(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)
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)
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.
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…
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)
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.
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)
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
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)
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)
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)
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.
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).
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
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)
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)
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)
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)
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)
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?
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 .
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) .
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)
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)
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
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)
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)
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)
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 .
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)
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)
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)
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
“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)
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)
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.
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 .
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)
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)
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)
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.
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