The Family Medical Herbalist - Polio or AFP?
The Family Medical Herbalist - Holistic medical herbalism, mycotherapy and immunonutrition

POLIOMYELITIS OR ACUTE FLACCID PARALYSIS (AFP)?

Stephen Hawkins on poliomyelitis and acture flaccid paralysisHere is the disease profile I researched at the University of Westminster in 2005. These concepts are nowadays better explored by a major scientist, Stephen Hawkins and I feel this subject is worth reflecting upon as it has major international safety implications. "Stephen Hawking has told reporters that he believes vaccinations pose a threat to the existence of humanity in the near future"

INTRODUCTION & EPIDEMIOLOGY
Poliomyelitis (polio) is inflammation of the myelin sheaths covering neurons and the grey matter of the central nervous system (CNS) that causes infantile paralysis (Oxford Concise Medical Dictionary 2002:545). It is considered a contagious disease transmitted via the nasopharynx (Hunter 2002:1198) after inhalation of air particles or by touching surfaces that have been in contact with faeces (Polio Eradication 2005). However, contagion may occur only through a non-paralysed person (Werner, 1999:61) up to 2 months after incubation (Sussman & Sussman 2003:62).
Polio may cause paralysis within hours, particularly in babies and young children under 5, whose CNS is not fully formed (Polio Eradication 2005). Although those vaccinated become virus carriers and may transmit the disease, Polio Eradication (WHO, UNICEF, Rotary Int. & US Centre for Disease Control) insist on global immunization (2005).
The American continent was certified free of polio in 1994, the Western Pacific regions followed suit in 1997 (PostPolio 2005) and the rest of the world now seem close to eradication. As of the first quarter of 2005, the only reports of polio are from Nigeria (29), Pakistan (4), Sudan (18) and India (12) (Polio Eradication 2005).
However, polio counts exclude acute flaccid paralysis (AFP), a condition indistinguishable from polio, except by viral specimen and serum antibodies analyses (Polio Eradication 2005). AFP cases are thousands in South East Asia and the Eastern Mediterranean and a few hundreds in all other regions, including America. Hence, it may be hard to establish whether AFP counts include poliomyelitis in vaccinated virus carriers (Bruno: 2002:129).

AETIOLOGICAL THEORY
Despite general suggestions that polio spreads due to poor sanitation (Polio Eradication 2005), the opposite has been argued (Bruno 2002:39). As polio epidemics did not exist before the XIX century, it has been alleged that virtually every person before that was immune, thanks to poor sanitation allowing contact with mild poliovirus (39). Hygiene theories appear, however, debatable, as polio epidemics occurred in the US mid XIX-mid XX century, irrespectively of sanitation (42).
With the first US mass vaccination programmes of 1957-1958 and 1959, polio rose by 50% and 80%, respectively, thus casting doubts on the efficacy of Sabin’s inactivated poliovirus (IPV) inoculation (McTaggart 1996:133). In the US, epidemics declined thereafter and success has been attributed to the introduction of Sabin’s attenuated live oral poliovirus (OPV) vaccine in 1963 (Bollenbach 1999).
However, polio has continued to increase amongst populations with the highest vaccination compliance (Lancet Neurology 2004:383), so that Polio Eradication has been withdrawing OPV and re-introducing new IPV inoculation on a country by country basis since 1999 (Franzini 2005) (383).
Controversially, dichlorodiphenyltrichloroethane (DDT) and organochloride-based pesticides had been known to provoke polio before mass vaccination (West 1999). Salk himself included the neurotoxins formaldehyde and methiolate in his IPV (1999), presumably as active constituents. Sabin’s later OPV contains mainly antibiotics, monkey kidney tissue and foetal tissue (Sussman & Sussman 2003:62).
Searching Medline reveals that neurotoxins like lead, arsenic or organophosphate pesticides are associated with paralysis in animal conditions such as “polioencephalomalacia” and “poliomyelomalacia”, thus supporting a possible aetiological relationship between neurotoxins and polio (West 1999). Poliovirus itself might be harmless but for heavy metals, ultraviolet light or other radiation accelerating genetic recombination and viral replication (1999).

PATHOGENESIS
Poliovirus measures 27mµ in diameter (Huckstep 1979:12) and has “canyon” shapes fitting human cells’ receptors (He et al 2005). Poliovirus is of the genus Enterovirus of the Picornaviridae family, which replicate fast once in the gastrointestinal tract; from the lymphoid tissue of the tonsils to the stomach and the intestinal Peyer’s patches (Bruno 2002:23).
After an incubation period of up to a fortnight, if the immune system fails to curb the viral infection, lymphocytic infiltrate spills into the circulation and travels to peripheral nerves, the spinal cord and the brain (Hunter 2002:1198).
Poliovirus then crosses the blood-brain barrier through leaky endothelial capillary cells and produces lymphocytic meningitis in the grey matter, brain stem and cortex (Hunter 2002:1198). Permanent dot-like lesions have been detected by magnetic resonance imaging (MRI) scans in individuals surviving paralytic as well as non-paralytic polio in the grey neurons of the reticular formation, basal ganglia and white myelin sheaths covering neurons, which connect the activating systems to the cortex of the brain (Bruno 164-165).

poliomyelitis, actute flaccid paralysis, AFP, bulbar polio, musce weaknessFrom the brain, the virus may continue to spread to the spinal cord and destroy anterior horn cells and lower motor neurons, thus causing failure of neuromuscular junctions and acute flaccid paralysis.

Type 1 viral strain:Lower and upper limb and sometimes breathing muscle paralysis (Bruno 2002:22).

Bulbar Polio, post polio, Type 3
Type 2 viral strain:Brainstem damage without paralysis; there may be fever but most infected individuals develop no symptoms (Bruno 2002:22).
Type 3 viral strain:“Bulbar polio”: Complete damage of the brainstem, lower and upper limbs and, in extreme cases, difficulties swallowing and respiratory paralysis leading to death (Bruno 2002:22).


  • Minor illness:Fever, headaches and sore throat lasting 1-2 days (Goldman L & Ausiello D 2005:2336).
  • Major illness:Diarrhoea, vomiting, pleocytosis in cerebrospinal fluid and aseptic meningitis lasting 5-10 days (Goldman L & Ausiello D 2005:2336). About 5% of individuals may develop neck, back stiffness and fibromyalgia and asymmetrical paralytic features (2336) (Werner 1999:61).

Post-polio Syndrome (PPS):Concentration and memory decline and muscle weakness lasting many years after contagion (Bruno 2002:228-233). PPS following non-paralytic polio, Chronic Fatigue Syndrome (CFS) and Myalgic encephalomyelitis (ME) are indistinguishable (228-233). Also, Enterovirus “Coxsackie B” caused polio-like paralysis in 1948 in New York and was considered ME (291-292).

PROGNOSIS & MANAGEMENT
Most paralytic cases resolve within weeks; if paralysis persists beyond a month, 60% recovery can be expected by 3 months (Goldman L & Ausiello D 2005:2337). Muscle weakness affects the whole body, even in non-paralytic polio, as only 60% of motor neurons are spared (Bruno 2002:20).
Orthopaedic crutches, braces, wheelchairs and other aids are needed in paralytic polio (Bruno 2002: 266-276). Besides, avoidance of fatigue is advised, for muscular fatigue and emotional stress wear out the nervous system and remaining motor neurons (131). Only relaxing exercise should be medically instructed to prevent atrophy, osteoporosis and fractures (134-141).

GLOSSARY
Acute flaccid paralysis (AFP): Rapid dropping of paralysed muscles, due to nerve damage.
Anterior horn: Frontal horn-shape grey matter in spinal cord.
Aseptic meningitis: Inflammation of meninges (3 membranes covering the brain) which is not infectious.
Basal ganglia: masses of grey matter inside the white matter of the cerebrum (the largest part of the brain).
Blood brain barrier: Tight junctions of capillary cells separating blood from cerebrospinal fluid in the brain.
Brain stem: Part of brain just above spinal cord.Central nervous system (CNS): Brain and spinal cord.
Fibromyalgia: Pain in muscle fibres without inflammation that causes stiffness and fatigue.
Grey matter: Substance of cell bodies and dendrides of neurons and glial cells in the CNS.
Lymphocytes: White blood cells producing antibodies involved in specific immune response.
Nasopharynx: Tube section above the palate, where air passes after entering the nose.
Necrosis: Cell death caused by disease or injury.
Neuromuscular junction: Meeting point of neuron with muscle fibre where motor nervous impulses pass.
Osteoporosis: Loss of minerals from bone tissue.
Peyer’s patches: Masses of intestinal lymphoid tissue.
Picornaviridae: “Pico” = small; “RNA” = containing ribonucleic acid; viridae = virus family.
Pleocytosis: Abnormally large number of lymphocytes in cerebro-spinal fluid bathing the brain and spinal cord.
Reticular Formation: Connections in brain stem passing motor and sensory impulses from spinal cord to other areas.

REFERENCES
Adl-Tabataba, Sean (5 October 2016) Stephen Hawking has told reporters that he believes vaccinations pose a threat to the existence of humanity in the near future. News US. http://yournewswire.com/stephen-hawking-vaccinations-threaten-humanity [accessed 7/10/2016].
Baumbach et al. (2005) Poliomyelitis. University of Iowa College of Medicine.www.vh.org/adult/provider/ pathology/CNSInfDisR2/Text/209.html [accessed 2/4/2005].
Bollenbach, E (1999) The Polio War and Vaccine Strategy.  www.ott.zynet.co.uk/polio/lincolnshire/library/bollenbach/biology6.html [accessed 29/3/2005].
Bruno, R L (2002) The Polio Paradox. New York, USA: Warner Books.
Franzini, C (2005) Poliomielite. http://www.medicina-online.net/meo10001.htm. [accessed 3/4/2005].
Goldman, L & Ausiello, D (eds.) (2005) Cecil Textbook of Medicine. (22nd edn.). Philadelphia, USA: Saunders.He, Y, Bowman V D, Mueller S, Bator C M, Bella J, Peng X, Baker, T S, Wimmer E, Kuhn R J, Rossman MG (1999) Interaction of the poliovirus receptor with poliovirus. PNAS 97, 79-84.  http://bilbo.bio.purdue.edu/~baker/projects/picorna/polio/polio.html [accessed 6/4/2005].
Huckstep R L (1975) Poliomyelitis. Edinburgh London and New York: Churchill Livingstone.
Hunter, JAA (ed.) (2002) Davidson’s Principles & Practice of Medicine (19th edn). Edinburgh, London, New York, Oxford, Philadelphia, St Louis, Sydney, Toronto: Churchill Livingstone.
Lancet Neurology (2004) Polio Eradication: the beginning of the end.
The Lancet 3, 383-383.
Oxford Concise Medical Dictionary (2002). (6th edn.). Oxford, New York: Oxford University Press.
McTaggart, L (1996) What Doctors Don’t Tell You. London, San Francisco: Thorsons.Polio Eradication (2005). WHO http://polioeradication.org/disease.asp. [accessed 6/4/2005] PostPolio (2005) Epidemiliogia recente della poliomielite. http://postpolio.it/epidemiologia_recente_della_poli.htm. [accessed 3/4/2005].
Sussman W & Sussman L (2003) Vaccinations. Seaview, Isle of Wight: The Merrydown Publishing Company.Werner, D (1999) Disabled Village Children. (2nd edn.) Berkeley: The Hesperian Foundation.
West J (1999) Images of Poliomyelitis. Overview / The Salk Vaccine. www.geocities.com/harpub/ [accessed 3/4/2005].