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Free Living Amoeba & The Effects of Anti-amoebic Drugs on

Rheumatoid Disease

The Cause of Rheumatoid and Autoimmune Diseases?

by ROGER WYBURN-MASON

Christ’s College, Cambridge, England

[Reprinted by permission of Arthritis News Today, Yorba Linda,

CA August 1981; from a paper presented at the 15th International

Congress of Rheumatology in Paris this June]

Roger Wyburn-Mason, M.D., Ph.D.

Historical Note

A letter from Professor Roger Wyburn-Mason

(Formerly published in The Journal of the Rheumatoid Disease

Foundation, Volume 1, Number 1)

The Roger Wyburn-Mason and Jack M. Blount Foundation

for the Eradication of Rheumatoid Disease

AKA The Arthritis Trust of America

, 7376 Walker Road,

Fairview, Tn 37062

Rheumatoid Disease is a generalized condition, not just one of

joints and muscle spasm. The occurrence of rheumatoid granulo-

matous nodules subcutaneously, at the sites of pressure or even on

the meninges or sclera or of rheumatoid lung, heart, liver, and

kidney lesions or of involvement of the parotid and lacrimal glands

and skin lesions can only be found in a systemic pathology.

The autonomic neurogenic cause of the disease was exploded

many years ago by the fact that complete sympathectomy was repeat-

edly found to have no effect on the disease. This is not a “one-of”

finding, but has been repeatedly confirmed. The nervous system

may be involved in producing the inflammatory changes in rheuma-

toid disease.

Years ago I showed that inflammation in a tissue is dependent

on the integrity of the unmyelinated C fibers of the posterior nerve

roots and mixed peripheral nerves. If these are destroyed, as in gun-

shot wounds, leprosy, tabes or syringomyelia then injury to the part

normally supplied by these nerve fibers results not in inflammation

but in necrosis. While in the condition of causalagia resulting from

injury to the median or sciatic nerves, mild trauma in the painful area

may result in an exaggerated inflammatory response as compared

with that in normal tissues of the patient. Inflammation depends on

antidromic impulses passing down from the spinal cord to the in-

flamed area through these special nerve fibers, in the case of rheuma-

toid arthritis, to the region of the joints.

Such cases as the following:

All were fit middle-aged men, ploughing the dry fields on windy

days — one in the Middle West of USA, one in Ontario and one in

Rhodesia. During the ploughing, there was a great deal of dust being

blown about from the dry surface soil and this was inhaled by the

subjects. During the next night, all three were wakened by drench-

ing night sweats, general malaise and next morning were found to

have temperatures of 105° F. Every joint in the body was painful,

swollen and immobilized even including the cryoarytenoids and

temporo-mandibular. They had a cough, sputum, severe headache

and muscular aching. All were admitted to the hospital and eventu-

ally found to be suffering from acute rheumatoid disease. In spite of

intensive treatment, their symptoms only very gradually diminished

over the next 3-4 months, but they were left at this time with severe

pain and swelling of the joints which did not respond to any treat-

ment over the next year or more. These cases are typical of severe

infection and NOT of a disturbance of the autonomic nervous sys-

tem. The origin of their infection would seem to lie in something

inhaled from the copious surface soil dust (which contains free liv-

ing amoeba).

I isolated free-living amoebae from all the body tissues in cases

of active rheumatoid disease, cultured them from the laboratory, found

that antiamoebic substances killed them and then treated cases of

active rheumatoid disease with various antiamoebic substances.

Incidentally, the eminent protozoologists Kofoid and Swezy,

working in their laboratory at the University of California (LA) in

1922 found the same organism in the bone marrow of cases of

rheumatoid arthritis and suggested its aetiological relationship to the

disease some 40 years before my work. They reported this in a

zoological journal which never reached the medical profession.

Furthermore, any substance which in vitro kills the organism

when given to active cases of rheumatoid arthritis often produces a

transient Herxheimer reaction, that is an exaggeration of the inflam-

matory changes of rheumatoid arthritis and often the appearance of

lesions in previously unaffected tissues, just like mercury exagger-

ated the symptoms of syphilis. When given to healthy subjects,

these antiamoebic drugs have no such effect, and Herxheimer reac-

tions do not occur when antibiotics or antiviral substances are used

against sufferers from bacterial or virus diseases. This observation

alone shows the presence in rheumatoid arthritic lesions of an organ-

ism more complex than a bacterium, namely an amoeba. This is the

complete proof of the amoebic causation of rheumatoid arthritis.

[Subsequent studies were unable to confirm this amoeba theory, but

strongly suggested that the treatment worked to normalize or stop

auto-immune activity of macrophages which happened to resemble

amoeba. Thomas McPherson Brown, M.D. felt that he'd isolated

mycoplasm from arthritic joints. Historical research clues lead to a

conclusion that perhaps many different organisms can stimulate a

tissue sensitivity to themselves, thus creating arthritic symptoms.

Ed.]

Local anesthetics have two effects — they are anti-protozoal

and also paralyze the unmyelinated C fibers, the discharge of which

is responsible for inflammation. Both these effects could explain

some of the benefits from procaine therapy in rheumatoid disease.