Bird-Flu Fear Mongering and Disease Mongering

Bird Flu Basics

     Taubenberger and Morens provide a good overview of bird flu:

Taubenberger, J K and Morens, D M (2017). H5Nx Panzootic Bird Flu—Influenza’s Newest Worldwide Evolutionary Tour, Emerging Infectious Diseases, 23(2):340-342. https://doi.org/10.3201/eid2302.161963.

They inform us that influenza A viruses are a common feature of the environment, causing annual epidemics, sometimes pandemics, and various common infections in numerous animals. Wild aquatic birds (including ducks and geese) are the natural hosts where influenza A viruses live, multiply, and get transported over great distances during bird migrations. 

     These common viruses usually cause mild or no apparent symptoms in their animal hosts, but sometimes they switch to domestic birds like chickens and turkeys, where they can mutate in ways that they do not usually do in wild animals. The H5 and H7 subtypes can spontaneously mutate to become "highly pathogenic avian influenza" (HPAI) viruses that typically cause fatal infections in poultry and sometimes in wild birds that come into contact with poultry.

     In this context, the phrase "highly pathogenic" refers only to bird infections and has no bearing on whether humans can acquire symptoms or develop severe disease. The word, "pathogenic", by itself, means "capable of causing disease". The phrase, "highly pathogenic", then, essentially means "highly capable of causing disease". When used with "avian influenza", "highly pathogenic" describes the capability of the virus to cause disease in the particular animal that it has adapted to infect. Even though the HPAI (Highly Pathogenic Avian Influenza) classification is usually associated with high death rates in the species that it attacks, again, it does not apply to death rates or even severity of illness in humans.

     Fatal outbreaks of HPAI in domestic-chicken and turkey flocks are not new phenomena — they have been described for over 225 years. Such fatal outbreaks today attract more attention, probably because of the great demand for chicken and turkey products in the current, enormously-populated world of demanding consumers. A fatal outbreak can disrupt production and supply chains for these products, thus causing consumer panic and media hype on a large scale. 

     Human infection with bird flu is relatively rare. When human infection does happen, the reason is because certain people have a greater susceptibility, either because they work in close contact with animals and/or their individual makeup predisposes them to an opportune infection by a virus that takes advantage of this predisposition. Deaths in humans, although alarming, have happened precisely due to this ability of the virus to take advantage of individual differences in susceptibility, not because the virus has naturally adapted to humans.

If Rare in Humans, Then Why Fear Bird Flu?

     Today, academic journals, news media, internet discussions, and government information sources portray bird flu (also called "avian influenza" and "H5N1") as a virus dangerously poised to mutate into a catastrophically-lethal, human pathogen. Hellsten and Nerlich present valuable insight into this development:

Iina Hellsten and Brigitte Nerlich (2010). Bird Flu Hype: The Spread of a Disease Outbreak Through the Media and Internet Discussion Groups, Journal of Language and Politics, 9(3).

These authors queried multiple data bases to determine how many articles were being published on the subject of bird flu. Of the data bases they queried, from 1997 up until 2003, the number of medical-journal articles on the subject of H5N1 remained at around a steady 20-30 articles per year. After 2003, this number increased dramatically. From 2004 to 2006, the number of articles rose from 77 to 848 (an increase of over 1100% in two years). This more-than-exponential increase indicates that interest in the H5N1 virus had grown extraordinarily, which suggests that increased funding opportunities in epidemiological research had emerged to help drive such interest.

     Hellsten and Nerlich also found that, in a large sample of newspapers from around the world, between September and October of 2005 alone, stories about "bird flu" and "H5N1" increased from 412 per month to 2,495 per month (an increase of over 600% in that one month). The 10-times-greater publicity for bird flu in newspapers seemed driven by the enormous interest demonstrated in medical research. Such an explosion of interest on all fronts during such a relatively short time further suggests that major incentives and cooperative arrangements (out of general public view) had reached an unprecedented peak.

     Fear appears to have been an underlying driver of this massive surge in published articles on bird flu. The following two science-journal articles played a key role in highlighting this fear and leading popular news media to stoke this fear:

Taubenberger, J; Reid, A; Lourens, R et al. (2005). Characterization of the 1918 Influenza Virus Polymerase Genes, Nature, 437: 889–893. https://doi.org/10.1038/nature04230

Here we present sequence and phylogenetic analyses of the complete genome of the 1918 influenza virus and propose that the 1918 virus was not a reassortant virus (like those of the 1957 and 1968 pandemics), but more likely an entirely avian-like virus that adapted to humans.

Tumpey, T M; Basler, C F; Aguilar, P V; Zeng, H et al. (2005). Characterization of the Reconstructed 1918 Spanish Influenza Pandemic Virus, Science, 310(5745): 77-80.

Since 1918 virus gene sequences are related more closely with avian H1N1 viruses than any other mammalian H1N1 strains, it was of interest to determine whether the 1918 strain would be lethal for fertile chicken eggs, a pathogenic feature of avian H1N1 viruses. After serial titration in 10-day-old embryonated chicken eggs, the 1918 virus was lethal for chicken embryos ...

Taubenberger worked at a military pathology research facility at the time, and Tumpey was with the Centers for Disease Control and Prevention (CDC). One of the primary interests of both Taubenberger and Tumpey was and still is vaccine development for newly-emerging viral infections. Their two articles from 2005 demonstrated the structural similarity between the pathogenic H5N1 virus (the virus causing bird flu) and the Spanish Flu virus, popularly cited as causing the deaths of 40 million or more humans in 1917-1918. Their work in this area, no doubt, gave impetus to vaccine development for an as-of-yet non-existent viral mutation, with the resultant accelerated interest in profitable patents and profitable vaccines. Profit, thus, also appears to have been an underlying driver of the surge in scientific-journal and news articles about bird flu.

     Fear of a deadly bird-flu pandemic on the scale of the 1918-flu pandemic drives funding for research on vaccines and investments in developing vaccines against such a threat. But is such a threat real?

Fallacy of Comparing 1918 Flu Pandemic to a Potential Bird-Flu Pandemic

     When a new breakthrough in knowledge becomes solidified into one frame of reference (shared and promoted vigorously by interlocking, cooperating organizations), other frames of reference can be ignored, which seems to be the case here. The frame of reference portraying bird flu as a dire threat in need of future vaccines directs all resources towards this one goal — a goal that also promises great financial gains or career-advancement for many of the people involved. There is, however, another frame of reference more in tune to how people conduct their lives from day to day, where fear of catastrophic disease does not drive their actions. This frame of reference considers less-publicized facts about the 1918 pandemic.

     The 1918 flu pandemic incorrectly serves as the bedrock of current bird-flu fear. Why? First, scientists, researchers and doctors at the time did not even know that a virus caused the illness to which so many deaths have been famously attributed.  Second, World War I resulted in extreme overcrowding in both the military and civilian populations, which fostered an ideal landscape for the proliferation of bacteria that caused pneumonia. Third, proper, widespread use of antibiotics did not exist to treat pneumonia, which, if they had existed (and had doctors understood the connection), then many deaths would not have happened.

     Consider the following key quotes from two scholarly references on this subject:

Brundage J F, Shanks G D (2008). Deaths From Bacterial Pneumonia During 1918-19 Influenza Pandemic, Emerging Infectious Diseases, 14(8):1193-9. doi: 10.3201/eid1408.071313. PMID: 18680641; PMCID: PMC2600384.

... healthcare providers, medical experts, and published data from the 1918 period suggest that most deaths were caused by secondary bacterial pneumonias —  hemorrhagic pneumonitis that rapidly progressed to death was considered an alarming but uncommon clinical manifestation.

... contemporaneous reports suggest that the pathophysiologic effects of the virus, in and of themselves, did not directly cause most (or even many) of the deaths during the pandemic.

We have identified epidemiologic and clinical characteristics of the 1918–19 pandemic that are not readily consistent with the view that most deaths were caused by the direct effects of an inherently hypervirulent virus ... 

Undoubtedly, factors other than the inherent virulence of the virus or the robustness of the host’s immune response affected the clinical expressions of influenza infections. 

Care providers and experts of the day in epidemiology, pathology, bacteriology, and infectious diseases clearly concurred that pneumonias from secondary bacterial infections caused most deaths during the pandemic.

The exclusive focus on the prevention and treatment of a novel strain of influenza virus is risky because it unnecessarily limits options and opportunities for other potentially effective prevention and treatment methods ...

Aligne, CA (2022). Lost Lessons of the 1918 Influenza: The 1920s Working Hypothesis, the Public Health Paradigm, and the Prevention of Deadly Pandemics, American Journal of Public Health, 112(10), 1454-1464. doi:https://doi.org/10.2105/AJPH.2022.306976

On the basis of the timing and geographic pattern of the pandemic, they hypothesized that an “essential cause” of the pandemic’s extraordinary lethality was the extreme, prolonged, and industrial-scale overcrowding of US soldiers in World War I, particularly on troop ships. 

Even to the general public, it was obvious that extreme overcrowding contributed to these deaths.

In other words, humans can manufacture virulence in (avian) influenza virus by creating conditions of industrial-scale prolonged extreme overcrowding. Furthermore, it is well-established that human activity can select for dangerous traits, such as antiviral resistance, in human influenza virus. 

World War I altered the daily lives of entire populations with shortages of essentials, even in the United States. For example, the rush to build ships in Philadelphia exacerbated crowding in squalid tenements with several families to each apartment. In cities across the United States, people living in slums had the highest flu mortality. In or out of cities, mortality was highest for those, like coal miners and factory workers, who lived in overcrowded conditions even though these occupations enjoyed relatively high incomes during the war. 

From Iran to Iceland, the common markers for flu mortality were environments associated with crowding or poverty. Taken together, the findings presented here from history, public health, military medicine, veterinary science, molecular genetics, virology, immunology, and epidemiology are consistent with a virus that was immunologically similar throughout the World War I pandemic, but varied intensely in virulence in response to war-related environmental factors such as industrial-scale, prolonged, extreme overcrowding.

     Interestingly, Dr. Anthony Fauci was aware of all this for many years prior to the COVID-19 vaccine debacle that he championed, as evidenced by the following article:

David M Morens, Jeffery K Taubenberger, Anthony S Fauci (2008). Predominant Role of Bacterial Pneumonia as a Cause of Death in Pandemic Influenza: Implications for Pandemic Influenza Preparedness, The Journal of Infectious Diseases, 198(7):962–970.

     The extreme reaction to COVID-19 and the resulting single-minded rush to create a vaccine were fueled by unjustified fear of a relatively unremarkable coronavirus, which faulty, misguided analysis erroneously projected would cause an event similar to the 1918-influenza pandemic. 

     Comparing the present time to 1918 carelessly overlooks critically important facts. 1918 simply was a different time from the current era (2024 and beyond). We know more about disease than we did back then. Antibiotics exist. Doctors are better today. Many experts not captured by the pharmaceutical industry also understand the dangers of single-minded approaches to public health, strongly tied to financial gains by drug developers. Consequently, promoting the fear of a naturally-mutating bird flu virus as the next "big one" (i.e., catastrophic pandemic) is nothing less than a further exercise of disease mongering.

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