By Professor Martin Neil - September 16, 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 who have 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.

But how 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 it be 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 so why 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 . . .

[SNIP]