It was pneumonia, not Covid, what done it

Martin Neil | 11 Sep 2023

THE first victim of what became known as Covid-19 was ‘Patient Zero’, whose case was recorded on December 26, 2019, in Wuhan, China. He was admitted to hospital with respiratory symptoms including fever, dizziness and a cough. Patient Zero was relatively young and without significant health problems, yet he was subjected to a battery of tests, including genetic sequencing of fluid from his airways. We are told this led to the discovery of a new coronavirus subsequently dubbed SARS-CoV-2. As described in the seminal paper in Nature from February 3, 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 quite typical of regular bacterial pneumonia. Given that he showed no unusual symptoms, clearly this was not a routine medical response to what looks like a typical respiratory infection.

This is not all that is odd about the narrative. Have you ever read much discussion of pneumonia vaccines? Researchers have found that a purported preventive of one of the major causes of bacterial pneumonia, the pneumococcal vaccine, is sometimes given to the elderly and vulnerable. Researchers whohave looked at the interaction between bacterial pneumonia and SARS-CoV-2 have found that bacterial pneumonia vaccination reduced the risk of Covid-19 by a statistically significant margin.Buthow can a vaccine for a bacterium reduce the risk from a virus?

Research into the etiology of community-acquired pneumonia concludes that it is often observed that viral species colonise the nasopharynx of patients after they have contracted bacterial pneumonia, suggesting that sequential pneumonia infection followed by viral infection, or parallel infection, where the infections occur together, are both possible. However, the default operating assumption in the medical literature and in practice is the opposite: viral followed by bacterial infection, and since 2020 with SARS-CoV-2 identified as the ‘novel’ root cause.

These research results suggest 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,might itbe the case that bacterial pneumonia is acquired in the community rather than in hospital, and that the signal of viral infection follows bacterial pneumonia infection? And if sowhy was the focus on a virus and not on the perennial risk of bacterial pneumonia?

Many of the frightening images 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 while being ventilated. Ventilator associated pneumonia (VAP) is a well-known condition in which ventilated patients have a significantly higher chance of dying after contracting ‘secondary’ pneumonia during ventilation. Many patients dying of VAP in spring 2020 were recorded as having died from SARS-CoV-2. 

High rates of ventilator-induced pneumonia are acknowledged by the authorities but their use continues to be defended as necessary. Even Anthony Fauci admitted that ventilation was overused. This overuse of ventilation was accompanied by changes in protocols, delays in admission and changes to medication and testing. Given that most people suffering death by ‘Covid-19 with respiratory symptoms’ died in ICUs, blaming these deaths on SARS-CoV-2 seems unscrupulous. The observational data is heavily confounded, and these deaths are just as likely to have involved, inter alia, bacterial infection and changes in treatment protocols as by detected or undetected pathogens. 

In a 2008 article in the Journal of Infectious Diseases (on the Spanish Flu pandemic), Anthony Fauci concluded: ‘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.’ 

Regardless of whether such stockpiles of antibiotics were created, community antibiotic prescriptions were reduced dramatically in spring 2020. Recall that in spring 2020 people were told to self-isolate if they suffered Covid symptoms. This would therefore buy time for pathogens to multiply and for a more severe condition to develop, which might subsequently be harder to manage. Many people would have presented late to ICU, with incipient or lingering pneumonia (perhaps from the previous normal flu season), disguised as Covid-19, and may have been left untreated with antibiotics until their condition deteriorated further.

A reluctance to perform bacteriological investigations in ICUs (and expose staff to a supposedly deadly pathogen) may have been a further contributory factor. Patients would therefore have suffered higher levels of respiratory distress than would have been seen historically. The lateness of presentation to ICU, and the very late administration of antibiotics, may have failed to save them from a (detected or undetected) bacterial pneumonia infection.

Conflating pneumonia and Covid-19 repeats an official longstanding tactic of conflating the attribution of influenza and pneumonia. There is evidence to suggest that a 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.

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

A (pneumonia) hypothesis, that a proportion of Covid-19 deaths in 2020, specifically those with associated respiratory symptoms, were caused by bacterial pneumonia, and that bacterial pneumonia may have been the primary, not the secondary, infection, starts to look rather strong. It matters because it challenges received wisdom about the true causative agent of the deaths resulting from the ‘pandemic’ – a bacterium or a virus, both or neither? It also brings into question how the agent was spread and, most significantly, it challenges how and if the illness was appropriately treated. 

Further confirmation that bacterial pneumonia, not Covid, is the real danger has come from two groups of doctors who have had 100 per cent success using antibiotics to treat ‘Covid’.

In allegorical terms it is akin to a scene from an Agatha Christie novel:  SARS-CoV-2, a bystander used as a decoy, is found guilty of the crime with ventilation as his accomplice, but the actual criminal, who has got off scot-free, is in fact bacterial pneumonia (undetected until the denouement).  In other words, SARS-CoV-2 has been framed.

This article is based on Whodunnit? (unabridged) by Professor Martin Neil, Jonathan Engler, Dr Jessica Hockett and Professor Norman Fenton.

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