There are 3 main strains of poliovirus. They are known as PV1
(poliovirus1), PV2 and PV3.
PV1, the most common in epidemics, produces the most severe paralysis and is known to be the culprit in WA's 1948 (311 cases) and 1956 (401 cases) epidemics. It is classed as the most severe because more deaths are likely to result. (In WA 1948 - 25 deaths, 1956 - 15 deaths). The 1954 epidemic was the PV2 strain and although there were more cases (434) there were only 5 deaths. However, like many other viruses, there are a number of smaller differences producing substrains of each of them. In fact by the time an epidemic finished, the PV had changed as a substrain from how it had been at the start of the
PV2 is more likely to cause meningitis. People with PV2 were often first diagnosed as having meningitis and may have gone into a coma, but often the paralysis was less severe
PV3 was more likely to be found where there were sporadic cases occurring, not in epidemics.
There are 12 other viruses that are closely related to polio and can cause paralysis. If they had been discovered before polio vaccines stopped polio they would probably have been recorded as other polio types. At present there is no vaccine for the other types as everything is geared at eliminating the 3 known polio strains. But people are still being paralysed by these other strains, now called acute flaccid paralysis.
|Polio belongs to the picornavirus family - see table right
- Rhinoviruses are the common cold. Apthovirus is foot and mouth disease. Hepatovirus causes Hepatitis A. Any of the enteroviruses as well as causing a sore tummy, can cause paralysis.
Only humans can catch polio. PV attaches at special receptor sites on the cells that line the gut and the central nervous system which are encoded by a gene on chromosome 19. Antigens HLA3 and HLA7 are believed to increase the risk of paralysis occurring.
The incubation period is 3-5 days for minor illness and 1-2 weeks
for paralysis symptoms. Onset from ingestion of virus can be 3 -
35 days. So a large number of people may have had a minor dose of
polio without really being aware of it unless it got to the paralysis stage.
The more severe the original flu-like illness, the more chance there is
of deterioration occuring later in life (fatigue & weakness).
Major polio illness includes aseptic meningitis, polio encephalitis, bulbar polio and paralysis alone or in any combination of these. Rarely this can lead to ceberal palsy-like and transverse myelitis-like symptoms. Less commonly recognised by medicos but familiar to many polio patients were urinary retention, decreased limb temperature, altered sensation, sweating, sleep, cardiac and blood pressure abnormalities. With cranial nerve involvement there could have been facial, voice and swallowing weakness, blindness and deafness.
Those who had PV2 were more likely to have had encephalitic polio and possible coma (may remember bad headache). Damage to the brain can give poor memory, problems keeping awake or falling and staying asleep.
Those who had PV3 (ie more likely if had polio in non-epidemic years) seem to be more prone to develop Chronic Fatigue or Parkinson's later in life.
Any areas damaged at original polio are likley to cause problems again now as we age more.
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