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-polio 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 the NPEVs are more widely distributed in 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 to150 post mortems done in 1948 on US Army veterans with a history of polio (JAMA, 1947; 134: 1148-54).

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, 1992:111-6).

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.

The 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, but an increased response to polio vaccine strains 2 and 3 (Lancet, 1958;1:370-71). 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).

Enteroviruses easily 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 Postviral 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).

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