Reasons to consider bacteria in the pathophysiology in Covid-19

@sanchak74 did much of the research here. I'll mostly compile and summarize the evidence and arguments provided, while make some additions if needed.

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In late January, computational biologist @sanchak74 analyzed the metagenomics data of covid patient samples.

He found in addition to the SARS-CoV-2 virus, anaerobic bacteria such as Prevotella numbers has been enhanced.

This implies the microbiome homeostasis was disrupted.
He later matched covid symptoms to a rare anaerobic bacterial infection called Lemierre syndrome (LS).

LS is characterized by fever, chills, and septic embolism that can "travel through the bloodstream to other organs", causing hypoxemia or even stroke. https://osf.io/usztn/ 
Because of the difference of the initial site of infection: internal juglar vein v.s. lungs, and other specifics of SARS-CoV-2, the details of LS may not exactly match Covid-19.

However, this demonstrates that bacterial infections can cause damage similar to what is seen Covid.
2. Endotoxins and bacterial DNA detected in the blood

Endotoxins are cell-walls of gram-negative bacteria that are released as a normal physiological activity or when the bacteria is destructed.

They are key triggers of septic shock and cytokine storms. https://twitter.com/sanchak74/status/1267783134910705664?s=20
In the study, endotoxins were detected in the blood of every patient, with significant portion having high levels.

Bacterial DNA was also detected in most of them.

These can trigger the immune response of Covid-19.
Note, the culturing of bacteria have fail with all but one of the patients.

This may be due to the problems of detecting anaerobic bacteria.

Or the bacteria infection can be local, but still disseminate the bacterial products into the blood stream, triggering immune reaction.
Press release and comment: https://twitter.com/sanchak74/status/1294103633177403392
3. Antibiotics works (observational study)

Harvard study shows antibiotics can help against Covid ARDS, even when taken months before.

This could not be attributed to its anti-inflammatory properties. Antibiotics can lower the bacteria load prior. https://twitter.com/joshux321/status/1295141982176567296?s=20
There were some controversies with whether some antiviral works or not.

However, a common denominator of many (supposedly) effective treatments are antibiotics.

Azithromycin:
https://twitter.com/LotusOak2/status/1297789658483560449
https://twitter.com/Damkyan_Omega/status/1278597088964739072
Doxycycline: https://twitter.com/Dover63A/status/1297631122638147591?s=20
Anecdotal evidence:
https://twitter.com/robinmonotti/status/1293965722541064198?s=20

Brazil president after positive for the coronavirus on July 7 and then negative July 25
“I just did a blood test. I was feeling kind of weak yesterday. They found a bit of infection also. Now I’m on antibiotics”
https://www.reuters.com/article/us-health-coronavirus-brazil-bolsonaro-idUSKCN24V3SH
4. Inverse relationship between viral load and the severity of symptoms:

Severe patients have low viral load:
https://twitter.com/sanchak74/status/1229781516797931520

Below picture showed host viral response (host is detecting the virus) is disjunct with host inflammatory response. https://twitter.com/sanchak74/status/1271032663575539712
It is certainly possible the virus is triggering the body to do weird things. (How it did that is currently not found)

However, as we've shown via various arguments and evidence, bacteria can certainly do these things.

Why not consider that?
A more rational explanation is the virus carved out a way to let bacteria thrive, while itself is been cleared by the immune system . https://twitter.com/joshux321/status/1294963606249824256?s=20
You can follow @joshux321.
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