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Dr Frederick Lamont Gates, Rockefeller Institute and swine influenza in 1918
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118275/
The first potential blow to Pfeiffer's theory came from Peter Olitsky and Frederick Gates at The Rockefeller Institute. Olitsky and Gates took nasal secretions from patients infected with the 1918 flu and passed them through Berkefeld filters, which exclude bacteria. The infectious agent—which caused lung disease in rabbits—passed through the filter, suggesting that it was not a bacterium (3, 4). Although the duo had perhaps isolated the influenza virus (which they nevertheless referred to as an atypical bacterium called Bacterium pneumosintes), other researchers could not reproduce their results. One of the doubters was Oswald Avery (Rockefeller Institute), who developed a culture media—chocolate agar—that optimized the growing conditions for B. influenzae and thus minimized false negative results from patient samples. Thus, the idea that flu was transmitted by a filterable agent (or virus) was dismissed.
Pig farmers in Iowa had reported two outbreaks—one in 1918 and another in 1929—of a highly contagious, influenza-like disease among their animals. The disease bore such a remarkable resemblance to human flu that it was named swine influenza. Shope and his mentor Paul Lewis took mucus and lung samples from the infected pigs and attempted to isolate the disease-causing agent. They quickly isolated a bacterium that looked exactly like Pfeiffer's human bacterium (and was thus called B. influenzae suis), but when they injected the bacteria into pigs, it caused no disease (5).
Did a Military Experimental Vaccine in 1918 Kill 50-100 Million People Blamed as “Spanish Flu”?
https://australiannationalreview.com/state-of-affairs/did-a-military-experimental-vaccine-in-1918-kill-50-100-million-people-blamed-as-spanish-flu/
Summary
The reason modern technology has not been able to pinpoint the killer influenza strain from this pandemic is because influenza was not the killer.
More soldiers died during WWI from disease than from bullets.
The pandemic was not flu. An estimated 95% (or higher) of the deaths were caused by bacterial pneumonia, not influenza/a virus.
The pandemic was not Spanish. The first cases of bacterial pneumonia in 1918 trace back to a military base in Fort Riley, Kansas.
From January 21 – June 4, 1918, an experimental bacterial meningitis vaccine cultured in horses by the Rockefeller Institute for Medical Research in New York was injected into soldiers at Fort Riley.
During the remainder of 1918 as those soldiers – often living and traveling under poor sanitary conditions – were sent to Europe to fight, they spread bacteria at every stop between Kansas and the frontline trenches in France.
One study describes soldiers “with active infections (who) were aerosolizing the bacteria that colonized their noses and throats, while others—often, in the same “breathing spaces”—were profoundly susceptible to invasion of and rapid spread through their lungs by their own or others’ colonizing bacteria.” (1)
The “Spanish Flu” attacked healthy people in their prime. Bacterial pneumonia attacks people in their prime. Flu attacks the young, old and immunocompromised.
When WW1 ended on November 11, 1918, soldiers returned to their home countries and colonial outposts, spreading the killer bacterial pneumonia worldwide.
During WW1, the Rockefeller Institute also sent the antimeningococcic serum to England, France, Belgium, Italy and other countries, helping spread the epidemic worldwide.
https://de.findagrave.com/memorial/35217973/frederick-lamont-gates
On the declaration of war in 1917, Mr. Gates volunteered for the U.S. Army Medical Corps, was accepted and commissioned a first lieutenant. He was assigned to duty on the Rockefeller Institute staff where he gave lectures to military groups selected to attend training there. He was also assigned to visit training camps, in the interest of preventive medicine, and traveled widely. He continued at the institute after the war and his researches, especially those on influenza, received worldwide recognition. His health failed in 1927 and he was required to undertake a less demanding schedule. He continued his research at Harvard and moved his family to Cambridge, MA where he died, June 17, 1933, at age forty-six, after suffering a concussion from a fall.