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Medical data is for informational purposes only. You should always consult your family physician, or one of our referral physicians prior to treatment.
Roger Wyburn-Mason, M.D., Ph.D.
The Free-living Amoebic Causation and Cure of
Activity in Rheumatoid and Auto-Immune Diseases
by ROGER WYBURN-MASON
Editor’s Note: This is from the last manuscript by Doctor
Roger Wyburn-Mason. While it repeats information previously
published, it also includes material inserted shortly before his
death and an updated bibliography to 1979. As a basis for the
research work at three schools of medicine and the clinical
practice of over 250 physicians throughout the world and the
formation and function of the Rheumatoid Disease Foundation
[now The Arthritis Trust of America], it has historical as well as
medical value.
However, numerous species of free-living amoebae are known.
Most fall into two genera, Acanthamoeba and Naegleria and some
are pathogenic to man and animals; they are found on the surface soil
preferring warm, moist conditions and proliferate in warm stagnant
pools and at the bottom of rivers and lakes, particularly around the
entry sites of warm effluents. They have been found in the domestic
water supply, in human feces and in unpasteurized milk. Pathogenic
free-living amoebae are readily isolated from chlorinated swimming
pools, potable water, sewage and human nasal and throat cavities.
They often contaminate tissue cultures. In inimical conditions, they
form hollow spherical cysts which are present in the air in most parts
of the world and can easily be found on agar plates exposed to air.
Free-living amoebae prefer warm surroundings, and they tend to
migrate from cool environments to body temperature, a property
known as thermotropism.1
All terrestrial animals and plants and those inhabiting fresh
water and also probably the sea, live in a world surround by many
species of free-living amoebae, which certainly pass into the mam-
malian respiratory passages as cysts or trophozoites in the gastrointes-
tinal tract of many animals, including man, since they are found in
their feces. As the organisms are motile, it would be unreasonable to
suppose that, once they had entered the orifices of man or other
warm-blooded animals, they would not migrate under the thermotro-
pic influences into the body tissues. Since the amoebae may prove to
be either non-pathogenic to animals, the same must also apply should
the organisms reach human tissues.1
Recently it has been shown10 that the sera of all humans, in-
cluding that of the cord blood, contain antibodies to either
Acanthamoeba or Naegleria, indicating universal present or past
infection of man and the newborn with these organisms. Textbooks
on protozoology state that “unspecified types of amoebae have been
isolated at times from every tissue in the body,”3 or “there is hardly
an organ in the body from which somebody has not obtained amoe-
bae.”4 Thus, all human bodies appear to contain free-living amoe-
bae somewhere in the tissues. A few cases of leisons due to species
of such organisms have been described in plants and man, in particu-
lar amoebic meningo-encephalitis.5,6
The whole syndrome resembles syphilis. Waldenstrom and
others, indeed, state that “if the spirochaete had not been discovered,
syphilis could be taken to be the ideal model of an autoimmune
disease. The variety of tissue reaction antibodies, the wide-spread
lymphocytic tissue damage and the vasculitis are characteristic fea-
tures.”21 Rheumatoid disease closely resembles the rheumatic mani-
festations in leprosy22 which may present with an acute arthritis
affecting one or a number of joints, polymyositis, skin leisons, fever
raised ESR, etc., with increase in circulating gammaglobulins and
positive serological tests for autoantibodies, RF and ANF, as in
rheumatoid disease. This is an immune complex syndrome with
antigen provided by disintegrating M. leprae. The reaction may be
precipitated by antileprosy drugs, a reaction known as Lucio’s phe-
nomenon, which is identical in nature with the Herxheimer reaction.
The syndrome confirms the deductions made regarding rheumatoid
disease. Such observations prove that every tissue in the body may
contain unsuspected free-living amoebae, which, if pathogenic, may
cause tissue infiltration by lymphocytes with germinal centers and
often plasma cells in genetically susceptible subjects as governed by
their tissue types. They are the source of Glynn’s previously postu-
lated unknown chronic antigenic stimulation,23 as the cause of rheu-
matoid disease. [See "The Herxheimer Effect,"
http:www.arthritistrust.org.]
References
15. Wyburn-Mason, R. The free-living amoebic causation of
rheumatoid and autoimmune diseases. International Medicine 1:
20-25; 1979.
16. Wyburn-Mason, R. New views on the aetiology of rheu-
matoid arthritis. British Medicine 12-14; August 21, 1979.
17. Wyburn-Mason, R. The Naeglerial causation of rheuma-
toid disease and many human cancers. A new concept in medicine.
Medical Hypotheses 5: 1237-49; 1979.
18. Williams, H.D., Lockwood, G.M., Russell, B.A. Inhibi-
tion of reticuloendotheial function by gold and its relation to post-
injection reactions. Brit. Med. J. 2: 235-7; 1979.
19. Levamisole in rheumatoid arthritis. Multicentre Study
Group, Lancet ii: 1007-12; 1978.
20. Herxheimer, K. Ueber eine Syphilitischen vorkommende
Quecksilberreaktion. Dtsch. Med. Wchsch. 28: 895-6; 1902.
21. Quoted in Doniach, D., Roitt, I.M., Taylor, K.B. Autoim-
mune phenomena in pernicious anaemia. Serological overlap with
thyroiditis, thyrotoxicosis and systemic lupus erythematosus. Brit.
Med. J. i: 1374-9; 1963.
22. Glynn, L.E. The chronicity of inflammation and its signifi-
cance in rheumatoid arthritis. Ann. Rheum. Dis. 27: 105-11; 1968.
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