Discover more from Where are the numbers? by Norman Fenton and Martin Neil
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.
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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 beeb 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.
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 (which are coded together as ICD-10 codes J09-J18 by the WHO) 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, 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?
Note that in this article we are not attempting to explain all cases and deaths coded as covid-19; rather, we are focusing only on cases and deaths where people presented with respiratory symptoms associated (according to our hypothesis) with bacterial pneumonia, distress and death. After all, it is these cases that were used as the spark to create fear of the ‘pandemic’, via news videos and reports. As such, they deserve special attention. Of course, many other causes of death other than bacterial pneumonia were misattributed as covid-19. This is simply one distinct category.
déjà vu - Does this story sound familiar?
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.
When medics say ‘pneumonia’ they can mean cause, effect and/or mechanism (all at once or single or in arbitrary pairings). This confusion and conflation of causality is typical in medicine and leads to both muddled definitions and a vulnerability that is exploitable by people with a sharper appreciation of the power of language and definitions. (Names have power, after all).
Mens Rea - "the act is not culpable unless the mind is guilty".
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.
At the event Rick Bright suggests the problem of long-term development might be sidestepped if:
“….there were an urgent call for an entity of excitement that is completely disruptive and is not beholden to bureaucratic strings and processes.”
Anthony Fauci says in response:
“So, we really do have a problem of how the world perceives influenza and it’s going to be very difficult to change that unless you do it from within and say, I don’t care what your perception is, we’re going to address the problem in a disruptive and in an iterative way because she does need both.”
And continues by saying:
“But it is not too crazy to think that an outbreak of a novel avian virus could occur in China somewhere. We could get the RNA sequence from that to a number of regional centers if not local, if not even in your home at some point, and print those vaccines on a patch of self-administer.”
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 26th 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 relatively young age and absence of 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 patient’s X-ray / CT findings also seem to suggest an unremarkable pneumonia: "bilateral focal consolidation, lobar consolidation and patchy consolidation, especially in the lower lung."
Chest radiographs were abnormal with air-space shadowing such as ground-glass opacities. However, this is not unique to covid-19. Ground glass opacities are also commonly associated with influenza infections and with a wide range of other lung conditions, including pneumonia.
Given this evidence, it is reasonable to ask whether patient zero may have been a case of bacterial pneumonia?
It is worth noting that this Nature paper was circulated widely to medical practitioners worldwide and has subsequently earned a place in the top 100 most widely cited scientific papers to date. Despite the importance of the findings, it remains largely unchallenged in academic literature and has simply been accepted at face value.
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:
“People keep describing this as like the flu. It’s worse than that, no?”
“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?
In another interview, Dr Cosentini says his hospital has admitted "900 patients with a pneumonia needing oxygen" and that "the virus circulated among us before we recognized it." He advises that UK hospitals “prepare for the struggle” by reorganizing emergency departments “to become great respiratory units with different level of intensity” and mentions needing to “pre-empty the hospital” in this effort. He also mentions “a young patient with severe pneumonia,” but makes no connection to covid-19 or to whether the young patient has tested positive for the virus.
Of course, as we’ve observed with the Wuhan patient zero, a possible explanation is that bacterial pneumonia was 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.
Which 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.
(In relation to this section, readers should not miss the inclusion of the word “purported” in the above, and should pay particular attention to the 2nd footnote below.)
Lewnard et al 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.
“Evidence that upper respiratory commensal bacteria promote viral infection dates at least to 1987 , with studies demonstrating that enzymes expressed by bacteria (including pneumococci ) enhance influenza virus replication and pathogenicity. More recently, blunting of innate immune responses to influenza virus during pneumococcal colonization has been demonstrated in human challenge studies . Such mechanisms of interaction may account for epidemiologic observations of enhanced virus acquisition and symptom risk among carriers of pneumococci and other respiratory commensal pathogenic bacteria [9, 13]”
This raises an interesting question: Does pre-existing exposure to bacterial pneumonia lead to a higher propensity to acquire, and/or fail to mount a strong immune response to, a viral infection, such as influenza or SARS-CoV-2? If this were the case, then bacterial pneumonia might be better considered to be the primary infection and the virus the secondary, rather than the other way around. If we put the chicken before the egg, the root cause of illness, hospitalisation or death might be pneumonia (inadequately treated), and not whatever virus occupies the nasopharynx or lungs at the time.
Note that the main aim of their study was to examine the effects of pneumonia vaccinations, of two types PCV13 and PPSV23, on Covid-19 diagnosis, hospitalisation and mortality. Here is what they found (aHR is the hazard ratio – any value below one shows the vaccines had a beneficial effect):
Clearly the authors claim the 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.
Vardhaam et al say this about the etiology of community acquired pneumonia (CAP):
“It is often observed that viral species colonize nasopharynx of patients with CAP. Whether they are the primary cause or contribute to the pathogenesis by secondary bacterial causes is still being investigated.”
Howard et al say:
“interactions between viruses and pneumococci in the nasopharynx during asymptomatic periods might have a role in onset of subsequent acute respiratory illness. The mechanisms for these interactions, along with other potentially associated host and environmental factors, and their role in ARI pathogenesis and pneumococcal transmission require further elucidation.”
Also, this paper by Lu et al found that the presence of Prevotella bacterium, and other bacteria, in SARS-CoV-2 patients:
The oropharyngeal microbiome characterization was different between SARS-CoV-2 infection and infections caused by other viruses. Prevotella could act as a biomarker for COVID-19 diagnosis and of host immune response evaluation in SARS-CoV-2 infection. In addition, the cross-talk among Prevotella, SARS-CoV-2, and sphingolipid metabolism pathways could provide a basis for the precise diagnosis, prevention, control, and treatment of COVID-19.
Finally, Upadhyay et al report on the use of an expanded PCR panel testing for the identification of respiratory pathogens and coinfections in influenza-like illness:
A detailed analysis of the detected pathogens showed that S. aureus was the most prevalent on both platforms (~30%) followed by SARS-CoV-2 (~25%), HRV (~15%) and HHV-6 (~10%)…..Coinfections between viruses and bacteria were the most common (~69%), followed by viral–viral (~23%) and bacterial–bacterial (~7%) coinfections.
They go on to say:
S. aureus was the most prevalent bacterial coinfecting pathogen, where SARS-CoV-2/S. aureus coinfections were the most common (~30%)
S. aureus (Staphylococcus aureus) is a Gram-positive spherically shaped bacterium, is frequently found in the upper respiratory tract and on the skin. It is a recognised cause of bacterial pneumonia.
These are recent papers so are representative of the state of medical knowledge around bacterial and viral interaction. And 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!
Zahin et al (UK) and Langford et al (USA) 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 (3.5% of patients with confirmed covid), co-infections were mainly in intensive care patients (8.1%). Hedberg et al found the coinfection rate for bacteria with SARS-CoV-2 was 4% in 2020, compared to 27% for influenza. So, one might conclude that there is no reason to blame deaths on pneumonia because it was largely absent.
However, Weidmann et al found that hospitalised patients with Covid-19 were 1.5-fold more likely than non-covid-19 patients 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. After all, as Monotti, notes:
“if we were to have routinely tested everyone for spike proteins or other coronavirus target genes before 2020, we would have found them in approximately one third of what we call winter colds or flus if not higher.
This is just to say that there is no public health emergency any different than any other year. There are approximately 200 respiratory viruses that can lead to respiratory disease. Many are coronaviruses.”
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.
Let’s look at other studies. From Korea Hyobin et al found results that stand in stark contrast to those presented by Langford and Zahin:
…..(COVID-19 associated co/secondary infection prevalence is up to 45.0%). In the COVID-19 pandemic, Streptococcus pneumoniae is the most common coinfecting pathogen. Half of the COVID-19 mortality cases showed co-infection, and pneumonia-related COVID-19 mortality in patients >65 years was 23%.
So, the Korea researchers found 45% of the patients showed coinfection but, in the USA, it was reported as significantly less at 3.5%. How can the same pathogen have such a different coinfection profile? And from the Korean study the fatality rate for elderly was 23% if they had pneumonia coinfection, but it was much less in the USA.
Again, things don’t add up. Pneumonia coinfection rates might be reported as low, but this could be artefactual. Is there any evidence of selection and observational biases that might explain misleadingly low coinfection rates?
We have teams of researchers claiming wildly different coinfection and mortality rates for pneumonia and covid-19 and these differences get little attention in medical academic literature. This has not gone unnoticed with Weidmann et al, who published a highly detailed paper looking at the rates of microbial testing, for covid-19 and non-covid-19 cases, who say this about other studies:
“.....none of these studies have assessed the concurrent rate of bacterial CAP, HAP, and VAP rates compared to non-COVID patients for whom respiratory cultures were ordered during the same period. In addition, no previous studies have assessed whether respiratory culture ordering was appropriate based on rates of positivity in the setting of COVID-19 for these groups. This lack of a direct comparison between COVID-19 and non-COVID-19-infected patients makes it difficult to determine whether the highly disparate reported rates of bacterial coinfection represent the heterogeneity of the patient populations studied or a truly elevated risk of bacterial pneumonia associated with SARS-CoV-2 infection.”
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.
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.
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.
Was ventilation an accomplice?
The claim of higher covid-19 mortality (in comparison to previously experienced respiratory viral infections), despite the best and most expensive treatment regimens (intensive care units – ICUs) that modern healthcare systems have to offer, 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.
“a type of lung infection that occurs in people who are on mechanical ventilation breathing machines in hospitals. As such, VAP typically affects critically ill persons that are in an intensive care unit (ICU) and have been on a mechanical ventilator for at least 48 hours. 1]. VAP is a major source of increased illness and death. Persons with VAP have increased lengths of ICU hospitalization and have up to a 20–30% death rate. Critical care physician Paul Mayo summarized the risk well saying, “Putting a person on a ventilator creates a disease known as being on a ventilator”.
Typical of these is the study by Rouyer et al who examined patients in the ICU of a 350 acute-care bed hospital in the Ile de France region in France from 1 March 2020 to 1 May 2020, and compared them with non-Covid-19 patients who developed VAP in the ICU from 2011 to 2019 and with patients who did not develop VAP from 1 March 2020 and May 2020. Their hypothesis is that covid-19 is novel and more deadly:
“The main hypothesis to verify is that VAP in COVID-19 is a new ‘pathology’ with some peculiarity that needs different healthcare than VAP in non-COVID-19 patients.”
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.
However, there are lots of problems with this paper, although some of these were inevitable and a consequence of it being a retrospective and not a controlled study. Things to note include:
The VAP non-covid-19 group, comprising 37 patients, from spring 2020 disappears from the paper as soon as they are introduced. This means there is no basis for directly comparing treatment regimens in spring 2020 (i.e., during the same period) for non-covid-19 patients against covid-19 patients. The justification for this is nonsensical:
“The choice of comparing two different timeframes was motivated by the following: (i) during the COVID-19 pandemic, the ICU of our hospital was exclusively reserved for COVID-19 patients; (ii) VAP in non-COVID-19 patients is less frequent than COVID-19 patients, and our ICU’s capacity is limited. For these reasons, we were forced to select non-COVID-19 patients during a longer timeframe.”
They describe the populations they set out to compare in their study as:
“From 1 March 2020 to 1 May 2020, 346 patients were hospitalised in the ICU. Among them, 100/346 (29%) were SARS-CoV-2 PCR-positive, 79/100 (79%) received mechanical ventilation, 42/79 (53%) experienced VAP, and 12/42 (28%) had a VAP relapse. From 1 January 2011 to 31 December 2019, 188 patients experienced VAP in the ICU, and 8/188 (4%) had VAP relapse.”
So, over a two-month period in 2020 42 from 79 experienced VAP, yet over a 9-year period 188 patients experienced VAP in the same ICU (the authors fail to provide the denominator). This suggests the chance of a patient being ventilated in spring 2020 was significantly higher than at any time in the preceding decade.
Everyone in the ICU in March to May 2020 was a Covid-19 patient and all had acute respiratory distress syndrome (ARDS). This was because ARDS and a Covid-19 diagnosis was a mandatory criterion for hospitalisation in the ICU for all Covid-19 patients. Other patients with other conditions were not put in the ICU, whilst historically in the period 2011-2019 only 33% of patients in the ICU were suffering ARDS.
So, in the spring 2020 cohort all subjects had ARDS and all of them had SARS-Cov-2, yet it is SARS-CoV-2 that was found to be statistically significant. The mere act of universal labelling would achieve the same ends: mark everyone in the ICU with a red sticker and this would be found statistically significant.
When we look at the microbiological isolates taken from patients suffering from VAP we find that gram-positive bacteria are present in covid-19 patients at a statistically significantly higher rate compared to non-covid-19 patients. Staphylococcus pneumoniae (pneumococci) are gram-positive, hence there is significantly higher presence of pneumonia (caused by this pathogen) in this cohort, which the authors fail to discuss.
It looks like this study suffers heavily from selection bias; it ignores the potential role of bacterial pneumonia strongly suggested by the data, and it has intentionally discarded data that might contradict its conclusions. Given these facts any claim of a higher mortality rate for Covid-19 patients must be in question.
Rouze et al performed a multi-centre study of 1576 patients that had suffered VAP and who had been admitted with SARS-CoV-2, influenza or no-virus. They found that SARS-CoV-2 patients had significantly higher rates of VAP than those with flu or no-virus: SARS-CoV-2 (36%), influenza (22%) or no-virus (16%). Careful reading of the paper shows that the flu and no-virus cohorts were selected prior to spring 2020, before the pandemic. Therefore, again, the study suffers from retrospective selection bias, which at least the authors recognise:
“Fourth, 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.
Rouze et al also looked at the incidence of VAP and SARS-CoV-2 and found that SARS-CoV-2 patients were around twice as likely to develop lower respiratory tract infections (including VAP). However again we find selection bias and treatment differences. The authors say:
“During the pandemic it was impossible to have patients with diseases other than COVID-19, because ICUs were full of COVID-19 patients. Inclusions of patients with influenza or no viral infection, admitted to the ICU before the pandemic, allow a fair comparison of VA-LRTI incidence between COVID-19 patients and other at-risk patients.
…..the higher incidence of VA-LRTI in patients with SARS-CoV-2 pneumonia is probably related, at least in part, to the longer duration of mechanical ventilation.”
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. Lastly, hidden within this paper we also find that the rate of gram-positive microbial infection, including bacterial pneumonia, was twice as high in the SARS-CoV-2 patients (19.5%) than found in historical influenza patients (11%).
Henri-Wicky et al reviewed similarities and differences between ventilator associated pneumonia in SARS-CoV-2 infection and with acute respiratory distress syndrome (ARDS):
“The increased risk of VAP in SARS-CoV-2 infections, as compared to other ARDS, may have been due to multiple factors including less rigorous use of standard prevention strategies during COVID-19, disease and therapy-associated immune impairment, more prolonged duration of mechanical ventilation, prolonged use of sedation, more frequent need for prone ventilation, and higher risk for pulmonary infarction with associated superinfection. Although ICU overcrowding could also have been a factor, the study of Blonz et al. was done in an “uninundated” region where ICUs had adequate facilities for providing usual level of patient care, and thus there were less potential breaches in contact isolation. Similarly, in another single center study, a VAP rate reaching 74% was observed during both the first overcrowded wave and during the second wave where the ICU beds were sufficient .”
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. Gao et al looked at the relationship between length of ICU stay and unresolved VAP in a Chicago hospital, using 2018-2020 as a comparison, and concluded that:
“Unsuccessful treatment of VAP is associated with higher mortality. The relatively long length of stay for patients with COVID-19 was primarily due to prolonged respiratory failure, placing them at higher risk of VAP.”
The investigators found nearly half of patients with COVID-19 develop a secondary ventilator-associated bacterial pneumonia:
“Those who were cured of their secondary pneumonia were likely to live, while those whose pneumonia did not resolve were more likely to die,” Singer said. “Our data suggested that the mortality related to the virus itself is relatively low, but other things that happen during the ICU stay, like secondary bacterial pneumonia, offset that.”
“The importance of bacterial superinfection of the lung as a contributor to death in patients with COVID-19 has been underappreciated, because most centers have not looked for it or only look at outcomes in terms of presence or absence of bacterial superinfection, not whether treatment is successful or not”.
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.
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.
Weidmann et al say:
“Bacterial pneumonia in COVID-19 patients was much more likely to be ventilator associated and less likely to be community acquired when compared to non-COVID patients”
Table 4 in their study shows the categorization of SARS-CoV-2 and pneumonia cases:
From the table, and comments made by the authors about testing and record keeping, it should be clear that it would take only some small shifts in the number of cases from community or hospital acquired pneumonia to make it appear that VAP rates are significantly worse for SARS-CoV-2 positive patients. Delaying or accelerating the culture testing until after a patient has been admitted or intubated might make a big difference to how a patient is eventually categorised, especially during turbulent times or where staff are new or inexperienced.
To further illustrate how sensitive the classification is to secondary (VAP) pneumonia rather than primary (community), according to a report in the BMJ very often patients were rushed onto ventilation:
“Two thirds (132) of covid-19 patients who required critical care in the UK had mechanical ventilation within 24 hours of admission, an audit of patients from England, Wales, and Northern Ireland has found.”
Any community acquired bacteria pneumonia infection will therefore most likely not be detected for patients rushed into ICU and ventilated. Any hospital infection registered in the system for a patient now ventilated, but ventilated within 48 hours, would then be recorded as a VAP infection. In this way primary bacterial pneumonia infections might be recorded as secondary.
Note that overall similar numbers of pneumonia patients that have tested positive (249) for SARS-CoV-2 as have tested negative (219), in Weidmann et al, suggesting there is a 53% chance their symptoms would be attributed to a positive SARS-CoV-2 test result when in fact pneumonia was always the underlying risk.
In contrast with Italy in spring 2020 there was no evidence of excess mortality in Germany in those months. Was this due to a different policy on ventilation? This report in the Frankfurter Allgemeine suggests this might just be the case. Lung specialist Thomas Voshaar, said:
“Of the ventilated Covid-19 patients, unfortunately, only between 20 and 50 percent have survived so far. If this is the case, we have to ask: Is this due to the severity and course of the disease itself or perhaps the preferred treatment method? When we read the first studies and reports from China and Italy, we immediately wondered why intubated so often was done there. This contradicted our clinical experience with viral pneumonia.”
On the use of ventilators to protect doctors and nurses from the virus he said “We cannot subordinate the well-being of the patient to the well-being of the staff. In terms of content, it is also nonsensical. Experienced pulmonologists and intensive care nurses can keep the aerosol load low.’”
The sedative, painkiller and muscle relaxant drugs needed to keep patients on ventilators were running low in spring 2020 showing that there was a huge spike in demand for use with the high number of patients put on ventilation in places like New York City.
Lastly, even Anthony Fauci admitted that ventilation was over-used:
“We very, very readily would put people on mechanical ventilation. When we found out through clinical experience it might have been better just to make sure we position them properly in the prone or supine position, and not necessarily intubate somebody so readily, which might have actually caused more harm than good.”
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 (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.
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 those 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 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.
King et al reported that outpatient antibiotics prescriptions changed dramatically during the period January to May 2020, exceeding expected seasonal reductions:
Note that we are not claiming that this mechanism would have caused a massive increase in national mortality figures attributed to pneumonia, but it is enough to cause a temporary spike in pneumonia cases/deaths, which would look to hospital staff like it was caused by a novel and deadly new virus for which they were testing, and finding, with a newly launched PCR test.
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).
Likewise in Romania a physician, Flavia Groșan, was reported in the media as approaching covid-19 as “atypical pneumonia”, saying there were huge mistakes with excessive oxygen therapy and intubation:
“Too much oxygen for too lengthy periods at a time, says Groșan, can lead to cerebral edema which in turn can cause death.”
She gave her patients ‘enough’ oxygen for their needs, antibiotics and other cheap medicines. On the choice of antibiotics she said:
“There are only three antibiotics in the macrolide class, erythromycin, which everyone knows, azithromycin and clarithromycin. I don’t like azithromycin because it’s a weaker copy of clarithromycin. I worked in some very interesting clinical studies on pneumonia and there I learned about the viral tropism of clarithromycin, as well as the anti-inflammatory role of clarithromycin, which no antibiotic has. I have been working with this antibiotic in viral and atypical pneumonias for 10 years. When the pandemic hit I went for an etiological treatment, clarithromycin. Of course, in addition to this antibiotic, there are several adjuvant treatments, because it can’t cope alone. It is a treatment scheme that is my own.”
She reported healing 100% of some 1,000 patients using this approach.
Pneumonia has ‘previous’
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.
As Lewnard et al have said, upper respiratory commensal bacteria promote viral infection. Infection with a virus might therefore be a necessary but not a sufficient condition for illness and death, and in the absence of serious bacterial infection a viral infection, in itself, may not present a serious hazard to health. Given there are literally millions of (known and unknown) circulating viruses and virus variants it might not even matter what the virus is. It is the severity of the bacterial infection and the vulnerability of the host to this infection that matters.
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,
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?
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. Furthermore, given that these tests generated exceptionally high positivity rates, that climbed to 70% and higher, it should be clear that the observed covid-19 case count was dominated by testing rather than a genuine respiratory illness. However, we can see that genuine bacterial pneumonia cases remain prominent in NYC despite the explosion of covid-19 cases generated by PCR testing.
In the UK the ICNARC report for Covid-19 in critical care charts the “all pneumonias” and covid-19 admissions for 2020 to January 2023. It shows that pneumonia was effectively replaced with covid-19 diagnosis (the majority of the covid-19 admissions may have been simply positive PCR tests rather than symptomatic respiratory conditions).
The global downward trend in bacterial infections, as well as in virtually all other infections during spring 2020 is amply illustrated by a screenshot of a respiratory pathogen prevalence in the USA. The chart was published by the BioFire syndromic trends reporting system and shows the USA percentage detection rate of pathogens by BioFire clinical diagnostic systems (PCR), from 2019 through to 2021. The reported rate of bacterial pathogens detected at least halved after SARS-Cov-2 appears on the scene in the USA, UK and Europe in February 2020.
Given that the claim of interference frequently made refers to interference between viral (and not bacterial) infections, then any claim that SARS-CoV-2 out-competed pneumonia does not hold water. The reduction in bacterial infections can only be attributed to changes in diagnostic testing, treatment and case definitions.
A pinpoint pandemic?
Bacterial pneumonia is said to be the most common kind of pneumonia and is claimed to spread by droplets and fomites. It is also generally viewed as the most serious kind of pneumonia. It doesn’t spread like a respiratory virus, through the air, but spreads by touch or via surfaces. Therefore, outbreaks are highly localised.
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.
Given pneumonia spreads by droplets we searched for experiments that attempted to determine how bacterial pathogens spread through a population over a geographical area.
Luckily for us (but not for the unwitting and unknowing participants in the experiments) the US Navy conducted such experiments (in secret). One was called Operation Sea Spray, which was a 1950 U.S. Navy secret biological warfare experiment in which Serratia marcescens and Bacillus globigii bacteria were sprayed over the San Francisco Bay Area in California, to determine how vulnerable a city like San Francisco may be to a bioweapon attack.
None of these experimental results have been released so we have no evidence to determine whether and how a bacterial pneumonia outbreak might occur and spread. It certainly doesn’t look like the experiments caused any global bacterial outbreaks or pandemics. We suggest that, under modern sanitary conditions, very large-scale pneumonia outbreaks in highly concentrated areas look to be unlikely to occur naturally. After all, we haven't seen one since 1918, which was also a time of malnutrition and insanitary post war conditions, combined with huge movements of people and experimental vaccination in at least a few U.S. locations. We must therefore 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 then, changes in ventilation policy and practices coupled with new PCR testing, would be enough to cause the pin-point pandemic effect.
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.
We asked: 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. Therefore, was SARS-CoV-2 a coincidental, bystander, infection simply present at the time of presentation or testing and the actual burden of risk to patients is not SARS-CoV-2 (or other viruses) at all but bacterial pneumonia?
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. Under modern sanitary conditions large scale pneumonia outbreaks in highly concentrated areas are unlikely to occur naturally. Changes in ventilation policy and practices coupled with new PCR testing, would be enough to cause the pin-point pandemic effect.
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.
Where are the numbers? by Norman Fenton and Martin Neil is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.
Pneumonia is a malleable and manipulable term. It covers viral and bacterial infection and resulting inflammation and other symptoms. The cause or type of pneumonia is dependent on what microbial or viral agents were detected in testing or by cultural growth from a sample. Hence the attribution of cause is entirely dependent on whether or when a sample is taken and the number and kinds of tests done to identify what is in the sample. There are dozens of species of bacteria, and some undergo genetic transformation, as do the thousands of known and unknown viruses.
After publication a reader deposited a critique of our work on github and pointed out that the metagenomic sequencing of Wuhan-Hu-1 lung samples of COVID patients run discovered a large number of Prevotella reads (Prevotella is a gram-negative bacteria).
Note that we are not making any claims here about the efficacy or safety of pneumonia vaccination but are instead simply pointing out evidence that contradicts the central covid narrative. In common with many others, we are extremely doubtful that the immune response against any respiratory illness can be usefully and safely augmented by an intramuscular injection. Based on what we have observed in relation to other vaccine trials, we certainly do not take the results reported at face value.
The important point being made here is nothing to do with whether pneumococcal vaccines work or should actually have been rolled out. No, it is that those who DO have an almost religious-like acceptance of any pro-vaccine data reported ignored this study, despite the fact that (for those who would have been inclined to believe the data) it should have resulted in discussions over urgent policy change.
The role of financial incentives such as those described here may have fuelled the number of people tested for SARS-CoV-2 and ensured covid-19 appeared on death certificates. This is more or less confirmed by this article in USA Today. Amounts received by hospitals for a portion of these incentives can be found in this online database.
Some have asserted that the increase in deaths that list a non-covid respiratory disease deaths as underlying cause on their death certificates were “missed” covid deaths. Yet when we look at hospital deaths that list a non covid-19 respiratory disease, as underlying cause, alongside those deaths with both a J00-98 code and an U07.1 code (covid-19) on the death certificate, we see that these respiratory disease deaths were very likely to have covid-19 listed elsewhere on the death certificate. Hence, they cannot be categorized as “missing” covid-19 deaths.
To date the global mortality burden shows that covid-19 is a respiratory illness comparable to and less risky than flu for all but the sickest/oldest people. However, from this chart we can the respiratory disease mortality burden exponentially increased— and did so toward the end of flu season, when the people most susceptible to a respiratory illness would have already succumbed to flu or similar. This NYC data is entirely inconsistent with previous viral or pneumonia outbreaks, including that seen in 1918, suggesting some other mechanism is needed to explain the entirety of the mortality pattern.
This is no ‘conspiracy theory’: it is widely and thoroughly documented in online science magazines such as Discover and Smart News and Wikipedia provide an overview of the experiments and notes the US Senate subcommittee hearings on the subject. In the UK similar experiments continued until 1979, as reported by the Guardian newspaper, including experiments using anthrax. Mathew Crawford wrote an article and made special notice of the increased pneumonia rates reported after these experiments.