I have in my possession a book of my aunt who worked in the polio wards at Shenton Park in 1948.
 
This book "Nursing in Acute Infectious Diseases" is written by the Medical  Superintendent of Fairfield Infectious Diseases Hospital in Melbourne, Dr Frank Scholes, and was first published in April 1940, revised 1945.
 
This is an interesting book because it was written just after the major Victorian epidemic of 1937-38, by someone in the thick of polio, so we can expect this to be accurate in detail for the time.  The chapter on polio lists the symptoms experienced at onset of polio and its progress.
 
The commonest form, spinal, could expect -

1.  Fever  2.  Drowsiness  3.  Irritability  4.  Vomiting, constipation or diarrhoea  5.  Pain - head, back of neck, spine  6.  Stiffness - of back of neck then also the back  7.  Sensitivity to touch or pressure  8.  Weakness  9.  Paralysis

 
Other common problems he lists included insomnia, restlessness, giddiness, retention of urine, tremor of hands, sweating, loss of appetite, fear of pain on movement
 
This is a typical picture of a gastro-enteritis, leading to nerve and then muscle involvement.
 
The Bulbar form affects the top of the spinal column and can involve polio-encephalitis.
If the cranial nerves are involved there could be problems with eyes, facial muscles, tongue, swallowing, voice, heart, stomach or breathing.  These are the form of polio that may result in death or iron lungs.  (Amongst the 1500 we have registered in WA to date, we have seen or heard of polio affecting all of these areas, including deaths from cardiac involvement.  He doesn't mention ears but we have seen deafness too.) One area clearly mentioned is bowel and urinary dysfunction that is not often
acknowledged.
 
Dr Scholes also talks about subclinical polio, making the point that 90% of those with measles have symptoms, 50% of those with chickenpox, but in epidemic polio only 5% display symptoms.
So he lists 5 categories of polio.
 

1.  Acute - with extensive paralysis  2.  Acute - with very slight paralysis  3.  Sub Acute - viral (flu' like) with no paralysis  4.  Sub Acute - vague illness  5.  Subinfection - no symptoms - self immunise

 
So 5% of the population had 1 or 2 and 95% had 3, 4 or 5 thus gaining protection from polio.
 
This is interesting then when compared to the work of cell biologists, Marcia Falconer & Addie Bollenbach, Canada,1999.  Their list reads
 

1.  Paralytic - Spinal & Bulbar  2.  (slight paralysis is not differentiated)  3.  Non-paralytic - flu' like with muscle irritability  4.  Abortive - flu' like symptoms  5.  Sub-Clinical - no symptoms

 
How polio is categorised may have an effect on gaining recognition today of the late effects of polio.  A history consistent with previous polio is required.  This is usually assumed to include a history of paralysis.  Autopsies performed on non-paralytic polios who died of other causes, showed some nerve damage consistent with paralytic polio even though none had been apparent (Howe and Bodian, 1942).  And Sharrard, 1955 says "damage may have been sufficient to cause weak muscles but not enough to manifest as paralysis."
 
Most people fronting up to doctors regarding late effects of polio, assume they have to have had original visible paralysis to qualify.  The question now raised is - Can people with other categories of polio also suffer "late effects"?
 
Falconer in her article documents a "typical" presentation of non-paralytic polio.
"As a child I was very ill with a high fever and a headache.  I was hospitalised for a few days (or quarantined and not hospitalised).  My mother says I was never paralysed.  I had cramps and pains in my back and legs, and was very weak for some months then recovered completely and forgot all about polio.  I wasn't good at sports, but then nor were lots of other people.  About 10 years ago I began tripping on smooth floors and occasionally falling.  Now everyday jobs like vacuuming tire me and I may have to lie down for a bit.  When I am this tired I can't think straight.  My legs ache after I walk a short distance and at night the muscles in them 'jump' or twitch.  My feet are always cold.  I have trouble climbing a flight of stairs.  My legs feel weak.  I saw a post polio neurologist and he says he saw no evidence that I had ever had polio and suggests my problems are arthritis or fibromyalgia."
 
The problem here is that the damage is unlikely to be as extensive as with paralytic polio and EMG tests can "appear" normal unless the exact area of denervation is found by the examiner.  A diagnosis in this fashion assumes that late effects can only derive from motor unit abnormalities and that no other metabolic or virological problems play any role - a fact which has not yet been established.  EMG testing is valuable for ruling out other neurological causes and may establish damage due to acute polio but should not be used to prove you don't have late effects of polio.  Anyone having symptoms in any category from 1-4 during the time of polio epidemics can be assumed to be a possible and probable case of polio and therefore liable to late effects at some stage.
 
A 1951 study on twins with polio (Hemdon & Jennings) and follow-up by (Nee et al 1995) showed that 71% of the twin with polio had PPS and surprisingly 42% of the unaffected twin have also developed symptoms of PPS.  Based on this study, we could assume around half of people with non-paralytic polio could develop late effects.
 
Polio is an enterovirus (ie gut virus) and other closely related strains could inflict similar damage and late effects.  There are a number of strains of polio and some are less virulent than others.  Virulance was usually accorded by the number of deaths occurring not on the numbers affected.
 
In WA, our 1954 epidemic is said to be a less virulent strain because there were only 5 deaths, compared to 25 in 1948 and 15 in 1956.  But, the number of notified cases for 1954 was greater - 436, compared to 1948 - 311 and 1956 - 401.  As well there were probably unreported cases that were not recognised at the time or others that were deleted when paralysis did not occur.
 
This information on "late effects" in non-paralytic polio would suggest that siblings, friends and relatives of polio survivors, who may have been offcolour around the time you got polio, should maybe wonder about late effects too, if they are experiencing fatigue, pain or weakness now. Data collection in WA includes history of polio contraction, and on speaking to many of our members, a history consistent with poor immune function at the time of obvious polio is apparent with most.
 
Possible reasons for under-par immune function include - previous illness or vaccination, allergies, surgery, fracture, adverse exposure to the elements, exhaustion from excessive exercise (sport, work or play), pregnancy, stressful episodes in life around that time - all factors that can stress the immune system.  The reason other family members were OK would have been better immune systems at the time.  They probably all had polio as well, in one of the 5 listed categories.
 
Statistically there is a minimum of 10 non-paralytic cases of polio to every paralytic case.  Polio support groups are reporting up to 10% of their members with late effect symptoms, had non paralytic polio.  We could feasibly expect that around 50% of non paralytic polios could develop late effects.  So does this mean that for every case of paralytic polio there could be another 5 who had non paralytic polio, out there in the community unaware that their problems now are actually caused by the late effects of polio?  The mind boggles.

Falconer concludes her article with
"In the case of non-paralytic polio, some amount of damage to neurones almost certainly took place and this may be sufficient to cause PPS symptoms of new muscle weakness, fatigue and pain."
 
We may be well advised to look at our old friends and relatives in a new light, recommending further investigation if they are experiencing deterioration too.
 
This makes even more important, the work we are doing in WA on carnitine levels.  The reduction of red meat intake in our diet may prove detrimental to more than presently recognised polio survivors.