Is Human Poliomyelitis Caused By An Exogenous Virus?

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Is Human Poliomyelitis Caused By An Exogenous Virus?

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Images Of Poliomyelitis

A Critique Of Scientific Literature

From Science (1954) v51, p117:

Is Human Poliomyelitis

Caused By An

Exogenous Virus?

Ralph R. Scobey, M.D.

Syracuse, NY

Note: This article was originally published as a 2-part

series (April and May, 1954). Throughout, Scobey does not mention

pesticides, pollution, or industrial culpability. He argues two

points: 1) for recognition of non-virus causes of poliomyelitis,

primarily the concept of toxic causality, and 2) for the concept of

an endogenous poliovirus, i.e., a virus which is generated from cells

as a response to toxins. The publication of this comprehensive

article coincides with the rushed and highly promoted Salk Vaccine

Field Trials in the spring of 1954.

Contents (HARpub)

Introduction Antibody Formation

Relationships Of Toxicology To Virology Koch's Postulates

The Nature Of A Virus Biochemical Factors

Human vs. Experimental Polio (Chart) Experimental Animal

Poliomyelitis

Toxic Activating Factors Comment

Virus Incubation Periods Summary

Precipitators Of Human Polio References

Comparative Pathology

TEXT HARpub Commentary

Introduction

It is now nearly half a century since Landsteiner2 and Flexner

and 3 established the basis for the virus theory of the cause of

poliomyelitis. Since that time the virus has been isolated, purified,

classified into strains, photographed, cultured, and vaccines

prepared with it in the experimental laboratory. However, human

poliomyelitis remains still an enigma and many things concerning it

cannot be explained by the exogenous virus theory. Landon4 stated, in

1938, that experimental evidence points to a filtrable virus as the

causative agent of poliomyelitis, although so far as the human

subject is concerned the theory still is not definitely proved. Van

Rooyen and 5, ten years later (1948), make the following

significant remark concerning this fact: " Theories of the

pathogenesis of human poliomyelitis have resulted largely from

experimental work on monkeys rather than on observations on the

patient. " A theory is valid only if it explains all facts without

exception. Poliovirus causality has definitely not been proven as of 1954.

The writer6,8 has emphasized repeatedly, as have others, that,

despite the finding of a virus associated with cases of human

poliomyelitis, the fundamental cause of this disease appears to be a

poisonous or toxic activator and that the fundamental problem, as far

as the human disease is concerned, is one of chemistry. The clues are

numerous, well known, and too strong to be ignored; they have not

been followed adequately. It is the purpose of this report to

simplify, as much as possible, this concept of the cause of human

poliomyelitis and to show that there may be an intimate relationship

between virus diseases and diseases resulting from toxic causes.

Relationship Between Toxicology And Virology

The association of viruses with cases of poisoning is a well

recognized fact. It is illustrated by the herpes simplex that follows

the injection of vaccines, milk, colloidal metals, ingestion of

foodstuffs, general anaesthesia, etc.5, 19-21 and the herpes zoster

that follows the intake or injection of arsenic, bismuth and

sulfonamides, and carbon monoxide, alcohol, or phenobarbital

poisoning22-24. Ritchen and Kantor25 (1947) reported herpes zoster as

a toxic manifestation from the administration of antimony in the

treatment of schistosomiasis. Both herpes simplex and herpes zoster

occur at times in association with infectious diseases which appears

to indicate that toxins produced in the course of these specific

diseases may be responsible. The lesions of both herpes simplex and

herpes zoster, regardless of the primary cause, are histologically

characterized by intranuclear inclusion bodies, and a virus can be

isolated from the lesions. Fixation occurs between the sera of cases

of arsenical or bismuth zoster and zoster antigen26. " ...a well

recognized fact. "

Modern explanations are that herpes manifest during periods of stress.

In 1900, there occurred an epidemic of arsenical poisoning in

and around Manchester, England, involving several thousand beer

drinkers27-29. For fully six months the etiology was not discovered

and the patients exhibited in sequence digestive symptoms, nasal and

pharyngeal catarrh, bronchitis, acute skin lesions, disturbances of

sensibility, motor paralysis, pigmentation and keratoses, Reynolds28,

toward the end of this period, observing an unusually large number of

cases of herpes zoster during the epidemic and recalling numerous

reports of this type of eruption occurring in association with

arsenical poisoning, came to the conclusion that this drug must be

the source of the epidemic. Investigations revealed that the arsenic

originated from Spanish pyrites that war used in the making of

sulfuric acid which was employed for the preparation of sugars used

in the brewing of beer. Thus, the cause of a mysterious epidemic with

many protean features, viz, gastro-intestinal, respiratory,

dermatological, and nervous symptoms was eventually unraveled by

finding the clue in a: virus disease which was a concomitant feature.

There was clearly a cause and effect relationship.

In the earlier literature there appeared many reports of cases

of poliomyelitis complicating or following the common infectious

diseases, viz, measles, scarlet fever, influenza, smallpox, etc.,

which were interpreted as resulting from the effects of the toxins of

the original disease on the anterior horn cells of the spinal cord.

More recent work, which indicates a similar situation, is the

poliomyelitis following the injection of toxic antigens, viz,

pertussis vaccine and diphtheria toxoid. The writer already has

discussed this form of human poliomyelitis in a previous report 8.

HARpub: All of these diseases can also be associated with

polluted regions (see Miscellaneous Epidemiology for some examples).

A clue to a relationship between virus diseases and diseases

resulting from toxic causes appears to exist in the inclusion body.

These bodies were considered to occur only in virus diseases and to

be composed of numerous virus particles or elementary bodies.

However, it is now known that inclusion bodies occur not only in

virus diseases but also in a variety of other diseases, including

those resulting from poisons and toxins. Although transfer

experiments with experimental animals have not always been possible

with material containing inclusion bodies, the reason why viral

material is present in some cases and not in others has not been explained.

Blackman30 (1936) found intranuclear inclusion bodies in the

kidneys and livers of children dying from the effects of acute lead

poisoning and lead encephalitis. He was able to produce them

experimentally in the kidneys and livers of white rats by

administering lead carbonate in water mixed with the food that was

fed to the animals.

Wolff and Orton31 (1932) found intranuclear inclusion bodies

similar to those found in poliomyelitis in a number of conditions,

including toxemia of pregnancy, tuberculous meningitis, chronic

basilar meningitis, myasthenia gravis, tetanus, acute suppurative

leptomeningitis, chronic epidemic encephalitis, meningeal

fibroblastoma, pernicious anemia, dissecting aneurism, chronic

pulmonary tuberculosis, cerebral epidermoid, suppurative

thrombophlebitis of uterus and pelvic veins, aneurism of the right

anterior cerebral artery (ruptured), spongioblastoma multiforme, and

protoplasmic astrocytoma.

Hembacker and O'Leary32 (1930) showed that repetitive

stimulation by electricity of the axon brings about granulation of

the chromatin and its clumping about the nucleolus. The chromatin

mass resembled the nuclear inclusions which have been considered

pathognomic of several virus infections. Davenport et al22 (1931)

found that nuclear inclusions occurred with great regularity in

extirpated ganglia in hypertonic solutions. They attributed them to

disturbed osmotic conditions in the cells. Lee34 (1933) observed

nuclear changes following the intravenous injection of various

solutions. These included 50 per cent sodium chloride, distilled

water and salyrgan. Intranuclear inclusion bodies were observed which

simulated those described by Covell35 (1930) in the nerve cells of

acute anterior poliomyelitis.

and Olitsky36 (1934), in studies on the prevention of

experimental equine encephalitis in guinea pigs by means of virus

adsorbed on aluminum hydroxide, observed intranuclear inclusion

bodies characteristic of encephalitis virus infections in the

phagocytic mononuclear and giant cells of the induced subcutaneous

nodules. When the chemical alone, free from the virus, was introduced

under the skin of guinea pigs, similar inclusions were seen in the

resulting foreign body reaction. Olitsky and Harford37 (1937) were

able to produce intranuclear inclusion bodies, indistinguishable from

those observed in virus infections, by the injection of aluminum

compounds, ferric hydroxide and carbon. Brain tissue derived from

apparently healthy guinea pigs produced similar inclusion bodies when

it was injected. Birch and Lucas38. (1948) produced intranuclear

inclusion bodies consistently with aluminum oxide injections. Van

Rooyen and 5 (1948) point out: " Histological changes similar to

those seen in infective encephalitis may be produced by carbon

monoxide poisoning, brain injury, arteriosclerosis, uremia, pregnancy

toxemia, and toxic agents like alcohol and lead. " HARpub:

encephalitis can be be clinically indistinguishable from polio.

The Nature Of A Virus

The word " virus " was originally used only in the singular and

meant a poison. Later, with the establishment of a difference between

poisons and infectious agents, the word " virus was used only in

connection with the latter entities. The word was eventually applied

only to those infectious agents capable of passing through filters

that retarded ordinary bacteria. The relationship of poisons and

viruses was not considered, but, in view of more recent developments,

there appears to be a vast field yet to be explored between these two

extremes. Originally " virus " meant that the patient was poisoned.

" ...a vast field yet to be explored... "

Following the discovery of a virus in association with cases of

human poliomyelitis, it was generally accepted, at least as a working

hypothesis, that this virus is a small exogenous organism. This

hypothesis led to attempts to establish a portal of entry, mechanism

of dissemination within the body, and communicability in order to

confirm this concept. However, these facts have not been conclusively

established after nearly half a century of research. It is now known

that the most intimate contacts - such as healthy and sick

individuals in one bed, the attendance of physicians and nurses upon

the sick, the use of unclean linen, clothes, or beds, unsanitary

conditions, insects and animals, post-mortem examinations of

poliomyelitis victims, and other factors - have in no wise

contributed to the spread of the disease. Yet, the original concept,

i.e., that the poliomyelitis virus is an exogenous organism is so

deep-rooted in the minds of many physicians, as well as the public,

that ineffective and obsolete measures to control human poliomyelitis

continue to be employed. " ...the most intimate contacts... have in

no wise contributed to the spread of [polio]. "

Medical approaches to polio are ineffective because of the

ingrained concept of the exogenous virus.

The conspicuous achievements of Dr. Wendell M. Stanley39, a

chemist, show clearly how unlimited research can bring about

remarkable scientific advances, whereas the general acceptance of and

adherence to a theory can cause retardation. Stanley reported in

1935, that the tobacco mosaic virus, which had been considered to be

a small organism, is a crystalline protein of high molecular weight.

Rivers40 (1941), a bacteriologist, described Stanley's work as

follows: " While a few investigators had stated that a chemical agent

instead of a microorganism is responsible for tobacco mosaic, Stanley

was the first to bring a respectable amount of proof that infectious

diseases are not of necessity caused only by microorganisms.

Stanley's findings, which have been confirmed, are extremely

important because they have induced a number of investigators in the

field of infectious diseases to forsake old ruts and seek new roads

to adventure. As much as bacteriologists hate to admit it, Stanley's

proof that tobacco mosaic virus is a chemical agent instead of a

microorganism is certainly very impressive. Moreover, every one

admits that the agent of tobacco mosaic is transmissible indefinitely

in series from plant to plant, a fact beyond dispute, indicating

abundant multiplication or reproduction of the virus. Inasmuch as

reproduction is usually considered an attribute of life, great

confusion and consternation has been caused. In fact, the results of

Stanley's work had the effect of demolishing bombshells on the

fortress which Koch and his followers so carefully built to protect

the idea that all infectious maladies are caused by living organisms

or their toxins. In addition, his findings exasperate biologists who

hold that multiplication or reproduction is an attribute only of

life. " Scobey is struggling with some of the knowledge gaps

that Carrel also experienced to a greater degree, in 1927. The

finding that viruses are chemicals, which can be crystallized, that

they are genetic entities, was becoming firmly established at the

time this article was written.

It was thought, long before Stanley's discovery was reported,

that viruses are the product of tissue cells which have suffered the

action of some deleterious influence, this new product in turn being

capable of engendering the same change in other cells. Stanley41

emphasized in 1939, that the all important and fundamental problem of

virus activity is one of chemical structure, and that it is a

straightforward problem of structural chemistry. Enter,

virology as molecular biology.

Rivers42 (1932) had stated seven years earlier, before Stanley's

amazing discovery: " The confused state of our knowledge of the

viruses at the present time makes it exceedingly difficult to define

the nature of these active agents. The easiest way out of the

dilemma, however, would be the acceptance of the presumptive evidence

that viruses are minute microorganisms. Yet, the easiest way and the

one that best fits the experience of the day might not be the right

one. " Subsequent developments showed that this presumptive evidence

was untenable.

Stanley's work showed that the tobacco mosaic virus could not

only be crystallized but the virus activity is a specific property of

the nucleoprotein of which it is composed. Many strains of the mosaic

virus have been isolated and these consist of closely related

nucleoproteins. All viruses thus far purified have been found to

contain or to consist of nucleoprotein and this fact has led some

workers to consider it possible that viruses may be derived from

genes or nuclear material. Since Stanley's discovery, many workers

believe that the particles of certain viruses are protein

macromolecules that may multiply in their hosts by a process of

autocatalysis.

The concept that is now generally accepted to explain herpes

manifestations is that sometime during the life of an individual the

herpes viruses enter the human body and remain latent until some

factor or factors activate them. The evidence to support this view,

however, is still necessarily indirect and it is largely derived from

seriological studies. On the other hand, there is much to support the

concept presented by Doerr43, a Swiss bacteriologist, in 1938. The

exogenous latent (or dormant) virus.

He considered the herpes virus to be endogenous in origin

produced within the cells by certain physiological stimuli. Once the

agent has been produced it will act on the cells of susceptible

animals of different species as a true virus exciting in them, when

appropriately injected, the production of an antiserum specifically

antagonizing the virus of herpes infection. According to this view,

the virus is primarily a derivative of the physiologically modified

cells. Jenner44 (1804) speaks about the herpetic fluid as one of the

morbid poisons which the body is capable of generating and when

generated it may be perpetuated by contact. In a letter dated October

25, 1804, he says: " Children who feed on trash at this season of the

year are apt to get distended bellies and on them it often appears

about the lips. " The endogenous virus.

Reports of experimental work have appeared, leading to claims

that normal cells have been induced to manufacture certain viruses.

Carrel45 (1926) was able to produce tumors resembling Rous' sarcoma

and transmissible by cell-free filtrates with indol, arsenic, or tar

in chicken embryo. Carrel's observations have been confirmed by other

workers. Fischer46 (1926), by treating cultures of normal cells with

arsenic obtained on one occasion a filtrable virus capable of causing

tumors. Copisarow47 (1939) says: " The predominance of infection over

spontaneity cannot remain indefinitely a stereotyped assumption and

tends to swing pendulum-like (at least in the domain of viruses) back

to synthetic inception, with an intermediate position as an ultimate

restpoint. " " Spontaneous " disease vs. cause ( " infection " ).

There is much evidence to indicate that the poliomyelitis virus

is synthesized or activated within the human body instead of entering

it as commonly assumed. Each poliomyelitis victim evidently develops,

as a result of an exogenous factor, an autogenous infectious agent

which is not transmissible under natural conditions to other human

beings. However, when this infectious agent is concentrated it can be

inoculated into experimental animals to produce experimental animal

poliomyelitis. Thus, there is a chain of chemical reactions from the

time that a human is exposed to a poison or toxin until a virus is

synthesized or activated. The experimental disease, on the other

hand, using the product (virus) resulting from the poison activator,

is purely a virus infection. The failure to demonstrate in the

prevention and treatment of natural human poliomyelitis the efficacy

of blood serum, the vaccines of Kolmer and Brodie, zinc sulfate nasal

sprays, the sulfa drug, darvisul (phenosulfazole), and gamma

globulin, although their value was proven conclusively in

experimental animal poliomyelitis, appears to indicate clearly an

entirely different mechanism in the natural human disease in contrast

to the artificial disease in experimental animals. These facts are

represented in Chart 1. Scobey refers to " ...a chain of

chemical reactions... " extending to virus synthesis or activation,

however, he stays clear of virus causality. " Infection " is not

causality. " See HARpub interpretation.

[scobey's Chart 1 describes orthodox laboratory

virus research as a search for preventative serums and vaccines

rather than cause. Such research begins where causal analysis ends,

with the virus, yet is often provided as evidence for cause. See an

analogous analysis.]

Chart 1

The Mechanism of Production of Human Poliomyelitis vs.

Experimental Animal Poliomyelitis

Human Poliomyeltis

Activator Precipitator Biochemical Factors

Poison/Toxin Fatigue

Chilling

Trauma

Heat and Humidity

Operative Procedures

Pregnancy Genetic Agents

Enzymes

Hormones

Mutation

Physical/Chemical Virus

Experimental Animal Poliomyelitis

Virus Strains Transfer

Experiment Purification Culture

Preventative Agents

Poison And Toxic Activating Factors

There are potential poisonous and toxic activating factors

present in food and water during epidemics of poliomyelitis that can

account for much that has been thus far unexplainable by the

exogenous virus theory. Fruits, vegetables, milk and water have been

mentioned many times in relation to the cause of human poliomyelitis

by medical writers, and they are suspected frequently by the laity.

Specific instances of an etiological relationship between fruits,

vegetables, milk and water and human poliomyelitis have been reported

infrequently, however, because of the fact that epidemiological

studies are limited almost exclusively to possible person to person

contacts and carriers of an exogenous virus. Sabin48 (1951), although

insisting on the exogenous virus etiology of human poliomyelitis,

implicates food and drink as important factors in the cause of the

disease. However, little attention has been given to the kind or the

source of the food or drink used by poliomyelitis patients prior to

or during epidemics of this disease, even in the search for an

exogenous virus. In this section, in terms of the dominant theory of

poliovirus causality, Scobey presents the case for poliovirus

activation by toxins.

'...little attention has been given to the kind or the source of

the food or drink used by poliomyelitis patients prior to or during

epidemics... " This is important, as Scobey begins to list epidemics

where food was found was suspected to be a possible cause.

Dr. H. C. Emerson49 (1909 [date of article]), Massachusetts

State Inspector of Health, District 14, investigating an epidemic of

poliomyelitis in that state [date of epidemic is 1908], made careful

inquiries regarding the food that had been eaten by the patients. He

found in six cases that fruit and berries had been a large item of

the diet. In the case 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 supplies were bought from fruit and vegetable

peddlers in their localities. Draper50 (1935) recorded a series of

cases of poliomyelitis which he considered to have originated from

the fruit purchased from a Greek fruit dealer. Barber51 (1939)

reported four cases of poliomyelitis that developed simultaneously on

the same day from the eating of strawberries in a single house of an

English boarding school. Barber points out that the simultaneous

onset of these cases resembled food poisoning. Goldstein et al52

(1946) reported an epidemic of polioencephalitis at a naval training

school among 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. A

HARpub analysis of Herbert C. Emerson's 1908 report and maps of the

period reveal that the disease epicenter was a small industrial town

with 3 cotton mills, situated close together on a river, upstream

from all of the polio cases. Circa 1908, large scale production began

of carbon tetrachloride which was commonly used to extract oil from

cotton seeds and it was used as an agricultural fumigant. Emerson

states that not a single case of polio was found in children who were

exclusively breast-fed. In the 1950s, Sabin discovered that milk

confers protection against polio. See dairy milk analysis.

Gebhardt and McKay58 (1946) investigated an epidemic of

poliomyelitis in Utah in 1946. The only food in common in all cases

in the survey were fresh fruits and vegetables. The writers point out

that the peach, pear, apple and tomato production peaks closely

parallel peaks of epidemics of poliomyelitis and that when several

cases of this disease occur in a family at about the same time, it

can be explained by a common food source. The authors state that

their data appears to fit into the jigsaw puzzle of epidemic

poliomyletitis. Produce, as a source of toxins.

Lepine et al54 (1952) point out that during the occupation of

France by the Germans, adults, and even young children, ate large

amounts of salads, as no other food was easily available, and the

incidence of poliomyelitis was about twice as great as usual. Raw

milk and even butter may be the cause of some cases of poliomyelitis,

they state. Investigations in France, they point out, favor the

digestive origin of poliomyelitis and the cases in the region of

Paris are best explained by the ingestion of foods, such as green

vegetation. HARpub: Fresh, unwashed, unprocessed, pesticides?

Wickman55 (1913) first suggested milk in connection with an

outbreak of poliomyelitis. In the parish of Ukla a case appeared on

October 6, 1905. The father of the patient had a dairy farm. Another

son and four other children of the neighborhood were stricken with

the disease on October 20. Altogether six families were attacked, and

ten cases occurred; all were supplied with milk by the father of the

initial case. HARpub: Dairy products can be primary carriers of

pesticides because of their lipid content. Virologist, Stefan Lanka

states that dairy products are beneficial except to the degree that

they are denatured.

Dingman5 (1916) reported a small outbreak of poliomyelitis in an

institution which resulted from the use of milk from a common source.

The cases occurred in three different and widely separated Jewish

boarding homes at Spring Valley, N.Y. The house mothers of these

homes were quite positive, even before the diagnosis of poliomyelitis

was made, that the milk was the cause. The eight cases of the disease

were the only ones which had developed in or about Spring Valley up

to that time and for some weeks after. Many milk examples follow.

Knapp et al. (1926) reported an outbreak in December of ten

cases of poliomyelitis in Cortland, N.Y. which was traced to the milk

supplied by one dealer. The epidemic started abruptly and ceased with

the discontinuance of the milk.

Aycock58 (1927) reported a poliomyelitis epidemic of unusual

severity caused by milk in Broadstairs, England, in October 1926. The

outbreak started and subsided suddenly, 62 cases being reported

between October 14 and 29, 31 of these appeared on October 14 and the

five days following. Multiple cases occurred in private boarding

schools having little communication with the town or with each other.

Four visitors, who had left Broadstairs just prior to the epidemic,

developed the disease at the height of the epidemic in Broadstairs in

widely separated places practically simultaneously with each other

and with the majority of the cases in Broadstairs. Investigation

disclosed that practically all the cases of poliomyelitis in this

epidemic were supplied with milk from the same dealer and from a

single farm.

H. e59 (1928) reported a small outbreak of poliomyelitis in

North Sweden caused by milk.

Rosenow60 (1932) described an outbreak of poliomyelitis

traceable to milk and cream in a midwestern college. Most of the

students roomed in the six dormitories on the campus; a few lived in

town near the campus. All ate their meals in large dining rooms in

three of the dormitories. The epidemic occurred abruptly in the late

autumn. There were eight frank and several abortive cases which

developed within a period of six days. The epidemic disappeared as

suddenly as it appeared after the discontinuation of the milk and

cream. The milk and cream supplied by the college dairy was served at

only one of the dining rooms for women from which two cases of

poliomyelitis developed and at the dining room for men from which six

cases developed. Numerous students eating in these particular dining

rooms had symptoms that comrnonly occur during the early stages of

poliomyelitis, chiefly gastro-intestinal and nervous system manifestations.

Rosenow et al.61 (1933) described an epidemic of poliomyelitis

at White Bear Lake, Minnesota, which was caused by milk. The

incidence of multiple cases in family groups was unusually high. The

epidemic occurred late in the autumn in several explosive outbreaks

during and immediately after spells of warm weather.

Kling62 (1928) supported the theory that poliomyelitis could be

spread by means of water supplies. He observed that the disease first

broke out near the water supply in the hills, cases occurring

successively as the stream descended. Gard63 (1938) stressed the

importance of increased rainfall and mentioned a laborer who was

alleged to have contracted poliomyelitis a few days after drinldng

water from a ditch. and Trask64 (1941) found, during an epidemic

of poliomyelitis, that the distribution of cases followed a water

course. Casey65 (1945) incriminated the water supplies for sporadic

cases occurring in a small parish in Alabama, in one village out of

numerous areas involved. They point out that a connection between

water and epidemic poliomyelitis cannot be disregarded. McFarland et

al.66 (1946) described an epidemic of poliomyelitis, explosive in

character, which began in Mauritius, in February, and terminated in

April. Three cyclones hit the island, one before and two during the

epidemic period, and rainfall was less than average. Flour and

vegetables were the staple diet because of the war. There was an

increasing prevalence of intestinal complaints when the poliomyelitis

epidemic began. In fact, there was an explosive rise in them in the

second half of February. In one village, Triolot, an explosive

epidemic of poliomyelitis appeared to have been caused by the eating

of ices.

In order to understand the relationship of fruits, vegetables,

milk and water to poliomyelitis. we must realize that under certain

conditions they may contain poisons or toxins which can constitute

activating factors. During droughts, for example, the incidence of

poliomyelitis is usually very much increased. It is this lack of

water from rainfall, which is necessary for the proper growth and

maturity of vegetation, that causes the development of toxic products

in fruits and vegetables. They are to be found in greater

concentration in unripened than in ripened fruits and vegetables

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Incubation Period Of Human Poliomyelitis Versus

Experimental Animal Poliomyelitis

Agreement regarding the incubation period of cases of human

poliomyelitis has been based almost entirely on the results of animal

experiments with the virus of the disease. It is a well known fact

that cases of human poliomyelitis in a home, institution or community

occur almost simultaneously and are often described as explosive in

character. This fact is typical of the effects of poisoning. On the

other hand, where experiments on animals in the laboratory are

carried out with the virus, a definite incubation period can be

established according to the manner in which the virus is

administered, its concentration, and the species of animal that is

employed. It has always been difficult to reconcile the fact that

human poliomyelitis has a short incubation period of one to three

days. according to Wickman55 and others, where the virus would

necessarily have to traverse the natural barriers in order to set up

infection in the central nervous system and an incubation period of

as long as nine or more days in the experimental disease, where the

virus is inoculated directly into the central nervous

system. Incubation period in humans is 1 to 3 days, yet more

than 9 days in lab animals.

Multiple cases in families present the nearest approach to the

grouping of epidemiologically connected cases. There is no conclusive

proof that the disease spreads under such circumstances like a

contagious or infectious disease. The cases in these families occur

simultaneously as in cases of poisoning. Avcock and Eaton71 (1925)

collected the records of 576 multple cases in 253 families. They

found that the proportion of secondary cases is highest on the day of

the appearance of the first case, and the proportion tends to

diminish steadily as time elapses.

Precipitators Of Human Poliomyelitis

Certain factors appear to be necessary in many cases for

precipitating the manifestations of human poliomyelitis. These

include fatigue, chilling, trauma, heat and humidity. operative

procedures, or pregnancy. Similar factors are well known

precipitators of the manifestations of lead toxicity. Neurological

manifestations of lead poisoning, and presumably other poisons, occur

more frequently in hot weather than during any other season of the

year. Suzuki and Kanako72 (1924), Fukushima and Matsumato73 (1928).

Blackman74 (1937), Rappaport and Rubin75 (1941), and Guannattasio et

al.76 (1951) have all pointed out this fact. It is well known that

the neurological manifestations of alcohol poisoning (delirium

tremens) can be precipitated by overexertion, exposure, operations,

trauma, shock, fright and acute inflammatory disease.

Comparative Pathology Of Human Versus

Experimental Animal Poliomyelitis

The differences between human poliomyelitis and the experimental

animal disease is definitely shown by the divergence of the

pathological lesions in the two diseases. It must be admitted that

the pathological lesions in the nervous system of experimental animal

poliomyelitis are similar to, if not identical with, those in cases

of human poliomyelitis. However, the visceral lesions that occur in

cases of human poliornyelitis cannot be reproduced in the

experimental animal with the virus regardless of the manner of

administration or its concentration. Thus, there are to be found in

human poliornyelitis many evidences of pathology besides the presence

of a virus and viral reaction. In the stomach there is a very high

incidence of submucosal petechial hemorrhage associated with intense

congestion of the mucosa. Myocarditis, accompanied by mycardial

degeneration, has been found in a high percentage of cases. In the

parenchymatous organs, especially the liver and kidneys, there is

usually demonstrated degeneration of the sort usually described as

cloudy swelling. Landon and 77 (1934 ) pointed out that the

granular degeneration of the parenchyrnatous cells, as well as fatty

degeneration represent toxic changes. They state also that the

kidneys in cases of human poliomyelitis show changes that may be

attributed to a general systemic toxemia. In practically all cases of

human poliomyelitis there is intense congestion of the blood vessels

throughout the body. Laboratory polio is not human polio.

The widespread lymphoid hyperplasia found consistently in gross

and microscopic autopsy examinations in cases of human poliomyelitis

never has been explained on the basis of a virus infection. There is

involvement of Fever's patches and the solitary follicles of the

gastro-intestinal tract, mesenteric and retroperitoneal lymph nodes,

peribronchial lymph nodes, thymus, malpighian corpuscles of the

spleen, tonsils, adenoid tissue of the nose and throat, and the lymph

nodes of the neck, axilla, groin, and other parts. Burrows78 (1931)

in a series of about fifty autopsies, noted that the maximum amount

of lymphoid hyperplasia was in Peyer's patches and the solitary lymph

follicles of the gastro-intestinal tract and the mesenteric lymph

nodes. He felt that the nerve tissue changes were secondary to those

existing in the lymph channels of this tissue. It is a well known

fact that lymphoid hyperplasia can occur as a result of poisons and

toxins. Doubtless the lymphoid hyperplasia in human poliolmyelitis is

an expression on the part of the body to poisons and toxins in which

protection is afforded by hyperplasia of its reserve forces, the

lymphatic apparatus.

The intense reaction in the gastro-intestinal tract not only

exp)lains the reaction to a poison but likewise the clinical

manifestations of gastro-intestinal irritation that so frequently

occur in cases of human polionwelitis. Although many workers have

postulated that the gastro-intestinal tract is the portal of entry of

the poliornyelitis virus into the human body, this never has been

lroven conclusively. Numerous investigators have failed to infect

monkeys when the virus has been administered orally even in high

concentration and in no case have the gastro-intestinal tract lesions

Ot human poliomyelitis been duplicated in experimental animals. The

virus that is recovered from the feces of human poliomyelitis is

probably synthesized or activated within the gastro-intestinal tract

and is excreted therefrom without gaining entrance to the hody. This

conclusion appears to be justified by the failure to infect animals

orally, and by the work of Gards of Sweden. Gards extensive studies

suggested that intestinal protein is an avirulent or non-neurotropic

varient of the poliornyelitis virus, a normal inhabitant of the

intestines. This intestinal protein (virus), according to Gard, is

non-pathogenic, but under the influence of exogenous factors is

pathogenic when injected into experimental animals. Fuirther proof

that the virus in the intestinal tract does not enter the human body

to cause human poliomyelitis is indicated by repeated failures to

isolate a virus from the blood stream, although human poliomyelitis

is generally considered to be a generalized systemic infection. The

isolation of a virus from the blood stream would not necessarily

indicate that it gained access to the body from the external environment.

Antibody Formation And Human Poliomyelitis

There has been much controversy regarding the interpretation of

the presence of poliomyelitis virus neutralizing antibodies in human

sera. It is now assumed that these antibodies develop following

non-paralytic and probably non-symptomatic infection with the virus

(hiring childhood as well as in frank cases of paralytic

poliomyehitis. Some workers have tried to prove the contagiousness of

human poliomyelitis by demonstrating elevated antibodies in contacts.

Other workers have been unable to find the antibodies increased in

contacts80. Poliomyelitis can develop in the presence of neutralizing

antibodies and many patients convalescent from the disease show no

antibody. The serums of guinea-pigs and rabbits do not contain

neutralizing antibody for monkey passage virus, though it is well

known that these animals possess an absolute immunity to the virus.

Further, antibodies are found in a high percentage of natives of

lands in which poliomyelitis is unknown and paradoxically in a much

smaller percentage of the population where the disease occurs in

epidemic form. The extent of natural resistance to human

poliomyehitis is utterly disproportionate to the quantities of virus

which is postulated to he present in the general population by

analogy with the results of experimental animal

poliomyelitis. Antibodies bear no relationship to presence of polio.

It is noteworthy that the appearance of neutralizing antibodies

in the blood after the injection of the poliomyelitis virus is very

uncertain evidence of parallel immunity to the natural disease81.

This fact was shown clearly by Kramer82, in 1936. He vaccinated a

group of children with vaccine and two months later found that 50 per

cent had developed neutralizing antibodies. However, in a parallel

uninoculated group of children, 41 per cent had also developed

antibodies. Kramer's results were in essential agreement with those

of Aycock and Hudson83, who found an increase of 28.6 per cent of

immunes among the vaccinated children in their series as compared

with an increase of 22.8 per cent of inimunes in the unvaccinated

control group. Neither of these writers considered the small

difference of any practical value in favor of the vaccinated

group. No significant difference in antibody formation between

vaccinated and control groups.

Koch's Postulates And Human Poliomyelitis

Koch's first and one of his most important postulates emphasizes

that a parasite must be found in every case of the disease in order

to state that that particular parasite is the cause of the disease.

In 1952, there were nearly 58,000 cases diagnosed as poliomyelitis in

the United States, 75 per cent of which were paralytic. Attempts to

isolate the virus from the excretions were carried out in little more

than one per cent. In the remaining 99 per cent, a virus was merely

assumed to have been present. That the paralysis in this large group

might have had many causes is obvious. It is not to be overlooked

that a significant number of spinal cords removed from children dying

in the acute stage of poliomyelitis are incapable of producing

paralysis after intracerebral inoculation in the monkey. Poliovirus

not found in a significant number of paralytic polio cases, using

intracerebral inoculation test..

Korns84 (1953), N. Y. State Public Health Officer, states that

the isolation of the poliomyelitis virus for diagnostic purposes is

almost never done and is of little practical value, while at the same

time being a very difficult procedure. He points out further that

isolation of the poliomyelitis virus from the patient by no means

establishes the diagnosis since the virus is widely prevalent in the

population during epidemic periods without producing disease. Bell85,

epidemiologist, National Institutes of Health, states that the

isolation of a virus from poliomyelitis patients is not a routine or

reportable procedure; it is carried out only in conjunction with

research studies. Serological tests of acute and convalescent blood

specimens, he says, are often of no value for determining the cause

of the current infection in poliomyelitis because in this disease the

antibodies are usually in good titer at the time of onset of

symptoms. Isolation of poliovirus has no diagnostic value.

Poliovirus antibody tests have no diagnostic value.

Biochemical Factors In Human Poliomyelitis

There appear to be certain physiological and chemical factors

which seem to be necessary for the development of human poliomyelitis

and for the synthesis or activation of the virus. Hormonal imbalance

has been suggested as an important factor by a number of writers in

predisposing an individual to poliomyelitis. Stern86 (1911) found

that a considerable number of cases of this disease showed some

symptom's of Basedow's disease. i.e., goiter, tachycardia, tremor,

nervousness, etc. Wynkoop87 (1916) suggested that human poliomyelitis

is a disease caused by negation of glandular efficiency. Draper88

(1932) noted signs in his patients that tended to point toward

endocrine deficiencies. The mothers of these poliomyelitis patients

not infrequently had moderate or marked exophthalmos or thyroid

enlargement. Inglessi89 (1932) found hypocholesterolemia in thirty

children with poliomyelitis during the acute stage and for some time

in the paralytic stage. Jungeblut90 (1932) suggested that the mass

protection enjoyed by the adult human population rests primarily on

the normal function of the endocrine balance characteristic of mature

age. Later91 (1935) he stated that the protective action against

poliomyelitis probably lies in the normal physiological function of

the organism and that the main cause for susceptibility is a hormonal

dysfunction. Prophylaxis he suggests must consist mainly in

correcting the individual susceptibility on a general

physiologic-hygienic basis. Aycock92 (1940) stated that the

susceptibility to poliomyelitis is determined by an inherent

endocrinopathy which is largely subclinical. Aycock93 (1940) found a

higher average excretion of estrogenic substance in a group of

poliomyelitis patients from one to twenty years after an attack of

this disease and noted that there was nothino to indicate that this

was a sequel of poliomyelitis. This fact suggested to him that

endocrinopathy as a basis of susceptibility does not lie in a simple

deficiency in the elaboration of estrogenic substance, but rather in

some discrepancy in its economy. Aycock pointed out the frequency

with which the paralytic disease tends to parallel certain seasonal

and climatic fluctuations in physiologic processes. " Such a

correlation suggests, " he says, " that susceptibility to paralytic

poliomyelitis does not lie in any fixed anatomical character, but is

dependent on some physiological process. " HARpub: Children

rather than adults usually acquire polio. Children up to age 7 have a

growing, exposed, unsheathed CNS.

The well known fact that virus activity, as well as the reaction

to poisons and toxins, produces chromatolysis in an affected nerve

cell indicates the necessity for knowledge of the localization of

materials and chemical reactions within the cell. Chromatolysis

suggests a shift in the balance of a steady state by differential

inhibition or acceleration of complex enzyme-regulated reactions94.

" In addition to the specific production of chromatolytic changes by

toxins and neurotropic viruses, interference with enzyme mechanisms

by homonal imbalances or dietary deficiencies might conceivably in

extreme cases produce the phenomenon of chromatolysis. " 94 Aycock and

Foley95 (1945) stress the fact that motor neurone disease may be

brought about by an enhancing or inhibiting action on one or more of

the enzyme systems.

A study of the biochemical changes that arise during the course

of human poliomyelitis has not been followed adequately, but a few

important clues have been reported. One of these consists of the

presence of coproporphyrin III in the urine of poliomyelitis

patients96; another is the appearance in the blood of increased

amounts of guanidine.98 It is not to be overlooked that both of these

chemicals are present in the body in increased amounts in cases of

poisoning by a number of toxic agents.

Kaplan et al.100 (1938-39) described an increase of proteases in

the cerebrospinal fluid of cases of human poliomyelitis. Kovacs101

found (1953) in this disease that there are no changes of acid

soluble inorganic phosphorus resulting from the interaction of

enzymes and phosphorus-containing organic material in the

cerebrospinal fluid. In acute bacterial meningitis, on the other

hand, a great increase of phosphorus was usually evident. Kovacs102

(1953) studied the nucleases in the cerebraspinal fluid in cases of

human poliornyelitis and found consistently high values. His findings

suggested some direct connection between chromatolvsis and

ribonuclease activity.

The fact that ascorbic acid103-105, thiamin106-113. methylene

blue114, as well as iodine115 have been successfully employed by some

workers in the treatment of human poliomyelitis. suggests that

certain biochemical disturbances within the body during the course of

the disease can be corrected with chemotherapy. In the treatment of a

case of hulbar poliomyelitis, Eskwith116 (1951) postulated that

dimercaprol (PAL) might be effective because in heavy metal poisoning

it combines with the metals and protects certain enzymes - those

containing a sulfhydryl group - from combination with the poison and

because viruses seem to cause necrosis by destroying or inhibiting

certain intracellular enzyme systems. He reasoned that if glutathione

and other sulfhydryl containing enzymes and tissue protein can be

injured by heavy metals, it seems quite possible that they can

combine with and be injured by other substances besides metals.

Similarly, it is quite possible, he thought, that since dimercaprol

contains two sulfhydryl groups, it may protect the enzymes from these

non-metallic toxic agents. Eskwith's patient was a 4 1/2 year old

girl who had required a tracheotomy and oxygen therapy and whose

clinical course was steadily downhill until the dimercaprol

injections were given. At the end of 24 hours after therapy was

begun, the patient was clinically improved and consciousness rapidly

followed. Eskwith learned subsequently that some work had been done

with dimercaprol in relation to neurotropic virus infections in

experimental animals and that there was no evidence of its efficacy.

This fact appears to confirm the belief that human poliomyelitis and

the artifically produced experimental animal disease are two entirely

different entities.

Experimental Animal Poliomyelitis In Human Beings

Once the poliomyelitis virus is recovered from human and

extrahuman sources many (diversified experiments can be carried out

in the laboratory with experimental animals. The unfortunate thing,

however, is that these laboratory experiments on animals are

interpreted as being applicable to the human disease from whence the

virus was obtained and that unjustified conclusions are drawn.

Realizing that an animal will develop experimental poliomyelitis

from a virus introduced into its body in an abnormal manner, one can

expect that a human being also can develop poliomyelitis of the

experimental animal type under the same conditions. Thus, there is to

be found in the medical literature reports of the development of

poliomyelitis in technicians117-120 working in laboratories with

concentrated forms of the poliomyelitis virus. In these cases the

portal of entry of the virus is doubtless an abrasion, scratch,

laceration or needle prick. A case of poliomyelitis in a

technician118, which followed the contamination by a virus of a

scratch, failed to show at autopsy the pathological lesions

characteristic of human poliomyelitis arising in a natural manner. It

is significant that in this case the gastro-intestinal tract revealed

no lesions and no virus was present in the intestinal contents. Over

the past 40 years these are the only reported cases of poliomyelitis

developing in laboratory workers. Essentially, there have been

no polio cases in laboratory workers in 40 years.

If humans are injected with a concentrated form of active virus,

it is natural to expect that they would develop the same type of

poliomyelitis that occurs in experimental animals following the

injection of the virus. Actually, this did occur in 1935, when some

children who received a poliomyelitis vaccine prepared with the virus

obtained from experimental animals developed poliomyelitis; half of

them died.121 Significant facts of great importance in these cases

were that the incubation period of 6 to 14 days following the

injections corresponds with the incubation period of experimental

animal poliomyelitis; the fact that the level of the spinal cord

first affected corresponded with the extremity in which the injection

was made. i.e., the same limb or the contralateral limb parallels

recent observations. It is now known, for example, that poliomyelitis

con occur following the injection of toxic antigens during the summer

months, i.e., pertussis vaccine and diphtheria toxoid and that the

paralysis occurs in the same limb or the contralateral limb where the

antigen is injected. Injections create a highly abnormal

situation. Injections of many things, such as cellular material or

peach skin can cause disease.

Comment

The evidence never has been strong nor very convincing that an

exogenous virus enters the human body to cause poliomyelitis.

Consequently. year after year, new concepts are presented and old

ones discarded that are intended to show where the virus originates

outside the body and to establish its portal of entry into the body.

Clearly evident are the facts that there is more to indicate that the

virus of poliomyelitis is of endogenous origin. " Clearly

evident... the virus of poliomyelitis is of endogenous origin. "

Whether or not one is of the opinion that a poison or virus, or

both, are responsible for human poliomyelitis, it is obvious that the

fruit, vegetables, milk, and water used by the poliomyelitis patient

prior to his or her illness should be carefully considered. If by

careful inquiry a fruit, vegetable, milk, or water source is found,

prevention of other cases of this disease can be brought about by

warning the public. Regarding the unsaid word: Pollution.

Since a poison or virus will cause damage by disturbing normal

chemical relationships within the body, particularly enzyme systems,

it is imperative. theretore, to determine what chemical changes take

place in human poliomyelitis and how they may be restored to normal.

It is at this point that much research can be done. A preventive and

therapeutic agent could doubtless be developed to maintain or restore

normal chemical relationships within the human body to prevent and

cure poliomyelitis. It must be seriously considered that if it were

possible with a vaccine to prevent the synthesis or activation of the

poliomyelitis virus within the human body, it does not follow that a

poisonous or toxic activator would be deprived of its ability to

cause neurotoxic damage to the lower motor neurone with resulting

paralysis. A preventive agent would be an antidote, not a vaccine.

Summary

1. The exogenous virus theory of cause of human poliomyelitis

fails to explain all facts without exception and cannot be considered

to be entirely valid.

2. It is emphasized in this report that the fundamental cause

of human poliomyelitis appears to be a poison or toxin and that the

virus is synthesized or activated within the human body as a result

of the poisoning.

3. There appears to be an intimate relationship between virus

diseases and diseases resulting from toxic causes. This fact,

illustrated by examples, has been stressed.

4. It is pointed out that the poisonous activating factor in

cases of human poliomyelitis can originate from fruits, vegetables,

milk, and water during epidemics of this disease.

5. The locality influences, seasonal incidence, simultaneous

development of multiple cases in homes, institutions and communities,

as well as the visceral lesions and other facts, all indicate the

association of a poison or toxin with human poliomyelitis.

6. Normal chemical relationships within the body are disturbed

in cases of human poliomyelitis; a preventive and therapeutic agent

could doubtless be developed to maintain or restore these

relationships and thus prevent and cure the disease.

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