Infection Control, Emergency Management, Safety, and General Thoughts

There have been many reports of unusually high case counts of pneumonia in children and some of this appears to be related to Mycoplasma pneumoniae. Some are calling this white lung syndrome. h/t to @celestial_bean_ for this list of different locations.

• China
• South Korea
• Denmark
• France
• Ireland
• Netherlands
• Switzerland
• Ohio
• Massachusetts

The review article Infection with and Carriage of Mycoplasma pneumoniae in Children provides an excellent background on this problem (Meyer Sauter et al., 2016).

An eight-year study beginning in the 1960s in Seattle found carriage rates that varied between endemic (2%) and epidemic (35%) periods (Foy et al., 1979). One study found that 21% of asymptomatic children carried M. pneumoniae in their upper respiratory tract at a single study site (Spuesens et al, 2013). In a separate study, 24% of children with pharyngitis were found to have M. pneumoniae on testing as well (Esposito et al., 2014).

A 2023 study of children with recurrent respiratory tract infections found that 68% carried M. pneumoniae (Koenen et al., 2023). Why is this rate doubled of that a few years ago? Could COVID be a driving factor?

This organism is more likely to cause severe disease in an immunocompromised host (Yacoub et al., 2016). One problem is that colonization may not drive a mucosal antibody response (de Groot et al., 2022). I have a number of studies linked on this page indicating immune system damage from COVID.

Think of the immune system as a chemical defense system against pneumonia. Another defense system is mechanical. “Mucociliary clearance (MCC) is the primary innate defense mechanism of the lung. The functional components are the protective mucous layer, the airway surface liquid layer, and the cilia on the surface of ciliated cells. The cilia are specialized organelles that beat in metachronal waves to propel pathogens and inhaled particles trapped in the mucous layer out of the airways.” (Bustamante-Marin and Ostrowski, 2016).

In a hamster model, “SARS-CoV-2 infection is followed by a severe loss of cilia.” (Schreiner et al., 2022). Part of the mechanism of spread to other cells in the respiratory epithelium has been described and illustrated (Su et al., 2023).

The mechanism of the loss of cilia has also been described (Fonseca and Chakrabarti, 2022).

This damage can clearly be seen in both transmission and scanning electron microscopy.

The authors also showed the impact of infection on the ability of the cilia to sweep away low density 30 µm-sized polystyrene microbeads. The first video is of mock-infected cells where “beads deposited on mock-treated epithelia moved generally in the same direction, consistent with coordinated beating of the underlying cilia.”

“In contrast, beads deposited on infected epithelia were mostly immobile or showed randomly-oriented limited movements, indicating an impairment of the mucociliary clearance function.”

It’s clear that both immune system dysfunction and respiratory epithelial damage could be contributing to the M. pneumoniae problem in the pediatric population. The question then becomes one of why this seems to be surging now. Could it be that a new variant is driving this? The answer seems that this seems to be a distinct possibility. “Omicron variants dramatically accelerate spread via the ciliary transport/microvilli reprogramming pathway, which explains the increase in its attack rate compared to previous variants.” (Wu et al., 2022).

What variants do the impacted countries have in common currently? 23F (EG.5) and its sublineages (HV.1 is one of them).

This variant is also dominant in Ohio…

…as well as Massachusetts.

However, the HV.1 sublineage seems to be what is becoming dominant in the US which correlates with the M. pneumoniae cases. It’s interesting that the EG.5 is dominant in the world.

Of course, this could all be correlation with the variants. It’s possible that there is ascertainment bias and that much of the pneumonia in pediatric populations is a combination of COVID, RSV, influenza, and M. pneuomoniae which are all on the rise. Even more concerning is the possibility that this is a new virus. The rapid rise in cases would certainly suggest that. It’s also worth learning about the concepts of sufficient and necessary causes in epidemiology if one has that level of interest in this topic.

Mainly though, I hope to impress on people that COVID not only is a causal pathway for a number of chronic diseases, but I think I’ve made a case that it is also causal for infectious diseases as well, with a special focus here on respiratory ones. We need to be doing far more to protect children.

Tackled another myth today. You can read the entire piece here. Robert F. Kennedy Jr. and Steve Kirsch are singled out.

*Update: I pulled the data today again and this disappeared. Sorry about any confusion. I’m just as dumbfounded. I didn’t change anything in the query I used. (10/1/23).

A big surprise happened today. I pulled variant data for the US from the CDC and plotted it. When I plotted a graph showing relative proportions of each variant, P1 and P2 were present again. These had pretty much disappeared from the radar in 2021. They are the black regions on the left and bottom right of this graph.

Why is this important? I can come up with three reasons that this might be happening.

1. An immunosuppressed person who never cleared the infection reintroduced it into the community.
2. An animal reservoir of it reintroduced it into the human population. This seems the least likely because it seems like this would have occurred sooner with other variants.
3. My biggest concern is that SARS-CoV-2 may remain somewhere in tissue and reemerge under the right conditions. We see something similar with VZV, which causes chickenpox initially, but the virus remains within the person and can later reemerge as shingles. If that is truly the mechanism, we have much longer to go with this virus than I had originally thought at the beginning of the pandemic. I expected it to be about a 5-8 year problem at the time.

The reemergence of Delta or a hybrid has been hypothesized as well. We really need to be bracing for the long haul of the pandemic. Until we get a much more effective vaccine that can be distributed globally, we are going to face repeated waves of new, and possibly reoccurring variants. That makes it all the more important to keep up to date on vaccination, using respirators while in the presence of others, increased ventilation and filtration, and social distancing measures.

There are many indicators that we are entering the next surge in the US, but most people seem oblivious, due to the lack of messaging from the CDC and mass media sources.

US Wastewater

Positivity

Estimated cases based on wastewater data

Climbing COVID Hospital Admissions (roughly a 3-week lag behind new cases)

This preprint study has some stunning findings. The short version is that even among those who had COVID but no symptoms, there is tissue damage.

When cells die, their contents are released into the surrounding tissue. Parts of the DNA of the cell are also released and can be detected in the bloodstream. That’s what is meant by cell-free DNA (cfDNA). Epigenetic liquid biopsies study the cfDNA and can determine the type of cells that it came from, based on characteristic molecular structures. The authors state “Patients with severe COVID-19 had a massive elevation of circulating cell-free DNA (cfDNA) levels, which originated in lung epithelial cells, cardiomyocytes, vascular endothelial cells and erythroblasts, suggesting increased cell death or turnover in these tissues.”

Cardiomyocytes are the muscle cells of the heart that contract to provide the heartbeat. When a large area of these become damaged, it is called a myocardial infarction, or commonly called a heart attack. This is normally due to either fatty plaques forming in the blood vessels that feed the heart or a clot that enters one of them. Keep that in mind for the part on vascular endothelial cell damage.

Endothelial cells line the inside of tissue. Epithelial cells line the outer surface. Damaged lung epithelium means that the cells that take up oxygen in the air sacs of the lungs (alveoli) which gets diffused into the bloodstream and carbon dioxide to flow into the alveoli no longer function. Erythroblasts are the cells that become red blood cells when mature. The damage to these just these two cell types means that other tissues will be supplied less oxygen, but that is just part of the widespread damage.

The damage to the vascular endothelium is really one of the most critical things to understand about COVID. It is the layer of cells lining blood vessels.

Capillaries become small enough that they only allow for a single red blood cell to pass at a time, as illustrated video.

That is the problem with endothelial damage. When that occurs, capillaries can be occluded, which would lead to reduced (or no) oxygen flow to the tissue supplied by the capillary. These blockages are what are referred to as microthrombi.

An important finding of this study is “Patients with severe COVID-19 have a higher concentration of cfDNA, originating in affected tissues.” When endothelial damage occurs and microthrombi form on a large scale, such as in severe COVID, it leads to acute organ damage and potentially organ failure.

The damage of clot formation is evident in a stroke. (The other common type of stroke, where a blood vessel ruptures, is called a hemorrhagic stroke). When a clot causes a stroke, it’s called an ischemic stroke, because the clot deprives the downstream brain tissue of oxygen, as illustrated in this animation.

There was an autopsy study of patients who had died of COVID. “151 autopsies were included, and 91 cases presented microthrombi in the lung (73%), heart (11.2%), kidney (24%), and liver (16.3%). The age range was between 27 and 96 years.” Clearly the COVID microthrombi risk is real across many organs.

Endothelial damage is not only dangerous due to clot formation, but also because the endothelial cells are responsible for the transfer of oxygen from red blood cells into the surrounding tissue, which can also lead to that tissue being starved of oxygen and potential death of those cells, which is called ischemia.

The preprint also refers to erythropoiesis, which is simply the production of new red blood cells. Why would this increase? Because the body recognizes that parts of it are starving for oxygen.

There is more to the study, but this is the basic biology that is important to understand in how COVID causes damage.

I suspect that part of the reason that COVID seems less damaging in younger or healthier populations is that they can more easily handle some tissue damage since the surrounding unaffected tissue can take on some of the load of the damaged tissue. However, as that unaffected tissue ages, it won’t work quite as efficiently as when it was young and healthy, and the impacts of the COVID infection will start manifesting themselves as a number of chronic diseases. The fact that we are seeing many of these in such a short time is extremely concerning. It suggests that we will see massive amounts of chronic diseases among people who had COVID infections in the future. You can find information on some of these broken down by organ system on this page. Click the link of the system to see some of the studies.

There is another round of disinformation around COVID vaccines related to the Amish, originating from people like Steve Kirsch, who doesn’t have a science or medicine background and makes false vaccine claims, which are easily debunked.

What does a real source say about COVID in this population?

Closed but Not Protected: Excess Deaths Among the Amish and Mennonites During the COVID-19 Pandemic (2021)

Closed religious communities also resist epidemiological surveillance. The same factors that put these communities at high risk for infectious disease outbreaks—lack of trust in medicine and the state, reluctance to receive routine and preventative healthcare, and closed communication networks—also make their members less likely to avail themselves of testing for COVID-19. Even among those tested, it may be difficult to connect their tests back to their religious communities without information about religious affiliation. Moreover, it is difficult to distinguish their COVID-19 transmission and death rates from surrounding communities.

CRCs are sectarian groups in tension with their environment’s dominant culture. This tension leads these communities to erect boundaries between themselves and outsiders, limiting interaction.

These communities warrant close monitoring, given their history of infectious disease outbreaks. However, some community members distrust state officials and medical providers, which undermine efforts to monitor public health. Additionally, since some groups prefer natural remedies to modern medicine, their members avoid routine medical care and are less likely to be tested for COVID-19. After a COVID-19 outbreak in an Amish community in Ohio, the local health department set up a testing site to track the spread. According to Ali et al, more traditional community members did not participate in the testing clinic, implying they won’t seek testing independently.

Our findings reflect the older Amish and Mennonites’ vulnerability in the population, as the average age of death is consistently higher after June 2020. The results indicate the average age of death during the first wave (March through May) was lower than the baseline average, suggesting the initial two waves of COVID-19 may have impacted people in the population with underlying health risks. In general, the Amish and the Mennonites were subject to government guidelines in March and April limiting religious gatherings. Many groups complied with the CDC’s recommendations to limit contact. However, when restrictions were lifted during the summer of 2020, many of these communities resumed church services. The importance of face-to-face rituals in CRCs and Amish groups’ general resistance to mask-wearing and other CDC guidelines makes them especially vulnerable to COVID-19. Indeed, we see the number of excess deaths spike in October and November when many governmental restrictions relaxed and many of the Amish and Mennonite groups were engaging in face-to-face interactions.

The large number of excess deaths among the Amish and Mennonite community is concerning, as it indicates not only the presence, but the impact of COVID-19 on this community. 

Addendum

Steve Kirsch was caught lying yet again.

I saw a long Twitter thread this week that was very interesting and well done. I wrote to Dr. Jose-Luis Jimenez who graciously agreed to allow me to copy it all here. I wanted it to be easily accessible for those without Twitter. I’ve only made minor edits to remove abbreviations and changed some punctuation for a non-Twitter space. The content has not changed except for where I have added wording for clarity.

What were the historical reasons for the resistance to recognizing airborne transmission during the COVID-19 pandemic? Our peer-reviewed open-access paper is now published.

Soon after COVID-19 pandemic started, it was clear to many scientists (inc. those who understand aerosols) that AIRBORNE transmission was an important contributor, e.g. as soon as we talked to the Skagit choir, it was obvious that was airborne-dominated.

However, major public health organizations such as the WHO and CDC were in complete denial, saying that airborne transmission was MISINFORMATION! (Disgracefully, the WHO has not deleted this tweet (below) or clearly stated that it was an ENORMOUS error).

How was that possible?

• Many scientists are concluding that airborne transmission is important.

• Major public health organizations such as the WHO say that it is misinformation!

Historical trends and errors (this thread) are important to explain this, but NOT the only reason.

This major error (IMHO one of most important errors in the entire history of Public Health) has had major consequences:

• In early pandemic we focused on surfaces, which are minor or negligible.
• We ignored air, which was the dominant mode.

[These led to a] lack of controlling transmission

Since then, research has clearly shown that airborne transmission is the DOMINANT mode of transmission of COVID-19:

To this day, zero proven cases of surface transmission and droplet transmission has NEVER been demonstrated, not just for COVID-19…but for ANY disease in the history of medicine! (Paper from Prof. Yuguo Li, member of WHO IPC Committee)

So how did we get into this mess?

Public health organizations tell us that unproven transmission mechanisms are dominant, and that the dominant transmission mechanism is misinformation. We’ll soon delve into the history in our paper.

But before we go into the history, there are other reasons to review. Most importantly, surface-droplet transmission is very CONVENIENT to those in power. And AIRBORNE transmission is an inconvenient truth (just like climate change, dealt with similarly).

The 2,000-year-old airborne disease theory that blinded Covid experts

There is at least one more reason for the resistance: those who made this enormous error at the WHO, its IPC committee, and at the CDC, & health ministries around the world DO NOT WANT to admit their error

A government advisor privately: “we need to find a way to allow us to save face.”

Those Public Health officials that continue to resist and obfuscate about airborne transmission are in control of the PH institutions. Aerosol scientists are almost complete outsiders, and have been almost systematically excluded to this day.

Orthodoxy, illusio, and playing the scientific game: a Bourdieusian analysis of infection control science in the COVID-19 pandemic

So what about the contribution of history to the denial of and resistance to airborne transmission by Public Health authorities worldwide? It is summarized in this diagram, which I’ll explain in this thread.

So to understand the errors that led to the denial and resistance of #COVIDisAirborne, we need to go back to Hippocrates! (~400 BCE).

Hippocratic writings in ancient Greece first proposed that diseases were caused by imbalance of humors in the body, which could be triggered by a “miasma” transmitted through the air.

Throughout much of subsequent human history, the belief persisted that diseases were transmitted through air Because the actual agents remained a mystery for centuries, explanations were given in general terms such as “miasmas,” or “bad air.”

For example, the etymological root of the term “malaria” (a disease that we now know is transmitted by mosquitos) is “mala aria,” medieval Italian for “bad air.”

Some origin theories were more specific, e.g. Roman scholar Varro (116–27 BCE) wrote that swamps were a particular breeding ground for minute creatures that “float in the air and enter the body through mouth and nose and there cause serious diseases.”

Thus it became a policy of the Roman Empire to drain swamps, removing breeding grounds for mosquitos, reducing malaria, an example of a mistaken theory giving good results and increasing faith on the theory. We see this many times through history.

Bad air, amulets and mosquitoes: 2,000 years of changing perspectives on malaria

The concept of person-to-person contagion came much later, most clearly in work of Italian physician Girolamo Fracastoro in 1546 (This is actually a subject of current debate, with some scholars thinking that the role of Fracastoro may have been overstated.

What ensued after Fracastoro, however, was a centuries-long debate between “miasmatists,” who held fast to the idea that diseases floated through the air over distances, and “contagionists,” who accepted person-to-person spread of disease.

Airborne infection with Covid-19? A historical look at a current controversy

Because it was (and it still IS) very difficult to determine how, why, and from where someone became infected, the miasmas vs. contagion debate failed to reach a resolution and persisted for centuries. A middle ground was proposed, “contingent contagionism”: malaria, or cholera might be contagious in an impure atmosphere, but not in a healthy atmosphere. This idea therefore captured some grains of truth (e.g. now we know ventilation reduces airborne).

Miasma theory was dominant till the mid/late 19thy Century. Florence Nightingale (1820–1910) like most Victorians was raised to believe that diseases were caused by ‘miasma’ or foul air.

In her Notes on Hospitals, Nightingale referred to the idea of contagion as absurd. She was nevertheless very practical and effective in reducing disease, e.g. with ventilation and phys. distance, and later accepted germ theory, as we’ll see later.

We enter a critical period around 1850. Miasma theory is still dominant, although contagion (mostly through the air) also has proponents. Microorganisms have been observed for two centuries since the invention of the microscope, but haven’t clearly been connected to disease.

Cholera strikes London in 1854. The public health establishment believed it to be caused by a miasma. English sanitary reformers (e.g. Chadwick), who initiated many modern public health practices, found miasma appealing, as it appeared to explain the prevalence of diseases in the undrained, filthy, and foul-smelling areas where the poor lived, and helped justify their efforts to address those conditions. (They had made a huge error, and they resisted accepting it, just as the WHO today).

Death and miasma in Victorian London: an obstinate belief

John Snow was a wealthy doctor but outsider to public health. His work in anesthesia made him familiar with the behavior of gasses. He realized that the spread of cholera was NOT consistent with what would be expected for a gas.

John Snow

Snow noticed how cases had clustered in a specific London borough and persuaded the local council to remove the handle of the Broad street water pump, which halted the epidemic.

John Snow and the Broad Street Pump on the Trail of an Epidemic

However, cholera was already in decline. The Board of Health refused to accept contaminated water, stating: “we see no reason to adopt this belief [that cholera was water-borne]” and dismissing Snow’s conclusions as mere “suggestions.”

The Board of Health had strong incentives for rejecting water as the source of cholera. To remove the sources of the miasma (filth), they had spearheaded the effort to build sewers that dumped raw sewage into the Thames, the source of much of London’s drinking water, thus effectively helping the spread of cholera. They had much to lose by admitting cholera transmitted through water. (Technology has advanced, but human nature has changed less. The WHO has avoided saying LOUD & CLEAR that #COVIDisAirborne, as their denials helped it spread.

Also around 1850, Ignaz Semmelweis in Vienna showed that handwashing greatly reduced deaths by childbed fever in a maternity clinic.

These are some of Semmelweis’ data, which would seem worth following up on: However, his ideas conflicted with established medical and scientific beliefs that STILL described diseases as due to an imbalance of humors triggered by a miasma in the air.

However, he was dismissed from his hospital and harassed by Vienna medical community, forced to move to Budapest. There he broke down, was interned and beaten by the guards, and ultimately died from an infected wound Like Snow, he died years before his theories were accepted.

Ironically, Semmelweis’ name lives on not only for advances of hand sanitation, but also in “Semmelweis reflex,” which describes the reflex-like tendency to reject new knowledge or evidence when it contradicts established beliefs, norms, or paradigms

That is especially ironic, as the chief deniers of airborne transmission (John Conly — chairman of key IPC WHO committee, Dr. Seto, Didier Pittet, and Peter Collignon) are handwashing experts following Semmelweis’ scientific advances, while forgetting about the reflex.

The 2nd half of the 19th Century is a period of rapid progress on disease transmission. Pasteur and Koch proposed the GERM THEORY of disease. Microscopic germs enter the body and are the cause of many diseases.

Germ theory was NOT accepted overnight, e.g. experiments by others in which water containing organic matter was boiled in a vessel, but microorganisms still appeared (later shown to be an imperfect seal or insufficient boiling) created controversy.

However, by the late 1880s, miasma theory was waning in popularity, and in 1888, the Institut Pasteur was created in Paris, reflecting the ascendancy of germ theory.

Florence Nightingale did accept the new ideas of germ theory, in fact before many physicians did. In 1882, she wrote

Initial results on plant pathogens in 1890s & the identification of bacteriophage in 1917 paved the way for recognition of viruses. A “golden era” followed, with the identification of the actual microorganisms that cause many infectious diseases.

The discovery and identification of the organisms causing different diseases did NOT, however, eliminate the great difficulty in conclusively determining the mode by which they transferred from one person to another. Malaria was still thought to go through the air in 1880

French physician Charles Laveran identified the pathogen responsible for malaria in 1880 (got Nobel Prize in 1907), but the manner of transmission was still thought to be through the air.

American physician Albert King proposed that malaria was transmitted by mosquitos, but encountered general skepticism In 1883, he presented a list of 19 facts supporting malaria as vector of malaria (Reminds me of 10 scientific reasons for #COVIDisAirborne).

In 1898 British surgeon Roland Ross provided definitive evidence, confirming the presence of the malarial parasites in mosquitoes, and demonstrating transmission of bird malaria by mosquitoes. World Mosquito day commemorates him.

Looking back at period 1850-1900, belief on transmission of many diseases through AIR was still strong But cholera, malaria, puerperal fever had been shown to transmit OTHERWISE. It was a fluid time. It was debated if air was actually important

In the 1890s, Carl Flügge in Germany set out to disprove the then-dominant transmission theory for tuberculosis, one of the major infectious diseases of the time. Most experts believed that tuberculosis was transmitted when dust of dried sputum that had landed on floors, blankets, bowls, and other objects was dispersed into air. In contrast, Flügge thought that it was not DRIED secretions from sick that caused infection, but rather FRESH secretions that people were exposed to IN AIR BEFORE they reached the ground.

Some contemporaries of Flügge such as Cornet argued that tuberculosis was transmitted only through large droplets, which were easily visible to the naked eye. Perhaps because droplets were more CONVENIENT and airborne disease VERY INCONVENIENT?

However, although term “Flügge’s droplets” has been used to describe ONLY those large particles that fell to the ground quickly near the infected person and that were assumed to dominate transmission, that does NOT accurately capture Flügge’s results.

Rather, Flügge and collaborators used the term “droplet” to refer to fresh particles of ALL SIZES, including AEROSOLS for which the researchers waited five hours to settle from the air on their collection plates.

In 1905, microbiologist M.H. Gordon was commissioned to study the atmospheric hygiene of the UK House of Commons after an epidemic of influenza among members. He famously performed the following experiment: after gargling with a broth culture of Serratia marcescens he loudly recited passages from Shakespeare in an empty House to an audience of agar plates. Although growth of colonies was more numerous on plates near the speaker, cultures were apparent on some plates over 21 meters away.

However, experimental progress in early 1900s was hampered by the limitations of the experimental techniques available at the time. In particular high-quality measurements of large droplets & aerosols would only be routinely available decades later.

We get to the CRITICAL POINT of this history. Throughout most of human history, the dominant belief was transmission of many diseases through the air. The last half of the 19th Century proves otherwise for major diseases. Strong debate ensues: “is air major or minor?”

Charles V. Chapin was a prominent American epidemiologist. He worked only a couple of decades after Germ Theory was accepted, during a period of intense research on pathogens and their transmission.

Charles V. Chapin

The period when Chapin’s worked on disease transmission was a fluid one, following a major paradigm shift, in which it was easier to change the dominant scientific discourse than during normal times

He summarized the evidence of transmission of different diseases in his 1910 seminal book, “The Sources and Modes of Infection.” (A must read if you are interested in this subject, esp. chapter on airborne transmission).

Chapin conceptualized “contact infection,” infection by germs that did NOT come from the environment, but from other PEOPLE through DIRECT CONTACT OR CLOSE PROXIMITY.

Chapin believed contact was main mode of transmission of many diseases But he encountered resistance: “I have sometimes been told I lay too much emphasis on contact infection [although] until recently very little attention has been paid to it.”

Chapin also reviewed the possibility of airborne infection, which he conceived especially as infections from afar. Lingering belief on air infection was making it difficult to promote contact infection.

Chapin realized that airborne infection may explain infection in close proximity (CP). However, he argued that ease of infection in CP was better explained by “spray-borne” droplets, large visible droplets considered by Cornet, the same as the WHO’s droplets.

This is the key. The evidence was insufficient, but Chapin turned absence of evidence into evidence of absence, and stated that airborne disease was almost impossible, and that “mouth spray” (large droplets) are only effective at short distances.

As we have explained in another recent paper, Chapin conflates an empirical fact (“distance reduces transmission”) with a mechanism: GRAVITY, which makes the droplets fall close to the infected person.

Problem: the more correct explanation (of why distance reduces transmission) is NOT gravity but DILUTION. Like exhaled smoke, you breathe less exhaled air farther from someone. And error in PHYSICS made by MEDICAL professionals who do not study physics!

Despite the lack of evidence, Chapin was too successful. He was much better positioned than Snow or Semmelweis as the long-serving Health Officer of Providence and with success of reducing contact transmission iin a new hospital. In 1927, he became President of the APHA.

Chapin was described in 1967 as “the greatest American epidemiologist” by Alexander Langmuir, first and long-time director (1949–1969) of epidemiology branch of the CDC. As late as the 1980s, Chapin’s views were dominant there.

CRITICALLY, Chapin’s unproven hypothesis was accepted as true: Ease of infection in close proximity is accepted proof of transmission from sprayed droplets. This KEY ERROR conditioned the evolution of this field over the next century, and into the COVID-19 pandemic.

The 1918 flu led to lots of work and discussion in this area, but did not blunt the ascendance of of Chapin’s theory.

In the 1930s, Harvard engineering professor William Wells and physician Mildred Wells, his wife, started applying more contemporary experimental methods to the investigation of airborne transmission.

But Chapin had successfully shifted the paradigm and his theory was now viewed as scientific progress. The Wellses were accused of a retrograde approach to science, which sought to bring back the miasma theory.

Wells was 1st to rigorously study size of sprayborne droplets vs. airborne aerosols and conceptualized dichotomy of sprayborne droplets (≳100 μm), which reach the ground before drying versus aerosols (≲100 μm) which dry before they reach ground (“droplet nuclei”).

Wells understood connection w/ meteorology where this is common knowledge, stating: “A raindrop 2 mm in diameter can fall miles without completely evaporating under conditions which would cause a 0.2 mm droplet to evaporate before it had fallen from the height of a man.”

Shockingly, Public Health and Infectious Diseases have published for decades that large droplets are those heavier than 5 microns (!!), including in the latest WHO Scientific Brief on COVID Transmission that addresses this issue.

We pointed out this glaring error many times. i.e. see that even at 50 microns, they don’t fall quickly: Not too important per se, but makes glaringly obvious the ignorance of physics by those in charge at WHO and its IPC committee.

We investigated the history of the 5 micron / 2 meters error in a previous paper led by @linseymarr and the extraordinary @katierandall, with support from @EThomasEwing, Lydia Bourouiba of @MIT and yours truly.

How did we get here: what are droplets and aerosols and how far do they go? A historical perspective on the transmission of respiratory infectious diseases

I am getting slightly out of order. I’ll explain the reason for the “5 micron particles fall within the meters of the person” enormous error later in the thread, once I have explained the background. So we were talking about the work of William Wells on airborne infection.

The Wellses suspected that tuberculosis and measles were airborne, but BOTH were already believed to be droplet diseases, and they encountered intense resistance from the epidemiological community.

Measles was thought to be a droplet/fomite disease. At the time of Wells, and as late as 1985, because of: – ease of transmission in close proximity (= sprayborne droplets per Chapin) – cases of lack of infection with shared air.

Wells thought that measles was airborne (and now we know he was correct, though he died 2 decades before this was accepted). Wells has some initial success showing that UV lights installed in the ceiling of classrooms greatly reduced measles infection.

Air Disinfection in Day Schools

However, subsequent attempts to replicate these findings produced mixed results. In retrospect, in schools where UV prevented measles transmission, children were together indoors only in the school, not elsewhere. In other schools, children shared other spaces (e.g. buses).

Wells established the scientific basis of airborne infection But he was working in a period of intense hostility in public health and infectious diseases towards airborne transmission, ushered by the success of the 1910 paradigm shift of Chapin after 2 millenia of belief in miasmas.

General skepticism against airborne tr. is illustrated by 1951 quote of Langmuir (first and longtime director of epidemiology at the CDC). “It remains to be proved that airborne infection is an important mode of spread of naturally occurring disease.”

Langmuir worked preventing disease transmission among US military in World War II. Substantial resources were dedicated to the effort, generating knowledge “which would have taken decades to accumulate under peacetime conditions” and established leaders for decades.

Langmuir et al. studied airborne transmission, but MISINTERPRETED the results of their own studies: Distance reduced transmission, therefore it was droplets. Ignoring that distance reduces airborne transmission by dilution.

Airborne Disease: Including Chemical and Biological Warfare

Systematic way to understand and classify the shared-room airborne transmission risk of indoor spaces

However, Langmuir’s work renewed interest in airborne infection, as he concluded that WEAPONS of airborne disease could be created, which became a topic of intense interest during the cold war.

Despite stubborn resistance to the idea that airborne transmission had relevance for natural diseases, Wells, Robert Riley, and Cretyl Mills succeeded in demonstrating airborne transmission of tuberculosis (TB) in 1962 through extensive efforts.

They routed air from TB hospital ward to 150 guinea pigs for two years. About three guinea pigs/month were infected No guinea pigs were infected in the control group where the only difference was that the air was irradiated with germicidal ultraviolet light, killing the TB bacterium.

Because of this, TB was the first important natural disease to be accepted as airborne in modern times It was shown that pulmonary TB can ONLY infect if bacterium-containing aerosols reach the alveoli, for which they need to be smaller than 5 microns.

Here is when we think that the ERROR of “5 micron particles fall to the ground in 1-2 m” originated: Only TB and bioweapons were important, someone at the CDC confused the size that goes to alveoli with size that falls to ground. This was repeated until 2020.

The fascinating story of how @katierandall,@linseymarr et al. figured out the cause of the 5 micron error was told in this article in @WIRED by @MeganMolteni. Reads like a spy novel, one of the best of the pandemic!

In a paper we characterize the years after the demonstration of TB as “Reluctant acceptance of as little airborne transmission as possible (1962–2020).” Airborne disease was not impossible, but required an extremely high (undeniable) standard of proof.

Unfortunately, standards of evidence were very different for different routes of transmission. Many diseases accepted as “droplet” without any substantive proof—let alone extensive and time-consuming experiments. Only the hypothesis of Chapin, ease of infection in close proximity = droplets.

Remember, large droplet transmission has NEVER been demonstrated DIRECTLY for ANY disease in the entire history of medicine (Paper from Prof. Yuguo Li, lone airborne specialist in @WHO IPC Committee).

An example of the resistance to airborne, an obvious case of long-distance airborne transmission of smallpox in [occured in] Germany in 1970. SP airborne transmission debated for centuries, only definitely accepted in the complete absence of community transmission.

An infected person arrived from in Germany from Pakistan, where there were no cases at all. Only possible explanation was transmission through air. In latter tests, smoke from index case room went to rooms of secondary cases.

The recent outbreak of smallpox in Meschede, West Germany

An airborne outbreak of smallpox in a German hospital and its significance with respect to other recent outbreaks in Europe

The case report shows the prevailing bias against airborne in Public Health: “The only remaining route of transmission considered reasonable was airborne spread of a virus-containing aerosol, **a possibility against which all of the investigators were initially prejudiced**”

Measles and chickenpox were similar, described as droplet diseases till mid-1980s, and only accepted when superspreading events with long-distance transmission made airborne undeniable.

Interestingly the WHO IPC commitee members stated that COVID could not be airborne as it was much less transmissible than measles. Otherwise they would have recognized it quickly Except… it took their profession 70 years to recognize it…

Note that it is always the same error, going back to Chapin. Assuming that ease of transmission in close proximity (and decreasing transmission with distance) is proof of large droplets, and that airborne is very unlikely. For TB, measles, chickenpox… and COVID-19.

SARS-1 in 2003 brought renewed attention to airborne transmission Superspreading was clearly observed. Airborne spread was implicated in several outbreaks in hospitals, and also in large Amoy Gardens outbreak in Hong Kong.

The same dynamic played out for SARS-1, observed ease of infection in close proximity was considered evidence of droplet transmission. Airborne transmission was considered unlikely, and only accepted if evidence was undeniable.

From IPC member: Airborne transmission and precautions: facts and myths

During last several decades, until the COVID-19 pandemic, with available antibiotics, vaccines, and no major respiratory pandemics, studies further probing the details of droplet vs. airborne transmission had NOT been a major public health priority.

High standards of ventilation and filtration in modern hospitals mean that airborne risks have been substantially mitigated in these settings, where many key infection control scientists work.

Adherents of droplet transmission were in control of all key public health institutions. Scientists proposing airborne transmission were typically ignored (as we saw later for COVID-19, and explaining persistence of errors).

How did we get here: what are droplets and aerosols and how far do they go? A historical perspective on the transmission of respiratory infectious diseases

Orthodoxy, illusio, and playing the scientific game: a Bourdieusian analysis of infection control science in the COVID-19 pandemic

This schematic qualitatively captures the situation before COVID-19 appeared:

Importantly, substantial scientific evidence had accumulated (BEFORE COVID) of airborne transmission of the flu, as reviewed in this paper in @ScienceMagazine (led by @ChiaWang8 and @kprather88).

But the evidence of airborne transmission of the flu had been ignored, and @WHO and@CDCgov pages on the flu ONLY mention droplets and surfaces.

WHO Influenza (Seasonal)

CDC Influenza (Flu)

Airborne transmission is well accepted in veterinary medicine, including several coronaviruses and flu viruses, and sometimes over many kilometers (facilitated by large animal concentrations). Every veterinarian I’ve talked to is dismayed about COVID

Finally we get to the COVID-19 pandemic. It is so massive and disruptive that every researcher that can contribute in some way gets to work doing so. It includes lots of aerosol researchers (e.g. yours truly), with fast collaboration with medical researchers, virologists etc.

Some early scientific and public health reports out of China state that COVID-19 has airborne transmission:.

Despite a lack of direct evidence in favor of droplet or fomite transmission of COVID, by Mar 2020, @WHO concluded that ease of transmission in close proximity proved that COVID-19 was transmitted by those mechanisms, continuing Chapin’s 1910 error

The same errors described for other diseases are repeated for COVID-19 and the bar is moved higher. Unlike TB, animal transmission is not enough. Unlike measles, superspreading and long-distance transmission is not enough.

However, accumulating evidence in favor of airborne, and critical LACK of evidence for droplets or surfaces tilts the balance. Airborne transmission is (reluctantly and slowly) accepted.

E.g. one summary of evidence for #COVIDisAirborne: TEN SCIENTIFIC REASONS IN SUPPORT OF AIRBORNE TRANSMISSION OF SARS-CoV-2

@WHO commissioned some reviews on the modes of transmission of COVID-19. The one on airborne included no airborne experts, and has been rejected by the reviewers: SARS-CoV-2 and the role of airborne transmission: a systematic review [version 2; peer review: 1 approved with reservations, 2 not approved]

Shockingly, no review has appeared (to my knowledge) on the evidence in favor of large droplet transmission, despite @WHO being so sure for a long time that it was dominant.

A @WHO-sponsored review has been written on “close contact transmission” equals “close proximity,” but that is a measurement of distance, NOT a mechanism of transmission! Still carrying the error of Chapin, confusing close proximity w/ spray droplets

That @WHO-sponsored review on close prox. transmission has also NOT been accepted for publ., and remains in limbo after over a year Even though THEY GET TO CHOOSE REVIEWERS! Read the comments that we posted on both articles:

SARS-CoV-2 and the role of close contact in transmission: a systematic review [version 2; peer review: 1 approved with reservations, 1 not approved]

SARS-CoV-2 and the role of airborne transmission: a systematic review [version 2; peer review: 1 approved with reservations, 2 not approved]

“Aerosol-generating medical procedures” were the only accepted cause of airborne transmission for over a year (e.g. by @WHO). They originated from low-quality research in SARS-1. Research has show that real AGPs are talking, singing…

@WHO has finally accepted airborne transmission, including the fact that transmission in close proximity includes short-range airborne transmissionut only in Dec. 2021, after we pushed them a lot.

But both @WHO and @CDCgov communicate poorly about this, not explaining it to the public, and avoiding the word “airborne” (which is the clearest for the public) as much as they can, e.g. no mention of airborne COVID in @WHO’s extensive Twitter feed and especially no clear description of the control measures. As @kprather88 keeps saying, it is totally doable to majorly reduce transmission, once we accept it and get serious about it. But it is a really inconvenient truth for those in power…

My pinned tweet has a good summary of those protection measures against transmission (also in many other sources such as @CleanAirCrewOrg, or the @CDCgov web pages if you actually read them in detail):

So where does that leave us in mid-2022: – PH institutions such as @CDCgov have given up on explaining or preventing transmission. Too inconvenient for those in power. Scientifically, the cat is out of bag. Tons of evidence of airborne, some medical and public health people understand it.

Measures to improve ventilation are favored (e.g. by the @WhiteHouse) since they don’t face resistance from public, but they are inconsistently applied. Carbon dioxide meters are resisted by institutions, because they make poor ventilation obvious.

Not sure how this will evolve. But as it becomes scientifically clearer, it will be harder to justify lack of action. As we know from climate change (follow https://twitter.com/i/lists/1053067173961326594…), the scientific evidence can be overwhelming & those in power still resist inconvenient actions.

This is the final (hopeful) paragraph of this historical paper. Wells lamented in 1945 the ignorance of airborne transmission in public health. Let’s hope that ends with COVID-19 (& fight to make it reality – we need to be activists).

I didn’t do this alone. I got involved in COVID-19 transmission research in early 2020, and was shocked and confused by the stubborn and impatient resistance we faced.

E.g. Conly’s (@WHO IPC Chair) rudeness on our Apr. 2020 call with @WHO]

I’ve been lucky to work with the Morawska/@Don_Milton group of 36 scientists & with many others

@Don_Milton made me curious about history, mentioning Chapin and his impact. I was perplexed an “ancient” researcher could influence @WHO advisors today so much and started reading.

As we investigated many aspects of transmission, I kept an eye on the history. The paper on the 5 micron error with @katierandall and @linseymarr made me learn a lot, and also see more clearly the pendulum of history.

Contributors to the paper include @linseymarr, @katierandall, @EThomasEwing, @zeynep, @trishgreenhalgh, Raymond Tellier, Julian Tang, Yuguo Li, Lidia Morawska, @jmcrookston, @DFisman, @Orla_Hegarty Stephanie Dancer, Philo Bluyssen, Giorgio Buonanno,, @Marcel_Loomans, @WBahnfleth.
@pkubioaerosol, Chandra Shekhar, @WargockiPawel Arsen Kritov Melikov, and @kprather88. The authors contributed majorly to the paper. If there are any remaining mistakes, they are mine.

As always, if you think that something is incorrect, or if you have a paper that contradicts (or further supports) anything I am saying here or in the paper, please send it my way.