The Myth of Secondary Infection (in Covid-19)

A standalone post regarding the secondary bacterial infection myth

Part of the series “Tolerance and severe disease.”

Contents:

• Part 1:

  • The myth of “cytokine storm.” (go)

  • The confusion over IgG4 tolerance in light of the myth. (go)

  • Innate antiviral suppression causes severe “Covid-19.” (go)

• Part 1.5 (this post):

  • The myth of secondary bacterial pneumonia.

  • Sky-high rates of antibiotic use among hospitalized “Covid-19” patients.

• Part 2:

  • The case for inflammation being (mostly) a bystander to Covid-19 pneumonia, not the cause.

• Part 3:

  • Severe “Covid-19” in turn causes adaptive immune suppression. (go)

  • Other examples of T Cell suppression and immune “stalemate” in persistent disease. (go)

  • The likely implications of IgG4 tolerance in light of the reality of severe “Covid-19”: persistent infections, ADE? (go)

Note that this post was originally written as a sub-section of Part 2; so the presentation is a bit compressed. The evidence for abundant antibiotic use is more extensive than what I have quoted below; see footnote 3.

The Myth of Secondary Infection (in Covid-19)

In Pt. 2, we will look at the features of Diffuse Alveolar Damage and “Organizing Pneumonia.” It is therefore useful at the start to distinguish the latter from the concept of “secondary [bacterial] pneumonia.”

The modern pre-expectation that Next Pandemic™ deaths would be driven by secondary bacterial infections originates from the same trio behind the recent “Rethinking vaccines” paper (see Igor’s excellent review), Morens, Taubenberger, and Fauci. It is one of the many 21st-Century predictive-programming breadcrumbs leading up to SARS-CoV-2’s appearance.

Morens, DM. Taubenberger, JK. Fauci, AS. (2008)

Unlike “cytokine storm,” however, the contemporary understanding of 1918 flu deaths strongly supported this modern reappraisal — so that all the trio were doing was providing a historical refresher. From Edwin O Jordan’s Epidemic Influenza:¹

There is no doubt that in nearly all fatal influenza there is a pneumonic process in the lungs, although occasional patients are observed who die soon after the onset and in whom only hemorrhage of the lungs is apparent. [Several thousand examples later:]

The factors operative in the production of influenza pneumonia may be summarized as follows:

1. The influenza virus weakens the resistant power of the pulmonary tissues so that various bacteria are able to play the role of secondary invaders;

2. The precise nature of the secondary—and tertiary—invaders is largely a matter of accident, dependent on the occurrence of particular bacteria in the respiratory tract of individuals at the time of infection, and, in the case of group outbreaks, on their occurrence in contacts

3. The character of the resulting pneumonia, clinical and pathologic, is largely determined by the nature of the secondary invaders, whether Pfeiffer bacillus, streptococcus, pneumococcus or other organisms;

4. There seems little doubt that the influenza virus, besides depressing the general pulmonary resistance, also acts directly on the pulmonary tissues, causing capillary necrosis, edema and hemorrhage

Morens, Taubenberger, and Fauci affirm the same; and thus recommend intense preparation of antibiotic treatments before the Next Pandemic™. And by all appearances this occurred. So why didn’t antibiotics stave off “Covid-19 deaths”?

Despite recent rumors, it in fact happens that antibiotics were administered aggressively to hospitalized Covid-19 pneumonia patients all over the world, in absence of strong guidance (in the US at least) promoting the same:

https://emergency.cdc.gov/coca/ppt/2021/111821_slide.pdf

Hat-tip, by the way, to Modern Discontent for helping me locate some of these materials:

From the citation in the slide above:²

Among 213,338 Inpatients with “Covid-19”*

All, received antibiotics: 77.3%

Ventilated, received antibiotics: 95.9%

Died in hospital, received antibiotics: 91.7%

*primary or secondary ICD-10-CM B97.29 February–April 2020 or primary or secondary U07.1 (COVID-19) April–October 2020, 716 hospitals

Antibiotics were used “empirically,” i.e. in absence of PCR or culture-confirmed bacterial infection; but they didn’t improve outcomes in any apparent manner. Altogether, secondary infections were uncommon (either because of or regardless of abundant antibiotic use):³

For COVID-19, 62/806 (8%) patients were reported as experiencing bacterial/fungal coinfection during hospital admission. […]

Despite frequent prescription of broad-spectrum empirical antimicrobials in patients with coronavirus-associated respiratory infections, there is a paucity of data to support the association with respiratory bacterial/fungal coinfection.

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1. pp. 268, 271. Jordan, Edwin O. (1927.) “Epidemic Influenza: A Survey.” Archived online at https://quod.lib.umich.edu/f/flu/8580flu.0016.858

2. Rose, AN. et al. “Trends in Antibiotic Use in United States Hospitals During the Coronavirus Disease 2019 Pandemic.” Open Forum Infect Dis. 2021 Jun; 8(6): ofab236.

3. Rawson, TM. et al. “Bacterial and Fungal Coinfection in Individuals With Coronavirus: A Rapid Review To Support COVID-19 Antimicrobial Prescribing.” Clin Infect Dis. 2020 May 2 : ciaa530.

See also:

Hughes, S. et al. “Bacterial and fungal coinfection among hospitalized patients with COVID-19: a retrospective cohort study in a UK secondary-care setting.” Clin Microbiol Infect. 2020 Oct; 26(10): 1395–1399.