Whodunnit {abridged}

Was SARS-CoV-2 or Pneumonia the primary cause of respiratory Covid-19 deaths?

A ‘whodunnit’ (a colloquial elision of "Who [has] done it?") is a complex plot-driven variety of detective fiction in which the puzzle regarding who committed the crime is the main focus. The reader or viewer is provided with clues to the case, from which the identity of the perpetrator may be deduced before the story provides the revelation itself at its climax. The investigation is usually conducted by an eccentric, amateur, or semi-professional detective.

THIS IS THE SHORTER- ABRIDGED - VERSION OF THIS ARTICLE, FOR THE UNABRIDGED VERSION VISIT HERE.

Summary

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 whichSARS-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 been 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?

Allegorically speaking, 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.

Introduction

After three years of research, we find ourselves as akin to the role of the “eccentric, amateur, or semi-professional detective” in a whodunnit detective thriller, trying to identify the pathogen that caused the respiratory deaths in hospitals that were attributed to Covid-19. Was the culprit, that is, the primary cause, a new novel, deadly virus called SARS-CoV-2, secondary bacterial pneumonia, brought on by exposure to one or both above?

In a series of previous posts, we have looked at what happened with flu (the latest post is here), finding that there was a collective and systemic failure in (if not manipulation of) flu surveillance and flu death reporting systems. We also found that deaths from influenza/ pneumonia continued during 2020 and, in the UK and USA, were reported at levels similar to previous years, proving that influenza/pneumonia did not actually disappear as a cause of death, despite the appearance of SARS-CoV-2.

This investigation looks at bacterial pneumonia specifically and presents the ‘pneumonia hypothesis’ that a proportion of Covid-19 deaths - namely 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 pneumonia, and that pneumonia was the primary, not the secondary, infection.

This hypothesis is important because it challenges what the true causative agent behind the ‘pandemic’ was – a bacterium or a virus, both or neither? It also brings into question how the agent was spread, and challenges how and if it was appropriately treated. Ultimately, we ask: do we really know what happened and is there a risk we have everything wrong or back to front?

The seminal work of Rancourt et al from October 2021 is perhaps the first to identify a strong link between covid-19 and bacterial pneumonia, making the case that many covid-19-assigned deaths may be misdiagnosed bacterial pneumonia deaths and attributing observed excess deaths as partially explainable by a reduction in antibiotic prescriptions.

Whodunnit opening scene – the first victim

Let’s look at the opening scene of our whodunnit. The first victim is: “Patient Zero” in China. On 26^th December in Wuhan, China, patient zero was admitted to hospital experiencing a ‘severe’ respiratory syndrome that included fever, dizziness, and a cough.

Patient zero’s symptoms are typical of any respiratory infection. Patient zero is of relatively young age and without significant health problems. Yet patient zero was subjected to a battery of tests, including very expensive genetic sequencing of fluid removed from his airways, that (we are told) ultimately led to the discovery of a new coronavirus subsequently dubbed SARS-CoV-2. This is not a routine medical response to a typical respiratory infection.

As described  in the seminal paper in Nature published 3 February 2020, the clinical features of the illness of the alleged patient zero, from whom the genome of the “novel virus” was said to have been sequenced, are perhaps more suggestive of a regular, bacterial pneumonia: the clinical features of the illness of the alleged patient zero, from whom the genome of the “novel virus” was said to have been sequenced, are perhaps more suggestive of a regular, bacterial pneumonia:

Scene two: Panic!

Weeks later, Sky News' Chief Correspondent Stuart Ramsay reporting from the main hospital in Bergamo, Italy, provided a series of apocalyptic warnings of what was to come, but this puzzling statement also slipped out:

“It is not like flu, it is chronic pneumonia, and it is killing hundreds each day.”

You can find this statement at 1:16 in his video report on YouTube:

And at 1.40 he interviews the head of emergency care, Dr Roberto Cosentini:

Ramsay: “People keep describing this as like flu. It’s worse than that, no?”

Cosentini: “No, it’s totally another thing. I think it is (mumbles) pneumonia because most people get pneumonia, and as I have said before it is a very severe pneumonia…"

Makes you think, doesn’t it? Here we have one of the most widely promoted videos from Spring 2020, one that helped trigger pandemic response globally, and the first word which springs to mind describing what is going on is pneumonia, not covid-19. Further, they are at pains to confirm that it isn’t flu.

Given they are confirming it is pneumonia, we can see why they would treat it with oxygen (the right thing). But why move to intubation (the wrong thing)? And why are they at pains to say it isn’t caused by flu? Are such pains a red herring – or are they genuine clues as to what was really going on?

Of course, as with Wuhan patient zero, a possible explanation is that bacterial pneumonia is a secondary consequence of the initial viral infection. If this is the case, why didn’t Dr Cosentini make this clear? Moreover, if bacterial pneumonia was the proximate cause of illness and deaths witnessed in the hospital, then surely this would relegate covid-19 to the class of ‘just another respiratory virus’, like flu, that can weaken the immune system to the extent that it may help pneumonia flourish, but is eminently treatable in most cases with antibiotics?

The patient zero evidence along with what happened, and what was said, in Bergamo, is an indication that bacterial pneumonia may have been the primary infectious pathogen, and that SARS-CoV-2 was a coincidental infection simply present at the time.

Who was first on the crime scene:  SARS-CoV-2 or pneumonia?

What else is odd about the narrative? Have you ever read much discussion of pneumonia vaccines? No?

A purported preventative of one of the major causes of bacterial pneumonia is said to be the pneumococcal vaccine, which is sometimes given to the elderly and vulnerable, though as we understand it, pneumonia vaccines get much less public attention than influenza vaccines (readers should not miss the inclusion of the word “purported” in the above; we aren’t making any claims or recommendations here about pneumococcal vaccines).

Researchers have looked at the interaction between bacterial pneumonia and SARS-CoV-2 and found some interesting results, especially when investigating whether vaccination for pneumonia reduced the risk of covid-19 disease. They found that bacterial pneumonia vaccination reduced the risk of Covid-19, and by a statistically significant margin. Given this, why didn’t the authorities consider rolling out a bacterial pneumonia vaccine globally?

This might show that the actual burden of risk to patients is not SARS-CoV-2 at all but bacterial pneumonia. And that SARS-CoV-2 is secondary to bacterial pneumonia, or it masks bacterial pneumonia, not the other way around. Given this, it might be the case that bacterial pneumonia is acquired in the community rather than in hospital, and that viral infection follows bacterial pneumonia infection.

Other researchers say that the pathogenesis by bacterial causes are still being investigated, and acknowledge that the mechanisms for the interactions between viruses and pneumococci require further elucidation. If recent papers are representative of the state of medical knowledge around bacterial and viral interaction, what is the state of knowledge? It is obvious that, despite billions in research funding, the medical community really knows very little with any certitude!

However, research does suggest that sequential infection - pneumonia infection followed by viral infection, or parallel infection, both at once, are both possible. However, the default operating assumption in the medical literature and in practice is the opposite - viral then bacterial infection.

But pneumonia could not have done it because the pneumonia coinfection rates were low!

Researchers in the USA and the UK report that the risk of death increases many-fold for those patients co-infected by SARS-CoV-2 and bacterial pneumonia but note that despite the rate of coinfection being low, co-infections were mainly in intensive care patients.  So, one might conclude that there is no reason to blame deaths on pneumonia because it was largely absent.

One study found that hospitalised patients with Covid-19 were 1.5-fold more likely than non-covid-19 to have positive respiratory cultures, which was higher for patients requiring intubation. They also noted that a significantly higher proportion of patients had ventilator acquired pneumonia relative to non-covid-19 patients,

One might think this proves that SARS-CoV-2 is the deadly causative agent and not pneumonia. But if SARS-CoV-2 was (relative to bacterial pneumonia) a benign but very widely prevalent coronavirus, or if most cases in intensive care are simply PCR false positives or are from a ‘bystander’ virus, then the opposite conclusion can conceivably be true.

Let us explain. Many people will be in hospital for a non-respiratory comorbidity but labelled as suffering from covid-19 because of a PCR positive test and may go on to die of that comorbidity. These deaths will be categorised as SARS-CoV-2 virus deaths without pneumonia coinfection. However, those people carrying pneumonia as a primary pre-condition, but as yet undetected, may also receive the covid-19 label by the same mechanism and die of what looks like secondary pneumonia. In aggregate the percentage of coinfections will appear small because the proportion of detected pneumonia cases was small to begin with. The same would occur if we labelled everyone in the hospital as “human genome” positive: then all deaths would be caused by the “humanity virus”.

In case this isn’t clear, consider this example scenario. Imagine out of 100 “covid-19” deaths 10 were actually found to have bacterial pneumonia, and 90 didn’t. But of that 90, 85 die of a comorbidity, having been classified as covid-19 merely by virtue of a positive test. (In this regard it is to be noted that tests in hospital were frequently repeated until a positive one was “found”.)

Simplistically, one might conclude that 10%, i.e., 10 out of 100 covid deaths, were bacterial.  But the correct way of looking at this is to exclude the deaths which really had no respiratory component at all, which leaves 15.  So, in fact, 10 out of 15 (i.e., 2/3) of true covid deaths had a bacterial component.

Here is another mechanism. In published observational studies those suffering pneumonia will have an intrinsically higher mortality risk because they are already in intensive care. This introduces the obvious potential for selection bias. If the background mortality rate in intensive care is higher for pneumonia patients than for patients suffering other non-respiratory or other conditions, then it is inevitable that mortality for ‘pneumonia plus covid-19’ will be higher than for ‘another non-respiratory or other condition plus covid-19’. Especially if other selection factors are at play.

We also found 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. For instance, coinfection rates were dramatically higher in the far east compared to the USA.

Was ventilation an accomplice?

The claim of higher covid-19 mortality (in comparison to previously experienced respiratory viral infections) was based on direct firsthand reports in the media. Fortunately, retrospective studies have now been performed to codify the experience. But unfortunately, they paint a grim picture, not of a pandemic but of potential data bias. Much of this bias involves a medical intervention called ventilation, which we might view as playing the role of the accomplice in our whodunnit.

Many of the frightening images being circulated in the media in spring 2020 were from ICUs showing patients being treated on ventilators. It was claimed that people were dying of acute respiratory distress caused by SARS-CoV-2 whilst being ventilated, including non-elderly adults age groups for which the infection fatality rate of the virus is known to be relatively low. 

Ventilator associated pneumonia (VAP) is a well-known condition, where ventilated patients have a significantly higher chance of dying after contracting ‘secondary’ pneumonia during ventilation.  The majority of patients dying of VAP in spring 2020 were recorded as having been caused by SARS-CoV-2.  However several researchers have acknowledged that other microbiologic and polymicrobial cultures are to be found in patients on ventilators yet are not directly implicated in the deaths. SARS-CoV-2 is named as the guilty culprit.

ICU triage criteria, ICU efficiency, and isolation measures differed between the pandemic and the non-pandemic periods. It is therefore entirely conceivable that the differences in lethality may be entirely explainable by changes in practice. There are also reports that people were kept on ventilators longer to protect staff.

Clearly ICU patient care is very complex and challenging. There are myriad factors that affect rates of VAP, including patient positioning, sedation, oxygenation, medication, etc. Outcomes will inevitably be sensitive to any deviation from well-established practices as they relate to any of these parameters. Two other 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.

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

In contrast with Italy, in spring 2020 there was no evidence of excess mortality in Germany. Was this due to a different policy on ventilation?  This report in the Frankfurter Allgemeine suggests this might just be the case, given that it questioned whether ventilation was at all appropriate and, also asked whether it was right to put patients on ventilators to protect staff.

Even Anthony Fauci admitted that ventilation was over-used.

But it couldn’t have been pneumonia because they were given antibiotics!

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 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.

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. 

In his 2008 article in the Journal of Infectious Diseases (which reported on autopsies of well-preserved victims of the Spanish Flu pandemic), Anthony Fauci concluded that:

“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.”

What happened to the stockpiles during the covid ‘pandemic’, or were these never actually created?

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 acute respiratory distress syndrome (ARDS) than would have been seen historically. Given the lateness of presentation to hospital, and despite the administration of antibiotics, this maybe 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.

Outpatient antibiotics prescriptions changed dramatically during the period January to May 2020, exceeding expected seasonal reductions:

In contrast to the evidence presented above physicians in Toledo, Spain, empirically administered antibiotics to covid-19 patients during spring 2020, contrary to official guidance. This resulted in zero hospitalizations or deaths in their care homes after they started routine administration. Their resulting mortality over spring 2020 was approx. 7% versus 28% in other comparable care homes (and the 7% died before they started routine antibiotic use).

Pneumonia has ‘previous’

Bacterial pneumonia has a track record of previous 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 in 1918 and 2020-2023 the historical lesson from public health is that people need to fear viruses, yet pneumonia does not get public attention.

Evidence from the crime scene

The chart below shows the data for respiratory disease as an underlying cause of death for New York City hospitals for 2020 (J00-J98). This does not include Covid-19 (code U07.1 in the ICD Chapter "Codes for Special Purposes”). Digging further into specific codes, we find much of the increase in deaths was accounted for by deaths attributed to other non-influenza viral and bacterial pneumonias:

Could a high proportion of these deaths be ventilator associated pneumonia deaths?

Now look at the hospital deaths that list covid-19 as the underlying cause versus those that list a respiratory death code (J00-J98). 

The next chart shows the weekly number of hospital deaths with respiratory disease as a cause, compared against covid-19 deaths:

This may look startling but given that New York City’s largest healthcare systems reported administering thousands of SARS-CoV-2 PCR tests a day early on, both in hospitals and in other settings, it should not be a surprise. However, we can see that genuine bacterial pneumonia cases remain prominent in NYC despite the explosion of covid-19 cases generated by PCR testing.

A pinpoint pandemic?

The pattern of spread, and the geographical concentration of the Covid-19 mortality toll is not what one would expect from a respiratory virus. Deaths were highly localised in care homes and hospitals, within elderly age groups and those suffering multiple comorbidities and in specific cities and regions such as New York, Lombardy and Madrid.

For instance, by May 2020 the 'pandemic' in the USA had only occurred around a few points that could have been pinned on a map, and everywhere else failed to experience it.

"A pinpoint pandemic?”

If the pneumonia was caused by the newly-named pathogen, then how was it introduced to “localised populations”? If we cannot count on a natural explanation, then perhaps a man-made one is worth considering.

Discussion

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.

Does pre-existing exposure to bacterial pneumonia lead to a higher propensity to acquire a viral infection, such as influenza or SARS-CoV-2? We suggest that maybe SARS-CoV-2 infection (or at the very least a positive test for it) can be secondary to pneumonia, or it can mask pneumonia, and not necessarily the other way around.

We have found that high rates of ventilator induced pneumonia, attributed to SARS-CoV-2, are confounded by changes in protocols, delays in admission, overuse of ventilation and classification biases and therefore any claim that SARS-CoV-2 was uniquely dangerous cannot be relied upon. Bacterial infection is ever present at the scene.

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 respiratory virus. It is highly localised in specific geographically distant regions and cities. It is a pin-point pandemic.

The central question remains: Was SARS-CoV-2 used as a decoy and were bacterial pneumonia deaths used as proof that SARS-CoV-2 was a deadly respiratory pathogen?

Allegorically speaking, 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.