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]

REFERENCES

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, : 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. pe and Gauthard: Quoted by R. W. Lovett, Ref. 24

13. Gossage: Quoted by R. W. Lovett, Ref. 24

14. Edsall, E.: Osler’s System

of Medicine, Vol. 1, p. 144, 1907

15. , 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, W.: Boston M. &

S. J., 159: 131-138, July 23. 1908

25. , 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. : 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

Sydenbam on Acute and Chronic Diseases by XVallis, Vol. 1. 1788

48. Cruvelier, P. J.: Abstr. Am. J. Med. Sc.. 12: 442-456. 1833

49. Rush, : Medical

Inquiries and Observations, Vol. 4, 2nd. Ed., 1805

50. Law, : Dublin J. V. Sc., 15: 1-86, Aug. 1849

51. Purefoy. T.: Dublin J. M. Sc.. 16: 318-331, 1853

52. , 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, : 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. on, 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.; , A. J.

and Ewing, A. C.: Brit. M. J., 298-3O1, Aug. 30. 1941

80. Dalldorf, G. and , R.

12.: Science, 102: 668.670, Dec. 28, 1943

81. Blackman, S. S. Jr.: Bull. s

Hopkins Hosp., 38: 384-404, 1936

82. , H. R.. and Olitsky, P. K.: Science, 79: 439, 1934

83. Van Rooyen, C. E. and , 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. , W. J.A.M.A. 60: 1948.1950, June 21, 1913

86. s, A. A.: The Practice of Medicine, pp. 294-295, 1922

87. Drake, : Quoted by Jordan,

E. O. and , 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 , 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. , G. D. Carlyle,

Executive Officer, State Board of Health. State of

Montana: Personal Communication

96. Editorial: Time Magazine, Jan. 2. 1950

97. , W. Ritchie: J. Bone & Joint Surg., 32B: 748.750, 1930

98. Landsteiner, K.: Wein. klin. Wchnschr., 21: 1830, 1918

99. Flexner, S. and , 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

102 Rosenau, M.J.: Preventive

Medicine and Hygiene, 4th Ed.. p. 389, 1921

103. Toomey, J. A.: 3. Pediat., 19: 103, July 1941

104. Toomey, J, A.: Science, 82: RU, Aug. 30, 1935

105. Jungeblut, Claus W.: J. Pediat.. 37: 109-13. July 1950

106. Jelliffe, S. K.: J. Nerv. & Ment. Dis., 49: 522. May 1919

107. Hoyne1 A. L.: Med. Clin. North

America, Chicago Number, 175-188, Jan. 1951

108. Editorial: Lancet: 2: 1173.1174. Dec. 22, 1951

109. Dauer, Carl C.: Pub. Health Rep., 33 1013.1034, June 24, 1938

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