Further evidence that treatable pneumonia was significantly under-diagnosed in the covid era.

A number of people, including

Martin Neil

,

Jessica Hockett

,

Norman Fenton

and I, have written extensively about the possibility that bacterial pneumonia was a significantly under-diagnosed, and therefore under-treated, feature associated with the clinical syndrome called covid:

Whodunnit? {unabridged}

This situation would have arisen primarily because the covid treatment protocols would have ensured that a positive PCR test meant that the patient’s illness was regarded as “purely viral” and therefore not amenable to treatment with antibiotics.

It is impossible to underestimate the cataclysmic shift in medicine which has befallen us lately:

• In 2019 the following mantra would have been drilled into medical students: Always go primarily by signs and symptoms; even established tests should be regarded merely as an adjunct to diagnosis; treat the patient, not a diagnosis.

• Now on the other hand, as regards “covid” at least, the following seems to be the case: Whatever the signs and symptoms, a novel test identifying a genetic sequence cranked up to maximum sensitivity signifies a definite diagnosis; treat strictly using this protocol.

In our “whodunnit” article we posited that in many of these cases, antibiotics could have either treated incipient or actual bacterial pneumonia, or prevented its development.¹

This paper - out of Memphis - adds further fuel to our argument:

The study comprised a “convenience sample” of all cases referred to 3 institutions for autopsy during the sample period. A total of 55 cases with proven SARS-CoV-2 testing were included.

For each subject the authors:

• Determined whether pulmonary co-infection had been diagnosed during life by a retrospective chart review using criteria previously validated in critically ill patients with respiratory insufficiency or failure [25] and “consistent with society guidelines for the diagnosis of hospital-acquired and ventilator-associated pneumonias”.

• Performed histology on lung tissues looking for bronchopneumonia. The authors say that they looked for “the presence of neutrophil infiltrates in alveolar spaces and bronchioles” to diagnose pulmonary co-infection, “as this finding is not observed in the diffuse alveolar damage (DAD) pattern seen in COVID-19 pneumonia alone".

Results:

Of the 36 cases (out of 55 in the study) with a postmortem diagnosis of pulmonary co-infection, 11/36 (30.6%) had a diagnosed pulmonary co-infection, while 25/36 (69.4%) had an undiagnosed pulmonary co-infection.

Put differently:

In more than 2/3 of cases a pulmonary coinfection found at postmortem had not been diagnosed before death.

Other findings:

• The patients with undiagnosed pulmonary co-infections also had significantly shorter times from symptom onset to death.

• While the rates of antibiotic use were high in both groups (11/11 vs. 23/25) there was a strong trend towards lower usages of combinations of antibiotics appropriate for the coverage of hospital-acquired or ventilator-associated pneumonia in patients with undiagnosed pulmonary co-infections (14/25 (56%) vs. 10/11 (91%), p = 0.0828)

• Five cases of invasive fungal pulmonary co-infection were found on autopsy, none of which had been identified during life, although fungal infection at other sites had been diagnosed in three of the five cases.

Conclusions (by the authors):

We found that in our case series, pulmonary co-infection was more common than previously believed, that the rates of pulmonary co-infection were significantly higher than those recognized premortem, that bacterial co-infections were predominantly caused by nosocomial pathogens, and that invasive fungal infections are under-recognized in this population.

The patients with undiagnosed pulmonary co-infections had shorter hospital and ICU stays, fewer extra-pulmonary infections, and tended to receive potentially inappropriate antibiotic therapy.

These findings suggest that in critically ill patients with COVID-19, there should be high index of suspicion for pulmonary bacterial co-infection, supporting empiric antibiotic use to covering nosocomial pathogens in this population.

Interestingly, this paper in Nature reports on a study of facemasks donated by 109 healthy volunteers in Japan. In nearly all cases colonies of bacteria and fungi could be cultured, many of which were potentially pathogenic species².

“We observed bacterial colonies in 99% of samples on the face-side & 94% on the outer-side; fungal colonies in 79% of samples on the face-side and 95% on the outer-side.”

It is more than likely, therefore, that the combination of mask usage and policies which inhibited treatment with antibiotics were synergistically harmful.

It must be remembered that we’ve been here before - as stated in this paper reviewing the causes of death in 1918-19:

However, healthcare providers, medical experts, and published data from the 1918 period suggest that most deaths were caused by secondary bacterial pneumonias (5–12); hemorrhagic pneumonitis that rapidly progressed to death was considered an alarming but uncommon clinical manifestation (8,11–13)

The authors go on to recommend use of “antimicrobial drugs” “during the next pandemic”.

I am leaving the question as to whether 1918-19 was primarily a flu pandemic for another day; suffice it to say the official narrative about “Spanish Flu” is riddled with holes.

1. Note that we do not think this contradicts our view that the data for certain places - N Italy and NYC in particuar - looks fraudulent.

2. Most pneumonias are caused by pathogens which live in symbiosis with the host in the mouth and / or nose and only become pathogenic in certain circumstances.