The Poison Cause of Poliomyelitis And Obstructions To Its Investigation

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The Poison Cause of Poliomyelitis And Obstructions To Its Investigation

From 1952

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Images Of Poliomyelitis

From Archive Of Pediatrics (April, 1952)

The Poison Cause of Poliomyelitis

And Obstructions

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.

Ralph R. Scobey, M.D.

Syracuse, N.Y.

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 accidentally and was admitted to the hospital. The primary effects

of the poison had been successfully combated 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. sburg, 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. pe 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. 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. "

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 of the neck. About eight days after the onset of the

illness, he became paralyzed. In discussing 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,

Mississippi and other states an epidemic of paralysis.16,17 The patients

gave a history of drinking commercial extract of ginger. 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 ginger, the symptoms appeared two to ten days later. In some cases

a longer time elapsed. This latent period 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 immediately

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 paralysis

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. 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, aniline, 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 origin 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

indiscretions 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 compounds 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. Various 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 in the 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, ( exclusion of children under

16 years of age from movies, churches, or schools, and © 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

acid 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 80 (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.

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 83, 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. 85 (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 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 milk sickness in man resemble those of influenza 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 occurring 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.

1. 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 97 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 practitioners. An outstanding example is the work of Dr.

Jenner, a general practitioner 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.

2. 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 99 (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 parallelism 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. R. , 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. 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. Jungeblut, 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 artifact 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 sackie 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 sackie virus, as

follows: " A crop of new snags is coming along as every week brings new

tidings of the sackie viruses. "

Many diseases have been considered to be caused by viruses but virus

studies constitute only a portion of the investigations 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 source 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 97, 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 epidemiology 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. "

SUMMARY

[Omitted]

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--------------------------------------------------------

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