Would We Survive the Spanish Flu if it Returned Today? Apparently, we would, as most of us have become ancestrally immune to dying from just about every strain going & yet to come…

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(Note that all the quotes are referenced with clickable links at the end of this article)

WHATEVER HAPPENED TO THE SPANISH FLU AND WOULD WE EVER SEE ITS LIKES AGAIN?

Just to put Influenza into perspective in terms of its impact across our emerging modern nations, the following quote will give you an idea of the sort of numbers of deaths we are talking about. Bear in mind that the world by the early 20th Century is much more heavily populated than it was back in the Middle Ages when the Great Plague ran rampant.

The influenza pandemic of 1918

The influenza pandemic of 1918-1919 killed more people than the Great War, known today as World War I (WWI), at somewhere between 20 and 40 million people. It has been cited as the most devastating epidemic in recorded world history. More people died of influenza in a single year than in four-years of the Black Death Bubonic Plague from 1347 to 1351. Known as “Spanish Flu” or “La Grippe” the influenza of 1918-1919 was a global disaster…

Bodies pil[l]ed up as the massive deaths of the epidemic ensued. Besides the lack of health care workers and medical supplies, there was a shortage of coffins, morticians and gravediggers… The conditions in 1918 were not so far removed from the Black Death in the era of the bubonic plague of the Middle Ages.

 Billings, M. (1997)

[1]

Why this major pandemic Flu came to be known as the Spanish sort is revealed in the following along with a very interesting pattern of the different waves of Influenza and what may have fueled its rage when it hit nearly all of the world between 1818-1819.

Limerick City and the Spanish Influenza Epidemic, 1918-19

The name ‘Spanish Influenza’ came about not because it originated in Spain but because Spain was the first country to report, uncensored and unbiased, on the spread of the disease, due to its neutrality in World War I.  It occurred in three waves; the first in spring 1918, the second in October/ November 1918 and the third in spring 1919…

. The demobilisation of troops in November 1918 (Armistice Day) could possibly account for the second wave of influenza which proved to be more deadly than its predecessor…

Buckley, M., (2014, 81)

[2]

Children in America even came up with a rhyme about this great pandemic as it swept across America and people could be arrested in the street if they sneezed as documented by Buckley in the following:

Limerick City and the Spanish Influenza Epidemic, 1918-19

…in Chicago, the police were instructed to arrest anybody who sneezed in public…

as the epidemic in America gathered speed, school children even came up with a rhyme about it to skip by…

I had a little bird and its name was Enza,

I opened the window and in-flew-Enza.

[ibid]

The situation in Ireland as recorded at the time and established from the historical accounts since reveals the impact felt across our nations as we were going through a near-déjà vu of the Great Plague of the Middle Ages many centuries earlier.

Recall the rhyme that children used to recite ‘ring-o ring-a rosies… and they all fall down…’ about the Great Plague of old? Essentially, the first wave of Influenza is also described as being mostly confined to the main ports and then it appeared to become more aggressive and wider spread – impacting our entire nation by the second wave that had reached even the far reaches of the country by Christmas time (just as the Great Plague of the similar pattern for the Great Plague?). This can be seen in the following documenting the Flu’s arrival on Ireland’s shores.

Limerick City and the Spanish Influenza Epidemic, 1918-19 continued…

In Ireland, the first verifiable outbreak of the first wave can be traced to Cobh, when a US Naval ship, the USS Dixie, docked there in May 1918.

It seems that the first wave was somewhat more contained th[a]n the subsequent waves as it did not affect the entire country …

Confirmation of the onset of the second wave came from Howth during late September and this time all areas of the country were infected.

By Christmas, all counties had suffered an outbreak in both rural and urban areas…

[ibid]

The death toll was massive for such a small nation as Ireland. However, it was proportional to what other regions all around the world, both great and small, were feeling. Just to put this into perspective, it is estimated that hundreds of thousands had become ill from the Flu and maybe as many as 21,000 died in Ireland from the Spanish Flu of 1918-19. For such a small nation, this had a significant impact

Review of: The Last Irish Plague: The Great Flu Epidemic in Ireland 1918-19, by Catriona Foley

…between spring 1918 and early summer 1919, resulted in the sickness of over 800,000 people on this island, and the related death of almost 21,000 of them (statistics of the Registrar General of Ireland 1918-19)…

Jones, M. (2016, Ill-Prepared)

[3]

Interestingly, the rest of the excerpted article goes on to describe how, running concurrently with this great pandemic, our scientists were frantically trying to find a solution, to what they obviously believed would keep killing relentlessly, unless we could stop it in its tracks, although, it proved unsuccessful as outlined below.

Review of: The Last Irish Plague: The Great Flu Epidemic in Ireland 1918-19, by Catriona Foley

From the early months of the Influenza Pandemic – in Ireland as elsewhere, attempts were underway in universities and laboratories in pursuit of a therapeutic vaccine for influenza.

They did not succeed: this influenza type infection was undoubtedly lethal, and they knew that it was not a bacteria; but they simply did not know, at this stage in the pandemic, precisely what order of complexity they were dealing with.

[ibid]

 

The Taming of the Flu

Now, when we assess the overall mortality for this spectacularly severe pandemic of 1918-1919, we can see that as bad as the statistics are worldwide and within our respective populations, we should bear in mind that for much of the greater proportion of those who got the Flu and fell ill, the result was not a death sentence. However, for its victims and their loved ones, it certainly would not have looked that way. The case to fatality rate is given in the following excerpt and it might surprise you just how many actually survived the Spanish Flu.

1918 Influenza: the mother of all pandemics. Could a 1918-like Pandemic Appear Again? If So, What Could We Do About It?

In its disease course and pathologic features, the 1918 pandemic was different in degree, but not in kind, from previous and subsequent pandemics.

Despite the extraordinary number of global deaths, most influenza cases in 1918 (>95% in most locales in industrialized nations) were mild and essentially indistinguishable from influenza cases today.

Taubenberger, J. K., & Morens, D. M. (2006)

[4]

Therefore, as tragic and ultimately devastating as the Spanish Flu was for so many families and communities, the vast majority survived the infection and even got off quite lightly in terms of suffering. It is hard to believe just how many survived the great Flu epidemic.

Furthermore, nobody knew that soon after, almost as suddenly as Enza flu in, this great pestilence flew out again. We know this from accounts on the ground at the time within Ireland as indicated within a newspaper article in the ‘Irish Times’ dating to the era.

November 9th, 1918: Relief as deaths from 1918 Spanish flu epidemic began to decline

Irish Times

IT WAS authoritatively stated yesterday that the influenza epidemic in Dublin is abating. The statement was based on the fact that there are very few fresh cases within the past few days…

On the whole, he stated, there was a decline.

Joyce. J (2009, Nov. 9th)

[5]

A similarly dramatic decline in deaths was beginning to occur around the world and as indicated below, it seems that rapidly developing immunity was emerging depending upon the degree of previous exposure individuals were experiencing. This begins to give us a very strong clue to why the deaths from Influenza were declining almost as rapidly as they had risen in the second wave.

Pathogenic Responses among Young Adults during the 1918 Influenza Pandemic

During the 1918 pandemic period, military nurses and medical officers were intensively and repeatedly exposed to the influenza A (H1N1) pandemic strain in clinics, in ambulances, and on crowded open wards. However, during the lethal second wave, nurses and medical officers of the Australian Army had influenza-related illness rates similar to, but mortality rates lower than, any other occupational group …

Similar observations were made in other groups of military and civilian health care workers … These findings suggest that the occupational group with the most intensive exposure to the pandemic strain had relatively low influenza-related pneumonia mortality rates during the second wave …

During the fall of 1918, all 40 large mobilization/training camps throughout the United States and Puerto Rico were affected by influenza epidemics…

During the camp epidemics, influenza–pneumonia mortality rates were inevitably highest among the soldiers with the least military service.

In the US Army overall, 60% of those who died of influenza-related pneumonia were soldiers with <4 months of military service …

Shank, D. & Brundage, J.F (2012)

[6]

In other words, the more exposed, the greater your resistance to the worst effects of these pathogens you became, and conversely, the least exposed and most naïve your immune system the more vulnerable you were in the face of the pathogen. Another dimension to this immunity conferred by natural exposure is addressed next:

How historical disease detectives are solving mysteries of the 1918 flu

The pattern of deaths by age was also intriguing. Young adults in their late 20s were at heightened risk. In contrast, influenza infections were frequent among teenagers, but these infections were mild. Senior adults were also less likely than young adults to die from influenza …

Why were older adults spared? One popular explanation is that well-connected populations who had seen influenza in the 19th century would be protected upon the return of a similar virus decades later. This is known as the “antigen recycling” hypothesis.

This hypothesis gained more traction during the 2009 pandemic, when older populations had higher levels of prior antibodies and therefore were less likely to die than younger populations.

…Moreover, patterns of infection and death may depend upon people’s prior immunity, imprinted by circulation of similar viruses within the last century.

The Conversation (2018, 5th March)

[7]

As indicated above, we may be looking at protection gained from previous exposure to a similar strain of Influenza in the face of another, even if it is much more potentially devastating. A type of memory imprinting may occur. This phenomenon may go some way to explaining the unusual age distribution of those impacted the worst during the Spanish Flu pandemic of 1918-1919, which appears to echo far down into the future.

Now, for instance, as highlighted above, it was some of our strongest, healthiest and fittest members of our populations who suffered the greatest fatalities during the Spanish Flu pandemic and we can perhaps apply this imprinting phenomenon to explain this to some extent. We can perhaps imagine that the equally unusual circumstances of high mobility and returning troops and medical personnel  (nurses and doctors) as the war drew to a close may help explain such a pattern.

For instance, these circumstances may have given this strain of Influenza unprecedented opportunities to expand beyond their previously more restrictive horizons to previously unexposed fresh victims who had very little experience at all with any of the Flu strains either, the first wave of Influenza that was milder or pandemic Influenza from the earlier era before they were born. Thus, they would have been ripe for the picking. Recall also that their more seasoned comrades caught up in the war effort would have been more familiar with the virus strains from working in the field longer than themselves. It was the newest recruits that were the most vulnerable due to lack of previous exposure as documented earlier.

In other words, if you didn’t have any previous exposure to the Flu viruses in general, or exposure to previous epidemics/pandemics, or became relatively immune to dying from the second wave because you experienced the first less severe wave, then, you would have been the pockets of the population most vulnerable to dying when the second wave hit.

The greater detrimental impact of the young adult and fittest population may therefore, not only reflect the fact that compared to their more seasoned counterparts who had been exposed to Flu viruses in general, or their older counterparts who were old enough to remember other great Flu outbreaks, but, the circumstance of returning home from the war itself may have caused them to miss the window of opportunity to become naturally immunised when the Spanish Flu was milder (the first wave) and metaphorically and literally missed the boat on this one.

They may have been shielded from the first Flu wave (milder form) due to being so dispersed around the world and mostly confined to either the front or barracks when it circulated around the world. Their particular infantry may not have had the opportunity to be immunised in the first round; unlike their younger siblings safely tucked up at home.

This begins to also explain how teenagers tended to get off so lightly (as noted in the above excerpt discussing the unusual age distribution of attack), perhaps simply, as they were too young to go off to war in the first place and therefore, having to stay at home, they did get the opportunity to become exposed to the milder first wave of Influenza that their older siblings didn’t.

Even the younger infant types fared relatively well comparatively speaking as seen in some studies of the unusual demographic.  However, this may also be explicable to some extent as this age group would have been protected to some degree from the worst effects of the Flu if she herself had experienced a little of the first wave whilst at home. Although, pregnant mothers may have been a little more susceptible as indicated in some of the literature, as this is a vulnerable time for their immune systems anyway.

In other words, if you didn’t have any previous exposure, either before the rise of the Spanish Flu, or from frequent exposure to a more usual circulation of Influenza or, became relatively immune to dying from the second wave because you experienced the first less severe wave (as suggested in the previous excerpt), then, this would have been the very population most vulnerable to dying when the second wave hit – the young and otherwise healthy and fit adult population returning from war.

We find further clues to this phenomenon of rapid resistance built up from prior natural exposure with strong and incredibly long-lasting molecular imprinting – even in elderly people who had experienced the Spanish Flu first hand as children and who were still alive within our modern era to tell the tale as documented in the following excerpt.

Neutralizing antibodies derived from the B cells of 1918 influenza pandemic survivors.

Nature

Little is known about naturally occurring adaptive immunity to this virus; however, some elderly survivors are still living. We sought to determine whether survivors exhibited evidence of acquired immunity to the virus. Expression of the 1918 HA antigen allowed us to identify and characterize protective antibodies induced by natural exposure of humans to the 1918 pandemic virus.

We identified a panel of 32 subjects aged 91-101 years (i.e., aged 2 to 12 years in 1918), many of whom recalled a sick family member in the household during the pandemic, which suggested direct exposure to the virus. Of the subjects tested, 100% exhibited serum neutralizing activity against the 1918 virus .., and 94% had serologic reactivity to the 1918 HA (…), even though these samples were obtained nearly 90 years after the pandemic.

-Thus, these studies reveal that survivors of the 1918 influenza pandemic possess highly functional, virus-neutralizing antibodies to this uniquely virulent virus, and that humans can sustain circulating B memory cells to viruses for many decades after exposure – well into the tenth decade of life.

Yu, X., et al. (2008).

[8]

This relationship between exposures to different strains over the course of the 20th Century and into the early 21st Century giving cross-protection is summarised in the following.

Your flu risk may be linked to the year you were born
CNN

Scientists stunned by own discovery
Influenza A viruses can be categorized into two groups, and within these groups, there are subtypes: H1, H2 and H5 are in group 1, and H3 and H7 are in group 2. Only three subtypes — H1, H2 and H3 — have circulated in humans worldwide from 1918 to 2015, according to the study.

As it turned out, the researchers found that people born before 1968 were more likely to be exposed to the group 1 viruses H1N1 or H2N2 and were less likely to suffer or die from infections with the group 1 virus H5N1 infections later in life. In 1968, there was an influenza pandemic that had a multinational impact.

The 1968 pandemic marked the transition from an era of group 1 viruses to a group 2-dominated one, the researchers wrote in the study.
Therefore, people born after 1968 were more likely to be exposed to the group 2 virus H3N2 at a young age and were less likely to suffer or die from infections with the group 2 virus H7N9 later in life. For both groups, exposure at a young age not only lowered the risk of a severe infection with either H5N1 or H7N9, it reduced the risk of death by up to 80%, the researchers wrote in their study.

Howard, J., (2016, 10th November)

[9]

However, some Flu strains began behaving quite unnaturally as outlined in the following. Although, this may have something to do with an accidental escape whilst we were trying to create a means of stopping the Flu from circulating entirely.

The Problem Child of Seasonal Flu: Beware This Winter’s Virus H3N2 is deadlier than many other influenza strains

For a long time, it was flu dogma that only one influenza A virus could circulate at once. The H1N1 virus that caused the 1918 Spanish flu disappeared when the H2N2 virus that touched off the Asian flu pandemic emerged in 1957. Then in 1968, H3 muscled out H2.

But in 1977, something odd happened. H1N1 reappeared—likely as the result of a laboratory accident. And what was thought to be impossible—two influenza A strains circulating at the same time—was shown to be possible. When the 2009 pandemic started, flu researchers hoped it would push the reset button.

They hoped the new virus—an H1N1 virus that had been circulating in pigs—would drive out both the old H1N1 and H3N2. The old H1N1 viruses did disappear. But H3N2 viruses didn’t budge. For the time being, we’re stuck with this unpleasant virus.

Branswell, H. (2018, 9th January)

[10]

As highlighted by the title of the above article, the persistent strain was to be feared the most, but, this season has come and gone as of the time of writing here, so thankfully, it didn’t cause massive death-tolls and besides, as discussed previously, having exposure to this particular type conferred fairly solid protection in the face of other strains (cross-protection) against other similar group strains that might be encountered later in life.

Therefore, our latest problem child (N3N2), as it only erupted in the late 1960s, may eventually disappear (or become less obvious) like its older counterparts, it is seemingly just a matter of exposure and time, until almost all of us become immune to that one as well.

Furthermore, we can gain a real-time insight into such infections from natural exposure and subsequent immunity during different Flu seasons in the following study which reveals just how quickly and robustly our immune systems adapt to all sorts of strains, including cross-protection from more familiar types to even those that have morphed rather dramatically and how the natural immune response can even deal with less than natural strains too; the returned A H1H1 hybrid (possibly escaped lab) strain of the 1970s.

Infection with influenza A H1N1: Effect of past experience on natural challenge

Following its reintroduction in 1978 influenza A HIN1 spread widely in the child population. By the autumn of 1979, 75 % of 11-year olds entering a boys’ boarding school had detectable antibody. The protective effect of previous experience could be assessed during two outbreaks in the school. In the first outbreak in 1979, 90 % of those known to have been infected in the previous year were protected against reinfection…

Previous experience conferred over 90 % protection against infection. Between the 1979 and the 1983 outbreaks there was no overt evidence of A HIN1 activity in the school although a few sporadic infections were identified in those investigated routinely or in connection with other infections…

First, with the re-emergence of A HINt in 1978, infections were virtually confined to young people. Those old enough to have had experience of strains before 1957 seemed to be immune.

Secondly, our own observations on A H3N2 in the school (Hoskins et al. 1979) suggested that natural infection gave good protection even against strains which had undergone considerable antigenic drift.

Thirdly, the 1979 outbreak showed that recent infection with A HINt gave good protection against reinfection.

Davies, J.R, Grill, E.A., & Smith, A.J (1985, Summary)

[11]

Not only did the boys survive their ordeal and were now almost all immune for life from being directly exposed to a strange attenuated mutant gone wild, most definitely, by all accounts manipulated by man (whatever the actual point of origin, it was humanly manipulated – that much everyone agrees), but, they also showed immunity to Flu strains upon re-exposure in other Flu seasons.

Also of interest, as also noted in the above article, is that it was observed from other related studies that exposure to the A H3N2 strain (that newer tricky type which appears to have morphed considerably by fully natural means, what is called antigenic drift) resulted in fairly robust resistance even though these boys had no previous exposure to that particular variant before. This is what is called cross-protection from being exposed to another Flu strain that is not too dissimilar.

All in all, it would appear that we have built up quite an arsenal of immunity against all sorts of strains over the course of our life due to continual exposure, sometimes not even knowing it and the really good news is that these seasonal exposures can give you lifelong protection, but also set you up with some mighty protection against a pandemic strain that you haven’t even experienced yet as highlighted in the excerpt below.

Age-dependence of the 1918 pandemic

Birth year dependence of H5N1 and H7N9 avian flu cases

A growing body of epidemiological evidence indicates reduced risk of pandemic infection in those with previous seasonal exposure, and lifelong protection against viruses of different subtypes but within the same HA Group

Woo, G (2018, 11)

[12]

That is fairly impressive cross-protection due to exposure to naturally circulating Flu viruses when we see that these exposures can provide protection to future pandemic strains (new mutations that impact the world) that haven’t even happened yet!

It certainly is beginning to look like our immune systems have been doing a fine job defending us over the generations and it may be worth being exposed to the real thing as it seems that at the very least, we are ensuring protection directly and indeed, indirectly against future strains. This becomes clearly evident when we take a closer look at our most recent pandemic – the first one of the 21st Century.

As we revisit our most recent worldwide pandemic, the 2009 Swine Flu outbreak, more research has emerged that demonstrates the possible cause of such low mortality figures across our nations (we will discuss the low mortality of this most recent pandemic shortly) may relate to the strains of Flu you were exposed to throughout your life, whether you knew it or not as indicated above and specifically from epidemiological data as indicated in the following

Immunity to Pre-1950 H1N1 Influenza Viruses Confers Cross-Protection against the Pandemic Swine-Origin 2009 A (H1N1) Influenza Virus

The 2009 H1N1 influenza virus outbreak is the first pandemic of the twenty-first century.

Epidemiological data reveal that of all the people afflicted with H1N1 virus, <5% are over 51 y of age. Interestingly, in the uninfected population, 33% of those >60 y old have pre-existing neutralizing Abs against the 2009 H1N1 virus.

This finding suggests that influenza strains that circulated 50–60 y ago might provide cross-protection against the swine-origin 2009 H1N1 influenza virus.

Skountzou, I., et al. (2010)

[13]

This dynamic protection across our lifespans and preparing us for future outbreaks due to exposure is perhaps the very reason why we see such a dramatic decline in deaths from Influenza since the Spanish Flu era within Ireland as seen in the graph below (Fig. 1).  It really does look like we have become robustly resistant, if not fairly immune, to just about all the strains that have been circulating over the last century?

Flu Mortality Ireland

FIGURE. 1: Individual number of annual Deaths from Influenza in Ireland from 1864 until the mid-1990s when the cause of death was classified differently,  being combined with Pneumonia in the registrar. Arrow denotes when the vaccine began to be offered to ‘at risk’ groups.  It was noticed that deaths from Pneumonia were significantly declining across death registers from different regions when assessed (although not specifically dealt with in this present study) and presumably deaths from Pneumonia would also fully resolve in time following the same near-universal pattern seen for Influenza across our industrialised nations.

Notice that in Figure 1 shows the individual number of deaths recorded from Influenza alone, annually in Ireland since official records began that there were epidemic years prior to the more significant rise in deaths during the Spanish Flu pandemic of 1918-19. You will see that the overall longer-term trend of the major spikes representing deaths from pronounced epidemics thereafter become less and less as we progress through the 20th Century.

Note also that the Irish data does not record deaths from Influenza after the mid-nineteen-nineties as the official cause of death changed at that point to include Pneumonia. Furthermore, we know from the continued data recorded from other sources that deaths from Influenza after this point or even for the first pandemic of the 21st Century would hardly register on the above graph compared to what went before. It is only really since the 2009/10 (Swine Flu era) that the vaccine has been offered in Ireland to a broader range of individuals beyond the elderly and their carers.

This overall decline in deaths since the Spanish Flu era to marginal figures in our modern era is a pattern shared across our diverse nations where statistics of this kind are available. For instance, if we examine the graphs generated from statistics relating to deaths resulting from Influenza within the U.S. and compare this data directly with the Irish graph, the only difference between them is one of scale.

The proportion of deaths for a massive population in the U.S. would obviously be greater than a relatively tiny population within a country like Ireland. See Figure 1, Crude mortality per 100000 population, by influenza season (July to June of the following year), for seasons 1900–1901 to 2003–2004 (a) in, Doshi, P. (2008), Trends in Recorded Influenza Mortality: United States, 1900–2004  [14].

Similarly, near-identical patterns of proportional deaths from Influenza over the same essential timeframe can be found in, Twentieth-century mortality trends in England and Wales, Figure 5, showing the age-standardised mortality rates for Influenza in England and Wales from 1901 to 2000 by Griffiths C and Brock A (2003) [15].

Indeed, the pattern of declining deaths from Influenza since the great pandemic of 1918-19 would appear to be a near-universal pattern experienced across our developing nations where an investigation into any of the relevant studies and statistics that are available recording deaths from this once deadlier contagion over a related timeframe consistently demonstrates.

This commonality of a dramatic decline is further supported by the worldwide estimates of deaths recorded for each of the major Influenza pandemics that near-simultaneously swept across almost all our nations commencing with the mother of them all, the Spanish Flu of 1918 until around 1920.

Influenza Virus (Flu)

There were three influenza pandemics in the 20th century – the “Spanish” flu of 1918-19, the “Asian” flu of 1957-58, and the “Hong Kong” flu of 1968-69.

The 1918 flu, caused by a strain of H1N1, was by far the most deadly. More than 500,000 people died in the United States as a result of the Spanish flu, and up to 50 million people may have died worldwide…

The 1957 pandemic was due to a new H2N2 strain of influenza virus that caused the deaths of two million people, while the 1968 pandemic resulted from an H3N2 strain that killed one million people.

One pandemic has occurred so far in the 21st century. This was due to the novel swine-origin H1N1 virus which emerged in 2009.

Baylor College of Medicine (1998-2008)

[16]

And our most recent Swine Flu pandemic of 2009/10 produced worldwide statistics as low as just under 20,000 deaths as seen in the excerpt below.

Pandemic (H1N1) 2009 

WHO: Weekly update

6 AUGUST 2010

– As of 1 August 2010, worldwide more than 214 countries and overseas territories or communities have reported laboratory confirmed cases of pandemic influenza H1N1 2009, including over 18449 deaths.

World Health Organisation (2010, update no. 12)

[17]

Since, the time of the above report, as this figure was so unexpectedly low – just over 18,000 deaths worldwide for the greatest pandemic of the 21st Century, there has been much debate and different estimates have since been projected using various mathematical modelling with widely divergent results. Perhaps we will never know the true figure of our most recent Flu pandemic. However, we do have some statistics from Ireland that would appear to suggest that the worldwide figure was not that far off.

For instance, as tragic as this was for the family and loved ones of those that did die directly from the 2009/10 Swine Flu pandemic, it turns out that the combined number of documented deaths for the Swine Flu pandemic in Ireland over this same period through to 2014 totalled just over twenty (as obtained from tracking the main stories at the time and statistics that were given from our major news outlets) – a figure that is so low that it would virtually not be visible on the graph above if we plotted it.

Now, if we review the figures for the preceding influenza season (2007/08), just before the Swine Flu outbreak of 2009/10 we can see just two registered deaths in the over 65s (usually the elderly – much older group – are the most susceptible, but, bearing in mind that the Swine Flu and its ancestor, the Spanish Flu impacted the younger adult population most) in the whole of Ireland reported as follows.

Summary Report of 2007/2008 Influenza

Mortality Data

(Ireland)

During the 2007/2008 influenza season, two deaths attributed to influenza were registered with the General Register Office. These deaths were both in adults over 65 years of age, one in HSE-NW registered in week 8 2008 and one in HSE-S registered in week 14 2008. It should be noted that the death registered in HSE-S was not a laboratory confirmed case of influenza.

The Health Protection Surveillance (2009)

[18]

Further support for the fact that deaths from Influenza have continued to plummet to historic lows in our modern era since the Spanish Flu, statistics are also available for the actual incidence of cases of Influenza itself that would tend to suggest that we are not even catching the Flu as often these days.

For instance, a study out of the UK which followed Flu seasons spanning forty years, (just prior to the last pandemic starting in 2009) also noted that the cases of Influenza have also gradually receded as highlighted in the following with an indication that the ability of the viruses to adapt to multiple strains may, in fact, have their limit

Lessons from 40 years’ surveillance of influenza in England and Wales

We show a gradually decreasing trend in the incidence of respiratory illness associated with influenza virus infection (influenza-like illness; ILI) over the 40 years and speculate that there are limits to how far an existing virus can drift and yet produce substantial new epidemics.

Fleming, D. M., & Elliot, A. J. (2007)

[19]

Therefore, perhaps it is a good thing that our rates of mortality and morbidity had already dwindled along with our cases of Influenza significantly due to this highly robust cross-immunity protection well before we began to intervene with the natural immunity cycle to any great extent, as where would we be then without our exposure?

However, it seems that we haven’t been able to come up with a good alternative to natural immunity anyway, as you will see in the following article, therefore, perhaps our failures are a blessing in disguise

Are Flu Viruses Smarter than us?

Here’s why it’s so hard to make a better flu vaccine

Imagine you work in a high-security building. It uses facial recognition technology to keep out known intruders. It works well, until someone figures out how to use clever makeup, or even just grow a moustache to game the cameras. No matter how often the intruders are caught, new infiltrators find new disguises to help them get in.

That’s a little bit how the immune system works, and the flu virus is gaming that recognition technology. It sneaks past the body’s immune system to cause misery and mayhem, even as new vaccines update the biological equivalent of facial recognition software. Each year, a new influenza vaccine is formulated and distributed, and each year, viruses develop ways to evade them. Flu vaccines are never as effective as other vaccines, and the current vaccine only provides partial protection against the ongoing flu epidemic.

It’s an annual guessing game of sorts, one backed by data but also plagued with uncertainty. And when the guesses don’t exactly match the reality, as happened this past year, it can mean a dismal and deadly flu season. “We’ll do the best we can,” said Daum, a Chicago doctor who heads the Food and Drug Administration advisory committee that makes the recommendations. But “the virus is smarter than we are at this point. I don’t know of any disease that plagues us more. It’s very, very frustrating and a very inexact science. . . . We do it with varying luck, and I think the luck is mostly the virus’s whim.

Fox, M. (2018 Feb. 14th)

[20]

The reason I suppose our health officials worry so much about protecting us from Influenza is that not many of them think to look at the actual mortality statistics that paint a somewhat more reassuring, and certainly more realistic picture of what is going on from the ground up. By all accounts discussed thus far, we are almost all already fairly resistant against all strains of these pathogens.

But, you may not blame them if you realise the type of statistical estimates and projections that they follow, which are essentially built upon assumptions modelled on Spanish Flu-like proportions pandemics lurking behind every normal Flu season. These models have been criticised as being often too broad, ill-defined and frequently contradictory and vary widely from one another depending upon the systems used as discussed in some detail by, Doshi, P. (2008), in Trends in Recorded Influenza Mortality: United States, 1900–2004  [21].

As noted earlier, in reality, as you will see from a recent study below, getting the actual Flu isn’t even as common as you might think and for almost all of us, it isn’t even that problematic. Just because the Flu circulates each season, doesn’t mean you’ll get it; most of us don’t and those that do, don’t even know they have the infection because it is so mild (asymptomatic) according to a long-term study as excerpted below:

Three-quarters of people with flu have no symptoms

“‘77% of flu infections’ have no symptoms, say experts,” reports ITV News. The news is based on a large community-based study carried out in England, which found that most people with influenza (“flu”) don’t have symptoms, and even if they do, only a small proportion go to a doctor.

The study was part of Flu Watch – a larger, ongoing study to assess the impact of flu on public health in England – and analysed five groups of people over six periods of influenza transmission, between 2006 and 2011. Participants provided blood samples before and after the influenza season, so that the amount of antibodies in the blood could be measured. They were then contacted every week so that cough, cold, sore throat, or any “flu-like illness” could be noted down. If any of these were experienced, participants were asked to complete a symptom diary and to take a nasal swab to test for the influenza virus.

Approximately 20% of people had an increase in antibodies against influenza in their blood after an influenza “season”. However, around three-quarters of infections were symptom-free, or so mild that they weren’t identified through weekly questioning. This is very much a “good news, bad news” story. It is good news in that so many people with a flu infection are spared the burden of a nasty infection. However, limiting the spread of a future pandemic could be challenging, as it would be unclear who is infected.

NHS, News (2014, 17th March)

[22]

 

 

Thankfully, as we have already been exposed to so many strains of Influenza over the generations, it seems that we are, for the most part, ready for just about any form that those influenza viruses can morph into.

Why Revive a Deadly Flu Virus?

New York Times Magazine

Flu viruses mutate very rapidly, and each season’s version is a little different. But your immune system preserves a memory of its previous encounters with a flu, which are dragged up, like old photographs from the back of a closet, every time your system responds to a new flu invasion.

Shreevejan, J. (2006, Jan. 29th)

[23]

The name of the game would appear to be, exposure and the more exposed you are, the greater your resilience and ultimate immunity, even to strains (cross-strain protection) that you may not have directly encountered as studies discussed above strongly suggest.

And certainly, this long-term memory is very encouraging indeed, as although there doesn’t appear to be any fundamental distinction between the Spanish Flu of 1918-19 and 2009 some ninety years later that would make one genetically more virulent than the other, the main difference appears to be our level of innate and generational resilience to the virus and all its variants due to simple exposure.

This gives us hope, particularly if someone released something like the Spanish type Flu upon our populations in say, a bioterrorist attack, which, is addressed in the next excerpt.

Scientists Believe They Have Explained The Great Flu Outbreak Of 1918

…The good news here is that much of the population has now been immunized against numerous strains of flu. While these might not be enough to stop people getting sick from a novel version, it should keep the death rates down if we experience something as potentially devastating as the 1918 outbreak again.

Luntz, S. (2014, 4th May)

[24]

So, essentially, nothing happened to the Spanish Flu; it never went anywhere in particular; it is just probably finding it difficult to infiltrate our mighty defences thanks to our sophisticated protein recognition system. In other words, we have been naturally immunised, now, isn’t that reassuring?

But, it gets better, as even more reassuring is the fact that overall, these Influenza viruses may have already lost a great deal of their earlier killing power by virtue of the fact that they have been circulating within us as their host over so many generations, further supporting the ideas that if Spanish Flu was genetically engineered and released out into the public, most of us may not even notice.

A clue came when investigating some communities who had gotten off rather lightly as the most virulent eruptions of the Spanish Flu reached its tentacles into some of remotest parts of the world, but yet, many communities survived relatively unscathed who had no previous exposure, mild or otherwise to this viral pathogen. How?

The Places that Escaped the Spanish Flu

BBC

“These communities basically shut themselves down,” explains Howard Markel, an epidemiological historian at the University of Michigan who was one of the authors of the study. “No one came in and no one came out. Schools were closed and there were no public gatherings. We came up with the term ‘protective sequestration’, where a defined and healthy group of people are shielded from the risk of infection from outsiders.”

…When these measures were lifted in November 1918, as reports of cases in San Francisco were on the decline, the base experienced only mild cases, but at least three people did die…

But there may be some benefit to keeping the virus out for as long as is possible. American Samoa implemented a five-day quarantine for all boats that kept influenza from its shores until 1920. When it finally did arrive, the virus appears to have lost much of its sting and there were no deaths attributed to influenza in a population of more than 8,000. The main island of Samoa to the northwest, however, lost around a fifth of its population to the pandemic…

A similar story unfolded on the on the Australian island of Tasmania, which implemented strict quarantine measures for boats arriving on its shores that required all passengers and crew to be isolated for seven days. When the infection penetrated the island in August 1919, medical officers reported that it was a milder infection than that on the mainland. The death rate on Tasmania was one of the lowest recorded worldwide.

Gray, R., (2018, 24th October)

[25]

What happened? Quarantine should have meant that these people were just as vulnerable whether they were exposed to the pathogen at the beginning of the invasion or about a week later and had only delayed the inevitable. But, that is not what occurred. The cause of this strange, but, very reassuring anomaly of the timing and decreasing impact of the Spanish Flu pandemic becomes clearer when we look to other similar patterns as documented from epidemiological studies and observations on the ground at the time summarised next:

The Story of Influenza 1918 Revisited

One of the more interesting epidemiologic findings in 1918 was that the later in the second wave someone got sick, the less likely he or she was to die, and the more mild the illness was likely to be.

This was true in terms of how late in the second wave the virus struck a given area, and, more curiously, it was also true within an area. That is, cities struck later tended to suffer less, and individuals in a given city struck later also tended to suffer less. Thus west coast American cities, hit later, had lower death rates than east coast cities, and Australia, which was not hit by the second wave until 1919, had the lowest death rate of any developed country.

Again, more curiously, someone who got sick 4 days into an outbreak in one place was more likely to develop a viral pneumonia … than someone who got sick 4 weeks into the outbreak in the same place…

The best data on this comes from the U.S. Army. Of the Army’s 20 largest cantonments, in the first five affected, roughly 20 percent of all soldiers with influenza developed pneumonia. Of those, 37.3 percent died…

In the last five camps affected—on average 3 weeks later—only 7.1 percent of influenza victims developed pneumonia. Only 17.8 percent of the soldiers who developed pneumonia died…

Inside each camp the same trend held true. Soldiers struck down early died at much higher rates than soldiers in the same camp struck down late. Cities struck later in the epidemic also usually had lower mortality rates… The same pattern held true throughout the country and the world… places hit later tended to suffer less…

Barry, J. M (2005)

[26]

As discussed in the rest of this article, it was difficult to reconcile some of the hypotheses offered for this strange phenomenon and, therefore, another explanation was required. One hypothesis that is offered by the author of the above study, albeit admittedly highly speculative, does appear to fit the evidence a whole lot better and is therefore excerpted in summary form below:

The Story of Influenza 1918 Revisited continued…

…At the peak of the pandemic, then, the virus seemed to still be mutating rapidly, virtually with each passage through humans, and it was mutating toward a less lethal form.

We do know that after a mild spring wave, after a certain number of passages through humans, a lethal virus evolved. Possibly after additional passages it became less virulent. This makes sense particularly if the virus was immature when it erupted in September, if it entered the human population only a few months before the lethal wave.

[ibid]

In other words, this rapid mutation to increased virulence and ultimately, a much less lethal form, may have been due to the number of pathogen passages (infections in individuals and their spread to others) through their human hosts. That doesn’t mean that this strain became genetically mutated, it just means that something may have occurred within the behaviour of the viral pathogens in the context of their human host – a dilution or filtering effect as the viruses passed through and between more and more people (hosts) during the outbreak.

Now to take this a little further, none of this would show up genetically, so we have to infer a plausible scenario from what we know of the behaviour of viruses within a host and some of the defences we might put up to defend ourselves against them.

For instance, we could say that the very fact that viruses require cells/hosts to begin replicating, unlike bacteria, viruses are not actually free-living independent organisms, perhaps they took a while to establish the full takeover (hijacking) of the host’s molecular machinery to get going (the first wave milder form), but once the immune system identified what they were doing (wreaking havoc in the second wave), it found a way to begin disarming these viral replicators and we find the milder impact again during the third wave.

This would explain how those exposed later in the pandemic, even in the same army barracks, towns and cities would fare better than those exposed earlier. It would also begin to explain how those remote islanders were able to protect themselves just long enough to only encounter the much attenuated/filtered viral form of the infection and still gain immunity.

We could call this the generational immunising effect, which completely concurs with McNeill’s hypothesis regarding the same as highlighted in the introduction of this present study [27].

This immunising effect over generations may have made these viruses more and more attenuated each time they passed through generations. Is this why our mortality graphs all look so similar and all the strains of Influenza look weaker and weaker on each passing season and pandemic over the course of the last hundred years?

Moreover, there is also an indication that Nature has taken care of our future resilience and immunity too. For instance, recently emerging molecular evidence takes this dynamic of non-inherited transference of protection somewhat further. It is now looking quite likely that our immune systems can memorise past battles with pathogens, even well into the future, across the generations even when the threat is no longer present in an obvious way as indicated in the excerpt below.

RETHINKING THE ORIGIN OF CHRONIC DISEASES

Some modern-day diseases reflect the capacity of organisms to “memorize” responses to external signals and transmit them across generations …

the original causative agent may not be extant today, but “memory” of the infection has persisted.

Shoja, M.M et al, (2012)

[28]

This type of generational imprinting, passing on environmental information, and all the necessary adaptations to all sorts of threats and experiences gleaned from past battles with a vast array of pathogens that can be passed on to our offspring obviously, tells us that it is not all in the genes as we once thought.  As the title and rest of the following excerpt suggest, our ancestral battles with the bugs is not a genetic one.

Your Immune System Is Made, Not Born

New research dispels the belief that the strength of the body’s defense system is genetically programmed

Landhuis, E. (2015)

[29]

We have only in more recent times began to gain deeper insights into just how adaptable and responsive the immune system actually is. Seemingly, just about every living thing can rapidly respond and defend itself from danger and threats, particularly infectious disease, without having to wait around for millions of years in hope that we might end up with the lucky genes that will save us.

Now, it looks very likely that we can inherit this hard-fought-for immunity, not just from our mother’s directly, but from their mother’s and perhaps generations of mothers before them as suggested by the following study – at least in pigeons, but that’s only because we haven’t looked yet, at least not in terms of generational immunity transference, but, we can certainly pass on just about everything else via molecular imprints for just about everything else that has been studied. And, these memory molecules are looking increasingly like they go back further; it is just simply that our scientists have not thought to look further than indicated next.

GRANDMOTHERS CAN PASS IMMUNITY TO THEIR GRANDCHILDREN, AT LEAST IN PIGEONS

At the moment of birth, a newborn leaves behind its safe protective environment and enters a world teeming with bacteria, parasites, viruses, and infectious agents of all sorts. However, the babies do have one trump card: antibodies and immune compounds passed across the placenta from their mothers. These short-lived molecules can dip into mom’s immunological experience to protect the newborn until the immune system gets up to speed.

Now, a new study in pigeons suggests that some baby birds owe their early immunity not just their mothers, but to their grandmothers as well.

…previous research has suggested that these early maternal immune compounds may have “educational effects” on the newborn’s developing immune profile—that they may somehow be priming the system to be on the lookout for common local diseases or parasites…

Shultz. D (2015)

[30]

In other words, as indicated in the excerpt above, adaptation and resistance to disease appear to be handed down through generations – and presumably, this also applies to humans. This, of course, goes directly against our current dogma of genetically driven adaptation, but, with so many studies emerging supporting this non-genetic inheritance, this dogma is finally changing and more studies are exploring such adaptive forms of evolution.

This gives us hope that even if a great infectious contagion of the past that once devastated our communities and loved ones, that due to natural immunity across the generations, even our children’s children may not have to face the same again. This could be the very reason why we don’t hear of those once deadlier and thankfully, for most of us, long-forgotten diseases. Maybe Influenza will ultimately go the same way. In other words, we may have now forgotten those once deadlier diseases that our ancestors battled with, but our immune systems have thankfully not.

So, the future looks brighter perhaps than we had imagined. Therefore in answer to the question posed at the beginning, would we survive the Spanish Flu if it re-emerged today, I think we most certainly would and it seems our children and their offspring might actually become fully immune to it in the not too distant future and would also survive the Spanish Flu if it re-emerged even generations later. Therefore, perhaps it would be prudent to leave this natural generational immunity cycle well alone so that we can continue to pass on those long-lived memory molecules to our offspring! We may be becoming immune to dying from Influenza along with just about every other once deadlier contagion of the past and within our more modern era.

THIS ARTICLE IS TAKEN FROM A CHAPTER IN A NEW BOOK ENTITLED: Plague to Polio in Ireland & Beyond. ‘Don’t Count Your Children ’til they’ve had the Pox: Becoming Ancestrally Immune to Dying from Once Deadlier Contagions?’ by M. B. O’Hare

You can read more chapters on this blog from previous articles posted here (there is also a full version PDF for review if you want to request it at the end of the linked article).

And, or, you might like to find out more about the published book by visiting Amazon.com by clicking on the images of your preferred version (Paperback or Kindle) below.

 

Paperback: 'Don't Count Your Children 'til they've had the Pox
Click on the book to find out more on AMAZON.COM
Kindle Book 'Don't Count Your Children 'til they've had the Pox'
Click on Kindle version of the book to find out more on Amazon.com

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[2] Buckley, M. (2014) Limerick City and the Spanish Influenza Epidemic, 1918-19, Critical Social Thinking, Vol. 6, p. 81. School of Applied Social Studies, University College Cork, Ireland. [Available online as PDF]: https://www.ucc.ie/en/media/academic/appliedsocialstudies/cstpdfs/vol6/MargaretBuckley.pdf

[ibid]
[ibid]

[3] Jones, M. (2016) Ill-Prepared, Review of: The Last Irish Plague: The Great Flu Epidemic in Ireland 1918-19, by Catriona Foley, Dublin Book Reviews http://www.drb.ie/essays/ill-prepared

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[4] Taubenberger, J. K., & Morens, D. M. (2006) 1918 Influenza: the mother of all pandemics. Could a 1918-like Pandemic Appear Again? If So, What Could We Do About It? Emerging infectious diseases, Vol.12, [1], pp. 15-22 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3291398/

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[6] Shanks, D., & Brundage, J. F. (2012) Pathogenic Responses among Young Adults during the 1918 Influenza Pandemic, Journal of Infectious Disease. Vol.18, [2]: pp. 201-207.  doi: 10.3201/eid1802.102042 [Available online]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310443

[7] The Conversation (2018), How historical disease detectives are solving mysteries of the 1918 flu, http://www.theconversation.com (5th March 2018) [Available online]: https://theconversation.com/how-historical-disease-detectives-are-solving-mysteries-of-the-1918-flu-91887

[8] Yu, X., Tsibane, T., McGraw, P. A., House, F. S., Keefer, C. J., Hicar, M. D., Tumpey, T. M., Pappas, C., Perrone, L. A., Martinez, O., Stevens, J., Wilson, I. A., Aguilar, P. V., Altschuler, E. L., Basler, C. F., … Crowe, J. E. (2008). Neutralizing antibodies derived from the B cells of 1918 influenza pandemic survivors. Nature, Vol. 455, [7212], pp. 532-6.  [Available online]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848880/

[9] Howard, J., (2016) Your flu risk may be linked to the year you were born
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[10] Branswell, H. (2018) The Problem Child of Seasonal Flu”: Beware This Winter’s Virus
H3N2 is deadlier than many other influenza strains, Scientific American, (9th January 2018) [Available online]: https://www.scientificamerican.com/article/ldquo-the-problem-child-of-seasonal-flu-rdquo-beware-this-winter-rsquo-s-virus/

[11] Davies, J. R., Grill, E. A., & Smith, A. J. (1985) Infection with influenza A HlNl: The effect of past experience on natural challenge effect of past experience on natural challenge, Journal of Hygiene, Vol. 96, Summary, pp. 345-352. [Available online]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2129641/

[12] Woo, G (2018) Age-dependence of the 1918 pandemic, 4. Birth year dependence of H5N1 and H7N9 avian flu cases, Paper presented to the Institute & Faculty of Actuaries, p. 11, London. [Available online as PDF]: https://www.actuaries.org.uk/documents/age-dependence-1918-pandemic

[13] Skountzou, I., Koutsonanos,  D.G., Kim, J. H., Powers, R., Satyabhama, L., Masseoud, F., Weldon, W.C., Martin, M del P., Mittler, R.S., Compans, R and Jacob, J.(2010) Immunity to Pre-1950 H1N1 Influenza Viruses Confers Cross-Protection against the Pandemic Swine-Origin 2009 A (H1N1) Influenza Virus, Journal of Immunology, Vol. 185 [3], pp. 1642-1649; doi: https://doi.org/10.4049/jimmunol.1000091 [Available online]: http://www.jimmunol.org/content/185/3/1642

[14] Doshi P. (2008). Trends in recorded influenza mortality: United States, 1900-2004. American journal of public health, Vol. 98 [5], pp. 939-45. Figure, 1. [Available online]:   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2374803/

[15] Griffiths C., & Brock A (2003) Twentieth Century Mortality Trends in England and Wales. Health Statistics Quarterly, Issue 18, Figure, 5: age-standardised mortality rates for Influenza in England and Wales from 1901 to 2000, pp. 5–17. [Available online as PDF] https://www.ons.gov.uk/ons/rel/hsq/health-statistics-quarterly/no–18–summer-2003/twentieth-century-mortality-trends-in-england-and-wales.pdf

[16] Baylor College of Medicine (1998-2008) Influenza Virus (Flu), [Available online]: https://www.bcm.edu/departments/molecular-virology-and-microbiology/emerging-infections-and-biodefense/influenza-virus-flu

[17] WHO (World Health Organisation) (2010) Pandemic (H1N1) 2009, WHO: Weekly update (2010, update no. 12) [Available online]: https://www.who.int/csr/don/2010_08_06/en/

[18] Health Protection Surveillance Centre (HPSC) (2009), Summary Report of 2007/2008 Influenza HPSC Influenza Summary Report v1.0 season, Mortality Data, [Available online]: https://www.hpsc.ie/a-z/respiratory/influenza/seasonalinfluenza/surveillance/influenzasurveillancereports/seasonsummaries/File,3418,en.pdf

[19] Fleming, D. M., & Elliot, A. J. (2007). Lessons from 40 years’ surveillance of influenza in England and Wales. Epidemiology and infection, Vol. 136 [7], pp. 866-75. [Available online]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2870877/

[20] Fox, M. (2018) Are Flu Viruses Smarter than us? Here’s why it’s so hard to make a better flu, nbcnews.com (Feb. 14th 2018) [Available online]: https://www.nbcnews.com/health/health-news/here-s-why-it-s-so-hard-make-better-flu-n848081

[21] Doshi, P. (2008). Trends in Recorded Influenza Mortality: United States, 1900–2004, American Journal of Public Health. Vol. 98 [5]: pp. 939–945. [Available online]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2374803/doi: 10.2105/AJPH.2007.119933 PMCID: PMC2374803

[22] NHS, News (2014) Three-quarters of people with flu have no symptoms, National Health Service Medical News (17th March 2014) [Available online]:  https://www.nhs.uk/news/medical-practice/three-quarters-of-people-with-flu-have-no-symptoms/

[23] Shreevejan, J. (2006), Why Revive a Deadly Flu Virus? New York Times Magazine online, (Jan. 29th 2006),  [Available online]: http://www.nytimes.com/2006/01/29/magazine/why-revive-a-deadly-flu-virus.html

[24] Luntz, S. (2014), Scientists Believe They Have Explained The Great Flu Outbreak Of 1918, IFLScience.com (May 4th 2014) [Available online]: http://www.iflscience.com/health-and-medicine/scientists-believe-they-have-explained-great-flu-outbreak-1918 

[25] Gray, R., (2018) The Places that Escaped the Spanish Flu, BBC (24th October 2018) [Available online]: http://www.bbc.com/future/story/20181023-the-places-that-escaped-the-spanish-flu

[26] Barry, J. M (2005) The Story of Influenza 1918 Revisited: Lessons and Suggestions for Further Inquiry, in, eds., Knobler, S. L., Mack, A., Mahmoud, A & Lemon, S. M. The Threat of Pandemic Influenza: Are We Ready? Workshop Summary, National Academies Press 2005 Academies Press, p. 63  [Available online]: https://www.ncbi.nlm.nih.gov/books/NBK22148/

[ibid]

[27] McNeill, W. H., (1976) Plagues and Peoples. Anchor Books, New York, USA. [Available online Google books]: https://books.google.ie/books?id=dJvuAAAAMAAJ&source=gbs_book_other_versions

[28] Shoja, M.M., Tubbs, R. S., Ghaffari, A., Loukas, M. & Agutter, P.S. (2012) Rethinking the Origin of Chronic Diseases, BioScience, Vol. 62, [5], Abstract, pp. 470–478, doi: 10.1525/bio.2012.62.5.8 [Available online]: https://academic.oup.com/bioscience/article/62/5/470/236430/Rethinking-the-Origin-of-Chronic-Diseases

[29] Landhuis, E. (2015), Your Immune System Is Made, Not Born, Discovery Magazine (Jan., 29th 2015)  [Available online]: http://discovermagazine.com/2006/nov/cover

[30] Shultz. D (2015) Grandmothers can pass immunity to their grandchildren, at least in pigeons, Sciencemag.com  (Nov. 10th 2015), [Available online]:

 

 

Measles: Are we following the right ‘HERD’?

“To those who ask me ‘Why do you wish to eradicate measles?’” … “Because it is there.”… “ and it can be done.”..

Are we following the right herd?

Fig 1: Measles: Are we following the right herd?

…Measles immunity as estimated for the United States (and presumably, most industrialised nations would be broadly comparable), shows that in the pre-vaccine era that almost everyone was naturally immunised prior to the greater availability of vaccines to prevent the circulation of Measles.

(note that all the quotes are referenced with clickable links at the end of this article).

Epidemiology and Prevention of Vaccine-Preventable Diseases

Before a vaccine was available, infection with measles virus was nearly universal during childhood, and more than 90% of persons were immune by age 15 years…

CDC (2015, 209)

[1]

Now, as we can tell from these estimated natural immunity statistics, it seems that hardly a child born in the pre-vaccine era had grown to maturity without having the Measles and therefore, at a population (community immunity) level, almost everyone had become immune to death and disabilities from having been naturally exposed to the Measles virus as children. It was in this context that we see the beginning of our efforts to eradicate the Measles as indicated in the following excerpted article.

Vaccination Before the Measles-Mumps-Rubella Vaccine

US and UK IMMUNIZATION POLICY, 1963–1968

Any decision to begin mass measles vaccination in the early 1960s thus involved numerous uncertainties. Was the disease serious enough? Would parents feel it worth having their children vaccinated? And if mass vaccination did seem justified, should the live or the killed vaccine (or a combination of both) be used?

In the United States, experience with the polio vaccines played a major role in shaping the consensus that gradually emerged.

…Approximately 15 million children were given one of the new measles vaccines starting with their licensing in 1963 and continuing until mid-1966, and the reported incidence of the disease fell by half… On the basis of this success, with material and financial support from the Centers for Disease Control and Prevention, and inspired by the social and political climate of the time, in 1967 a campaign was launched to eliminate measles from the United States…

Mass measles immunization began in Britain in 1968. In Sweden it began in 1971 and in the Netherlands not until 1976.

Hendriks, J., & Blume, S. (2013)

[2]

As you can see from the excerpt above, the vaccine was made widespread and Measles became yet another vaccine-preventable disease. Other regions followed suit at varying times – some rather late as indicated above, but none as late as Ireland. Ireland was the latecomers to the anti-Measles party. It was the mid-1980s before we introduced the Measles vaccine for the first time (National Immunisation Office, 2018) [3].

Measles IrelandFigure. 2: Graph showing the annual number of deaths in Ireland from Measles since official records began in 1864. Source for raw data since records began sourced from, “Annual Reports on Marriages, Births and Deaths in Ireland, from 1864 to 2000” An Phríomh-Oifig Staidrimh, Central Statistics Office CSO. Arrow indicates when Ireland first introduced a vaccine against the Measles.

Now, as the vaccine against Measles was introduced in Ireland at a time when hardly a child passed to adulthood without having the Measles growing up. And the mortality graph has almost flat-lined (Fig. 26), perhaps, we can begin to see how other regions would have seen a near-flat lining of deaths from Measles by the mid-1980s too if they had not have introduced a vaccine to prevent Measles earlier. It seems that if none of our respective regions had tried to stop this common and virtually benign infection of childhood, the deaths would have ceased entirely as we left the 20th Century behind.

One can imagine that Measles would have become much like Scarlet Fever (the slightly older plague of children that also became a benign infection of childhood and seemed to disappear entirely) and perhaps infections of Measles would have become increasingly rare as well and like Scarlet Fever that we never tried to eradicate using vaccination (recall that antibiotics against this bacterial disease only became widely available after it had seemingly become eradicated on its own), if it did ever return, it was only to make sure that the children got their much needed natural immunising boosters to protect them and their offspring for the future.

In other words, one has to ask: did we really need such an intervention for Measles, considering that Nature had obviously done such a great job on her own? Perhaps now you can see that full resolution of natural infectious contagions comes down to one thing: mass exposure to the real authentic pathogen (and the more exposure, the better), not mass lack of exposure, and nature will do the rest. However, our health officials thought otherwise. We thought we could do it better than Nature herself as clearly indicated in the following quote.

Vaccination Before the Measles-Mumps-Rubella Vaccine

US and UK IMMUNIZATION POLICY, 1963–1968

“To those who ask me ‘Why do you wish to eradicate measles?’” wrote Alexander Langmuir, chief epidemiologist at the Centers for Disease Control and Prevention from 1949 to 1970, I reply with the same answer that Hillary used when asked why he wished to climb Mt. Everest. He said “Because it is there.” To this may be added, “… and it can be done.”…

Hendriks, J., & Blume, S. (2013)

[4]

In other words, we had this mass vaccination policy because we had the weapon of choice at the ready, and eradication of wild Measles was seemingly within our grasp.

The only problem was as indicated above, that, as you will see as we proceed, vaccine immunity came nowhere near the life-long and generational immunity/protection of naturally acquired Measles. As you will see as we continue, vaccine failures and waning turned out to be a big issue for Measles – just as it had with so many others including Jenner’s vaccine against Smallpox back in the day.

However, where our efforts may have been somewhat justified regarding Smallpox, as health officials were not in possession of the full facts regarding how tame this had actually become compared to generations previous, with Measles, we really could have known better.

Now reviewing all of this in retrospect, it would appear that we may have actually created more problems for ourselves in the long run and we may have been highly misguided in believing that we could conquer Nature in this way.

In order to assess this fully, we need to return to the pre-vaccine era in the light of the sheer numbers of children getting the Measles whilst growing up compared to the likelihood of dying or having disabilities from the infection.

Evidence of Number of Cases of Measles in the Pre-Vaccine Era

It is only really from the 1940s onwards that many of our industrialised nations started to make Measles a notifiable disease, that we begin to get a glimpse into the numbers of infections (at least the ones we have official records for) as seen in one account from England and Wales in the following:

Atlas of Epidemic Britain: A Twentieth-Century Picture

During the first three full years of notification, 1940-42, over 1.15 million cases of measles were reported.

With this new information to hand, William Butler could inform a meeting of the Royal Statistical Society that:

“In looking through the Annual Reports of a number of Medical Officers of Health for the year 1940, I was impressed by the small number of deaths recorded in proportion to the number of cases notified in the districts to which they related.”

Smallman-Raynor, M and Cliff, A (2012, 50)

[5]

We are talking about over a million cases of Measles within a fairly short timeframe, which wasn’t unusual back in these days and yet, as the statistician remarked, there were so relatively few deaths. This observation is supported by historical accounts of the massive amount of Measles cases – almost every child had the Measles whilst growing up across many of our now modernised nations with correspondingly decreasing number of deaths, where available, as plotted on our respective mortality graphs for this era right up to 1950s/1960s. This simply reminds us that having an infection does not correspond in any way to your chances of dying from the disease.

It would appear, as based upon more in-depth research by the present writer that it depends upon the era of the pathogen and how long it has been circulating amongst our populations. The longer our ancestors were exposed over the generations, the greater the generational immunity resulting in less and less death until a contagion finally stops plaguing us altogether.

Moving forward in time, we begin to fill out the picture of the pre-vaccine era regarding the actual ratio of expected deaths to notified cases (remember that many cases of Measles would have been so mild that they may not have been officially notified at all).

For instance, we have a more specific indication of the ratio of deaths to reported cases of Measles from around the 1950s as an average across our developed or industrialised nations of about 1 death in every 10.000 reported cases as indicated in the following excerpt which also compares this relatively low rate with the larger rate in less developed nations.

Measles deaths in the 1950s in industrialized countries

Whatever its toll in industrialized countries, where the measles fatality rate is 1 per 10,000 cases (Babbott and Gordon, 1954), measles has been a far greater scourge in developing countries, with case fatality rates as high as 1,000 per 10,000 cases (Morley, 1974).

Institute of Medicine (US)

(1994, Chapter 6, Measles and Mumps Vaccines)

[6]

The importance of the figures of deaths from Measles from less developed nations given above, is that although a thousand deaths in every 10.000 reported cases of Measles, is that with this increasing immunity due to massive exposure, it is reasonable to suggest that it would not be long before they too would also experience similarly low fatality rates to the more industrialised nations – it would simply be a matter of time. But, alas, we may never know as mass vaccination swept across all of theses nations almost as virulently as the Measles virus.

Mass Vaccination Against Measles Some Years On

The great triumph that ushered in the mass vaccination starting in the United States, although, this led to a fairly remarkable coverage – but, their hopes were dashed as the virus proved rather difficult to control, even by having such a highly vaccinated school-aged population as seen in the following article excerpted next.

Measles Control in the United States: Problems of the Past and Challenges for the Future

…during the 1970s, all states passed laws mandating documentation of immunization against measles and other childhood diseases for entry into school. By the early 1980s, high immunization rates were achieved for school-age children; more than 95% of children were completely immunized by the time of school entry.

…Immunization efforts during the 1980s, however, failed to eradicate indigenous measles, and the number of reported cases averaged 3,700/year until 1989…

Wood, D.L & Brunell, P. A., (1995, 260)

[7]

Such outbreaks amongst highly vaccinated populations culminated in the United States in the most severe epidemic of the late 1980s, early 1990s as continued from the above article as outlined in the following:

Measles Control in the United States: Problems of the Past and Challenges for the Future

During the 1970s and 1980s, measles outbreaks in schoolage children accounted for the majority of reported measles cases… From 1985 to 1988 there were a median of 47 outbreaks among school-age populations and only 8 outbreaks among preschool populations…

In 1989, the number of outbreaks among school-age children swelled to 170 and the number of total reported measles cases increased to more than 18,000, with 41 deaths. The epidemic continued unabated through 1990, when 27,786 cases were reported, with more than 60 deaths…

In 1989, the majority of reported cases were in school-age or college-age individuals and a minority were in preschool children… Approximately 80% of the affected school-age children were appropriately vaccinated.

Studies have documented that epidemics of measles can be sustained in school-age populations despite their having very high vaccination rates.

(ibid)

Note the age shift of those infected by Measles in these post-vaccine era epidemic outbreaks has shifted from younger children (usually pre-school age); the age group who typically got the Measles infection naturally, to the older school-age and even college-age students who had grown up without immunity against the Measles. This shift in the older age group pattern of those most commonly now infected in the post-vaccine era is like history repeating itself (recall vaccine waning immunity and Smallpox).

It was the school children and college-age young adults group who were most commonly the source of the post-mandated vaccination epidemics of Measles who got infected themselves, who would not be the typical age group in which Measles would naturally erupt in the pre-vaccine era as most of them would already have had the infection as younger children and grown up with life-long immunity.

As you can see, this major epidemic within the United States was particularly tragic and hugely infuriating and massively disappointing for our well-intentioned public health officials as they slowly came to terms with the possibility that perhaps the slogan ‘Stop Measles with One Shot’ was becoming as irrelevant to parents as it was to the bugs themselves.

Now with these first-generation Measles outbreaks erupting within highly vaccinated populations, for the most part, one has to ask, did the long-term suppression of restricting the natural circulation of the wild Measles virus resulting in an entire generation of children who had grown up unexposed for the most part to the natural immunising of boosting effect of naturally circulating Measles, amplify the severity of such outbreaks?

Consider the following, where for instance, you can see below the case to death ratio – the actual deaths calculated from the numbers of reported infections of Measles, just a short generation after the introduction of mass vaccination against the Measles is remarkably high; 55,622 cases of Measles over the course of this epidemic (1989-1991) and a total of 123 deaths resulting in just over 2 deaths per 1000 cases as established by calculating the statistics recorded by the CDC Pinkbook tabulations from May 2019 [8].

No wonder it was this Measles epidemic more than most that had culminated in 1989 through to 1990 in the United States that urgently prompted the recommendation second dose MMR:

One has to ask, how come the risk of deaths/disabilities to cases of Measles in the 1950s in the same industrialised region was so much less (at 1 in 10,000 cases of Measles and decreasing thereafter) than getting it in the late 1980s/early 1990s?

Now, I also noticed that this is the very same risk ratio of 1 or 2 deaths per 1000 cases of Measles averaging out over the series of Measles outbreaks prior to and including the late 1980s – early 1990s epidemic in the United States and as documented statistically elsewhere in similarly severe post-mass vaccination Measles epidemics is the presumed risk ratio that many parents seeking medical advice regarding the case for vaccinating against Measles versus getting the wild version. This is truly not justified, as this high risk for catching the Measles of 1 or 2 in every 1000 doesn’t apply to natural Measles under normal circumstances.

I only mention it, as I feel we are being very disingenuous to nature herself, as after all, these figures are based upon a very unusually severe eruption after a long artificial suppression of the natural infections via vaccination – i.e., they are from outbreaks of Measles that first erupted within highly vaccinated populations in the first place due to the inadequacies of both long-term and rather poor protection in a sizable portion of the vaccinated population that the single-dose MMR offered as is now broadly acknowledged by most of our public health officials and infectious disease control experts.

Do also bear in mind, that this rather alarming estimated number of deaths to cases of Measles also contrasts with regions such as Ireland that didn’t see the Measles vaccine until the mid-1980s (a few years prior to this particularly severe post-mass vaccination eruption of Measles culminating in the late 1980s through to the early 1990s) where the case rate in Ireland was virtually zero deaths/disabilities to hundreds of thousands of cases as most children had the Measles growing up.

Seemingly, anywhere in the industrialised world that had relatively early and mass vaccination coverage experienced similarly severe epidemics a few decades after the implementation of the first MMR/Measles vaccine. Even Ireland experienced a relatively severe eruption in the early 2000s with a few infant casualties. But, thankfully nothing as serious has occurred since – even though we have seen outbreaks of wild Measles since. This brings us to another fall out of our respective mass vaccination coverage to attempt to eradicate Measles, which we will review in the next section.

Vaccinated Mothers can no longer protect their most vulnerable infants the way they used to in the Pre-Vaccine Era

Now we find when we dig deeper into the deaths that resulted from the major Measles outbreaks of the later 1980s and early 1990s in the United States as documented in the next excerpt (and seen elsewhere subsequent to our mass vaccination policies), that when we review the statistics, it turns out that it was the infants who became the greatest casualties in our war on the Measles bug, which itself prompted the call for infants and small children under one year old to be vaccinated earlier to help protect this most vulnerable group.

Measles Control in the United States: Problems of the Past and Challenges for the Future

… During the 1989 to 1991 epidemic, the attack rate for children under 1 year of age in urban communities reached 119/100,000, the highest of any age group…

In addition, the morbidity and mortality were highest among this age group. Therefore, a vaccine effective in preventing measles in infants less than 1 year of age is greatly needed worldwide …

Wood, D. L. & Brunell, P. A., (1995, 265)

[9]

In order to put this in context, we have to understand that this was unusual as in the pre-vaccine era, this is the age group that typically did not get the full-blown Measles as they were for the most part protected by their mother’s maternal antibodies (a type of attenuated or weakened version of the Measles virus that would familiarise the infant without causing an actual more life-threatening attack), Niewiesk, S., (2014) [10].

Maternal Antibodies: Clinical Significance, Mechanism of Interference with Immune Responses, and Possible Vaccination Strategies, that their mothers’ would have due to having the wild Measles infection herself whilst growing up when she was at an appropriate age to deal with it.

Essentially, infants were becoming increasingly the most vulnerable as they were too young to be vaccinated themselves as highlighted in accumulating studies, although the second dose MMR as prompted by the inadequate protection of the single dose, the infant population still remained the most vulnerable as we can see from the following more recent assessments of this situation.

Loss of Passively Acquired Maternal Antibodies in Highly Vaccinated Populations…

Measles outbreaks in countries with high measles vaccine coverage have demonstrated a shift in measles incidence to children <12 months of age …

As with previous studies, the authors note significantly lower measles antibody titers in infants born to women from the highly vaccinated populations in comparison to those born to mothers with presumed naturally induced immunity.

Gans, H. A. &. Maldonado, Y. A. (2013)

[11]

This is further echoed in the following studies dating again to our more modern vaccine era such as that highlighted in the following excerpt relating to our more recent experiences in the European Union, which is becoming a near-universal theme of late across all of our first world nations as seen in the growing number of science papers addressing similar issues.

New measles vaccination schedules in the European countries?

…Measles is a highly infectious disease …

Old studies on measles infection showed that infants were protected against measles with maternal antibodies over the first year of their lives. Vaccination of infants after 12 months of age aimed at avoiding the neutralizing effect of maternal antibodies and in turn improving measles vaccine effectiveness …

Based on the results of measles outbreaks, especially age of affected patients, we should consider changing measles vaccination schedules in all EU countries…

vaccinated mothers aged between 30 and 40 years old provide very low levels of antibodies to their infants, not sufficient to protect them over the first 12 months of their lives …[also] the prevalence of breast feeding is lowering or at least reduced in duration all over the EU countries… Maternal milk provides antibodies which offers major protection for infants against many bacterial and viral infections including measles …

…In conclusion, administrating the first dose of measles vaccine in the EU countries should be considered before 12 months of age, most probably at 9 months of age.

Allam M. F. (2014, Summary)

[12]

As indicated above, this issue of significantly lesser protective duration and quality of maternal antibodies from increasingly vaccinated populations of mothers has not gone away. Hence, we are beginning to grasp that there is a correspondingly greater need for earlier vaccination. The following example of another relatively recent paper dating to 2013 again addresses similar issues emerging within highly vaccinated populations within the Netherlands.

Waning of Maternal Antibodies Against Measles, Mumps, Rubella, and Varicella in Communities With Contrasting Vaccination Coverage

…Mothers who received MMR vaccine tend to have a lower concentration of measles virus–specific antibodies than mothers who naturally acquired measles…

Infants born to measles-vaccinated mothers are hence likely to have lower levels maternal antibodies at birth and a shorter period of protection than infants of mothers who acquired measles naturally …

In countries with high MMR vaccination coverage, such as the Netherlands, most women of childbearing age are vaccinated against measles and have avoided natural infection. …

Sandra Waaijenborg, S. et al. (2013)

[13]

The moral of this story is that we appear to have shot ourselves in the foot regarding mass vaccination as a means of protection against Measles. You see, Nature appears to have already found a means of protecting newborn infants right up to a year old and beyond in some cases via their mother’s own experience with the Measles and indeed, all other infectious type diseases that we have investigated in this way.

The only requirement is that she herself had exposure whilst growing up and it is this natural immunisation process, or becoming increasingly familiar with certain pathogens, that helped to ultimately resolve these vulnerabilities either well before a vaccine became available, or certainly on the cusp of a fuller resolution within our industrialised nations as we began introducing mass vaccination against such diseases.

But, all may not be as gloomy after all, as you will see as we further investigate our more current insights into the fall out of living in a world which has become heavily dependent upon vaccine protection against the Measles virus which is equally applicable to all the major and once deadlier infectious diseases that we now recommend as vaccine-preventable.

Are We Becoming Generationally Resilient to Dying from Measles Once Again?

Now it wasn’t long after we started giving the second MMR dose that a whole generation of highly vaccinated children grew to maturity with ever-decreasing protection against the Measles as is becoming abundantly clear, particularly in more recent years due to the significantly decreasing effect of natural boosting from the wild Measles circulation – one could argue, due to the success of high vaccination coverage across our first world populations.

It turns out, as you will see from the following studies investigating such issues, that even after being fully vaccinated as a child with at least two doses of MMR, your protection will seemingly wear off significantly by the time you reach adulthood and it is very likely that you would get the infection if you encountered it in an outbreak.

The next study, is a case in point where it has recently specifically investigated this issue of the longevity of 2 dose MMR within highly vaccinated populations in Taiwan and demonstrated with statistical significance that these young adults would not be able to avoid getting the Measles in an outbreak and this has consequences for many other regions where high vaccination coverage and uptake rates have been maintained for a significant period of time.

Waning population immunity to measles in Taiwan

To evaluate the population immunity to measles in Taiwan where the coverage rate of the measles vaccine was >95% for more than a decade…

In subgroups aged 2-25 years, to whom at least 2 doses of measles-containing vaccine were given, there was a declining trend of seropositivity with age from 94.5% at 2 years to 50.6% at 21-25 years (p<0.0001)…

Seroprevalence was uniformly >95% in the older population (≥ 35 years) who had not been immunized against measles.

The waning vaccine-induced immunity may have impact on the control of measles in the future, especially when the vaccinated population becomes older.

Chen C. J. et al (2012, Abstract)

[14]

These findings are supported from around the world within increasing investigations demonstrating that the longer-term use of 2 doses of MMR doesn’t actually appear to have resolved the issues of vaccine waning over time since the date of last immunisation, leaving the young adult population the most vulnerable to getting the Measles and indeed other infections that the MMR is supposed to protect against as exemplified in the next study from Finland, particularly with the absence of natural boosting from the wild Measles virus.

The study also suggests that in the light of these findings that a third dose MMR should be considered. However, as you will see further on, studies that have investigated such are far from encouraging with regard to the length and strength of protection that this might offer.

MMR vaccination and disease elimination: The Finnish experience

An increasing part of the Finnish population is MMR-vaccinated. Over 95% of the population up to 35 years of age has been vaccinated twice…

A study on the immunity of the whole population against measles, mumps and rubella, carried out among different groups, showed that vaccinated age groups have antibody levels significantly lower than those of naturally infected individuals… These findings are in line with the results of antibody-persistence studies, which confirm that in the absence of natural boosters, a decline in vaccine-induced antibodies takes place…

The MMR vaccine was believed to induce life-long immunity against measles, mumps and rubella, although that has not proved to be true … Our antibody follow-up studies among the vaccinated cohort strongly suggest that immunity wanes…

On the basis of the decline in antibodies observed after the administration of two doses of the MMR vaccine, a third dose may be needed at the time of young adulthood…

Davidkin, I., et al (2010)

[15]

Now, as the excerpted investigations given above within highly vaccinated populations suggest, in the face of an outbreak, it would be unlikely that even full vaccination compliance would hold up and this is borne out in the following outbreaks of Measles that are presented throughout the rest of this section.

Fortunately, however, the characteristics of much more recent outbreaks commonly now impacting highly vaccinated populations due to vaccine failures have turned out to be rather tame; certainly, when we compare such Measles outbreaks across our first-world nations with the second generation post-vaccination era eruptions discussed previously, deaths and injuries from such recent outbreaks are notable by their absence from all of the reports investigated here.

All in all, as you will see from the samples of fairly recent Measles eruptions presented here, it looks like we may becoming quite resilient to the Measles virus once again and we may in part, have to thank our vaccination failures for this most welcomed return to more robust immunity.

Take for example the outbreak of Measles in Korea mostly impacting children less than one year old (and therefore, too young to be vaccinated) and yet, this population appear to have survived rather well as no deaths or disabilities were reported as a result. Furthermore, the other age group most impacted in the Measles outbreaks were adolescents and young adults whose vaccination protection against the Measles (two-dose MMR) given in childhood had seemingly worn off (waned) are not reported as having suffered greatly due to the outbreaks.

Essentially, it looks like all of the cases not only survived unscathed but, ended up with life-long immunity to the Measles as a result. Could vaccine waning immunity be providing a strange means of natural boosting and building up an ever-increasing population dependent upon real exposure for full, robust and generational protection?

An increasing, potentially measles-susceptible population over time after vaccination in Korea

Waning levels of measles antibodies with increasing time post-vaccination suggests that measles susceptibility is potentially increasing in Korea. This trend may be related to limitations of vaccine-induced immunity in the absence of natural boosting by the wild virus, compared to naturally acquired immunity triggered by measles infection. This study provides an important view into the current measles herd immunity in Korea…

In Korea, the measles-containing vaccine (MCV) became available in 1965, and the trivalent measles, mumps, and rubella (MMR) vaccine was introduced in early 1980s. A 2-dose MMR vaccination schedule was recommended beginning in 1997, with the first dose given at 12–15 months of age and the second dose given at 4–6 years of age…

Although measles had been eliminated in Korea, the resurgence of measles outbreaks related to imported and import-associated measles cases occurred during 2013–2014. Most patients with measles were infants aged <1 year, but measles cases were also identified in patients aged 13–24 old who had received a 2-dose measles vaccination…

Measles outbreaks among highly vaccinated populations have been observed in many countries…

… Our data showed good agreement between the incidence of measles and the susceptible age groups (adolescents and young adults) with measles seronegativity observed, suggesting the potential accumulation of measles-susceptible individuals in the population due to waning immunity, which may pose increased risk for measles outbreaks following measles importation from other endemic countries.

Kang, H. J. et al (2017, Conclusions)

[16]

The tameness of such recently emerging Measles outbreaks impacting highly vaccinated populations in particular (and thankfully not negatively impacting infants too young to be vaccinated to any concerning extent within first-world nations) may be accounted for by the fact that the type of Measles encountered most frequently is often described as fairly mild and even without obvious symptoms and has come to be known as modified Measles which are most common amongst highly vaccinated young people whose vaccination since childhood have waned. These outbreaks are also often described as self-limiting and another recent example is given in the following from Israel.

Measles Outbreak in a Highly Vaccinated Population — Israel, July–August 2017

On August 6, 2017, the Israeli Defense Force Public Heath Branch (IDFPHB) was notified of two suspected measles cases. IDFPHB conducted an epidemiologic investigation, which identified nine measles cases in a population with high measles vaccination coverage.

All measles patients had signs and symptoms consistent with modified measles (i.e., less severe disease with milder rash, fever, or both, with or without other mild typical measles symptoms). A total of 1,392 contacts were identified, and 162 received postexposure prophylaxis (PEP) with measles-mumps-rubella (MMR) vaccine; the remaining contacts were followed for 21 days (one incubation period). No tertiary cases were identified.

Avramovich E, et al (2017, Abstract)

[17]

Another case in point of both an outbreak of Measles impacting highly vaccinated young people in particular who presented with the mild form (Modified Measles for the most part) and an outbreak that was self-limiting is outlined in the following recent cases of Measles in Taiwan.

Occurrence of modified measles during outbreak in Taiwan in 2018

To the editor: We read with great interest the rapid communication by Mizumoto et al … regarding modified measles in Japan, 2018. In particular, we discovered that the index case in Japan was epidemiologically linked to an outbreak in Taiwan […]; measles was transmitted on board an aircraft while the case returned to Taiwan from Thailand, before travelling on to Japan while febrile and contagious.

Measles was confirmed in three members of the cabin crew and one passenger that shared the same aircraft as the index case. Further transmission by the infected cabin crew members occurred and involved an additional seven staff. One passenger that contracted measles in the airport caused a secondary cluster of four cases with ca 1,000 contacts in Chang Gung Memorial Hospital, Taiwan…

In 2018, during the outbreak in Taiwan, from March to April involving 24 cases.., we found that in the aircraft cluster 12 of 13 measles cases were young adults aged 20–40 years who had been immunised with two doses of measles-containing vaccine during childhood…

The presentation of measles was modified in these cases, making the clinical suspicion of measles very difficult; in the serological tests… In cases presenting with modified measles transmission was limited, as further infections occurred in only three cases among 1,000 contacts in the hospital cluster and these cases had close and long-time contact with the modified measles cases.

Although the uptake of two-dose measles vaccine in children was maintained at > 95% for 40 years in Taiwan, the measles outbreak in younger age groups was not unexpected. We have shown that vaccine-induced humoral immunity to measles can wane to a very low level (50–60%) in young adults…

The measles outbreak in Taiwan seems to have mainly resulted from secondary vaccine failure rather than suboptimal vaccination coverage.

Chen, C-J., Lin, T-Y., & Huang, Y-C. (2018)

[18]

The spread of Measles was remarkably self-limiting, even the wild type with more obvious symptoms, and rather self limiting also within the confined space of the aircraft where only a handful of fully-vaccinated young adults were infected, even if they did manage to pass it on to some hospital staff who were in close quarters with them.

And as also noted above, this outbreak in the younger age group – fully vaccinated with two doses of MMR, was not unexpected, as the authors had previously demonstrated (secondary vaccine failure).

This next case, again relating to Japan, is also of interest because although it had quite a sizable proportion of infected individuals who presented with more typical Measles symptoms and were unvaccinated (although more than half were fully vaccinated in this outbreak and tended to spread the infection less and had the milder and less obvious form of the Measles infection), it is really surprising how little the outbreak spread amongst the populations in general, particularly, considering the many opportunities for the virus to do so.

The following account also points out, there was a strong association between the number of MMR doses that those infected had received and the mildness of having the Measles.

The Largest Measles Outbreak, Including 38 Modified Measles and 22 Typical Measles Cases in Its Elimination Era in Yamagata, Japan, 2017

The incidence of modified measles (M-Me), characterized by milder symptoms than those of typical measles (T-Me), has been increasing in Japan. However, the outbreak dominated by M-Me cases has not been thoroughly investigated worldwide. .. This phenomenon was observed after Japan had achieved measles elimination in 2015.

We confirmed 60 cases by detecting the genome of the measles virus (MeV). Among the cases, 38 were M-Me and 22 were T-Me. Thirty-nine (65.0%) patients were 20–39 years of age. Three out of 7 primary cases produced 50 transmissions, of which each patient caused 9–25 transmissions. These patients were 22–31 years old and were not vaccinated.

Moreover, they developed T-Me and kept contact with the public during their symptomatic periods. Considering that M-Me is generally caused by vaccine failure, some individuals in Japan may have insufficient immunity for MeV. Accordingly, additional doses of measles vaccine may be necessary in preventing measles importation and endemicity among individuals aged 20–39 years…

… Outbreak description: During the outbreak, 60 measles cases were confirmed from March 3 to April 15, 2017… The index case involved a man in his twenties who had traveled to Bali Island, Indonesia, from February 20 to February 26, 2017… After the index case, 25 second-generation cases, 27 third-generation cases, 2 fourth-generation cases, and 5 cases of unknown origin were reported…

On May 17, 2017, measles epidemic had ended because no additional cases were observed for 4 weeks… Approximately 65.0% of the patients were 20–39 years. Among the 36 vaccinated patients, 83.3% presented with M-Me… Asymptotic linear-by-linear association test indicated a trend in which the proportion of M-Me cases increased with increasing vaccination doses…

Transmission pathways: We confirmed that 54 of 59 cases had a direct or indirect epidemiological association with the index case… In conclusion, the measles outbreak in Yamagata Prefecture, Japan, in 2017 was caused by importation and was transmitted primarily by 3 unvaccinated patients… including the index case.

Komabayashi, K. et al (2018, Summary)

[19]

These infections of Measles would presumably produce life-long immunity, not just for those who were not vaccinated even if they tended to be more infectious and spread the virus more than their vaccinated counterparts, but, those with vaccine waning immunity would also have become immune for life – even if the symptoms are expressed in a more mild form due to having at least some familiarity with the pathogen as a result of their vaccination history.

You see many people are not actually aware that they have the Measles when exposed unwittingly to infection. We can see this particularly within highly vaccinated situations such as hospitals as exemplified in the following reports amongst health workers and patients, starting with a recent outbreak in Portugal:

Challenging measles case definition: three measles outbreaks in three Health Regions of Portugal

We report three simultaneous measles outbreaks with 112 confirmed cases in three Health Regions of Portugal, from February to April 2018. The mean age of cases was 30 years, 79% worked in a healthcare setting and 87% were vaccinated… Several cases presented with modified measles, highlighting the importance of rethinking the measles case definition for vaccinated cases.

We present preliminary findings and implemented control measures of three simultaneous measles outbreaks that occurred in Portugal between February and April 2018. One of the outbreaks took place in a hospital and represented a particular challenge for epidemiological and laboratory investigations as a substantial number of vaccinated healthcare workers (HCWs) developed benign clinical signs and symptoms of measles. We discuss these findings and highlight the need to expand the European Union (EU) measles case definition, in order to increase sensitivity in case capture among vaccinated individuals with modified measles and who do not meet the current European Union (EU) case definition…

Since the measles vaccine was introduced in the Portuguese National Immunisation Programme in 1974, the country has achieved a consistent and sustained high immunisation coverage against measles (> 95%) [11,14]. HCWs are at higher risk of measles exposure because the high intensity of the exposure and subsequent transmission to vulnerable patients… According to the National Measles Elimination Programme, HCWs are recommended to receive two doses of measles vaccine (either single measles-containing vaccine or MMR) or to have evidence of previous measles infection… However, measles outbreaks in healthcare settings are becoming more frequent in the European Region…

Countries, such as Portugal, which maintained a high vaccination coverage for many years and had eliminated measles, are at greater risk of modified measles cases emerging during outbreaks… Modified measles mainly affect young adults who were adequately vaccinated but with the last dose of the vaccine administered more than 10 years prior.

In one chain of transmission, a hospital cluster was identified and most cases were HCWs vaccinated with two or more doses of MMR vaccine. This was described in other outbreaks… and may be related to waning of vaccine-induced immunity in the absence of natural boosting by the wildtype virus…

The outbreaks described here, which included a number of cases with modified measles and a large number of cases among vaccinated HCWs, highlight the need for further investigation in order to recommend innovative approaches in future outbreaks: Nearly half of these cases would not have been identified using the current EU case definition.

Augusto, G. F., et al (2018, Abstract)

[20]

Another outbreak in a hospital situation has recently been reported in the Netherlands, again, amongst fully vaccinated health workers with very little spread and the typical presentation of modified and milder Measles as documented below.

Measles Outbreak Among Previously Immunized Healthcare Workers, the Netherlands, 2014

We investigated a measles outbreak among healthcare workers (HCWs) by assessing laboratory characteristics, measles vaccine effectiveness, and serological correlates for protection…

Cases were laboratory-confirmed measles in HCWs from hospital X during weeks 12–20 of 2014…

Eight HCWs were notified as measles cases; 6 were vaccinated with measles vaccine twice, 1 was vaccinated once, and 1 was unvaccinated… Among 106 potentially exposed HCWs, the estimated effectiveness of 2 doses of measles vaccine was 52%…

Measles occurred in 6 twice-vaccinated HCWs, despite 2 having adequate pre-exposure neutralizing antibodies. None of the twice-vaccinated cases had severe measles, and none had onward transmission, consistent with laboratory findings suggesting a secondary immune response…

Results of long-term follow-up studies of measles virus immunity among twice-vaccinated cohorts who have not been exposed to wild-type measles virus show considerable waning of immunity, raising the question whether a booster MMR vaccination is necessary…

Recent results by Fiebelkorn et al, however, suggest that administering a third dose of MMR to twice-vaccinated individuals has a limited long-term effect on the height and quality of the immune status… Larger studies to further explore the effects of MMR-3 are urgently needed.

… Enhanced surveillance and detailed laboratory characterization of measles vaccine failures will be crucial to establish the long-term effectiveness of measles vaccination programs.

Hahné, S. J. M. et al (2016)

[21]

However, as noted above, a third dose MMR may not be the solution to the waning vaccine immunity crisis as apparently, due to a more recent study indicates that this may not be that effective or particularly long-lasting either. Perhaps, given the increasing mildness of such outbreaks, to the point where we are finding it increasingly difficult to even spot the outbreaks these days, we should not worry so much.

Take for example, the two physicians who contracted Measles without knowing it and because they were fully vaccinated they never thought for one minute they had the Measles and then, they went on to expose their patients, but everyone was fine, including unvaccinated individuals and at least now, these doctors won’t have to worry about having to keep getting vaccinated or, passing their infection on to their patients.

Two Case Studies of Modified Measles in Vaccinated Physicians Exposed to Primary Measles Cases: High Risk of Infection But Low Risk of Transmission

In 2009, measles outbreaks in Pennsylvania and Virginia resulted in the exposure and apparent infection of 2 physicians, both of whom had a documented history of vaccination with >2 doses of measles-mumps-rubella vaccine. These physicians were suspected of having been infected with measles after treating patients who subsequently received a diagnosis of measles.

The clinical presentation was nonclassical in regard to progression, duration, and severity. It is hypothesized that the 2 physicians mounted vigorous secondary immune responses typified by high avidity measles immunoglobulin G antibody and remarkably high neutralizing titers in response to intense and prolonged exposure to a primary measles case patient. Both of the physicians continued to see patients, because neither considered that they could have measles. Despite surveillance for cases among contacts, including unvaccinated persons, no additional cases were identified.

Rota, J. et al (2011, Abstract).

[22]

Where does all this leave herd immunity? After all, we are so often told that if only we could achieve at least 95 per cent vaccination uptake, there would be no Measles outbreaks and everyone, including those who cannot be vaccinated, would be protected.

However, in a strange sort of way we may be witnessing a means of bringing about more solid and robust community immunity back to pre-vaccine era levels (certainly to levels seen in Ireland before we introduced the vaccine against Measles), but, in a sort of ironic twist in all of this – we may already have greater community immunity than we realise, due in large part to vaccine failure, and we so firmly believed and hoped that One-Shot Would Be For Life, never mind, three or four and still counting.

All in all, secondary Measles vaccine failure is now recognised as more common than previously thought as more and more of our populations are growing up fully dependent upon vaccine-derived protection and not being boosted by naturally much these days, unless an outbreak occurs and then, they might end up with a modified form ultimately leading to lifelong immunity in the long run.

Now, as Jenner’s vaccine protection against Smallpox waned significantly within a fairly short period, this ironically may have allowed the natural pathogen to fully resolve itself by more natural means in the end. Therefore, for much of its history, and despite our best efforts, almost nobody grew to maturity without having the Pox in the end and ultimately became immune to dying as a result of having the infection whilst growing up, or as their vaccines wore off.

Well, it now looks like the story of our remarkable resistance to dying from the Measles may be due to maternal protective antibodies becoming increasingly attenuated (weakened) and a much less virulent virus as each generation is exposed is somewhat similar – only its story began a little later in history than Smallpox and, because of this, we are making its particular history as we speak.

Therefore, although we do not have the full picture as yet, it is hoped that nature will fully resolve the whole thing, despite our best efforts to eradicate this virus by more artificial means, in the end.

THIS ARTICLE IS BASED UPON CHAPTER 14 of ‘Don’t Count Your Children ’til they’ve had the Pox: Becoming Ancestrally Immune to Dying from Once Deadlier Contagions’

Plague to Polio in Ireland and Beyond by M.B. O’Hare

…Read more chapters by directly downloading the PDF version available on the previous blog on this website here (there is also an option to get the full version PDF of the entire book for review upon request at the end of the blog post).

And, or, you could take a look on Amazon.com for the published book by clicking on either the paperback or Kindle version below:

Paperback: 'Don't Count Your Children 'til they've had the Pox
Click on the book to find out more on AMAZON.COM
Kindle Book 'Don't Count Your Children 'til they've had the Pox'
Click on Kindle version of the book to find out more on Amazon.com

References:

[1] CDC (2015) Epidemiology and Prevention of Vaccine-Preventable Diseases, 13th Edition, CDC.gov p. 209 [Available online as PDF]: https://www.cdc.gov/vaccines/pubs/pinkbook/downloads/meas.pdf

[2 Hendriks, J., & Blume, S. (2013). Measles Vaccination Before the Measles-Mumps-Rubella Vaccine. American Journal of Public Health, Vol. 103 [8], pp.1393–1401. doi.org/10.2105/AJPH.2012.301075 [Available online]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007870/

[3] National Immunisation Office, (2018) Previous vaccine schedules, hse.ie. [Available online]: https://www.hse.ie/eng/health/immunisation/whoweare/vacchistory.htm

[4] Hendriks, J., & Blume, S. (2013). Measles Vaccination Before the Measles-Mumps-Rubella Vaccine. American Journal of Public Health, Vol. 103 [8], pp.1393–1401. doi.org/10.2105/AJPH.2012.301075 [Available online]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007870/

[5] Smallman-Raynor, M, and Cliff, A (2012), Atlas of Epidemic Britain: A Twentieth Century Picture, Oxford University Press, Oxford. p. 50. [Available online Google Books]: https://books.google.ca/books?id=iMnN4fZrj70C&pg=PA48 – v=onepage&q&f=false

[6] Institute of Medicine (US) (1994). 6, Measles and Mumps Vaccines; in, (eds.) Stratton KR, Howe CJ, Johnston RB Jr., Adverse Events Associated with Childhood Vaccination, Evidence Bearing on Causality. Vaccine Safety Committee Washington (DC): National Academies Press (US). [Available online]: https://www.ncbi.nlm.nih.gov/books/NBK236288/

[7] Wood, D.L & Brunell, P. A., (1995) Measles Control in the United States: Problems of the Past and Challenges for the Future. Clinical Microbiology Reviews, American Society for Microbiology, Vol. 8, [2], Introduction, Conclusions, p. 260, [Available online as PDF]: https://cmr.asm.org/content/cmr/8/2/260.full.pdf

[ibid]

[8] CDC (2019) Reported Cases and Deaths from Vaccine Preventable Diseases, United States CDC pinkbook tabulations from May 2019 [Available online as PDF]: https://www.cdc.gov/vaccines/pubs/pinkbook/downloads/appendices/e/reported-cases.pdf

[9] Wood, D.L & Brunell, P. A., (1995) Measles Control in the United States: Problems of the Past and Challenges for the Future. Clinical Microbiology Reviews, American Society for Microbiology, Vol. 8, [2], p. 265 [Available online as PDF]: https://cmr.asm.org/content/cmr/8/2/260.full.pdf

[10] Niewiesk, S., (2014) Maternal Antibodies: Clinical Significance, Mechanism of Interference with Immune Responses, and Possible Vaccination Strategies, Immunology, Vol. 3 [446], doi:  10.3389/fimmu.2014.00446 PMCID: PMC4165321 [Available online]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4165321

[11] Gans, H. A. & Maldonado, Y. A. (2013) Loss of Passively Acquired Maternal Antibodies in Highly Vaccinated Populations: An Emerging Need to Define the Ontogeny of Infant Immune Responses, The Journal of Infectious Diseases, Vol. 208, [1], pp. 1–3. doi.org/10.1093/infdis/jit144 [Available online]: https://academic.oup.com/jid/article/208/1/1/796926

[12] Allam M. F. (2014). New measles vaccination schedules in the European countries?. Journal of preventive medicine and hygiene, Vol. 55 [1], Summary, pp. 33-34. [Available online]: http://www.ncbi.nih.gove/pmc/articles/PMC4718332/

[13] Waaijenborg, S., Hahné, S. J., Mollema, L., Smits, G. P., Berbers, G. A., van der Klis, F. R., de Melker, H. E., & Wallinga, J. (2013) Waning of Maternal Antibodies Against Measles, Mumps, Rubella, and Varicella in Communities With Contrasting Vaccination Coverage, Journal of Infectious Diseases, Vol. 208, [1], pp. 10–16, doi.org/10.1093/infdis/jit143 [Available online]: https://www.ncbi.nlm.nih.gov/pubmed/23661802

[14] Chen C. J., Lee P. I., Hsieh Y. C., Chen P.Y., Ho Y. H., Chang C. J., Liu D.P., Chang F.Y., Chiu C.H., Huang Y. C., Lee C. Y., & Lin T. Y. (2012), Waning population immunity to measles in Taiwan, Vaccine, Vol. 30, [47], pp. 6721-7. Abstract, doi: 10.1016/j.vaccine.2012.05.019. [Available online]: https://www.ncbi.nlm.nih.gov/pubmed/22634294/

[15] Davidkin, I., Kontio, M., Mikko P & Heikki P. (2010) MMR vaccination and disease elimination: The Finnish experience. Expert Review of Vaccines. Vol. 9. pp. 1045-53. [Available online]: https://www.researchgate.net/publication/46169080_MMR_vaccination_and_disease_elimination_The_Finnish_experience

[16] Kang, H. J., Han, Y.W., Kim, S. J., Kim, Y-J., Kim, A-R., Kim, J. A., Jung, H-D., Eom, H. E., Park, O., & Kim, S. S. (2017) An increasing, potentially measles-susceptible population over time after vaccination in Korea, Vaccine, Vol. 35, [33], Conclusion, pp. 4126-4132, doi.org/10.1016/j.vaccine.2017.06.058. [Available online]: http://www.sciencedirect.com/science/article/pii/S0264410X17308551

[17] Avramovich E, Indenbaum V, Haber M, Amitai Z, Tsifanski E, Farjun S, Sarig A, Bracha A, Castillo K, Markovich M. P and Galor I. (2017) Measles Outbreak in a Highly Vaccinated Population – Israel, MMWR Morbidity and Mortality Weekly Report, Vol. 67, [42]: pp. 1186-1188. doi: 10.15585/mmwr.mm6742a4. PMID: 30359348; PMCID: PMC6290812. [Available online] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6290812/

[18] Chen, C. J., Lin, T. Y., & Huang, Y. C. (2018). Letter to the editor: Occurrence of modified measles during outbreak in Taiwan in 2018. Euro Surveillance: Bulletin European sur les maladies transmissibles – European communicable disease bulletin, Vol. 23, [37], doi:10.2807/1560-7917.ES.2018.23.37.1800485, [Available online]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6144468/

[19] Komabayashi, K., Seto, J., Tanaka, S., Suzuki, Y., Ikeda, T., Onuki, N., Yamada, K., Ahiko, T., Ishikawa, H. & Mizuta K. (2018) The Largest Measles Outbreak, Including 38 Modified Measles and 22 Typical Measles Cases in Its Elimination Era in Yamagata, Japan, 2017, Japanese Journal of Infectious Disease, Vol. 71, Summary, pp. 413–418, [Available online]: https://www.jstage.jst.go.jp/article/yoken/71/6/71_JJID.2018.083/_pdf/-char/en

[20] Augusto G. F., Cruz D., Silva A., Pereira N., Aguiar B., Leça A., Serrada E., Valente P., Fernandes T., Guerra F., Palminha P., Vinagre E., Lopo S., Cordeiro R., Sáez-López E., Neto M., Nogueira P. J. & Freitas G. (2018) Challenging Measles Case Definition: Three Measles Outbreaks in Three Health Regions of Portugal, February to April 2018. Euro Surveillance. Vol. 23, [28], Abstract: doi: 10.2807/1560-7917.ES.2018.23.28.1800328. [Available online]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6152152/

[21] Hahné, S. J. M., Nic Lochlainn, L. M., van Burgel, N., Kerkhof, J., Sane, J., Yap, K. B., van Binnendijk, R. S. (2016) Measles Outbreak Among Previously Immunized Healthcare Workers, the Netherlands, 2014, The Journal of Infectious Diseases, Vol. 214, [12], pp. 1980–1986, doi.org/10.1093/infdis/jiw480 [Available online]: https://academic.oup.com/jid/article/214/12/1980/2631197

[22] Rota, J., Hickman, C., Bae, S. S., Rota, P., Mercader, S., & Bellini, W. (2011). Two Case Studies of Modified Measles in Vaccinated Physicians Exposed to Primary Measles Cases: High Risk of Infection But Low Risk of Transmission. The Journal of infectious diseases. Vol. 204 Supplement 1. Abstract. pp. 559-63. doi:10.1093/infdis/jir098. [Available online]: https://www.researchgate.net/publication/51212588_Two_Case_Studies_of_Modified_Measles_in_Vaccinated_Physicians_Exposed_to_Primary_Measles_Cases_High_Risk_of_Infection_But_Low_Risk_of_Transmission

Why Nature Deserves the Credit for the Dramatic Decline in Deaths from Once Deadlier Infectious diseases – NOT US – & Why this Matters More than Ever Today!

PDF

Don’t Count Your Children ’til they’ve had the Pox, Becoming Ancestrally Immune to Dying from Once Deadlier Contagions_ 

Click above to read a substantial PDF with full chapters and sections (taken from a recently published book) which, will give you the essentials of confirming why Nature should be given all the credit for the dramatic decline in deaths from once deadlier contagions and why this matters so much today…

Request a REVIEW COPY of the full version of: ‘Don’t Count Your Children ’til they’ve had the Pox’ by filling out the form below the book cover.

Cheers & Enjoy!

MariaBrigit

1 front cover plague2polio final artwork

 

Epigenetics explains why it is Nurture, not so much Nature (your genes), that changes your destiny…

As you will see throughout much of the research within this blog and as presented in the videos below, our scientific insights into epigenetics are the game-changer in the genetic Roulette of life. Your genes are not your destiny – your experience is. This certainly changes the old Nature vs. Nurture debate towards Nurture being the main-driver. Only thing is, it comes with quite a big bit of responsibility – but, epigenetics turns out to be very empowering and highly relevant to all of our lives.

This, of course, couldn’t be further from living under the old regime of the Neo-Darwinian dogma that claimed that your genes were selfishly and slavishly-driven survival machines and there wasn’t a jot you could ever do to change them! (Anyone familiar with Richard Dawkins’ perspective should know what I am referring to).

You might also like to watch my own little video about my background and how I got to researching everything about epigenetics and how this led to me questioning the entire science behind the old Neo-Darwinian dogma and perhaps bringing back Lamarck instead! If you don’t know what I am on about, take a look around this blog and you should come to understand.

Cheers

MariaBrigit

Would We Survive the Spanish Flu if it Returned Today? Apparently, we would, as most of us have become ancestrally immune to dying from just about every strain going & yet to come…

Link to Source Image

(Note that all the quotes are referenced with clickable links at the end of this article)

WHATEVER HAPPENED TO THE SPANISH FLU AND WOULD WE EVER SEE ITS LIKES AGAIN?

Just to put Influenza into perspective in terms of its impact across our emerging modern nations, the following quote will give you an idea of the sort of numbers of deaths we are talking about. Bear in mind that the world by the early 20th Century is much more heavily populated than it was back in the Middle Ages when the Great Plague ran rampant.

The influenza pandemic of 1918

The influenza pandemic of 1918-1919 killed more people than the Great War, known today as World War I (WWI), at somewhere between 20 and 40 million people. It has been cited as the most devastating epidemic in recorded world history. More people died of influenza in a single year than in four-years of the Black Death Bubonic Plague from 1347 to 1351. Known as “Spanish Flu” or “La Grippe” the influenza of 1918-1919 was a global disaster…

Bodies pil[l]ed up as the massive deaths of the epidemic ensued. Besides the lack of health care workers and medical supplies, there was a shortage of coffins, morticians and gravediggers… The conditions in 1918 were not so far removed from the Black Death in the era of the bubonic plague of the Middle Ages.

 Billings, M. (1997)

[1]

Why this major pandemic Flu came to be known as the Spanish sort is revealed in the following along with a very interesting pattern of the different waves of Influenza and what may have fueled its rage when it hit nearly all of the world between 1818-1819.

Limerick City and the Spanish Influenza Epidemic, 1918-19

The name ‘Spanish Influenza’ came about not because it originated in Spain but because Spain was the first country to report, uncensored and unbiased, on the spread of the disease, due to its neutrality in World War I.  It occurred in three waves; the first in spring 1918, the second in October/ November 1918 and the third in spring 1919…

. The demobilisation of troops in November 1918 (Armistice Day) could possibly account for the second wave of influenza which proved to be more deadly than its predecessor…

Buckley, M., (2014, 81)

[2]

Children in America even came up with a rhyme about this great pandemic as it swept across America and people could be arrested in the street if they sneezed as documented by Buckley in the following:

Limerick City and the Spanish Influenza Epidemic, 1918-19

…in Chicago, the police were instructed to arrest anybody who sneezed in public…

as the epidemic in America gathered speed, school children even came up with a rhyme about it to skip by…

I had a little bird and its name was Enza,

I opened the window and in-flew-Enza.

[ibid]

The situation in Ireland as recorded at the time and established from the historical accounts since reveals the impact felt across our nations as we were going through a near-déjà vu of the Great Plague of the Middle Ages many centuries earlier.

Recall the rhyme that children used to recite ‘ring-o ring-a rosies… and they all fall down…’ about the Great Plague of old? Essentially, the first wave of Influenza is also described as being mostly confined to the main ports and then it appeared to become more aggressive and wider spread – impacting our entire nation by the second wave that had reached even the far reaches of the country by Christmas time (just as the Great Plague of the similar pattern for the Great Plague?). This can be seen in the following documenting the Flu’s arrival on Ireland’s shores.

Limerick City and the Spanish Influenza Epidemic, 1918-19 continued…

In Ireland, the first verifiable outbreak of the first wave can be traced to Cobh, when a US Naval ship, the USS Dixie, docked there in May 1918.

It seems that the first wave was somewhat more contained th[a]n the subsequent waves as it did not affect the entire country …

Confirmation of the onset of the second wave came from Howth during late September and this time all areas of the country were infected.

By Christmas, all counties had suffered an outbreak in both rural and urban areas…

[ibid]

The death toll was massive for such a small nation as Ireland. However, it was proportional to what other regions all around the world, both great and small, were feeling. Just to put this into perspective, it is estimated that hundreds of thousands had become ill from the Flu and maybe as many as 21,000 died in Ireland from the Spanish Flu of 1918-19. For such a small nation, this had a significant impact

Review of: The Last Irish Plague: The Great Flu Epidemic in Ireland 1918-19, by Catriona Foley

…between spring 1918 and early summer 1919, resulted in the sickness of over 800,000 people on this island, and the related death of almost 21,000 of them (statistics of the Registrar General of Ireland 1918-19)…

Jones, M. (2016, Ill-Prepared)

[3]

Interestingly, the rest of the excerpted article goes on to describe how, running concurrently with this great pandemic, our scientists were frantically trying to find a solution, to what they obviously believed would keep killing relentlessly, unless we could stop it in its tracks, although, it proved unsuccessful as outlined below.

Review of: The Last Irish Plague: The Great Flu Epidemic in Ireland 1918-19, by Catriona Foley

From the early months of the Influenza Pandemic – in Ireland as elsewhere, attempts were underway in universities and laboratories in pursuit of a therapeutic vaccine for influenza.

They did not succeed: this influenza type infection was undoubtedly lethal, and they knew that it was not a bacteria; but they simply did not know, at this stage in the pandemic, precisely what order of complexity they were dealing with.

[ibid]

 

The Taming of the Flu

Now, when we assess the overall mortality for this spectacularly severe pandemic of 1918-1919, we can see that as bad as the statistics are worldwide and within our respective populations, we should bear in mind that for much of the greater proportion of those who got the Flu and fell ill, the result was not a death sentence. However, for its victims and their loved ones, it certainly would not have looked that way. The case to fatality rate is given in the following excerpt and it might surprise you just how many actually survived the Spanish Flu.

1918 Influenza: the mother of all pandemics. Could a 1918-like Pandemic Appear Again? If So, What Could We Do About It?

In its disease course and pathologic features, the 1918 pandemic was different in degree, but not in kind, from previous and subsequent pandemics.

Despite the extraordinary number of global deaths, most influenza cases in 1918 (>95% in most locales in industrialized nations) were mild and essentially indistinguishable from influenza cases today.

Taubenberger, J. K., & Morens, D. M. (2006)

[4]

Therefore, as tragic and ultimately devastating as the Spanish Flu was for so many families and communities, the vast majority survived the infection and even got off quite lightly in terms of suffering. It is hard to believe just how many survived the great Flu epidemic.

Furthermore, nobody knew that soon after, almost as suddenly as Enza flu in, this great pestilence flew out again. We know this from accounts on the ground at the time within Ireland as indicated within a newspaper article in the ‘Irish Times’ dating to the era.

November 9th, 1918: Relief as deaths from 1918 Spanish flu epidemic began to decline

Irish Times

IT WAS authoritatively stated yesterday that the influenza epidemic in Dublin is abating. The statement was based on the fact that there are very few fresh cases within the past few days…

On the whole, he stated, there was a decline.

Joyce. J (2009, Nov. 9th)

[5]

A similarly dramatic decline in deaths was beginning to occur around the world and as indicated below, it seems that rapidly developing immunity was emerging depending upon the degree of previous exposure individuals were experiencing. This begins to give us a very strong clue to why the deaths from Influenza were declining almost as rapidly as they had risen in the second wave.

Pathogenic Responses among Young Adults during the 1918 Influenza Pandemic

During the 1918 pandemic period, military nurses and medical officers were intensively and repeatedly exposed to the influenza A (H1N1) pandemic strain in clinics, in ambulances, and on crowded open wards. However, during the lethal second wave, nurses and medical officers of the Australian Army had influenza-related illness rates similar to, but mortality rates lower than, any other occupational group …

Similar observations were made in other groups of military and civilian health care workers … These findings suggest that the occupational group with the most intensive exposure to the pandemic strain had relatively low influenza-related pneumonia mortality rates during the second wave …

During the fall of 1918, all 40 large mobilization/training camps throughout the United States and Puerto Rico were affected by influenza epidemics…

During the camp epidemics, influenza–pneumonia mortality rates were inevitably highest among the soldiers with the least military service.

In the US Army overall, 60% of those who died of influenza-related pneumonia were soldiers with <4 months of military service …

Shank, D. & Brundage, J.F (2012)

[6]

In other words, the more exposed, the greater your resistance to the worst effects of these pathogens you became, and conversely, the least exposed and most naïve your immune system the more vulnerable you were in the face of the pathogen. Another dimension to this immunity conferred by natural exposure is addressed next:

How historical disease detectives are solving mysteries of the 1918 flu

The pattern of deaths by age was also intriguing. Young adults in their late 20s were at heightened risk. In contrast, influenza infections were frequent among teenagers, but these infections were mild. Senior adults were also less likely than young adults to die from influenza …

Why were older adults spared? One popular explanation is that well-connected populations who had seen influenza in the 19th century would be protected upon the return of a similar virus decades later. This is known as the “antigen recycling” hypothesis.

This hypothesis gained more traction during the 2009 pandemic, when older populations had higher levels of prior antibodies and therefore were less likely to die than younger populations.

…Moreover, patterns of infection and death may depend upon people’s prior immunity, imprinted by circulation of similar viruses within the last century.

The Conversation (2018, 5th March)

[7]

As indicated above, we may be looking at protection gained from previous exposure to a similar strain of Influenza in the face of another, even if it is much more potentially devastating. A type of memory imprinting may occur. This phenomenon may go some way to explaining the unusual age distribution of those impacted the worst during the Spanish Flu pandemic of 1918-1919, which appears to echo far down into the future.

Now, for instance, as highlighted above, it was some of our strongest, healthiest and fittest members of our populations who suffered the greatest fatalities during the Spanish Flu pandemic and we can perhaps apply this imprinting phenomenon to explain this to some extent. We can perhaps imagine that the equally unusual circumstances of high mobility and returning troops and medical personnel  (nurses and doctors) as the war drew to a close may help explain such a pattern.

For instance, these circumstances may have given this strain of Influenza unprecedented opportunities to expand beyond their previously more restrictive horizons to previously unexposed fresh victims who had very little experience at all with any of the Flu strains either, the first wave of Influenza that was milder or pandemic Influenza from the earlier era before they were born. Thus, they would have been ripe for the picking. Recall also that their more seasoned comrades caught up in the war effort would have been more familiar with the virus strains from working in the field longer than themselves. It was the newest recruits that were the most vulnerable due to lack of previous exposure as documented earlier.

In other words, if you didn’t have any previous exposure to the Flu viruses in general, or exposure to previous epidemics/pandemics, or became relatively immune to dying from the second wave because you experienced the first less severe wave, then, you would have been the pockets of the population most vulnerable to dying when the second wave hit.

The greater detrimental impact of the young adult and fittest population may therefore, not only reflect the fact that compared to their more seasoned counterparts who had been exposed to Flu viruses in general, or their older counterparts who were old enough to remember other great Flu outbreaks, but, the circumstance of returning home from the war itself may have caused them to miss the window of opportunity to become naturally immunised when the Spanish Flu was milder (the first wave) and metaphorically and literally missed the boat on this one.

They may have been shielded from the first Flu wave (milder form) due to being so dispersed around the world and mostly confined to either the front or barracks when it circulated around the world. Their particular infantry may not have had the opportunity to be immunised in the first round; unlike their younger siblings safely tucked up at home.

This begins to also explain how teenagers tended to get off so lightly (as noted in the above excerpt discussing the unusual age distribution of attack), perhaps simply, as they were too young to go off to war in the first place and therefore, having to stay at home, they did get the opportunity to become exposed to the milder first wave of Influenza that their older siblings didn’t.

Even the younger infant types fared relatively well comparatively speaking as seen in some studies of the unusual demographic.  However, this may also be explicable to some extent as this age group would have been protected to some degree from the worst effects of the Flu if she herself had experienced a little of the first wave whilst at home. Although, pregnant mothers may have been a little more susceptible as indicated in some of the literature, as this is a vulnerable time for their immune systems anyway.

In other words, if you didn’t have any previous exposure, either before the rise of the Spanish Flu, or from frequent exposure to a more usual circulation of Influenza or, became relatively immune to dying from the second wave because you experienced the first less severe wave (as suggested in the previous excerpt), then, this would have been the very population most vulnerable to dying when the second wave hit – the young and otherwise healthy and fit adult population returning from war.

We find further clues to this phenomenon of rapid resistance built up from prior natural exposure with strong and incredibly long-lasting molecular imprinting – even in elderly people who had experienced the Spanish Flu first hand as children and who were still alive within our modern era to tell the tale as documented in the following excerpt.

Neutralizing antibodies derived from the B cells of 1918 influenza pandemic survivors.

Nature

Little is known about naturally occurring adaptive immunity to this virus; however, some elderly survivors are still living. We sought to determine whether survivors exhibited evidence of acquired immunity to the virus. Expression of the 1918 HA antigen allowed us to identify and characterize protective antibodies induced by natural exposure of humans to the 1918 pandemic virus.

We identified a panel of 32 subjects aged 91-101 years (i.e., aged 2 to 12 years in 1918), many of whom recalled a sick family member in the household during the pandemic, which suggested direct exposure to the virus. Of the subjects tested, 100% exhibited serum neutralizing activity against the 1918 virus .., and 94% had serologic reactivity to the 1918 HA (…), even though these samples were obtained nearly 90 years after the pandemic.

-Thus, these studies reveal that survivors of the 1918 influenza pandemic possess highly functional, virus-neutralizing antibodies to this uniquely virulent virus, and that humans can sustain circulating B memory cells to viruses for many decades after exposure – well into the tenth decade of life.

Yu, X., et al. (2008).

[8]

This relationship between exposures to different strains over the course of the 20th Century and into the early 21st Century giving cross-protection is summarised in the following.

Your flu risk may be linked to the year you were born
CNN

Scientists stunned by own discovery
Influenza A viruses can be categorized into two groups, and within these groups, there are subtypes: H1, H2 and H5 are in group 1, and H3 and H7 are in group 2. Only three subtypes — H1, H2 and H3 — have circulated in humans worldwide from 1918 to 2015, according to the study.

As it turned out, the researchers found that people born before 1968 were more likely to be exposed to the group 1 viruses H1N1 or H2N2 and were less likely to suffer or die from infections with the group 1 virus H5N1 infections later in life. In 1968, there was an influenza pandemic that had a multinational impact.

The 1968 pandemic marked the transition from an era of group 1 viruses to a group 2-dominated one, the researchers wrote in the study.
Therefore, people born after 1968 were more likely to be exposed to the group 2 virus H3N2 at a young age and were less likely to suffer or die from infections with the group 2 virus H7N9 later in life. For both groups, exposure at a young age not only lowered the risk of a severe infection with either H5N1 or H7N9, it reduced the risk of death by up to 80%, the researchers wrote in their study.

Howard, J., (2016, 10th November)

[9]

However, some Flu strains began behaving quite unnaturally as outlined in the following. Although, this may have something to do with an accidental escape whilst we were trying to create a means of stopping the Flu from circulating entirely.

The Problem Child of Seasonal Flu: Beware This Winter’s Virus H3N2 is deadlier than many other influenza strains

For a long time, it was flu dogma that only one influenza A virus could circulate at once. The H1N1 virus that caused the 1918 Spanish flu disappeared when the H2N2 virus that touched off the Asian flu pandemic emerged in 1957. Then in 1968, H3 muscled out H2.

But in 1977, something odd happened. H1N1 reappeared—likely as the result of a laboratory accident. And what was thought to be impossible—two influenza A strains circulating at the same time—was shown to be possible. When the 2009 pandemic started, flu researchers hoped it would push the reset button.

They hoped the new virus—an H1N1 virus that had been circulating in pigs—would drive out both the old H1N1 and H3N2. The old H1N1 viruses did disappear. But H3N2 viruses didn’t budge. For the time being, we’re stuck with this unpleasant virus.

Branswell, H. (2018, 9th January)

[10]

As highlighted by the title of the above article, the persistent strain was to be feared the most, but, this season has come and gone as of the time of writing here, so thankfully, it didn’t cause massive death-tolls and besides, as discussed previously, having exposure to this particular type conferred fairly solid protection in the face of other strains (cross-protection) against other similar group strains that might be encountered later in life.

Therefore, our latest problem child (N3N2), as it only erupted in the late 1960s, may eventually disappear (or become less obvious) like its older counterparts, it is seemingly just a matter of exposure and time, until almost all of us become immune to that one as well.

Furthermore, we can gain a real-time insight into such infections from natural exposure and subsequent immunity during different Flu seasons in the following study which reveals just how quickly and robustly our immune systems adapt to all sorts of strains, including cross-protection from more familiar types to even those that have morphed rather dramatically and how the natural immune response can even deal with less than natural strains too; the returned A H1H1 hybrid (possibly escaped lab) strain of the 1970s.

Infection with influenza A H1N1: Effect of past experience on natural challenge

Following its reintroduction in 1978 influenza A HIN1 spread widely in the child population. By the autumn of 1979, 75 % of 11-year olds entering a boys’ boarding school had detectable antibody. The protective effect of previous experience could be assessed during two outbreaks in the school. In the first outbreak in 1979, 90 % of those known to have been infected in the previous year were protected against reinfection…

Previous experience conferred over 90 % protection against infection. Between the 1979 and the 1983 outbreaks there was no overt evidence of A HIN1 activity in the school although a few sporadic infections were identified in those investigated routinely or in connection with other infections…

First, with the re-emergence of A HINt in 1978, infections were virtually confined to young people. Those old enough to have had experience of strains before 1957 seemed to be immune.

Secondly, our own observations on A H3N2 in the school (Hoskins et al. 1979) suggested that natural infection gave good protection even against strains which had undergone considerable antigenic drift.

Thirdly, the 1979 outbreak showed that recent infection with A HINt gave good protection against reinfection.

Davies, J.R, Grill, E.A., & Smith, A.J (1985, Summary)

[11]

Not only did the boys survive their ordeal and were now almost all immune for life from being directly exposed to a strange attenuated mutant gone wild, most definitely, by all accounts manipulated by man (whatever the actual point of origin, it was humanly manipulated – that much everyone agrees), but, they also showed immunity to Flu strains upon re-exposure in other Flu seasons.

Also of interest, as also noted in the above article, is that it was observed from other related studies that exposure to the A H3N2 strain (that newer tricky type which appears to have morphed considerably by fully natural means, what is called antigenic drift) resulted in fairly robust resistance even though these boys had no previous exposure to that particular variant before. This is what is called cross-protection from being exposed to another Flu strain that is not too dissimilar.

All in all, it would appear that we have built up quite an arsenal of immunity against all sorts of strains over the course of our life due to continual exposure, sometimes not even knowing it and the really good news is that these seasonal exposures can give you lifelong protection, but also set you up with some mighty protection against a pandemic strain that you haven’t even experienced yet as highlighted in the excerpt below.

Age-dependence of the 1918 pandemic

Birth year dependence of H5N1 and H7N9 avian flu cases

A growing body of epidemiological evidence indicates reduced risk of pandemic infection in those with previous seasonal exposure, and lifelong protection against viruses of different subtypes but within the same HA Group

Woo, G (2018, 11)

[12]

That is fairly impressive cross-protection due to exposure to naturally circulating Flu viruses when we see that these exposures can provide protection to future pandemic strains (new mutations that impact the world) that haven’t even happened yet!

It certainly is beginning to look like our immune systems have been doing a fine job defending us over the generations and it may be worth being exposed to the real thing as it seems that at the very least, we are ensuring protection directly and indeed, indirectly against future strains. This becomes clearly evident when we take a closer look at our most recent pandemic – the first one of the 21st Century.

As we revisit our most recent worldwide pandemic, the 2009 Swine Flu outbreak, more research has emerged that demonstrates the possible cause of such low mortality figures across our nations (we will discuss the low mortality of this most recent pandemic shortly) may relate to the strains of Flu you were exposed to throughout your life, whether you knew it or not as indicated above and specifically from epidemiological data as indicated in the following

Immunity to Pre-1950 H1N1 Influenza Viruses Confers Cross-Protection against the Pandemic Swine-Origin 2009 A (H1N1) Influenza Virus

The 2009 H1N1 influenza virus outbreak is the first pandemic of the twenty-first century.

Epidemiological data reveal that of all the people afflicted with H1N1 virus, <5% are over 51 y of age. Interestingly, in the uninfected population, 33% of those >60 y old have pre-existing neutralizing Abs against the 2009 H1N1 virus.

This finding suggests that influenza strains that circulated 50–60 y ago might provide cross-protection against the swine-origin 2009 H1N1 influenza virus.

Skountzou, I., et al. (2010)

[13]

This dynamic protection across our lifespans and preparing us for future outbreaks due to exposure is perhaps the very reason why we see such a dramatic decline in deaths from Influenza since the Spanish Flu era within Ireland as seen in the graph below (Fig. 1).  It really does look like we have become robustly resistant, if not fairly immune, to just about all the strains that have been circulating over the last century?

Flu Mortality Ireland

FIGURE. 1: Individual number of annual Deaths from Influenza in Ireland from 1864 until the mid-1990s when the cause of death was classified differently,  being combined with Pneumonia in the registrar. Arrow denotes when the vaccine began to be offered to ‘at risk’ groups.  It was noticed that deaths from Pneumonia were significantly declining across death registers from different regions when assessed (although not specifically dealt with in this present study) and presumably deaths from Pneumonia would also fully resolve in time following the same near-universal pattern seen for Influenza across our industrialised nations.

Notice that in Figure 1 shows the individual number of deaths recorded from Influenza alone, annually in Ireland since official records began that there were epidemic years prior to the more significant rise in deaths during the Spanish Flu pandemic of 1918-19. You will see that the overall longer-term trend of the major spikes representing deaths from pronounced epidemics thereafter become less and less as we progress through the 20th Century.

Note also that the Irish data does not record deaths from Influenza after the mid-nineteen-nineties as the official cause of death changed at that point to include Pneumonia. Furthermore, we know from the continued data recorded from other sources that deaths from Influenza after this point or even for the first pandemic of the 21st Century would hardly register on the above graph compared to what went before. It is only really since the 2009/10 (Swine Flu era) that the vaccine has been offered in Ireland to a broader range of individuals beyond the elderly and their carers.

This overall decline in deaths since the Spanish Flu era to marginal figures in our modern era is a pattern shared across our diverse nations where statistics of this kind are available. For instance, if we examine the graphs generated from statistics relating to deaths resulting from Influenza within the U.S. and compare this data directly with the Irish graph, the only difference between them is one of scale.

The proportion of deaths for a massive population in the U.S. would obviously be greater than a relatively tiny population within a country like Ireland. See Figure 1, Crude mortality per 100000 population, by influenza season (July to June of the following year), for seasons 1900–1901 to 2003–2004 (a) in, Doshi, P. (2008), Trends in Recorded Influenza Mortality: United States, 1900–2004  [14].

Similarly, near-identical patterns of proportional deaths from Influenza over the same essential timeframe can be found in, Twentieth-century mortality trends in England and Wales, Figure 5, showing the age-standardised mortality rates for Influenza in England and Wales from 1901 to 2000 by Griffiths C and Brock A (2003) [15].

Indeed, the pattern of declining deaths from Influenza since the great pandemic of 1918-19 would appear to be a near-universal pattern experienced across our developing nations where an investigation into any of the relevant studies and statistics that are available recording deaths from this once deadlier contagion over a related timeframe consistently demonstrates.

This commonality of a dramatic decline is further supported by the worldwide estimates of deaths recorded for each of the major Influenza pandemics that near-simultaneously swept across almost all our nations commencing with the mother of them all, the Spanish Flu of 1918 until around 1920.

Influenza Virus (Flu)

There were three influenza pandemics in the 20th century – the “Spanish” flu of 1918-19, the “Asian” flu of 1957-58, and the “Hong Kong” flu of 1968-69.

The 1918 flu, caused by a strain of H1N1, was by far the most deadly. More than 500,000 people died in the United States as a result of the Spanish flu, and up to 50 million people may have died worldwide…

The 1957 pandemic was due to a new H2N2 strain of influenza virus that caused the deaths of two million people, while the 1968 pandemic resulted from an H3N2 strain that killed one million people.

One pandemic has occurred so far in the 21st century. This was due to the novel swine-origin H1N1 virus which emerged in 2009.

Baylor College of Medicine (1998-2008)

[16]

And our most recent Swine Flu pandemic of 2009/10 produced worldwide statistics as low as just under 20,000 deaths as seen in the excerpt below.

Pandemic (H1N1) 2009 

WHO: Weekly update

6 AUGUST 2010

– As of 1 August 2010, worldwide more than 214 countries and overseas territories or communities have reported laboratory confirmed cases of pandemic influenza H1N1 2009, including over 18449 deaths.

World Health Organisation (2010, update no. 12)

[17]

Since, the time of the above report, as this figure was so unexpectedly low – just over 18,000 deaths worldwide for the greatest pandemic of the 21st Century, there has been much debate and different estimates have since been projected using various mathematical modelling with widely divergent results. Perhaps we will never know the true figure of our most recent Flu pandemic. However, we do have some statistics from Ireland that would appear to suggest that the worldwide figure was not that far off.

For instance, as tragic as this was for the family and loved ones of those that did die directly from the 2009/10 Swine Flu pandemic, it turns out that the combined number of documented deaths for the Swine Flu pandemic in Ireland over this same period through to 2014 totalled just over twenty (as obtained from tracking the main stories at the time and statistics that were given from our major news outlets) – a figure that is so low that it would virtually not be visible on the graph above if we plotted it.

Now, if we review the figures for the preceding influenza season (2007/08), just before the Swine Flu outbreak of 2009/10 we can see just two registered deaths in the over 65s (usually the elderly – much older group – are the most susceptible, but, bearing in mind that the Swine Flu and its ancestor, the Spanish Flu impacted the younger adult population most) in the whole of Ireland reported as follows.

Summary Report of 2007/2008 Influenza

Mortality Data

(Ireland)

During the 2007/2008 influenza season, two deaths attributed to influenza were registered with the General Register Office. These deaths were both in adults over 65 years of age, one in HSE-NW registered in week 8 2008 and one in HSE-S registered in week 14 2008. It should be noted that the death registered in HSE-S was not a laboratory confirmed case of influenza.

The Health Protection Surveillance (2009)

[18]

Further support for the fact that deaths from Influenza have continued to plummet to historic lows in our modern era since the Spanish Flu, statistics are also available for the actual incidence of cases of Influenza itself that would tend to suggest that we are not even catching the Flu as often these days.

For instance, a study out of the UK which followed Flu seasons spanning forty years, (just prior to the last pandemic starting in 2009) also noted that the cases of Influenza have also gradually receded as highlighted in the following with an indication that the ability of the viruses to adapt to multiple strains may, in fact, have their limit

Lessons from 40 years’ surveillance of influenza in England and Wales

We show a gradually decreasing trend in the incidence of respiratory illness associated with influenza virus infection (influenza-like illness; ILI) over the 40 years and speculate that there are limits to how far an existing virus can drift and yet produce substantial new epidemics.

Fleming, D. M., & Elliot, A. J. (2007)

[19]

Therefore, perhaps it is a good thing that our rates of mortality and morbidity had already dwindled along with our cases of Influenza significantly due to this highly robust cross-immunity protection well before we began to intervene with the natural immunity cycle to any great extent, as where would we be then without our exposure?

However, it seems that we haven’t been able to come up with a good alternative to natural immunity anyway, as you will see in the following article, therefore, perhaps our failures are a blessing in disguise

Are Flu Viruses Smarter than us?

Here’s why it’s so hard to make a better flu vaccine

Imagine you work in a high-security building. It uses facial recognition technology to keep out known intruders. It works well, until someone figures out how to use clever makeup, or even just grow a moustache to game the cameras. No matter how often the intruders are caught, new infiltrators find new disguises to help them get in.

That’s a little bit how the immune system works, and the flu virus is gaming that recognition technology. It sneaks past the body’s immune system to cause misery and mayhem, even as new vaccines update the biological equivalent of facial recognition software. Each year, a new influenza vaccine is formulated and distributed, and each year, viruses develop ways to evade them. Flu vaccines are never as effective as other vaccines, and the current vaccine only provides partial protection against the ongoing flu epidemic.

It’s an annual guessing game of sorts, one backed by data but also plagued with uncertainty. And when the guesses don’t exactly match the reality, as happened this past year, it can mean a dismal and deadly flu season. “We’ll do the best we can,” said Daum, a Chicago doctor who heads the Food and Drug Administration advisory committee that makes the recommendations. But “the virus is smarter than we are at this point. I don’t know of any disease that plagues us more. It’s very, very frustrating and a very inexact science. . . . We do it with varying luck, and I think the luck is mostly the virus’s whim.

Fox, M. (2018 Feb. 14th)

[20]

The reason I suppose our health officials worry so much about protecting us from Influenza is that not many of them think to look at the actual mortality statistics that paint a somewhat more reassuring, and certainly more realistic picture of what is going on from the ground up. By all accounts discussed thus far, we are almost all already fairly resistant against all strains of these pathogens.

But, you may not blame them if you realise the type of statistical estimates and projections that they follow, which are essentially built upon assumptions modelled on Spanish Flu-like proportions pandemics lurking behind every normal Flu season. These models have been criticised as being often too broad, ill-defined and frequently contradictory and vary widely from one another depending upon the systems used as discussed in some detail by, Doshi, P. (2008), in Trends in Recorded Influenza Mortality: United States, 1900–2004  [21].

As noted earlier, in reality, as you will see from a recent study below, getting the actual Flu isn’t even as common as you might think and for almost all of us, it isn’t even that problematic. Just because the Flu circulates each season, doesn’t mean you’ll get it; most of us don’t and those that do, don’t even know they have the infection because it is so mild (asymptomatic) according to a long-term study as excerpted below:

Three-quarters of people with flu have no symptoms

“‘77% of flu infections’ have no symptoms, say experts,” reports ITV News. The news is based on a large community-based study carried out in England, which found that most people with influenza (“flu”) don’t have symptoms, and even if they do, only a small proportion go to a doctor.

The study was part of Flu Watch – a larger, ongoing study to assess the impact of flu on public health in England – and analysed five groups of people over six periods of influenza transmission, between 2006 and 2011. Participants provided blood samples before and after the influenza season, so that the amount of antibodies in the blood could be measured. They were then contacted every week so that cough, cold, sore throat, or any “flu-like illness” could be noted down. If any of these were experienced, participants were asked to complete a symptom diary and to take a nasal swab to test for the influenza virus.

Approximately 20% of people had an increase in antibodies against influenza in their blood after an influenza “season”. However, around three-quarters of infections were symptom-free, or so mild that they weren’t identified through weekly questioning. This is very much a “good news, bad news” story. It is good news in that so many people with a flu infection are spared the burden of a nasty infection. However, limiting the spread of a future pandemic could be challenging, as it would be unclear who is infected.

NHS, News (2014, 17th March)

[22]

 

 

Thankfully, as we have already been exposed to so many strains of Influenza over the generations, it seems that we are, for the most part, ready for just about any form that those influenza viruses can morph into.

Why Revive a Deadly Flu Virus?

New York Times Magazine

Flu viruses mutate very rapidly, and each season’s version is a little different. But your immune system preserves a memory of its previous encounters with a flu, which are dragged up, like old photographs from the back of a closet, every time your system responds to a new flu invasion.

Shreevejan, J. (2006, Jan. 29th)

[23]

The name of the game would appear to be, exposure and the more exposed you are, the greater your resilience and ultimate immunity, even to strains (cross-strain protection) that you may not have directly encountered as studies discussed above strongly suggest.

And certainly, this long-term memory is very encouraging indeed, as although there doesn’t appear to be any fundamental distinction between the Spanish Flu of 1918-19 and 2009 some ninety years later that would make one genetically more virulent than the other, the main difference appears to be our level of innate and generational resilience to the virus and all its variants due to simple exposure.

This gives us hope, particularly if someone released something like the Spanish type Flu upon our populations in say, a bioterrorist attack, which, is addressed in the next excerpt.

Scientists Believe They Have Explained The Great Flu Outbreak Of 1918

…The good news here is that much of the population has now been immunized against numerous strains of flu. While these might not be enough to stop people getting sick from a novel version, it should keep the death rates down if we experience something as potentially devastating as the 1918 outbreak again.

Luntz, S. (2014, 4th May)

[24]

So, essentially, nothing happened to the Spanish Flu; it never went anywhere in particular; it is just probably finding it difficult to infiltrate our mighty defences thanks to our sophisticated protein recognition system. In other words, we have been naturally immunised, now, isn’t that reassuring?

But, it gets better, as even more reassuring is the fact that overall, these Influenza viruses may have already lost a great deal of their earlier killing power by virtue of the fact that they have been circulating within us as their host over so many generations, further supporting the ideas that if Spanish Flu was genetically engineered and released out into the public, most of us may not even notice.

A clue came when investigating some communities who had gotten off rather lightly as the most virulent eruptions of the Spanish Flu reached its tentacles into some of remotest parts of the world, but yet, many communities survived relatively unscathed who had no previous exposure, mild or otherwise to this viral pathogen. How?

The Places that Escaped the Spanish Flu

BBC

“These communities basically shut themselves down,” explains Howard Markel, an epidemiological historian at the University of Michigan who was one of the authors of the study. “No one came in and no one came out. Schools were closed and there were no public gatherings. We came up with the term ‘protective sequestration’, where a defined and healthy group of people are shielded from the risk of infection from outsiders.”

…When these measures were lifted in November 1918, as reports of cases in San Francisco were on the decline, the base experienced only mild cases, but at least three people did die…

But there may be some benefit to keeping the virus out for as long as is possible. American Samoa implemented a five-day quarantine for all boats that kept influenza from its shores until 1920. When it finally did arrive, the virus appears to have lost much of its sting and there were no deaths attributed to influenza in a population of more than 8,000. The main island of Samoa to the northwest, however, lost around a fifth of its population to the pandemic…

A similar story unfolded on the on the Australian island of Tasmania, which implemented strict quarantine measures for boats arriving on its shores that required all passengers and crew to be isolated for seven days. When the infection penetrated the island in August 1919, medical officers reported that it was a milder infection than that on the mainland. The death rate on Tasmania was one of the lowest recorded worldwide.

Gray, R., (2018, 24th October)

[25]

What happened? Quarantine should have meant that these people were just as vulnerable whether they were exposed to the pathogen at the beginning of the invasion or about a week later and had only delayed the inevitable. But, that is not what occurred. The cause of this strange, but, very reassuring anomaly of the timing and decreasing impact of the Spanish Flu pandemic becomes clearer when we look to other similar patterns as documented from epidemiological studies and observations on the ground at the time summarised next:

The Story of Influenza 1918 Revisited

One of the more interesting epidemiologic findings in 1918 was that the later in the second wave someone got sick, the less likely he or she was to die, and the more mild the illness was likely to be.

This was true in terms of how late in the second wave the virus struck a given area, and, more curiously, it was also true within an area. That is, cities struck later tended to suffer less, and individuals in a given city struck later also tended to suffer less. Thus west coast American cities, hit later, had lower death rates than east coast cities, and Australia, which was not hit by the second wave until 1919, had the lowest death rate of any developed country.

Again, more curiously, someone who got sick 4 days into an outbreak in one place was more likely to develop a viral pneumonia … than someone who got sick 4 weeks into the outbreak in the same place…

The best data on this comes from the U.S. Army. Of the Army’s 20 largest cantonments, in the first five affected, roughly 20 percent of all soldiers with influenza developed pneumonia. Of those, 37.3 percent died…

In the last five camps affected—on average 3 weeks later—only 7.1 percent of influenza victims developed pneumonia. Only 17.8 percent of the soldiers who developed pneumonia died…

Inside each camp the same trend held true. Soldiers struck down early died at much higher rates than soldiers in the same camp struck down late. Cities struck later in the epidemic also usually had lower mortality rates… The same pattern held true throughout the country and the world… places hit later tended to suffer less…

Barry, J. M (2005)

[26]

As discussed in the rest of this article, it was difficult to reconcile some of the hypotheses offered for this strange phenomenon and, therefore, another explanation was required. One hypothesis that is offered by the author of the above study, albeit admittedly highly speculative, does appear to fit the evidence a whole lot better and is therefore excerpted in summary form below:

The Story of Influenza 1918 Revisited continued…

…At the peak of the pandemic, then, the virus seemed to still be mutating rapidly, virtually with each passage through humans, and it was mutating toward a less lethal form.

We do know that after a mild spring wave, after a certain number of passages through humans, a lethal virus evolved. Possibly after additional passages it became less virulent. This makes sense particularly if the virus was immature when it erupted in September, if it entered the human population only a few months before the lethal wave.

[ibid]

In other words, this rapid mutation to increased virulence and ultimately, a much less lethal form, may have been due to the number of pathogen passages (infections in individuals and their spread to others) through their human hosts. That doesn’t mean that this strain became genetically mutated, it just means that something may have occurred within the behaviour of the viral pathogens in the context of their human host – a dilution or filtering effect as the viruses passed through and between more and more people (hosts) during the outbreak.

Now to take this a little further, none of this would show up genetically, so we have to infer a plausible scenario from what we know of the behaviour of viruses within a host and some of the defences we might put up to defend ourselves against them.

For instance, we could say that the very fact that viruses require cells/hosts to begin replicating, unlike bacteria, viruses are not actually free-living independent organisms, perhaps they took a while to establish the full takeover (hijacking) of the host’s molecular machinery to get going (the first wave milder form), but once the immune system identified what they were doing (wreaking havoc in the second wave), it found a way to begin disarming these viral replicators and we find the milder impact again during the third wave.

This would explain how those exposed later in the pandemic, even in the same army barracks, towns and cities would fare better than those exposed earlier. It would also begin to explain how those remote islanders were able to protect themselves just long enough to only encounter the much attenuated/filtered viral form of the infection and still gain immunity.

We could call this the generational immunising effect, which completely concurs with McNeill’s hypothesis regarding the same as highlighted in the introduction of this present study [27].

This immunising effect over generations may have made these viruses more and more attenuated each time they passed through generations. Is this why our mortality graphs all look so similar and all the strains of Influenza look weaker and weaker on each passing season and pandemic over the course of the last hundred years?

Moreover, there is also an indication that Nature has taken care of our future resilience and immunity too. For instance, recently emerging molecular evidence takes this dynamic of non-inherited transference of protection somewhat further. It is now looking quite likely that our immune systems can memorise past battles with pathogens, even well into the future, across the generations even when the threat is no longer present in an obvious way as indicated in the excerpt below.

RETHINKING THE ORIGIN OF CHRONIC DISEASES

Some modern-day diseases reflect the capacity of organisms to “memorize” responses to external signals and transmit them across generations …

the original causative agent may not be extant today, but “memory” of the infection has persisted.

Shoja, M.M et al, (2012)

[28]

This type of generational imprinting, passing on environmental information, and all the necessary adaptations to all sorts of threats and experiences gleaned from past battles with a vast array of pathogens that can be passed on to our offspring obviously, tells us that it is not all in the genes as we once thought.  As the title and rest of the following excerpt suggest, our ancestral battles with the bugs is not a genetic one.

Your Immune System Is Made, Not Born

New research dispels the belief that the strength of the body’s defense system is genetically programmed

Landhuis, E. (2015)

[29]

We have only in more recent times began to gain deeper insights into just how adaptable and responsive the immune system actually is. Seemingly, just about every living thing can rapidly respond and defend itself from danger and threats, particularly infectious disease, without having to wait around for millions of years in hope that we might end up with the lucky genes that will save us.

Now, it looks very likely that we can inherit this hard-fought-for immunity, not just from our mother’s directly, but from their mother’s and perhaps generations of mothers before them as suggested by the following study – at least in pigeons, but that’s only because we haven’t looked yet, at least not in terms of generational immunity transference, but, we can certainly pass on just about everything else via molecular imprints for just about everything else that has been studied. And, these memory molecules are looking increasingly like they go back further; it is just simply that our scientists have not thought to look further than indicated next.

GRANDMOTHERS CAN PASS IMMUNITY TO THEIR GRANDCHILDREN, AT LEAST IN PIGEONS

At the moment of birth, a newborn leaves behind its safe protective environment and enters a world teeming with bacteria, parasites, viruses, and infectious agents of all sorts. However, the babies do have one trump card: antibodies and immune compounds passed across the placenta from their mothers. These short-lived molecules can dip into mom’s immunological experience to protect the newborn until the immune system gets up to speed.

Now, a new study in pigeons suggests that some baby birds owe their early immunity not just their mothers, but to their grandmothers as well.

…previous research has suggested that these early maternal immune compounds may have “educational effects” on the newborn’s developing immune profile—that they may somehow be priming the system to be on the lookout for common local diseases or parasites…

Shultz. D (2015)

[30]

In other words, as indicated in the excerpt above, adaptation and resistance to disease appear to be handed down through generations – and presumably, this also applies to humans. This, of course, goes directly against our current dogma of genetically driven adaptation, but, with so many studies emerging supporting this non-genetic inheritance, this dogma is finally changing and more studies are exploring such adaptive forms of evolution.

This gives us hope that even if a great infectious contagion of the past that once devastated our communities and loved ones, that due to natural immunity across the generations, even our children’s children may not have to face the same again. This could be the very reason why we don’t hear of those once deadlier and thankfully, for most of us, long-forgotten diseases. Maybe Influenza will ultimately go the same way. In other words, we may have now forgotten those once deadlier diseases that our ancestors battled with, but our immune systems have thankfully not.

So, the future looks brighter perhaps than we had imagined. Therefore in answer to the question posed at the beginning, would we survive the Spanish Flu if it re-emerged today, I think we most certainly would and it seems our children and their offspring might actually become fully immune to it in the not too distant future and would also survive the Spanish Flu if it re-emerged even generations later. Therefore, perhaps it would be prudent to leave this natural generational immunity cycle well alone so that we can continue to pass on those long-lived memory molecules to our offspring! We may be becoming immune to dying from Influenza along with just about every other once deadlier contagion of the past and within our more modern era.

THIS ARTICLE IS TAKEN FROM A CHAPTER IN A NEW BOOK ENTITLED: Plague to Polio in Ireland & Beyond. ‘Don’t Count Your Children ’til they’ve had the Pox: Becoming Ancestrally Immune to Dying from Once Deadlier Contagions?’ by M. B. O’Hare

You can read more chapters on this blog from previous articles posted here (there is also a full version PDF for review if you want to request it at the end of the linked article).

And, or, you might like to find out more about the published book by visiting Amazon.com by clicking on the images of your preferred version (Paperback or Kindle) below.

 

Paperback: 'Don't Count Your Children 'til they've had the Pox
Click on the book to find out more on AMAZON.COM
Kindle Book 'Don't Count Your Children 'til they've had the Pox'
Click on Kindle version of the book to find out more on Amazon.com

Bibliography

[1] Billings, M. (1997) The influenza pandemic of 1918, Stanford Education [Available online]: https://virus.stanford.edu/uda/

[2] Buckley, M. (2014) Limerick City and the Spanish Influenza Epidemic, 1918-19, Critical Social Thinking, Vol. 6, p. 81. School of Applied Social Studies, University College Cork, Ireland. [Available online as PDF]: https://www.ucc.ie/en/media/academic/appliedsocialstudies/cstpdfs/vol6/MargaretBuckley.pdf

[ibid]
[ibid]

[3] Jones, M. (2016) Ill-Prepared, Review of: The Last Irish Plague: The Great Flu Epidemic in Ireland 1918-19, by Catriona Foley, Dublin Book Reviews http://www.drb.ie/essays/ill-prepared

[ibid]

[4] Taubenberger, J. K., & Morens, D. M. (2006) 1918 Influenza: the mother of all pandemics. Could a 1918-like Pandemic Appear Again? If So, What Could We Do About It? Emerging infectious diseases, Vol.12, [1], pp. 15-22 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3291398/

[5] Joyce. J (2009) November 9th, 1918: Relief as deaths from 1918 Spanish flu epidemic began to decline, The Irish Times (Nov. 9th, 2009) [Available online]: https://www.irishtimes.com/opinion/november-9th-1918-relief-as-deaths-from-1918-spanish-flu-epidemic-began-to-decline-1.768576

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[ibid]

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