The Spanish flu and underlying questions

To say that what I do is compulsive is akin to saying a Marathon runner really enjoys running. He/she doesn’t enjoy the suffering, I don’t imagine, but feels a need to conquer some madness inside, some burning desire to excel at something that most people don’t think or care about, running. I read a lot, but not compulsively, that is, I feel no urge to complete a book start to finish, and if I don’t like what I’m reading, I set it aside. If I really don’t like what I’m reading, I ceremoniously toss the damned thing in the recycle bin. I would easily drop out of the marathon at mile marker 3.0. I don’t suffer that burning desire, and don’t understand those so motivated.

Anyway, when I encounter a book I like, I shortly thereafter forget its contents. I can actually read it again and it will hit me as brand new. So, long ago, I developed the habit of revisiting a book I liked not too long after finishing it, and transcribing passages I had read and flagged. The idea was that manually typing out those passages would seal them inside my cranium with some permanence.  It works! Sort of. These days I use transcription software, so typos abound, often comical, often hard to rectify without going back to the page of the crime.

The book I read recently is called “Can You Catch a Cold?”, Untold History of Human Experiments, by Daniel Roytas. (Video link here, Amazon link here.) I’m not big on credentials, but do note that the author lacks a “Dr.” before or a “PhD” after his name. But that does not matter if the only thing that matters is content. I also note that the book is not indexed, a true defect in my mind. Indexing is a time-consuming but worthy exercise. There are also some annoying typos  contained within, not uncommon in this time of self-published works. The “Forward by Dr. Samantha Bailey” helps some, as I like her and her husband Mark, but living on the outside of their chosen fields must be degrading, with the resultant preaching while in exile being more like circle jerking than actually reaching anyone. Nonetheless, truth is where it is found, and I tip my hat to those who labor onward.

All that in mind, I am going to cite a long passage from this book on the Spanish flu of the post-World War I era, as I found it revealing and gripping. Read it too if you can, or not. I seldom follow orders, and when someone tells me I need to read this or that, I usually continue on doing what I am doing without heeding the advice. I made it through high school in that manner, and yes, I missed a lot in the process, but agree with Paul Simon that most of it was crap.

So, if you start to read what follows and then say “Ah, fook this,” I get it.

Have fun! Or not. There is a payoff at the end, so skip there if you want. Or skip it all and go to my own brief observations at the very end, and share your own in the comments. I know of one person, not sure who, claiming that the Spanish Flu was a hoax. I do not believe that. I believe it real, and just as with polio and micro encephalitis and God only know what else, was blamed on a virus as a cover-up. That is, really, the true function of viruses.

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Begins at page 149:

Just like the Russian influenza pandemic of 1889, there are several peculiarities surrounding the Spanish flu. The first being its unusual pattern of spread. The pandemic was said to have appeared in Boston and Bombay on the same day, despite the city’s being separated by more than 12,000 km. Stranger still, the flu somehow took over three weeks to travel 300 km from Boston to New York, and more than a month to spread a mere 60 km from Joliet to Chicago. This period of spread seems inconsistent with human to human contact.

Even in desolate places, the dissemination of the disease seemed rather peculiar. In 1919, the governor of Alaska, Thomas Riggs, wrote a report to the U.S. Senate detailing the situation that was unfolding there. To prevent the spread of the disease, Riggs ordered the seaports closed. The very last ship to dock in Nome before the winter set in, was the Victoria, a steamship carrying mail and 30 passengers. Although the passengers were in a good state of health after the 11-day voyage, they were examined by three different doctors before disembarking. Once on dry land, they were placed in hospital quarantine for another five days. Every precaution was taken to protect the townsfolk, even the mail was fumigated for 10 hours before being collected by the Postal Service. Despite these measures, the people of Nome soon became ill. Apparently the quarantined passengers were “asymptomatically infected” at this time, spreading the disease throughout the town upon the release. The weather conditions were some of the worst in living memory. Travel was incredibly difficult and restricted entirely to snow-ready dog teams. The terrain was unforgiving, the days were short, and the temperature was freezing. This meant even experienced travelers could cover no more than 50 km on a good day. But to put things in perspective, some towns were so remote, that even in optimal conditions it took over a month for news to arrive that World War I had ended. Yet, the pandemic still managed to sweep across the state, allegedly carried by mailman and hunters as they went from town to town. Despite having a population of just 50,000 people, who were thinly dispersed across a vast area of wilderness roughly the size of Europe, Alaska suffered one of the highest mortality rates per capita of anywhere in the world.

The second peculiarity is that there were three waves of Spanish flu in the first year alone. The pandemic spread back and forth across the Earth for the first time in the spring of 1918; a second time in the autumn just a few months later; and a third time in the winter of 1918-19. The fourth and final wave occurred between late 1919 and mid-1920. The waves were relatively brief, lasting just three or so months, disappearing for three months, and then returning for the same amount of time. Many considered it unusual that distinct waves could re-occur in such a timeframe, especially when it took more than three years for the same number of waves to hit during the Russian influenza pandemic. This is atypical of influenza more generally, which normally hits during a single season each year.

The third. Here peculiarity is that about half of the people who died of Spanish flu were young adults, specifically males between 20 and 40 years of age. This is rather unexpected considering mortality rates in previous and subsequent pandemics were highest among children and older adults. Though the scientific and medical communities put forth different explanations (e.g. the “cytokine storm” hypothesis), none were properly substantiated, so this anomaly remains a mystery. Another puzzling piece of information is that civilian and military healthcare workers such as doctors, nurses, and ambulance officers had mortality rates lower than any other occupation. How did the front-line workers evade the most infectious and lethal form of flu the world had ever seen, despite regular close contact with sick and dying patients? Given their heightened risk, it is miraculous that they were found to have the best chances of surviving the pandemic.

Even in the face of these three peculiarities, the most perplexing aspect of the pandemic was the greatest disparity of symptoms experienced by those struck down by the disease. Much like the Russian flu, doctors described a wide variety of “strange” and “inconsistent” forms of Spanish flu [Table 2, page 152]. These forms were protean enough to convince doctors there must be multiple pandemics of different diseases occurring simultaneously. In fact, the symptoms were so unusually diverse, that doctors were mistaken into thinking the Spanish flu was the bubonic plague, while others misdiagnosed it as typhoid fever, dengue fever, or cholera.

There were at least four different types of Spanish influenza described in the literature: (1) a normal form indistinguishable from the seasonal flu, characterized by typical symptoms (e.g. chills, fever, headache, sore throat, nasal congestion) lasting 3 to 4 days, (2) a severe form characterized by more significant respiratory symptoms (e.g. pneumonia and bronchitis), (3) gastrointestinal form characterized by respiratory symptoms plus nausea, vomiting and diarrhea, and (4) a phthisic form resembling tuberculosis (i.e. coughing up blood). As stated previously, germ theory subscribes to the premise that “one germ causes one disease”. If this is true, how then is it possible that the same influenza virus could cause such a broad and varied array of symptoms?

In addition to varying considerably in form, the Spanish flu also appeared to vary dramatically in severity. During the first wave, doctors around the world reported the pandemic could not be influenza because the symptoms were so mild. However, subsequent waves struck with much greater intensity. In September 1918, Col. William Welch, who was stationed at Camp Devens in Massachusetts, examined the lungs of a dead soldier and stated the disease must be a new kind of infection or plague. Similarly, a pathologist for the United States Public Health Service, remarked that the lungs of the dead were unlike any other form of pneumonia he had ever come across. Every day, hundreds of people dropped dead in the street, despite waking up completely healthy just a few hours prior. To confuse matters even further, a very well-known medicine manufacturer of cold and flu remedies (who are still manufacturing the same product to this day) published newspaper advertisements claiming that authorities were in agreement that the disease was nothing more than an old-fashioned flu masquerading under a new name.

The worst case of Spanish flu started as what seem like any normal bout of the flu. Before long, mild symptoms like dyspnoea would rapidly progress to bronchitis and then pneumonia. By the time people had been rushed to hospital, they already had dark “mahogany” spots on their cheekbones – the beginning of cyanosis (i.e. skin color changes from lack of blood oxygen). The spots on the cheekbones soon expanded over the entire face, before spreading to the rest of the body in just a few short hours. Cyanosis – a hallmark symptom of the Spanish flu – may have been caused by thick, purulent yellow sputum blocking the airways. Some describe it as “the most vicious type of pneumonia that has ever been seen”. The cyanosis was very distinct in that the whole body would turn a deep-purple color, making it impossible to tell dark skinned people from light-skinned. Hence it was often named “Black Flu”, or “Purple Death”.

In the most extreme cases of Spanish flu, people bled from the ears, eyes, mouth and nose. People’s hair and teeth fell out and, in many instances, their bodies emitted a strange smell reminiscent of musty hay or straw, symptoms which are atypical of influenza. Few were lucky to survive once they had become cyanotic, as they often developed right-sided heart failure. The main symptom of Spanish flu was haemorrhagic tracheobronchitis (respiratory tract inflammation and bloody sputum), which appeared suddenly and was often fatal. It was not uncommon for people to die within as little as 24 hours after the onset of symptoms. However, the average time of death was around 10 days – a consequence of a so-called secondary bacterial pneumonia “superinfection”.

PAYOFF (My title) (Pages 153-159)

The Spanish flu was also unique in that it coincided with World War I. In the summer of 1918, American troops approaching the Western Front slowed to a crawl after experiencing an unprecedented number of casualties among the ranks. More than 43,000 had already died at that point, not due to combat, but because of pandemic influenza. Such losses were by no means insignificant, amounting to 80% of the total number of combat deaths recorded for the entire war. Indeed, the Spanish flu crippled military efforts by incapacitating up to 40% of the United States Army and Navy personnel with illness.

As previously mentioned, there is much debate as to where and how the pandemic began. Some historical records point to the first cases emerging from military posts, such as a British base camp at Etaples in Northern France during the winter of 1916, or a British barracks at Aldershot in March 1917. Coincidentally, at these two bases, more than 100,000 soldiers were stationed in treacherous and unsanitary conditions. Inhabitants huddled together in cramped tents pitched on ground contaminated with thousands of tons of chemical warfare agents known as “battle gas”. Battle gas had been deployed by German forces as early as 1915 and was used unforgivingly throughout the entire duration of the conflict. Living in such conditions would have undoubtedly had deleterious effects on even the most robust and battle-hardened soldiers.

During the Great War, over 150,000 tons of chemical warfare agents were produced worldwide, with approximately 125,000 tons being deployed on the battlefields. These gases persist in the environment for weeks, possibly months, after being deployed because they were heavier than air and not readily soluble in water. The gases were so poisonous, doctors were forced to evacuate entire wards if a man was brought in still wearing contaminated clothing. The gas residue on the affected individuals’ clothing readily dispersed into the air and would irritate the eyes of medical workers, making it impossible to see.

Despite its widespread use, the military was tight-lipped about battle gases and shared little or no information about the consequences of human exposure with doctors on the frontline. The only way for doctors to learn about the horrific effects was by treating victims in the field. They frequently encountered the most widely used battle gas, phosgene. This weapon was preferred because it was easy to manufacture, rapidly fatal at high concentrations, and exceptionally hard to detect. Upon detonation, phosgene gas was usually colorless and odorless – a true invisible enemy. However, it could present as a pale yellow or pale green cloud, with some reporting it had a smell reminiscent of musty hay, or freshly mown grass. Of the 90,000 men who died from exposure to battle gases during the war, 85% were killed by phosgene. Military forces also employed mustard, chlorine, and lewisite gases, but did so far less than phosgene because these were not typically colorless or odorless. This made them much easier to detect and evade. Alongside phosgene, the military implemented lacrimatory gases – also known as “blue gas” – throughout the war. Although not fatal, blue gas was originally thought to be fine enough to pass through a gas mask filter, causing violent irritation of the respiratory tract. The intention was to force soldiers to remove their gas masks, after which the enemy would deploy more lethal gases like phosgene. It was soon realized, however, lacrimatory gases could not penetrate gas mask filters, nevertheless, they were still widely used for strategic purposes.

Although inhaling large quantities of phosgene was almost instantly fatal, it could take up to 24 hours for victims to succumb to their injuries. To make matters worse, there were no effective treatments available for gas poisoning apart from oxygen therapy, which afforded only a minor reprieve. Records from an open-air hospital in Boston showed that patients with access to fresh air, sunlight, and hygienic facilities fared much better than their counterparts in enclosed wards. This contrasts markedly with the experience of frontline doctors and nurses who could do little more than comfort soldiers while they suffered an agonizing death. Gas-afflicted men who felt better after laying down for several hours would often die within minutes of getting up and moving about. Other victims ripped their clothes from their bodies as they asphyxiated to death, with some even committing suicide to escape the unbearable suffering.

Symptoms of severe gas poisoning were initially mild, presenting as a flu-like illness, before progressing rapidly over several hours to bronchitis, pneumonia, and pulmonary edema (an acute-respiratory-distress-like syndrome). Eventually, those severely poisoned with gas would die. Dyspnoea and cyanosis were hallmarks of gas poisoning. Men clutched their chests as they gasped for air. They coughed up blood and frothy yellow sputum as their bodies turned deep blue-purple color – a serious condition known as “heliotrope cyanosis”. The cyanosis was so pronounced, that many medical practitioners feared the Black death had returned. Despite the wide range of serious side effects, the lethal effects of poison gas were primarily due to respiratory failure and right-sided heart failure.

In instances of mild phosgene exposure, it could take up to 48 hours or longer for symptoms to develop. Mild cases presented as flu -like illness with delayed onset of symptoms including, but not limited to a persistent cough, bloodied and frothy yellow sputum, sneezing, general weakness lasting several weeks to months, irritated eyes and throat, chest tightness, pulmonary edema, nausea, vomiting, headache, runny nose, sinus pain, shortness of breath, hair loss, and heliotrope cyanosis. In moderate to severe cases, exposure to battle gases rapidly eroded the mucous membranes of soldiers, resulting in bleeding from the eyes, mouth, and nose.

Medical personnel believed poor living conditions, the stress of war and exposure to chemical agents all lowered soldiers’ immunity, making them more susceptible to an infection with Spanish influenza virus (H1N1). Although this is a plausible story, many other doctors at the time were unconvinced that military flu deaths were largely attributable to the pandemic. This is because, as the first gas victims began arriving at field hospitals, attending doctors could not help but draw parallels between the pathology of Spanish influenza and battle gas exposure.

When pathologists examined the lungs of soldiers poisoned with phosphene [should this read “phosgene”?] gas at autopsy, they were astonished to find that damage to the respiratory tract was remarkably similar to that of Spanish flu victims. Meanwhile, at world-leading universities, bacteriologists and pathologists also noted how closely the effects of influenza resembled poison gas inhalation when they examined tissue samples obtained during autopsy. Even revered influenza experts acknowledged a how reminiscent the lesions of Spanish flu infection were to poison gas inhalation. After the war had ended, doctors continued to learn about the effects of phosgene gas. They found that, when it was inhaled by soldiers, phosgene mixed with water vapor in the lungs to form hydrochloric acid (HCl), resulting in significant tissue damage. In follow-up animal experiments, they showed that inhaling HCl produced lesions in the lungs identical to those observed in patients who died of pandemic influenza. It’s no wonder, then, why people describe the pandemic as an “attack” or “invasion” that was “as dangerous as poison gas shells”. As illustrated in table 1.3 [Page 157], the symptoms of battle gas victims align very closely with those of Spanish flu patients. The two presented in a way exceedingly difficult to distinguish from one another.

The conflation of gas and flu is worsened by the fact they coincided in history. That is, the Spanish influenza pandemic occurred around the same time the companies were mass-producing and shipping chemical warfare agents for Armed Forces to deploy extensively on the front lines. As previously mentioned, over 150,000 tons of poison gases were produced worldwide during World War I. Of this, 68,000 tons were produced by the Germans, 36,000 tons by the French, 25,000 tons by the British and 2,500 tons by the Americans. Soldiers were regularly afflicted with phosgene poisoning and, therefore, the potential for a mixed diagnosis was significant. Unsurprisingly, there was also a higher incidence of Spanish influenza among employees working at phosgene gas manufacturing facilities, but not for workers at facilities manufacturing other types of battle gases, who were largely unaffected. Much like the military, it is possible that workers poisoned by phosgene gas manufacturing plants were also misdiagnosed with the Spanish flu.

Beyond exposure from battlefields and supply chains, there are other ways battle gas might have caused illness in distant locations. On 9 March 1918, in noxious pale-yellow gas cloud emanated from the Fort Riley military base in Kansas. Two days later, the first reported outbreak of Spanish flu in North America occurred at that very base. The official story states that the yellow cloud was a result of manure being burned, of which 9,000 tons per month were produced by the innumerable horses stabled there. Just as the manure was being incinerated, a sandstorm kicked up, blowing the stinking cloud across the base and surrounding areas. The cloud was claimed to contain an equine virus that infected the soldiers stationed there. Strange occurrences like this weren’t restricted to military installations. There were claims that German forces have been infiltrating allied countries around the world releasing “airborne agents” in cities and ports. In September 1918, Lieut. Col. Philip S. Doane – the head of Health and Sanitation Section of the Emergency Fleet Corporation – announced that the outbreaks of Spanish flu in the United States may have been the result of covert German military operations. He suspected German submarines had deployed spies along the coastline under the cover of night, who would then release “flu germs” in theaters or other crowded places. According to Doane, the Germans had already achieved this in Europe, so it was not unreasonable to think the same thing could happen on American soil.

Indeed, eyewitness accounts from civilians described camouflaged German ships sneaking into ports of major American cities under the cover of darkness and releasing “greasy looking gas clouds” into the air that wafted ashore. Similar claims were also made by media outlets in Brazil. For example, a prominent newspaper in Rio de Janeiro reported that Germans had put “germs” in bottles which were then dropped into the ocean near coastlines of allied countries. The bottles were then carried ashore by the current, dispersing the contents onto innocent civilians unfortunate enough to pick them up. Of course, it is impossible to confirm what these clouds and bottles contained, or if such events ever actually transpired. However, if these reports are true, it seems more plausible from a technological and logistical standpoint to release poison gas instead of flu germs, especially given the fact both afflicted people in the same way.

Many pertinent questions remain unanswered concerning the relationship between poisonous phosgene gas and Spanish influenza. First, if doctors could not tell one from the other, to what extent was gas poisoning mistakenly attributed to the flu? The highest Spanish flu mortality was recorded among males aged between 20 and 40 years – those most likely to have been exposed to chemical weapons in combat. Second, why did doctors, nurses, and those transporting the “infected” have the lowest mortality rates of any profession? It’s possible “sick” soldiers were frequently dying of gas poisoning – not influenza – meaning healthcare workers caring for them were being exposed to poisoned people, not infected people. Given that poisoning isn’t contagious, the lack of disease transmission in such cases could have been confused as “immunity” or “asymptomatic infection”. Third, and finally, why was the Spanish flu orders of magnitude deadlier than every other influenza before or after it? This influenza killed up to 100 million people, which is significantly more than the Russian flu three decades prior (up to 1 million deaths) and the Asian flu four decades later (slightly over 1 million deaths). Coincidentally, the worst year of the pandemic was 1918 – the final and deadliest year of the war, occurring in a narrow window in history where phosgene gas was widely dispersed into the atmosphere. Though these questions are difficult to resolve a century later, the connection between gas and flu is nonetheless interesting to ponder.

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OK, that’s it for transcription. Just a few observations: First, why any mention by the author of H1N1,  a virus not ‘discovered’ until 1931? The word “virus” existed prior to its formal introduction into the lexicon, but in those days there were no electron microscopes, so viruses could not have been thought to be anything more than very small particles, perhaps tiny, tiny bacteria. There could not have been any debate about H1N1 during the time of the Spanish influenza.

Second, how did the supposed deadly gases travel so far and linger so long as to be able to infect so many people so severely? The author mentions German agents deliberately infecting America from submarines, etc., and that would certainly explain its presence. In addition, it is safe to say it was being manufactured at Fort Riley in Kansas and so likely other places too. It just happens that at Riley we had the initial American outbreak of H1N1, excuse me, the Spanish influenza pandemic.

It’s a given in the practice of propaganda that official enemies are capable of dastardly deeds, like spreading poison gas, but unthinkable that our own people would do such a thing.

But go ahead and think it. I do.