'Spikeopathy' does not explain the 'novel' symptoms associated with COVID-19
An investigation into competing alternative explanations
Recently two of the authors were involved in a WhatsApp conversation with two ‘frontline’ doctors:1 and Dr Jackie Stone2 in which the conversation focused on differences of opinion on the topic of whether covid-19 was ‘novel and deadly’ and whether there was indeed a ‘pandemic’ (by any reasonable definition) at all.
Dr Kory and Dr Stone’s summary of the signs and symptoms associated with covid-19 are:
Happy hypoxia; diarrhoea; fever; raised D Dimers (blood clot marker); CRPs of over 200 (marker of inflammation); Raised LDH (sign of tissue damage) and very low lymphocytes, anosmia, and ageusia (loss of taste and smell); CT scans – acute fibrous organising, bilateral pneumonia with ground glass opacities; CT scans - evidence of peripheral, subpleural predominance; CT scans - Diffuse alveolar damage (DAD) (perhaps indicative of alveolar haemorrhage); Lungs were dry – zero extravascular lung water.
They attribute these symptoms to ‘spikeopathy’, associated with the spike protein in the SARS-CoV-2 virus. In this article we look at some other explanations and weigh the evidential support for these competing explanations.
We reviewed the medical literature and found that most of the papers on covid-19 CT findings actually suggest findings indistinguishable from those associated with influenza or bacterial pneumonia; it appears to be very difficult (or impossible) to reliably differentiate between influenza and bacterial pneumonia and covid-19 on CT scans.
We also reviewed the medical literature to look for supporting evidence relating for ‘happy hypoxia’ and ‘dry lung’ in covid-19 patients. We did not find any compelling evidence reported linking happy hypoxia to covid-19. Neither did the literature confirm that dry lung was strongly diagnostic of SARS-CoV-2 infection. Likewise, many of the papers and reviews we reviewed made no mention of diarrhoea, loss of taste and smell and micro clotting or other ‘blood issues’.
Thus, we do not think that these symptoms can be explained by a single over-arching cause, that of a novel spikeopathy mechanism associated with SARS-CoV-2. We therefore believe that prior to the “‘pandemic’” many/most covid-19 cases would have been diagnosed as ‘ordinary’ influenza and bacterial pneumonia cases, as this is the most likely mechanism that explains the evidence reported in the medical literature.
None of the symptoms attributed to SARS-CoV-2 need be explainable by spikeopthy, except for those cases where blood problems, happy hypoxia and dry lung and diarrhoea were observed, either more frequently or severely. But even here there are alternate explanations.
One explanation that might better explain some observed symptoms, in some patients, and perhaps in localised geographies such as NYC, is that people were subject to toxicological poisoning events, perhaps from vapes. It is worth considering this despite the medical literature being largely blind to the possibility. The symptoms related to VALI (vaping associated lung injury) match those attributed by some to covid-19: CT scans showing consolidation with subpleural sparing seen in a significant proportion of cases, accompanied by dyspnoea, diarrhoea, a non-productive (dry) cough, haemorrhage, fever and severe hypoxic respiratory failure requiring mechanical ventilation.
It is suspected that VALI is caused by the adulteration of vapes with solvents, fungicides and pesticides. It is therefore conceivable that some cases attributed to covid-19 were actually vaping injuries caused by illegal & adulterized ingredients. Cases might then present themselves in a highly localised fashion, in particular cities and geographical areas, much like we have historically seen with ‘bad batches’ of adulterated heroin. Also note that toxic poisoning cases would be resistant to anti-bacterial and anti-viral treatments.
These two alternative explanations for covid-19 symptoms – ‘ordinary’ pneumonia encountered in the elderly and vulnerable, mixed with vaping cases in younger people, can potentially explain the heterogenous nature of some covid-19 ‘outbreaks’, and might have been each attributed to a single cause - SARS-CoV-2, via a ‘group think’ diagnosis.
We might also speculate about an alternative hypothesis - that it is within the realm of possibility that similar toxins to those found in illegal vapes might have been accidentally, or otherwise, spread as aerosols, indoors, and perhaps could have given rise to the so-called super spreader events reported in early 2020, and then either inadvertently or otherwise have been attributed to SARS-CoV-2. We view this as a low probability scenario, but not one to be discarded.
Competing hypotheses under scrutiny
“There is nothing more deceptive than an obvious fact.”
― Arthur Conan Doyle, The Boscombe Valley Mystery - a Sherlock Holmes Short Story
In our whodunnit substack article we investigated the ‘bacterial 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 concluded that it was and believe this evidence contradicts the idea that SARS-CoV-2 was both ‘novel and deadly’, and hence there was no ‘pandemic’.
Fauci et al believe that the 1918 ‘pandemic’ was largely caused by pneumonia, and in 2020 the number of influenza and pneumonia deaths in the UK and USA were relatively unchanged from historical patterns, at a time when ‘flu’ was said to have disappeared (see here for details). This suggests that the mortality risk presented by these respiratory conditions had not changed in 2020 despite it supposedly being a ‘pandemic’ caused by a competing novel pathogen.
Both Dr Kory and Dr Stone firmly believe that the world saw a novel pathogen in 2020 and that this pathogen was SARS-CoV-2. They attribute the symptoms of covid-19 to ‘spikeopathy’, associated with the spike protein of the SARS-CoV-2 virus.
This article is not an exposition on the discussion we had but is instead an investigation into the evidence about the novelty and deadliness of covid-19 illness that they presented to us, weighed up against the evidence easily found in the scientific and medical literature.
Evidence from Dr Stone and Dr Kory
Dr Stone’s evidence:
It is not possible that this was a flu virus. It was not only a respiratory virus. It was transmissible and could enter through the gut and respiratory tract and could first present as diarrhoea, or flu, or fever, or unstable blood sugar. It was a disease of the endothelium and nothing else I have seen causes the clotting I saw.
Fear does not cause low saturation, chest X-ray and CT chest findings, and raised D Dimers and CRPs of over 200, or raised LDH and very low lymphocytes which were among the myriad of novel and objective findings seen.
Those who were "spiked" responded in a myriad of ways depending on the state of their immune system.
We treated for bacterial pneumonia in the first half of 2020, and they still died. Bacterial pneumonia complicated some patients and the neutrophil count responded to IV antibiotics.
They only stopped dying when we added Ivermectin and the most noticeable and objective findings were the increase in sats, the increase in D Dimer with clot breakdown and the restoration of a good pulse waveform on the monitors, suggesting reperfusion. I have countless photos that I have presented on this. Ivermectin stopped coagulation, and clinically, patients survived hypoxia because of its effects on the mitochondria.
Dr Kory’s evidence:
My paper shows extremely high incidence of organizing, pneumonia on CAT scans, and my early paper shows extremely high incidence of wickedly severe clotting.
Extremely high rates of anosmia, and ageusia.
I wholeheartedly agree that "they" use viral spikeopathy to blame everything on the virus and not the vax, my practice specializes in treating patients with Long Covid and Long Vax
They found that the predominant finding was an "organizing pneumonia" pattern. Yes, this pattern has been associated with viruses before, but never to such a high incidence and so reproducibly - I suddenly was rounding in an ICU where everyone’s chest x-ray and CT scan were identical, oxygen requirements and vent settings maximal, it was impossible to remember the patients’ names as so little differentiated their disease.
Organising pneumonia - ground glass is non-specific as a general finding on CT scans, but pneumonia is not typically bilateral, and the ground glass is not typically seen in an "organizing" pattern of lung injury, but is more typically seen in patchy or consolidative or micronodular patterns - organizing pneumonia (oddly well demarcated with a peripheral, subpleural predominance) is a somewhat rare disease, and suddenly we had ICU wards full of patients with organizing pneumonia patterns of lung injury.
Bacterial pneumonias requiring hospitalization do not present with "happy hypoxia" (a puzzling finding to many doctors that was widely discussed even in newspapers), reason being is that the lungs are typically "heavy" with accumulated fluid/pus, they are not "dry" as they were with Covid. My partner Paul Marik, using a sophisticated device, measured the "extravascular lung water" (EVLW) in like the first 5 Covid patients he admitted on vents to the ICU. They had zero EVLW.
Secondly, in ICUs most ICU docs have a hair trigger for empiric antibiotics with either a fever, raised white counts, increasing phlegm or unilateral or asymmetric consolidations. I saw a lot of antibiotics being used in patients in my NYC ICU in the spring - didn’t help. However, reading your article, you do make a strong case for Patient zero having a bacterial pneumonia based on his CT scan finding.
The Covid patients were crashing on vents with organizing pneumonia as the inciting cause (organizing pneumonia is not associated with bacteria).
None were suggestive of a bacterial process (typically unilateral abnormalities) preceding the viral syndrome (typically bilateral). Also, they had dry lungs and happy hypoxia - i.e. not bacterial.
Now the 2nd aspect you analysed, whether lots of secondary bacterial pneumonia or VAP as we call it in the ICU went unrecognized and contributed to the mortality rates, that certainly maybe true……as it has always been true. VAP is and has always been a shitshow of a topic in ICU medicine.
Happy Hypoxia does not refer to a specific level of saturation, rather it refers to someone who evidences low to very low blood oxygen saturations, but the low saturations are not accompanied by a significant increase in the "work of breathing,", i.e. they look oddly and discordantly comfortable. Most patients with an acute lung injury or infection which leads to low oxygen saturation will be struggling to breathe (especially bacterial pneumonia leading to hypoxia). These Covid patients (on presentation only as with time they did eventually develop respiratory distress, just not on arrival to the ER or in the first days) were not overtly struggling to breathe initially, thus the term "happy hypoxia".
Covid has two phases, the first is a viral syndrome, typical as any other, except the high incidence of severe anosmia (which then persisted beyond the acute phase) but then on like day 6-10, a minority of patients went into what I call the "pulmonary phase" where the lungs would get inflamed with ground glass opacities in an organizing pattern, their sats would drop, they would come to hospital, often relatively comfortable, but then, without treatment (i.e. corticosteroids), they would then start the slow steady Covid trajectory towards worsening oxygenation, increased shortness of breath, high flow oxygen devices or non-invasive ventilators and then would get intubated. But again, it was the latter pulmonary phase, which was so unique, not the earlier acute viral syndrome phase - that one, as you guys point out, was relatively indistinguishable from other acute viral illness (with the exception of severe and more frequent anosmia/ageusia in some). Otherwise, yes, the acute phase was relatively indistinguishable, but the later hospital phase was not - i.e. the organizing pneumonia, happy hypoxia, the microclotting etc.
Also, obviously, I cannot describe hospital phase Covid occurring in other places, I can only describe what I saw in ICU's in Madison, NYC, Milwaukee, South Carolina, and Central Wisconsin - they were all similar/identical, but the incidence of severe clotting waned over time during that first year and a half.
Note that Dr Stone and Dr Kory approved of our summary of their views and for us to include it in a public article.
To summarise Dr Kory and Dr Stone’s view on the signs and symptoms associated with covid-19 are:
Happy hypoxia (saturating between 51% and 90%)
First present as diarrhoea, or flu, or fever, or unstable blood sugar.
Raised D Dimers (blood clot marker) and CRPs of over 200 (marker of inflammation)
Raised LDH (sign of tissue damage) and very low lymphocytes.
Anosmia, and ageusia (loss of taste and smell)
CT scans – Acute fibrous organising, bilateral pneumonia with ground glass opacities
CT scans - Evidence of peripheral, subpleural predominance
CT scans - Diffuse alveolar damage (DAD) (indicative of alveolar haemorrhage)
Lungs were dry - They had zero EVLW "extravascular lung water".
Micro clotting severe but waned over course of the ‘pandemic’.
This article does not address treatments, which were a fast-moving and controversial topic early in the ‘pandemic’. Illustrative of this is Dr Kory’s testimony to the Homeland Security & Governmental Affairs senate committee meeting in May 2020, where he recommended that the ‘life threatening’ ventilator shortage be addressed, that medicines like remdesivir or hydroxychloroquine be administered at home to keep patients away from hospital and that corticosteroids, which he says were lifesaving in prior ‘pandemics’, should be given to anyone beyond mild illness. Currently the FLCCC (Front Line COVID-19 Critical Care Alliance), of which Dr Kory is the President and Chief Medical Officer, recommends a panoply of treatments, including ivermectin and the FLCCC have published a factsheet on remdesivir suggesting its use is now known to result in a higher risk of sickness and death.
Evidential support for ‘novel’ covid-19 signs and symptoms
We assume a sceptical stance as to whether these signs and symptoms are caused exclusively by SARS-COV-2 and will investigate a subset of them, looking at contradictory and confirmatory evidence, as well as alternative explanations for what may have caused disease in 2020, but which was then (wrongly, in our view) associated with the deadly and novel virus.
Initial reporting of the signs and symptoms of covid-19 from Wuhan, in the form of the study of 1,099 patients by Guan et al appeared in the NEJM in April 2020 and was very widely reported (17,901 citations). They say:
It surely says something about the suspension of normal critical faculties within the scientific community that this paper became so widely cited and, apparently, played a major role in the propagation of the ‘pandemic’ narrative, given that:
The median age of the subjects was 47 – dramatically lower than that observed elsewhere.
Within 3 weeks of the “sequence” for the novel virus being identified, they were able to find more than 1000 patients infected by it across 552 hospitals.
They assume all these hospitals were capable of a reliable diagnosis of covid-19 in so short a period from its ‘discovery’ to the implementation of diagnostic tests.
It should be noted that diarrhoea was uncommon, and the most common CT findings were ground glass opacities (GGO - this can be a manifestation of a wide variety of clinical features, including malignancies and benign conditions, such as focal interstitial fibrosis, inflammation, and haemorrhage). In the appendixes to their paper, they present a case fatality rate (CFR) comparable to the lower end of that reported for seasonal influenzas. Likewise, the CT scan reports do not differentiate from flu or bacterial pneumonia. It does not report dry throat or happy hypoxia as unusual symptoms, nor are either microvascular thrombosis (micro clotting) or alveolar haemorrhage reported at all.
In their July 2020 paper Kory and Kane, identify a set of Computed Tomography (CT)3 imaging descriptors that they claim are diagnostic of covid-19 in the six patients they examined: an acute bilateral fibrinous and organising pneumonia. The paper mentions a rapidly progressive course exhibiting imaging findings similar to diffuse alveolar damage (DAD)4. Note also that in Dr Kory’s testimony he mentions the presence of subpleural predominance – “oddly well demarcated with a peripheral, subpleural predominance” - but the paper says, “which can extend to the subpleural regions”, which we assume to be equivalent.
In April 2020 Kory’s co-author Kanne identified the CT imaging descriptors that correlated with covid-19. He recorded the usual ground glass opacities, consolidation, bilateral and peripheral distribution, as shown in their table below, but no pleural effusion or other findings related to the pleural cavity.
Note that Kanne says:
“The long-term imaging features of 2019-nCoV are not yet known but presumably will resemble those of other causes of acute lung injury.”
In October 2021 Zarei et al5 compared chest CT imaging descriptors from influenza pneumonia (H1N1) and Covid-19 patients and conducted an interobserver agreement study of radiologists to determine whether they could consistently differentiate between one disease or the other from the scan alone. They found that:
They reported that radiologists found that the similarities of lung involvement in both diseases meant it was very hard to differentiate between them. Their statistical results show that ground glass opacities and consolidation are not useful to diagnostically distinguish the two conditions from each other, and the only features that shows on a CT scan that might practically assist in this regard are subpleural sparing, effusion and banding.
They did not mention any symptoms related to DAD (diffuse alveolar damage), microvascular thrombosis (micro clotting) or alveolar haemorrhage.
The March 2020 study by Fu et al retrospectively analysed CT features in covid-19 patients and confirmed that ground glass opacities and consolidation were common features in covid-19 disease. However, interestingly they did record that the age variable had a mean of 45 (range was 20-67), only 14.5% had shortness of breath and only 0.02% had diarrhoea. They also said 5% of patients had severe progression with “white lungs”. They did also make these comments when comparing to other diseases:
They reported this experience about CT scans for covid-19:
“The common CT features of COVID-19 pneumonia are multiple lung opacities, multiple types of the opacity (ground-glass, ground-glass and consolidation, and consolidation alone), and multiple lobes especially the lower lobe involved.”
Note that they did not report any findings of happy hypoxia, subpleural sparing, subpleural band or pleural effusion nor did they mention any symptoms related to DAD (diffuse alveolar damage), microvascular thrombosis (micro clotting) or alveolar haemorrhage. They emphasised that their reported CT features of covid-19 should be considered preliminary rather than definitive.
In April 2020 Hani et al performed a systematic review on a large series of 1014 patients and reported a 97% sensitivity of chest CT for the diagnosis of covid-19 but said nothing about specificity (meaning that nearly all covid-19 patients had abnormal CT scans, but the question as to how many of those with abnormal CT scans had covid-19 was left unanswered.) The common features for CT findings in covid-19 cases reported were similar to the papers discussed above. All cases were verified by PCR test which was often repeated until they got a positive test result. They even say:
“when the viral load is insufficient, RT-PCR can be falsely negative while chest CT shows suggestive abnormalities. RT-PCR remains needed for final confirmation, but its positivity can be delayed, with the need to repeat the test if the CT features are suggestive.”6
They did not mention any symptoms related to DAD (diffuse alveolar damage), microvascular thrombosis (micro clotting) or alveolar haemorrhage.
In May 2020 Yin et al also performed a comparison study of H1N1 influenza patients versus covid-19 patients (30 patients in each cohort) and found the CT scan results to be similar, except that plural effusion was more evident in influenza patients. They also found that time from symptom onset to CT was much higher with covid-19 patients7. They did not mention any symptoms related to DAD (diffuse alveolar damage), microvascular thrombosis (micro clotting) or alveolar haemorrhage.
Sharif et al, 2020, performed a systematic review, on papers from December 2019 until April 2020, and did a meta-analysis, reporting that:
“COVID-19 cases had a higher risk of having ground glass opacities, but there was no significant difference between the presence of pleural effusion, positive CT findings, and bilateral involvement in two groups. However, non-COVID-19 patients showed an increased risk of having consolidation”.
“CT results in patients with COVID-19 were comparable with those of people having pneumonia from other causes”.
They did not mention any symptoms related to DAD (diffuse alveolar damage), microvascular thrombosis (micro clotting) or alveolar haemorrhage.
In the BMJ, from July 2020, Cleverly et al reported (in a study referring to chest X-rays rather than CTs) that:
“Covid-19 pneumonia can be classed as an atypical pneumonia because of the radiographic appearances of multifocal ground glass opacity, linear opacities, and consolidation. These changes are also seen in other atypical pneumonias, including other coronavirus infections (severe acute respiratory system, SARS, and Middle East respiratory syndrome, MERS).”
“No single feature on chest radiography is diagnostic of covid-19 pneumonia”.
Unlike many of the previous reviews Cleverly et al reported that evidence suggests a high prevalence of thrombotic complications in covid-19 patients.
A Dutch study by Klak et al from patients in April 2020 reported a 31% incidence of thrombotic complications in ICU patients with proven COVID-19 infections, which they say is remarkably high. The mean age of patients was 64 years old.
In April 2020 Revel et al, from the European Society of Radiology (ESR) and the European Society of Thoracic Imaging (ESTI), describe typical findings in CT scans for early diagnosis of covid-19 (* means presence is disconformity and suggests other infectious disease of superinfection):
“Presence of (bilateral, diffuse, confluent, patchy) ground glass opacities with /a rounded morphology/a crazy paving pattern/a peripheral distribution without subpleural sparing &
Presence of ground-glass opacities admixed with perilobular consolidations /linear consolidation &
Presence*/Absence of tree-in-bud pattern/centrilobular nodules/endobronchial secretion/lobar or segmental consolidation &
Presence*/Absence of adenopathy/significant pleural effusion”
However, they say findings of diffuse alveolar damage (DAD) are nonspecific.
The only paper we could find on CT and bacterial pneumonia was published in 2001 by Franquet, which reported that consolidation was indicative of community acquired bacterial pneumonia.
In 2020 Dhont et al investigated the pathophysiology of ‘happy’ hypoxia in covid-19, noting that it occurred in around 20% of hospitalised patients, but the condition was also observed in patients with atelectasis, intrapulmonary shunt (i.e. arterio-venous malformations) or right-to-left intracardiac shunt.
In 2020 Laredo et al failed to find any strong evidence of happy hypoxia:
“The RR/SpO2 relationship before oxygen administration does not differ between patients with COVID-19 and those without COVID-19, except in elderly patients.”
As did Plummer at al in 2022:
“Patients with COVID-19 display a more symptomatic phenotype in response to hypoxaemia than those with other causes of hypoxaemic respiratory failure, however individual patients exhibit a wide range of responses. As such although asymptomatic hypoxaemia may be a phenomenon in any individual patient with hypoxaemic respiratory failure, it is no more frequently observed in those with SARS-CoV-2 infection than without.”
“Our results therefore refute the notion of COVID-19 infected patients being any more “happy” with hypoxaemia than non-COVID-19 patients”
“The mechanism of severe hypoxaemia in COVID-19 … remains poorly understood”.
In 2023 Lardet et al looked at Extravascular lung water (EVLW) and covid-19 and found no correlation between this condition and covid-19 patients experiencing acute respiratory distress:
“our main objective was to investigate the relationship between extravascular lung water (EVLW) and/or pulmonary vascular permeability index (PVPI) and respiratory mechanic variables in patients with COVID-19-induced ARDS.
We found no clinically relevant correlations between EVLW and the respiratory mechanics variables…..driving pressure…., respiratory system compliance… or positive end-expiratory pressure. Similarly, there were no relevant correlations between PVPI and these same respiratory mechanics variables”.
It is worth pointing out that some doctors sometimes refer to imaging characteristics (e.g. ‘ground glass opacities’) without specifying whether they are referring to findings from x-rays or CT scans. The Cleverly study above talks about GGOs, but in x-rays, yet the majority of papers refer to CT scan findings. In most places, plain x-rays are in much more frequent use, CT scans for suspected pneumonia being used infrequently.
We do not know if GGOs found on x-ray have the same significance as those found on CT. Yet, interestingly, there are few papers suggesting concordance between x-rays and CT yet generally speaking doctors talk as if there is. In a 2015 review Claessens et al found that CT scanning changed the diagnosis which had been made after x-ray alone in 58% of cases, concluding that:
"In CAP-suspected (community-acquired pneumonia) patients visiting the emergency unit, early CT scan findings complementary to chest radiograph markedly affect both diagnosis and clinical management."
A 2008 review by Hayden and Wrenn also found that CT scans ‘found’ considerably more cases of pneumonia than x-rays alone.
One is left wondering firstly whether faulty assumptions made about the concordance of findings between these two technologies may have been significant, secondly whether the increased use of CT scans in some places may have affected perceptions about the novelty of covid-19 and thirdly whether this, like PCR testing, is a further example of the increased reliance on expensive technologies in lieu of clinical acumen.
Some evidence about CT is hard to fathom. In April 2020 Rubin et al reported that:
“…. CT screening of 82 asymptomatic individuals with confirmed COVID-19 from the cruise ship “Diamond Princess” showed findings of pneumonia in 54% (11).”
So here we have asymptomatic patients showing findings of pneumonia. Perhaps this suggest a higher false positive rate than practitioners might assume given we might conclude many of these were perfectly well people. Furthermore, it is worth considering the possibility that an increase rate at which CT scans were being done would have resulted in higher numbers of patients suspected of having covid-19.
All studies have limitations, especially observational studies. However, it is worth noting a few significant issues in the papers in our literature review:
Many of the academic papers written about diagnosing covid-19 disease use a positive PCR test as the definitive diagnosis of SARS-COV-2 infection. In at least one study these tests were repeated until a positive was found.
There are no standard terminology, definitions, or causal descriptors in CT. This introduces the potential for interpretation bias and variability in interpretation.
In many of the papers potentially confirmatory biopsies were not taken from the lungs. For instance, in the Kory and Kane paper, the authors say they never took tissue biopsies ante mortem, and that the majority of autopsies were carried out after patients had died post ventilation, hence represent the most severely ill patients:
Setting aside issues with terminology, gold standard verification of covid and the lack of biopsies we can summarise what we know about the ability of CT findings for covid-19 and the extent to which they are genuinely diagnostic of this disease in isolation of other tests and indications. Most CT imaging descriptors appeared to be shared with influenza and bacterial pneumonia, as meta-analysis shows, and most papers acknowledge how difficult it is to differentiate one from the other from CT scans.
The only imaging descriptor that appeared to differentiate between covid-19 and influenza was subpleural sparing, subpleural effusion (contra-indicating) and subpleural banding. Only Zarei et al and Revel et al reported these as features of covid-19.
We also have little evidence to support differences in oxygen saturation between influenza and covid-19 patient groups. Happy hypoxia is not identified in any of the papers reviewed, except for Kane and Kory. Likewise, there are no reported high incidences of diarrhoea in covid-19 patients subject to CT scans.
Symptoms related to DAD (diffuse alveolar damage), microvascular thrombosis (micro clotting), alveolar haemorrhage are not consistently reported, with only the one Dutch study and the Kory paper both citing it as a specific finding related to Covid-19.
‘Dry lung’ was also reported but this does not appear to be confirmed by the one study that looked for evidence of it.
We conclude that CT cannot differentiate between any of the respiratory diseases, and in the absence of objective confirmation can only ever be suggestive. Furthermore, objective confirmation cannot be obtained by PCR test because of the inability of swabs to reliably collect and identify causative agents (as reported by the CDC EPIC study in two 2015 NEJM articles - one done on adults and one on children). Hence a positive result gained from a sample taken from the upper throat or the nose does not mean an infection in the lung is caused by the detected pathogen. Hence, just because a patient is PCR positive, we cannot conclude it is covid-19 and this conclusion should be reinforced by the fact that patients have been repeatedly retested, most times at high CT values, to establish positivity.
Credible alternative explanations
“How often have I said to you that when you have eliminated the impossible, whatever remains, however improbable, must be the truth?”
― Arthur Conan Doyle, The Sign of Four
The evidence presented here strongly suggests that none of the symptoms discussed are necessarily wholly and easily explainable by a single cause, that of a novel spikeopethy mechanism associated with an infection from SARS-CoV-2.
So, where does this leave us? We can speculate that there are several non-mutually exclusive, potentially interacting, explanations. There look to be two or more sets of observed disease manifestations, with distinct groups of symptoms seen in some patients caused by one or more different pathogens entirely, where:
Many/most covid-19 cases would have been ‘ordinary’ influenza and bacterial pneumonia cases.
Some were not viruses or diseases at all but caused by toxicological events.
Each of these were misattributed to covid-19 either deliberately or through a process of human error.8
In our view the first explanation is the most likely, for the majority of cases, especially given there was a panic over covid-19 which would have created an overwhelming psychological pressure leading to confirmation bias.
However, the second possibility, a toxicological cause, is worth considering despite the medical literature being largely blind to the possibility. Such an explanation would potentially explain the dry lung, happy hypoxia and diarrhoea as well as the rarer CT scan result - subpleural sparing. It might also explain the haemorrhagic and vascular events. This is worth discussing in a little more detail.
A very interesting review paper by Chong et al on subpleural sparing was published in 2021 which reviews a number of causes of this CT identifier, including nonspecific interstitial pneumonia (NSIP), organizing pneumonia (OP), pulmonary alveolar proteinosis (PAP), diffuse alveolar haemorrhage (DAH), vaping-associated lung injury (EVALI/VALI9), cracked lung, pulmonary oedema, pneumocystis jirovecii pneumonia (PJP), pulmonary contusion, and more recently, Coronavirus disease 2019. And inhalational lung injury, associated with vaping and cracked lung. The relevant section is:
Notice the symptoms related to VALI (vaping associated lung injury) are consolidation with subpleural sparing seen in a very high percentage of cases, accompanied by dyspnoea, a non-productive cough (dry), fever and severe hypoxic respiratory failure requiring mechanical ventilation.
In March 2020 Layden et al reported in the NEJM that:
“In July 2019, the Wisconsin Department of Health Services and the Illinois Department of Public Health received reports of lung injury associated with the use of e-cigarettes (also called vaping) and launched a coordinated public health investigation……There were 98 case patients, 79% of whom were male; the median age of the patients was 21 years. The majority of patients presented with respiratory symptoms (97%), gastrointestinal symptoms (77%), and constitutional symptoms (100%). All case patients had bilateral infiltrates on chest imaging. A total of 95% of the patients were hospitalized, 26% underwent intubation and mechanical ventilation, and two deaths were reported. A total of 89% of the patients reported having used tetrahydrocannabinol products in e-cigarette devices, although a wide variety of products and devices was reported. Syndromic surveillance data from Illinois showed that the mean monthly rate of visits related to severe respiratory illness in June through August of 2019 was twice the rate that was observed in the same months in 2018.”
Clearly many of the symptoms of VALI appear to be shared by a subset of covid-19 patients, including GGO, and perhaps those in Spring 2020 more than others. Might it be possible that these ‘covid-19 events’ were toxicological in nature and not caused by a viral or bacterial pathogen at all?
In an interview in the NEJM Christiani points out that the ingredients in vapes are largely unknown and unregulated:
Xantus reports on the situation around VALI up to November 2019. This report identifies a new syndrome characterised by respiratory distress with bilateral (sometimes haemorrhagic):
“Vast majority (98%) of the patients presented with respiratory symptoms; however, most (81%) had gastrointestinal (diarrhoea and vomiting) problems as well. Almost one-third progressed rapidly to respiratory distress needing intubation and mechanical (mostly positive pressure) ventilation. Imaging often revealed bilateral infiltration; however, the pathology was very diverse, varied from chemical pneumonitis (with one case of lipoid pneumonia) to certain degree of acute respiratory distress syndrome with bilateral infiltrates (sometimes haemorrhage)”
Specifically, it also mentions:
“An investigation commissioned by National Broadcasting Company analysed 18 legal and illegal samples were analysed. The samples were analysed by CannaSafe Analytics LLC, the world first accredited cannabis laboratory. At least 10 samples had unacceptable level of pesticides and myclobutanil. Latter is a fungicide, which turns into the hydrogen cyanide and hydrogen chloride when heated: both compounds may result in lung damage if inhaled.”
Rossana Segreto (a former DRASTIC contributor) produced this paper in 2022 comparing VALI and SARS-CoV-2, concluding that there is evidence to support the hypothesis that VALI cases were actually early manifestations of infections caused by early circulating SARS-COV-2. However, one commentator noted that:
“People with EVALI were presenting to the ED...chest x-ray and chest CT bore a striking resemblance to what was claimed to be CoV-2. They either get documented as 'suspected covid' or tested positive only a hypersensitive PCR. Boom! EVALI gets categorized as CoV-2.”
As well as pesticides and fungicides illegal vapes have also included solvents which may have acted as effective super-warfarins leading to alveolar haemorrhage (and might show as DAD on CT).10
Note that VALI patients are typically younger. Might this explain some of the young patients in New York and elsewhere – they were suffering from vaping lung injuries, and this was being misattributed to covid-19? And the rest of the elderly patients may have been succumbing to untreated bacterial pneumonia?
Might Segreto and frontline doctors got things the wrong way around? Perhaps VALI cases were being wrongly attributed to covid-19, and physicians were mistakenly believing that the symptoms of VALI were symptoms of SARS-CoV-2 infection, also believing that since VALI occurred predominately in the young that covid-19 was ‘deadly’ for the young as well as the elderly?
A more speculative hypothesis
Another, perhaps more conspiratorial, hypothesis is worth considering – a toxic poisoning event affecting, not individuals using e-cigarettes or vapes, but crowds of people in enclosed spaces.
How might such toxicological events manifest themselves? A lot has been written about the transmission of SARS-COV-2 as an aerosol, such as this article written by Dr Pierre Kory in the USA Today:
“However, it has recently been determined that a major mode of transmission of SARS-CoV-2 is via aerosol droplets, exhaled by presymptomatic, asymptomatic or symptomatic persons. These small aerosol particles remain airborne indoors for extended periods and can infect those nearby who inhale them into their lungs.”
The article argues for masks but in very special circumstances – in ‘at risk environments’:
“The key point is that, for standard masks to be effective, there needs to be near universal wearing of these masks by all persons when in any poorly ventilated, air-recirculated, confined indoor, or highly congested outdoor environment.”
These at-risk environments are ‘indoors’.
The article also goes onto describe super-spreader events at choir practice, in nightclubs, at karaoke, in ships and aircraft carriers and meat-packing plants. All indoors.
If someone was intending to release a pathogen that might mimic a respiratory disease, we might speculate that this might be more manageable in indoor spaces. And to maximise the negative psychological aspect of this it would also be helpful to label these as super-spreader events.
This alternative hypothesis - that it is within the realm of possibility that similar toxins to those found in illegal vapes might have been accidentally, or otherwise, spread as aerosols. That this occurred indoors, and potentially could have given rise to the so-called super spreader events reported in early 2020 and then (deliberately?) attributed to SARS-CoV-2. We view this as a low probability scenario but not one to be discarded.
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Dr Kory is the President and Chief Medical Officer of the Front Line COVID-19 Critical Care Alliance. He is a pulmonary specialist who focused his discussion mainly on the evidence he saw from his time in New York City in late April and May 2020, and elsewhere in the US during and after the NYC ‘first wave’.
Dr Jackie Stone is a UK trained general practitioner located in Zimbabwe and developed extensive experience in applying early treatments to covid-19 patients, partly based on her extensive experience treating malaria, TB and HIV infection.
This might relate to microvascular thrombosis (micro clotting) or alveolar haemorrhage.
Note that in this study none of the influenza patients were not in ICU whereas almost half of covid patients were in the ICU. Almost all Covid patients were given antibacterial and antivirals and none of the Influenza got antivirals and only half got antibacterials. There was no difference in oxygen saturation between groups.
Readers may well – like the authors – raise their eyebrows, or worse, at the bias introduced here in by the investigators repeating negative tests until a positive was found, on the implied assumption their CT scan findings provided a definitive diagnosis.
Note this may be because patients did not attend hospitals until symptoms became severe.
Fame, status, and financial reward might have created a ‘gold rush’ effect, especially when this was coupled with propaganda and a new ‘infallible’ medical test.
EVALI and VALI are used interchangeably. The ‘E’ stands for E-cigarette.