could mean that the ‘isolates’ used by Salk to make a vaccine injected into over a hundred million people, had no relationship to the human disease it was supposed to counter.

Then, in 1948 Gilbert Dalldorf and Grace Sickles of the New York Department of Health triumphantly claimed that they had found the virus in the excrement of paralysed children. They had spun a sample to remove larger particles, diluted it and injected it into the brains of mice. The animals unsurprisingly became dangerously ill and paralysed.

The news of Dalldorf and Sickles’ experiment was nevertheless welcomed by the vaccine scientists. Up to now they had struggled to find the poliovirus in human spinal tissue. It would now be vastly easier to collect the poliovirus they believed they had identified from human excrement than from human spinal tissue. But why was it so hard to find it in the nerve cells in the spinal column that it supposedly damaged – that is where it had to be, if it really were the cause of infantile paralysis?

In 1951 they discovered a reason why. Quite simply, it was not always there. Instead a different virus might be present eg the Coxsackie virus. This news was grimly received. Their planned polio vaccine would not work against the Coxsackie. There was ‘some feeling of dismay … [this] added one more problem to the nebulous conditions surrounding poliomyelitis… the more we learn about poliomyelitis, the less we know,’ wrote AL Hoynel in the journal The Medical Clinics of North America. A Lancet editorial in the same year said this discovery brought ‘a crop of new snags’ to developing a vaccine.

Soon they discovered that it was possible for many different viruses to be present in these damaged nerve cells. If toxins caused the disease, this would be easy to explain. Many kinds of viruses are attracted to toxin-damaged cells. More bad news for the polio vaccine scientists. The public expected them to deliver vaccines that would stop the epidemics, but it was now evident that their polio vaccines would, at the very best, only prevent some cases, the ones with their poliovirus present.

And yet despite all the doubts and contrary findings, the vaccine research continued. In 1949 John Enders and Thomas Weller discovered how to grow the poliovirus in cell cultures, rather than only in the brains of living animals. This made possible the commercial production of virus-based vaccines. Then it was discovered how to grow their poliovirus on cheap monkey kidney and testicle cells. Monkeys soon became the ‘growing bed’ for the virus. They would be trapped, imported and slaughtered by the hundreds of thousands to make the polio vaccines, and are still caught in the wild today for the purpose of testing the UK vaccine.

By 1954 Salk had his polio vaccine ready for testing. (He confessed to ‘sacrificing’ some 17,000 monkeys in the process of developing it) He based the vaccine on his theory that children would gain immunity to living poliovirus if dead poliovirus were injected into them. He hoped our sensitive immune system would react by creating antibodies to these viral corpses that would also protect us against living wild poliovirus. To kill the virus he poisoned it with formaldehyde before putting it into his vaccine.

In 1954 he tested this concoction on more than 400,000 US children. It was reported afterwards that ‘only’ 112 of the children who received three jabs of his vaccine contracted polio within the next few months. Salk judged his experiment a success. But his safety-test results omitted all cases of children who were paralysed after one or two doses of the vaccine – or within two weeks of taking the third dose. These were counted as cases of polio in the non-vaccinated control group and thus in my view cast doubt on the validity of his results, for it made it impossible to tell just what impact his vaccine had had. It could have been that many of the cases of polio in the control group were caused by one dose of his vaccine – there was nothing in the published accounts I have seen to say that this was not so.

Salk claimed that his vaccine protected ‘30 to 90 per cent’ of those who received it (a remarkably vague statistic). But more than 60 per cent could have been immune already, at least according to the theory of the US federal agency the Centers for Disease Control and Prevention (CDC) that working-class children were already immune as a result of exposure to the virus in dirt. It is not known if Salk ever checked to see if children were already immune before he vaccinated them, but Hilary Koprowski reported in 1957 that the inhabitants of the Congo were 85 per cent immune before they ever saw a dose of polio vaccine. (Amazingly this didn’t stop Koprowski. He went on to uselessly administer to them hundreds of thousands of doses of his experimental vaccine.)

The Salk vaccine could have been derailed if a 1954 report by Dr Bernice Eddy, the scientist in charge of the US government safety-testing lab, had been taken seriously. Eddy stated that when she tested the Salk vaccine it caused severe paralysis in monkeys. She photographed the diseased monkeys, took these photos to her boss – and was reprimanded as an alarmist. She was not sure what it was in the vaccine that caused the paralysis: was it a virus, cellular debris or a toxin? Something quite deadly was clearly present. (One year later, after her warnings proved true, she was stopped from working on polio.)

On April 12 1955, Salk’s polio vaccine was pronounced totally safe and effective in providing complete protection against poliomyelitis (infantile paralysis), when it was launched by the National Foundation for Infantile Paralysis before an invited audience of 500 doctors and 200 journalists. The launch ceremony was relayed by closed-circuit television to some 54,000 doctors in cities throughout the US and Canada.

Salk was immediately awarded a Congressional Medal by US president Dwight Eisenhower. Church bells were rung in celebration of Salk’s victory. In The Manchester Guardian, Alistair Cooke wrote: ‘Nothing short of the overthrow of the Communist regime in the Soviet Union could bring such rejoicing to the hearts and homes in America as the historic announcement last Tuesday that the 166-year war against poliomyelitis is almost certainly at an end.’

Medical Fraud

The triumph following the launch of the Salk vaccine was short-lived. The medical historian Dr M Beddow Baily recorded what happened next: ‘Only 13 days after the vaccine had been acclaimed by the whole of the US press and radio as one of the greatest medical discoveries of the century, and two days after the British ministry of health had announced it would go right ahead with the manufacture of the vaccine, came the first news of disaster. Children inoculated with one brand of the vaccine had developed poliomyelitis. In the following days more and more cases were reported, some of them after inoculation with other brands.’

Within two weeks of the launch the number of cases of polio in vaccinated children had nearly reached 200. This created near panic in the White House. President Eisenhower had publicly endorsed the vaccine at its launch, so he sent the US health secretary Oveta Hobby to make it very plain to the Surgeon General that the president needed to be spared the embarrassment of further such cases.

On 8 May 1955 the Surgeon General suspended the entire US production of the vaccine. After hurried meetings between Salk, manufacturers and the surgeon general, distribution of the vaccine was resumed five days later, with new regulations in place to ensure better standards in the vaccine laboratories. The general consensus was that these cases had been caused by viruses in the vaccine that had survived the formaldehyde, despite evidence that repeated injections can cause paralysis.

However, despite these new regulations, four months later more than 2,000 cases of infantile paralysis were recorded in Boston, despite the vaccination of 130,000 children in the city. The previous year it had seen only 273 cases. The number of cases doubled in vaccinated New York State and Connecticut, and tripled in Vermont. They increased by five times in both Rhode Island and Wisconsin. Many were paralysed in the injected arm.

It seemed that the vaccine would soon be totally discredited. So, to protect the President, Salk, the vaccine manufacturers and themselves from the humiliation of an unmitigated failure, the US health authorities had to dramatically slash the incidence of poliomyelitis. They managed this by simply changing the way they recorded the incidents of poliomyelitis. It worked like this:

Prior to 1956, the authorities recorded a patient as having paralytic polio (infantile paralysis) if they suffered from paralytic symptoms for 24 hours.

After 1956 patients had to have these paralytic symptoms for at least 60 days to be counted as having polio. As many people recovered within 60 days, this measure alone dramatically cut the official number of cases. This ‘drop’ in polio cases was publicly credited to the vaccine. Furthermore, all cases of polio occurring within 30 days of vaccination (such as the first 200 cases that had so alarmed the White House) were in future not to be blamed on the vaccine but to be recorded as ‘pre-existing’.

But Salk continued to worry. Despite its regulatory and statistical ‘success’, the reputation of his vaccine was plummeting. In June 1955 the British doctors’ union the Medical Practitioners’ Union wrote: ‘These misfortunes would be almost endurable if a whole new generation were to be rendered permanently immune to the disease. In fact, there is no evidence that any lasting immunity is achieved.’

The following month Canada suspended its distribution of Salk’s vaccine. By November all European countries had suspended distribution plans, apart from Denmark. By January 1957 17 US states had stopped distributing the vaccine. The same year The New York Times reported that nearly 50 per cent of cases of infantile paralysis in children between the ages of five and 14 had occurred after vaccination.

So, more regulatory and statistical changes were needed in order to give the polio vaccine the appearance of a triumph of modern medicine. What better way to achieve this than to reclassify all the cases of polio into numerous other diseases resulting in a massive reduction in polio cases, and a host of other diseases to attract funding. And this is exactly what they did.

Prior to 1958 the definition of infantile paralysis (polio) included cases in which paralysis was minimal: perhaps manifesting itself as a very stiff neck, often accompanied by widespread pain. Polio also included cases of ‘meningitis’, or of inflammation of the membrane that protects the brain and spinal neurons. The CDC describes such cases as ‘serious but rarely fatal’.

Prior to 1958 these cases were scientifically referred to as ‘non-paralytic poliomyelitis’, or polio for short. Henceforward, they would be reclassified. The Los Angeles County health authorities stated: ‘Most cases reported prior to July 1 1958 of non-paralytic poliomyelitis are now reported as viral or aseptic meningitis.’ The incidence of meningitis soared as official polio cases declined, as the following table (compiled from national surveillance reports) shows.

Non-paralytic polio cases | Aseptic meningitis cases:

  • 1951-1960:    70,083 | 0
  • 1961-1982:    589       | 102,999
  • 1983-1992:   0            | 117,366

(Jim West, Images of Poliomyelitis)

These classifications are still used today. Last year the US National Center for Infectious Diseases reported no cases of poliomyelitis but 30,000 to 50,000 cases of aseptic meningitis requiring hospitalisation. There are probably several times this number of incidents of aseptic meningitis that did not require hospitalisation, but statistics are no longer kept for such cases.

Then another scam was enacted to massage down the poliomyelitis figures. It took advantage of the 1951 discovery that different viruses could be present in cases of infantile paralysis. Prior to 1958 this did not matter. A doctor diagnosed a person with polio by taking note of their evident symptoms. They did not investigate to see if the poliovirus were present. In 1958 a new regulation was put in place requiring doctors to only register a patient as having polio if the poliovirus were present, something that was very difficult to establish for sure. For a start, it was impossible to tell by looking at symptoms. The Textbook of Child Neurology reported: ‘Coxsackie virus and echoviruses can cause paralytic syndromes that are clinically indistinguishable from paralytic poliomyelitis.’ This new requirement for doctors caused a vast drop in the number of cases registered as poliomyelitis – a drop that ever since has been credited solely to the vaccine.

So, when patients diagnosed as having polio in a 1958 epidemic in Detroit were re-tested as required by this new rule, 49 per cent were found to have no poliovirus. They had to be reclassified as having ‘non-poliomyelitis acute flaccid paralysis’ even though they were suffering from symptoms identical to poliomyelitis with the same paralysis and the same pain. Other polio cases were reclassified as ‘Guillian-Barré syndrome’, which some researchers now think is what crippled Roosevelt. Yet more cases are now referred to as ‘Hand, Foot and Mouth Disease’, which can also cause paralysis. And last year the Coxsackie virus was found in cases of Chronic Fatigue Syndrome (CFS), which sometimes shows polio-like symptoms of muscle damage; in the past CFS might have been classified as a form of polio.

If this process of reclassification had not occurred, it would have been impossible to hide the fact that infantile paralysis cases had sharply increased after the introduction of Salk’s vaccine. Without the Coxsackie and aseptic meningitis reclassifications, for example, the number of reported cases of paralytic polio would have doubled from 2,500 in 1957 to 5,000 in 1959.

This deliberate fraud did not go entirely unnoticed, however. Dr Bernard Greenberg, the then head of the Department of Biostatistics at the University of North Carolina, testified at a 1962 Congressional hearing that infantile paralysis cases had increased after the introduction of the vaccine by 50 per cent from 1957 to 1958, and by 80 per cent from 1958 to 1959. He concluded that US health officials had manipulated the statistics to give entirely the opposite impression.

Milk paralysis

Many infantile paralysis outbreaks between 1905 and the 1940s would be linked by doctors to supplies of contaminated milk, including one in 1927 in Broadstairs in Kent. The Broadstairs outbreak was fairly typical. It affected institutions such as boarding schools that had little contact with each other, but which took milk from a common source. These epidemics ended when suspected milk supplies were stopped. Lead arsenate was being used as a cattle dip, but the formaldehyde that used to be added to milk to prolong its ‘shelf life’ may also have been responsible. (In 1897 The Australian Medical Gazette reported that formaldehyde in milk had caused several cases of paralysis.)

Vaccine Paralysis

1 Muscles can be poisoned and paralysed by being repeatedly injected with vaccines or antibiotics; this is now called ‘provocation paralysis’, and was no secret in the 1950s. In 1952 vaccinations had been suspended for the summer in the UK and US (the ‘infantile paralysis season’) as the injected arms of many children had been paralysed. The Lancet had reported: ‘Clinically, the cases associated with recent immunisations were indistinguishable from the acute cases of paralytic poliomyelitis.’ By 1955 US children were receiving three injections with Salk’s polio vaccine, as well as the smallpox and whooping cough vaccines.

2 Also, the Salk vaccine was far from pure. We now know that it was contaminated with a small amount of formaldehyde and viral debris.

What are viruses?

The pharmaceutical industry makes vast profits by exploiting paranoia about viruses, so it is important to understand just what viruses are. When viruses were first discovered they were presumed to be enemies. (The word ‘virus’ is Latin for ‘poisonous fluid’.) This was a serious misconception.

We now know that human bodies need and create viruses. Our cells contain tiny molecular engineers, known as transposons, which cut and adapt our DNA. Sometimes we may need to send genetic code from one cell to another – perhaps so as to resolve genetic problems or to deal with toxins. Cells can do this by turning transposons into messengers that carry genetic code from cell to cell. Traveling transposons are called ‘endogenous’ viruses: we manufacture them ourselves. They are essential to our genetic information highway. We make millions of such viruses.

Other viruses are ‘exogenous’: they originate from outside the human body. They must enter (infect) cells in order to ‘reproduce’. Some kill the cells they use to do this – others do not. If they are viruses that we have never met before, then they are more likely to be dangerous to us. Such a virus has recently been found present in 85 per cent of all cases of a cancer, mesothelioma, which is caused by asbestos. This virus, SV40, seemingly makes this toxin more dangerous to us, by switching off a human gene, p53, which protects us against cancer. And yet many exogenous viruses also do us no harm. We sometimes welcome them by making their genetic code part of our DNA. As such these harmless viruses are likely to have been around humanity for a long time. We have become adapted to each other.

Polio: are pesticides to blame?

Endocrinologist Morton Biskind said the spread of polio after WWII was caused by the ‘most intensive campaign of mass poisoning in human history’ – the spraying of some 3.1 billion pounds of pesticides.

The first epidemic of poliomyelitis in a tropical nation was contemporaneous with the introduction of the pesticide DDT in that country. Towards the end of WWII, US military camps in the Philippines started to be sprayed daily with DDT in order to kill flies. Writing in The Journal of the American Medical Association two years after the war, Albert Sabin reported that poliomyelitis became, after conflict, the major cause of death among the troops stationed at these camps. And yet unsprayed neighbouring populations were not affected by the disease. At the end of the war, the US military’s stocks of DDT were sold onto the public – despite the gravest warnings from establishment scientists.

In 1944, the US federal research centre the National Institutes of Health reported that DDT damaged the same part of the spinal cord (the anterior horn cells) that is damaged in infantile paralysis. Endocrinologist Dr Morton Biskind further described in 1949 how DDT caused ‘lesions in the spinal cord resembling those in human polio in animals’. He commented: ‘Despite the fact that DDT is a highly lethal poison for all species of animals, the myth has become prevalent among the general population that it is safe for man in virtually any quantity. Not only is it used in households with reckless abandon so that sprays and aerosols are inhaled, the solutions are permitted to contaminate skin, bedding and other textiles.’ The same year in Germany, Daniel Dresden found that acute DDT poisoning produced ‘degeneration in the central nervous system’ that seemed identical to that reported in severe cases of infantile paralysis.

Yet DDT was used to replace lead arsenate as a pesticide in fruit farming and with which to wash dairy cows. Heavy levels of DDT were soon reported in milk supplies. The organochlorine pesticide DDE (which is several times more dangerous than DDT) was also widely used in the US. Both were known to penetrate the blood-brain barrier that protects the human brain from viral invasion. Housewives were actually advised to spray DDT to stop infantile paralysis. Children’s bedrooms had wallpaper pre-soaked in DDT. Epidemics of infantile paralysis started to occur every year.

By 1952 the number of cases of infantile paralysis was three times higher than the figure for 1940.

Biskind treated over 200 patients affected with such neurological disorders. He found that many of these patients recovered when foods contaminated with pesticides were removed from their diets; this applied particularly to milk products. Biskind found high concentrations of DDT in butter purchased in New York. In 1949 he wrote: ‘Though it was originally observed in 1945 that DDT is absorbed through the skin, accumulates in the body fat and appears in the milk of animals, it has recently become almost universal practice to spray cattle with DDT… Although young animals are much more susceptible to the effects of DDT than adults, so far as the available literature is concerned, it does not appear that the effects of such concentrations on infants and children have even been considered.’

Despite the official complacency about substances like DDT and DDE, a few doctors did consider the effects of toxins. Some reported successfully treating paralysed patients with dimercaprol, an anti-toxin that is still used in hospitals since it ‘binds’ heavy metal poisons such as arsenic and lead and renders them non-toxic. In 1951 Dr Irwin Eskwith reported successfully using dimercaprol to cure a child suffering from bulbar paralysis, the most severe form of infantile paralysis. A medical journal also reported that 17 acute cases of polio were cured after treatment with very large doses of another anti-toxin – ascorbic acid.

3 thoughts on “Polio – A Shot in the Dark

  1. I 1947 I had polio menengitis in the brain and spinal chord.
    I was told then that only two people in the U.S. survived the desease that year.I and a girl in L.A. My repecustuions from the desease were not physical but psychological. I would like to know if the facts that were told to mme are true that i and that girl were the only two who survived that particular polio infection

  2. RTB presents a reprint of the great Neenyah Ostrom’s seminal article on polio, asking all the right questions.

    Was there a particular ‘virus?’ What were the environmental and toxicological factors at work? What were the laboratories doing to demonstrate that they had a ‘virus’ and not a toxicological poisoning?

    Poliovirus Isolation:  No Evidence
    Originally this article was online at chronchronicllnet dot org.  That site is now defunct, and so I have posted the article here, as a public service.
    Howard Urnovitz, Ph.D., microbiologist, referred me to this study of poliovirus isolation during our meeting at the office of Nicholas Regush, ABC headquarters, in Manhattan, April 2001.  Howard is the authority behind this article, which, by the way, was published one year after publication of my DDT/polio article in Townsend Letters, 2000.

    Will The Poliovirus Eradication Program ?Rid the World of Childhood Paralysis?
    With So Little Poliovirus Detected Around the World, What Is Causing Today’s Outbreaks of Acute Flaccid Paralysis?
    By Neenyah Ostrom ?(NONYN@aol.com)?April 20, 2001

    Every child of the early ’50s surely remembers the polio panics that swept the nation, invariably during the hottest days of summer, closing public pools and resulting in doctor visits at the first sign of a stiff neck or leg prone to falling asleep. My memory of the terror induced by the whispered word “polio” resides in a spot in the pit of my stomach just distal to the one recalling the Cold War era duck-and-cover drills we practiced in grammar school.
    In retrospect, it seems darkly hilarious that we ever believed plywood desks and plump little arms would protect school children from a nuclear attack. Our not-quite-rational fear of the poliovirus, however, endures despite World Health Organization eradication programs in the corners of the developing world where poliovirus is thought to lurk. One reason for this lingering concern is the continuing prevalence of acute flaccid paralysis, polio’s most crippling symptom that can leave its victims unable to control entire muscle groups, even those that allow us to breathe.

    Worldwide polio-related public health alarms sounded on the first day of 2001 when a new epidemic was reported to have broken out on the island of Hispaniola, on which Haiti and the Dominican Republic are located. David Brown reported in the Washington Post that a “mutant” poliovirus, derived from strains present in the oral polio vaccine, appeared to have run amok on this Caribbean island during the latter half of 2000.3
    When the US Centers for Disease Control and Prevention (CDC) examined these cases, another mystery was revealed: Only about one-third of the paralysis cases were associated with poliovirus. The CDC identified 19 individuals in the Dominican Republic who developed acute flaccid paralysis (AFP, the hallmark symptom of poliovirus infection as well as a syndrome unto itself) between July 12 and November 18, 2000. However, poliovirus was detected in only six of those individuals. The cause of the other cases of paralysis remains unknown.25

    The mystery deepens when we examine World Health Organization (WHO) statistics on AFP and poliovirus infection in the Dominican Republic for the last several years.  Although the number of cases of AFP in the Dominican Republic from 1996 to 1999 range from 4 to 24, not a single case of poliovirus was detected.
    If we further examine other WHO statistics on poliovirus-associated AFP and those in which the virus is not detected, a striking fact becomes clear: Most acute flaccid paralysis diagnosed around the world today is NOT associated with poliovirus.
    This fact raises new, disturbing questions, including whether there ever was  an epidemic of poliovirus infection in the United States and Canada. There was a greatly increased prevalence of AFP, to be sure, during which many children (and some adults) tragically were paralyzed or died. Since many of those cases showed all the hallmarks of a typical poliovirus infection fever, stiff neck and back, severe headache, muscle pain, sore throat and, in severe cases, paralysis and occurred in clusters, they were assumed to be caused by the easily-transmitted poliovirus.

    But were they? If not, what is the cause of so much misery today in areas of the world least-equipped to be able to deal with it? Is it correct to assume that poliovirus causes most cases of paralysis?

    What Is Poliomyelitis?

    The word poliomyelitis comes from two Greek words:  polio, which means gray, and myelitis,  inflammation of the spinal cord. Poliomyelitis can cripple and kill vulnerable individuals, especially children, within days. It often affects the very young, which is why it is also called infantile paralysis. Some individuals develop only flu-like symptoms without paralysis; aseptic meningitis (swelling of the membranes surrounding the brain) can result. This minor illness of poliomyelitis (as it is called) is characterized by slight fever, malaise, headache, sore throat, and vomiting; patients usually recover completely in 24-72 hours. Non-paralytic poliomyelitis cannot be differentiated clinically from aseptic meningitis caused by other transmissible agents. Surprisingly, fewer than one in 100 cases (and possibly as few as one in 1,000 cases) of infection with poliovirus produces any obvious disease, even during outbreaks.23,24
    The major illness of poliomyelitis usually develops suddenly, with fever, stiff neck and back, severe headache, and muscle pain. Major illness can progress to loss of tendon reflexes and asymmetrical weakness or paralysis. Poliomyelitis is generally diagnosed clinically by the concurrent presence of high fever and acute, asymmetrical flaccid paralysis, which develops in 2-4 days following the fever and muscle aches. Approximately 50% of people stricken with paralytic poliomyelitis remain disabled throughout their lives.24
    The paralysis produced by poliomyelitis results from inflammation and destruction of motor neurons in the gray matter of the spinal cord and brain. The type or degree of paralysis induced depends upon the location and extent of motor neuron destruction, and can range from minor to severe limb paralysis, to paralysis of the muscles that allow us to breathe. The iron lung was used in the 1940s and 50s to assist children who could not breathe on their own. As frightening as iron lungs look in the old photos, many children recovered completely. However, paralytic poliomyelitis is fatal in 2-10% of cases. 24

    With the exception of patients who go into respiratory failure, poliomyelitis treatment is symptomatic: non-narcotic pain killers, application of hot packs, and physical therapy.
    What Is Poliovirus?

    Despite the damage it causes to nerve tissue, the poliovirus has been placed in the enterovirus family of viruses that live in the gastrointestinal system. It is formed of a single strand of RNA enclosed in a protein coat that protects it from environmental attack (inactivation). Poliovirus is quite small by viral standards (22-32 nanometers). Humans are thought to be poliovirus’s only host, which is why the WHO launched an eradication program. According to the CDC, the only confirmed cases of poliovirus-associated paralysis in the US since 1979 have been associated with the oral, live-virus vaccine.24,31 In fact, the CDC now concludes that both laboratory surveillance for enteroviruses and surveillance for polio cases suggest that endemic circulation of indigenous wild polioviruses ceased in the United States in the 1960s.24 Other investigators question the CDC’s conclusion that wild poliovirus circulation truly ceased in the United States four decades ago.
    The Search for the Transmissible?Agent of Poliomyelitis

    Poliomyelitis became an important public health concern when it first spread along the eastern seaboard of the United States, as well as in industrialized areas of Europe, in the early 1900s. Its inexplicable outbreaks were frightening to the public and medical personnel alike, as Simon Flexner and Paul A. Lewis (both of the Rockefeller Institute for Medical Research in New York) demonstrated when they wrote in the Journal of the American Medical Association in 1909, “The cause and mode of dissemination of the disease [poliomyelitis] are unknown; and hence there exists no intelligent means of prevention. While the severity and fatality of the disease fluctuate widely, its effects are always so disastrous as to make it of the highest medical and social importance.”14??Just a year earlier, Austrian researchers Karl Landsteiner and Erwin Popper had made a historic breakthrough in the study of poliomyelitis. Landsteiner had a nine-year-old poliomyelitis patient who died on November 18, 1908, after just four days of illness. With his colleague Popper, Landsteiner created a suspension from the child’s spinal cord and injected it into two monkeys, as well as a number of rabbits, guinea pigs, and mice. While the other animals were unaffected by the injections of spinal cord material, the two monkeys developed lesions in their spinal cords and brains that appeared indistinguishable from those found in humans suffering from poliomyelitis. One of the monkeys developed acute flaccid paralysis in both legs. Although Landsteiner and Popper attempted to transmit paralysis to other monkeys using the sick monkeys’ nervous system tissues which is called “passaging” of the transmissible agent they were unsuccessful.10,20

    The following year, Flexner and Lewis succeeded where Landsteiner and Popper had not: Flexner and Lewis reported in the Journal of the American Medical Association that they had successfully passaged poliomyelitis through several monkeys (i.e., from monkey to monkey). They began, like Landsteiner and Popper, by injecting diseased human spinal cord tissue into the brains of monkeys. After a monkey fell ill, a suspension of its diseased spinal cord tissue was injected into other monkeys. Flexner and Lewis’s 1909 work was considered a breakthrough because the second monkey (and the third, and fourth, through at least six by the time of publication) developed poliomyelitis. Flexner and Lewis had successfully passaged the disease’s transmissible component from animal to animal.14

    But what was the passaged agent? “We failed utterly to discover bacteria, either in film preparations or in cultures, that could account for the disease, Flexner and Lewis reported.” Therefore, they concluded, “..the infecting agent of epidemic poliomyelitis belongs to the class of the minute and filterable viruses that have not thus far been demonstrated with certainty under the microscope.”14??Did Flexner and Lewis succeed in isolating poliovirus in 1909? Hindsight being 20/20, it is possible to see that early experiments attempting to create purified poliovirus preparations might well have contained other agents. ??The debate over the nature of the causative agent of poliomyelitis continued. One research team speculated in 1919 that a type of bacteria, cautiously named “poliococcus”, was either the culprit or a co-factor.7 In early experiments, all kinds of biological materials spinal cord, brain, fecal matter, even flies were ground up and injected into monkeys to induce paralysis.4,7,15,21,22,33 These early “virus preparations” were known to contain bacteria. The amount of bacteria was determined by seeding a tissue culture plate with some of the spinal cord (or fecal matter) emulsion to measure how long it took for bacterial colonies to appear. As F.B. Gordon and colleagues pointed out in a paper published in the Journal of Infectious Diseases, “If there was no [bacterial] growth after approximately 22 hours incubation at 37 C., the specimen was considered suitable for inoculation into monkeys. This was not an actual sterility test, since growth would usually occur on longer incubation; it was rather an indication of the amount of bacterial contamination in the specimen.”15

    Early poliovirus researchers, then, knew that the “virus” they were injecting into monkeys also contained an undetermined amount of bacteria. They had no way of determining what else might be present.

    While Flexner and Lewis may have been incorrect in assuming they had transmitted a purified form of “filterable virus” into their monkeys, they certainly transferred a disease-causing agent or agents from animal to animal. Although they could not actually visualize this agent, they described it in the greatest detail that they could. In doing so, which they undoubtedly meant to be a service to other researchers, they may have voiced their conclusions in ways that would haunt poliomyelitis research for decades.
    At the beginning of the 20th century, as scientists began trying to understand and characterize viruses and viral diseases, many of them including poliomyelitis researchers like Flexner and Lewis overstated their findings.

    Early poliomyelitis researchers were true scientific pioneers: Flexner, Lewis, Dalldorf, Landsteiner, Popper, Dulbecco, Sabin, Salk, and many others worked with unknown agents. They didn’t understand the properties of the contaminated tissues they handled, and they didn’t know how to protect themselves from the diseases those tissues might contain. Their bravery in undertaking these risks should never be underestimated, especially in our era when latex gloves, biosafety cabinets, and many other methods of protecting scientists from dangerous transmissible agents are readily available.
    Nevertheless, these early 20thcentury researchers should not get a free pass for their lack of precision in describing experiments and their results.

    For example, in 1948, Gilbert Dalldorf and Grace M. Sickles from the New York State Department of Health published a research report that illustrates some problems in virology that persist even today. Dalldorf and Sickles described an “unidentified, filterable agent” that they had “isolated” from the feces of paralyzed children.6
    The problems become clear when Dalldorf and Sickles described how they “isolated” this agent:
    “Twenty per cent fecal suspensions, prepared by ether treatment and centrifugation, were inoculated intracerebrally into albino mice of the laboratory strain. Suckling mice, 3-7 days of age, became paralyzed, while mice 10-12 gm in weight did not. The isolations were repeated several times.”6
    Dalldorf and Sickles used the word “isolation” to describe their creation of a suspension of fecal matter which was a vast overstatement, to put it mildly.
    Dalldorf and Sickles then attempted to identify the agent. In 1948, antibodies, like viruses, could not be characterized as they now can. “Neutralizing serum”-the non-cellular portion of the blood, taken from a person or animal presumed to be infected with the agent-was used to differentiate between viral strains. This neutralizing serum probably contained antibodies against the agent.

    According to Dalldorf and Sickles, neutralizing serum from paralyzed children inhibited paralysis in mice when they were injected simultaneously with it and the unidentified agent. This absence of evidence-that the mice did not develop paralysis, was interpreted to mean that the agent injected into the mouse had been successfully stopped by the neutralizing serum (i.e., the immune response generated by the sick child). There was no proof, as Dalldorf and Sickles asserted, that the neutralizing serum was reacting with and inhibiting one specific agent.

    Dalldorf and Sickles believed they’d “isolated” a novel agent that could infect people, although they did not argue that it was responsible for producing the paralysis seen in their patients. “The patients we studied may possibly have been coincidentally infected with the new agent and classical poliomyelitis virus, although isolations were not successful in [causing disease in] the rhesus monkey,” they write.6 Again, they write of “isolation” when they are referring to taking a partially processed specimen (spinal tissue or feces) from a paralyzed person and injecting it into an animal to see if the diluted specimen produced paralysis. True isolation did not take place.

    Has Poliovirus Ever Really Been Isolated?

    ßIt is an article of faith in modern medicine that poliovirus has been isolated, characterized, is fully understood and on its way to extinction, thanks to aggressive vaccination/eradication programs. As the recent outbreak in the Dominican Republic illustrates, however, we may be further from eradicating poliomyelitis than we are generally led to believe.
    Furthermore, while the agent identified as poliovirus was certainly cultured in the late 1940s, do we know for sure that it was truly isolated, i.e., grown in a pure form containing no contaminants? We now know that adventitious (“passenger”) viruses like SV40 are common in the monkey tissues that early poliovirus researchers used for cell cultures. While these agents apparently cause no harm to the monkeys, their long-term effects on humans remain to be determined.

    Some 90 years after Landsteiner and Popper”s report of successful transfer of poliomyelitis to monkeys, Dr. Wolfgang K. Joklik reviewed the great leaps forward during the 20thcentury by its defining discipline, virology.19 The occasion was the concurrent 100thanniversaries of the American Society for Microbiology and the field of virology itself. Having served as editor-in-chief of Virology and an editor of Journal of Virology over his long career as a professor of microbiology, Joklik was uniquely placed (as he noted) to evaluate what had been learned since early experiments in virology.

    Before the founding of Virology and Journal of Virology in the 1950s and “60s, respectively, Joklik noted, a number of “epoch-making discoveries in virology” appeared in journals not devoted to the field. Among the seven discoveries he singled out were two related to paralysis research. The first was “the discovery by Enders et al. in 1949 that poliomyelitis virus could be grown in human embryonic tissue cells cultured in vitro, which formed the basis of the technique of tissue culture (single cell culture)”; the second, “”the demonstration by Dulbecco, also in 1952, that an animal virus ” was capable of forming plaques in monolayers of cloned cultured cells, which opened up the field of molecular animal virology.”19 While Dulbecco’s 1952 study did not involve poliovirus, it led directly to his 1954 paper in which he extended the new methodology to the study of poliovirus.8,9

    In 1949, as Joklik recounted, Harvard Medical School researcher John F. Enders, along with his colleagues Thomas H. Weller (a Fellow of the U.S. Public Health Service) and Frederick C. Robbins (a Senior Fellow in Virus Diseases of the National Research Council) showed not only that poliovirus could grow in cultured cells, but also that it could replicate in non-nervous system tissues, a stunning discovery at the time.13 It was already suspected that poliovirus was often present in the intestines of affected individuals. However, no one had been able to propagate the virus in gut tissue, primarily because of the bacteria that naturally live there. Enders and colleagues were successful in part because they added antibiotic (penicillin and/or streptomycin) to their cell cultures to kill the bacteria” a technique that had not, of course, been available to researchers working in the pre-World War II era.

    While Enders and colleagues” 1949 paper is widely acknowledged to be a turning point in poliomyelitis research” many, including World Health Organization poliovirus eradication researchers, credit this piece of science with paving the way for the development of both the Salk and Sabin polio vaccines” poliovirus was not actually isolated by these investigators, either. They successfully grew “filterable agents,” which they assumed to be poliovirus, in human embryonic tissues. Like Landsteiner and Popper 40 years earlier” and like just (jump to rest of article)

    The Dulbecco “Isolation” Experiment

    In 1954, Dulbecco and his colleague Margaret Vogt published a classic research paper that is credited with having set the standard for purifying poliovirus for decades.9 In it, they introduced a technical innovation to the process of “purifying” viruses from tissue culture. This new technique was called “plaque purification”; a single plaque (a circular area of cells that stained differently from the surrounding culture) was considered to represent a pure virus population. Plaque purification utilized trypsinization, which involves treating the cells” in this case, monkey kidney cells” with the enzyme trypsin, breaking up any clumps of cells that might have formed and resulting in a single-cell suspension. 
    In the early days of poliovirus research, tissue culture was usually conducted using monkey kidneys (or, sometimes, monkey testes). Dulbecco and Vogt explained where the “virus” they grew came from:

    “The virus was supplied as a 20 per cent suspension of spinal cord of rhesus monkey in distilled water. Type 1 virus obtained from passage through the monolayer kidney cultures was used. Type 2, Yale-SK strain, and Type 3, Leon strain, were kindly supplied by Dr. J.L. Melnick in form of tissue culture supernatants.”9

    That passage clearly demonstrates that Dulbecco and Vogt did not isolate pure poliovirus in any of the experiments described in this 1954 report. While they write of seeding their cultures with “virus,” they actually used unpurified suspensions, not pure viral isolates.

    Once the monkey kidneys were ground up into “single cells, cell clusters, and cell debris,” they were seeded with the monkey spinal cord emulsion. The appearance of the plaques was evidence that the virus was growing, according to the model Dulbecco had developed in 1952.8 

    The control for these experiments was to treat the cultures with monkey antiserum (derived from monkeys infected with Type 1, 2, or 3 poliovirus); if Type 1 antiserum inhibited plaque formation but Type 2 or 3 (or normal monkey) antiserum didn’t, then Type 1 poliovirus was assumed to be exclusively present in the culture. In other words, it was assumed that no other organism or disease-associated agent was growing in the culture.

    Once again, what Dulbecco and Vogt describe as “isolation” of the poliovirus is not isolation in the way we would understand it in modern microbiology. To perform their “plaque purifications,” they simply pipetted some liquid (“plaque stock”) from one culture plate and replated it onto other culture plates. When the second-generation cell cultures showed evidence of viral growth (i.e., plaques), monkeys were inoculated with the plaque stock. The inoculated monkeys developed paralysis and, subsequently, most died. Since the plaque purified viral stock both grew new plaques in second-generation cell culture and caused monkeys to develop flaccid paralysis, Dulbecco and Vogt concluded they had “isolated” poliovirus. 

    Like poliovirus researchers before them, it is clear that Dulbecco and Vogt were propagating disease-associated substances in their tissue cultures, and that they later transferred these substances to monkeys in whom acute flaccid paralysis developed. These were impressive accomplishments.

    Dulbecco and Vogt’s claims, however, went further than they had evidence to support. They asserted not only that they had isolated poliovirus, but that, “Since each plaque stock originated from a single virus particle (as proved in the Discussion), these stocks constitute the purest lines of virus presently available.”

    How could they possibly know that a “single virus particle,” something they had never seen or measured, was causing the growth of exactly one plaque in their cultures? The evidence Dulbecco and Vogt supplied to “prove” that a single virus particle produced each plaque is contained in a mathematical equation: They extrapolated the cell culture’s assumed “virus concentration” from the number of times the original fluid (for example, monkey spinal cord suspension) was diluted. The fewer times the fluid was diluted, the more plaques grew in laboratory cultures; the more times it was diluted, the fewer plaques grew. Dulbecco and Vogt’s mathematical model assumed this linear relationship between dilution of virus stocks and number of plaques formed and, when they reached the greatest possible dilution that still caused a single plaque to grow, they assumed that only one “virus particle” was present therein. And how did they prove that assumption, as promised? They provided their mathematical model. This is a perfectly tautological proof. Its most apparent flaw is that the mathematical model “could not” distinguish between a “single virus particle” and a biological complex that may have contained a single virus. This is made clear in Dulbecco and Vogt’s description of the plaque-forming “single virus particle” they claim to have isolated:

    “Having arrived at this point, it is now possible to define properly the characteristics of the virus particle detected by a plaque. Owing to its all-or-none effect, it has the character of a particle. It corresponds to a unit of the virus which is not further subdivisible at high dilution. From the property by which it is recognized, we call it a plaque-forming particle. We do not know its morphological or genetic properties. It might be a single elementary body, or a clump of them, provided that the clump persists indefinitely at high dilution….”9

    It is puzzling, in retrospect, that Dulbecco and Vogt raised the possibility that they were detecting a “clump” of material, but thereafter ignored it. What if another type of virus was also included in these particles? Or, what if host genetic material attached itself to the particle to form a “clump”? 

    Although electron microscopy “which would have allowed them to visualize a single viral particle” existed in 1954, Dulbecco and Vogt did not use it. Instead, they employed the time-honored technology in which viruses were assumed to be present in cultures if certain chemicals stained them, or if fluids thought to contain them produced characteristic patterns of growth, like the poliovirus-related plaques described here. Dulbecco and Vogt could not possibly determine that they were viewing single viruses in their cultures and, therefore, their assumption that they had isolated a “single virus particle” was a vast overstatement. Dulbecco and Vogt did not isolate poliovirus.

    about everyone else in the field during its first 60 years or so Enders and co-workers called this disease-transmitting suspension of tissue “virus.”

    Despite this overstatement, Enders, Weller, and Robbins were the first to prove that a transmissible agent associated with poliomyelitis could be propagated in cells in the laboratory, and that cell cultures could be substituted for live animals in studying such transmissible agents. In 1954, their ground-breaking work was rewarded with a Nobel Prize.

    Renato Dulbecco’s 1952 paper lauded by Joklik is considered to have made a significant contribution to viral research in general and, by extrapolation, to poliovirus research. Working at the California Institute of Technology (in Pasadena), Dulbecco developed a method of growing plates of cells so that “virus plaques” could be visualized.  He grew Western Equine Encephalomyelitis virus plaques on a substrate of chicken embryo cells and, when he published his paper, he pointed out that it was still unknown whether all viruses could be cultured in this manner. These were truly the very earliest days of modern virological research, and Dulbecco expressed hope that investigators would some day be able to distinguish between various viruses grown in cell culture by using his methodology and examining the resulting plaques under the microscope.8

    In 1954, Dulbecco and his colleague Margaret Vogt published a classic research paper [see sidebar, “The Dulbecco Isolation Experiment,” above] that set the standard for purifying poliovirus cultures for decades.9Dulbecco and Vogt, like their colleagues, used monkey kidney cells to culture tissues thought to contain poliovirus. Dulbecco and Vogt explained where the “virus” they grew came from:

    “The virus was supplied as a 20 per cent suspension of spinal cord of rhesus monkey in distilled water. Type 1 virus obtained from passage through the monolayer kidney cultures was used. Type 2, Yale-SK strain, and Type 3, Leon strain, were kindly supplied by Dr. J.L. Melnick in form of tissue culture supernatants.”9

    In other words: Dulbecco and Vogt did not isolate pure poliovirus in any of the experiments described in this 1954 report. While they write of seeding their cultures with “virus,” they actually used unpurified suspensions, not pure viral isolates.

    It is clear from this historical review of early poliovirus research papers that none of these poliomyelitis researchers truly isolated poliovirus. Additionally, they were injecting monkeys with experimental fluids that were probably contaminated with other disease-associated agents.

    Further confusing the picture (but not reviewed here) is the fact that enteroviruses other than poliovirus are associated with AFP. For example, as recently as February 2001, it was shown that Coxsackie A24 is associated with nonpolio AFP.5

    How Much Flaccid Paralysis Is NOT Caused by the Poliovirus?

    There is an astonishing number of cases of paralysis around the world not associated with poliovirus. If you visit the World Health Organization website that tracks acute flaccid paralysis (AFP), polio and non-polio, you will see that the world is not rid of the scourge of AFP. For example, India reported 9,580 cases of AFP in 1999; 2802 of them, fewer than one-third, were associated with poliovirus. China reported 5,064 cases of AFP to WHO in 1999; only one of those cases was associated with poliovirus. Poliovirus eradication and vaccination programs have not eliminated paralysis.

    WHO recently declared Egypt on the threshold of eradicating poliovirus. “We are now at the end of a polio era,” a UN Children’s Fund Project Officer told Reuter’s news service in late February 2001. Egypt had “not a single case of the crippling virus reported so far this year” or in 2000, according to Reuters.17

    According to the WHO AFP/polio surveillance web site, however, there were 54 cases of acute flaccid paralysis in Egypt in 2000 (the most recent year for which statistics are available). In 1999, although there were 9 AFP cases classified as due to poliovirus, 276 were classified as nonpolio. During 1998, Egypt had 295 cases of AFP, 35 of which were classified as poliovirus-related; in 1997, Egypt reported 217 cases of non-polio paralysis compared to 14 cases in which poliovirus infection was confirmed; and in 1996, the earliest year for which statistics are available, Egypt reported 309 cases of acute flaccid paralysis. One hundred of those were classified as poliovirus-related, leaving 209 cases “two-thirds of the total” probably due to a cause other than poliovirus (with the caveat that epidemiological statistics are not perfectly accurate in every country of the world).

    Afghanistan is another country in which there is an increasing prevalence of AFP compared to a decreasing incidence of poliovirus. As the U.S. Centers for Disease Control and Prevention’s Morbidity and Mortality Weekly Report (MMWR) notes on March 2, 2001, “During 1999-2000, the number of AFP cases [in Afghanistan] increased from 230 to 253, and the number of wild polioviruses isolated from AFP cases decreased from 63 to 28.”28 

    How does the CDC explain the increase in AFP cases in Afghanistan, in the face of a vigorous poliovirus eradication campaign? Well, it doesn’t. In fact, the MMWR report almost makes the increase in nonpolio AFP sound like a triumph of public health: “During 1999-2000, the nonpolio AFP rate almost doubled and the number of districts reached by NIDs [National Immunization Days] increased steadily. Careful planning and supervision of house-to-house vaccination and support from an increasing number of local partners resulted in the largest number of children ever being reached. Monitoring by nongovernment organizations, United Nations” agencies, and local authorities has increased the quality of NIDs”.”28 In other words, the more National Immunization Days there were, the more cases of paralysis appeared. Does this mean immunizations were causing paralysis? No, but neither was increased immunization preventing children from becoming paralyzed.

    The Western Hemisphere has also been impacted by an increased case load of AFP. As mentioned earlier, the island of Hispaniola (the Dominican Republic and Haiti) experienced what the CDC called an “outbreak of poliomyelitis” that began in July 2000. There were 54 cases in the Dominican Republic, 12 of which were

    Polio Vaccination Recommendations, U.S. Centers for Disease Control and Prevention

    Recommendations for children in the United States include a 4-dose vaccination series with inactivated poliovirus vaccine (IPV) at ages 2, 4, 6″18 months, and 4″6 years. Unvaccinated adults should receive three doses of IPV, the first two doses at intervals of 4″8 weeks and the third dose 6″12 months after the second. If three doses cannot be administered within the recommended intervals before protection is needed, alternative schedules are proposed. For incompletely vaccinated persons, additional IPV doses are recommended to complete a series. Booster doses of IPV may be considered for persons who previously have completed a primary series of polio vaccination and who may be traveling to areas where polio is endemic.

    Morbidity and Mortality Weekly Report, March 2, 2001, Vol. 50, No. 8, p. 147

     “laboratory-confirmed poliomyelitis cases attributed to vaccine-derived poliovirus type 1,” according to the CDC. Although the oral polio vaccine is known to cause polio in about 1 of every 750,000 infants who receive it or their mothers.  Unlike the inactivated Salk vaccine “shot,” the Sabin oral vaccine contains live viruses.  The 45 cases reported in January 2001 in the Washington Post are, if confirmed, clearly outside the realm of this statistic.3

    As of the end of February 2001, the cause(s) of 33 AFP cases in the Dominican Republic and three in Haiti remained undetermined.27 All of these cases might be due to the oral polio vaccine, in which case the mystery would be solved, leaving unanswered, however, the question of what factors contributed to such a large vaccine-associated outbreak of paralysis. 

    If these 36 AFP cases are not related to the polio vaccine, however, then what is causing them?  What is causing other nonpolio outbreaks of AFP identified by WHO all over the world?

    And in cases in which poliovirus is fingered as the culprit in an outbreak, how sensitive are the current methodologies that virologists use to isolate and identify it?

    How Is Poliovirus Detected Today?

    It is nearly unimaginable how sensitive and sophisticated laboratory technology has become over the last 30 years. As we examine the entire sequence of the human genome in early 2001, it’s difficult to imagine that it was only in the 1970s that scientists first developed the technology that allowed the rapid sequencing of genes, including genetic sequences from transmissible agents like bacteria and viruses. 

    This new sequencing methodology was immediately applied to poliovirus research. During the 1970s, the CDC began routinely performing genotypic testing (“molecular sequencing” or “oligo-nucleotide fingerprinting”) on stool samples collected in suspected poliovirus outbreaks to determine whether the virus was present. Using findings from the new technology to extrapolate to the prior decade, CDC documents now state that, “Both laboratory surveillance for enteroviruses and surveillance for polio cases suggest that endemic circulation of indigenous wild polioviruses ceased in the United States in the 1960s.”24

    To detect poliovirus today, according to CDC and WHO guidelines, two stool samples should be collected from each patient, 24-48 hours apart within 14 days of the onset of paralysis, and they must arrive at the laboratory in “good condition.” While WHO’s target is to obtain two good samples in at least 80% of all AFP cases, some areas of the world fall short of this, approaching only 50%.28

    The CDC provides the following guidelines on how to detect poliovirus:

    “The following tests should be performed on appropriate specimens collected from persons who have suspected cases of polio: a) isolation of poliovirus in tissue culture; b) serotyping of a poliovirus isolate as serotype 1, 2, or 3; and c) intratypic differentiation using DNA/RNA probe hybridization or polymerase chain reaction to determine whether a poliovirus isolate is associated with a vaccine or wild virus.

    “Acute-phase and convalescent-phase serum specimens should be tested for neutralizing antibody to each of the three poliovirus serotypes. A fourfold rise in antibody titer between appropriately timed acute-phase and convalescent-phase serum specimen is diagnostic for poliovirus infection. The recently revised standard protocol for poliovirus serology should be used. Commercial laboratories usually perform complement fixation and other tests. However, assays other than neutralization are difficult to interpret because of inadequate standardization and relative insensitivity.”24

    While this procedure is a time-honored method of detecting the poliovirus and the body’s response to it, it does not “isolate” the poliovirus, it simply detects poliovirus. The samples tested by the CDC and WHO should be described as “poliovirus reactive material,” not as samples that contain isolated, pure poliovirus.

    Once again, we have no proof that poliovirus has been isolated.

    If Not Poliovirus, Then What Is Causing Today’s Cases of Flaccid Paralysis?

    “The history of the etiology of poliomyelitis is a history of errors.”

    J.F. Eggers, Medicine, 1954

    If the majority of the U.S. population has been immunized since the 1950s, why did it take until 1979 to “eradicate” poliovirus within the United States?24,31

    And what is causing the nonpolio cases of paralysis that continue to occur all over the world?

    It is becoming clear that one culprit capable of causing not only paralysis but also other neurological conditions is organophosphate pesticides. Recent research has tied chronic organophosphate pesticide exposure to development of Parkinson’s disease signs and symptoms in an animal model.2 And researchers in Paraguay have good evidence that an outbreak of AFP among children in 1990-1991 was associated with organophosphate pesticide exposure.

    The 50 Paraguayan children identified in this study, given that it was conducted in a rural, isolated area meant that quite a number of affected children might have been excluded from the study, as investigators noted, developed a type of AFP named Guillain-Barré Syndrome, or GBS. As is the case in other forms of AFP, the myelin sheath that surrounds and protects nerves is damaged in GBS. The disease’s causes are unknown, but it’s generally believed to be an autoimmune condition provoked by infections, toxins, or a combination of both.16

    The children became ill during the Paraguayan summer (January to April), with weakness, upper respiratory tract infection, fever, and gastrointestinal symptoms. Three children developed difficulty breathing, and two of them required mechanical help to breathe (intubation). “Weakness progressed in an ascending pattern in 95% of the children, and simultaneously in all limbs in 5%; the average time to reach the nadir was 7 days (range, 2-12 days),” the investigators reported. Of the 35 children observed while they were in the acute stage of AFP, 18 were unable to walk, 10 walked with assistance, four walked independently, and three were too young to walk. The children exhibited full or partial paralysis of facial muscles and their bladders; they also experienced autonomic nervous system changes that created fluctuations in blood pressure, erratic heartbeat, flushing of skin, and intestinal motility. One child died.16

    The study was conducted as part of the Pan American Health Organization’s effort to eradicate poliomyelitis. David E. Hart of the U.S. National Institute of Neurological Disorders and Stroke at the National Institutes of Health was the lead investigator working alongside researchers from the Paraguayan Ministry of Health.16 The majority of cases, they point out, were clustered in a rural, farming province named Concepcion.

    “The clustering of patients in Concepcion could be related to the use of organophosphate pesticides in the cotton fields,” Hart and colleagues suggest. “Farmers use great amounts of these pesticides, often in concentrated form, and empty containers serve as toys. Also, the maximum usage of organophosphates occurs during the summer (December-March),” when these children became ill.16

    Although they note that retrospective measurement of organophosphate exposure is very difficult, Hart and co-workers cite a report that the cotton industry officially spent approximately US$ 6.7 million on organophosphate pesticides in 1991. However, more than half of the pesticides used in Paraguay are obtained “unofficially,” according to this report.

    “Four children were excluded from this study because of definite exposure to this product and presentation with concurrent acute cholinergic syndrome,” the severe disease produced by organophosphate pesticide exposure. Hart and colleagues added, “Their clinical course, however, was similar to that of the children included” in the study.16

    By examining the possibility that the AFP observed in these Paraguayan children might be associated with organophosphate pesticides, Hart and colleagues took that extra step that is so often omitted. Clusters of illnesses in communities can arise from any number of causes; they are not exclusively due to transmissible agents. Toxins in the environment are significant factors in many illnesses.

    Since the time of Koch, bacteriologists have used the gold standard he described for the assignment of the disease process to single organisms. Bacteria and fungi can be truly isolated and grown independently on artificial media; they don’t require the presence of human or other cells. One problem that researchers have faced in describing non-bacteriologic related diseases has been the assumption that a single entity can cause them, without interaction from the cells in which they are grown, the human genome, or the environment. 

    We live in a important time: We are about to redefine much of what we know about medical science. In early 2001, two stunning reports on the Human Genome Project, published simultaneously in February issues of Science and Nature, turned much of what we thought we knew about the human genome on its head.  Instead of possessing 100,000 genes, for example, we learned that the human genome is made up of only about 30,000 genes, fewer than the number possessed by rice.1

    Our new understanding of the human genome was produced, in part, by new technologies that we can now apply to revisiting many of the assumptions of modern medicine. One of the most important lessons learned from the challenge of decoding the human genome is that scientists need to describe laboratory experiments and results accurately. Technologically advanced tools can provide detailed and precise information, but the researchers using them must describe those results with equal precision. When a sample is laboratory reactive, it should not be assumed to be infectious. Likewise, suspensions of diseased brain tissue should not be called “virus” and dilutions of brain tissue material should not be called “isolations.”

    As the human genome comes more precisely into focus, our understanding of how our genes interact with one another, the environment, and other organisms will also become more precise. 

    Precision should also be applied to research objectives. Clearly, it is incorrect to state that poliomyelitis has been eradicated from many countries. The surprisingly large number of cases of nonpolio acute flaccid paralysis around the world warrants continued pursuit of the original objective of the March of Dimes: the elimination of infantile paralysis. On its website, the March of Dimes takes some well-deserved credit for helping to limit the amount of paralysis in the world today. “Historians have called the conquest of polio one of the great achievements of this century,” a fact sheet on the website states. “Thanks to the March of Dimes, and the millions of people who supported it, we no longer have the devastating epidemics that terrorized generations.”

    Clearly, the original objective of the March of Dimes has not yet been met, or there would not be so much acute flaccid paralysis around the world today. Examining the last 50 years of poliomyelitis research shows that the objective of eliminating infantile paralysis has been replaced with the objective of eliminating poliovirus. As governments, international health organizations, and charitable foundations pour hundreds of millions of dollars into poliovirus eradication efforts, shouldn’t we also invest in basic research that will prevent all cases of childhood paralysis?

    Acknowledgement: The author wishes to thank Dr. Howard Urnovitz, Science Director of the Chronic Illness Research Foundation, for bringing this story to her attention and approving the scientific content of this article.

    Literature Cited

    1. Abate, Tom. February 11, 2001. Genome discovery shocks scientists. San Francisco Chronicle.
    2. Betarbet, R., T.B. Sherer, G. MacKenzie, M. Garcia-Osuna, A.V. Panov, and J.T. Greenamyre. December 2000. Chronic systemic pesticide exposure reproduces features of Parkinson’s disease. Nature Neuroscience 3(12):1301.
    3. Brown, David. January 1, 2001. Ready to let go of polio? Mutant virus in Caribbean outbreak alarms health experts. Washington Post, p. A7.
    4. Burnet, F.M. and J. MacNamara. 1931. Immunological differences between strains of poliomyelitic virus. The British Journal of Experimental Pathology 12(2):5.
    5. Chaves, S.S., S. Lobo, M. Kennett, and J. Black. February 24, 2001. Coxsackie virus A24 infection presenting as acute flaccid paralysis. The Lancet 357:605.
    6. Dalldorf, G. and G.M. Sickles. 1948. An unidentified, filtrable agent isolated from the feces of children with paralysis. Science 108:61.
    7. Davis, W.M. 1919. The demonstration of immune opsonins for the pleomorphic streptococcus in the experimental poliomyelitis in monkeys. Journal of Infectious Diseases 24:176.
    8. Dulbecco, R. 1952. Production of plaques in monolayer tissue cultures by single particles of an animal virus. Proceedings of the National Academy of Sciences USA 38:747.
    9. Dulbecco, R. and M. Vogt. 1954. Plaque formation and isolation of pure lines with poliomyelitis viruses. J. Exp. Med. 99:167-182.
    10. Eggers, H.J. 1999. Milestones in early poliomyelitis research (1840-1949). Journal of Virology 73(3):4533.
    11. Enders, J.F. 1954. Some recent advances in the study of poliomyelitis. Talk given on the occasion of receiving the Passano Award, June 3, 1953. Published in Medicine 33:87, May 1954.
    12. Enders, J.F. 1972. Early observations on cytopathogenicity of poliovirus. American Journal of Clinical Pathology    57(6):846.
    13. Enders, J.F., T.H. Weller, and F.C. Robbins. 1949. Cultivation of the Lansing strain of poliomyelitis virus in cultures of various human embryonic tissues. Science 109:85.
    14. Flexner, S. and P.A. Lewis. 1909. The transmission of acute poliomyelitis to monkeys. Journal of the American Medical Association 53:1639.
    15. Gordon, F.B., F.M. Schabel, Jr., A.E. Casey, and W.I. Fishbein. 1948. Laboratory study of the epidemiology of poliomyelitis. Journal of Infectious Diseases 82:294.
    16. Hart, D.E. et al. 1994. Childhood Guilliain-Barré Syndrome in Paraguay, 1990 to 1991. Annals of Neurology 36(6):859.
    17. Hassan, Abdalla. February 22, 2001. Egypt appears close to wiping out polio scourge. Reuters News Service.
    18. International Human Genome Sequencing Consortium. February 15, 2001. Initial sequencing and analysis of the human genome. Nature 409:860.
    19. Joklik, W.K. When two is better than one: Thoughts on three decades of interaction between Virology and the Journal of Virology. 1999. Journal of Virology 73(5):3520.
    20. Landsteiner, K. and E. Popper. 1909. Uebertragung der poliomyelitis acuta auf affen. Z. Immunitatsforsch 2:377.
    21. Melnick, J.L. and R. Ward. 1945. Susceptibility of vervet monkeys to poliomyelitis virus in flies collected at epidemics. Journal of Infectious Diseases 77:251.
    22. Melnick, J.I. and N. Ledinko. 1952. Vaccination as a provoking factor in poliomyelitis: An experimental approach. Journal of Infectious Diseases 90:279.
    23. Merck Manual, Fifteenth Edition. 1987. Merck & Co., Inc., Rahway, NJ, USA.
    24. Morbidity and Mortality Weekly Report. May 19, 2000. Poliomyelitis prevention in the United States: Updated Recommendations of the Advisory Committee on Immunization Practices (ACIP). U.S. Department of Health & Human Services, Centers for Disease Control and Prevention, Atlanta, GA 30333.
    25. Morbidity and Mortality Weekly Report. December 8, 2000. Outbreak of poliomyelitis, Dominican Republic and Haiti, 2000. U.S. Department of Health & Human Services, Centers for Disease Control and Prevention, Atlanta, GA 30333.
    26. Morbidity and Mortality Weekly Report. January 26, 2001. Circulation of a Type 2 vaccine-derived poliovirus. Egypt, 1982-1993. U.S. Department of Health & Human Services, Centers for Disease Control and Prevention, Atlanta, GA 30333.
    27. Morbidity and Mortality Weekly Report. March 2, 2001. Outbreak of poliomyelitis, Dominican Republic and Haiti, 2000- 2001. U.S. Department of Health & Human Services, Centers for Disease Control and Prevention, Atlanta, GA 30333.
    28. Morbidity and Mortality Weekly Report. March 2, 2001. Progress toward poliomyelitis eradication, Afghanistan, 1999- 2000. U.S. Department of Health & Human Services, Centers for Disease Control and Prevention, Atlanta, GA 30333.
    29. Morales, E.G. 1930. Acute anterior poliomyelitis at Vega Baja, Porto Rico. Journal of Infectious Diseases 46:32.
    30. Schabel, F.M., Jr., H.T. Smith, W.I. Fishbein, and A.E. Casey. 1950. Stool virus recovery in subclinical poliomyelitis during  incubation, febrile, and convalescent periods. Journal of Infectious Diseases 82:294.
    31.     Strebel, P.M., R.W. Sutter, S.L. Cochi, et al. 1992. Epidemiology of poliomyelitis in the United States one decade after the  last reported case of indigenous wild virus-associated disease. Clin. Infect. Dis. 14:568.
    32. Venter, J.C., et al. February 16, 2001. The sequence of the human genome. Science 291:1304.
    33. Wenner, H.A., R.W. Menges, and G.S. Harshfield. 1954. Sporadic bovine encephalomyelitis: 3. Reproduction of the   disease, with particular reference to the role of poliomyelitis viruses in experimental infection in calves. Journal of Infectious Diseases 94:284.
     

  3. Images Of Poliomyelitis

    Poliovirus Isolation:  No Evidence
    Originally this article was online at chronchronicllnet dot org.  That site is now defunct, and so I have posted the article here, as a public service.
    Howard Urnovitz, Ph.D., microbiologist, referred me to this study of poliovirus isolation during our meeting at the office of Nicholas Regush, ABC headquarters, in Manhattan, April 2001.  Howard is the authority behind this article, which, by the way, was published one year after publication of my DDT/polio article in Townsend Letters, 2000.

    Will The Poliovirus Eradication Program ?Rid the World of Childhood Paralysis?
    With So Little Poliovirus Detected Around the World, What Is Causing Today’s Outbreaks of Acute Flaccid Paralysis?
    By Neenyah Ostrom ?(NONYN@aol.com)?April 20, 2001

    Every child of the early ’50s surely remembers the polio panics that swept the nation, invariably during the hottest days of summer, closing public pools and resulting in doctor visits at the first sign of a stiff neck or leg prone to falling asleep. My memory of the terror induced by the whispered word “polio” resides in a spot in the pit of my stomach just distal to the one recalling the Cold War era duck-and-cover drills we practiced in grammar school.

    In retrospect, it seems darkly hilarious that we ever believed plywood desks and plump little arms would protect school children from a nuclear attack. Our not-quite-rational fear of the poliovirus, however, endures despite World Health Organization eradication programs in the corners of the developing world where poliovirus is thought to lurk. One reason for this lingering concern is the continuing prevalence of acute flaccid paralysis, polio’s most crippling symptom that can leave its victims unable to control entire muscle groups, even those that allow us to breathe.

    Worldwide polio-related public health alarms sounded on the first day of 2001 when a new epidemic was reported to have broken out on the island of Hispaniola, on which Haiti and the Dominican Republic are located. David Brown reported in the Washington Post that a “mutant” poliovirus, derived from strains present in the oral polio vaccine, appeared to have run amok on this Caribbean island during the latter half of 2000.3

    When the US Centers for Disease Control and Prevention (CDC) examined these cases, another mystery was revealed: Only about one-third of the paralysis cases were associated with poliovirus. The CDC identified 19 individuals in the Dominican Republic who developed acute flaccid paralysis (AFP, the hallmark symptom of poliovirus infection as well as a syndrome unto itself) between July 12 and November 18, 2000. However, poliovirus was detected in only six of those individuals. The cause of the other cases of paralysis remains unknown.25

    The mystery deepens when we examine World Health Organization (WHO) statistics on AFP and poliovirus infection in the Dominican Republic for the last several years.  Although the number of cases of AFP in the Dominican Republic from 1996 to 1999 range from 4 to 24, not a single case of poliovirus was detected.

    If we further examine other WHO statistics on poliovirus-associated AFP and those in which the virus is not detected, a striking fact becomes clear: Most acute flaccid paralysis diagnosed around the world today is NOT associated with poliovirus.

    This fact raises new, disturbing questions, including whether there ever was  an epidemic of poliovirus infection in the United States and Canada. There was a greatly increased prevalence of AFP, to be sure, during which many children (and some adults) tragically were paralyzed or died. Since many of those cases showed all the hallmarks of a typical poliovirus infection fever, stiff neck and back, severe headache, muscle pain, sore throat and, in severe cases, paralysis and occurred in clusters, they were assumed to be caused by the easily-transmitted poliovirus.

    But were they? If not, what is the cause of so much misery today in areas of the world least-equipped to be able to deal with it? Is it correct to assume that poliovirus causes most cases of paralysis?

    What Is Poliomyelitis?

    The word poliomyelitis comes from two Greek words:  polio, which means gray, and myelitis,  inflammation of the spinal cord. Poliomyelitis can cripple and kill vulnerable individuals, especially children, within days. It often affects the very young, which is why it is also called infantile paralysis. Some individuals develop only flu-like symptoms without paralysis; aseptic meningitis (swelling of the membranes surrounding the brain) can result. This minor illness of poliomyelitis (as it is called) is characterized by slight fever, malaise, headache, sore throat, and vomiting; patients usually recover completely in 24-72 hours. Non-paralytic poliomyelitis cannot be differentiated clinically from aseptic meningitis caused by other transmissible agents. Surprisingly, fewer than one in 100 cases (and possibly as few as one in 1,000 cases) of infection with poliovirus produces any obvious disease, even during outbreaks.23,24

    The major illness of poliomyelitis usually develops suddenly, with fever, stiff neck and back, severe headache, and muscle pain. Major illness can progress to loss of tendon reflexes and asymmetrical weakness or paralysis. Poliomyelitis is generally diagnosed clinically by the concurrent presence of high fever and acute, asymmetrical flaccid paralysis, which develops in 2-4 days following the fever and muscle aches. Approximately 50% of people stricken with paralytic poliomyelitis remain disabled throughout their lives.24

    The paralysis produced by poliomyelitis results from inflammation and destruction of motor neurons in the gray matter of the spinal cord and brain. The type or degree of paralysis induced depends upon the location and extent of motor neuron destruction, and can range from minor to severe limb paralysis, to paralysis of the muscles that allow us to breathe. The iron lung was used in the 1940s and 50s to assist children who could not breathe on their own. As frightening as iron lungs look in the old photos, many children recovered completely. However, paralytic poliomyelitis is fatal in 2-10% of cases. 24

    With the exception of patients who go into respiratory failure, poliomyelitis treatment is symptomatic: non-narcotic pain killers, application of hot packs, and physical therapy.
    What Is Poliovirus?

    Despite the damage it causes to nerve tissue, the poliovirus has been placed in the enterovirus family of viruses that live in the gastrointestinal system. It is formed of a single strand of RNA enclosed in a protein coat that protects it from environmental attack (inactivation). Poliovirus is quite small by viral standards (22-32 nanometers). Humans are thought to be poliovirus’s only host, which is why the WHO launched an eradication program. According to the CDC, the only confirmed cases of poliovirus-associated paralysis in the US since 1979 have been associated with the oral, live-virus vaccine.24,31 In fact, the CDC now concludes that both laboratory surveillance for enteroviruses and surveillance for polio cases suggest that endemic circulation of indigenous wild polioviruses ceased in the United States in the 1960s.24 Other investigators question the CDC’s conclusion that wild poliovirus circulation truly ceased in the United States four decades ago.

    The Search for the Transmissible?Agent of Poliomyelitis

    Poliomyelitis became an important public health concern when it first spread along the eastern seaboard of the United States, as well as in industrialized areas of Europe, in the early 1900s. Its inexplicable outbreaks were frightening to the public and medical personnel alike, as Simon Flexner and Paul A. Lewis (both of the Rockefeller Institute for Medical Research in New York) demonstrated when they wrote in the Journal of the American Medical Association in 1909, “The cause and mode of dissemination of the disease [poliomyelitis] are unknown; and hence there exists no intelligent means of prevention. While the severity and fatality of the disease fluctuate widely, its effects are always so disastrous as to make it of the highest medical and social importance.”14??Just a year earlier, Austrian researchers Karl Landsteiner and Erwin Popper had made a historic breakthrough in the study of poliomyelitis. Landsteiner had a nine-year-old poliomyelitis patient who died on November 18, 1908, after just four days of illness. With his colleague Popper, Landsteiner created a suspension from the child’s spinal cord and injected it into two monkeys, as well as a number of rabbits, guinea pigs, and mice. While the other animals were unaffected by the injections of spinal cord material, the two monkeys developed lesions in their spinal cords and brains that appeared indistinguishable from those found in humans suffering from poliomyelitis. One of the monkeys developed acute flaccid paralysis in both legs. Although Landsteiner and Popper attempted to transmit paralysis to other monkeys using the sick monkeys’ nervous system tissues which is called “passaging” of the transmissible agent they were unsuccessful.10,20

    The following year, Flexner and Lewis succeeded where Landsteiner and Popper had not: Flexner and Lewis reported in the Journal of the American Medical Association that they had successfully passaged poliomyelitis through several monkeys (i.e., from monkey to monkey). They began, like Landsteiner and Popper, by injecting diseased human spinal cord tissue into the brains of monkeys. After a monkey fell ill, a suspension of its diseased spinal cord tissue was injected into other monkeys. Flexner and Lewis’s 1909 work was considered a breakthrough because the second monkey (and the third, and fourth, through at least six by the time of publication) developed poliomyelitis. Flexner and Lewis had successfully passaged the disease’s transmissible component from animal to animal.14

    But what was the passaged agent? “We failed utterly to discover bacteria, either in film preparations or in cultures, that could account for the disease, Flexner and Lewis reported.” Therefore, they concluded, “..the infecting agent of epidemic poliomyelitis belongs to the class of the minute and filterable viruses that have not thus far been demonstrated with certainty under the microscope.”14??Did Flexner and Lewis succeed in isolating poliovirus in 1909? Hindsight being 20/20, it is possible to see that early experiments attempting to create purified poliovirus preparations might well have contained other agents. ??The debate over the nature of the causative agent of poliomyelitis continued. One research team speculated in 1919 that a type of bacteria, cautiously named “poliococcus”, was either the culprit or a co-factor.7 In early experiments, all kinds of biological materials spinal cord, brain, fecal matter, even flies were ground up and injected into monkeys to induce paralysis.4,7,15,21,22,33 These early “virus preparations” were known to contain bacteria. The amount of bacteria was determined by seeding a tissue culture plate with some of the spinal cord (or fecal matter) emulsion to measure how long it took for bacterial colonies to appear. As F.B. Gordon and colleagues pointed out in a paper published in the Journal of Infectious Diseases, “If there was no [bacterial] growth after approximately 22 hours incubation at 37 C., the specimen was considered suitable for inoculation into monkeys. This was not an actual sterility test, since growth would usually occur on longer incubation; it was rather an indication of the amount of bacterial contamination in the specimen.”15

    Early poliovirus researchers, then, knew that the “virus” they were injecting into monkeys also contained an undetermined amount of bacteria. They had no way of determining what else might be present.

    While Flexner and Lewis may have been incorrect in assuming they had transmitted a purified form of “filterable virus” into their monkeys, they certainly transferred a disease-causing agent or agents from animal to animal. Although they could not actually visualize this agent, they described it in the greatest detail that they could. In doing so, which they undoubtedly meant to be a service to other researchers, they may have voiced their conclusions in ways that would haunt poliomyelitis research for decades.

    At the beginning of the 20th century, as scientists began trying to understand and characterize viruses and viral diseases, many of them including poliomyelitis researchers like Flexner and Lewis overstated their findings.

    Early poliomyelitis researchers were true scientific pioneers: Flexner, Lewis, Dalldorf, Landsteiner, Popper, Dulbecco, Sabin, Salk, and many others worked with unknown agents. They didn’t understand the properties of the contaminated tissues they handled, and they didn’t know how to protect themselves from the diseases those tissues might contain. Their bravery in undertaking these risks should never be underestimated, especially in our era when latex gloves, biosafety cabinets, and many other methods of protecting scientists from dangerous transmissible agents are readily available.

    Nevertheless, these early 20thcentury researchers should not get a free pass for their lack of precision in describing experiments and their results.

    For example, in 1948, Gilbert Dalldorf and Grace M. Sickles from the New York State Department of Health published a research report that illustrates some problems in virology that persist even today. Dalldorf and Sickles described an “unidentified, filterable agent” that they had “isolated” from the feces of paralyzed children.6

    The problems become clear when Dalldorf and Sickles described how they “isolated” this agent:

    “Twenty per cent fecal suspensions, prepared by ether treatment and centrifugation, were inoculated intracerebrally into albino mice of the laboratory strain. Suckling mice, 3-7 days of age, became paralyzed, while mice 10-12 gm in weight did not. The isolations were repeated several times.”6

    Dalldorf and Sickles used the word “isolation” to describe their creation of a suspension of fecal matter which was a vast overstatement, to put it mildly.

    Dalldorf and Sickles then attempted to identify the agent. In 1948, antibodies, like viruses, could not be characterized as they now can. “Neutralizing serum”-the non-cellular portion of the blood, taken from a person or animal presumed to be infected with the agent-was used to differentiate between viral strains. This neutralizing serum probably contained antibodies against the agent.

    According to Dalldorf and Sickles, neutralizing serum from paralyzed children inhibited paralysis in mice when they were injected simultaneously with it and the unidentified agent. This absence of evidence-that the mice did not develop paralysis, was interpreted to mean that the agent injected into the mouse had been successfully stopped by the neutralizing serum (i.e., the immune response generated by the sick child). There was no proof, as Dalldorf and Sickles asserted, that the neutralizing serum was reacting with and inhibiting one specific agent.

    Dalldorf and Sickles believed they’d “isolated” a novel agent that could infect people, although they did not argue that it was responsible for producing the paralysis seen in their patients. “The patients we studied may possibly have been coincidentally infected with the new agent and classical poliomyelitis virus, although isolations were not successful in [causing disease in] the rhesus monkey,” they write.6 Again, they write of “isolation” when they are referring to taking a partially processed specimen (spinal tissue or feces) from a paralyzed person and injecting it into an animal to see if the diluted specimen produced paralysis. True isolation did not take place.

    Has Poliovirus Ever Really Been Isolated?

    ßIt is an article of faith in modern medicine that poliovirus has been isolated, characterized, is fully understood and on its way to extinction, thanks to aggressive vaccination/eradication programs. As the recent outbreak in the Dominican Republic illustrates, however, we may be further from eradicating poliomyelitis than we are generally led to believe.
    Furthermore, while the agent identified as poliovirus was certainly cultured in the late 1940s, do we know for sure that it was truly isolated, i.e., grown in a pure form containing no contaminants? We now know that adventitious (“passenger”) viruses like SV40 are common in the monkey tissues that early poliovirus researchers used for cell cultures. While these agents apparently cause no harm to the monkeys, their long-term effects on humans remain to be determined.

    Some 90 years after Landsteiner and Popper”s report of successful transfer of poliomyelitis to monkeys, Dr. Wolfgang K. Joklik reviewed the great leaps forward during the 20thcentury by its defining discipline, virology.19 The occasion was the concurrent 100thanniversaries of the American Society for Microbiology and the field of virology itself. Having served as editor-in-chief of Virology and an editor of Journal of Virology over his long career as a professor of microbiology, Joklik was uniquely placed (as he noted) to evaluate what had been learned since early experiments in virology.

    Before the founding of Virology and Journal of Virology in the 1950s and “60s, respectively, Joklik noted, a number of “epoch-making discoveries in virology” appeared in journals not devoted to the field. Among the seven discoveries he singled out were two related to paralysis research. The first was “the discovery by Enders et al. in 1949 that poliomyelitis virus could be grown in human embryonic tissue cells cultured in vitro, which formed the basis of the technique of tissue culture (single cell culture)”; the second, “”the demonstration by Dulbecco, also in 1952, that an animal virus ” was capable of forming plaques in monolayers of cloned cultured cells, which opened up the field of molecular animal virology.”19 While Dulbecco’s 1952 study did not involve poliovirus, it led directly to his 1954 paper in which he extended the new methodology to the study of poliovirus.8,9

    In 1949, as Joklik recounted, Harvard Medical School researcher John F. Enders, along with his colleagues Thomas H. Weller (a Fellow of the U.S. Public Health Service) and Frederick C. Robbins (a Senior Fellow in Virus Diseases of the National Research Council) showed not only that poliovirus could grow in cultured cells, but also that it could replicate in non-nervous system tissues, a stunning discovery at the time.13 It was already suspected that poliovirus was often present in the intestines of affected individuals. However, no one had been able to propagate the virus in gut tissue, primarily because of the bacteria that naturally live there. Enders and colleagues were successful in part because they added antibiotic (penicillin and/or streptomycin) to their cell cultures to kill the bacteria” a technique that had not, of course, been available to researchers working in the pre-World War II era.

    While Enders and colleagues” 1949 paper is widely acknowledged to be a turning point in poliomyelitis research” many, including World Health Organization poliovirus eradication researchers, credit this piece of science with paving the way for the development of both the Salk and Sabin polio vaccines” poliovirus was not actually isolated by these investigators, either. They successfully grew “filterable agents,” which they assumed to be poliovirus, in human embryonic tissues. Like Landsteiner and Popper 40 years earlier” and like just (jump to rest of article)

    The Dulbecco “Isolation” Experiment

    In 1954, Dulbecco and his colleague Margaret Vogt published a classic research paper that is credited with having set the standard for purifying poliovirus for decades.9 In it, they introduced a technical innovation to the process of “purifying” viruses from tissue culture. This new technique was called “plaque purification”; a single plaque (a circular area of cells that stained differently from the surrounding culture) was considered to represent a pure virus population. Plaque purification utilized trypsinization, which involves treating the cells” in this case, monkey kidney cells” with the enzyme trypsin, breaking up any clumps of cells that might have formed and resulting in a single-cell suspension. 
    In the early days of poliovirus research, tissue culture was usually conducted using monkey kidneys (or, sometimes, monkey testes). Dulbecco and Vogt explained where the “virus” they grew came from:

    “The virus was supplied as a 20 per cent suspension of spinal cord of rhesus monkey in distilled water. Type 1 virus obtained from passage through the monolayer kidney cultures was used. Type 2, Yale-SK strain, and Type 3, Leon strain, were kindly supplied by Dr. J.L. Melnick in form of tissue culture supernatants.”9

    That passage clearly demonstrates that Dulbecco and Vogt did not isolate pure poliovirus in any of the experiments described in this 1954 report. While they write of seeding their cultures with “virus,” they actually used unpurified suspensions, not pure viral isolates.

    Once the monkey kidneys were ground up into “single cells, cell clusters, and cell debris,” they were seeded with the monkey spinal cord emulsion. The appearance of the plaques was evidence that the virus was growing, according to the model Dulbecco had developed in 1952.8 

    The control for these experiments was to treat the cultures with monkey antiserum (derived from monkeys infected with Type 1, 2, or 3 poliovirus); if Type 1 antiserum inhibited plaque formation but Type 2 or 3 (or normal monkey) antiserum didn’t, then Type 1 poliovirus was assumed to be exclusively present in the culture. In other words, it was assumed that no other organism or disease-associated agent was growing in the culture.

    Once again, what Dulbecco and Vogt describe as “isolation” of the poliovirus is not isolation in the way we would understand it in modern microbiology. To perform their “plaque purifications,” they simply pipetted some liquid (“plaque stock”) from one culture plate and replated it onto other culture plates. When the second-generation cell cultures showed evidence of viral growth (i.e., plaques), monkeys were inoculated with the plaque stock. The inoculated monkeys developed paralysis and, subsequently, most died. Since the plaque purified viral stock both grew new plaques in second-generation cell culture and caused monkeys to develop flaccid paralysis, Dulbecco and Vogt concluded they had “isolated” poliovirus. 

    Like poliovirus researchers before them, it is clear that Dulbecco and Vogt were propagating disease-associated substances in their tissue cultures, and that they later transferred these substances to monkeys in whom acute flaccid paralysis developed. These were impressive accomplishments.

    Dulbecco and Vogt’s claims, however, went further than they had evidence to support. They asserted not only that they had isolated poliovirus, but that, “Since each plaque stock originated from a single virus particle (as proved in the Discussion), these stocks constitute the purest lines of virus presently available.”

    How could they possibly know that a “single virus particle,” something they had never seen or measured, was causing the growth of exactly one plaque in their cultures? The evidence Dulbecco and Vogt supplied to “prove” that a single virus particle produced each plaque is contained in a mathematical equation: They extrapolated the cell culture’s assumed “virus concentration” from the number of times the original fluid (for example, monkey spinal cord suspension) was diluted. The fewer times the fluid was diluted, the more plaques grew in laboratory cultures; the more times it was diluted, the fewer plaques grew. Dulbecco and Vogt’s mathematical model assumed this linear relationship between dilution of virus stocks and number of plaques formed and, when they reached the greatest possible dilution that still caused a single plaque to grow, they assumed that only one “virus particle” was present therein. And how did they prove that assumption, as promised? They provided their mathematical model. This is a perfectly tautological proof. Its most apparent flaw is that the mathematical model “could not” distinguish between a “single virus particle” and a biological complex that may have contained a single virus. This is made clear in Dulbecco and Vogt’s description of the plaque-forming “single virus particle” they claim to have isolated:

    “Having arrived at this point, it is now possible to define properly the characteristics of the virus particle detected by a plaque. Owing to its all-or-none effect, it has the character of a particle. It corresponds to a unit of the virus which is not further subdivisible at high dilution. From the property by which it is recognized, we call it a plaque-forming particle. We do not know its morphological or genetic properties. It might be a single elementary body, or a clump of them, provided that the clump persists indefinitely at high dilution….”9

    It is puzzling, in retrospect, that Dulbecco and Vogt raised the possibility that they were detecting a “clump” of material, but thereafter ignored it. What if another type of virus was also included in these particles? Or, what if host genetic material attached itself to the particle to form a “clump”? 

    Although electron microscopy “which would have allowed them to visualize a single viral particle” existed in 1954, Dulbecco and Vogt did not use it. Instead, they employed the time-honored technology in which viruses were assumed to be present in cultures if certain chemicals stained them, or if fluids thought to contain them produced characteristic patterns of growth, like the poliovirus-related plaques described here. Dulbecco and Vogt could not possibly determine that they were viewing single viruses in their cultures and, therefore, their assumption that they had isolated a “single virus particle” was a vast overstatement. Dulbecco and Vogt did not isolate poliovirus.

    about everyone else in the field during its first 60 years or so Enders and co-workers called this disease-transmitting suspension of tissue “virus.”

    Despite this overstatement, Enders, Weller, and Robbins were the first to prove that a transmissible agent associated with poliomyelitis could be propagated in cells in the laboratory, and that cell cultures could be substituted for live animals in studying such transmissible agents. In 1954, their ground-breaking work was rewarded with a Nobel Prize.

    Renato Dulbecco’s 1952 paper lauded by Joklik is considered to have made a significant contribution to viral research in general and, by extrapolation, to poliovirus research. Working at the California Institute of Technology (in Pasadena), Dulbecco developed a method of growing plates of cells so that “virus plaques” could be visualized.  He grew Western Equine Encephalomyelitis virus plaques on a substrate of chicken embryo cells and, when he published his paper, he pointed out that it was still unknown whether all viruses could be cultured in this manner. These were truly the very earliest days of modern virological research, and Dulbecco expressed hope that investigators would some day be able to distinguish between various viruses grown in cell culture by using his methodology and examining the resulting plaques under the microscope.8

    In 1954, Dulbecco and his colleague Margaret Vogt published a classic research paper [see sidebar, “The Dulbecco Isolation Experiment,” above] that set the standard for purifying poliovirus cultures for decades.9Dulbecco and Vogt, like their colleagues, used monkey kidney cells to culture tissues thought to contain poliovirus. Dulbecco and Vogt explained where the “virus” they grew came from:

    “The virus was supplied as a 20 per cent suspension of spinal cord of rhesus monkey in distilled water. Type 1 virus obtained from passage through the monolayer kidney cultures was used. Type 2, Yale-SK strain, and Type 3, Leon strain, were kindly supplied by Dr. J.L. Melnick in form of tissue culture supernatants.”9

    In other words: Dulbecco and Vogt did not isolate pure poliovirus in any of the experiments described in this 1954 report. While they write of seeding their cultures with “virus,” they actually used unpurified suspensions, not pure viral isolates.

    It is clear from this historical review of early poliovirus research papers that none of these poliomyelitis researchers truly isolated poliovirus. Additionally, they were injecting monkeys with experimental fluids that were probably contaminated with other disease-associated agents.

    Further confusing the picture (but not reviewed here) is the fact that enteroviruses other than poliovirus are associated with AFP. For example, as recently as February 2001, it was shown that Coxsackie A24 is associated with nonpolio AFP.5

    How Much Flaccid Paralysis Is NOT Caused by the Poliovirus?

    There is an astonishing number of cases of paralysis around the world not associated with poliovirus. If you visit the World Health Organization website that tracks acute flaccid paralysis (AFP), polio and non-polio, you will see that the world is not rid of the scourge of AFP. For example, India reported 9,580 cases of AFP in 1999; 2802 of them, fewer than one-third, were associated with poliovirus. China reported 5,064 cases of AFP to WHO in 1999; only one of those cases was associated with poliovirus. Poliovirus eradication and vaccination programs have not eliminated paralysis.

    WHO recently declared Egypt on the threshold of eradicating poliovirus. “We are now at the end of a polio era,” a UN Children’s Fund Project Officer told Reuter’s news service in late February 2001. Egypt had “not a single case of the crippling virus reported so far this year” or in 2000, according to Reuters.17

    According to the WHO AFP/polio surveillance web site, however, there were 54 cases of acute flaccid paralysis in Egypt in 2000 (the most recent year for which statistics are available). In 1999, although there were 9 AFP cases classified as due to poliovirus, 276 were classified as nonpolio. During 1998, Egypt had 295 cases of AFP, 35 of which were classified as poliovirus-related; in 1997, Egypt reported 217 cases of non-polio paralysis compared to 14 cases in which poliovirus infection was confirmed; and in 1996, the earliest year for which statistics are available, Egypt reported 309 cases of acute flaccid paralysis. One hundred of those were classified as poliovirus-related, leaving 209 cases “two-thirds of the total” probably due to a cause other than poliovirus (with the caveat that epidemiological statistics are not perfectly accurate in every country of the world).

    Afghanistan is another country in which there is an increasing prevalence of AFP compared to a decreasing incidence of poliovirus. As the U.S. Centers for Disease Control and Prevention’s Morbidity and Mortality Weekly Report (MMWR) notes on March 2, 2001, “During 1999-2000, the number of AFP cases [in Afghanistan] increased from 230 to 253, and the number of wild polioviruses isolated from AFP cases decreased from 63 to 28.”28 

    How does the CDC explain the increase in AFP cases in Afghanistan, in the face of a vigorous poliovirus eradication campaign? Well, it doesn’t. In fact, the MMWR report almost makes the increase in nonpolio AFP sound like a triumph of public health: “During 1999-2000, the nonpolio AFP rate almost doubled and the number of districts reached by NIDs [National Immunization Days] increased steadily. Careful planning and supervision of house-to-house vaccination and support from an increasing number of local partners resulted in the largest number of children ever being reached. Monitoring by nongovernment organizations, United Nations” agencies, and local authorities has increased the quality of NIDs”.”28 In other words, the more National Immunization Days there were, the more cases of paralysis appeared. Does this mean immunizations were causing paralysis? No, but neither was increased immunization preventing children from becoming paralyzed.

    The Western Hemisphere has also been impacted by an increased case load of AFP. As mentioned earlier, the island of Hispaniola (the Dominican Republic and Haiti) experienced what the CDC called an “outbreak of poliomyelitis” that began in July 2000. There were 54 cases in the Dominican Republic, 12 of which were

    Polio Vaccination Recommendations, U.S. Centers for Disease Control and Prevention

    Recommendations for children in the United States include a 4-dose vaccination series with inactivated poliovirus vaccine (IPV) at ages 2, 4, 6″18 months, and 4″6 years. Unvaccinated adults should receive three doses of IPV, the first two doses at intervals of 4″8 weeks and the third dose 6″12 months after the second. If three doses cannot be administered within the recommended intervals before protection is needed, alternative schedules are proposed. For incompletely vaccinated persons, additional IPV doses are recommended to complete a series. Booster doses of IPV may be considered for persons who previously have completed a primary series of polio vaccination and who may be traveling to areas where polio is endemic.

    Morbidity and Mortality Weekly Report, March 2, 2001, Vol. 50, No. 8, p. 147

     “laboratory-confirmed poliomyelitis cases attributed to vaccine-derived poliovirus type 1,” according to the CDC. Although the oral polio vaccine is known to cause polio in about 1 of every 750,000 infants who receive it or their mothers.  Unlike the inactivated Salk vaccine “shot,” the Sabin oral vaccine contains live viruses.  The 45 cases reported in January 2001 in the Washington Post are, if confirmed, clearly outside the realm of this statistic.3

    As of the end of February 2001, the cause(s) of 33 AFP cases in the Dominican Republic and three in Haiti remained undetermined.27 All of these cases might be due to the oral polio vaccine, in which case the mystery would be solved, leaving unanswered, however, the question of what factors contributed to such a large vaccine-associated outbreak of paralysis. 

    If these 36 AFP cases are not related to the polio vaccine, however, then what is causing them?  What is causing other nonpolio outbreaks of AFP identified by WHO all over the world?

    And in cases in which poliovirus is fingered as the culprit in an outbreak, how sensitive are the current methodologies that virologists use to isolate and identify it?

    How Is Poliovirus Detected Today?

    It is nearly unimaginable how sensitive and sophisticated laboratory technology has become over the last 30 years. As we examine the entire sequence of the human genome in early 2001, it’s difficult to imagine that it was only in the 1970s that scientists first developed the technology that allowed the rapid sequencing of genes, including genetic sequences from transmissible agents like bacteria and viruses. 

    This new sequencing methodology was immediately applied to poliovirus research. During the 1970s, the CDC began routinely performing genotypic testing (“molecular sequencing” or “oligo-nucleotide fingerprinting”) on stool samples collected in suspected poliovirus outbreaks to determine whether the virus was present. Using findings from the new technology to extrapolate to the prior decade, CDC documents now state that, “Both laboratory surveillance for enteroviruses and surveillance for polio cases suggest that endemic circulation of indigenous wild polioviruses ceased in the United States in the 1960s.”24

    To detect poliovirus today, according to CDC and WHO guidelines, two stool samples should be collected from each patient, 24-48 hours apart within 14 days of the onset of paralysis, and they must arrive at the laboratory in “good condition.” While WHO’s target is to obtain two good samples in at least 80% of all AFP cases, some areas of the world fall short of this, approaching only 50%.28

    The CDC provides the following guidelines on how to detect poliovirus:

    “The following tests should be performed on appropriate specimens collected from persons who have suspected cases of polio: a) isolation of poliovirus in tissue culture; b) serotyping of a poliovirus isolate as serotype 1, 2, or 3; and c) intratypic differentiation using DNA/RNA probe hybridization or polymerase chain reaction to determine whether a poliovirus isolate is associated with a vaccine or wild virus.

    “Acute-phase and convalescent-phase serum specimens should be tested for neutralizing antibody to each of the three poliovirus serotypes. A fourfold rise in antibody titer between appropriately timed acute-phase and convalescent-phase serum specimen is diagnostic for poliovirus infection. The recently revised standard protocol for poliovirus serology should be used. Commercial laboratories usually perform complement fixation and other tests. However, assays other than neutralization are difficult to interpret because of inadequate standardization and relative insensitivity.”24

    While this procedure is a time-honored method of detecting the poliovirus and the body’s response to it, it does not “isolate” the poliovirus, it simply detects poliovirus. The samples tested by the CDC and WHO should be described as “poliovirus reactive material,” not as samples that contain isolated, pure poliovirus.

    Once again, we have no proof that poliovirus has been isolated.

    If Not Poliovirus, Then What Is Causing Today’s Cases of Flaccid Paralysis?

    “The history of the etiology of poliomyelitis is a history of errors.”

    J.F. Eggers, Medicine, 1954

    If the majority of the U.S. population has been immunized since the 1950s, why did it take until 1979 to “eradicate” poliovirus within the United States?24,31

    And what is causing the nonpolio cases of paralysis that continue to occur all over the world?

    It is becoming clear that one culprit capable of causing not only paralysis but also other neurological conditions is organophosphate pesticides. Recent research has tied chronic organophosphate pesticide exposure to development of Parkinson’s disease signs and symptoms in an animal model.2 And researchers in Paraguay have good evidence that an outbreak of AFP among children in 1990-1991 was associated with organophosphate pesticide exposure.

    The 50 Paraguayan children identified in this study, given that it was conducted in a rural, isolated area meant that quite a number of affected children might have been excluded from the study, as investigators noted, developed a type of AFP named Guillain-Barré Syndrome, or GBS. As is the case in other forms of AFP, the myelin sheath that surrounds and protects nerves is damaged in GBS. The disease’s causes are unknown, but it’s generally believed to be an autoimmune condition provoked by infections, toxins, or a combination of both.16

    The children became ill during the Paraguayan summer (January to April), with weakness, upper respiratory tract infection, fever, and gastrointestinal symptoms. Three children developed difficulty breathing, and two of them required mechanical help to breathe (intubation). “Weakness progressed in an ascending pattern in 95% of the children, and simultaneously in all limbs in 5%; the average time to reach the nadir was 7 days (range, 2-12 days),” the investigators reported. Of the 35 children observed while they were in the acute stage of AFP, 18 were unable to walk, 10 walked with assistance, four walked independently, and three were too young to walk. The children exhibited full or partial paralysis of facial muscles and their bladders; they also experienced autonomic nervous system changes that created fluctuations in blood pressure, erratic heartbeat, flushing of skin, and intestinal motility. One child died.16

    The study was conducted as part of the Pan American Health Organization’s effort to eradicate poliomyelitis. David E. Hart of the U.S. National Institute of Neurological Disorders and Stroke at the National Institutes of Health was the lead investigator working alongside researchers from the Paraguayan Ministry of Health.16 The majority of cases, they point out, were clustered in a rural, farming province named Concepcion.

    “The clustering of patients in Concepcion could be related to the use of organophosphate pesticides in the cotton fields,” Hart and colleagues suggest. “Farmers use great amounts of these pesticides, often in concentrated form, and empty containers serve as toys. Also, the maximum usage of organophosphates occurs during the summer (December-March),” when these children became ill.16

    Although they note that retrospective measurement of organophosphate exposure is very difficult, Hart and co-workers cite a report that the cotton industry officially spent approximately US$ 6.7 million on organophosphate pesticides in 1991. However, more than half of the pesticides used in Paraguay are obtained “unofficially,” according to this report.

    “Four children were excluded from this study because of definite exposure to this product and presentation with concurrent acute cholinergic syndrome,” the severe disease produced by organophosphate pesticide exposure. Hart and colleagues added, “Their clinical course, however, was similar to that of the children included” in the study.16

    By examining the possibility that the AFP observed in these Paraguayan children might be associated with organophosphate pesticides, Hart and colleagues took that extra step that is so often omitted. Clusters of illnesses in communities can arise from any number of causes; they are not exclusively due to transmissible agents. Toxins in the environment are significant factors in many illnesses.

    Since the time of Koch, bacteriologists have used the gold standard he described for the assignment of the disease process to single organisms. Bacteria and fungi can be truly isolated and grown independently on artificial media; they don’t require the presence of human or other cells. One problem that researchers have faced in describing non-bacteriologic related diseases has been the assumption that a single entity can cause them, without interaction from the cells in which they are grown, the human genome, or the environment. 

    We live in a important time: We are about to redefine much of what we know about medical science. In early 2001, two stunning reports on the Human Genome Project, published simultaneously in February issues of Science and Nature, turned much of what we thought we knew about the human genome on its head.  Instead of possessing 100,000 genes, for example, we learned that the human genome is made up of only about 30,000 genes, fewer than the number possessed by rice.1

    Our new understanding of the human genome was produced, in part, by new technologies that we can now apply to revisiting many of the assumptions of modern medicine. One of the most important lessons learned from the challenge of decoding the human genome is that scientists need to describe laboratory experiments and results accurately. Technologically advanced tools can provide detailed and precise information, but the researchers using them must describe those results with equal precision. When a sample is laboratory reactive, it should not be assumed to be infectious. Likewise, suspensions of diseased brain tissue should not be called “virus” and dilutions of brain tissue material should not be called “isolations.”

    As the human genome comes more precisely into focus, our understanding of how our genes interact with one another, the environment, and other organisms will also become more precise. 

    Precision should also be applied to research objectives. Clearly, it is incorrect to state that poliomyelitis has been eradicated from many countries. The surprisingly large number of cases of nonpolio acute flaccid paralysis around the world warrants continued pursuit of the original objective of the March of Dimes: the elimination of infantile paralysis. On its website, the March of Dimes takes some well-deserved credit for helping to limit the amount of paralysis in the world today. “Historians have called the conquest of polio one of the great achievements of this century,” a fact sheet on the website states. “Thanks to the March of Dimes, and the millions of people who supported it, we no longer have the devastating epidemics that terrorized generations.”

    Clearly, the original objective of the March of Dimes has not yet been met, or there would not be so much acute flaccid paralysis around the world today. Examining the last 50 years of poliomyelitis research shows that the objective of eliminating infantile paralysis has been replaced with the objective of eliminating poliovirus. As governments, international health organizations, and charitable foundations pour hundreds of millions of dollars into poliovirus eradication efforts, shouldn’t we also invest in basic research that will prevent all cases of childhood paralysis?

    Acknowledgement: The author wishes to thank Dr. Howard Urnovitz, Science Director of the Chronic Illness Research Foundation, for bringing this story to her attention and approving the scientific content of this article.

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