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What You are Not Hearing about COVID-19

By Kelley Herring

With “social distancing” as the new norm, and nationwide closures of schools, businesses and public places, tensions and fear around COVID-19 are high.

Today, I hope to bring some perspective by sharing how pandemics of the past compare with COVID-19. Plus, we will discuss the two leading causes of death in viral pandemics like COVID-19 – and why the secondary (non-viral) component of this disease is cause for even greater concern…

What We Can Learn from Past Pandemics

During the last 100 years, four well-documented influenza pandemics have impacted the world.

The most infamous and deadly of these was the 1918 influenza A H1N1 virus, which is believed to have infected 500 million people worldwide.i It is important to note that only about five percent of those who died during that outbreak, did so in the early phase of the infection. On the other hand, 95 percent of deaths occurred between days 7-14.

Similar patterns were observed in the pandemics of 1957 and 1968, as well as the 2009 H1N1 Swine Flu outbreak.ii, iii

So, why do so few deaths occur during the early phase of the infection compared to the later stages of the illness?

The reason is that there are two potentially deadly pathways the disease can traverse…

It’s Not the Virus, It’s “the Storm”

Severe viral infection can cause what is known as a “cytokine storm”.

As the body is overwhelmed with viral infection, the immune system produces an onslaught of inflammatory chemicals meant to destroy the invaders. However, this virally-driven hyper-inflammation can also backfire and create what is known as “acute respiratory distress syndrome” (ARDS). This critical state requires ventilator support and often results in death.iv

However, cytokine storms only represent a very small number of total deaths.

Now let’s take a look at…

antibiotic resistance, boost immunity, immune system

Bacterial Superinfection: The Primary Killer in Pandemics

We’ve long known that respiratory viruses pave the way for bacterial pneumonia.v

When it comes to death related to viral infections, most people don’t die from the virus itself. They die from secondary bacterial infections that develop after the viral infection has been established.

In fact, in the 1918 flu pandemic, it is estimated that 90% of the fatal cases manifested as acute bronchopneumonia – confirmed by bacteria cultured on

Researchers who analyzed the data from the previous four influenza pandemics, found two key bacterial organisms – Staphylococcus aureus and Streptococcus pneumoniae – were those most commonly found in viral-associated pneumonia.vii

These data strongly implicate influenza virus infection combined with bacterial superinfection as the primary cause of mortality during that influenza pandemic.”

In the 1957 pandemic, bacterial pneumonia accounted for 44% of deaths.viii Similarly, in the 2009 influenza pandemic, pneumonia complicated up to 50% of severe infections in both children and adults. And those with bacterial superinfections experienced higher morbidity and mortality.ix, x, xi

The difference between the two later pandemics and the one that occurred in 1918 is that those which occurred more recently resulted in FAR fewer deaths. This is undoubtedly due to the development of antibiotics, used to counter the deadly bacterial infections.

Now, that sounds like good news…

But as you know, the advent (and the overuse) of antibiotics has come at a considerable cost. Like all living creatures, bacterial microbes have an innate will to survive. And the way that bacteria survive in the face of antibiotics is by mutating and evolving to achieve resistance to those threats.

In fact, in the U.S. alone, there are nearly three million antibiotic-resistant infections each year, resulting in more than 35,000 deaths. And most experts believe those numbers to be quite conservative.xii

And it turns out that this is the REAL and most concerning threat posed by a virus like Covid-19. It makes the body vulnerable to bacterial superinfections in the respiratory tract, which are virtually untreatable due to antibiotic resistance.

In a recent article, former Director of the CDC, Julie L. Gerberding, M.D., writes:

There is an even larger threat lurking behind the current outbreak, one that is already killing hundreds of thousands of people around the world and that will complicate the care of many Covid-19 patients… the hidden threat from antibiotic resistance.”xiii

She goes on to say that these bacteria have become more widespread. They are more deadly than ever before. And they are difficult to treat. And while mainstream medicine is calling for new and better antibiotics, it is clear that these drugs are as much a part of the problem as they are part of the solution.

In my next article, I will discuss the growing concern of antibiotic resistance… why the bacteria that cause pneumonia are of special concern… plus a “stealth” antimicrobial – with no side effects! – that may have the ability to save lives when antibiotics fail.

Read more of Kelley Herring’s health & wellness articles on our Discover Blog.

kelley herring


Kelley Herring is the author of the brand new book Keto Breads – which includes more information you need to know about why it is so important to avoid wheat and grains in your diet, plus how to use healthy replacements for these foods to create all the breads you love… without the gluten, carbs and health-harming effects. Click here to learn more about Keto Breads


i Chien YW, Klugman KP, Morens DM. 2009. Bacterial pathogens and death during the 1918 influenza pandemic. N Engl J Med 361:2582–2583. doi:10.1056/NEJMc0908216

ii Trotter Y, Jr, Dunn FL, Drachman RH, Henderson DA, Pizzi M, Langmuir AD. 1959. Asian influenza in the United States, 1957–1958. Am J Hyg 70:34–50.

iii Dawood FS, Iuliano AD, Reed C, Meltzer MI, Shay DK, Cheng PY, Bandaranayake D, Breiman RF, Brooks WA, Buchy P, Feikin DR, Fowler KB, Gordon A, Hien NT, Horby P, Huang QS, Katz MA, Krishnan A, Lal R, Montgomery JM, Molbak K, Pebody R, Presanis AM, Razuri H, Steens A, Tinoco YO, Wallinga J, Yu H, Vong S, Bresee J, Widdowson MA. 2012. Estimated global mortality associated with the first 12 months of 2009 pandemic influenza A H1N1 virus circulation: a modelling study. Lancet Infect Dis 12:687–695. doi:10.1016/S1473-3099(12)70121-4

iv Mehta P1, McAuley DF2, Brown M3, Sanchez E4, Tattersall RS5, Manson JJ6; HLH Across Speciality Collaboration, UK.COVID-19: consider cytokine storm syndromes and immunosuppression.Lancet. 2020 Mar 28;395(10229):1033-1034. doi: 10.1016/S0140-6736(20)30628-0. Epub 2020 Mar 16.

v Jakab GJ.Mechanisms of bacterial superinfections in viral pneumonias.Schweiz Med Wochenschr. 1985 Jan 19;115(3):75-86.

vi Morens DM, Fauci AS. 2007. The 1918 influenza pandemic: insights for the 21st century. J Infect Dis 195:1018–1028. doi:10.1086/511989.

vii Rynda-Apple A1, Robinson KM2, Alcorn JF3.Influenza and Bacterial Superinfection: Illuminating the Immunologic Mechanisms of Disease.Infect Immun. 2015 Oct;83(10):3764-70. doi: 10.1128/IAI.00298-15. Epub 2015 Jul 27.

viii Trotter Y, Jr, Dunn FL, Drachman RH, Henderson DA, Pizzi M, Langmuir AD. 1959. Asian influenza in the United States, 1957–1958. Am J Hyg 70:34–50

ix Gill JR, Sheng ZM, Ely SF, Guinee DG, Beasley MB, Suh J, Deshpande C, Mollura DJ, Morens DM, Bray M, Travis WD, Taubenberger JK. 2010. Pulmonary pathologic findings of fatal 2009 pandemic influenza A/H1N1 viral infections. Arch Pathol Lab Med 134:235–243

x Martín-Loeches I, Sanchez-Corral A, Diaz E, Granada RM, Zaragoza R, Villavicencio C, Albaya A, Cerdá E, Catalán RM, Luque P, Paredes A, Navarrete I, Rello J, Rodríguez A; H1N1 SEMICYUC Working Group. 2011. Community-acquired respiratory coinfection in critically ill patients with pandemic 2009 influenza A(H1N1) virus. Chest 139:555–562. doi:10.1378/chest.10-1396

xi Rice TW, Rubinson L, Uyeki TM, Vaughn FL, John BB, Miller RR, III, Higgs E, Randolph AG, Smoot BE, Thompson BT. 2012. Critical illness from 2009 pandemic influenza A virus and bacterial coinfection in the United States. Crit Care Med 40:1487–1498. doi:10.1097/CCM.0b013e3182416f23.