The following article appeared in the pages of Pediatrics in the early 50s. The evidence was obvious that Polio was NOT an infectious, transmissible disease. It was only after the criminal elements in organized medicine and the vaccine industry conspired that Polio was then presented as an infectious epidemic disease in order to sell vaccines.
One of the largely unknown criminal acts committed by organized medicine immediately after Polio vaccines were put in use, was to advise doctors not to report new cases of Polio until tbirty days after the onset of symptoms. This of course helped make the vaccines look good by eliminating the cases misdiagnosed early on. Doctors often labeled every kid with a stiff neck and fever as a Polio statistic, waiting thirty days eliminated those mistakes from the overall count. Another ruse was to rename Polio and call it Aseptic Meningitis. It has been known by 200 names over the years.
A very significant effect on the early Polio numbers resulted from the efforts of Benjamin Sandler MD who conclusively proved that sudden high doses of dietary sugar caused Polio. His diet was widely published in every major newspaper in the country and summer sales of high sugar junk foods were outlawed in his small North Carolina community stopping new cases of Polio. He published a book entitled, “Diet Prevents Polio” another proof of the poison cause of Polio.
Australian medical doctors killed half of the Polio-vaccinated Aborigine children until one MD tried using vitamin C before the shots. The Book, “Every Other Child” tells the story. It was vitamin C that eventually stopped the wholesale slaughter of Australian Aborigine children by the medical quacks.
When the Japanese stopped vaccinating their infants and waited until the children were two years old, Japan immediately moved up into first place in infant mortality, proving conclusively that vaccinations kill babies.
When Dr Vieara Scheibner of Australia discovered that DPT shots were causing crib deaths, the medical fraternity ignored her but the public demand for the DPT shots, which are strictly voluntary in Australia, dropped by approximately 50% and the crib death rate immediately dropped about the same amount, again proving that vaccination kills babies.
It is my opinion, based upon my knowledge, experience and historical proof, that any doctor who vaccinates an infant belongs in jail not in practice.
In my opinion, vaccination is the quintessential quackery of the 21st century and the fact that it is MANDATORY in some areas is the most repulsive, unacceptable act that has ever been forced on free peoples anywhere at any time in history.
Everyone must educate themselves on the facts, often hard to find, and then make their own decisions on whether or not to subject themselves, their children, and their loved ones to vaccination.
VIOXX causes Aseptic Meningitis – the current euphemism under which POLIO masquerades these days.
VIOXX is one of the current poisons that cause Polio.
Check your Physicians Desk Reference (PDR).
Other drugs that can cause POLIO are IBUPROFEN, NAPROXEN, SULINDAC and TOLMETIN.
(Polio was renamed Aseptic Meningitis after the vaccines went into use, thereby effecting a partial reduction in Polio by euphemistic redefinition.)
In our age, redefining 25 old diseases as AIDS helped create the fake AIDS epidemic of today.
Before getting into the POISON CAUSE OF POLIO article one more comment to help drive home the point. The following is from John at whale.to in answer to an article I sent to one of the anti-vaccination websites – I added the bold print and underline [DHD Sr].
Talking of various polio terms I came across some GBS (another polio one) ones. Amazing really:
GBS is short for Guillain-Barré-Strohl syndrome which is long for just plain Guillain-Barré.
The point is that GBS is Also known by the following names:
Glanzmann-Saland syndrome (misnomer)
Synonyms for the above named:
Acute ascending polyradiculoneuritis, acute polyneuritis, acute febrile polyneuritis, acute idiopathic polyneuritis, acute infectious polyneuritis, acute inflammatory demyelinating polyradiculoneuropathy, acute plexitis, acute polyneuritis with facial diplegia, acute polyneuronitis, acute polyneuropathy, acute polyradiculitis, ascending paralysis, acute postinfectious polyneuropathy, celluloradiculoneuritis, encephalomyeloradiculoneuritis, febrile polyneuritis, idiopathic polyradiculoneuritis, infectious neuronitis, infectious polyneuritis, infectious polyneuronitis, inflammatory polyneuropathy, myeloradiculitis, neuritis with albuminocytologic dissociation, neuromyelitis hyperalbumenotica, neuronitis, paralysis spinalis ascendens acuta, polyneuritis with facial diplegia, polyradiculitis, polyradiculoneuritis, polyradiculonévrite inflammatoire (aiguê), postinfectious radiculoneuropathy, radiculoneuritis, schwannosis. All are believed to be the same syndrome. This disturbance has been described by various eponymic terms, which are now all believed to be the same disease. The term Glanzmann-Saland syndrome (severe polyneuritis following diphteriae) has also been used, but that is a misnomer – for more information along these lines go to – http://www.whonamedit.com/synd.cfm/1766.html
The Poison Cause of Poliomyelitis
To Its Investigation
Statement prepared for the Select Committee
to Investigate the Use of Chemicals in Food Products,
United States House of Representatives, Washington, D.C.
Archives of Pediatrics, April 1952
Ralph R. Scobey, M.D.
The disease that we now know as poliomyelitis was not designated as such until about the middle of the 19th Century. Prior to that, it was designated by many different names at various times and in different localities.1,2 The simple designations, paralysis, palsy and apoplexy, were some of the earliest names applied to what is now called poliomyelitis.
Paralysis, resulting from poisoning, has probably been known since the time of Hippocrates (460-437 B.C.), Boerhaave,3 Germany, (1765) stated: “We frequently find persons rendered paralytic by exposing themselves imprudently to quicksilver, dispersed into vapors by the fire, as gilders, chemists, miners, etc., and perhaps there are other poisons, which may produce the same disease, even externally applied.” In 1824, Cooke,4 England, stated: “Among the exciting causes of the partial palsies we may reckon the poison of certain mineral substances, particularly of quick silver, arsenic, and lead. The fumes of these metals or the receptance of them in solution into the stomach, have often causes paralysis.”
Colton5 (1850) mentions the case of a patient who swallowed some arsenic accidently and was admitted to the hospital. The primary effects of the poison had been successfully combatted with proper remedies, but seven days afterward he became paralyzed. It is significant to note that there was a latent period of several days before the paralysis appeared since this delayed reaction is comparable to the incubation period in infectious diseases.
Vulpian6 (1879) experimentally produced paralysis of the extensor muscles of a dog by lead poisoning. The lesions, consisting in colloid degeneration and cell atrophy of the anterior horn cells of the spinal cord were pronounced by Vulpian as poliomyelitis. Adamkiewitz7 (1879) reported two parallel cases, one of poliomyelitis and one of lead poisoning.
In 1881, Popow8 of St. Petersburg, published an essay upon the pathological anatomy of arsenical paralysis as produced artificially in animals. The work of Popow was carried out under the guidance of the distinguished neurologist and microscopist, Professor Mierzeyeski. Popow concluded that arsenic, even in a few hours after its ingestion, may cause acute central myelitis or acute poliomyelitis.
During an epidemic of poliomyelitis in Australia in 1897, Altman9 pointed out that phosphorus had been widely used by farmers for fertilizing that year. This observation may be of significance since in recent years organic phosphorus insecticides, such as parathion, have been suspected as possible causes of poliomyelitis.
Onuff10 (1900) reported a case of a painter with flaccid paralysis of both legs, in whom the autopsy showed lesions characteristic of poliomyelitis.
Obsrastoff11 (1902) reported a case of acute poliomyelitis resulting from arsenic poisoning. Phillippe and Gauthard12 (1903) reported a case of anterior poliomyelitis from lead poisoning.
Gossage13 (1902), writing on infantile paralysis, says: “The nerve cells or fiber may be acutely disabled by the action of some poison circulating in the blood, and it is possible that such poison would only temporarily impair their functions or so seriously affect them that recovery would be impossible.”
Dr. David E. Edsall14 (1907), writing on the pathology of carbon monoxide poisoning in Osler’s System of Medicine, states: “Peripheral neuritis had repeatedly been described and poliomyelitis and disseminated encephalitis have been seen.”
Collins and Martland15 (1908) reported a case of poliomyelitis in a man, 38 years of age, which resulted from the use of cyanide as a silver polish. The illness began with diarrhea, followed by headache and pain and stiffness in the back fo the neck. About eight days after the onset of the illness, he became paralyzed. In discussing collins and Martland’s paper, Larkin stated that he had seen one instance of this disease following potassium cyanide poisoning.
In the spring of 1930, there occurred in Ohio, Kentucky, Alabama, Missippi and other states an epidemic of paralysis.16,17 The patients gave a history of drinking commercial extract of giner. It is estimated that at the height of the epidemic there were 500 cases in Cincinnati district alone. The cause of the paralysis was subsequently shown to be triorthocresyl phosphate in a spurious Jamaica ginger. Death resulted not infrequently from respiratory paralysis similar to the bulbar paralysis deaths in poliomyelitis. On pathological examination, the anterior horn cells of the spinal cord in these cases showed lesions similar to those of poliomyelitis.
These incidents show that epidemics of poisoning occur and furthermore, that epidemic diseases do not always indicate that they are caused by infectious agents. Moreover, following the ingestion of the spurious Jamaica giner, the symptoms appeared two to ten days later. In some cases a longer time elapsed. This latent peior is comparable to the incubation period of infections diseases. As a matter of fact, the incubation period of poliomyelitis is commonly stated to be seven to 10 days on the average with considerable variation in either direction. The so-called incubation period in poliomyelitis and the latent period in these cases of poisoning, therefore, are strikingly similar in length.
Leenhardt et al.18 (1951) described acrodynia in the course of three cases of acute poliomyelitis. Some authorities have considered acrodynia to be caused by a poison. Elmore19 (1948) reported two cases of this disease following the ingestion of mercury and Warkany and Hubbard20 (1951) found mercury in the urines of 38 (92.7 per cent) of 40 acrodynia patients. Meyerhofer21 (1939) reported that infantile acrodynia may immeidiately follow certain forms at atypical poliomyelitis, especially encephalomyelitis. Mercury is used as an insecticide and a fungicide and the above clinical observations indicate that it might be a factor in producing some cases of poliomyelitis.
Gougerot22 (1935) reported that during arsenical therapy for syphilis, poliomyelitis developed in two patients, and lethargic encephalitis followed by Parkinson’s disease in one.
In 1936, during a campaign to eliminate yaws in Western Samoa by the injection of arsenicals, an epidemic of poliomyelitis appeared simultaneously.23 In one community all of the patients developed payalysis in the same lower limbs and buttocks in which they had received the injections and this pattern was repeated in 37 other villages, whereas there was no paralysis in uninoculated districts. The natives accused the injections as the cause of the epidemic of poliomyelitis. Most of the cases of paralysis occurred one to tow weeks after the injection of the arsenic.
The foregoing reports indicate that poisons can cause poliomyelitis. It would appear that not any one poison in particular would be responsible for all cases of poliomyelitis but the effect of any one of several could produce the same ultimate result. When a disease is known to be caused by a poison, it is obvious that a search for a germ or virus in relation to it would not be made. Conversely, if a so-called virus is believed to be associated with the disease, then the possibility of poisoning as the cause of the disease would not be considered. It will be shown, moreover, that some so-called virus diseases and virus inclusions can be caused by poisons.
Dr. Robert W. Lovett24 of the Massachusetts State Board of health (1908), describing the epidemic of poliomyelitis in Massachusetts in 1907, and after reviewing the medical literature on experimental poliomyelitis, states: “The injection experiments prove that certain metallic poisons, bacteria and toxins have a selective action on the motor cells of the anterior cornua when present in the general circulation; that the paralysis of this type may be largely unilateral; that the posterior limbs are always more affected than the anterior; and that the lesions in the cord in such cases do not differ from those in anterior poliomyelitis.” It appears to be of great importance that various poisons, lead, arsenic, mercury, cyanide, etc., found capable of causing paralysis are employed in relation to articles of food that are used for human consumption.
There are two abnormal findings in cases of poliomyelitis that point strongly to poisoning as the cause of this disease. One consists in the appearance of increased amounts of porphyrin in the urine; the other is the presence of increased amounts of guanidine in the blood. It is a well-known fact that porphyria can follow poisoning by a number of chemicals. Guanidine has been found in increased amounts in the blood in arsenic, chloroform, and carbon tetrachloride poisonings.
The fact that ascorbic acid has been effective in the treatment of poliomyelitis appears justly to imply that this disease has a poison cause. Ascorbic acid has been used as a reducing agent in the treatment of poisoning resulting from a number of toxic agents, including coal tar antipyretics, nitro compounds, analine, cyanide, benzene, lead, arsenic, etc.32-40 Paralleling these modern scientific investigations is the observation over a century ago that lime juice and lemon juice were protective against the poisoning by fish which sometimes resulted in paralysis,41,42. This early observation is perhaps the principle reason why lemon juice is customarily served today when fish are eaten.
The fact that methylene blue,43 another reducing agent, is effective in the treatment of poliomyelitis also points to the poison cause of this disease. Methylene blue has been used as an antidote in the treatment of nitrite, cyanide, carbon monoxide and other poisonings.
Another fact that strongly implies that human poliomyelitis is caused by a poison is found in the recent report (1951) by Dr. Irwin S. Eskwith44 of Bridgeport, Conn., that BAL (dimercaprol) was effective in bringing about complete recovery in a moribund 4 1/2 year-old girl with bulbar poliomyelitis. BAL counteracts the effects of poisons; it has been shown not to be effective in infectious diseases.
RELATIONSHIP OF HARVEST TO POLIOMYELITIS
In 1907, Dr. H. C. Emerson54, Massachusetts State Inspector of Health, District 14, investigating an epidemic of poliomyelitis in that state, made a careful inquiry regarding the diet. No infant who was fed exclusively on the breast developed poliomyelitis. He found in six cases that fruit and berries had been a large item of the diet. In the cases of two infants, bananas and berries had been given in the diet in addition to breast milk. In three cases of poliomyelitis, the illness was attributed to the eating of large amounts of blackberries and blueberries. In one case the illness was credited to eating heartily of English mulberries. In 39 instances it was stated that food supplied were bought from fruit and vegetable peddlers in their localities.
Dingman55 (1916) reported a milk-borne epidemic of poliomyelitis and several similar outbreaks have been reported since then that were traceable to milk.
Chapman58, raised the question of food poisoning to explain the epidemic of poliomyelitis in England in 1947, when he stated: “Is it not possible that the present prevalence of infantile paralysis may, in part at any rate, be due to some article in our restricted and modified dietary?”
Toomey and August59 (1932) pointed out that some authors thought that poliomyelitis is a disease of gastrointestinal orgin which might follow the ingestion of foodstuffs. In 193360, they noted that the epidemic peak of poliomyelitis corresponds with the harvest peak of perishable fruits and vegetables. They called attention to the fact that the disease occurs only in those countries which raise the same type of agricultural products. Dr. C.W. Burhans60, one of the colleagues of the authors, thought that green apples might be a factor in the etiology of poliomyelitis. Toomey et al61. (1943) points out that there is frequently a history of dietary indeiscretions previous to an attack of poliomyelitis. They suspected that a virus could be found on or in unwashed fruit or in well water during epidemics of poliomyelitis. Every year for eight years, therefore, grapes, apples, peaches, and pears were collected from the vineyards and trees in Northern Ohio at the time of the ripening. In none of their studies was the so-called virus of poliomyelitis demonstrated when the washings of the fruit or the well water were injected into experimental animals. However, no chemical tests were made to determine whether or not a chemical substance on or within the fruit or in the well water, acting by oral ingestion top produce poliomyelitis, was present.
Draper62 (1935) recorded a series of cases of poliomyelitis which he postulated originated from a Greek fruiterer. All of the cases were in contact with the Greek as business associates, relatives or customers, and there was nothing in the evidence to point to infection being carried by the Greek himself other than the fruit he supplied.
Barber64 (1939) reported four cases of poliomyelitis that developed simultaneously on the same day from the eating of strawberries in a single house of a boarding school. He says that the simultaneous onset of these cases resembled food poisoning. The seasonal and climatic incidence of poliomyelitis, he points out, agree closely with the seasonal increase in the consumption of fresh garden production. He says that the epidemiological distribution of poliomyelitis resembles food poisoning.
Chenault65 (1941) noted that the history of poliomyelitis points to a “suggested parallelism between a number of epidemics and the appearance of fresh fruits and vegetables.” [With regard to these numerous statements regarding fruit and milk, note the high production of pesticides in the form of lead and arsenic coumpounds during this pre-DDT period, graphed]
Goldstein et al66 (1946) reported an epidemic of polioencephalitis at a naval training school among the cadets. The epidemic was explosive in character and involved over 100 persons. Epidemiological evidence suggested that some food served in the mess hall was the cause of the disease.
Gebhardt and McKay68 (1946) found during an epidemic of poliomyelitis in Utah that of a total of 206 persons surveyed, 192 persons, or 93.2 per cent, had one to two weeks prior to the onset of the disease eaten fresh fruits. The authors found in Utah, New York and California, during 1943, that the cases of poliomyelitis paralleled the harvest peaks. Most of the multiple cases in families were found to have developed at the same time, suggesting means other than contact as the mode of spread. Among the fruits more commonly eaten were apples, peaches and pears; tomatoes headed the list of vegetables. The authors stated that the data appeared to fit into the jigsaw puzzle of epidemic poliomyelitis.
Abbott71 (1948), of Auckland, New Zealand, stated: “The public has always been fully convinced that they caught poliomyelitis from one another by direct infection. The ‘germ’ idea is indeed deeply ingrained in both the profession and the public. It will be many years before our prolific writers of medical textbooks attain the degree of sophistication that would enable them to understand how and why poliomyelitis would be more likely to be contacted from the flour-bag, or some homely article of food, rather than from their neighbors.”
Barondes72 (1949) points out that a study of the epidemiology of poliomyelitis shows a definite correlation with the harvesting of fruit and vegetable crops and to changes in climate, weather and humidity. The harvesting of such fruits as cherries, grapes, berries, apricots, etc. and the edible vegetables, as lettuce, radish, cucumbers, etc. usually from June to September, corresponds with the period of poliomyelitis epidemics, Barondes points out.
Toomey et al74 (1949) made some important experimental observations that appear to show a correlation of the poison and virus theories of poliomyelitis. They considered it possible that a food (fruit) which enters the gastrointestinal tract could in some way act as a precursor of catalytic enzyme on a normal constituent of the tract and accelerate the production of poliomyelitis. Varous materials, together with fruit extracts, were tested.
When supernates of peach skin mash were injected intracerebrally into cotton rats, followed at intervals with intracerebral injections of the so-called poliomyelitis virus, accelerated production of paralysis occurred. Because of the presence of cyanophore glucosides in peach skins, a synthetic preparation, succinotrile, was injected intracerebrally into the experimental animals. This chemical accelerated the production of the disease similar to that produced with the peach supernates. Toomey et al. emphasize that the injections of fruit supernates were made in a manner that does not occur under natural circumstances.
Sabin75 (1951), although insisting on the virus etiology of poliomyelitis, implicates food and drink as important factors inthe cause of this disease. He points out that measures which are often advocated to combat poliomyelitis epidemics are not warranted, such as (a) avoidance of crowds, large gatherings or sports events, (b) exclusion of children under 16 years of age from movies, churches, or schools, and (c) exclusion of poliomyelitis patients and suspects from general hospital wards.
The implications [of the foregoing] should be obvious that investigations of foods eaten by the poliomyelitis victim prior to his or her illness should be carefully considered.
THE PRODUCTION OF SO-CALLED VIRUS DISEASES
AND “VIRUS” INCLUSIONS BY POISONS
The public, as well as many physicians, is under the impression that viruses are living organisms comparable to a germ that enters the human, animal or plant to cause the disease. The scientists, who are authorities on virus diseases, are in disagreement as to the nature of a virus.
It is not generally realized that some so-called virus diseases may result from the effects of poisons on the human body, thus, herpes zoster may follow exposure to carbon monoxide or the administration of arsenic, bismuth, lipiodol, gold, mercury, tuberculin, alcohol, etc. An epidemic of herpes zoster and peripheral neuritis, similar to the “jake” paralysis epidemic in this country, followed the ingestion of arsenic in beer in Manchester, England in 1900.76-78 The toxic agent was determined to be arsenic arising from dextrose made from starch by the use of crude sulfuric acide containing this poisonous substance.
Herpes simplex, another so-called virus disease, has followed the ingestion of alcohol, benzol, arsenobenzol, mercury, and the inhalation of either, among other poisons. Van Rooyen79 noted its appearance after sulfapyridine therapy. Herpes simplex has followed the injection of vaccines, milk and colloidal metals.
Inclusion bodies have been defined as products of virus activity or the elementary virus bodies themselves. Inclusion bodies have been found in poisoned humans and experimental animals.
Dalldorf and Williams80 (1945) found large acidophilic inclusion bodies in the kidneys of rats poisoned by lead. Blackman81 (1936) found intranuclear inclusion bodies in the tubular epithelium of the kidney and in the liver cells of 21 children dying from the effects of acute lead poisoning and lead encephalitis.
Cox and Olitsky82 (1934) found that the injection into animals of aluminum hydroxide produced inclusion bodies similar to those seen in infectious encephalitis.
Van Rooyen and Rhodes83, in their textbook (1948), “Virus Diseases in Man,” state: “Histological changes similar to those seen in infectious encephalitis may be produced by carbon monoxide poisoning, brain injury, arteriosclerosis, uremia, pregnancy toxemia and toxic agents like alcohol and lead.”
Olitsky and Harford84 (1937) were able to produce inclusion bodies indistinguishable from those observed in virus infections by the injections of aluminum compounds, ferric hydroxide and carbon.
MISTAKES THAT HAVE BEEN MADE IN THE PAST
Several commissions, appointed during the first quarter of this century to investigate the cause of pellagra, concluded from their studies that pellagra was an infectious, contagious disease. Harris85 (1913) was able to inject Berkefeld filtered tissue material from pellagra victims into monkeys to cause a corresponding disease in these animals. He concluded from these experiments that a virus was present in the injected material and that it was the cause of pellagra. If the work of Harris had been followed exclusively, various strains of this “virus” might have been discovered and a vaccine, effective in experimental animals, might have been developed, as in the case of poliomyelitis. Today, as a result of unlimited research, however, we know conclusively that pellagra is not caused by a virus but rather that it is a vitamin deficiency disease. It is obvious that if the investigations of pellagra had been restricted to the virus theory, it would still be a mystery.
The symptoms of milksickenss in man resemble those of influenze or grippe, gastritis, and so-called ptomaine poisoning. As a matter of fact, so-called summer grippe or flu often occurs during epidemics of poliomyelitis. There were 10,000 cases in Cincinnati in 194789-90, which were thought to be related to poliomyelitis and were considered, therefore, virus infections. However, Matson91 (1950), writing about poisonous plants, says that some physicians have expressed the opinion that mysterious outbreaks of so-called summer flu in the late summer are often due to milk contaminated with tremetol [a poison occuring in white snakeroot and rayless goldenrod].
The observation that human and bovine outbreaks of tremetol poisoning occur simultaneously corresponds with similar observations made during epidemics of poliomyelitis. Medical reports have shown repeatedly that paralytic diseases in horses, pigs, dogs, cats, ducks, chickens, etc. occur simultaneously in districts where epidemics of poliomyelitis are prevalent,… [even though “polio” affects only humans (except in laboratories), pesticide causality resolves these conflicts of data.]
FACTORS PRECLUDING INVESTIGATION
OF THE POISON CAUSE OF POLIOMYELITIS
It is obvious that in the study of poliomyelitis every possible cause, including the possibility of poisoning, should be investigated.
Since 1908 — for 44 years — poliomyelitis research has been predominantly directed along only one line of investigation, i.e., the infectious theory. This single line of study, precluding other possibilities, including the poison cause of the disease, has resulted from two factors, (1) The Public Health Law93, and (2) the insistence, based entirely on animal experiments, that poliomyelitis is caused by a virus.
- The Public Health Law. The inclusion of poliomyelitis in the Public Health Law as a communicable, infectious disease dates back to the early part of the 20th Century. At that time many diseases, now known to be neither communicable nor infectious, were considered to be caused by an infectious agent simply because they occurred in epidemics. The general attitude of that period is expressed by Sachs94 (1911) in his statement: “In general, the epidemic occurrence of any disease is sufficient to prove its infectious or contagious character.” The vitamin deficiency diseases, beriberi and pellagra, are outstanding examples of epidemic diseases that were formerly considered to be infectious and communicable according to the logic employed by Sachs. In fact, we find pellagra incorporated into the Public Health Law as a communicable disease in the State of Pennsylvania in the following rule and regulation adopted January 5, 1910: “That all physicians practicing within the limits of the state shall make immediate report of each and every case of uncinariasis duodenalis (hookworm disease) and pellagra and anterior poliomyelitis (infantile paralysis) occurring in their practice in the same manner that other communicable diseases are now by law and by rule and regulation of the State Department of Health reported to the health authorities.” A State Health Officer95 recently wrote to me as follows: “I think all of us will agree with you that in the past, as is still probably true, public health rules and regulations and sometimes even public health laws, were influenced too much by what we did not know rather than by what we did know. This was probably an acceptable line of reasoning in the past, but with increasing public health education and greater understanding and cooperation from citizens, this justification becomes less acceptable.”
The fact that an extensive epidemic of poliomyelitis was prevailing in the states of New York and Massachusetts in 1907, aroused the suspicion that the disease was infectious and communicable; it was therefore incorporated into the Public Health Law as such. However, conclusive evidence of contagiousness was not established during that epidemic nor in subsequent ones. Moreover, during the greatest epidemic of poliomyelitis in recorded history, as shown by the records of the U.S. Public Health Service and the New York State Department of Health. Time Magazine, commenting on these surveys, points out how, when and where people catch polio remained a mystery. In addition to the failure to prove contagiousness of human poliomyelitis, it has likewise been impossible to prove contagiousness of poliomyelitis in experimental animals. This fact will be considered in detail later.
As a result of the inclusion of poliomyelitis in the Public Health Law as a contagious, communicable or infectious disease, investigations regarding it are almost exclusively in the hands of specialists in virology and public health. The country doctor, general practitioner, and clinician have little or no opportunity to participate in poliomyelitis research under these circumstances. Yet, Dr. W. Ritchie Russell97 of the Department of Neurology, United Oxford Hospitals, Oxford, England stated in 1950: “Clinical research into this disease is so much neglected that there are exciting discoveries waiting for anyone with time to give to this type of investigation.”
Medical advances of the utmost importance have been made in the past by general practicioners. An outstanding example is the work of Dr. Edward Jenner, a general practioner in Gloucestershire, England, whose observations and deductions brought about vaccination against smallpox. All advances in medicine do not result from laboratory experiments. Any doctor in any community, however, small, and however limited his opportunities, may make a fundamental discovery, but he must be given the opportunity to participate in the program and his observations and deductions must be given adequate consideration.
- Virus Research. The more or less general acceptance of the idea that poliomyelitis is caused by a virus arose from experimental animal studies by Landsteiner98 (1908) in Austria, and Flexner and Lewis99 (1909) in the United States. These experiments showed that a substance obtained from poliomyelitis victims could produce a paralytic disease when administered to experimental animals. It has been assumed, as a result of these experiments that an exogenous [originating from without] virus is the cause of human poliomyelitis. Dr. Harold L. Amoss100 stated in 1928: “By reason of the parrellelism of the human and experimental disease it is believed that inferences drawn from experiments with monkeys may be accepted with a certain degree of safety as applicable to the solution of problems in connection with human cases.” The portal of entry of the so-called virus of poliomyelitis into the human body never has been established. The question of the portal of entry is summed up in the published reports of the International Poliomyelitis Congress that was held in New York City in 1948. The Modulator stated: “We do not know too much about the portal of entry in human beings,” and Dr. John R. Paul, of Yale University, stated: “I would say we do not know the portal of entry in human beings.”
It was mentioned in the foregoing that human poliomyelitis has not been shown conclusively to be a contagious disease. Neither has the experimental animal disease, produced by the so-called poliomyelitis virus, been shown to be communicable. Rosenau102(1921) stated: “Monkeys have so far never been known to contract the disease “spontaneously” even though they are kept in intimate association with infected monkeys.” Twenty years later (1941), Dr. John A. Toomey103, a poliomyelitis authority, stated: “No animal gets the disease from another no matter how intimately exposed.”
It is extremely difficult to understand how a human can contract poliomyelitis from another individual through dissemination of a virus by contact, carriers, excrement, unclean hands, unwashed fruits and vegetables, flies, etc. when a healthy animal in the same cage with an “infected” animal, exposed to all of these natural factors, remains unaffected. It appears obvious, therefore, that communicability should have been established conclusively both in humans and in experimental animals before poliomyelitis was incorporated into the Public Health Law as a communicable disease.
Some investigators have as a matter of fact pointed out that human poliomyelitis and the disease produced in experimental animals from human material, etc. are not the same disease. Toomey104 (1935), for example, stated that intranasal and intracerebral inoculation of poliomyelitis virus in the monkey does not produce the same disease that is seen in man. Dr. Claus W. Jungebut, a well-known bacteriologist who has worked on the poliomyelitis problem for many years, recently stated (1950): “Whatever the final answer may be, it seems a reasonable statement at this time that the highly specialized, neurotropically fixed virus, which has been maintained in the past by intracerebral passage in rhesus monkeys, is more likely a laboratory artefact than the agent which causes the natural disease in man.” The logical conclusion appears to be, therefore, that the laboratory experiments with the so-called virus of poliomyelitis are merely of academic interest and have no practical application to human poliomyelitis.
For almost half a century poliomyelitis investigations have been directed towards a supposed exogenous virus that enters the human body to cause the disease. The manner in which the Public Health Law is now stated imposes only this type of investigation. No intensive studies have been made, on the other hand, to determine whether or not the so-called virus of poliomyelitis is an autochthonous chemical substance that does not enter the human body at all, but simply results from an exogenous factor or factors, for example, a food poison. Analogous reactions are well-known as illustrated by the production of experimental sarcomas by indol, arsenic, tar, etc. and which have been transmitted by Berkefeld filtrates.
The discovery in recent years of the so-called Coxsackie virus has tended to further confuse the entire poliomyelitis problem. Hoyne107 (1951), for example, states that the announcement of this discovery “is accompanied by some feeling of dismay… In view of the foregoing announcement it seems that trained investigators have added one more problem to the nebulous conditions enveloping poliomyelitis. One might also be tempted to make the statement that the more we learn about poliomyelitis, the less we know.” Hoyne’s statement applies obviously to the confusion that has arisen from exclusive virus studies in poliomyelitis. A Lancet editorial108 (1951) also indicates the complexity of the problem brought about by the discovery of the Coxsackie virus, as follows: “A crop of new snags is coming along as every week brings new tidings of the Coxsackie viruses.”
Many diseases have been considered to be caused by viruses but virus studies constitute only a portion of the investiations intended to determine the cause of the disease. Poliomyelitis investigations, on the other hand, have been confined exclusively to virus studies. Because of this situation and the Public Health Law, those who maintain other opinions, including those concerned poisons as the cause of poliomyelitis, can neither obtain funds from any sourrce for research nor cooperation for investigating their ideas. Reappraisal and investigation of all theories, infectious and non-infectious, are imperative.
To epitomize, the following quotation from a talk on poliomyelitis given by Dr. Ritchie Russell97, Department of Neurology, United Oxford Hospitals, Oxford, England (1950) summarizes what has been pointed out in the foregoing: “The time is ripe for a survey of our knowledge of the disease, of the methods of treatment we are accustomed to use and our efforts to advance knowledge of the condition… Surely if the Americans with all their millions of dollars for research on poliomyelitis can do so little, we need not try… I do not intend here to praise good work that has been done, but more to emphasize the gaps in our knowledge of the disease in the hope that others may be encouraged to work on the subject which sorely needs some extra attention. There are at present several different groups of specialists working on the disease, including virologists, infectious disease physicians, orthopedic surgeons, physiotherapists and public health officers. This may be a reasonably adequate state of affairs as far as handling the individual case is concerned; but as a background for advancing knowledge of the disease it is not satisfactory for the members of each of these groups have many other interests, and have neither the time nor always the experience of other aspects of the disease to enable them to fit their piece into the whole picture in such a way as to advance research… Unfortunately, the disease gets worse as public health improves, and measures which are designed simply to avoid infection seem to be singularly ineffective in poliomyelitis.”
The statement is reminiscent of one made in 1938 by Dr. Carl C. Dauer109, Chief of the Bureau of Preventable Diseases, District of Columbia health Department, viz: “It seems rather remarkable in spite of all the time and effort spent in poliomyelitis studies during the past 20 years so little information in the epidemiologiy of the disease has been produced.”
The urgent need for cooperation between the clinician and laboratory worker, as well as an unprejudiced attitude toward the poliomyelitis problem, is emphasized by Jungeblut105 as follows: “The subject is of keen interest to clinicians and laboratory workers alike and progress will be measured by the extent of cooperation between the two. Until the final word has been said it is hoped that, in the future, students of poliomyelitis will preserve an open mind and maintain an open door in their efforts to unravel the mysteries of this baffling disease.” Jungeblut indicates the confusion that has been caused by the virus theory when he states: “Actually, the history of this disease has been marked by periods of violent disagreement among scientific workers and by sharp dissension within the ranks of the medical profession.”
|1.||Scobey, R. R.: Arch Pediat, 67: 29-46, Jan. 1930|
|2.||Scobey, R. R.: Arch Pediat, 67: 400-430, Sept. 1950; 462-482 Oct. 1950|
|3.||Boerhaave, Herman: Aphorisms of Dr. Herman Boerhaave by G. Van Sweeten, Vol. 10, 1765|
|4.||Cooke, John: Treatise of Nervous Diseases, 1824|
|5.||S. Coulton, F. P.: New York J. Med., 177-178, Sept. 1850|
|6.||Vulpian, A.: Quoted by R. W. Lovett, Ref. 24|
|7.||Adamkiewitz, A.: Charitê-Ann., 4: 430, 1879|
|8.||Popow: Quoted by C. K. Mills, Boston M. & S. J., 108: 248-250. March 15, 1883|
|9.||Altman: Quoted by L. Emmett Halt and F. H. Bartlett, Am. J. M. Sc., 135: 647-662, May 1908|
|10.||Onuff: Quoted by L. W. Lovett, Ref 24|
|11.||Obrastoff: Quoted by R. W. Lovett, Ref. 24|
|12.||Philhppe and Gauthard: Quoted by R. W. Lovett, Ref. 24|
|13.||Gossage: Quoted by R. W. Lovett, Ref. 24|
|14.||Edsall, David E.: Osler’s System of Medicine, Vol. 1, p. 144, 1907|
|15.||Collins, J. and Martland, H. S.: J. Nerv. & Ment. Dis., 35: 417-436, July 1908|
|16.||Vonderabe, A. R.: Arch. Neural. & Psychiat., 25: 29-43, 1931|
|17.||Gringer, R. R.: Arch. Neurol. & Psychiat., 25: 649-653, 1931|
|18.||Leenhardt, E.; Chaptel. and Dufoix, M.: Montpellier med., 74: 109. 1931|
|19.||Elmore, S. E.: Pediatrics, 1: 643-647, May 1948|
|20.||Warkany, J. and Hubbard, D. M.: Am. J. Dis. Child., 81: 335-373, March 1951|
|21.||Meyerhofer, E.: Ann. Paediat., 153: 144, June 1939|
|22.||Gougerot, H.: Rev. gen. de clin. et de therap., 49: 353. June 1. 1935|
|23.||Lambert, S. M.: J. Trap. Med. & Hyg., 39: 41, Feb. 15, 1936|
|24.||Lovett, Robert W.: Boston M. & S. J., 159: 131-138, July 23. 1908|
|25.||Watson, C. J.; Schuitze, W.; Hawkins, J. and Baker, A. B.: Proc. Soc. Exper. Biol. & Med., 64: 73-78, Jan. 1947|
|26.||Cascio. D.: Brasil-med., 61: 387-390. Nov. 1.15 1947|
|27.||Cascio. D.: N. V. State J. M., 49: 1685-1686, July 13, 1949|
|28.||Jungeblut, Claus XV: J. Exper. Med., 66; 459-477, Oct. 1, 1937|
|29.||Marshall, R.: Med. Rec., 144: 32. July 1, 1936|
|30.||Marshall, R.: Med. Rec., 157: 279-284. May 1944|
|31.||Klenner, F. R.: South. Med. & Surg. J., 111: 209-214. July 1949|
|32.||Cormia, F. E.: Canad. M. A. J., 36: 392-396, April 1937|
|33.||Landfisch, S.: Polska gaz. lek., 16: 575, July 18, 1937|
|34.||Damon, I.: Presse med., 45: 1670, Nov. 24. 1937|
|35.||Schopp. J. H.: Canad. M. A. J., 49: 515. Dec. 1943|
|36.||Linn, C.: Frumusan. P. and Sassier, R.: Bull. et mem. Soc. med. d. hop. de Paris, 55: 1194-1203, July 17, 1939|
|37.||Carmick, M.: Polis, B. D. and Klein, T.: Arch. Int. Med., 78: 296-302, Sept. 1946|
|38.||King, E. J.: Gilchrist: V. and White. J. C.: Biochem. J., 38: 8, 1944|
|39.||Vesting, C. S.: J. Biochem.. 143: 439.446. April 1942|
|40.||Gibson, 0. H.: Biochem. J.. 37: 615-618, 1943|
|41.||Chisholm, C.: Edinburgh V. & S. J., 4: 393-422, Oct. 1808|
|42.||Burrows. G. V.: London Med. Repos., 3: 445-476, June 1. 1815|
|43.||Massi, L. and Postorini: Riv. di clin. pediat., 44: 196-198. March 1948|
|44.||Eskwith. Irwin S.: Am. J. Dis. Child.. 81: 684-686. May 1951|
|45.||Creighton. Charles: History oi Epidemics in Britain, 1891|
|46.||Crookshank, F. G.: Boston V. & S. J., 182: 34.33, Jan. 8, 1920|
|47.||Sydenham. T.: The works of Thomas Sydenbam on Acute and Chronic Diseases by George XVallis, Vol. 1. 1788|
|48.||Cruvelier, P. J.: Abstr. Am. J. Med. Sc.. 12: 442-456. 1833|
|49.||Rush, Benjamin: Medical Inquiries and Observations, Vol. 4, 2nd. Ed., 1805|
|50.||Law, Robert: Dublin J. V. Sc., 15: 1-86, Aug. 1849|
|51.||Purefoy. T.: Dublin J. M. Sc.. 16: 318-331, 1853|
|52.||Harris, S.: “Food Poisoning”: Tice’s Practice 0f Medicine, Vol. 8. 1928|
|53.||Colton. M. H.: Virginia V. Semi-Monthly, 22: 437. 1917|
|54.||Emerson. H. C.: Boston M. & S. J.. 151: 115-119. July 22, 1909|
|55.||Dingman, J. C.: New York State J. Mcd., 16: 389. 1916|
|56.||Pitzman. Marsh: J. Missouri V. A.. 25: 249.257, June 19, 1928|
|57.||Bramfield, Louis: Out of the Earth. pp. 43.45. 1950|
|58.||Chapman. Col. P. F.: Brit. V. J., 2: 398, Sept. 6, 1947|
|59.||Tourney, J. A. and August. V. H.: J. Pediat.. 1: 601.607, Nov. 1932|
|60.||Tourney, J. A. and August, V. H.: Am. J. Dis. Child.. 46: 262.279, Aug. 1933|
|61.||Tourney, J. A.; Tackacs, XV. S. and Tischer. M. D.: J. Pediat.. 23: 172. Aug. 1943|
|62.||Draper, George: Infantile Paralysis, 1933|
|63.||Leavell, H. R..: Kentucky M. J., 34: 110, March 1936|
|64.||Barber, C. O.: Brit. M. J., 2: 1137, Dcc. 7, 1938|
|65.||Chenault, J. W.: J. Nat. M. A., 33: 220, Sept. 1941|
|66.||Goldstein, Lt. Col. 13. H.; Hammon, W. McD. and Vietes, H. R.: J. A. M. A., 131: 369.373. June 13, 1946|
|67.||Kovar, W. B.: Nebraska M. J., 30: 394, Oct. 1943|
|68.||Gebhardt, L. P. and McKay, M. H.: .J. Pediat., 28: 1.13, Jan, 1946|
|69.||Scobey, R. B..: Arch. Pediat., 63: 322-354, July 1946|
|70.||Scobey, B.. B.. Arch. Pediat., 63: 567-580, Nov. 1946|
|71.||Abbott, W. N.: “Poliomyelitis in Relation to the Recent Advances in Our Techiniques and Concepts Concerning Protein, Radiation and Viruses” (Monograph), 1948|
|72.||Adamson, J, D.: Moody, J. P.; Peart, A. F. W.; Smillie, R. A.; Wilt, J. C. and Waad, W. 3. L.: Canad. M. A. J., 61: 339.348, Oct. 1949|
|73.||Barondes, B. de Rohan: Mil. Surgeon, 103: 403.408, Nov. 1949|
|74.||Tooniey, J. A.: Takacs, W. S. and Pirone, P. P. Am. J. Dis. Child., 78: 1.13. July 1949|
|75.||Sabin, A. B.: J. Pediat., 39: 319.531. Nov. 1951|
|76.||Row, N.; Barent, F. H. and Warrington, W. B.: Brit. M. J., 1: 10, Jan. 3, 1901|
|77.||Reynolds, C. S. et al.: Brit. M. J., 2: 1044-1049, Oct. 12, 1901|
|78.||Editorial: Boston M. & S. J. 150: 49.50, Jan. 14, 1904|
|79.||Van Rooyen, C. K.; Rhodes, A. J. and Ewing, A. C.: Brit. M. J., 298-3O1, Aug. 30. 1941|
|80.||Dalldorf, G. and Williams, R. 12.: Science, 102: 668.670, Dec. 28, 1943|
|81.||Blackman, S. S. Jr.: Bull. Johns Hopkins Hosp., 38: 384-404, 1936|
|82.||Cox, H. R.. and Olitsky, P. K.: Science, 79: 439, 1934|
|83.||Van Rooyen, C. E. and Rhodes, A. J.: Virus Diseases in Man, 1948|
|84.||Olitsky, P. K. and Harfo.rd, C. G.: Am. J. Path., 13: 729-747, Sept. 1937|
|85.||Harris, W. J.A.M.A. 60: 1948.1950, June 21, 1913|
|86.||Stevens, A. A.: The Practice of Medicine, pp. 294-295, 1922|
|87.||Drake, Daniel: Quoted by Jordan, E. O. and Harris, N. M., J. Infect, Dis., 6: 401.491, Sept. 20, 1909|
|88.||Huffman, W. T. and Couch, J. F.: “Plants Poisonous to Livestock”,Yearbook of Agnculture, p. 366, 1942|
|89.||Sabin, A. B. and Steigmact, A. J.: Am. J. Hyg., 49: 176.193, March 1949|
|90.||Editorial: Good Housekeeping Magazine, p. 30, Aug. 1949|
|91.||Matson, V. F.: Today’s Health, 28: 28, May 1950|
|92.||Dixon: Quoted by Jordon, E. O. and Harris, N. M,: J. Infect. Dis., 6: 401.491.
Sept. 20, 1909
|93.||Scobey, R.. R.: Arch. Pediat., 68: 220.232, May 1951|
|94.||Sachs, B.: Am. J. Obst. & Gynec., 63: 703.710, April 1911|
|95.||Thompson, G. D. Carlyle, Executive Officer, State Board of Health. State of
Montana: Personal Communication
|96.||Editorial: Time Magazine, Jan. 2. 1950|
|97.||Russell, W. Ritchie: J. Bone & Joint Surg., 32B: 748.750, 1930|
|98.||Landsteiner, K.: Wein. klin. Wchnschr., 21: 1830, 1918|
|99.||Flexner, S. and Lewis, P. A.: J.A.M.A., 33: 639, Nov. 13 1909|
|100.||Amoss, Harold L.: Tice Practice of Medicine, Vol. 5, p. 335, 1928|
|101||Published Reports: International Poliomyelitis Congress, p, 292, 1948|