‘The most feared disease of childhood and adolescence’ and ‘a deafening silence’: Polio and post-polio in Australia

Frank B. (Ben) Tipton, The University of Sydney

Kerry Highley Dancing in My Dreams: Confronting the Spectre of Polio, Clayton, Monash University Publishing, 2015 (272 pp). ISBN 9781922235848 (paperback) RRP $39.95.

Joan London The Golden Age, North Sydney, Vintage Books Australia, 2015 (242 pp). ISBN 9780857989000 (paperback) RRP $19.99.

Kristina Olsson Boy, Lost: A Family Memoir, St. Lucia, Queensland University Press, 2013 (264 pp). ISBN 9780702249532 (paperback) RRP $29.95.


‘Uh, sorry, but what did you do to your leg?’

‘Oh. Well, I had polio when I was a kid, and now, well, it sort of comes back to bite you, later.’

‘Polio? What’s that?’

‘Oh. Well, it’s a virus, attacks the nerve ends in the spine, so you can’t use the muscles, and you get paralysed? You recover, some, but then, later, it sort of comes back, like I said, again? But you, you’re only, what, in your thirties? So you wouldn’t ever have had to worry about it, you’ll have been vaccinated, like everyone.’

‘Uh, um, well, yah, no, I guess. Still, I mean, for you, that’s a bit stiff, you know?’

That conversation, in the physiotherapy rooms of a rehabilitation hospital in Sydney in 2006, left me bemused. My well-meaning fellow outpatient, then 42 was born very shortly after the last reported case of ‘wild’ polio infection in Australia. He had been struck by a car turning illegally against a red light as he crossed a road in the crosswalk, and both knees had needed surgical reconstruction. Under instructions from his neurologist, the physiotherapists assigned him a program including time on an exercise bike and treadmill, workouts with a Swiss ball and leg lifts, all intended to strengthen his legs. I had been struck by polio in 1954, but after a long period of stability I had experienced increased difficulty walking and climbing stairs. Under instructions from my neurologist, the physiotherapists assigned me a program including time on an exercise bike and treadmill, workouts with a Swiss ball and leg lifts, all intended to strengthen my legs. To be honest I thought being blindsided in a crosswalk was a bit stiff, but I felt my own situation was a bit stiff as well, as I found myself repeating a process I had worked through 50 years before. Suddenly those 50 years seemed to weigh more heavily, with the realisation that awareness of the disease that touched so many of us had been so completely effaced for the next generation.

So I am intrigued to find three recent works that feature that old disease here in Australia, a history, a novel and an account of a broken family, all of them highly readable and rewarding. In Dancing in My Dreams: Confronting the Spectre of Polio, historian Kerry Highley aims to redress the ‘scant attention’ paid by social historians to what was once ‘the most feared disease of childhood and adolescence’ (p. 1). She begins with the first epidemic outbreaks in the early 20th century, but concentrates on the conflict over treatment in the 1920s and 1930s and on the research of the 1940s that led to the vaccines and the ‘victory’ over polio in the early 1960s. Very critical of contemporaneous medical and government leaders, she is quite willing to draw equally negative parallels with their descendants today. In The Golden Age, novelist Joan London takes an actual historical setting, a pub of that name in suburban Perth re-purposed in the early 1950s as a polio rehabilitation facility for children and the collected memoirs of its former patients, and uses them as an exotic backdrop for an imagined adolescent love affair. In Boy, Lost: A Family Memoir, journalist Kristina Olsson investigates her family history, a story that revolves around her missing half-brother, Peter. Taken from their mother by his violent father in 1950 when she makes her escape, Peter falls victim to polio as a young child, must cope with both the disease and ongoing abuse by his father, and finally locates the mother and her new family over 30 years later. In three very different genres, the books are closely connected by a shared theme: the impact of those now forgotten polio epidemics.

Extremely contagious and potentially fatal, polio reaped an annual harvest from the late 19th through the middle of the 20th centuries, with increasing peaks in Australia particularly in the years of the First World War (436 reported cases in 1916), the late 1930s (2,590 cases in 1938) and the early 1950s (4,940 cases in 1951) (Highley, Table 2, pp. 179–180). As such it posed extremely difficult problems for those charged with treatment of the victims. The next sections outline the features of the disease, its onset and spread and the conflict over early treatment. This leads to the process of recovery, rehabilitation and the psychological impact of the experiences of disease and survivorship. As the case of Olsson’s half-brother shows, the story does not stop, and the final section looks at the long term effects of polio, commonly referred to as post-polio syndrome.


Poliovirus is an enterovirus, entering through the mouth, moving to the throat, and settling in the gut. It may then spread into the bloodstream, for instance through the lymph glands. Once in the bloodstream the virus attacks the central nervous system, replicating itself in the motor neurons of the spinal cord, brain stem and motor cortex. In possibly 70 per cent of cases the body’s immune system resists successfully, and the resulting infection is asymptomatic. In a further 24 per cent of cases the virus causes minor symptoms such as fever, headache and sore throat. Some may experience more severe symptoms including a painful stiffness, but only in one per cent or less of cases—the majority of the cases actually reported—does the destruction of nerves cause serious damage. How and why this occurs is still not understood, but in these unfortunate cases the virus destroys significantly large numbers of motor neurons, leading to either temporary or permanent paralysis. The virus may also destroy large numbers of the neurons that control the respiratory system. In these ‘bulbar’ cases the resulting paralysis can be fatal, killing perhaps two to five per cent of children and fifteen to 30 per cent of adults who contract polio, although fatalities ranged even higher in some outbreaks.

Explanations of polio and its incidence therefore remained inferential and speculative.

In an early moment of intimacy in The Golden Age, Elsa shares her ‘onset story’ with Frank, but London’s Golden Age children are uniformly reluctant to speak or even to think of their time in the infectious diseases wards where they were originally confined. In paralytic cases, muscle pain and spasms frequently precede muscle weakness and paralysis. Many experience truly excruciating tenderness and pain over their entire bodies. Olsson’s half-brother Peter was two years old. She says, ‘It happens like this: one day his legs and throat simply fail him, leaving him prone in the dirt ... His body is all jagged sensation’. However, ‘he will not remember this precisely … Instead, memory short-circuits in his young brain, storing itself in his limbs, his muscles, waiting’ (Olsson, p. 84). Very young patients of course could only cry, and many remember the painful treatments as cruelty on the part of staff. Others remember with horror the needle used to extract spinal fluid to test for an increased presence of white blood cells, an indication of infection and again the terrible pain (Highley, p. 22).

The sudden rise and increasing height of the waves of polio cases mystified health professionals and terrified ordinary people. Understanding of all disease developed slowly; among scientists the germ theory still remained only one among several into the 20th century. Miasma or ‘bad air’ might cause disease. So might dirt, dust, or flies. The germ theory of course prevailed; the optical microscope allowed many pathogens to be identified as causes of specific diseases. However, although viral infections could be identified through observation and experiment, no virus could be directly observed until the development of the electron microscope in the late 1930s. Explanations of polio and its incidence therefore remained inferential and speculative. Among ordinary people, folk memory retained the other older theories in succeeding decades. Prejudice was common (Highley, pp. 33–34). Elsa’s aunt infuriates her mother by suggesting that her children do not wash their hands properly, and ‘The first time she’d walked into the butcher’s after Elsa went to hospital, some people walked out. It seemed to her that her home had a darkness about it, a mark on its door. She felt like an outcast when she pushed her pram up the road past the other houses’ (London, p. 104).

Today we know what causes polio, but in addition we would like to know how it develops from an individual to an epidemic infection, not least because this could help in combatting other epidemic diseases. Highley follows others, notably historian Naomi Rogers (Rogers 1992), in arguing that epidemic polio paradoxically resulted from improvements in sanitation in the late 19th century. Because the virus resides in the gut, it passes out of the patient’s body in the patient’s faeces. Polio victims may excrete the virus through their faeces for some weeks after recovery. In communities where human waste lay exposed in open drains or dung heaps, the likelihood of exposure to waste-born pathogens was extremely high. However, all survivors of polio infection retain lifelong immunity. Therefore, they argue, because of the high percentage of asymptomatic or very mild cases, widespread exposure had the effect of inoculating the entire community. But from the 1880s onwards cleaner water and indoor toilets meant that ‘Common diseases like typhoid became less frequent, but those same advances in public health reduced exposure of infants to the poliovirus. Epidemics of polio increased with improved sanitation’ (Highley, p. 16).

Richard Bruno, a leading practitioner in treatment of post-polio patients, disputes this ‘Central Dogma’ of polio, and argues that much of the detailed evidence does not fit. In the United States, from the first great epidemic in 1916 until the last in the 1950s, recent immigrants and those living in crowded unsanitary slums were much more likely to fall victim. Bruno links the American epidemics to the rapid growth of cities, fed by migration of susceptible populations, from southern Europe before the First World War, from the southern American states during the depression and then during the Second World War, and again from country to city in the 1950s. In addition there must have been paralytic cases before the 19th century, but they escaped notice because ‘ten cases of polio in a town of a thousand people would be equivalent to ten thousand cases in a city of one million’ (Bruno 2002, p. 41, 47, 59).

Control over the polio patient’s body was a necessity for the medical profession.

Bruno would also dispute Highley’s conclusion, following Rogers, that ‘the incidence of polio was not defined by class or race’ (Highley, p. 41). Poor people fell victim more often, but in addition so did those from Germanic and Southern European backgrounds, compared to those whose families had come from Britain, Northern Europe, or Eastern Europe. In African outbreaks, native Africans suffered far less than Europeans, and East Asians also have been less susceptible than Europeans (Bruno 2002, pp. 48–49). While Japan, Korea, the Philippines and China all had low rates of infection, India continued to report between 200,000 and 400,000 new cases of paralytic polio in children every year, and additional peaks every five to seven years, until the massive immunisation campaigns beginning in 1995 (John & Vashishtha 2013). Living in unhygienic conditions obviously did not protect Indian children.

Australia seems to fit Bruno’s model: highly urbanised, with half of the population concentrated in Sydney and Melbourne where the majority lived in notoriously unsanitary slums, and substantial flows in and out of the cities in response to economic fluctuations and wartime emergencies. For those living in congested slums or travelling to and from country towns, even high levels of personal hygiene could not offer protection. Children in a school, workers in factories or offices, families in apartment blocks, shearers in the shed, or anyone in any place that shares bathroom facilities where a single person has been infected, all may bathe and wash their hands fastidiously, but the minuscule amount required for infection means that they are all nevertheless at risk. Tragically, the major focus of the disease in Melbourne during the 1937 epidemic was the outpatient department of the Children’s Hospital (Highley, p. 43). Australia also shows a genetic component to susceptibility. Aboriginal Australians appear to have been resistant, partly because of widespread presence of antibodies, but in addition among those who did contract polio virtually none developed the severe paralytic condition (Highley, pp. 44–45). For all, as in India, vaccination offered the only certain defence, but that could only be known after decades of intensive research.


Highley is on firmer ground in her fascinating account of the dispute over early treatment of polio victims. In Australia the debate over the proper management of polio patients intersected with the interests of an emerging medical profession, personified in the enmity between conservative Jean Macnamara (1899–1968) and Elizabeth Kenny (1880–1952), advocate of a radical departure from accepted treatment. During the 1920s and 1930s Macnamara established herself as Australia’s foremost recognised authority on the treatment of polio. Central to her approach was her adamant insistence that the only proper treatment in the early phases of the disease was immobilisation of the patient’s limbs with splints or plaster casts. Only this, she argued, could prevent deformities of the bones or tendons developing due to the asymmetrical impact of muscular paralysis. ‘The number of cases in which recovery is to be obtained is very greatly extended by keeping the patients from walking during the first year, and in many cases during the second year’, she wrote in 1946, quoting a paper published in 1917. Her influence persisted. ‘All active or passive muscular movement should not only be avoided but forbidden for up to six weeks, and the patient not allowed to lift even a finger to do anything for himself’, an authoritative practitioner asserted confidently in 1954 (Highley, p. 170, 171).

Highley argues convincingly that control over the polio patient’s body was a necessity for the medical profession, precisely because the doctors’ hold on disease and its treatment was a recent and as yet incomplete achievement. The Medical Act of 1908 laid the foundation for the control of scientifically-trained doctors over the provision of health care, including supervision of subordinate paraprofessionals, particularly nurses and physiotherapists. However, given the large number of existing practitioners—chemists, dentists, midwives, homeopaths, herbalists and others—outside the new framework, medical dominance was still contested into the 1930s. Repeated polio epidemics required the provision of new and expanded hospitals, and professionalisation of their management, a process that ran parallel to the extension of doctors’ authority. Nurses, conceived as subordinate to doctors, now required training in hospitals under doctors’ control, and developed their own subaltern professional hierarchy. Physiotherapists, another emerging professional group, also allied with doctors as a support for their own claims to status (Highley, ch. 4).

Kenny emerged from the old framework. Trained as a nursing sister, but not in the new style of approved institutions, she set up a practice and began to treat patients. She travelled widely in Queensland and New South Wales during the 1920s, and her supporters convinced the Queensland government to establish a clinic using her methods in the early 1930s. She had determined that early application of ‘hot packs’, consisting of wool felt soaked in boiling water, wrung out and applied to the patient’s limbs, would loosen them and allow for stretching that would ‘re-educate’ the paralysed muscles. At some point she became actively hostile to the use of splints and casts, as well as to hydrotherapy and the testing of muscle strength to determine the extent of damage.

Nurse Elizabeth Kenny developed her own idiosyncratic theory of polio infection.

Not scientifically trained, Kenny developed her own idiosyncratic theory of polio infection. She believed that polio was a disease of the muscles, not the neurons. The disease, she said, caused the muscle to spasm, but when the spasm passed, the muscle still did not move, not because the neuron was damaged but because it was now ‘alienated’ from the muscle. Immobilising muscles, she said, increased paralysis by further ‘alienating’ muscles from the patient’s thoughts. Patients, or rather their neurons, simply forgot about a limb or how to use it. As such, she believed that she could treat and cure old paralysis cases, claims that could not be verified and which she later dropped (Highley, pp. 78–82, p. 170). A conference in Canberra in 1936 featured papers by both Macnamara and Kenny, but Kenny was isolated and attacked for her imprecise language, her lack of qualifications and accusations that her patients had ‘developed deformities’ (Highley, p. 88).

Kenny had, though, a brilliant instinct for what would now be termed public relations management. Her unshakeable belief in herself and glowing reports of her cures fed news media hungry for good news about polio. However, that same self-confidence and her refusal to listen to alternatives made her a terrible administrator. Her clinics uniformly failed. She attempted to forbid anyone not trained by herself personally to take the label of ‘Kenny method’, but was unwilling to allow her subordinates any freedom of action, and unwilling or unable to produce a coherent account of her methods, for either treatment or training. Attacked by Macnamara, undermined by self-serving careerists in the Queensland health administration and alienated from former supporters, she moved to the United States in 1940. There she rode a wave of media excitement, notably a link with President Franklin Roosevelt and the Warm Springs treatment centre in Georgia (Highley, chs 5–6). Roosevelt was the archetypal polio survivor, and the famous March of Dimes campaign, launched by his law partner in 1938, had inundated the White House with small contributions (Rogers 1992; Oshinsky 2005). However, as Highley shows in detail, Kenny continued to break with anyone who dared to disagree with her. Her authoritarian streak also affected patients:

Sister Kenny strode through the ward like General Patton, going from bed to bed examining each child, looking for something. When she got to my bed she apparently saw what she was looking for. She picked me up, put me under one arm, and walked down the hallway to the pool. She went to the side and threw me in, calling after me “sink or swim”. My legs were totally paralyzed so I sank. Two therapists had to jump in to fish me out (Respondent to 1995 survey, Bruno 2002, p. 74).

Kenny was revered in her lifetime and Rosalind Russell was nominated for an Academy Award in the 1946 film of her life. Macnamara dropped from public memory. However, in many ways Macnamara is the more interesting of the two. Kenny, as Highley shows, was cast out by the Australian medical profession because she was a mere nurse, and because she was female. Nurses were to take on the natural nurturing role of women, and not to involve themselves in the scientifically based diagnosis of disease or the prescription of treatment (Highley, p. 66). Macnamara, equally female but also a qualified physician, carved out a considerable professional niche for herself. Her approach suited the prejudices of political leaders. She was a convinced eugenicist, quite willing to intervene to prevent the ‘unfit’ from bearing children. She wrote from the United States in 1932, describing a home for disabled children as ‘lavishly endowed [but] some of the children were epileptic and spastic, and would be better knocked on the head than being treated like millionaires’ (Highley, p. 56).

The immobilisation of the limbs of polio patients to prevent ‘deformities’ aimed not to guarantee them a more comfortable life, but to guarantee that they would not become ‘crippled’ and therefore potential claimants of government support. Kent Hughes, an influential member of the Victorian parliament, believed that a disabled person was ‘not entitled to the same rights as someone who had laboured for twenty or thirty years in the service of the State’ (Highley, p. 52). Hughes appointed Macnamara as medical advisor to Victoria’s 1925 Joint State and Municipal Campaign Against Poliomyelitis. Twenty-six years old, she had previously gained a hospital position as one of two women allowed in grudging preference to potential war veteran applicants, but had a reputation as a specialist in the diagnosis of polio. The appointment acted as both a financial and a professional springboard, for her advocacy of injections of serum taken from the blood of polio patients, later dropped because of their ineffectiveness and a minor scandal regarding her use of the serum in her private practice (Highley, p. 59), but primarily for the use of splints and casts, as she said, to prevent ‘a condition which threatened to add 100 to 300 persons annually to the list of those eligible for invalid pensions’ (Highley, p. 62). In 1935 she was made Dame Commander of the British Empire.


In cases of paralytic polio, the primary paralysis may persist from days to weeks before recovery. Half of cases of ‘spinal’ polio recover fully, about a quarter suffer mild disability, and the remaining quarter may suffer severe ongoing disability. The most important mechanism in recovery from polio is nerve terminal sprouting. The process is spontaneous, but like the original damage, it is impossible to predict in advance. Surviving motor neurons develop new sprouts that can re-innervate muscle cells whose neurons have been destroyed by the virus. Estimates vary, but a single neuron that before controlled possibly 200 muscle cells might take control of from 800 to 1,000 cells in this way. However, as the damage is asymmetrical, so is the recovery. The nerves destroyed by the virus vary widely from case to case, and so do the numbers of ‘orphaned’ muscle cells adopted by surviving neurons. Therefore the muscles affected, and the degree to which they are affected, also vary widely, and the wide variation means that the effectiveness of any treatment will be difficult to evaluate.

Physician Jean Macnamara carved out a considerable professional niche for herself.

Until the late 1940s and 1950s, given the absence of knowledge of both infection and recovery, claims made for all treatments were necessarily impossible to verify. In retrospect, only experimental, science-based research would be able to uncover the truth of those processes. At the time, both the accredited doctor Macnamara and the unqualified nurse Kenny based their claims on ‘successful’ outcomes, where patients under their treatment had ‘recovered’. In addition, the staff of rehabilitation centres, families and the patients themselves, believed that hard work and willpower would enable the victim to ‘defeat polio’ and return to the ‘normal’ world. President Roosevelt said, ‘Once you have spent two years trying to wriggle one toe, everything is in proportion’ (Highley, p. 110). In fact Roosevelt could not wriggle his toes (Gallagher 1985), but his carefully concealed paralysed legs and other miraculous stories reinforced the myth.

As between Kenny and Macnamara, who won? Apparently, neither. Anyone unfortunate enough to contract polio today would most likely be treated with hot packs and stretching, but splints might still be used, for instance to stretch the Achilles tendon. Casts are also used in cases where children risk developing club foot. The children living in The Golden Age have no hot packs. Highley describes a sympathetic reception for Kenny by orthopaedic surgeon Reg McKellar Hall after the 1936 conference. He introduced Kenny’s methods into the Children’s Hospital in Perth, but in 1948 was accused by Macnamara of ‘operating a cripple factory’ (Highley, pp. 88–89). Some but not all of The Golden Age children have splints at night, but not during the day, and in flat contradiction to Macnamara’s principles, they exercise regularly. The recently acquired hydrotherapy tub, a point of pride for the staff, would have pleased neither Macnamara nor Kenny.

In Queensland, Kenny’s home state, Kristina Olsson’s brother Peter had hot packs applied, and like many others he still cannot stand the smell of damp wool, but he was also confined in a steel brace (Olsson, p. 83). It appears both Peter and The Golden Age children were treated with graded exercise, working towards the ability to walk. The staff aimed to get the patients out of the rehabilitation centre as quickly as possible. No one was expected to stay immobile for a year, let alone two. Peter and Elsa were given callipers and crutches, and Frank heavy orthopaedic boots and a walking stick. Practice, of course, was often exhausting, as we now see because it had run ahead of the recovery process.

None of London’s Golden Age children undergoes surgery. Indeed, surgery is never mentioned as an option, except for an irritated whisper from Elsa’s aunt to her father, asking whether there isn’t some sort of operation she can have. Peter, however, had extensive surgery, a series of operations in 1963 and 1964 to lengthen his short leg:

They lay him out on cold, narrow tables … doctors and students poke and prod him and pronounce him ripe for intervention, for experiment … After the first surgery when the pain has settled, there is once more the terrifying notion of walking again. But his legs are unfamiliar to him; they crumple as soon as the nurse lets go … Day after day he tries and fails and falls. Tries not to cry. It doesn’t matter if he does … Getting himself up is part of the recovery (Olsson, pp. 178–179).

The story Olsson tells about Peter is typical of severely affected patients. Peter’s story is also typical in that many of the surgical procedures were in fact experimental, and in that they were not always successful. Twenty years later, he still used a built up shoe to equalise his stance. Highley emphasises the need of the medical profession to control the patient’s body to maintain their monopoly of treatment (Highley, pp. 140–142). Peter, by this time, had become a multiple offender, runaway, truant and petty thief. As a Ward of the State and an inmate of juvenile detention centres, ‘his body is theirs’ (Olsson, p. 178). At the same time, however, Bruno (2002, ch. 7) notes the desire of families and patients themselves to become ‘normal’, to continue physiotherapy beyond the amount likely to benefit, and to agree to the range of surgeries when they were given the choice. ‘I knew that someday the doctor would come up with an operation my mother couldn’t refuse’, a woman remembers thinking before her spinal fusion (Bruno 2002, p. 97).

Peter, Frank and Elsa all look in mirrors, and all are distressed by what they see. For Frank, ‘Everything had changed: his image in the mirror, his thin leg, his lopsided shoulder’ (London, p. 197); Elsa ‘saw a thin, flat-chested girl with a clunky brace on her left calf, one shoulder higher than the other, the once fluid lines of her body now distorted’ (London, p. 220); Peter thinks to himself, ‘Look in the mirror: it’s still the same person—peg-leg, crip, wog; unlovely, unlovable, unloved’ (Olsson, p. 178). The real life Peter of course hated his callipers. The fictional Frank hates his shoes and walking stick and hopes he can give them up before he starts school (London, p. 198), while Elsa only uses her crutches on uneven surfaces outside, and moves around her family home ‘unaided’ (London, p. 218, 220). All discard their assistive devices as soon as they are able. As Richard Bruno puts it: ‘The braces, crutches and wheelchairs that had made mobility possible, that had been symbols of triumph over paralysis in the hospital, at home became stigmata of the dread disease’ (2002, p. 94).

It is not too much of a plot spoiler to reveal that Frank and Elsa do not stay together, and that Peter and his mother were ultimately unable to bridge the gap that had opened over the years of separation; there is much else of value in both of these very moving books. Frank and his mother and father are Hungarian Jews, among the very few who survived the Holocaust (London, p. 51; Tipton 2003, pp. 486–495). Seeing Elsa for what will be the last time, Frank thinks, ‘Whatever this force was it would never release him … He would always be alone’ (London, p. 231). London leaves us to decide which of his two survivorships determines his feelings. We discover in a final chapter that he becomes a public school teacher, but then leaves Australia for New York. He teaches at a university and has had a very successful career as a poet, following a calling mapped out early through his friendship with another boy, a bulbar polio victim, who died in an iron lung.

Until the late 1940s and 1950s claims made for all treatments were necessarily impossible to verify.

Elsa becomes a doctor, and her husband is also a doctor, as are two of their three sons. London tells us that Frank has written repeatedly over the years, and sent her his books as they appear, but that she has never replied. We are not allowed into Elsa’s mind after their final meeting, but her youngest son tells Frank that once when he was younger he saw her ‘climbing the sandhills after a swim and almost didn’t make it. Went up three paces and slipped back two, over and over again. He knew he mustn’t go to help her … The rule was that nothing was ever too much for her’. Frank nods, and thinks, ‘For years he too walked without a stick, raced along sidewalks, up and down flights of steps. Taught all day at Cooper Union, partied all night. Rejected any offer of assistance’ (London, p. 236). Peter’s dogged attempts to escape his father, dragging first his calliper and then the bad leg after him, mirrored Elsa’s and Peter’s. He finally does succeed; he is employed to design, build and then manage an upscale brothel. But the new business he attempts after finding his mother fails, as does his marriage. He is humiliated and runs away from her, but returns at her death and helps to carry her casket despite having fallen and broken his ankle (Olsson, pp. 235–236, p. 240).


Polio has been nearly eradicated by vaccination. Jonas Salk’s breakthrough vaccine made from killed virus was introduced to fanfare in 1954 in the United States and 1956 in Australia, and followed in the early 1960s by Albert Sabin’s version made from ‘attenuated’ but still live virus. The Salk vaccine is injected and hence relatively expensive to administer; the Sabin vaccine is oral and relatively cheap. The 88 million children vaccinated in the first of the annual programs in India in 1995 could not have been treated with the Salk version (John & Vashishtha 2013). However, the live virus vaccine has a danger; approximately one in 700,000 recipients on average contract polio despite the weakening of the virus. Currently in Africa a few dozen cases a year result from infection from the vaccine. Affluent countries therefore, after a period with live virus vaccine, have moved toward the injectable killed virus version. Highley gives an excellent, balanced account of the vaccines’ development, the rivalries and the competition. As with the dispute over treatment, there are very few unblemished heroes and a fair number of villains. Salk tested his vaccine on institutionalised handicapped children in Pennsylvania; Sabin tested his on children in the Soviet Union. Neither needed to obtain their consent (Oshinsky 2005). And as Highley also notes regarding the quite substantial Australian contributions, the loss of both talented individuals and promising research agendas because of the government’s unwillingness to provide sufficient funding is a depressing story that has since been repeated across a dispiritingly wide range of fields.

In her history of the Salk vaccine, Jane Smith (1990) describes the widespread tendency to treat the vaccine as a ‘cure’ for polio. Survivors were either forgotten entirely or treated as victims of their own poor timing. They did not go away, but as with Peter, Frank and Elsa they considered themselves isolated, inferior on one scale, that of ‘normal’ people without weakness, but superior on another scale, where their will and determination had allowed them to ‘defeat’ polio, the most feared disease of childhood and adolescence. Rejecting all offers of assistance, they developed ways of compensating for or concealing weakness. Bruno ticks off a series of contrasts. Told they would die, they lived; told they would never walk again, they walked; told they would never marry or have children, they married and had children; told their weakness would keep them from having genuine careers, they not only strove to succeed, but often became ‘the best and the brightest’ (Bruno 2002, pp. 105–106).

The pressure on polio survivors worked in both directions. They either succeeded, as Elsa and Frank did, or they could feel massive guilt if they did not, as in Peter’s case. Bruno argues that the experience of polio, onset, early treatment, rehabilitation, surgery, and the need to fit into ‘normal’ society all predisposed polio survivors to develop features of the ‘Type A’ personality. Type A individuals tend to be relatively competitive, ambitions, impatient and possibly aggressive. They are status conscious and yearn for success. On the positive side they are organised, proactive and concerned with time management. However, they are not necessarily good team players. Time management can become time urgency and impatience, leading to frustration. Their competitive drive can lead to stress, an achievement-driven mentality. The need to satisfy multiple demands may cause them to develop into workaholics, unable to relax. What are the consequences? Bruno is blunt: ‘No level of achievement, no stream of accolades, can make some polio survivors feel that they are anything but unclean and unacceptable, a hobbling child, a paralyzed pariah’ (Bruno 2002, p. 104).

Polio has been nearly eradicated by vaccination.

The fictional Frank and Elsa, more than 50 years after The Golden Age, both suffer from decreased mobility. Frank uses his stick again. Elsa’s husband has installed a lift in their house, and she goes out only infrequently. London does not use the term post-polio, and her characters appear to accept their weakness as a natural, if somewhat accelerated, ageing. ‘Their progress was always parallel’, thinks Frank (London, p. 236). Olsson is very aware of post-polio syndrome as something different from the original disease. Her half-brother Peter begins to feel ‘a new and needling pain’ that ‘pierces not just his leg but his whole body, arms, neck, back’ (Olsson, p. 232).

Thirty to 40 years after ‘defeating’ polio, some 25 to 50 per cent of survivors may find themselves suffering new weakness, not only in their affected limbs, but in previously unaffected muscles as well. Weakness, pain, sleep disturbance, sensitivity to cold and periods of extreme fatigue may all pose new problems. These vary, and onset can be gradual or sudden, but for ‘the best and the brightest’ the new symptoms can come as a severe shock. Denial is common (Bruno 2002, pp. 240–241). The fictional Elsa and Frank exist in slightly different states of denial, but neither it seems has come to terms with their new condition. Olsson says Peter dismissed the new pain as ‘self-pity’ and only acknowledged his condition after considerable time.

What has happened? Two things, it appears. Neurons that have sprouted and serviced four, five, or more times the normal number of muscle cells may fail. This may be the result of normal aging, since everyone loses neurons with age but polio survivors have fewer neurons to lose; it also might be the ongoing effects of the original disease, or failure of the surviving neurons due to years of overuse. In addition, the damage the poliovirus caused to the brain stem may cause either incorrect or inadequate messages to be sent to various glands, the possible origin for instance of the episodes of fatigue (Bruno 2002, chs 10–11).

Further, someone infected by the polio virus but with only minor or no polio symptoms has still lost significant numbers of neurons and may therefore develop post-polio symptoms. In the 1940s, David Bodian performed autopsies on several polio victims and discovered that all had suffered a kind of encephalitis, residual damage to the brain stem and some loss of motor neurons (Bruno 2002, p. 34). Bodian also showed that only muscles that had lost 60 per cent or more of their neurons would show weakness, while muscles that had lost up to 40 per cent of their neurons could nonetheless continue to function normally. A mild attack with few or no symptoms, or a paralytic attack from which the patient apparently recovered, therefore may still have resulted in the loss of a significant number of the motor neuron cells, predisposing to later post-polio symptoms (Bruno 2002, p. 29; Perlman 2000).

On balance the medical profession has been unhelpful. In the United States, the March of Dimes, rather than disbanding, reinvented itself as a campaigner for premature babies (see Oshinsky 2005; March of Dimes n.d.), and has given no support to research into post-polio or to post-polio victims apart from informational publications (March of Dimes 2001). Doctors frequently ignore the histories of polio infection and dismiss the experiences of their middle aged or elderly patients as ‘empty nest syndrome, laziness, sexual frustration, nerves, boredom’ or simply ‘all in your mind’ (Highley, p. 171). Highley’s summary is echoed by Bruno (2002) and by Olsson in her passionate review of Highley’s book (Olsson 2015).

For those fortunate enough to have physicians who recognise post-polio, the current situation parallels the 1930s. Experts give flatly contradictory advice, based on competing pardigms. A majority have tended as in my own case to refer patients to physiotherapists, who design programs of exercise to strengthen the weakened muscles (see Perlman 2000). This ‘use it or lose it’ approach derives from a belief that weakened muscles must be exercised or they will waste away. There is some clinical support for exercise; a recent small study by Indian physiotherapists reported improvement after four weeks of exercise five times a week (Sharma, Seth & Vyas 2014).

Bruno in contrast represents those who reject this approach. His advice regarding exercise of ‘affected’ muscles is—don’t. Rather than helping, he believes exercise will damage or destroy the remaining overworked neurons, actually making the muscles weaker. And, taking Bodian’s results into account, rather than attempting to strengthen ‘unaffected’ muscles he prescribes only very mild exercise, and by inference would prefer none at all. A psychologist by training, he advocates a change in attitude, away from the previous Type A behaviour. His patients are instructed to reorient their daily schedule to allow for periods of rest, and to begin again to make use of assistive devices, the very implements given up decades before when they ‘defeated’ polio (Bruno 2002, ch. 16).

The current discussion of post-polio syndrome awaits breakthrough research.

Information is sparse (see Bruno’s website, http://www.postpolioinfo.com). In 2015 a request by my arthritis specialist over his internet networks for information regarding interactions with post-polio symptoms resulted, he told me apologetically, in ‘a deafening silence’. Overseas, for example in India, the country with the largest number of post-polio sufferers in the world, the National Health Portal (2016) contents itself with a recycled definition, and an article from 2014 concluded with the anodyne advice that Indian post-polio patients should ‘get a good night’s sleep, maintain a balanced diet, avoid unhealthy habits such as smoking and overeating and follow a prescribed exercise program’ (Bhandari 2014).

In part this is because the current discussion of post-polio syndrome, like the debate over polio in the 1930s, awaits that same sort of breakthrough research. Currently there is no way to determine how many may suffer, to predict when the new symptoms may strike, or to determine the proper course of treatment in each case. The possibility that there are very large numbers of apparently normal healthy people who may develop post-polio syndrome suggests that governments should fund the necessary research and be prepared for future claims to support. Unfortunately in Australia neither major party supports the research and both continue the tradition of the 1930s in regarding treatment and support for the ‘disabled’ not as a right, but as a means of shifting them back into the workforce.

Polio itself, as my own experience shows, not only is in the past, but is also forgotten. However, forgetfulness carries a danger, because the virus still exists, and can and will strike the unprotected. Vaccination protects us, but Highley concludes with a rather discouraging discussion of the opposition to childhood vaccination in Australia (pp. 172–174). Governments also have an educational responsibility here, because the unfortunate tendency to arrogance of the medical profession, and their reflexive opposition to demands for choice in medical treatment, have opened the way for a combination of complacency, ignorance, suspicion and deliberate misinformation lead worryingly large numbers of parents to refuse to have their children vaccinated, with potentially tragic consequences. Unfortunately vaccination has been thrown together with the notion of parental choice, and some believe ‘the government in particular, and doctors, are trying to scare people into vaccinating their kids’, and have convinced themselves that a ‘healthy lifestyle’ will protect the children (Marriner 2016). It will not, and neither will washing your hands. Vaccinate your children, always, but don’t be afraid to ask for a second opinion, ever.


Bhandari, N. 2014, ‘After eradication: India’s post-polio problem’, British Medical Journal, vol. 348.

Bruno, R.L. 2002, The Polio Paradox: Uncovering the Hidden History of Polio to Understand and Treat ‘Post-Polio Syndrome’ and Chronic Fatigue, Warner Books, New York.

Gallagher, H. 1985, FDR’s Splendid Deception, Dodd, Mead, New York.

John, T. J. & Vashishtha, V.M. 2013, ‘Eradicating poliomyelitis: India’s journey from hyperendemic to polio-free status’, Indian Journal of Medical Research, vol. 137, no. 5, pp. 881–894.

March of Dimes n.d. Mission [Online], Available: http://www.marchofdimes.org/mission/mission.aspx [2016, Feb 13].

March of Dimes 2001, After effects of polio can harm survivors 40 years later, March of Dimes, Stories and Media [Online], Available: http://www.marchofdimes.org/news/after-effects-of-polio-can-harm-survivors-40-years-later.aspx [2016, Jan 24].

Marriner, C. 2016, ‘Parents keep mum on anti-vaccination’, The Sun Herald, 24 January, p. 5.

National Health Portal, India 2016, Post Polio Syndrome [Online], Available: htpp://www.nhp.gov.in/disease/neurological/post-polio-syndrome [2016, Feb 1].

Oshinsky, D. 2005, Polio: An American Story, Oxford University Press, Oxford.

Olsson, K. 2015, ‘An epidemic still tries its patients’, The Sydney Morning Herald, Spectrum, 7–8 November, pp. 26–27.

Perlman, S. 2000, ‘Polio above the neck’, Rancho Los Amigos Post-Polio Support Group Newsletter, April [Online], Available: http://www.skally.net/ppsc/neck.html [2016, Feb 13].

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Sharma, S.S., Seth, M.S. & Vyas, N.J. 2014, ‘Fatigue and functional capacity in persons with post-polio syndrome: Short-term effects of exercise and lifestyle modification compared to lifestyle modification alone’, Disability, CBR and Inclusive Development, vol. 25, no. 3, pp. 78–91 [Online], Available: http://dcidj.org/article/view/335 [2016, Feb 13].

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Frank B. (Ben) Tipton is Professor Emeritus of International Business in the University of Sydney Business School. As noted he contracted polio in 1954. He did not experience spasms or generalised pain at onset, but retained moderate weakness in his left leg, serious weakness and drop foot in his right leg, and asymmetric weakness in his back and abdominal muscles that threatened to produce severe S-curve scoliosis. Twelve of his vertebrae were fused, his Achilles tendons lengthened, and the right tendon split and anchored outside the ankle for stability. He used a calliper and crutches for a year and then discarded them. He earned an AB with Great Distinction and was elected to Phi Beta Kappa at Stanford, and received his doctorate from Harvard. He is married with two children. He has written eight books and some 50 articles. A colleague once described him as ‘a laid-back Type A’ which he accepts as both an apt description and a compliment. Stable into the mid-1990s, he began to suffer new weakness in his legs, new curvature in his spine below the fusion, sensitivity to cold, and periodic episodes of extreme tiredness. He now uses two walking sticks when outside, and a walker inside the house. His exercises include stretching, an exercise bike for his legs, and weights for the clinically unaffected upper body. He bench presses half his body weight, three sets of six reps, more than Bruno would recommend. He would like to thank the members of the Sydney Hills Post-polio Support Group for their friendship and support, especially Susan Ellis and Moya Adams who agreed to read a draft of this essay.