The advent of polio
immunization in 1955 caused changes in the balance of the gut viral population,
favouring the spread of ME.
No doubt polio immunization
(both the inactivated Salk vaccine and the live oral Sabin variety, introduced
worldwide between 1954-1959) reduced circulation of the wild polio virus 1-3.
However, it also altered the balance between enteroviruses, in favour of
non-polio1o enteroviruses (NPEVs) (BMJ, 1961: 1061).
For instance, in 1959, polio
caused 84 per cent of enterovirus associated paralysis; by 1961, its incidence
had fallen to 12 per cent. But after 1961, other enteroviruses such as old and
new varieties of Coxsackie caused 74 per cent of all enterovirus-associated
paralytic disease. Between 1959-65, concludes Nightingale Research Foundation,
there may have been a changeover from polio as the prevalent disease to ME and
other diseases caused by enteroviruses.
A similar changeover followed
the introduction of oral polio vaccine (OPV) in China since 1971. The prior
incidence of polio fell, while cases of Guillain Barre Syndrome (GBS), another
paralytic disease, rose sharply (The Lancet, October 8, 1994).
These produce a much greater
variety of symptoms, since NPEVs are more widely distributed m the body than is
polio (muscle, joints, heart, endocrine and lymphoid organs), according to ME
specialist Dr Elizabeth Dowsett. Otherwise, lesions in brain stem, mid and hind
brain and upper spinal cord are identical in polio and ME, according to 150 post
mortems done on US Army veterans with a history of polio (JAMA, 1947; 134:
In viral populations, the polio virus
can easily be displaced
by Echo or Coxsackie viruses, and this second enterovirus may be
more virulent than the polio virus it replaces (The Lancet, 1962: 548-51).
Post-1955 ME patients frequently have been shown to have severe muscle
failure (BM Hyde, The Clinical and Scientific Basis of ME/CFS,
Many gut viruses other than
polio virus 1-3 can cause paralytic polio and ME. This is because they can
attach to more than one set of tissue receptors found on different cells in the
brain, spine and other body areas, as can polio. Injury to such cells results in
ME symptoms, which also occur in polio and post-polio syndromes.
presence of these
non-polio gut bugs also appears to alter responses in the
population to the various vaccine strains of polio. During a 1955 polio epidemic in areas of Iceland that had been exposed to
the 1948-49 outbreak of epidemic neuromyasthenia (the early name for ME),
children had a lower antibody response to polio vaccine strain 1, but an
increased response to polio vaccine strains 2 and 3 (Lancet, 1958:I:370-71).
Later, it was discovered that other viruses can inhibit the pathological
effects of classic polio (IRSC Jnl Int Res Coms [Med Sc], 1974;2:22-26).
mutate - hence the polio
strain used in vaccines "wanders". There have been
countless reports of vaccine failure, polio contracted by fully vaccinated
populations and parents contracting polio from vaccinated infants (See the
WDDTY Vaccination Handbook). In these, the weakened, supposedly "safe"
vaccine strain of polio has transformed into a virulent enterovirus -
either one of the classic polio ones or a strange mutation of it. Over 64
epidemic outbreaks of ME have been published in the past 70 years, two
thirds after the introduction of polio immunization 40 years ago (Am Jnl
Med, 1959:569-95; AM Ramsay, Myalgic Encephalomyelitis and Post viral
Fatigue Syndromes, Gower Med Publ, 1988; SAMJ, 1988; 74: 448-52;
Postgrad Med J, 1988; 64: 559-67).
In epidemic form, this disease
strikes teaching and medical establishments (ME is more common in teachers than
in health care workers). The earliest epidemic outbreaks usually occurred in the
wake of a polio epidemic, the first at LA County General Hospital in 1934 (Publ
Health Bulletin 240, Washington DC, 1938), referred to as "Atypical Polio".
Another, which affected officers and men in Switzerland in 1939, was described
as "abortive poliomyelitis" (Helvetica Med Acta, 1949; 16: 170-72), as was a
1950 NY State outbreak (Neurology,1954;4:506-16).
Republished with permission of What Doctors Don't Tell
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