The Rise & Demise of Polio the Great Crippler
Polio is perhaps known more for its ability to cripple than its ability to kill. It must have been quite horrifying to see otherwise healthy older children for the most part – crippled – sometimes for life and often not being able to breathe for themselves, but many did also eventually recover either partially or fully.
To put this disease into perspective in relation to the other greater destroyers of the past, even at its peak, being infected with Polio didn’t always spell death and disability for the vast majority of the population that one might imagine. Indeed, most would not have known that they had the Polio infection at all as strongly suggested by the statistical data below.
Permanent paralysis, fortunately, occurs in only 0.5% of infections. The majority of infections (72%) do not lead to any symptoms. About a quarter of cases (24%) result in “abortive” poliomyelitis which leads to nonspecific symptoms for a few days, such as a fever or a cold, and 1-5% of cases lead to “non-paralytic aseptic meningitis”, in which the patient suffers from stiff limbs for up to 10 days.
Sophie Ochmann and Max Roser (2018)
A clue to how Polio, a previously benign infection that was commonly transmitted without any major complications, became a crippler for a small minority of the population dovetails well with the review of infectious diseases discussed throughout this study as it relates to natural exposure leading to long-term community resistance.
For instance, the article excerpted below highlights the fact that many plagues of old were commonly triggered by major shifts in social/economic change, and points out that the epidemic Polio (Poliomyelitis) was common to many of our industrialised nations due to modernity and one of the great shifts that occurred in our modern era, was that we became a good deal more sanitised.
The origin of plagues: old and new science
There are numerous examples of old viruses that have caused new epidemics as a consequence of changes in human practices and social behavior.
Epidemic poliomyelitis emerged in the first half of this century when modern sanitation delayed exposure of the virus …
Krause R.M., (1992)
This observation runs counter, of course, to our widely held belief that it was the lack of hygiene and sanitation that led to the eruption of many contagions of the past as addressed previously in this series, now the Polio epidemics may have been stimulated by a lack of exposure to naturally occurring background pathogens due to being improved sanitation too.
Again, we have supporting evidence to suggest that it may not be the pathogens themselves that are the culprits entirely, but our level of previous exposure and familiarity with them – a theme that runs throughout this study.
For instance, the tipping of the balance within our social and economic practices as a major trigger for Polio becoming more virulent is supported by a growing body of studies which strongly suggest that Polio paralysis, in particular, was a problematic contagion for older children who tended to be better-off and as such, Polio became referred to as a Middle-class Plague as indicated by the title of the following excerpt and of course, this would be the very social class who were becoming increasingly more sanitised and effectively with indoor running water and plumbing and toilets, were unwittingly becoming the most susceptible.
The Middle-class Plague: Epidemic Polio and the Canadian State, 1936-37
Thus, despite medical science-and, ironically, because of improving public health and personal hygiene standards that delayed what had earlier been an endemic, invisible, harmless and almost universal gastrointestinal infection-during the first half of this century epidemics of paralytic polio escalated throughout the industrialized world…
Rutty, J. C. (2006, 278)
This is a common theme seen throughout our near-fully modernised nations and Ireland, is no exception, as the following recollections of the Polio era reveal.
Polio the Deadly Summer of 1956
Polio, once the most feared of diseases, is about to be eradicated
Dr Gerard McCarthy, the medical officer for Cork county, pointed this out, saying:
“The higher the standard of living, the greater the tendency towards the disease. Generally the well- washed and well-laundered children are the more susceptible.”
Maureen O’Sullivan, a Red Cross nurse, noticed that
“80 per cent of the victims came from affluent or semi-affluent families.”
Cockburn, P., (2010, Oct. 27th The Independent)
Those that had always been the least vulnerable were the vast majority of people who had grown up exposed naturally to the Polioviruses (there are three main strains) and more often than not, they had Polio and passed it on silently to others without complications or even obvious symptoms for the most part and gained life-long immunity unbeknownst to themselves.
This would build up a shielding effect and there would have been strong robust community immunity. However, once small infants and young children were no longer playing in the dirt, living in close proximity to these pathogens, problems began to ensue later in their childhood as seemingly, as outlined in the following, it was much less problematic to get infected with these pathogens whilst in infancy versus facing your first infection as an older child.
The origin of plagues: old and new science
Before the introduction of modern sanitation, polio infection was acquired during infancy, at which time it seldom caused
paralysis but provided lifelong immunity against subsequent polio infection and paralysis in later life.
Krause R.M., (1992)
In this scenario, is embedded, the very reason why it seems we became generationally immune to a whole range of much deadlier pathogens over the course of generations. Nature seems to provide protection at times most needed and if we miss that opportunity whether growing up as an individual or as a nation developing towards modernity by shifting the delicate balance between pathogen and us as their natural host due to improved sanitation, booming populations in more urbanised settings and increased opportunities to spread such more virulent infections due to greater world interconnectedness – thus, cutting off essential exposures at the right time and to the correct degree, we have historically seen the disastrous consequences of upsetting this balance. Polio is a case in point, albeit on a much lesser scale.
This brings us to another interrelated factor that may have been the very reason why younger children tended to be less susceptible to paralysis from being infected with Polio and consequently, the very reason that may have led to a greater tendency for older children to be more susceptible to the worst impact of becoming infected for the first time with Polio.
How Mother’s Pass on Protection Against Disease to Their Offspring
PROTECTION OF INFANTS BY MATERNAL ANTIBODIES
As early as the 1930s, it was observed that mothers transfer antibodies to their infants, thus providing infants with some degree of protection against diseases such as measles, diphtheria and poliomyelitis…
Maternal antibodies can protect infants from infections and modify the severity of infectious diseases in infants for a varying period of time, depending on the level of placental transmission and the rate of decay of passively acquired antibodies.
Rie, A.V., Wendelboe, A.M. and Englund, J.A. (2005)
Generational protection afforded to infants and young children when first being exposed to natural environmental pathogens essentially, comes from their mothers as described above. Now, if mothers themselves were becoming less exposed to natural background polioviruses whilst growing up, then, their offspring could not benefit from maternal protective antibodies against the Polioviruses if their mothers hadn’t accumulated regular contact and increasing resilience to the pathogens themselves.
Therefore, the most vulnerable mothers and subsequently, the most vulnerable children growing up were typically those who were less and less exposed to such pathogens at an early age. During the Polio epidemic era within many of our industrialised nations, breastfeeding, also a well-recognised source of antibody protection to the environmental pathogens currently circulating, being another mode of protection for infants was also rapidly declining, if not becoming increasingly shorter in duration.
These factors would have, in combination, contributed significantly to the vulnerability of older children as they grew up and began to encounter the Polioviruses, potentially, in all three forms for the first time. They would not be primed to deal with them or had cross-protection from different strains. Some of these factors that conspired to fuel the flames of epidemic Polio are outlined in the article below:
The Spatial Dynamics of Poliomyelitis in the United States: From Epidemic Emergence to Vaccine-Induced Retreat, 1910–1971
According to the hygiene model, successive improvements in levels of sanitation during the late nineteenth and early twentieth centuries would account for a reduced level of faecal exposure to poliovirus in early infancy, thereby reducing the level of latent immunization in the population.
Contingent on these developments, Nathanson and Martin… postulate that the appearance of epidemic poliomyelitis resulted from several concomitant changes:
1) a reduction in levels of maternal antibody as booster infections became less common; and
2) a reduction in the frequency of antibody levels sufficient to produce cross-protection between virus types. . .
Both of these developments would reduce the average duration of passive protection of infants.
3) An increase in the average age of primary infections.
Together, these changes would drastically increase the proportion of children at risk of a paralytic infection.
Trevelyan, B., Smallman-Raynor, M., & Cliff, A. D. (2005)
So you can imagine what our health professionals were making of it all. They were indeed, rather perplexed as we were living in a world with renewed optimism just having come out of the second world war of the 20th Century, with all this modern living and people finally beginning to see light at the end of the contagion tunnel as more older children and younger adults began showing fairly extreme symptoms such as paralysis, and these same individuals were for the most part, as suggested above, typically from some of the best laundered and well-scrubbed homes.
However, it gets worse. Little did our health professionals think for one moment that the very medical modern marvels that have in some minds saved us from the plagues of the bad old days could be implicated in adding fuel to the already smouldering fire. As indicated by the chronology of when and to what degree vaccines were introduced, particularly in our more modern era, epidemic Polio came on the heels of our massive vaccination campaigns against Diphtheria in particular with Tetanus and Pertussis (Whooping Cough) vaccinations being combined a little later in the form of the DTP. This is discussed as a contributing factor in the excerpt below.
Polio provocation: solving a mystery with the help of history
During the summer of 1951, a medical mystery in the USA erupted into a crisis, stimulating professional debate and public anxiety. The issue was polio provocation, a health risk facing unvaccinated children in polio endemic regions. Leading specialists were at a loss to explain the condition.
As the poliovirus was widespread before the discovery of an effective vaccine in 1955, evidence that some paediatric injections could incite polio infection and paralysis led to extraordinary shifts in health policy and calculated efforts to mitigate the risk. At the core of this discussion were physicians and public health researchers, whose efforts to formulate a clinical theory drove both policy and the impetus for scientists to unravel the underlying mechanism.
During the 1940s and 1950s, physicians and public health researchers in the USA, UK, Canada, and Australia sought to understand the nature of polio and how it attacked the grey matter of the spinal cord… some physicians noticed a correlation between certain medical interventions and polio paralysis… it was not until the end of World War II that injection-induced polio emerged as a public health concern. The application of epidemiological surveillance and statistical methods enabled researchers to trace the steady rise in polio incidence along with the expansion of immunisation programmes for diphtheria, pertussis, and tetanus.
…Concern about polio provocation lay dormant for decades, but resurfaced in the 1980s when large international aid agencies, such as Rotary International and WHO, expanded their immunisation programmes in low-income nations. In some areas of Africa, where polio was endemic, public health workers began to report cases of paralysis after immunisations against common childhood diseases. Since these observations were decades removed from earlier published findings, many health professionals supposed they were witnessing a new phenomenon… Published historical accounts drew some attention to the matter, but it was not until severe epidemics erupted in India during the 1990s that fresh clinical evidence became available. …For the first time, health professionals working in polio endemic regions had scientific evidence that paediatric injections could incite paralysis.
Mawdsley, S.E., (2014)
The mechanism for this is documented in the following excerpt from one of these very important studies dating to the mid-nineteen-nighties.
Mechanism of injury-provoked poliomyelitis
Provocation poliomyelitis In persons incubating wild poliovirus infection, intramuscular injections (e.g. DTP) may provoke paralysis in the injected limb (…).
Skeletal muscle injury is known to predispose its sufferers to neurological complications of concurrent poliovirus infections. This phenomenon, labeled “provocation poliomyelitis,” continues to cause numerous cases of childhood paralysis due to the administration of unnecessary injections to children in areas where poliovirus is endemic.
Recently, it has been reported that intramuscular injections may also increase the likelihood of vaccine-associated paralytic poliomyelitis in recipients of live attenuated poliovirus vaccines. We have studied this important risk factor for paralytic polio in an animal system for poliomyelitis and have determined the pathogenic mechanism linking intramuscular injections and provocation poliomyelitis.
Skeletal muscle injury induces retrograde axonal transport of poliovirus and thereby facilitates viral invasion of the central nervous system and the progression of spinal cord damage. The pathogenic mechanism of provocation poliomyelitis may differ from that of polio acquired in the absence of predisposing factors.
Gromeier, M., & Wimmer, E. (1998)
And to make matters even worse, there was a growing realisation that potentially, some of our other newer medical interventions and sanitary measures to tackle the bugs may have also been further fanning the flames of Polio epidemics, this was tonsillectomies (removal of the tonsils in older children).
Polio provocation: solving a mystery with the help of history
One of the first medical procedures implicated in the causation of polio was tonsil surgery. A study of more than 2000 case histories in the 1940s by the Harvard Infantile Paralysis Commission concluded that tonsillectomies led to a significant risk of respiratory paralysis due to bulbar polio.
Although proponents of the theory did not entirely oppose tonsillectomies, they cautioned that such interventions should be avoided during epidemics. Reflecting the growing body of evidence that tonsillectomies could provoke polio, many doctors in the USA adjusted their surgical procedures to account for disease-endemic factors. “The policy of the United States Army”, Major-General E A Noyes acknowledged in 1948, “has been to stop tonsil and adenoid operations during epidemics”.
Even though laboratory technology at the time was not sufficiently advanced to unravel the mechanism, published evidence affected clinical practice.
Concerns about tonsillectomies coincided with indications that paediatric injections could also incite polio paralysis…
Mawdsley, S.E., (2014)
We are only now beginning to gain an insight into some plausible biological mechanisms that may have exacerbated the epidemic rise in paralytic Polio as outlined in the following.
A Wicked Operation’? Tonsillectomy in Twentieth-Century Britain.
Some academic surgeons also opposed tonsillectomy by building on earlier suggestions that the tonsils were protective against infectious diseases like poliomyelitis. They emphasised the immunological compromise created by ‘three open wounds’ and believed the tonsils conferred ‘immunity’ against such diseases, … as part of a circle of lymphoid tissue in the throat known as ‘Waldeyer’s ring’… Logically, it would follow that tonsillectomy could cause both a short-term risk and long-term predisposition to infectious diseases.
A retrospective study of the 1947–8 South Australian poliomyelitis epidemic vindicated these predictions. In over half of bulbar poliomyelitis cases, the individual had received tonsillectomy at least five years prior, supporting an increasingly popular theory: that susceptibility persisted after wounds healed…
Immunological and epidemiological arguments converged and provided mutual reinforcement. It was not enough to defer surgery until next year: tonsillectomy would require large-scale reduction.
Dwyer-Hemmings L. (2014).
Furthermore, we are only in more recent times beginning to understand how important the tonsils are in your first line of defence against many infectious diseases, but particularly against Polio due to the way in which it enters the body naturally, via the mouth in particular.
Moreover, there is also a clue to the age group most vulnerable to Polio (pre-puberty) as the tonsils seem to be most active at this time as indicated in the excerpt below, and removing them may have had a fairly big impact, leaving them wide open to attacks of the worst type, before the viruses could be dampened down by natural pathogen filters as their first line of defence had been removed surgically.
Tonsils produce certain types of disease-fighting white blood cells. Therefore, the tonsils are believed to act as the immune system’s first line of defense against bacteria and viruses that enter your mouth.
This function may make them particularly vulnerable to infection and inflammation. The problem is more common in children because the immune system function of tonsils is most active before puberty. Also, unlike an adult’s immune system, a child’s system has had less exposure to bacteria and viruses and has yet to develop immunities to them.
Mayo Clinic (2011)
Obviously, if these medical and generation improved hygienic factors did conspire to create the perfect storm of vulnerability, particularly amongst those who could afford to avail most easily from such medical procedures and interventions and came from some of the most modernised homes, for these particularly nasty Polio outbreaks to converge into larger epidemics, essentially being more manmade than naturally occurring, we should expect to see some variation between our respective nations (unlike the more closely matched pattern that we have observed for the more natural rise, fall, peaks and troughs if other much deadlier contagions of the past).
And this is what we do see when we examine the mortality graphs from different regions showing the impact of Polio within our respective nations. Take, for instance, the United States as shown in the following, Fig. 15.
Fig. 15: Polio vaccine first became widely available in the United States in 1955. Graph generated from statistics of annual mortality from Polio since official records began in the United States (with small data gap for deaths) source of raw data, Sophie Ochmann and Max Roser (2018) – “Polio”. Published online at OurWorldInData.org. https://ourworldindata.org/polioreported-paralytic-polio-cases-and-deaths-in-the-united-states-since-1910(1).csv
As you can see from the above graph (Fig. 15) from the United States with a small data gap for the early 1940s in relation to mortality rates for Polio (the light grey smaller curve) compared to Polio cases (the larger dark grey curve), there is a very pronounced spike corresponding to 1916 shortly after official records of Polio began. This seemingly came out of nowhere and at no time after, even at its height, did Polio cause such destruction in terms of deaths (not cases which are greater in the 1950s with mortality rates significantly lower in this era).
The other aspect of this large spike that makes it unusual, is its concentrated origin and confined regional impact (New York as its epicentre and only spreading to a limited range beyond. This and the virus’s unique signature has lead one scholar to investigate the possibility of it being an epidemic of unnatural origins as suggested in the abstract of the study below.
The 1916 New York City Epidemic of Poliomyelitis: Where did the Virus Come From?
Previous accounts of the 1916 devastating epidemic have been faulty. The unique features of the epidemic and its sudden appearance have never been explained. A New York laboratory was passaging poliovirus in primate brains, a technique which increased pathogenicity. I propose that highly virulent virus escaped and caused the epidemic. Scientists, technical and animal house staff were unaware that they could be infected by poliovirus which could then infect others. All laboratory workers must be constantly reminded of the dangers which can arise from the escape of pathogens from their work.
…An Extraordinary Epidemic
The definitive account of the epidemic from the US Public Health Service […] concluded that the outbreak had remarkable features: the extent and intensity was beyond all previous experience; the origin was remarkably definite in time and place; there was a strikingly uniform radial spread from this focus (…) with intensity progressively decreasing in proportion to the distance from the original focus; and a demonstrable mathematical regularity in its whole evolution.
These features were never experienced again. Three other aspects were not noted at the time: the number of children age 2 yr affected was the highest ever recorded […]; the case fatality rate of 25 % was the highest ever recorded… the epidemic started in early May, well before the normal summer polio season. p. 13
…Polio has a particularly hidden risk as it was not realised that adults with immunity could be infected and shed virus, infecting other adults as well as children. Most infected children would also shed virus, but without any symptoms. Some years ago I visited an Indian laboratory which monitored stools sent from paralysed children. The scientist in charge was unaware that staff who handled the stools could be infected and shed virus in the community even though they were themselves immune…
It is not possible to prove that the 1916 epidemic was caused by the escape of MV from the Rockefeller Institute… However it is a remarkable coincidence that a unique neurotropic strain of poliovirus was developed a few miles from an epidemic caused by a uniquely pathogenic strain of the virus.
Wyatt, H. V., (2011, 13-14)
In the absence of any other convincing causes of this Polio epidemic, and with all the evidence presented in the rest of the study excerpted above, the chart presenting the cases and death rate from Polio from the United States should perhaps be considered in the light of this potential anomaly (as you will see when we begin to examine the other charts from different regions, this large spike for the same general period is absent).
Now, setting this anomaly aside, when we review the more general era of eruption of Polio and its impact in the United States, we can clearly see some of its worst epidemics (after 1916) and greatest number of deaths occur from the late 1940s with a degree of decline and the last peak of a significant number of deaths occurs around 1952 (Fig. 15). Again, reviewing Figure 15 closely, we can see that the number of cases peaks also at this point (1952) followed by a steep decline and then the cases increase again followed by a sharp decline which is not reflected in the significantly declining number of deaths for the corresponding period of relatively high case incidences.
Note that in the terms of Polio in particular, and certainly as we have previously reviewed for the many other previously much deadlier contagions, increased number of cases/infections that are obvious, does not equal an increase in the number of deaths and disabilities – this is clear also for Polio when we see from the United States (Fig. 15) the overall number of deaths dropping dramatically after 1952, whilst the number of cases rise sharply again soon after but drops dramatically just slightly before the vaccine was made widely available in 1955.
Now if we review the Canadian mortality rates for the same broad period (Fig. 16), which also introduced a vaccine shortly after the United States within the same year, 1955, we find an even more dramatic decline in deaths from Polio just prior to our efforts to eliminate the disease. There is a small peaking after the vaccine was introduced in 1955, and deaths from Polio appear to return to the very low levels seen just prior to the vaccine becoming more widely available and continue to decline thereafter. (Note that we only have data for mortality and not paralysis or cases for Canada, but we can assume that number of cases does not equal proportional number of deaths).
Fig. 16: Polio vaccine became widely available in 1955, but after it was introduced into the United States. Statistics in graph derived from Figure 1, table showing annual mortality rate from Polio per 100,000 of population since official records began in Canada http://www.healthheritageresearch.com/Polio-Biologicals34-2-June2006sdarticle.pdf The Middle-class Plague: Epidemic Polio and the Canadian State, 1936-37, CHRISTOPHER J. RUTTY http://www.healthheritageresearch.com/cbmhbchm_v13n2rutty.pdf This graph was generated for Polio deaths across the Canadian states
It looks like Canada had seen the last of its most major impact of Polio in terms of deaths on the eve of the introduction of the vaccine in 1955 and really the major span of relatively and more consistently deadly Polio era in Canada was from the late 1920s and part of the 1930s. It fluctuates quite considerably thereafter, until the final spike over a few short years from the early 1950s, which peaks during 1953 and rapidly plummets just before the vaccine was introduced.
The Middle-class Plague: Epidemic Polio and the Canadian State, 1936-37
The many serious polio epidemics that occurred between the late 1920s and early 1950s have received minimal historical attention… During the 1950 – 55 period there were wide natural variations in incidence of paralytic polio in Canada that peaked in 1953 and then sharply declined in 1954 and 1955. National incidence remained low during 1956 and 1957, when it dropped to an attack rate level not seen since 1926.
Rutty, J. C. (2006, 279)
Fig. 17: Vaccine became widely available by about 1959 onwards. Graph produced using raw data statistics of rates of paralysis and mortality from Polio in the UK since official records began. http://www.post-polio.org/ir-eng.html Incidence Rates of Poliomyelitis in England, Incidence Rates of Poliomyelitis in Other Countries In the US, PHI thanks The British Polio Fellowship for obtaining the following records. Acute Poliomyelitis became notifiable in 1912. *Deaths include late effects Source: Annual Reports of the Registrar General. Communicable Disease Surveillance Centre, London. http://www.post-polio.org/ir-eng.html
Now comparing the later introduction of the new vaccine against the Polio paralysis cases and number of individual deaths in the United Kingdom, we find that when we examine the mortality/paralysis statistics (Fig. 17), that these have already declined significantly shortly after the terrible outbreaks of Polio of the later 1940s, peaking and dramatically declining after 1951. Polio paralysis spiked somewhat after deaths declined to increasingly smaller numbers, but, the worst was truly over by the time the vaccine eventual made its way out to the wider starting on the eve of the 1960s. This rather convoluted sage is summarised as much as possible in the following excerpt.
Vaccine innovation and adoption: polio vaccines in the UK, the Netherlands and West Germany, 1955-1965
IPV in the UK
Eventually, in 1956, a new vaccination programme was planned with British IPV, … However, only small amounts of vaccine were available from the British manufacturer. In May and June 1956 the vaccine was administered to children between two and nine years of age, whose parents had to register them beforehand… On the whole, 29 per cent of all British children in that age group had been registered for vaccination, but only 10 per cent of those registered, or 3 per cent of all children born between 1947 and 1956, could be inoculated in 1956 with the specified two injections. The limited supplies available extended no further than this.
Why did the British attitude, which had been so much in favour of the Salk vaccine, change so quickly in 1955 and why were the risks so radically reassessed that for two years imports of US vaccine were impossible? …An additional source of delay had to do with the supply of vaccine. For spring 1957, Glaxo had promised to put a certain amount of vaccine at the disposal of the health ministry, but there were again delays in production…. Growing public pressure for vaccination was a main factor leading to a change of views in the British health administration…
In the Ministry of Health the question “If British supplies are adequate, should we buy only British?” was discussed repeatedly in November and December 1958. Although Canadian and American products were much cheaper … and should therefore have been attractive to the NHS with its chronic shortage of funds, other criteria could clearly override cost considerations. These were partly to do with safety…
For 1958 the Ministry of Health agreed to administer vaccine to all children under fifteen. In order to meet this goal the imported vaccine would be used, provided it had undergone an additional British test. Furthermore, parents should be able to choose, and would have the right to refuse to allow their children to be inoculated with imported vaccine. This complicated scheme added to the relatively slow progress of vaccination in the UK…
Lindner, U., & Blume, S. S. (2006)
In Ireland, it should be noted that although the number of deaths was tragic and significant to those affected, these numbers are really very small indeed in the scheme of things with the greatest death toll peaking in some years between 50 and 60 individuals (Fig. 18).
Obviously, the paralysis cases would have been significantly higher judging by other statistics from regions such as the UK. Ireland, however, sees an earlier intensification of Polio (as seen in the relative death rates) than the UK. In Ireland, Polio has a greater impact rising as we approach the late 1930s and peaks rather aggressively during the earlier 1940s. Certainly, in this era, it must have terrifying indeed. But, finally, Polio impacted less and less soon after as seen in the ever-decreasing peaks of deaths since that time, with the final peak following soon after the vaccine trails begin in Ireland in 1957 (See excerpt below).
Fig. 18: Vaccine started to be used on a trial basis in 1957. Chart of the annual number of individual deaths in Ireland from Polio since deaths from the disease was first recorded (1922). Source: Chart generated using this tumultuous statistics reports since records began – “Annual Reports on Marriages, Births and Deaths in Ireland, from 1864 to 2000” courtesy of: An Phríomh-Oifig Staidrimh, Central Statics Office CSO, link. © Copyright dig-press.com.
Polio, once the most feared of diseases, is about to be eradicated
Official statistics show that overall 499 people got the disease in Ireland in 1956, of whom 220 were from the Cork area. The number admitted to hospital suspected of having polio was slightly larger. The figures seem low, but they conceal the fact that by the end of the year most people in Cork had got the disease, although very often without realising it. By 1957 the first trials of the Salk vaccine were taking place in Ireland …
Cockburn, P., (2010, Oct. 27th The Independent)
It would appear that much of the people were already fairly well immunised by natural means, as indicated within the excerpt above, at least in Cork, but presumably the rest of Ireland were well on their way to becoming more resilient to Polio’s worst effects as the ever-declining peaks in deaths appear to indicate as seen in Figure 18.
Bearing in mind that Polio had a greater negative impact in Ireland towards the latter half of the 1930s (deaths only began to be recorded from 1922 onwards – See Fig. 18), this ties in with observations on the ground at the time which also give us an insight into the ratio of Polio paralysis (many would have recovered from) across Ireland as a whole and the specific impact of Polio during the last recorded major eruption of 1956 (before the vaccine trials) from one medical officer.
The 1956 Polio Epidemic in Cork
In 1956, 499 cases of paralytic poliomyelitis, resulting in twenty deaths, were notified to the Department of Health for the entire country. …There were 220 cases and five deaths in Cork city and county, a comparatively low fatality rate of 2.3%, particularly if the 1942–3 epidemic is taken as the benchmark.
Dr Gerald P. McCarthy, MOH for County Cork, concluded, with some justification in the light of these figures, that the poliomyelitis outbreak in the city and county was no more than ‘a trifling epidemic’.
History Ireland (2006, May/June issue)
Similarly, we can see from the relative impact of Polio in Canada from the short history of previous Polio outbreaks, that the disease overall had a greater and more sustained impact in the earlier era and the worst was seemingly over by the time the vaccine was introduced (Fig. 16).
The United States shows a comparatively later rise in fatalities (leaving aside the 1916 anomaly) and correspondingly later decline in deaths compared to these other regions, yet, even with the relatively early introduction of a vaccine, deaths still to significantly decline well before this intervention (Fig. 15). And, certainly in the UK (Fig. 17) deaths from Polio, followed closely by a dramatic drop in paralysis was essentially indicating an overall resolution prior to the relatively delayed introduction of the vaccine to combat the disease.
However, our medical history books tend to only focus upon Polio deaths and paralysis at its worst as if the contagion would have continued to be a plague of our modern age if we had not have intervened and, understandably, therefore, everyone naturally associated this intervention with the remarkably positive turn of events (as seen in the rather dramatic declines in paralysis and deaths) soon after.
Although the first trials certainly looked promising, and I am sure that lives were saved and disabilities avoided initially, however, it seems that the honeymoon period was almost over before it ever started as highlighted in the following excerpt.
History of polio vaccination
In 1954, the inactivated vaccine was tested in a placebo-controlled trial, which enrolled 1.6 million children in Canada, Finland and the United States […]. In April 1955, Salk’s vaccine was adopted throughout the United States. The incidence of paralytic poliomyelitis in the United States decreased from 13.9 cases per 100 000 in 1954 to 0.8 cases per 100 000 in 1961[…].
Some disadvantages of the Salk vaccine in that time were the decrease of the titres of the circulating antibody within a few years of vaccination, the further circulation of wild PV and its implications in outbreaks, and the large number of monkeys (about 1500) needed to be sacrificed to produce every 1 million inactivated doses. .. Shortly after the licensing of Salk vaccine, the failure of inactivation of vaccine virus at Cutter Laboratories, Berkeley, was followed by 260 cases of poliomyelitis with PV type 1 and 10 deaths.
… The use of the highly virulent Mahoney strain in vaccine production has been controversial and after the Cutter incident, even more so. In Sweden, the Brunenders strain for type 1 was preferred. In 1980, concentration and purification of polio antigens were introduced into the manufacture of IPV and the immunogenicity of the vaccine was increased.
Baicus A. (2012)
As noted above, the rate of Polio paralysis dropped dramatically after this major trial of the injectable killed (Inactivated Polio Vaccine) IPV vaccine given to over one and a half million schoolchildren. Now without going into the ins and outs of all that actually unfolded regarding the few hiccups at the early stages of the rollout of the new Polio vaccine (IPV) and things like the Cutter incident and without mentioning the monkeys, we will fast-forward a few years and review why we started using the oral form of the competing vaccine OPV (Sabin attenuated/weakened virus oral type) instead of the IPV (Salk inactivated/killed virus injectable type). One of the reasons relates to what was eluded to above regarding the seemingly rather short-lived protection that Salk’s new vaccine against Polio provided and a few other things besides.
A Brief History of Polio Vaccines
Many virologists were of the opinion that Salk’s vaccine could not provide long-lasting protection and that this could only be achieved with Sabin’s live-attenuated version. Only a live vaccine, it was argued, had sufficient immunogenicity to provide protection. In contrast, an inactivated vaccine would have to be re-administered regularly…
On the basis of these trials, Sabin’s vaccine was deemed the better of the two. It was found to confer longer-lasting immunity, so that repeated boosters were not necessary, and acted quickly, immunity being achieved in a matter of days. Taken orally (on a sugar cube or in a drink), the vaccine could be administered more readily than the Salk vaccine, which had to be injected.
Most importantly, the Sabin vaccine offered the prospect of passive vaccination because it caused an active infection of the bowel that resulted in the excretion of live-attenuated virus. Thus, through fecal matter and sewage the Sabin vaccine could help to protect those who had not been vaccinated. In August 1960, the U.S. Surgeon General recommended licensing of the Sabin vaccine. The oral vaccine gradually supplanted its rival and by 1968, Salk’s vaccine was no longer being administered in the United States, and U.S. pharmaceutical companies had stopped producing it.
Blume, S., & Geesink, I., (2000, 1593-1594)
All in all, we went with some successful trials that promoted the OPV (Oral Polio Vaccine – Sabin oral form) vaccine as the front-runner. Quickly it became the mainstay vaccine shortly thereafter across most of our developed nations, first administered via sugar cubes if anyone is old enough to remember, then later and presently as drops into the mouth – and as noted above, in many ways it mimicked the natural form of the infection – but made it attenuated (less potent) and depended upon spreading the virus to unvaccinated people and the community at large – which is of course, somewhat different to what most other vaccines are intended to do – i.e., stop the actual spread of the infection.
So, in effect, the OPV was seen to provide much longer protection and given the nature of the way Polio circulated in its natural state (silently for the most part as most people who were infected wouldn’t know they had Polio and they could easily pass it along to others – more often than not giving them life-long immunity and even cross-strain protection, i.e., if you were immune to one or two strains this helped protect you against a third), it seemed like a sure bet that the oral vaccine could mimic nature and achieve something similar.
The idea of course was to attenuate the viruses (weaken them) and stop replication in the gut that might cause problems (called mucosal immunity) and indeed, the aim was to make enough people immune (even those unvaccinated could gain some immunity from coming into close contact with the vaccinated individual), thus producing broadly reaching community immunity (usually referred to as herd immunity) in a safer way than the wild virus infections as the vaccine virus was attenuated (much like how a mother can attenuate a pathogen for her new-born into infancy allowing their immune systems to get familiar with the bug without the danger) and it was believed that this was, therefore, a much safer way to gain protection for everyone. It was simply a case of reaching enough people (children for the most part) and soon the world would be entirely free of Polio the crippler for once and for all.
As you can imagine, things did not quite pan out in the way that had been hoped. Although, the OPV was deemed the weapon of choice when it came to stopping outbreaks in their tracks and indeed, it did seem to do this rather successfully in the early days when the vaccination coverage was very high (or, possibly as natural immunity was restored to much of our populations), but once natural Polio had essentially stopped circulating across our industrialised nations (at least in an obvious way as it would only become obvious that Polio was still viral and spreading amongst our communities by its ill effects such as paralysis or death from obvious symptoms – may be most had already become silently immune without anyone noticing?) and we could begin to see the woods for the trees, we noticed that the only ones getting paralysed were those who had gotten it from the vaccine itself.
When Can We Stop Using Oral Poliovirus Vaccine?
Why must OPV vaccination be stopped?
Vaccine-associated paralytic poliomyelitis was recognized shortly after the introduction of OPV, with cases occurring in both vaccinees and their contacts.
The time is coming when the only cause of polio is likely to be the vaccine used to prevent it.
Hull, H.F., & Minor, P.D., (2005, 2033 – 2035)
This was one of the main reasons why we and most other first world countries went back to using the IPV inactivated (killed) type vaccine around the 2000s, as the IPV vaccine seemed to be effective enough as long as Polio was no longer circulating when the risk of being infected by the wild virus was very low.
However, the OPV remained the mainstay vaccine of choice for low income or less industrialised nations, as it was easier to administer and was much cheaper. But, the long-term use of this revealed another issue, especially when natural wild Polio was still circulating in some pockets as discussed below, the OPV strain itself started to go viral and even evolve into new lineages.
Evolution of the Sabin Vaccine into Pathogenic Derivatives without Appreciable Changes in Antigenic Properties: Need for Improvement of Current Poliovirus Surveillance
Viruses constituting the Sabin oral polio vaccine (OPV) are inherently genetically unstable (…). Upon reproduction in vaccinees and their contacts, they tend to lose attenuating mutations. At a certain step in their evolution, vaccine-derived polioviruses (VDPV) have virtually no phenotypic distinctions from wild polioviruses and are able to circulate, especially in underimmunized communities, causing sporadic cases of the disease and outbreaks (…).
Such VDPV pose a serious challenge to the Global Polio Eradication Initiative (…) because the real eradication of polioviruses should obviously include not only “true” wild viruses but also VDPV (…). Since it is unlikely that the usage of OPV (inevitably producing new VDPV) will be discontinued soon, i.e., until its replacement by inactivated polio vaccine (…), the identification of VDPV is a key issue for the eradication program.
Yakovenko, M. L., Korotkova, E.A., Ivanova, O. E., Eremeeva, T.P., Samoilovich, E., Uhova, I., Gavrilin, G.V., & Agol1, V.I., (2009, 3402)
As you can tell from the above excerpt, this issue with the OPV going wild and turning out to be causing outbreaks and the recirculation of Polio in its newly evolved wild vaccine-derived state sort of defeats the purpose of trying to eliminate the wild type Polio in the first place.
It now looks like some of these OPV vaccine strains have evolved from humble origins in the lab, even having their own family tree and at the base of it is its common ancestor, the vaccine virus itself as excerpted below. It looks like it isn’t the Polioviruses in their original state that we need to pay attention to, but those of our own making.
“The evolutionary pathway to virulence of an RNA virus,”
In the past, all three oral polio vaccine (OPV) strains have reverted and caused outbreaks, but this occurs most commonly with the vaccine’s poliovirus type 2 (OPV2), as has happened dozens of times in places such as Belarus, China, Egypt, Madagascar, and Nigeria.
And because wild poliovirus type 2 was eradicated in 1999, public health workers began using a bivalent vaccine that used attenuated versions of only strains 1 and 3 in April 2016.
Using 424 sequences of circulating OPV2-derived virulent viruses, representing about 30 independent outbreaks of vaccine-derived poliovirus, the researchers created an evolutionary tree showing how the vaccine-derived viruses evolved in parallel from their common ancestor, the vaccine virus.
Through this analysis, the researchers could also determine the order in which the virulence-promoting mutations occurred…
Pathway to Polio Virulence Revealed
Using epidemiological and laboratory data, scientists have mapped out a sequence of mutations through which the attenuated oral polio vaccine reverts to a virulent virus.
Taylor, P., (The Scientist 2017, March 23rd)
The following excerpt highlights just how widespread these vaccine strains gone wild or, VDPVs (Vaccine-Derived Polioviruses) are, and it also points out the potential problem particularly for those that are not vaccinated or can’t be reached to vaccinate.
When Can We Stop Using Oral Poliovirus Vaccine?
Ample molecular data are now available to demonstrate that vaccine viruses can revert to full neurovirulence […]. Outbreaks of polio in China, Egypt, Haiti, Madagascar, and the Philippines caused by circulating, neurovirulent vaccine-derived polioviruses (VDPVs) demonstrate that these revertent strains are fully transmissible and pose significant population risks.
VDPV outbreaks are associated with incomplete vaccine coverage over a period of years, allowing a large population of susceptible children to accumulate […]. Worldwide, only 70%–80% of children receive 3 routine doses of diphtheria-tetanus-pertussis and OPV in their first year of life. Many of the poorest countries in the world are unable to vaccinate even 50% of their children.
Under these circumstances, continuing to use OPV after eradication is very risky
Hull, H.F., & Minor, P.D., (2005, 2033 – 2035)
It certainly would be a bit difficult to see who was even infected with these vaccine mutants gone wild, however, we may not have to worry too much as they seem to behave like the Polioviruses in that, if we recall that even at the height of the worst Polio epidemics, most people who got Polio, didn’t show symptoms or become paralysed and many more recovered from their ordeal.
Therefore, many people may already be immune from infections even from vaccine strains without even knowing they had ever been infected. But, yes this certainly makes the eradication of Polio worldwide quite a task. It would be like trying to find the proverbial needle in a haystack. So the plan of later years is to use a combination of both vaccines – the OPV and IPV to help stop the spreading to top it off for the final eradication.
Now since most of the world has been using the OPV, even if we changed to the IPV back in the day, where we would need boosters, certainly as adults, even if we were fully vaccinated with all four doses during childhood according to health officials, then, if the immunity from the OPV was believed to be very long-term, most of us who are old enough to remember the sugar cubes or at least anyone around up to the year 2000 who had the OPV should still be immune. But, as it turns out, the OPV lasts a surprisingly short time as seen in a number of large-scale studies as excerpted further on.
But, studies that have looked back at large populations who were previously vaccinated using detailed records and clinical testing of stool samples have discovered that the OPV may not be as long-lasting as previously thought. Indeed, it now looks like – at least in less industrialised regions where the wild Polioviruses were still circulating, that the OPV may have only provided mucosal (gut) protection for up to a year!
Waning Intestinal Immunity After Vaccination With Oral Poliovirus Vaccines in India
Infection with OPV (vaccine “take”) is highly seasonal in India and results in intestinal mucosal immunity that appears to wane significantly within a year of vaccination…
Waning intestinal mucosal immunity after vaccination with OPV is likely to make the interruption of wild-type poliovirus transmission more challenging. We have previously found frequent infection with wild-type polioviruses among healthy, OPV-vaccinated children in contact with children with poliomyelitis […].
Grassly N. C, Jafari H, Bahl S, Sethi, R., Deshpande, J. M., Wolff, C., Sutter, R. W., & Aylward R. B. (2012, Conclusion)
This gut immunity is important for how the OPV is intended to work, i.e., it is not that you don’t get an infection with Polio, it is simply that you get a much-weakened form and it should not keep replicating in your gut once you get it. Therefore, if the gut immunity doesn’t hold for long due to vaccine waning, then it is likely to start replicating again, but, that doesn’t mean that it isn’t still a mild form, but, it causes issues regarding the spread of the virus amongst the population where the endgame is eradication.
Asymptomatic wild-type poliovirus infection in India among children with previous oral poliovirus vaccination.
Mucosal immunity induced by oral poliovirus vaccine (OPV) is imperfect and potentially allows immunized individuals to participate in asymptomatic wild-type poliovirus transmission in settings with efficient fecal-oral transmission of infection.
We examined the extent of asymptomatic wild-type poliovirus transmission in India by measuring the prevalence of virus in stool samples obtained from 14,005 healthy children who were in contact with 2761 individuals with suspected poliomyelitis reported during the period 2003-2008…
Wild-type poliovirus serotypes 1 and 3 were isolated from the stool samples of 103 … healthy contacts, respectively. Among contacts of individuals with laboratory-confirmed poliomyelitis, 27 (12.7%) of 213 and 29 (13.9%) of 209 had serotypes 1 and 3, respectively, isolated from their stool samples. The odds ratio of excreting serotype 1 wild-type poliovirus was 0.13 (95% confidence interval, 0.02-0.87) among healthy children reporting 6 doses of OPV, compared with children reporting 0-2 doses. However, two-thirds of healthy children who excreted this virus reported >or=6 doses, and the prevalence of this virus did not decrease with age over the sampled range.
…Although OPV is protective against infection with poliovirus, the majority of healthy contacts who excreted wild-type poliovirus were well vaccinated. This is consistent with a potential role for OPV-vaccinated children in continued wild-type poliovirus transmission and requires further study.
Grassly, N. C., Jafari H, Bahl S, Durrani S., Wenger J,
Sutter R. W, & Aylward R. B
However, ironically perhaps, because our nations, for the most part, used the oral type vaccine for so long before switching back to the original injectable form, we may have been immunised via a combination of naturally attenuated and artificially attenuated strains anyway due to the overall freedom of the vaccine viruses had to mate and produce mutated forms of themselves. Certainly, if these studies are anything to go by, where our nations were ourselves not that long ago still living with wild Polio circulating, but, not causing too much harm, then if the OPV actually wore off so rapidly – did this leave our populations wide open to Polio returning in its own colours?
Seemingly not, as the nature of Polio meant that asymptomatic (infected individuals who showed no obvious signs of having Polio could spread it easily to others, who in turn may not show any symptoms) would mean that this facilitated the wide community spread of the wild Polioviruses as more and more became silently infected as the OPV wore off, with not too much mishap, then, we would not have had much evidence of wild Polio still being present and many more people would have been exposed (and therefore became fully immunised naturally) anyway without us necessarily being aware of it.
And as we used the OPV for so long and it tried to mimic the natural form of immunisation, perhaps, ironically, the fact that OPV may have conferred such surprisingly short term protection against the wild Polioviruses, and with those vaccine virus strains evolving and acting more like wild Poliovirus silently infecting whole communities without most of them even knowing it, we may have become naturally immune to even lab-created mutants by more natural means as well.
Please feel free to share your thoughts below…
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