The COVID-as-bacterial-pneumonia conspiracy theory rises again

To antivaccine conspiracy theorists, it is always of the utmost importance to find a way to explain deaths from the pathogens that cause vaccine-preventable diseases as somehow not being due to that pathogen. The reason is simple. If antivaxxers can spin a convincing-sounding narrative claiming that a specific pathogen isn’t causing disease and death that can be prevented by vaccines targeted against that pathogen, then they can add to that narrative the claim that the vaccine doesn’t work (because it’s not targeting the “true” cause of the disease and death) and is therefore unnecessary. Add to that claims that the vaccine is dangerous, and they can spin a narrative that seems compelling if you don’t know a lot about infectious disease. For COVID-19, we saw this narrative in the form of conspiracy theories falsely claiming that death certificates were misattributing deaths during the pandemic as being due to COVID-19 when they supposedly were not, leading to false claims that people were dying “with COVID-19” and “not of COVID-19” or that “only” 6% of deaths attributed to COVID-19 were actually caused by COVID-19. That latter lie was based figures showing that 94% of COVID-19 death certificates had multiple contributing factors but also involved conflating sequelae of COVID-19 infection that ultimately led to death with primary causes of death. As I like to say, everybody dies of cardiac arrest. Whatever ultimately kills you, your proximate cause of death will be cardiac arrest. That’s a trivial observation. The far more important thing to know is: What caused the cascade of events that led to your cardiac arrest and death.

Antivaxxers are still doing it, as I noticed over the weekend when I came across a Substack post published last Friday—because of course it was a Substack post spreading COVID-19 misinformation—by Mathew Crawford titled “The COVID-As-Pneumonia Hypothesis“. My first thought reading that title was that the word “hypothesis” is doing some very heavy lifting here, as in science the word “hypothesis” generally means a falsifiable prediction that has enough evidence behind it to make testing it through experimentation, and clinical testing in the case of medical hypotheses, reasonable. In reality, it was a conspiracy theory that what was “really causing” all those COVID-19 deaths wasn’t COVID-19 at all for the most part, but actually bacterial pneumonia that “They” somehow didn’t want to admit but rather attribute to SARS-CoV-2, the coronavirus that causes COVID-19. Why would they want to do this? Reasons. Nefarious reasons. Of course. Because it’s a conspiracy theory.

Mathew Crawford, Norman Fenton, and their antivax pals regurgitate an old antivax conspiracy theory. Again.

In his Substack, Crawford cites a number of “sources” to justify the conspiracy theory that it’s bacterial pneumonia, not viral pneumonia associated with COVID-19 that killed most COVID victims and that “They” are intentionally misclassifying these deaths as due to COVID-19. Unsurprisingly, nearly all of his sources are other Substack articles by COVID-19 cranks and antivaxxers, starting with this introduction:

At some point last year, I was emailing with Drs. Brian Tyson and George Fareed, telling them that it may very well be that most of the [true] COVID-19 deaths were due to pneumonia, and that the most important mechanism behind their protocol might be the antibiotic effects of both hydroxychloroquine and azithromycin/doxycycline. Brian’s response suggested that not only did they agree, but that they were ahead of me on that thought. And that’s good to see—the doctors who were sane enough to focus on early treatment in 2020 were open-minded and aware of the branching hypotheses over what they saw on a clinical level.

This week I was extremely glad to see Martin Neil, Jessica Hockett, Jonathan Engler, and Norman Fenton—a group in which I have high trust—take on what we might term “The Bacterial-COVID Hypothesis”.

The specific Substack that Crawford most relied upon was published on Norman Fenton’s Substack and titled “Whodunnit? {unabridged}“, which “boldly” asked, “Was SARS-CoV-2 or Pneumonia the primary cause of respiratory Covid-19 deaths?”

Personally, given the length and tendentiousness of Fenton’s post, I would have preferred the abridged edition. I like how Fenton and his merry band of antivaxxers and COVID-19 minimizers frame their “hypothesis” all as investigating a mystery, as if scientists and physicians had never before considered the question of differentiating viral pneumonia from bacterial pneumonia. Personally, I like to point out that, contrary to the entire argument being made by people claiming that most COVID-19 deaths were really due to bacterial pneumonia, it actually does matter if a viral pneumonia leads to lung damage that predisposes to a superimposed bacterial pneumonia and the bacterial pneumonia—or, more commonly, a combination of the viral and bacterial infection—ultimately leads to the patient’s death. Why? Because the bacterial pneumonia wouldn’t have been superimposed on the viral pneumonia if the lungs hadn’t been damaged by the viral pneumonia and also because, patients placed on ventilators for a viral pneumonia would not have been predisposed to ventilator-associated bacterial pneumonia if they damage to their lungs hadn’t necessitated the institution of mechanical ventilation in the first place. It isn’t rocket science to understand that if a viral infection damages the lungs enough to predispose them to a bacterial infection that results in sepsis that finishes the patient off, it was the viral infection that caused the death.

As is often the case in such arguments, the authors focus on choosing anything other than the virus as the “primary” cause of death, conveniently ignoring or downplaying what started the cascade of events leading to a patient’s death. I’m going to keep harping on this. For example, if advanced cancer filling a patient’s liver leads to liver failure, which ultimately leads to metabolic disturbances that kill the patient, yes, liver failure was a more proximal cause of death than the cancer, but it was still the cancer that killed the patient. Arguments like Fenton’s and Crawford’s rely on citing events further down the cascade of complications from COVID-19 as the “true” causes of death, not the virus that incited the cascade. (Hmmm. I might become as repetitive as the COVID-19 cranks, but damn if they don’t rather force me to.) Also, in most cases I’m sure that people like Fenton (for example) know this. What they also know is that most people without a medical background can be easily misled by specious arguments like theirs. Yes, after three years of observing them, I no longer give them the benefit of the doubt; in my opinion they are intentionally deceiving.

Let’s dig in.

Tell me you don’t understand viral respiratory diseases without telling me you don’t understand viral respiratory diseases

Let’s pivot over to the Substack by Fenton and friends. I’ve discussed Norman Fenton’s tendency to play fast and loose with definitions and defending antivax p-hacking before elsewhere (albeit, oddly enough, not on SBM until now), but I honestly did not recall any of his “coauthors.” Let’s just say that Fenton has gone from being a “new school” antivaxxer who spread fear, uncertainty, and doubt (FUD) about COVID-19 vaccines—e.g., here, where he spreads a common conspiracy theory that “they” altered COVID-19 death certificates to attribute non-COVID deaths to COVID and (of course!) deaths due to COVID vaccines to COVID—into someone who is increasingly becoming just plain antivaccine, as shown by his receptiveness to really old school antivax claims that vaccines cause autism:

As for the rest of the “co-authors,” Jessica Hockett is a Brownstone Institute author (because of course she is!) who’s used that platform to spread the lie that New York City hospitals were not overwhelmed by COVID-19 cases in the spring of 2020, a lie debunked here on more than one occasion. Indeed, our very own Dr. Jonathan Howard addressed the very claims made by Dr. Hockett, who in analyzing infectious disease epidemiological data shows that she’s an educational psychologist. She was still at it as of yesterday:

Jonathan Engler is co-chair of the HART Group (Health Advisory & Recovery Team), a group of UK-based “open everything up” COVID-19 minimizers and antivaxxers and prime spreaders of disinformation, while Martin Neil is a professor of computer science and statistics at Queen Mary University of London who is spreading the same message that it’s bacterial pneumonia, not COVID-19, that killed people:

Note the conspiracy mongering that links influenza to the same narrative that it’s bacterial pneumonia, not SARS-CoV-2, that killed people. In his post, Fenton claims he will show these things. I will reproduce his “summary” of bullet points, in order to go through them, noting that the point in the Tweet above is one that he and Fenton, along with Hockett and Angler, make in their post:

We have investigated the pneumonia hypothesis: that a proportion of covid-19 deaths, those with associated respiratory symptoms (rather than deaths coded as covid-19 because of a positive PCR test, that are absent symptoms), were caused by bacterial pneumonia, and that bacterial pneumonia was the primary, not the secondary, infection.

Our argument in favour of the hypothesis is:

Conflating pneumonia & covid-19 repeats an official longstanding tactic of conflating the attribution of influenza and pneumonia. The reduction in the public’s perceived threat of flu may have prompted the pharmaceutical industry to attempt a rebranding of the threat along with a new suite of marketable products to respond to that threat.
We investigated the hypothesis that a proportion of covid-19 deaths, those with associated respiratory symptoms (rather than deaths coded as covid-19 because of a positive PCR test, that are absent symptoms), were caused by bacterial pneumonia, and that maybe bacterial pneumonia was the primary, not the secondary, infection.
Does pre-existing exposure to bacterial pneumonia lead to a higher propensity to acquire a viral infection, such as SARS-CoV-2? And we suggest that SARS-Cov-2 infection may mask or be secondary to pneumonia infection and not necessarily the other way around, in which SARS-CoV-2 is assumed to lead to bacterial pneumonia as a secondary infection.
Given this the actual burden of risk to hospitalized patients may not have been SARS-CoV-2 (or other viruses) at all but bacterial pneumonia.
High rates of ventilator induced pneumonia are confounded by changes in protocols, delays in admission, and overuse of ventilation etc. and estimates of rates of attribution to SARS-CoV-2 cannot therefore be relied upon. Respiratory deaths in hospitals may therefore have beeb [sic] caused by bacterial pneumonia but wrongly attributed to SARS-CoV-2.
The pattern of spread of SARS-CoV-2 in spring 2020, and the geographical concentration of the SARS-CoV-2 mortality toll is not what one would expect from a spreading respiratory virus. It is highly localised in specific geographically distant regions and cities. It is a pin-point pandemic.
Under modern sanitary conditions large scale pneumonia outbreaks in highly concentrated areas are unlikely to occur naturally. We must look elsewhere for explanations, including the possibility of human agency.
Given that rates of pneumonia deaths in 2020 were similar to those seen in previous years, changes in ventilation policy and practices coupled with new PCR testing, would be enough to cause the pin-point pandemic effect.
The central question is therefore: Was SARS-CoV-2 a bystander or decoy virus and were bacterial pneumonia deaths mistakenly or intentionally used as proof that SARS-CoV-2 was a deadly respiratory pathogen?

Events are akin to a scene from an Agatha Christie novel where SARS-CoV-2, a bystander used as a decoy, is guilty of the crime, with ventilation as the accomplice, but the actual criminal, who has got off scot-free, is in fact bacterial pneumonia. In other words, SARS-CoV-2 has been framed.

I do like how in the very first bullet point Fenton and crew demonstrates exactly what I’m talking about while also demonstrating that to antivax cranks every accusation is a confession. That’s because it has been a longstanding trope of the antivax movement to claim that what kills many people who die of the flu is a superimposed bacterial pneumonia and then try to claim that the pneumonia was the “primary cause” of that person’s death, not the “harmless”—or “mostly harmless” (except to the old and debilitated and who cares about them anyway?)—flu. They even added Agatha Christie and tried to characterize COVID-19 as having been the innocent bystander dupe who’s been “framed.” They even cite James Lyons-Weiler:

False attribution/conflation of pneumonia deaths to a virus is not a new phenomenon. James Lyons Weiler reports on a long history of manipulation of definitions and statistics to inflate the perceived danger from the flu, when the actual danger is bacterial pneumonia. Pneumonia deaths were henceforth coded as influenza/pneumonia.

This leads to the conspiracy theory of why “they” would do such a thing as to intentionally blame deaths from bacterial pneumonia on COVID-19:

Before SARS-CoV-2 came on the scene, there was a belief in pharmaceutical circles that the flu wasn’t perceived to be dangerous enough and a concern that flu vaccination rates were dropping. To some it may have looked like the vaccine enterprise and pharmaceutical industry itself might be in danger of terminal decline. In October 2019, there were calls for a universal high-tech flu vaccine to face upcoming viral threats and ‘blow up’ the existing system, with the necessity of having many people dying for the sense of urgency to occur.”

The reduction in the public’s perceived threat of flu may have prompted the pharmaceutical industry to attempt a rebranding of the threat along with a new suite of marketable products to respond to that threat.

That’s right. To conspiracy theorists, it’s all about profit. Just as they accuse public health officials before the pandemic of ginning up the fear of influenza by falsely attributing deaths from pneumonia to the flu, all in order to sell vaccines and antivirals, they now accuse public health officials during the pandemic of ginning up fear of COVID-19 by falsely attributing deaths from pneumonia to COVID-19, all in order to—you guessed it!—sell vaccines and antivirals like remdesivir and Paxlovid (instead of the supposedly cheap and effective treatments that aren’t, like ivermectin and hydroxychloroquine.

They even try to claim that Anthony Fauci agrees with them:

Bacterial pneumonia has a track record of previous/prior convictions yet appears to get off the hook in 2020 as well as during previous influenza seasons.

We have argued that the steepness of the mortality spikes in Lombardy, Italy and New York City do not reflect those we might expect from a virus. Hence, we must look elsewhere for an alternative explanation. Might they be better explained as localised pneumonia outbreaks?

Fauci et al believe that the 1918 pandemic was largely caused by pneumonia:

The similarity of the mechanism between 1918 and 2020 is uncanny. The flu pandemic might be more accurately called a pneumonia pandemic. In 1918, influenza was blamed, but pneumonia did the deed. Yet with 1918 and 2020-2023, the historical lesson from public health is that people need to fear viruses, yet pneumonia does not get public attention.

Of course, if you actually read the 2008 Fauci paper cited, you’ll soon realize that Anthony Fauci and his coauthors say no such thing as “the 1918 pandemic was largely caused by pneumonia.” Rather, they wrote that most of the deaths during the 1918 pandemic were caused by complicating bacterial pneumonia:

The majority of deaths in the 1918-1919 influenza pandemic likely resulted directly from secondary bacterial pneumonia caused by common upper respiratory-tract bacteria. Less substantial data from the subsequent 1957 and 1968 pandemics are consistent with these findings. If severe pandemic influenza is largely a problem of viral-bacterial copathogenesis, pandemic planning needs to go beyond addressing the viral cause alone (e.g., influenza vaccines and antiviral drugs). Prevention, diagnosis, prophylaxis, and treatment of secondary bacterial pneumonia, as well as stockpiling of antibiotics and bacterial vaccines, should also be high priorities for pandemic planning.

They even manage to throw in some antimask claims:

It is also to be noted that in this study carried out in Japan and published in Nature, nearly all face coverings retrieved from a series of users in Japan had evidence of potentially pathogenic – and mainly commensal – bacterial and fungal colonies, which might have been particularly dangerous for the immunocompromised, such as the elderly,

If I were to swab Prof. Fenton’s throat, there’s a decent chance that there probably be potentially pathogenic bacteria there, too. There are also some pretty nasty bugs that normally live in our digestive tract and skin. As an amusing aside relevant to a recent post that I wrote, that very study cited by Fenton found that those who ate natto on a daily basis had a lot more of the spore-forming bacterium Bacillus subtilis on their masks, which made me laugh because COVID-19 quack Dr. Peter McCullough has been selling nattokinase, an enzyme made by this bacterial species, as “spike protein detox“, basically a cure for COVID-19. Sure, it’s theoretically possible that immunosuppressed people might be susceptible to their natural flora, but that’s not really what Fenton et al. are implying.

The argument being made by Fenton et al., again, assumes that the bacterial pneumonias recorded had nothing whatsoever to do with influenza infections, which any infectious disease doctor will tell you is not the case, which brings us to the second bullet point, the conspiracy theory that “they” coded COVID-19 deaths as COVID-19 deaths in patients who supposedly had an asymptomatic case of COVID-19 who just happened—by coincidence!—to die of a bacterial pneumonia. In fact, in the third bullet point, they reverse the polarity, so to speak, and claim that it’s exposure to bacterial pneumonia that predisposes to COVID-19. Of course, I can’t resist pointing out that their pulling this trick implicitly admits that the proximal cause is not necessarily “the cause” of death. To make this argument, Fenton et al. have to assume that SARS-CoV-2 is a nearly harmless virus, like viruses that cause the common cold.

At this point, I was beginning to wonder what evidence they actually had, because for the most part the whole Substack is one big load of handwaving and JAQing off, along with appeals to incredulity; e.g., the claim that “the steepness of the mortality spikes in Lombardy, Italy and New York City do not reflect those we might expect from a virus” and “pattern of spread, and the geographical concentration of the Covid-19 mortality toll is not what one would expect from a respiratory virus.” Of course, the pattern of spread of SARS-CoV-2 actually very much like what we would have expected from a novel respiratory virus that originated in a single place (around Wuhan, China) and then spread to different parts of the world along via infected travelers, where at each new location the infected travelers started spreading the infection to others, thereby causing “pinpoint” epidemics in highly populated areas like New York that spread and grew until all the mini-epidemics started to converge into one huge global pandemic.

Similarly, Fenton et al. argue from their incredulity that under “modern sanitary conditions large scale pneumonia outbreaks in highly concentrated areas are unlikely to occur naturally” and that therefore we “must look elsewhere for explanations, including the possibility of human agency” (bold text Fenton’s). Again, on what planet do these people live? Although very important in preventing the spread of water-borne disease or diseases spread by the fecal-oral route, sanitation appears not to play a major role in preventing outbreaks of transmissible highly infectious respiratory diseases, although simple handwashing can. Population immunity (e.g., vaccination) and population density do. When people live packed in small spaces with poor ventilation (as all too many humans do), even in “modern” cities, it’s a perfect setup for a respiratory virus to spread. What can slow the spread of respiratory viruses are long-used physical measures. As for the “possibility of human agency”, it sounds to me as though Fenton is implying some sort of cover-up or nefarious intervention of public health officials and government.

Pretty much all of what Fenton et al. express such incredulity about turns out to be nothing more than what we’ve long known that respiratory viruses do, how they spread, and how they can be complicated by a secondary bacterial pneumonia. The principles of virology and viral pneumonias didn’t change overnight when COVID-19 arrived. While COVID-19 had some unusual characteristics, it was (and is) still a respiratory virus, a subtype of coronaviruses, which had been fairly extensively studied before the pandemic, particularly after the SARS epidemic in 2003, which fortunately—and unlike COVID-19—fizzled out before becoming a pandemic.

But what evidence do Fenton and his antivaxxers have?

Cherry picking, thy name is Fenton (et al.)

As I have explained, pretty much everything that confuses Fenton and colleagues into thinking that COVID-19 could not be the primary cause of death and that bacterial pneumonia must have been the culprit has been consistent with what we know about viral pneumonia and how to treat it. The principles haven’t changed: Support the respiratory status of those suffering from viral pneumonia, with supplemental oxygen, pulmonary hygiene to loosen secretions, and even with mechanical ventilation if necessary. Use antivirals if there are any effective ones against the particular virus-causing pneumonia and treat secondary bacterial infections with appropriate antibiotics if they arise. It’s the same set of principles used to treat ARDS (acute respiratory distress syndrome). This, of course, brings us back to ventilators, because Fenton et al. blame ventilators for COVID-19 deaths. First, though, they muddy the waters by selectively interpreting and quoting a large retrospective cohort study of over 19,000 patients with COVID-19 and other respiratory diseases between March 10th, 2020 to December 31st, 2020, a study whose findings were actually fairly interesting and complex.

In brief, the authors found:

…a 2.6-fold increase (P < 0.001) in respiratory culture ordering in COVID-19 patients. On a per-patient basis, COVID-19 patients were 1.5-fold more likely than non-COVID patients to have positive respiratory cultures (46.8% versus 30.9%, P < 0.001), which was primarily driven by patients requiring intubation. Among patients with pneumonia, a significantly higher proportion of COVID-19 patients had ventilator-associated pneumonia (VAP) relative to non-COVID patients (86.3% versus 70.8%, P < 0.001), but a lower proportion had community-acquired (11.2% vs 25.5%, P < 0.01) pneumonia. There was also a significantly higher proportion of respiratory cultures positive for methicillin-resistant Staphylococcus aureus, Klebsiella pneumoniae, and antibiotic-resistant organisms in COVID-19 patients. Increased rates of respiratory culture ordering for COVID-19 patients therefore appear to be clinically justified for patients requiring intubation, but further research is needed to understand how SARS-CoV-2 increases the risk of VAP.

Basically, this study published in 2022 concluded that there’s something about SARS-C0V-2 that results in a higher rate of ventilator-associated bacterial pneumonia. Of course, VAP is a common complication during prolonged ventilation for respiratory failure, particularly if the lung is injured. This study concluded that the risk of VAP complicating ventilation for COVID-19 was most increased relative to that for non-COVID-19 ventilated patients after ten days of mechanical ventilation. Of course, this is not the only study looking at this question. If one looks at the overall evidence, it appears that COVID-19 does result in a higher risk of VAP compared to other causes of ARDS, a risk attributed thusly in one study:

In patients admitted in an intensive care unit (ICU) and ventilated for Acute Respiratory Distress Syndrome (ARDS) due to SARS-CoV-2, ventilator-associated pneumonia (VAP) is a common complication, ranging from 30% to 86% of patients [1,2]. The cumulative incidence among COVID-19 patients can reach approximately 35/1000 ventilator days in European cohorts, which is 50% to 80% higher than in ARDS from other etiologies [3,4]. Several mechanisms explain the higher incidence of these superinfections [5,6]. They involve mucus plugs favoring atelectasis, diffuse alveolar damages, viral-induced immunoparalysis, impaired lung perfusion due to endothelial dysfunction, altered coagulation, and immunothrombosis [7,8]. Of note, the risk truly induced by corticosteroids or other immunomodulator therapies remains debated [9]

How do Fenton et al. spin these results? First, they don’t like the fact that the definition of VAP precludes pneumonia acquired less than two days after intubation:

Likewise, it looks like the majority of respiratory culture tests were performed post intubation, and unfortunately, any positive culture tests found for intubated patients collected at least 2 days prior to intubation were excluded from the study (because they would not qualify under the class “ventilator acquired pneumonia” versus hospital or community acquired). It is thus possible that cases may have tested positive for competing pathogens contracted before ventilation but subsequently discovered during ventilation and classified as a secondary pneumonia were actually a primary pneumonia contracted in the hospital or in the community.

Now that’s some serious JAQing off, as in, “Hey, what if all these patients diagnosed with VAP actually had bacterial pneumonia when they were intubated but it was missed because VAP is defined as bacterial pneumonia that develops more than two days after intubation? And, hey, what about this:

When reporting for their own hospital, Columbia University Irving Medical Center (CUIMC) located in New York City, they report that respiratory cultures were ordered for test in 16% of SARS-CoV-2 positive patients compared to 6.2% in negative patients. So, as the overwhelming majority of covid-19 patients were not tested for competing pathogens, it cannot be ruled out that those showing respiratory symptoms attributed to SARS-CoV-2 might have been suffering from another viral or bacterial coinfection.

These people are clearly not clinicians. They don’t think like clinicians, nor do they think like clinical investigators. There’s a saying in medicine: When you hear hoofbeats, don’t look for zebras. (A “zebra” is slang for a rare or uncommon diagnosis in a given clinical situation.) Yes, sometimes you will find a zebra, but only rarely. When a patient has the symptoms of COVID-19 over a time period consistent with COVID-19 and tests positive for COVID-19, that patient has COVID-19 unless there are other things in their clinical picture that make us think that there might be something else going on. Moreover, in the middle of the first surge of the pandemic, testing all patients for “competing respiratory pathogens” would not have been justified given resource constraints. Indeed, look at it this way: Clinicians were testing COVID-19 patients for “competing pathogens” nearly three-fold more frequently than they were doing so for non-COVID-19 patients.

Fenton also can’t help but doing a bit more conspiracy mongering here:

They also say:

“….between March 10th and 23rd, testing was performed by clinical suspicion due to limited testing capacity….”

So, there was an absence of rigorous data collection at the height of the ‘pandemic’ in NYC and at other times the rates at which culture testing is done appears selective, and cases appear to have been removed from the analysis due to classification requirements. This suggests that the rates at which bacterial and viral coinfection, and the stage at which infections are detected (community, hospital ICU) are highly sensitive and dependent on local testing and record keeping practices, and also differences between practices extant prior to the ‘pandemic’ and during it.

See what I mean about resource constraints? Yet Fenton et al. use that admission to imply that somehow this means that many “co-infections” were missed.

In the rest of their Substack, Fenton et al. cite papers confirming what was found above, namely that COVID-19 appeared to be associated with a higher risk of VAP, with ventilation being portrayed as an “accomplice” in their fanciful murder mystery. They even cite one s tudy in order to imply that doctors were ignoring all the other microbes they found in patients with COVID-19:

They found that:

“…..morbidity was principally due to SARS-CoV-2 infection and some other microbiologic characteristics, such as an association with positive blood cultures and polymicrobial cultures rather than patients’ related risk factors, such as immune-depression and co-morbidities.”

So here the authors acknowledge that other microbiologic and polymicrobial cultures are to be found at the ‘crime scene’ yet are not directly implicated in the deaths. SARS-CoV-2 is named as the guilty culprit.

Yes, because, absent SARS-CoV-2, all the other polymicrobial infections wouldn’t have happened! Indeed, it is telling how Fenton et al. ignored this part of the study, which said:

In our study, VAP occurred in more than 50% of COVID-19 patients receiving mechanical ventilation, and it was associated with death in 50% of cases. These results are aligned with data presented by other authors [8,9,10]. Additionally, no significant difference in mortality rate was detected between COVID-19 patients with and without VAP. This result is encouraging, and it suggests that VAP can be managed in ICUs, and the risk of VAP should not be a limitation to mechanical ventilation in COVID-19 patients.

In actuality, this study supports not what Fenton claims, but rather that the bacterial pneumonias were secondary infections that could be managed and did not appear to be the primary drivers of mortality in COVID=19 patients. That, too, is why the authors concluded that SARS-CoV-2, not bacterial pneumonia, was the primary cause of death.

As for the repeated observation that the risk of VAP went way up the longer COVID-19 patients were kept on mechanical ventilation, Fenton et al. also spin a conspiracy theory. Citing another study looking at VAP in ventilated COVID-19 patients, they write:

The act of keeping people on ventilators for longer, perhaps to protect staff as an early FDA statement indicated, confounds any claim that SARS-CoV-2 was more deadly.

I encourage you to actually read the FDA statement. It says nothing about keeping people on ventilators for longer to protect medical staff. Go ahead. Click on the link. I’ll wait. The notice is from March 2020 and is all about increasing the supply of ventilators for patients by issuing “an Emergency Use Authorization (EUA) to allow for the emergency use in health care settings of certain ventilators, anesthesia gas machines modified for use as ventilators, and positive pressure breathing devices modified for use as ventilators (collectively referred to as “ventilators”), ventilator tubing connectors, and ventilator accessories that the FDA determines meet specified criteria for safety, performance and labeling.” and increasing the supply of personal protective equipment (PPE), such as respirators, N95 masks, etc. Fenton et al. are basically lying about what the FDA statement says, counting on the fact that most people won’t click on the link, much less read what the FDA statement says.

None of this stops them from citing two studies showing similar things (a higher rate of VAP and prolonged ventilator support) and then concluding:

Both of these studies suggest that any conclusion that SARS-CoV-2 was the primary causal factor in mortality is heavily confounded, inter alia, by bacterial infection and changes in treatment protocols. Patients were in the ICU for longer and the increase in bacterial pneumonia, from prolonged exposure to ventilation, may well have led to an increased mortality rate and the misattribution of this to SARS-CoV-2.

They also use the observation that fewer invasive procedures were done (e.g., bronchoscopy) to collect sputum samples in COVID-19 patients on ventilators in order to try to claim again that many bacterial pneumonias were missed:

Furthermore, it appears that established protocols for bacterial sampling were changed to reduce exposure of hospital staff to the virus:

“Additionally, VAP incidence may vary according to the bacteriological test used. Indeed, to avoid healthcare workers (HCW) contamination when the diagnosis of VAP is suspected, the use of bacteriological samples and bronchoscopy have been reduced, and gram stain examination not performed.”

This suggests that bacterial causes for acute respiratory distress might not have been detected at all in many cases, but not because it wasn’t present, but because it was never tested for.

Apparently, Fenton et al. have never heard of empirical treatment of VAP. As I learned back in my trauma days, you don’t always isolate the bug causing VAP, or sometimes you isolate several. In these cases, antibiotics are chosen empirically. Basically, if there is clinical suspicion for a bacterial pneumonia, ICU docs will institute empirical treatment for it. Just because there’s no culture doesn’t mean there’s no diagnosis. Indeed, Fenton cites research indicating that the vast majority of patients with severe COVID-19 were treated with antibiotics at some point during their course. That would seem to go against his “hypothesis,” but not if you’re a good conspiracy theorist:

In the VAP studies, cited earlier rates of first line antibiotic treatment were similar across groups, as was targeted treatment with antibiotics. At first glance this appears to falsify the claim (discussed here) that denial of antibiotics caused SARS-CoV-2 respiratory deaths. However, as with all medical treatments the important question is whether, if people had pneumonia, they were given antibiotics on time, in the community or in hospital, before they were presented to the ICU and experienced VAP. Langford et al report that “the majority of patients with Covid-19 received antibiotics” – estimated at 72%. But what if the wrong people got the antibiotics, and those with pneumonia did not? The study authors don’t say but the effect of any misallocation would naturally be to increase the mortality rate of those with pneumonia.

Pneumonia symptoms overlap heavily with SARS-CoV-2 symptoms and given the edict that antibiotics do not help in the treatment of SARS-CoV-2, it is inevitable that many patients suffering from pneumonia would have been denied antibiotics until it was too late for them to have a material effect.

Got it? Even though most ventilated COVID-19 patients did receive treatment with antibiotics, they didn’t get the right antibiotics at the right time, because that’s the only way Fenton et al. could JAQ off about it in a way to cast doubt on the rather obvious refutation of their conspiracy theory. They go beyond even this, though:

Furthermore, in spring 2020 people were told to self-isolate if they suffered covid symptoms. This would buy time for pathogens to multiply and for a more severe condition to develop, which might be subsequently harder to manage. Many people would have then presented late to ICU, with incipient or lingering pneumonia (perhaps from the previous normal flu season), disguised as covid-19, and were left untreated with antibiotics until their condition deteriorated further. The reluctance to perform bacteriological investigations may have been a further contributory factor. They would therefore have suffered higher levels of ARDS than would have been seen historically. Given the lateness of presentation to hospital, and despite the administration of antibiotics, this may have came too late to save them from what was a (detected or undetected) bacterial pneumonia infection. A proportion of these would have been attributed to SARS-CoV-2.

At this point I was getting tired. It was variation upon variation of the same misunderstanding regarding how viral pneumonias are often complicated by bacterial pneumonia during their clinical course. They express amazement that cases of pneumonia graphed against time overlap COVID-19 surges, as if that were evidence that it was bacterial pneumonia, not COVID-19, causing the waves of death during those surges, while citing antivaxxers like James Lyons-Weiler, who in his Substack claimed that a single study suggested that “the stunning potential that perhaps 58% of “COVID” cases were respiratory issues other than COVID (43% bacterial pneumonia, 16% non-pathogen causes of respiratory failure),” rendering them “doomed to a fate of non-treatment due to mis- or under-diagnosis.”

Oh, and Fenton also points to a study showing a large decrease in antibiotic prescriptions from January to May 2020, as though this were some sort of conspiracy not to treat bacterial pneumonia in favor of misclassifying it as COVID-19, when the study itself notes that the decrease was most likely due to pandemic mitigation measures.

Confusing cause and effect to spread antivax propaganda

During the pandemic, there have been a number of false messages promoted by pandemic minimizers and antivaxxers, including:

• That COVID-19 death tolls are being intentionally exaggerated by the media and government for nefarious purposes; for example, early in the pandemic it was claimed that the “true” toll was “only 6%” of the toll usually cited.
• That “only” the sick and the old are at risk.
• That you don’t have to worry about COVID-19 if you don’t have one or more of the comorbid conditions listed.
• That, because “only 6%” died of “only COVID-19,” lockdowns, social distancing, masks, etc., are unnecessary.

Fenton’s messaging is very much of a piece of this, specifically the common antivax claim heard from time immemorial that vaccine-preventable diseases are not actually dangerous. We’ve seen this claim many times before for influenza, measles, varicella, and a number of other vaccine-preventable diseases, and, predictably, we’re now seeing it for COVID-19. What Fenton and his buddies are doing is yet another strategy antivaxxers like to use to claim that vaccines are not necessary and/or that the vaccine is more dangerous than the disease: To downplay the severity of the disease by confusing a complication of the disease with the disease itself, and then to claim that the complication is the “true” cause of death, not the virus causing the disease.

The worst thing is, I believe it’s very likely that Fenton and his friends know that their arguments are a load of fetid dingos’ kidneys. What they are spreading is disinformation more than misinformation.