COVID-19 Vaccines Truth or Fiction?

If you are confused about COVID-19 vaccines, whether they are “good” or “bad”, effective or  ineffective, safe or unsafe, causing more deaths than COVID-19 itself, resulting in a new epidemic of “turbo cancer” or not, and whether you should consider getting an updated vaccine when they roll out around the country next month, this blog post is for you.

It will be helpful to your understanding if you read my blog from two posts ago entitled: “A (fairly) Comprehensive Review of What We Know, What We Think We Know and What You Should Consider about COVID-19,” but don’t worry if you don’t have time to do that, because I will pull pieces from that post into this one to help you out.

Let’s get the issue of conflicts of interest out of the way first:

  1. I do not own any individual shares of any pharmaceutical company. The only individual stock that I hold is that of an oil and gas company. I specified “individual,” because I do have investments in mutual funds, but I have no idea what stocks are in them and they are managed by professional managers, not me and the managers do not consult with me on which funds to invest in.
  2. I do not receive any payments from pharmaceutical companies (and never have) for advisory services, speaking engagements, participation on a board, research, or any other kind of service. You can verify this for yourself at openpaymentsdata.cms.gov.
  3. I do provide information on a weekly radio show (The Doctors Roundtable segment of the Idaho Matters show on Boise State Public Radio with host Gemma Gaudette), but I receive no payments for doing so, and they do not influence or control what I say.
  4. If you are reading this blog, you know that I make it free to everyone and do not charge any subscription fee to do so. I do not receive any advertising dollars or sponsorships for my blog or social media accounts.
  5. I have absolutely zero interest in running for elected office or serving in any current or future administration, so my positions on COVID-19 and COVID-19 vaccines are not influenced by attempting to attract attention or curry favor with any current or future politician.
  6. The only money even remotely related to COVID-19 I have made is the royalties off the book I published in 2023: Preparing for the Next Global Outbreak: A Guide to Planning from the Schoolhouse to the White House.

So, whether you get a COVID-19 vaccine or not makes no difference to me from a financial standpoint. All I want to do is give you information that is evidence-based that you can use to make your own decision and hopefully some tips for how you can evaluate claims being made so that your disinformation warning system goes off when it comes your way.

Two more points to be made before we dive in. First, not all COVID-19 vaccines are mRNA vaccines. The Pfizer and Moderna vaccines are, but the Novavax is not. Further, a number of countries have used non-mRNA vaccines (more on that below).

Second, let’s be sure we all have a common understanding as to what mRNA is. mRNA is not something we made synthetically until recently. It is naturally-occurring in every cell of our bodies and has been for all of creation. Our DNA that contains our genetic code is in the nucleus of our cells. I find that it helps to compare a cell to a freshly cracked egg that has been poured into a skillet. In this analogy, the yolk would represent the nucleus of the cell. That genetic material in the DNA in the nucleus contains the code (think of it like the recipe) of the precise instructions for how the cell should make its proteins. These proteins are vital for our cellular and bodily functions. The problem is that all the parts of the protein assembly plant within the cell are in the cytoplasm (think of that as the white part of the egg). So, how do we get the instructions in the genetic code of the DNA in the nucleus to the protein assembly plant in the cytoplasm? Answer: mRNA. mRNA can make a copy of those instructions for the particular protein that is needed directly from the DNA. Unlike the DNA, which cannot move between the nucleus and the cytoplasm, the mRNA can. mRNA takes that copy of the instructions (a transcript) and then travels to the cytoplasm to the protein-making factory so that those specific ingredients to make the protein can be assembled in precisely the correct order to end up with the functional protein that the cell needs. (By the way, the mRNA does not incorporate itself into or alter the DNA. Thus, the claims by certain prominent physician disinformation purveyors that mRNA is gene therapy is without any basis in biology or reality).

With that behind us, the most recent stir caused by RFK, Jr. as Secretary of HHS occurred on August 5, 2025 when the U.S. Department of Health and Human Services issued a press release entitled: “HHS Winds Down mRNA Vaccine Development Under BARDA” https://www.hhs.gov/press-room/hhs-winds-down-mrna-development-under-barda.html. Most readers will never have heard of BARDA – Biomedical Advanced Research and Development Authority. BARDA was formed in 2006 to fund the research, development and stockpiling of vaccines and other treatments to respond to public health emergencies such as a chemical, biological, radiation, or nuclear attacks, as well as to prepare for pandemics (especially influenza viruses) and for other emerging infectious diseases.

While I don’t think that mRNA vaccines are perfect, I believe, and many other experts believe, that mRNA vaccines currently offer the best and quickest option for a vaccine in the event of a novel virus emerging (very likely an avian influenza virus) that is associated with high mortality and high transmission rates that end up overwhelming our hospitals. All you have to do is look at Operation Warp Speed, a phenomenal and unprecedented success, under the first Trump Administration to see what I mean. The average time to development of a vaccine before Operation Warp Speed was roughly 5 – 10 years. With Operation Warp Speed, vaccines were available in just under 12 months.

Now, personally, I think COVID-19 was bad, but I understand that some feel differently. However, relatively speaking, while COVID-19 caused a huge number of deaths, it was not a high mortality rate virus. Even a low mortality-rate virus can cause a lot of deaths if it is highly transmissible and infects enough people. As I mentioned in my blog post on a review of COVID-19, the case fatality rate for COVID—19 after the availability of vaccines and treatments was about 2.1% worldwide and 1.6% in the U.S. There are viruses that do cause disease outbreaks in other parts of the world, but may or may not have pandemic potential, that have mortality rates in excess of 80%. Probably the most serious virus that we know does have pandemic potential (because it has happened in the past) is the avian influenza virus, and we have been watching two new strains (clades) spread in the U.S. – one among cattle and one among wild birds. Both have the potential (and there have been actual cases) to spread to humans. Historically, avian influenza infections in humans have resulted in case fatality rates of 40 – 60%, with an average of about 50%. I understand that some people are very distressed by the fact that during the COVID-19 pandemic there were times they felt pressured to take a vaccine they didn’t want to receive. We should address those concerns and make plans for the next pandemic (because there will be one), but overreacting to that concern by further feeding vaccine mistrust and by cutting off funding and development of vaccines could be a very costly mistake. Let me explain.

The field of vaccinology is exploding. We are learning so much, so fast. That field of knowledge rapidly expanded during the pandemic because of all the research done on vaccines. We are learning about the associated immunity from vaccines, as well. We have a better, but still as of yet, incomplete understanding as to why some vaccines provide life-long protection, and others require boosting or frequently updated vaccines. We are learning much more about mucosal immunity (the immune protection that occurs at the mucosal barriers that are the borders between the body and the outside – e.g., the gut and the mouth and nose) – likely a key to being able to protect from developing infection. We are learning more about adjuvants that can themselves significantly boost the immune response to a vaccine. We are learning more about the importance of the correct interval between first and second doses of a vaccine. Our knowledge is exploding, and with that knowledge, we will be able to develop even better vaccines in the future, including potentially nasal vaccines that may not require needles and new ways to protect against infection that may not even require a vaccine.

We have known that some viruses are oncogenic (meaning that they can cause cancer), and now we know that one vaccine (HPV vaccine) can essentially eliminate aggressive cervical cancer in women, and yet, I see the target on its back based on some of RFK, Jr.’s comments. In just the past couple of years, we are now seeing the evidence that some viruses can be responsible for certain neurological conditions, such as the Epstein Barr Virus’ (EBV) role in the development of multiple sclerosis (MS), and we may have just identified a virus that causes or can contribute to the development of Parkinson’s Disease.

We need to be realistic about what vaccines can and cannot do, but at the same time, abandoning areas of vaccine research means lost opportunity to learn, lost opportunity to increase our response to novel threats, and potentially lost opportunities to prevent disease and complications of disease. We also now make the U.S. more vulnerable to bioterrorism. It is not lost on our enemies that trust in our government and in vaccines is decreasing and the opportunities that creates for them.

Flash back to March of 2020 when COVID-19 was spreading to more and more states. Now, let’s assume that instead, it was one of the current clades of the H5 avian influenza virus that had transmitted from birds to humans and had picked up the mutations that allow for efficient transmission between people. Avian influenza virus shares some features with SARS-CoV-2, e.g., the fact that both are spread by airborne transmission (I cover what this is in my review of COVID-19 blog post). However, we have reason to believe (i.e., there is supporting evidence, but not proof) that unlike COIVD-19, older adults might have more protection against severe illness from avian influenza than children because we have been exposed through infection and/or vaccination over the years to a shared component of the virus between the avian influenza H5 strains and the seasonal influenza viruses that come around annually. I point all of this out to say that if we were experiencing an avian influenza pandemic with a case fatality rate of even half what it has historically been (let’s say 25%) and children were getting severely ill as often or even more often that older adults, then imagine the panic. Further, it has been well established that schools are the source of spread of influenza virus epidemics that we experience each year. Our schools would be closed and our pediatric hospital capacity would soon be overwhelmed (as a hospital administrator, I can tell you that it is much more difficult to quickly surge (expand) pediatric capacity than it was for us to expand adult capacity as was necessary in late 2021 and early 2022 with COVID-19). I doubt too many people would be advocating for the “let it rip” strategy to get people infected so that we could get to herd immunity (I explain the concept of herd immunity in the review blog piece and in my book) if that meant 1 in 4 of those infected persons would die. Do you want a mRNA vaccine in months or a traditional vaccine in years, or do you just want to take your chances?

Of course, if the Secretary’s announcement is because of some new information that mRNA vaccines are a “cure that is worse than the disease” so-to-speak, perhaps this is the reasonable thing to do. Let’s see what he says:

“We reviewed the science, listened to the experts, and acted,” said HHS Secretary Robert F. Kennedy, Jr. “BARDA is terminating 22 mRNA vaccine development investments because the data show these vaccines fail to protect effectively against upper respiratory infections like COVID and flu. We’re shifting that funding toward safer, broader vaccine platforms that remain effective even as viruses mutate.” (emphasis mine)

It is refreshing to know that HHS “reviewed the science” and “listened to the experts.” Let’s see who the experts were:

  1. The first on the list is Martin Wucher, MSC Dent Sc. Never heard of him or his credentials, so I looked him up. The MSC Dent SC refers to a Master of Science in Dental Sciences. Now, I have worked with a lot of dentists, I go regularly to a dentist, dentists are very important to our oral and overall health, but I have never gone to or referred my patients to a dentist for vaccines and never called a dentist in the middle of the night to manage a critically ill patient with COVID-19. With the resources of our federal government, is he the best of the best of our experts that we hope might have a background in vaccinology, virology, infectious diseases, and public health to be able to help us critically evaluate the data on mRNA vaccines? Well, it is certainly possible for a dentist to get advanced education and training in these areas. So, let’s look at Dr. Wucher’s bio. His dental practice is described as “nutritional therapy and orthomolecular medicine.” Orthomolecular medicine is a fancy and legitimate-sounding name for alternative medicine that is based on a concept that disease reflects an imbalance of the nutritional environment. Certainly, we well recognize diseases that are a consequence of nutritional or vitamin deficiencies, but there are no infectious diseases that I can think of that can be addressed solely by nutritional therapy. The other tip-off is that I didn’t recognize his credentials, and I am guessing that you didn’t either, and that is because we don’t grant that credential in the U.S. So where is Dr. Wucher’s practice? Answer: Namibia, just outside of South Africa.
  2. Bryam Bridle, Ph.D. Unfortunately, RFK, Jr. does not include any of the biographical information about these “experts” so that I can be confident that I have identified the right person, but I feel like the name is uncommon enough that I have probably have, especially as I look at his background. If so, he is an associate professor at the University of Guelph Ontario Veterinary College. He is a viral immunologist, so that is really good. According to his bio, he is working on a “research initiative aimed at modifying the research team’s optimized cancer vaccine platforms to target severe acute respiratory syndrome virus (SARS-CoV) – 2.” Now, the good part of this is that he obviously must not believe the nonsense being spread by a number of the prominent physician disinformation purveyors that the COVID-19 vaccines are causing cancer, in fact “turbo-cancer” (addressed below) if he uses SARS-CoV-2 in his vaccines in an attempt to prevent cancer. However, there is an obvious potential conflict of interest if he is developing a COVID-19 vaccine that I would assume he and the veterinary college would benefit from commercializing, but would also be benefitted by eliminating or reducing the competition from mRNA vaccines.
  3. Steven Hatfill, M.D. Assuming that I have identified the correct Dr. Hatfill, and I think I did because the biographical information indicates he has been hired by HHS, he went to medical school at the University of Rhodesia (Zimbabwe). He later pursued a Ph.D. program, but reportedly never completed it because he failed the thesis requirement. He was a strong advocate for the treatment of COVID-19 with hydroxychloroquine, even though data continued to show that it was not effective, and in fact, more recent data showed that thousands of people were harmed. Also see Washington Post, “Scientist who was part of covid treatment controversy returns to HHS,” May 4, 2025.
  4. Peter McCullough, M.D., Ph.D. – This is the first one on the list that I am familiar with and have followed fairly closely. According to multiple sources, his board certification was revoked for spreading disinformation, and one article indicates McCullough is currently listed as chief science officer of The Wellness Company, the owner of which was recently reported as also investing in an anti-vaccine dating site and launching a coffee brand for “anti-woke” consumers. The Wellness Company sells supplements, one of which is called “Ultimate Spike Detox.” It costs $89.99 for 120 capsules. https://www.namd.org/journal-of-medicine/3353-abim-revokes-certification-of-another-doctor-who-made-controversial-covid-claims.html. Obviously, Dr. McCullough’s supplement sales may create a potential conflict of interest.
  5. Harvey Risch, M.D., Ph.D., on paper appears to be very qualified. He is a professor of epidemiology at the Yale School of Public Health, though I found that his interests have been focused on cancer, and saw nothing to suggest any of his research interests have related to vaccines or infectious diseases.
  6. Kelly Victory, M.D. appears to be a trauma and emergency medicine specialist.
  7. Matt Bain, M.D. There are too many physicians with this name for me to be confident that I have identified the right person.
  8. James Thorp, M.D. I am assuming that this is a gynecologist who has been very outspoken against the COVID-19 vaccines, but I certainly could be mistaken. If so, here is a link to one of the fact checks addressing a number of his allegations, including his assertion that 350,000 – 400,000 people had died from the COVID-19 vaccines. https://healthfeedback.org/claimreview/james-thorp-false-claims-covid19-vaccines-harm-fertility-pregnancy-infant-survival-the-sentinel-report/.

Now, because the HHS supporting document does not provide the biographical information on this group of experts, I had to make educated guesses, in some cases, and that means I might have identified the wrong person, but other sources seem to be confirming the identities of at least some of these individuals. My point here is that you can do the same kind of research as I just did without any special scientific knowledge. One might assume if the credentials and reputations of this group were stellar and impressive that information likely would have been included. Furthermore, another strategy for evaluating credibility is to look at statements and actions that are internally inconsistent. Generally, when people are being sincere, clear-headed and truthful, their statements are internally consistent. In this case, on June 9, RFK, Jr. summarily dismissed all members of the Advisory Committee on Immunization Practices citing that at least a major factor in his decision was that the members had too many conflicts of interest. https://kffhealthnews.org/news/article/rfk-jr-acip-vaccine-advisory-committee-cbs-celine-gounder/. If that was not pretense, why not be extra careful to select “experts” who did not have such obvious potential conflicts of interest as I pointed out above?

On June 9, 2025, HHS released another press release titled: RFK, Jr.: HHS Moves to Restore Trust in Vaccines. In it, it states: … under my direction, the U.S. Department of Health and Human Services is putting the restoration of public trust above any pro- or antivaccine agenda.” That is certainly an encouraging statement, but then one must look to see if future words and actions match that. Given the outspokenness of some of these members expressing clearly strong anti-COVID-19 vaccine rhetoric on very public venues, at least one member with disciplinary action by the certifying board, why choose this group as the “experts” that you are going to shape U.S. vaccine policy if you are trying to restore the public trust? The fields of virology, vaccinology, immunology, infectious diseases and public health are replete with recognized experts, who have not been outspoken or taken public positions on this subject from which to choose a committee who could carefully sift through high quality data and provide the Secretary with recommendations and advice.

The selection of this group appears to be based on a bibliography for a book called TOXIC SHOT: Facing the Dangers of the COVID Vaccines. One would think that just from the title of the book, it is pretty clear what bias this group is coming to the table with, especially since there doesn’t appear to be anyone else on this list of experts other than the authors of this book. You can see this reference in the data document that is referenced in the HHS press release at https://zenodo.org/records/15787612. It is at the top of the list of references.

Further, it seems a bit insincere for RFK, Jr. (and also NIH Director Jay Bhattacharya – see his opinion piece in the Washington Post August 12, 2025) to attribute the termination of funding for mRNA vaccines to the loss of public trust without acknowledging their own out-sized influence on that deepening loss of public trust and promoting the spread of disinformation.

Now personally, I believe that people can be mistaken and learn from those mistakes and therefore, even if these members had previously spread misinformation or disinformation, they might now be on the right track given that we have so many more high-quality medical studies, much more data, and we have gained significant new knowledge about the disease and the vaccines. I also believe that potential conflicts of interest can oftentimes be managed when fully disclosed. I also believe that doctors who have been disciplined can go through the steps to be rehabilitated and safely reintroduced to the practice of medicine.

If the 181-page attachment of studies that support the decision to stop the investments into mRNA research were high-quality, peer-reviewed studies that clearly demonstrated that “these vaccines fail to protect effectively against upper respiratory infections like COVID and flu,” then that trumps everything and these other matters related to this group of experts don’t matter much. So, is that what the science shows when we examine that list of references? No.

Most of the papers referenced are studies conducted in test tubes and petri dishes. That can be important early information to inform subsequent studies in laboratory animals and then humans, but we often find that these results do not hold up in humans, and indeed, where tested, these did not hold up. Part of the problem is that it is easy to get much higher levels of a drug into a test tube or petri dish than you can safely get in the blood of a human. This was the big problem with ivermectin showing promising results in a test tube, but failing to be effective at doses that were safe in humans. Second, most of these studies tested the effects of the SARS-CoV-2 spike protein that comes from the virus, not from vaccination. Many studies have failed to separate out the effects of spike protein resulting from infection, which contains other proteins as well and is produced in much higher amounts for much longer periods of time than the spike protein that results from vaccination. We saw that many of the effects attributed to the spike protein and suggested to have resulted from the vaccine occurred in patients who were not vaccinated or who got infected prior to the time in which vaccines were available to the public. Rather than offer proof that the vaccine is dangerous, these studies contributed to the dangers of the SARS-CoV-2 causing natural infection.

A common strategy that I have observed by those who spread disinformation is to either avoid providing references so that their claims are difficult to refute, or, as in this case, flood the audience with a long list of studies that almost no one is likely to read and evaluate. Also, they will often claim that the study states one thing, when in actuality, it states the opposite.

For example, in reference number 16, the authors actually state: ”vaccines were efficacious against the Delta variant, especially reducing the severity of the disease.”

In reference number 26, the authors actually state: “several of these vaccines have proved to avoid severe disease symptoms.”

Reference number 48 is a study of a segment of the spike protein from the virus that was demonstrated to produce the toxic effects. The authors did not study vaccines or even mention them in the article.

There are many other specific examples I could provide. Some of these studies expressly state that the benefits of COVID-19 vaccination far outweigh the risks of complications from infection, including a review article that dir. ectly compares infection with vaccination and concludes that vaccination is “the more favorable option for protection.” What I want you to know is that we cannot trust this information coming out of this administration at face value. However, you also don’t have to have a deep understanding of the science and data interpretation. Just check some of the studies like I did, and go to the conclusion section to see if the authors say the same thing as what the person or persons citing the study says. You can also search the document for certain terms like vaccines, vaccination, etc.

Besides studies whose conclusions are limited because they used in vitro (in test tubes or in petri dishes as opposed to actual human beings) or in silico (computer simulations) methodologies, and others that used only laboratory mice (as opposed to actual humans – like with test tube and petri dish studies, we often find that encouraging findings in mice don’t pan out in humans), some of the study methodologies are suspect because they injected spike protein directly into the blood stream or even directly into the brains of laboratory animals – routes of vaccination that are never used in humans.

Finally, before we go into the data ourselves, one more common-sense clue that what we are experiencing is politically and ideologically motivated and not in fact based on science and evidence. The rest of the world is not following our lead. I have a lot of respect for the UK Health Security Agency. It’s technical briefs that were regularly issued throughout the pandemic were much higher quality and informative reports that those of the CDC. They are not abandoning or recommending abandoning mRNA vaccines. The European Centre for Disease Prevention and Control is an excellent public health organization and puts out excellent information. They are not recommending abandoning mRNA vaccines. The Israeli CDC, part of the Israeli Ministry of Health is similarly not abandoning mRNA vaccine technology. None of these organizations, nor the WHO, has endorsed, supported or shared the views of our HHS and this panel of “experts.” The science is the science. If these vaccines were not effective and if they were not relatively safe, we would be seeing similar conversations and actions across the globe. This is the first time in history that I can think of that the world is not following our lead on matters relating to medicine, health and science. That should be more reason for us to be skeptical.

So, let’s evaluate RFK, Jr.’s statement ourselves since his supporting data doesn’t really support his claims. As a reminder, here is what he states in the HHS press release: “…the data show these vaccines fail to protect effectively against upper respiratory infections like COVID and flu. We’re shifting that funding toward safer, broader vaccine platforms that remain effective even as viruses mutate.”

The first thing that I would note from this language is the phrase “upper respiratory infections like COVID and flu.” It is an interesting way to describe these two viral infections, because it is not the “upper” (which refers to the nose and throat) respiratory tract infection that kills people from either illness. The SARS-CoV-2 virus and influenza viruses do make their entry through the upper respiratory tract, however, unless the body’s immune system is able to contain the infection, it will progress down to the “lower” (lungs) respiratory tract, and this is when people get critically ill, and even die during the acute phase of COVID-19 or influenza. For COVID-19, that process takes about a week. That is why vaccinations give your body a head-start and an increased chance of preventing severe disease.

Here is the chronology of antibody response from a study of 30 patients who developed COVID-19 (https://pmc.ncbi.nlm.nih.gov/articles/PMC7129952/):

Remember, the SARS-CoV-2 virus can make its way down the respiratory tract to settle into the lungs and cause severe disease in as soon as a week. What you see from above is that the body’s antibody response takes about three days for the body to recognize the foreign invader and develop antibodies to it. However, it can be up to two weeks before the antibody response is fully ramped up. This is the advantage of being vaccinated prior to being infected with the virus. With vaccination, we have the opportunity to generate an antibody response prior to exposure, and therefore, the body can respond quicker and with a higher level of antibodies that better enable the virus to be contained in the upper airway.

Now, assuming that what I have just told you is true, then we should see that vaccinated persons have a much lower rate of developing severe disease and death. Is that what the data show us? Here are some examples of data taken from different points in the pandemic (these are the data from the CDC, though I think these have been removed from the website, at least I can’t find them):

Here is a graph showing the rate of hospitalization for COVID-19 in the U.S. by vaccination status. It is very clear that throughout this period from the end of January, 2021 through the end of November, 2021 at all points the rate of hospitalization was orders of magnitude higher in the unvaccinated relative to the rate in those fully vaccinated.

Here is a graph prepared by CDC staff for the Advisory Committee on Immunization Practices that shows the rates of COVID-19 deaths by vaccination status in the U.S. for the period of April 4, 2021 through October 30, 2021. The fall of 2021 is when we were seeing the Delta variant become predominant in the U.S. You can read from the CDC staffer’s notes that in October of 2021, an unvaccinated person had 5 times the risk of testing positive for COVID-19 compared to fully vaccinated persons (which means that the vaccine did in fact reduce the chances of being infected) and 14 times the risk of dying from COVID-19.

Here is another graph that at the period from where those above ended to April 1 of 2023 and plots the COVID-19 weekly death rate in the U.S. by vaccination status. Again, you can see that at all points, your chance of dying from COVID-19 was lower if you were vaccinated than if you were unvaccinated.

Now, I could take you through all the science of this, and some of the many studies demonstrating the same findings, but as they say, “a picture is worth a thousand words.” Further, I want you to be able to look at data and sources that you can find and understand on your own, if you are not trained in science or statistics yourself. You don’t need me to tell you whether the Secretary’s statement: ”the data show these vaccines fail to protect effectively against upper respiratory infections like COVID” is true or false; you tell me. In fact, if you have a middle schooler or high school student, show them these graphs and see how they interpret them.

I will write more on this subject in my next blog piece, including addressing the statement from the Secretary that: “We’re shifting that funding toward safer, broader vaccine platforms that remain effective even as viruses mutate.”

Science Is Under Attack

There is no question that science is under attack, and in a systematic and coordinated fashion. I have been studying this in the context of the pandemic for the past 5 years, and there were many recurring signs and patterns I could see that were tip offs that the person spreading disinformation was doing so intentionally rather than mistakenly and that the person, while touting expertise, was really an ideologue (rather than being scientifically curious and open to evolving evidence, they were committed to a particular point of view or belief and could not be swayed by contradictory evidence or faults in their own reasoning when pointed out to them. Sometimes they would state that a study showed X, but then when I reviewed the study they referred to, it didn’t say that at all and often contradicted what the disinformation purveyor asserted. Other times, it was far more devious with data or graphs displaying the data manipulated to try to prove the point they wanted, rather than what the study actually demonstrated).

To be clear, questioning the science and challenging it has always been at the very heart of science, but it has to be in good faith to be legitimate. As scientists, we come up with hypotheses, design studies to try to answer the question raised by the hypothesis, then collect data, and finally interpret the data. And, science evolves. Often, studies answer some questions, but then raise new ones. Rarely is a study so large, so comprehensive, that we can apply those findings to the entire population of people. For example, a study in adults may not necessarily apply to children, and vice versa. A study in immunocompetent persons (those without immune deficiencies or conditions or treatments that cause their immune systems to be suppressed or impaired) may not be applicable to immunocompromised patients. We gain confidence in the results of studies when those studies are reproduced by other scientists coming to the same or similar results, when the studies are subjected to rigorous peer review, and when we see the results and conclusions hold up over time as we continue to gain more experience with more patients with those conditions over time.

High quality science has always been subject to external peer review by experts in the field. Peer review seeks to determine whether potential biases that could have influenced the data or produced data that were not as generally applicable as the investigators may have asserted were accounted for or called out as limitations to the results of the study. [An example of bias could be a study to identify the effectiveness of air purifiers in the workplace in reducing the transmission of influenza conducted in the winter of 2020/2021 in comparison to transmission rates in prior years, but upon closer look, the study did not take into consideration that during that study time period, many workers were working remotely, which itself would reduce the risk of exposure of those in the workplace and did not consider the confounding factors that this was a time when people were physically distancing, having fewer large group meetings, etc.)  Peer review determines whether the design of the study was sufficient to answer the question being asked and whether limitations to the applicability of the results are identified and pointed out. Peer review also looks to determine whether a study is sufficiently powered (e.g., a sufficient number of study participants) to give confidence that the results are applicable to a broader population, whether the conclusions drawn were based upon data that were statistically significant to support those conclusions.

I write all this because I will continue to fight disinformation for as long as I can and as best I can, but realize that the rate of new disinformation and volume of disinformation is increasing dramatically, and disinformation groups have learned how to coordinate messages and social media activity so that they reinforce and further amplify disinformation. And, unfortunately, some algorithms may favor and disseminate that disinformation much more and wider than the post that tries to point out the errors and misinformation. Further, it takes me longer to explain why the information is wrong or misleading than it does for them to put it out there. The point being that I will continue to provide good information and explain why particular disinformation is wrong, but I cannot stay ahead of it, and frankly can’t even keep up with it, therefore, I need to teach you how to spot it and how to evaluate it for yourselves.

I do this because ever since I began my practice of medicine, my belief, philosophy, and ethics have been that I should present my patients with the facts as best as I know them, in an understandable way, with an explanation of the treatment options in the setting of a clear explanation of my best estimation of the risks of a particular treatment or not taking the treatment and the likely consequences of either approach so that my patients can make an informed decision as to what is best for them, as opposed to presenting the information in such a way as to manipulate them into making the decision that would cause them to select the option that I prefer or that would benefit me personally. What irritates me about the physicians who are spreading disinformation (that is, those relatively few, but outspoken, physicians who are repeatedly spreading information that they know or should know is false and doing so out of ideology or personal gain or both) is that they are using their credentials in an effort to manipulate people into making a decision aligned with that physician’s ideology or in a way as to promote that physician’s personal interests. I worked hard to become a physician, I consider it an honor and a privilege, and the thought that I would ever abuse that position of trust is abhorrent to me.

So, here are my tips as to how to spot these disinformation purveyors. In my experience, they tend to:

  1. Never admit that they have been wrong or mistaken about anything they stated or projected during the pandemic. I have been surprised and mistaken more than once, but I have also admitted publicly that I was mistaken and corrected myself. It is unreasonable to assume that any expert could be right about everything as a novel virus with which we have no experience is spreading and evolving over many years.
  2. They tend to make absolute statements. For example, a number of the physicians spreading disinformation claimed boldly that every patient they treated with such and such avoided severe illness and death. There is no medical condition that I can think of off the top of my head for which we have a treatment or preventive that is 100 percent effective. That is because an elderly patient is different than a young, healthy child; an immunocompetent patient is very different than an immunocompromised patient; and sometimes, women respond differently than men.
  3. Along the same lines, I cannot think of a time when one of these prominent purveyors of disinformation expressed doubt or that there were things we just don’t know yet.
  4. If you listen to them long enough or read what they write long enough, you tend to see common phrases being used that are not used by legitimate scientists. For example, early on it was very common to see these physicians using phrases like “crimes against humanity,” “violations of the Nuremberg Code” (which isn’t even applicable to the situation), and others, but also, you not infrequently see symbols or signs that are affiliated with certain political or religious groups. Legitimate scientists tend to avoid politics and religion like the plague.
  5. It takes time for the system to catch up to these doctors, but you also tend to see some of these physicians being disciplined by their state boards or losing their board certification by the national accrediting board.
  6. As I mentioned above, they also tend to misrepresent studies they refer to, misinterpret the data, or alter it. You will also rarely hear or see them state that a study that they offer for support of their position has any limitations.
  7. You can also frequently find fact checks by reputable organizations that help point out the flaws in the disinformation being circulated, and some of the better ones have nationally renown experts or even the authors of the study that is being misinterpreted interviewed and included in the fact check.

I am now working on a blog post in which we will go through line-by-line some of the disinformation being perpetuated by our HHS Secretary and our NIH director (and others) regarding the mRNA vaccines so that you can see for yourself how I analyze statements being made as to their veracity, using common sense, critical thinking, and simple data so that you don’t have to be an expert to spot it.

A (fairly) Comprehensive Review of What We Know, What We Think We Know and What You Should Consider about COVID-19.

A (fairly) Comprehensive Review of What We Know, What We Think We Know and What You Should Consider about COVID-19.

My intention here is to provide you with information. With this information, you can make your own decisions about your health care. Any recommendations that I make are just that – you can choose whether to take them or not. I am also going to refute some of the disinformation out there, but much of that will occur in the next part of this blog series.

  1. Transmission

COVID-19 is caused by infection with the SARS-CoV-2 virus, a novel coronavirus that was first recognized in late 2019 and sequenced in January of 2020 (or at least that is when the sequence was shared across the world). Infection occurs as a result of airborne transmission, that is to say that the virus is expelled through the nose and throat of an infected person in respiratory droplets (meaning droplets of saliva, mucus and other secretions containing the virus within them, which can then infect persons in proximity to the infected person as the infected person breathes, but the infected person produces more droplets when he or she talks and these droplets can be propelled even further when the person coughs, sneezes, sings or yells) and in aerosols (meaning much smaller particles that are light enough to be carried in airstreams and therefore can infect persons who are further away from the infected person such that respiratory droplets would have already landed on something or fallen to the ground and not be a threat to them, but the virus can still expose them to infection as they breathe in air in a room, plane, or building with the same ventilation (air inflow and outflow) supply, in which these aerosols containing virus are suspended until such time as the air is exchanged, filtered or treated. How long the virus remains viable (infectious) and suspended in air depends on a complex interplay of factors such as temperature, humidity, UV light exposure, the rate of air changes provided by the ventilation system, whether the air is recirculated or exhausted, and whether the ventilation system is equipped with MERV or HEPA filters.

[Note: Here is an easy way to understand the difference between respiratory droplets and aerosols. Stand in front of a handheld mirror held out in front of your mouth 4 – 6 inches or lean over the counter in front of your bathroom mirror. Now, sing a song or recite the pledge of allegiance rapidly. You will see little droplets accumulate on the surface of the mirror. If you have watched someone give a speech while viewing them from the side, you may have seen these droplets coming out of their mouth. In fact, every kid has noticed this phenomenon leading to the profound admonition of “Say it; don’t spray it.” These are respiratory droplets. Now, grab a can of hair spray or deodorant and spray it out into the room. You will see a fine mist of particles that ride in the air and eventually dissipate. That is similar to a respiratory aerosol, although respiratory aerosols include particles that are too small for you to see.]

We have ways through collecting epidemiological data and applying mathematical models to estimate how contagious a virus is when it first begins to spread and before the population acquires partial immunity through infection or vaccination. The index we use is called the basic reproductive number (R0). The most contagious virus we know of that infects humans is the measles virus with a R0 of 12 – 18, meaning that when everyone is considered susceptible to infection, one case of measles would be expected to infect 12 – 18 other people. The R0 for SARS-CoV-2 is generally thought to be between 2 and three, which would be consistent with the basic reproduction number for SARS-CoV-1, which emerged in 2003.[1] Readers may remember the outbreak of COVID-19 that occurred on the Diamond Princess cruise ship in early February of 2020. This was the first big outbreak outside of China and certainly caused me to begin preparing for the spread of this new disease in the U.S., as I realized it was only a matter of time, and probably not too much time. I like the estimate of R0 from a study of the outbreak on this ship because it was a confined setting with heightened awareness by an on-ship medical team. The researchers estimated R0 to be 2.28, consistent with many other later studies and estimates. Thus, we might expect a person infected with SARS-CoV-2 to infect 2 – 3 other persons on average, at least at the beginning of the pandemic.

However, we also soon realized that there were situations where a so-called superspreader event could occur in which one infected person could infect far greater numbers of people than the 2 or 3 that would be expected. We do know that it is the fact that SARS-CoV-2 is transmitted through aerosols, as opposed to only respiratory droplets, that enables superspreading events, but we think that it is characteristics of the infected person as opposed to the virus itself that predisposes to superspreading events.

The first time I realized that superspreading was possible with this novel virus was when I heard about an outbreak of COVID-19 following a choir practice in Mount Vernon, Washington in early March[2]. The practice lasted 2.5 hours and was attended by 61 people. With heightened awareness of the threat of this new infection, choir members had agreed not to shake hands or hug and tried to spread out in the room. Unfortunately, one of those 61 persons was symptomatic, however, chose to attend the event anyway. As a consequence, (recall as I stated above that singing will project respiratory droplets further and increase aerosol generation) 32 of the 61 attendees subsequently developed confirmed (tested + for the virus) and 20 additional attendees were considered probable (recall that testing was very limited at this point in the outbreak and generally required sending sample for testing to the CDC in Atlanta) secondary COVID-19 cases occurred. That is an astonishing attack rate of 53.3% (if you only include confirmed cases) to 86.7% (if you include all cases). Sadly. three patients were hospitalized and two of them died.

So, how could one sick person infect 52 people as opposed to the average of 2-3? No doubt the fact that they were in the same room for so long (2.5 hours), with presumably everyone sharing the same air from a common ventilation system and engaged in an event (singing) contributed, but the very high attack rate (percentage of those exposed who actually became ill) remained striking to me. A study published the following year may suggest the answer or part of the answer[3]. The investigators studied exhaled aerosols and noted that some individuals have a propensity to exhale many more aerosols (three orders of magnitude) than is average. An increase in number of aerosols would also mean more virus introduced into airstreams. As I previously mentioned, the virus is accompanied in droplets and aerosols by secretions including mucus. These investigators showed that the resistance of the mucus to breaking-up (which would in turn impair the viability of the virus as the mucus protects the virus from the temperature, humidity and UV light in the room) varies significantly among individuals and was more resistant with advancing degrees of infection and higher BMI-years (the product of multiplying body mass index by age in years). In other words, by the time someone is symptomatic from COVID-19 and the amount of virus in their nose, throat and lungs may be peaking, they can transmit more virus in their respiratory droplets and aerosols. Further, the combination of increase in age and BMI may result in greater resistance to breakdown of the mucus in which the virus is carried, which in turn may keep the virus viable for a longer period of time increasing the risk of infection of others who are exposed for a longer period of time.

  1. Incubation period

The incubation period is the interval between being exposed and infected until the development of symptomatic illness. The average incubation period in adults is 4 – 5 days (range 2 – 14 days), and 97.5% of people with symptomatic infection develop symptoms within 11.5 days. Most of this data is fairly dated, and I am not aware of more recent data with more recent variants in the setting of more extensive partial immunity related to prior infection and vaccination to know whether there has been any change to these numbers. I suspect that there is now a bit more variability in the data that might be influenced by your infection and vaccination history. Also, recall that early on in the pandemic, data suggested that around 40% of infections might be asymptomatic. I have not seen more recent data to know if that number has changed. Studies early on in the pandemic revealed that asymptomatic persons were no less likely to infect others, and in fact might pose more risk because they would not self-isolate as some of those who were symptomatic might. Furthermore, some people categorized as having asymptomatic infections might really have been pauci-symptomatic (meaning few and usually milder symptoms) rather than asymptomatic, as it was common for people with very mild COVID to ascribe their symptoms to a cold or allergies or simply overdoing things at work, especially when they were less likely to seek testing or test themselves.

The incubation period for children determined during Omicron was a bit shorter with a mean of 3 – 4 days.

  1. Case Fatality Rate

The case fatality rate (CFR) is the death rate among cases of a disease, in this case COVID-19, determined by dividing the number of deaths caused by the disease divided by the number of confirmed (test positive/diagnosed) cases[4]. With a novel virus (one we had not confronted before and therefore had not yet developed an understanding of its pathophysiology, nor did we have proven treatments), one expects the CFR to come down over time as we learn more about how to treat the infection and its complications, and that is what happened with SARS-CoV-2. In the first two months of the spread of this infection in the U.S., the CFR was 5.4% (that CFR would be higher in countries that don’t have the same health care infrastructure and advanced medical services). With our understanding of how to manage these patients better and the availability of proven therapeutics (steroids, monoclonal antibodies, antiviral agents, etc.), the CFR came down to 2.1% worldwide and to 1.6% in the U.S.[5]

  1. Current Epidemiology

While there are frequent comments made such as “the pandemic is over” or “we are now past COVID,” and while there can be no denying that at a high level, we certainly are in a better place relative to the social disruption and overwhelming of hospital capacity that we saw at the first two years of the pandemic, COVID-19 continues to impact Americans’ health. The CDC has issued preliminary estimates that the burden of COVID-19 in the U.S. from October 1, 2024 – August 2, 2025 was:

  1. 11.3 – 17.6 million COVID-19 illnesses;
  2. 2.7 – 4.2 million COVID-19 outpatient visits;
  3. 310,000 – 470,000 hospitalizations for COVID-19; and
  4. 36,000 – 54,000 deaths.[6]

The SARS-CoV-2 virus continues to mutate, and when these mutations (and/or recombinations in which two SARS-CoV-2 variants exchange parts of their genetic material) are significant enough to affect the virus’ biological characteristics (e.g., transmissibility, virulence and/or immune escape), that specific altered form of the virus may get the designation of being a “variant” by the World Health Organization. We speak of viral fitness in reference to those changes that enhance the ability of the virus to spread to more people, who in turn can spread the virus to more people. That form of the virus is more “fit.” We noted the first such increased fitness mutation in 2020 (D614G) that increased transmissibility (and thereby fitness) by increasing viral replication and thereby increasing viral loads (the amount of virus) in the oral and nasal passages, which in turn would result in infected persons expelling more virus in their respiratory droplets and aerosols, which in turn infected greater numbers of people[7]. There was and remains no evidence that this change resulted in immune evasion (the ability of the virus to evade the body’s immune response generated by past infection or prior vaccination).

We then saw a number of new variants (e.g., Alpha (B.1.1.7) and Delta (B.1.617.2)) over the course of early to mid-2021 that primarily seemed driven by increases in transmissibility, although Delta did demonstrate some degree of immune evasiveness evidenced by decreased neutralizing activity by convalescent sera (the part of the blood that contains antibodies, in this case, antibodies following prior infection with pre-Delta variants). We refer to these gradual changes in the properties of the virus due to mutations as antigenic drift. However, we got a shock in December of 2021 with the detection of the Omicron variant that presented antigenic shift (as opposed to drift) with the presence of 26 unique mutations in addition to ones accumulated along the way such that Omicron had 50 mutations relative to the wild-type virus (the original circulating form of virus)[8]. Soon hospitals became overwhelmed again with patients with severe COVID-19. Evolutionary biologists suspect that Omicron resulted from a long-term, ongoing infection in an immunocompromised patient that allowed the virus to evolve in that patient many more steps that would occur in a immunocompetent patient, such that by the time the immunosuppressed patient infected someone else, the virus had undergone extensive change.

Starting with Omicron and continuing on with its progeny to today, immune escape has been an increasing focus compared to pre-Omicron. The immune response to viruses, and to SARS-CoV-2 in particular, is very complicated. The immune system has numerous components and these components can play varying roles as to aspects of immunity – preventing infection, the early response to infection, containing the infection, and clearing the infection. When there is a reference to “immunity” or “immune protection” from prior infection or vaccination, that means that the person has some (not total) protection against some of these elements of infection (i.e., preventing infection, responding early to infection, containing infection and/or clearing infection) whereas someone who has never been exposed to the virus would not be expected to have any of these (for purposes of this explanation, I am ignoring the phenomenon of cross-protective immunity that may or may not result from prior infection with a different type coronavirus). However, there are few infections for which we have complete immunity (i.e., the ability to avoid infection at all) and certainly that is the case for SARS-CoV-2. “Immunity” from prior infection or vaccination remains limited in duration and limited in preventing infection altogether, such that the immunity that we do achieve is primarily enhancing our early response to infection, containing the infection and clearing the infection, which translates into a lower risk for severe disease or death and a reduced risk for long-term complications of COVID-19, such as Long COVID. (More on this below).

An immunological explanation has been proposed and demonstrated (the absence of inducing long-lived plasma cells in the bone marrow) as to why our immune responses to SARS-CoV-2 infection and vaccination are not more durable, but the continued evolution of the virus becoming more and more divergent from the original strain through the accumulation of mutations eventually resulting in Omicron and then the appearance of recombinations (swapping of gene segments between two different variants infecting the same person (likely immunocompromised individuals) leading to the XBB lineage in late 2023 and into 2024, and now further mutations as well as recombinations of variants that were themselves recombinants certainly has contributed to the need for booster vaccinations and changes in the formulation of the vaccines to better match more current lineages of the virus.

In the winter of 2023-2024, the long run of XBB.1.5 viruses and their progeny were completely replaced by JN.1-like viruses that persist to today. The SARS-CoV-2 viruses that have predominated since January 2025 are all descendants of JN.1, which accounts for the recommendation for this fall’s COVID vaccine to either provide the code for the JN.1 spike protein (this is the approach Novavax has taken) or to provide the code for KP.2, a more recent descendant of JN.1 (this is the approach Pfizer and Moderna are taking). There are arguments pro and con each approach. Basically, I think of the evolutionary tree of SARS-CoV-2 much as I think of a genealogical or family tree. In what I am sure will be an appalling oversimplification to evolutionary biologists, I think about it this way:

Let’s think about JN.1 as grandpa. JN.1 has several children, and each of those children have children (the grandchildren of JN.1). JN.1’s children are all past the point of having children and now the grandchildren are beginning to have their children (JN.1’s great grandkids). JN.1 has learned that there will be an addition to the family, but unfortunately, he has bad hearing and perhaps a poor memory, and he can’t remember which grandchild is due to have the new child. Now keep in mind, while JN.1 has been a source of genetic material for each child, and in turn, each grandchild, each child married someone unrelated to JN.1, and now the grandchild who is expecting has also married someone unrelated to JN.1. In fact, the children of JN.1’s different children (JN.1’s grandchildren) will have genetic diversity because their parents married different outsiders. So, the question becomes, will this new addition to the family have more in common genetically-speaking with great grandpa JN.1, or with their parent (KP.2) if it happens that the new expectant parent is KP.2 or alternatively, their aunt or uncle that is genetically distinct from KP.2 if the new arrival is from KP.2’s brother or sister?

If the next new significant variant (offspring) is a direct descendant of KP.2, then I think the bet of Pfizer or Moderna is a good one. If instead, it is a descendant of a sibling or cousin (so-to-speak) of KP.2, then it could be that Novavax’s bet is the best one. And, of course, because they are both closely related, it may be that it is a toss-up and really doesn’t matter which vaccine we use. We don’t know and can’t know the answer yet, but time will tell. Personally, I suspect that it won’t matter since we already have some new variants and they, as well as JN.1 and KP.2 pseudoviruses seem to be relatively well neutralized by sera  from participants who were vaccinated with the 2024-2025 COVID-19 vaccine, which was based on the JN.1 spike protein.

  • What about herd immunity?

Many suggested in 2020, dangerously so, in my opinion, including two current Trump appointees of U.S. public health agencies, that achieving herd immunity through natural infection would be a desirable way to bring the pandemic to a rapid end. In fact, the current Director of the FDA infamously and very publicly predicted that the U.S. would achieve herd immunity by April of 2021, an absolutely ridiculous assertion to those of us who were watching the pandemic play out. Herd immunity did not occur.

Herd immunity is the level of immunity to infection by a contagious organism (whether acquired through natural infection of vaccination) that results in such inefficient transmission of that infectious agent that the infection fails to spread to others in the population who remain susceptible (e.g., infants too young to be vaccinated or adults who are immunocompromised)[9].

There were a number of problems with the suggestion that we could achieve herd immunity against the SARS-CoV-2 virus. First, in the modern era of vaccines, the proponents of this idea were unable to offer an example of any other viral disease for which herd immunity had been achieved through natural infection, nor a plausible explanation as to why we should believe that SARS-CoV-2 would be different.

Second, herd immunity requires as its foundational elements durable immunity against infection (which as I stated above has not been achieved by either natural infection or vaccination in the case of SARS-CoV-2) and a sufficient percent of the population with such immune protection. Without both of these conditions being fulfilled, there was no reasonable basis to assume that the U.S. could achieve herd immunity. There are many evidences in the epidemiological data that demonstrate convincingly that we still have not achieved herd immunity – the continued waves of U.S. infections, the frequency of hospital admissions of infants and young children and older adults, and the reinfection rates. A convincing piece of evidence that demonstrates that immunity from infection is not durable is reinfection rate within a relatively narrow window of time. We have that data from the state of New York, where researchers monitored infections from January 2021 in which there were over 6 million cumulative first-time infections to August of 2023, during which period there were over 660,000 cumulative reinfections (a reinfection is a confirmed case of COVID-19 (positive test at least 90 days following a prior confirmed case of COVID-19). The reinfection rate was 9.8%[10].

Third, it was irresponsible. At the time natural infection was being advocated to achieve herd immunity, we did not fully understand the illness, nor had we identified the risks of infection with respect to long-term sequalae. As proposed, the proponents of this theory advocated for children and young adults to go about their normal lives and get infected to hasten the achievement of herd immunity. However, even by mid-to-late 2020, we were detecting the development in some persons of the condition that would later be referred to as Long COVID or PASC (post-acute sequelae of SARS-CoV-2 infection). Thus, infection in young people was not always inconsequential.

Finally, it was further irresponsible to promote this philosophy in mid-to-late 2020 when by this time, phase III clinical trials were already underway with promising COVID-19 vaccine candidates. Given the risks of infection, both known and unknown at that time, it would have been far more responsible, though still similarly misguided, to advocate for the theory once vaccines were widely available primarily by encouraging wide-spread adoption of the vaccine. As it is, no country has achieved herd immunity, and there is no reasonable basis for assuming it will be possible in the future.

  • Clinical course

There can be significant variation in how COVID-19 presents. As already mentioned, some people are asymptomatic and don’t present with symptoms. Some of those who are asymptomatic, may actually be presymptomatic, meaning they may have tested because a friend or family member with whom they had contact became ill and so they tested and were positive, yet without symptoms, making them “asymptomatic.” However, a certain number of these folks have simply not yet developed symptoms, and therefore are actually “presymptomatic,” with symptoms to follow in the next day or couple of days.

For those that are or become symptomatic, they may have one or more symptoms in any combination: fever, cough, shortness of breath, fatigue, decreased exercise tolerance, headache, sore throat, muscle aches, nasal congestion or runny nose, loss of smell (anosmia), loss of taste (ageusia), nausea, vomiting, and diarrhea. [Note of all these symptoms, shortness of breath should prompt immediate medical evaluation and attention. In addition, pregnant women and immunocompromised patients should contact their physician if testing positive and not wait for symptoms to occur.]

The acute course of COVID-19 is biphasic. Generally, the first week of illness is mild (does not require outpatient or inpatient medical care and can be managed at home with self-care). However, for those over age 50 and those with underlying chronic medical conditions that increase the risk for progression to severe disease (see below), this is the time at which antiviral therapy (see below) should be strongly considered, both to prevent progression to severe disease, but also to diminish the changes for the development of Long COVID. [Note: a common situation I deal with is someone in this group of at-risk patients who tests positive and contacts me for advice. I explain the risks and advise them to contact their physician or health care provider to consider beginning antiviral therapy ASAP – in that first week; the sooner, the better. However, some patients report back to me that their health care provider told them they were not sick enough for antivirals. That is a mistake and these patients are precisely the group who should take antivirals – ideally after testing positive, but before symptoms develop, but if symptoms have developed, as soon as possible, but within 5 days of the development of symptoms[11].

The purpose of COVID-19 vaccination prior to becoming infected and the purpose of antivirals soon after testing positive is to end the illness at this first phase/first week of illness and prevent progression to the second phase of illness – severe disease (severe disease means hospitalization has become necessary, most often due to low oxygen levels (hypoxia) related to lung inflammation and infection; ICU care is necessary for even more severe illness; or death from COVID-19 occurs). “Progression to severe disease, if it occurs, usually occurs 7 to 10 days after symptoms appear. It is caused by the virus directly damaging lung cells while pro-inflammatory cytokines (these are chemical messengers released by immune cells) cause the lungs to fill with immune cells and fluid.”[12] We now know that SARS-CoV-2 can also infect and disrupt the endothelial cells lining small blood vessels throughout the body, including in the lungs, which can further contribute to lung dysfunction and poor oxygenation of blood. Patients with severe COVID-19 may have disease manifestations not solely limited to the lungs, but experience high rates of kidney injury and may be at increased risk for blood clots, including more widespread thromboembolic (blood clots that develop in a blood vessel and then break off and travel in the blood circulation to land somewhere else other than the origin of the clot to cause tissue or organ damage) events than the most common events associated with critical illness and immobility (pulmonary emboli – blood clots that travel to the lungs). Patients with severe disease may develop myocarditis, myocardial infarction (heart attack), stroke or other neurological manifestations, renal insufficiency (poor kidney function), and multi-organ failure, as well as a range of other complications.

There are a host of complications that can occur following this acute course of illness, and some of those will be discussed below.

  • Risk factors for severe disease

Can we predict who will go on to develop the second phase of COVID-19 acute illness – severe disease? We can for most adults, but we are much more limited in children. Let’s take adults first:

  1. For adults, one of the strongest correlations with developing severe COVID-19 is advancing age. COVID-19 associated-hospitalizations increase with age and among all age groups are highest among those 75 years and older.
  2. Although deaths from COVID-19 can occur at any age, the distribution of COVID-19 deaths by age increases with each decade of life. The biggest jump in the distribution of deaths occurs after the fifth decade of life (ages 40 – 49) with those ages 40 – 49 accounting for 3.87% of all COVDI-19-related deaths (from January 1, 2020 to June 30, 2025) and those in the age range of 50 – 64 accounting for 17.07% of the COVID-19-related deaths. The percentage of COVID-19-related deaths by age in older age groups is 22.05 for those ages 65 – 74 and 54.55% for those ages 75 and above.[13]
  3. Another strong correlation to the development of severe disease can be drawn to being unvaccinated. (I’ll show some of the data on this in my next part of this blog series). Not staying up with booster/updated vaccines also increases the risk in older adults for developing severe COVID-19 and Long COVID.
  4. We also know that certain underlying health conditions can increase the risk for the person with that condition developing severe disease irrespective of age, although increasing age may further increase that risk. These are the underlying health conditions for which the evidence is the strongest[14]:
    1. Asthma
    1. Cancer, especially hematologic malignancies (cancers of the blood cells, e.g., leukemia)
    1. Cerebrovascular disease (e.g., strokes)
    1. Chronic kidney disease, especially those receiving dialysis
    1. Chronic lung diseases – specifically bronchiectasis, chronic obstructive pulmonary disease, interstitial lung disease, pulmonary embolism, and/or pulmonary hypertension.
    1. Chronic liver diseases – specifically cirrhosis, non-alcoholic fatty liver disease, alcoholic liver disease, and autoimmune hepatitis
    1. Cystic fibrosis
    1. Diabetes mellitus type 1
    1. Diabetes mellitus type 2
    1. A number of disabilities including Down syndrome (see citation above and link for full list)
    1. Certain heart conditions such as heart failure, coronary artery disease and cardiomyopathies.
    1. HIV infection
    1. Certain mental health conditions – specifically mood disorders (including depression) and schizophrenia spectrum disorders
    1. Dementia
    1. Parkinson’s Disease
    1. Obesity
    1. Physical inactivity
    1. Pregnancy or recent pregnancy. (I have highlighted this to bring your attention to it for our discussion that follows below and in the next part of this blog series about COVID-19 vaccination. In the CDC’s review of pregnant women admitted to the hospital for COVID-19 between April 2024 and March 2025, 92% had no record of COVID-19 vaccination since July 1, 2023 and 50% of the women had no underlying medical condition.)
    1. Primary immunodeficiencies (these are inherited or acquired disorders of the immune system itself as opposed to a medication or other medical condition that weakens the functioning of the immune system)
    1. Smoking (whether current of former)
    1. Solid organ or blood stem cell transplantation
    1. Tuberculosis
    1. Treatment with steroids or other medications that impair the functioning of the immune system

Now let’s look at children:

  1. Among all children and adolescents, rates of COVID-19-associated hospitalizations are highest among infants and children under the age of 2. (In fact, infants less than 6 months of age have slightly higher rates of COVID-19-associated hospitalizations than adults in the 65 – 74-year age range.
  2. As for adults, vaccination status is inversely correlated with risk for severe disease and hospitalization. 89% of children ages 6 months to 17 years admitted to the hospital for COVID-19 have no record of recent COVID-19 vaccination.
  3. Unlike adults, for children over age 2 years with severe COVID-19 and admitted to the ICU, 53% had no underlying medical conditions. (CDC ACIP briefing June 2025)
  4. One study[15] has reviewed pediatric hospitalizations between October 1, 2022 and April 30, 2024 and found that among children aged 6 to 23 months, severe disease was associated with underlying chronic lung and cardiovascular disease, and among children aged 2 years and older, severity was associated with chronic lung disease, diabetes, and neurologic disorders. However, even during this more limited period of time and looking more broadly at all COVID-19-related hospitalizations (as opposed to only those admitted to the ICU), these investigators could only identify an associated underlying medical condition in 58.9% of cases.
  • Long-term complications of COVID-19. (The following list is not exhaustive)
    • Beginning 30 days after apparent recovery from COVID-19, individuals are at increased risk for cardiovascular events for at least 1 year, including cerebrovascular events (including stroke), arrhythmias (disturbances of heart rhythm), ischemic heart disease (including heart attacks), pericarditis, myocarditis, heart failure and thromboembolic disease (blood clots and pulmonary embolism). These risks were elevated even in those who experienced mild infection, but the risks increased in correlation with the severity of the COVID-19 illness[16].
    • New Onset Diabetes after COVID-19 (NODAC)[17]
    • Long COVID (PASC – Post Acute Sequelae of COVID-19)

According to the CDC, Long COVID is a chronic condition that occurs after SARS-CoV-2 infection and is present for at least 3 months. Long COVID includes a wide range of symptoms or conditions that may improve, worsen, or be ongoing.[18] Most people with Long COVID experience symptoms days after first learning they had COVID-19, but some people who later develop Long COVID do not know when they were infected. Each time a person is infected with SARS-CoV-2, they have a risk of developing Long COVID, and there is some evidence that the risk may be cumulative. The symptoms and conditions of Long COVID can range from mild to severe, may require comprehensive care, and can even result in a disability. Some patients with Long COVID experience symptoms consistent with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) or another condition called POTS (postural orthostatic tachycardia syndrome). Certain populations appear to be at higher risk for the development of Long COVID, though Long COVID can occur in anyone and now has been identified as much more common than previously thought in children, including very young children:

  • Those with multiple COVID-19 reinfections
  • Women, especially those in the 35 – 49 age range
  • Hispanic and Latino people
  • People who have experienced more severe COVID-19 illness, especially those who were hospitalized or needed intensive care
  • People with underlying health conditions and adults who are 65 or older, especially those not treated with antivirals and/or metformin early in the course of their infection.
  • People who did not get a COVID-19 vaccine and those who have not kept up with boosters and updated COVID-19 vaccines.
  1. Vaccine Effectiveness

There is an overwhelming amount of misinformation and disinformation about the COVID-19 vaccines. I can’t cover it all here, but I am going to hit the topic of whether COVID-19 vaccines remain effective (spoiler alert – they do) and then in my follow-up blog post to this article, I will go through the information being put out by the HHS Secretary in detail and cover more aspects of the COVID-19 vaccines at that time because this is probably the longest blog post I have ever written already!

So, when we talk about “vaccine effectiveness” we have to qualify effectiveness as to what? Preventing infection? Preventing symptomatic infection? Preventing severe illness? Preventing death? The prevailing theme of organized COVID-19 vaccine disinformation is “COVID-19 vaccines don’t prevent infection; therefore, they are not effective.” That is incorrect and misleading. I will address this further in the follow-up post, but let’s look at some of the most current evidence for vaccine effectiveness in preventing urgent care/ emergency care utilization, severe illness, hospitalization and death for adults and vaccine effectiveness at preventing emergency department/urgent care encounters in children.

First of all, unlike in July of 2020, when the vaccine trials were designed to assess safety and vaccine effectiveness (VE) (and you may remember VE numbers in the mid and high 90s), VE effectiveness numbers are expected to be lower at this point in the pandemic, because almost everyone has some degree of immune protection related to prior infection/vaccination. Thus, we interpret VE studies now as the incremental benefit provided by COVID-19 vaccination.

CDC data reveals that in a study of children and adults from September 2023 – August 2024, the vaccine effectiveness of the 2023-2024 updated COVID-19 vaccine (added protection over whatever immune protection people already had acquired from past infections/vaccinations at 7 – 59 days post updated vaccine was:

For children 9 months to 4 years                                      53%

For children and adolescents ages 5 – 17 years           64%

For adults                                                                                 49%

And the same data for 60 – 299 days following the 2023 – 2024 updated COVID-19 vaccine was

For children 9 months to 4 years                                      23%

For children and adolescents ages 5 – 17 years           34%

For adults                                                                                 12%

What I conclude is that there was incremental benefit for persons at all ages following the updated vaccine, however, that benefit does wane, and wanes faster in adults (thus the recommendation for adults at high risk to receive a mid-year second dose (booster) of vaccine).

Interestingly, the data 7 – 179 days following the 2024 – 2025 updated vaccine was even better:

For children 9 months to 4 years                                      79%

For children and adolescents ages 5 – 17 years           57%

For adults                                                                                 34%

Now, that was VE at preventing the need for urgent care/emergency care with symptomatic COVID-19. What about the VE for preventing hospitalization in adults over the age of 65?

Here we have data from two networks of hospitals, so I will present both. This is data following the 2024-2025 updated COVID-19 vaccine:

7-59 days following vaccination                                        46%/42%

60 – 119 days following vaccination                                50%/53%

120 – 179 days following vaccination                              32%/40%

What about VE against those 65 years of age and older (not immunocompromised) from becoming critically ill?

7-59 days following vaccination                                        46%

60 – 119 days following vaccination                                45%

120 – 179 days following vaccination                              43%

Data from the other network of hospitals was broken down into more specific outcomes (all of these are for the period of 7 – 179 days following the updated vaccine):

Reduction in acute respiratory failure                                           44%

Reduction in ICU admission or death                                            56%

Reduction in invasive mechanical ventilation or death            70%

Did the 2024 – 2025 updated vaccine help protect adults against hospitalization over the age of 65 who are immunocompromised (answer: better than I had guessed)?

7-59 days following vaccination                                        25%

60 – 119 days following vaccination                                47%

120 – 179 days following vaccination                              39%

This kind of data is probably unfamiliar to you and may be confusing. So, here is the bottom line:

The data show that receiving the updated vaccine (compared to not receiving it) provided children and adults with added protection against

  • Emergency department and urgent care visits for children and adults;
    • Hospitalization for adults over age 65 whether they were immunocompromised or not;
    • Becoming critically ill for adults over age 65.
  • Outpatient treatment for Acute COVID-19
  • For persons who may be at high risk for severe disease and/or the development of Long COVID, you should discuss two options with your physician (I generally use them together) as a plan in the event you should test positive for COVID-19 due to the fact that these medications work best when started early, and most importantly before you become ill enough that hospitalization needs to be considered. The notion that someone must already be sick to start antivirals is completely backwards thinking.

The second option to be considered besides the antiviral is metformin. A study showed that when started early, especially within the first three days of COVID-19 symptoms, the course of metformin (a medication most often used to treat diabetes) could reduce the risk of long-term symptoms and Long COVID by as much as 40%, a result that is better than many of the studies on the use of antivirals.[19]

The first-line antiviral (Paxlovid) has many potential drug interactions, and for someone with significant underlying medical conditions for which stopping or decreasing those medications while taking the antiviral may be expected to worsen their underlying health condition, this could be a good option instead. This medication is also very expensive now that the government has stopped purchasing it and distributing it to Americans, so if that is an obstacle for the patient, metformin is relatively very inexpensive.

However, because the mechanisms of action are different and drug interactions are minimal, I often recommend the use of both medications, especially for those at very high risk and whose doctors determine that the patient has no contraindication for the antiviral.

A note of caution. I have noted on occasion that a provider seeing a patient with the first phase of illness (mild-to-moderate) without progression to severe disease and low blood oxygen levels will start the patient on steroids. Except for an uncommon underlying medical condition, this is a dangerous treatment as the steroids will impair the body’s immune response to the infection and can increase the potential for progression to severe disease and worsen clinical outcomes. Rather, the place for steroids in the treatment of COVID-19 is in that second phase of illness once the patient has developed low blood oxygen levels and is requiring supplemental oxygen, as this phase is generally associated with an over-aggressive immune response and immunopathology for which the steroids can be beneficial, but even in this situation, we give a brief course of steroid treatment to improve oxygenation and decrease the overactive immune response, but stop it after that to minimize the risk of the patient now developing a superimposed infection. [To my horror, this occurred early on in the pandemic in India where their protocols called for extremely high doses of steroids for a protracted period of time and then we received reports of patients developing an extremely aggressive fungal-type of infection that itself threatened the patient’s life and was extremely difficult to treat.]

  • For moderately to severely immunocompromised patients that are 12 years old and older, we have an option (although costly and with some degree of inconvenience of administration) to prevent illness (so-called pre-exposure prophylaxis) – pemivibart – a long-acting monoclonal antibody. It is administered intravenously every 3 months, and it must be supervised by medical professionals, because there is a risk (0.6%) of anaphylaxis – a severe, potentially life-threatening allergic-type reaction. There also needs to be coordination between receipt of a COVID vaccination and infusion of pemivibart so that the latter is not infused for at least 2 weeks following the immunization.

[1] R0 and Re of COVID-19: Can We Predict When the Pandemic Outbreak will be Contained?https://pmc.ncbi.nlm.nih.gov/articles/PMC7751056/.

[2] High SARS-CoV-2 Attack Rate Following Exposure at a Choir Practice — Skagit County, Washington, March 2020. CDC MMWR May 15, 2020 / 69(19);606–610.

https://www.cdc.gov/mmwr/volumes/69/wr/mm6919e6.htm

[3] Exhaled aerosol increases with COVID-19 infection, age, and obesity. Proceedings of the National Academy of Sciencesof the United States of America Feb. 9, 2021. https://www.pnas.org/doi/10.1073/pnas.2021830118

[4] Preparing for the Next Global Outbreak: A Guide to Planning from the Schoolhouse to the White House, Pate D. and Epperly T., Johns Hopkins University Press, 2023, p. 105.

[5] Essential Human Virology, second edition, Louten J. Academic Press, 2023, p. 284.

[6] https://www.cdc.gov/covid/php/surveillance/burden-estimates.html.

[7]Spike mutation D614G alters SARS-CoV-2 fitness. Nature 592, 116–121 (2021).

https://www.nature.com/articles/s41586-020-2895-3.

[8] A Detailed Overview of SARS-CoV-2 Omicron: Its Sub-Variants, Mutations and Pathophysiology, Clinical Characteristics, Immunological Landscape, Immune Escape, and Therapies. Viruses. 2023 Jan 5;15(1):167.

https://pmc.ncbi.nlm.nih.gov/articles/PMC9866114/.

[9][9] Preparing for the Next Global Outbreak: A Guide to Planning from the Schoolhouse to the White House, Pate D. and Epperly T., Johns Hopkins University Press, 2023, pp. 220 – 228.

[10][10] https://coronavirus.health.ny.gov/covid-19-reinfection-data.

[11] Timing of Antiviral Treatment Initiation is Critical to Reduce SARS‐CoV‐2 Viral Load https://pmc.ncbi.nlm.nih.gov/articles/PMC7323384/.

[12] Essential Human Virology, second edition, Louten, J. Academic Press 2023, p. 282.

[13] https://covid.cdc.gov/covid-data-tracker/#demographics. (accessed 8/11/25).

[14] https://www.cdc.gov/covid/hcp/clinical-care/underlying-conditions.html.

[15] Hospitalization for COVID-19 and Risk Factors for Severe Disease Among Children: 2022–2024. PEDIATRICS Volume 156, Issue 3, September 2025. https://publications.aap.org/pediatrics/article/doi/10.1542/peds.2025-072788/202525/Hospitalization-for-COVID-19-and-Risk-Factors-for?autologincheck=redirected.

[16] Long-term cardiovascular outcomes of COVID-19. Nat Med 28, 583–590 (2022). https://www.nature.com/articles/s41591-022-01689-3#citeas.

[17] New-Onset Diabetes After COVID-19. J Clin Endocrinol Metab. 2023 May 19;108(11). https://pmc.ncbi.nlm.nih.gov/articles/PMC11009784/.

[18] https://www.cdc.gov/long-covid/about/index.html.

[19] Covid-19: Metformin reduces the risk of developing long term symptoms by 40%, study finds. https://www.bmj.com/content/381/bmj.p1306.

A Note to My Readers

I’m back, and I want to thank everyone for their patience. As faithful readers of my blog know, I lost my wife – my best friend, my soulmate, and the person who kept me grounded – of nearly 45 years, suddenly and unexpectedly on May 5 due to a sudden cardiac arrest. She was 71 years old. While she had been in gradually declining health for many years, I thought we still had at least a few more years together. She had even had a thorough medical evaluation the month before, and her doctor was very impressed with the overall control of her medical problems. I am so grateful for our time together from my late college years all the way through 5 years of retirement; the fact that despite her deteriorating health, Lynette had a great quality of life filled with much happiness all the way up to the end; and that she went quickly, without suffering, and at home.

Nonetheless, I have needed this time to pause from writing my blog. I still am grieving, but the main problem with respect to writing has been a lack of motivation, a lack of ability to focus for extended periods of time, and much more difficulty in organizing my thoughts, especially around complicated matters. None of these have ever been challenges for me in the past. Fortunately, as I process my grief, as I learn to adapt to my new life, and as I receive comfort and encouragement from so many friends, family, neighbors and colleagues, I also feel that all of these impediments to writing are gradually improving; improving enough that I can return to writing.

It is important to me that if I am going to spend the time and effort to write my blog posts, that they are high quality in the mind of the readers. To me that means they have to be understandable, they have to give you new information or at least new insights or perspectives, and they need to be of value to you in terms of informing your own health care decisions or those that you provide information and advice to.

While my perhaps “writer’s block” is understandable under the circumstances, what I have not lost is a sense of urgency to get back at it. There is more disinformation than ever, still coming from social media and the usual suspects, but now also coming from some of the highest levels of our government and public health agencies, that I feel the pressing need to get facts and truth out to my readers, especially as our children and grandchildren will be soon be restarting school and in 2 – 3 months we will be experiencing the onset of respiratory virus (so-called cold and flu) season here in the U.S.

So, I am back at work and just wanted to let you know that next week I will post a comprehensive review for the lay person as to what we know, what we think we know, and what you need to consider about COVID-19, including updates and my recommendations about the COVID-19 vaccines. I will follow that with reviews and recommendations about influenza and RSV, since these are the major respiratory virus threats we will be facing for which we have vaccines.

So, thank you for your patience for the past three months and look for new blog posts to resume next week.

A Loving Tribute to My Wife

Mary Lynette Pate

November 2, 1953 – May 5, 2025

Our Love Story

I knew that I wanted to be a doctor from an early age. The problem is that anytime I went to the hospital for a visit, I would pass out. It wasn’t that I was squeamish about blood, it was that I had an overwhelming sense of empathy for my friends or family members we were visiting that would overwhelm me suddenly and intensely upon seeing them. In high school, for career day, I went to our local general hospital and we were taken to the neonatal intensive care unit. For some reason, I was the only boy in the group. When I saw a newborn with a gastroschisis (internal organs outside of the abdomen), I passed out, hitting an incubator on the way down. Unfortunately for me, none of the twenty-some girls who accompanied me on this tour day passed out, so I knew I was in for a razzing when I returned to school the next day.

My parents, of course, suggested a number of alternative careers that might suit me better. But, after consulting with a neighbor of ours who was a doctor, he told me to stick with it and one day, I would stop passing out (he turned out to be right). So, while an undergraduate student at Rice University in Houston, I went to the Texas Medical Center hospitals to see if any of them had a paying job for me during the summers that would allow me to begin a program of immersion that would hopefully result in fewer and fewer fainting spells over time. Failing that, I offered to volunteer, if they would just agree to assign me to the grossest unit in the hospital.

Memorial Hospital took me up on my offer and assigned me to the Surgical Intensive Care Unit (SICU), where the most severe surgical, trauma and burn patients were cared for. I was essentially an orderly and my duties were to assist the nurses with whatever they needed an extra pair of hands with. Sometimes, it would be bathing or lifting a patient; other times I might be holding pressure on a bleeding site or assisting with a burn scrub (my least favorite thing to do).

When accepted to Rice, it was with the condition that I live off campus since they had already run out of campus dorm living. So, I lived with my parents because I got a great deal on food and rent. One day, the SICU was particularly busy, and I was asked if there was anyway that I could stay past my assigned shift to help. I immediately agreed. I called my Mom on the unit’s phone (we didn’t have cell phones back then) and told her they needed me, I was planning to stay late, and so don’t hold dinner for me. Unbeknownst to me until she told me years later, Lynette, one of the SICU nurses, overheard my conversation and told one of the other nurses, “Whoever marries him is going to be a lucky woman.”

Back then, I played a lot of tennis. One day, I asked the head nurse, who happened to be Lynette’s roommate, whether she might like to play tennis the next weekend. She told me she couldn’t (a frequent refrain when I asked girls/women out in high school and college), but not surprising to anyone who knew her, Lynette stepped up and told me she was available that weekend. That was the start of our relationship 48 years ago. We played tennis, she let me beat her, preserving my fragile male ego, but I could already tell that there was something very special about Lynette that I had never seen or felt with prior dates or infatuations. She told me that what she first noted and appreciated about me was my thick hair and what she thought were beautiful eyelashes (I don’t think I had ever noticed my eyelashes). But, with Lynette, I can tell you that what set my heart on fire was her huge smile, made even better on those occasions that I or someone else made her laugh. (I had tried over the subsequent 48 years to convince her that I am hilarious, but she never could get herself to acknowledge that). Don’t misunderstand me- I thought Lynette was beautiful then and was always beautiful to me as we aged together, but her smile, her laugh, and her inner beauty was what set her apart from everyone else.

After that first tennis date, we continued to date, and before long, we were what we called in those days, “going steady.” I had bought a used red Volkswagen beetle convertible for $300 just before we started dating that had a lot of miles on it and a rusted out floor board in the back. I played in the Rice University MOB (Marching Owl Band) and so when we had home games, I put Lynette in the front seat with me and stood my 45 pound sousaphone in the backseat with the giant bell sticking up with the top down to drive to the games.

I continued to work in the SICU during summers, and the next year, finally achieved a paid position as the unit clerk processing doctors’ orders, requesting lab and radiology tests for patients, and ordering the supplies the unit would need. Meanwhile, knowing that I wanted to go to medical school, Lynette taught me how to read EKGs and laboratory results on the patients we had in the unit. She also began teaching me all the things that I should not do once I became a doctor. Chief among those things were: (1) don’t order weights on patients who are on a ventilator and in traction and then don’t even look at them when you make rounds; (2) don’t do a procedure and leave a mess for the nurses to clean up; and (3) don’t take out your frustrations or fatigue on the nurses. I can honestly say that I took everyone of those teachings to heart. I remember years later being at the hospital and conducting a spinal tap on a patient late at night when I was sleep deprived and very busy. I completed the procedure and began cleaning up everything, and the two nurses that were assisting me said, “that’s alright, doctor. We’ll clean this up.” I replied, “My wife will kill me if I don’t do this myself.”

While I was at Rice and while we were still dating, Lynette asked if I wanted to attend Sunday school with her. Lynette and a man co-taught a popular Sunday school class for single adults. At that point in my life, I was not interested in church, but I was interested in her, so I agreed to go. We continued to go every Sunday. At some point, the adult singles went on a ski trip with the pastor (Dick Stafford) who eventually would marry us. When I spoke with him just a few days ago following Lynette’s passing, he told me a story that I am pretty sure I never knew. He said that on that ski trip, I was off somewhere on the slopes, but he was standing with Lynette at the chair lift, and she told him, “He’s the one.” He had not anticipated this and asked, “He’s the one what?” Lynette replied, “He’s the one I am going to marry.” Dick, still unprepared for this and not connecting all the dots asked, “Who, David?” She confidently answered yes.

I suspect it was after about a year of attending Sunday school and church services with Lynette that she asked me, “Don’t you think it is about time for you to join the church?” Now, I had been raised in the Midwest in a very conservative church, and I did not have a full understanding of just what “joining the church” meant when you are talking about a Southern Baptist church. So, I immediately responded, “okay. What do I do?”

Well, that next Sunday, there was an invitation at the end of the service, so I walked down the aisle to the front of the church. They then directed us to another room where Lynette joined me. Several associate pastors began making their way through to each person who had accepted the invitation until one reached me and Lynette. We introduced ourselves and then he asked me to recount my salvation story. I really didn’t know what that was a reference to, but I answered, “Well, I believe in God and I try to be a nice person.” I think the pastor appeared a bit unprepared for that answer because there was a very long pause. Then, in typical Lynette fashion, she stepped in to intervene and said to me one sentence that would change my life and my assurance of eternal life: “You do know that the Devil believes in God, right?” That hit me like a sledge hammer.

She was right (as usual). Believing in God doesn’t make you a Christian or assure you of the promise of salvation. The problem is that I was like many today who profess to be Christians, but who never have read and studied the Bible. Lynette didn’t have to tell me the answer, she just planted that one sentence in my brain that made me realize the internal inconsistency in my thinking.

So, I began praying that God would help me understand, I began reading and studying the Bible in earnest, and I began praying that I could have the same joy that I noticed in those around me who were mature Christians. Before long, I came to several important passages from the Bible:

Matthew 7:21-23

21 “Not everyone who says to me, ‘Lord, Lord,’ will enter the kingdom of heaven, but the one who does the will of my Father who is in heaven. 22 On that day many will say to me, ‘Lord, Lord, did we not prophesy in your name, and cast out demons in your name, and do many mighty works in your name?’ 23 And then will I declare to them, ‘I never knew you; depart from me, you workers of lawlessness.’”

I realized that Lynette was exactly right. More is required than just believing there is a God. In fact, many people who tout themselves as Christians today claim a belief in God, but express hate for those who do not look like them or believe like them, ignore the needs of the poor and the vulnerable, and spend their time fighting culture wars and when they die, may find themselves receiving the same reply from Jesus on His throne as the “workers of lawlessness.”

So, then I began to understand what salvation really meant when I read the book of Romans:

Romans 3:23: “for all have sinned and fall short of the glory of God.”

First, I had to acknowledge that I was a sinner and as a consequence was not entitled to salvation.

Romans 6:23 “For the wages of sin is death, but the gift of God is eternal life in Christ Jesus our Lord.”

In fact, as a sinner, I would face eternal separation from God. To ask for God’s forgiveness and grace, I needed to admit I was a sinner, profess my sins, and repent of my sins.

I also realized that I was wrong about something else. I thought that the combination of me believing in God plus being nice and doing good things was the recipe for eternal life. However, that isn’t what the Bible teaches us. Romans 6:23 tells us that eternal life in Christ Jesus is a “gift.” It is not something we earn, because by virtue of being sinners, the same verse tells us that if we got what we deserved, it would be death.

Ephesians 2:8 “For by grace you have been saved through faith. And this is not your own doing; it is the gift of God, not a result of works, so that no one may boast.”

Ephesians also clarifies that salvation is achieved through faith and by grace. In other words, faith is required and specifically what we must have faith in is explained in Romans 10:9 below, but we only receive salvation through grace. Grace means that we are receiving something we don’t deserve. And, to make sure we understand this, the verse goes on to state explicitly that salvation is not of our own doing. Romans 3:23 above already made clear that we all have sinned and fallen short of the glory of God (i.e., salvation). Therefore, according to Romans 6:23, we all deserve death (not just physical death in this case, but worse – eternal separation from God. Salvation is not compensation, reward or something otherwise earned – none of us have earned it. It is a gift to which we are not entitled, and it is by grace that God gives us eternal life, even when we don’t deserve it. I realized that being nice and doing good things does not result in eternal life, but rather flows naturally from our faith and a true desire to follow His teachings.

So, what is the faith we need to have?

Romans 10:9  “If you declare with your mouth, “Jesus is Lord,” and believe in your heart that God raised him from the dead, you will be saved.”

In other words, we must have faith that Jesus is who the Bible says He is – the son of God, God incarnate, who died for our sins and was resurrected from the dead. If we believe it, we must profess it according to this verse. And, the reason we must believe in our heart that God raised Jesus from the dead after crucifixion is that if God could not raise His son from the dead, how can we have any assurance of eternal life following our own physical deaths. In fact, Christianity is the only religion for which there is a claim and evidence for the death and resurrection of the head of the Church.

That simple question that Lynette asked me set me on the path that ultimately led to my salvation and changed my life forever.

Lynette and I continued to date. I told her that I only planned to marry once, and thus, I wanted to make sure that she was the person that I wanted to be the mother of my children and that I would want to spend the rest of my life with. After a bit more than two years, I asked Lynette to marry me, and she accepted without reservation. I graduated from Rice University in 1979 and began medical school that summer.

We were married on September 13, 1980. My knees nearly gave out when I first saw her walking down the aisle holding her father’s arm. She was stunningly beautiful in her wedding gown and the glow of her face that I could see through her wedding veil. The Reverend Dick Stafford officiated our ceremony, but we had the special added treat that each of our brothers were ordained ministers and able to assist in the ceremony.

Given that I was in medical school, we could only take off a weekend for our honeymoon, which worked out fine since we didn’t have much money saved for the honeymoon.

My role model for the kind of physician I wanted to be was Dr. Richard Blakely, a general internist. Lynette left the ICU and worked for him as his hospital nurse. I continued my medical studies and Lynette decided to go back to school to get her BSN degree.

We eventually decided that we wanted to start our family. Lynette became pregnant and was due at the beginning of December 1982. Around six or seven months, Lynette was crossing the street between the medical office building and the hospital and began bleeding. She called me crying, fearful that we were losing our first child. I told her to get to the ER and I would meet her there. Thankfully, Lynette and the baby were fine, but they told her she had just worked her last day and would have to spend the remainder of the pregnancy in bed.

I was graduating from medical school on November 19, 1982, my birthday and two weeks before we anticipated the birth of our first child. We didn’t know if Lynette could make it to my graduation, however, she had improved so much with the bed rest that the doctors permitted it.

We were ready for our first baby with a decorated nursery and clothes for a baby boy, as the ultrasound had revealed fairly clear evidence of the baby being a boy, and I was glad because I could do all those father-son things, and had no idea what to do with a girl since I grew up with my brother, my sister being 11 years younger than me. On the other hand, my grandma kept telling us it was going to be a girl given the way the baby was lying. I explained to grandma that we had sophisticated tests now (even though the ultrasounds today are of far better quality than those we had 40 years ago), and the tests had revealed that the baby would be a boy.

Lynette had reached her due date without any indication that baby Richard, as we had planned to name him, had any intentions of coming out of the womb anytime soon. The obstetrician gave us another 10 days to see if the situation improved, but alas, it had not. Thus, induction of labor was begun. No dramatic results, so the induction was suspended overnight to begin anew the next day. Again, all day of induction, with little to show for it.

But it was worse. I had the brilliant idea that made perfect sense to me as a man, that I should go get the nurses lunch when I went to eat so that the nurses would be grateful to Lynette and in turn give her more attention and great care. I, again, thinking like a man, thought that I should get them What-a-burgers because, after all, those were my wife’s favorite hamburgers. The flaw in my thinking became exposed when I returned to the unit, dropped off the fresh What-a-burgers with the onions and distinctive mustard smell that I then discovered that a woman who is laboring and unable to eat or drink can smell and identify through the ventilation system. She quickly put two and two together and realized that I had brought her favorite hamburgers to the nurses. She was none too happy with me (which by the time of two days of induced labor, I already had the distinct impression she was planning a vasectomy for me), and in her state of starvation, had no appreciation for my intentions that seemed so clearly in her own best interests, and may have mentioned something about me being an idiot in between contractions.

Finally, after a third day of induced labor with artificially ruptured membranes, progressive doses of Pitocin, and a threat of having to undergo a C-section, the obstetrician delivered a healthy baby proclaiming, “It’s a girl!” “A girl?!?!?” I replied. And, yes, I could see that it was a girl and what the obstetrician and I thought we had seen on the ultrasound must have been the umbilical cord between her legs. I will never forget the cackle that my grandmother made when she learned of the news. She had been right all along. So, the name Richard was quickly changed to Lindsey, the nursery was redone and Lynette sewed lace on to the bottom of infant blue jean overalls that we had ready for her. Lindsey slept in a blue onesie.

I had two weeks left in the break between medical school graduation and the beginning of my residency in internal medicine. I was able to help rock, feed and diaper Lindsey. Then, I was gone for 36 hour periods of time while I took call at the hospital, and returned home with 8 hours to eat, sleep and talk to my wife before returning to the hospital to work a 12-hour day before returning to repeat the 36-hours of new admissions, patient rounds, conferences, pages, and code blues. (These were the days before there were limits on the number of hours residents could work in a row and in a week.)  But, while I was away taking care of patients, Lynette was at home taking care of Lindsey. And, Lindsey had colic every night between 11 pm and 2 am during which this little infant was capable of constant blood-curdling screaming and crying. I would walk in the door, barely able to keep my eyes open, and Lynette would hand me the baby. We would sit down to eat, talk a bit and then both try to go to bed, only to be awakened around 11 p.m. Lynette, God rest her soul, would get up first. She would try holding Lindsey, rocking her, applying a pacifier and various other techniques to get Lindsey back to sleep, almost always to no avail. Soon, both Lindsey and Lynette would be crying and pillows over my head could not obscure the distress of both. I would have to get up, go in and see what more I could possibly do to get them both to stop crying.

I tried everything I could think of. I even had another clever Dad idea. Let’s tape record her crying, then we will put headphones on her and play back the crying so that she thinks she is crying and doesn’t have the need to actually cry. (Well, you try going without sleep for nearly two days and nights and see if you come up with something better). To my disappointment, it didn’t work. Praise God, eventually, Lindsey grew out of it.

For survival of the species, God inflicts amnesia upon young parents so that the mother forgets the three days of labor she went through with the prior baby and the dad forgets all the sleepless nights (and Lynette forgot the visions of me undergoing a vasectomy while smelling What-a-burgers in the labor and delivery department). Nearly three years later, we decided to have another child. This time, the ultrasound would correctly identify that we were having another girl. The due date was projected to be in March of 1986, right after I completed my residency training in internal medicine and during the six-month period of time that I was given the privilege of serving in the prestigious position as Chief Resident in Internal Medicine for the hospital. Laurie was born in March after another three-day induction of labor that shaved only one hour off from the length of duration for Lynette’s labor with Lindsey.

I finished my Chief Residency and went into medical practice. Lynette asked the first patient I saw if he would mind paying part of his bill with a one-dollar bill. She then framed that for me. I still have it today.

There are some couples whose relationship could not withstand too much togetherness. That was not the case for Lynette and me. For a period of time, Lynette served as my office manager. It was wonderful. First, she was really good at her job. Secondly, being married to a doctor, especially back in those days when it was common for doctors to see patients all day in their office, but also have to run to the hospital to see a patient in the ER or to consult on another physician’s patient, and to take calls even once home, and occasionally have to get up from dinner, leave a social gathering or get up from bed and go to the hospital to see an emergency case. With Lynette working in the hospital, she understood the demands on my time, and understood the commitments we both had to make in order to make a medical practice successful. It also gave us brief moments throughout the day that we could see each other, smile at each other, have a quick hug, or go over a matter that just came up rather than having to wait until we were both exhausted at the end of the day.

By the time the girls were old enough to begin kindergarten, we were finally getting on our financial feet and Lynette wanted to work less and spend her time volunteering at the kids’ school. I thought it would be great for her to be actively involved in the school. She went all in. She became an invaluable asset for the school, leading the fund-raising effort to develop the school’s playground into a Spark Park – a program to expand and enhance the playground into a community park that enhanced the playground of the public school, while embracing and involving the community in the school by utilizing the grounds as a park when school was not in session. Lynette also did whatever else was needed to help out at the school – decorating rooms and hallways, buying and selling school supplies, organizing events, you name it. The principal and teachers loved Lynette. The elementary school our kids attended was a magnet school, meaning that attendance wasn’t determined solely by your geographic distance from the school, but children excelling in the areas for which the school was recognized as a magnet program were also eligible to attend.

I still remember the first day of elementary school for Lindsey. I can remember the shoes she was wearing, her backpack, and the way I fixed her hair. I had forgotten the first rule from husband school: do not show your wife that you know how to do anything that you don’t want to be assigned as your permanent job. When I would get the girls up for school, they would tell me whether they wanted a pony tail or pig tails (to this day, I still have no idea why these hair styles are named for these animals). After fixing Lindsey’s hair, she would run her hand across her hair to determine whether there were any “bumps,” which were completely unacceptable and required a revision. Being the first grandchild, not only were Lynette and I there to see her off to school, but my parents were there, as well.

It was a very different experience three years later when Laurie had her first day of elementary school. Keep in mind that schools typically have a fairly high tolerance on the first day of school for kindergarteners, realizing that this is a new experience and perhaps the first day away from home. Nevertheless, I received a call at my office from Lynette saying that we needed to come to the principal’s office. I couldn’t imagine why this would be the case. I met Lynette at the school and she explained that Laurie had called one of her fellow students a “bit…” I am quite certain I gave Lynette one of my looks as we walked into the school and down the hallway towards the principal’s office. On our walk, we ran into Mr. Lockley, the Magnet Coordinator. We both loved him. He was full of energy, vey funny and great with the kids. He knew Lynette well from her years of volunteering at the school, and asked, “What are you two doing here?” Lynette explained that Laurie had called (Lynette supplied the name of the girl) a “bit…” Mr. Lockley unhelpfully replied, “well, she is!”

On the way home, I could not help myself in asking Lynette where she thought Laurie would have picked up that word. Being a man, I never quite learned that trying to have the last word or assign fault will always backfire. Even as an attorney, when I thought I had an iron-clad case against her, even at times with a Perry Mason moment, it always seemed to end with me apologizing to her. I do think that I won one argument with her during the 48 years, I just unfortunately can’t remember what it was.

My favorite picture of the two of us was when she was pregnant with Lindsey and we were seated at a table with her to my right. She was even more beautiful with her pregnancy glow. The picture might as well have been a video as I can see it playing out with her pleading her case for something she wanted or wanted me to do, and me giving her the hand as though that might stop her incessant pleas. And, while I told her “no” many times, I turned around afterwards and did it or gave it to her anyway. She used to tell me that our two daughters had me wrapped around their little fingers, but she never acknowledged that in reality, all of the women in our household had me wrapped around their little fingers, none so more than her.

Through the years, Lynette was my confidant, a great resource for advice, and amazing mother. She served as the president of our kids’ PTA. She did countless fund-raisers for worthy causes. She wrote a song for a friend’s wedding. She and I planned, arranged for and chaperoned a group of Lindsey’s fellow students from the High School for the Performing and Visual Arts to go to Broadway to see some shows and to get a back stage tour of The Lion King and an after-performance Q&A with William H. Macy.

When Lindsey subsequently became a costume designer, there were many times, Lynette hopped on a plane at the last minute and went up to stay with Lindsey to work day and night in what she referred to as “Lindsey’s sweat shop.”

The girls went to Camp Ozark, a Christian camp in Arkansas during the summers. They offered two-week sessions, and Laurie would have stayed all five, if they would have let her. Most years that I can remember, she went for two sessions. We most often drove to camp in a suburban for the closing session. We would put down the seats in the back and lay sleeping bags down, and the girls usually slept the entire ride home.

Eventually, I started volunteering to be the camp doctor for one of the sessions. I always had a blast, and one summer I had to stitch Laurie’s knee up, but I don’t recall it slowing her down a bit.

I used to describe our marriage like that of Lucille Ball and Desi Arnez on I Love Lucy. I suspect that all wives have at one point or another done something their husbands might not have anticipated. But, at one point, we purchased a piece of property in Central Texas on a river that we could escape to on the weekends to get away from it all. Then, without telling me a thing, Lynette bought a house and had it moved onto the property. Of course, despite my protestations, I loved it, and it was just right for the property, but every day I had to be prepared for something totally unexpected.

Besides keeping me on my toes and never knowing what to expect, I continued to learn new things about Lynette even after 40 years of marriage. For her 69th birthday, her brother, sister-in-law, and Lynette and I went to Galveston for a birthday celebration. It turned out that there was a motorcycle convention in town at the same time. Everywhere we went, Lynette would go up to bikers and begin to learn all about them. She loved everyone she met and loved listening to the motorcycles going up and down the seawall in front of where we stayed. She told us she wanted to return for the next year’s event.

I soon began my plotting with brother-in-law Len and his wife Cathie. I found a company in Canada that would make a leather bike jacket with the inscription on the back – “Born to Ride. I just had to wait until I was 70.” Lynette’s birthday, November 2 is during the Dia de los Muertos, a Mexican holiday to honor the dead, and Lynette loved it, collected sugar skulls and various statutes or clothing with that style of decoration. I was able to get the company to add a sugar skull imprint below the inscription.

In the meantime, Cathie worked to find someone that we might know who drove a motorcycle and might be planning to attend that next year’s event. We wanted to surprise Lynette with the jacket and a short ride on the Seawall on a motorcycle.

We made our way to Galveston that next year to be there on her 70th birthday. The jacket made it just barely in time. However, when we arrived in Galveston, we learned that the friend of a friend of Lynette’s who was to take her on the ride was not going to be able to make it. Unfortunately, I had no Plan B. Lynette’s brother, Len, said, “follow me.” We headed to the lobby of our hotel. I could already see where this was headed. I explained to Len that I can’t very well tell the police that we asked a complete stranger to take my wife on a ride down the Seawall who then abducted her. After all, I have watched Dateline before. However, we both did decide that if someone did take her, he would likely be back soon begging us to take her back, after Lynette gave him a piece of her mind. So, we watched and waited. Len saw his target, a man with a biker vest on, staying at the same hotel we were staying at, which we surmised that not too many of America’s Most Wanted would hang out, who was at the desk to see if he could get late check-out the next morning. Then, we made our move. He was extremely nice. We explained our predicament, and he said he would be glad to fill in. It turned out that he was Timothy Paisley, the cousin of country music superstar Brad Paisley.

That next morning, we escorted Lynette out the back door of the hotel to the parking lot with the ruse that we were going out to eat. Timothy pulled up on his motorcycle, and I presented Lynette with her jacket. It fit perfectly, and she hopped (well, more like Len and I helped her climb) onto the back of the motorcycle, and she wrapped her arms tightly around this very handsome biker (not that I was jealous or anything). He drove her across the parking lot down the Seawall to the sound of the crashing waves of the ocean and back. I thought Lynette was as happy as she had ever been.

It is now a year-and-a-half later. In September we would celebrate our 45th wedding anniversary. In November it would be Lynette’s 72nd birthday. I was contemplating a return to Galveston for her birthday.

Last year for our anniversary, Lynette surprised me by getting me a used Volkswagen beetle convertible, just like the one I drove when I was dating her. Its not really a winterized car, so I kept it in our garage over the winter, and not surprisingly, the battery died. On Sunday, May 4th, it was a beautiful day, and God put on my mind that I should go ahead and replace the battery that day, which I did. The car was running. I went inside and told Lynette, “Let’s go for a ride. It’s a beautiful day.”

It was not a trivial event for Lynette to go out. She was weak to the point that I usually had to help her get up and get dressed. Her balance was not good, so I would have to hold on to her as she ambulated. A lot of times, I would suggest us going out to grab a bite to eat or run to the bookstore, or other such excuse to get us out of the house, but often Lynette thought it was more trouble than it was worth. But, this day, she didn’t protest, and she got right up and I walked her out to the car. Our grandson, Clif, hopped in the back seat, and I helped Lynette into the front passenger seat and buckled her in. We took off and I drove her to the park. Then we stopped for ice cream. On our way home, I placed my hand on her thigh and I said, “This is just like it was 48 years ago.”

We laid in bed that night and held hands and talked. When she was beginning to fall asleep, I tucked her in with her favorite blanket that I had given her from Christmas. I kissed her and gave her a hug, and told her “I love you and I will see you in the morning.” She replied with her last words: “I love you, too.” She passed away in the early morning hours of May 5, 2025.

Her mother had died of a heart attack in the early morning hours as she sat on the couch sipping her morning coffee. Lynette had always expected that she would die of a heart attack, as well. It appears that she did.

The pain of losing her at times seems almost unbearable. She has left such a huge hole in my life, because my life centered around her. I find myself at times seeing or hearing something and saying to myself, I have to remember to tell that to Lynette, only to quickly realize I can’t. I went to a choir concert that two of my grandchildren performed in. As they took the stage, I thought to myself, be sure to record this so I can share it with Lynette, again to then realize she isn’t here. But, as so many people have shared messages that they had observed our marriage over the years and realized that there was something special in our relationship, and shared that they had never found their soul mate, or that they thought they had, but the relationship didn’t last, I realized that what Lynette and I had is not ordinary; it is not common these days. So, as I long for what I had and grieve that I have it no longer, I also make an effort to express gratitude for what I had and express sorrow for those who have never experienced it.

I am a better man because of Lynette.

Over the past five years, I have felt that my main responsibilities were to protect her and keep her healthy, and equally important, to protect myself – not for me, but for her. I knew that if something happened to me, others would step in to care for Lynette, but I did not believe anyone could provide her with the same level of love and care that I provided.

I had always told my daughters when we were raising them to be sure that the man you marry is someone who will treat you like a princess. Later, I explained to them what I meant. That man should always treat you with respect. He should never lay a hand on you, never curse at you or call you a bad name. He should put your needs ahead of his own. Finally, that man should thank God for you every day and feel blessed to have you as his wife. I thank God for Lynette to this day. It doesn’t mean that Lynette was perfect, I was perfect, or our marriage was perfect. But I knew that I was loved and by accounts of her friends, adored; and I am confident that Lynette was reminded every day of how much I loved her, adored her and thanked my lucky stars that we got to make this journey together.

I hope that I was that example for my daughters of how a man should treat his wife. In turn, now, I am trying to set the example for my grandsons of what a man is and how he should treat his wife. It may be working. A couple nights after Lynette passed, after an exhausting day of visits to the funeral home, looking at venues for her memorial service, receiving friends and family, and making so many decisions as to our plans for the days ahead, Laurie and her four boys and I finally had a chance to sit down for dinner together hours past the usual dinner time. As we were eating and talking, my youngest grandson, age 7, said, “Papa, you took really good care of Gigi.” My heart overflowed with joy at seeing that a boy so young could see that.

I want for my grandchildren to have the kind of relationship that I had with their grandmother. I want them to know that being a man doesn’t mean being right, being controlling, being harsh, or being emotionless. For me, being a man meant loving my wife more than myself and willing to protect her at all costs for as long as I could. Being a man never was about winning an argument or being right for me. In fact, I learned that it didn’t matter who was right or wrong if I was not meeting my wife’s needs or if what I did was not caring for her and making her happy. Being a man was never about control. Our relationship was special because we respected each other’s views and opinions and tried to reach better decisions because we both had valuable input into the important decisions we made. I don’t recall being harsh with Lynette, mostly because I loved her so much that I couldn’t stand the thought of hurting her. I tried to show Lynette affection every day, in my words and in the little things I did for her. I want my grandsons to treat their future wives like princesses, and I want my granddaughter to know that she is special and deserves that treatment from her future husband. I think Lynette was right. If you want to know whether a man will make a good husband, look at how he treats his mother. For me, the advice is marry your best friend.

As her health declined over the past few years, I would prepare all of her meals other than when we went out to eat. I awoke much earlier in the day than she did and worked in the living room or my office so as not to awaken her. Once she did wake, she would text me with her breakfast request. I would stop what I was doing and prepare it and bring it in to her, and she would always ask me to sit down and review the world news with her while she ate.

One day, I came into the bedroom with her breakfast, and I told her, “You know that I am on to you, right?” She involuntarily smiled and asked what I meant. I replied that I knew that many days she was probably capable of making her own breakfast. She said that was true but she liked it better when I did it, because she knew that I did it for her because I loved her.

She was right, and I never again brought it up as I prepared her breakfast every day after for the rest of our time together. I would give anything if I could make breakfast for her tomorrow.

The Loss of Control of Measles in the U.S.: A Harbinger of Bad Things to Come

For the past five years, we have been seeing the impacts of decades of coordinated anti-vaccine, and more generally and more recently, anti-science campaigns on a grand scale. When writing the previous sentence, I initially used the phrase “we have been seeing the end results,” but then I replaced “end results” with “impacts.” That is because, sadly and tragically, I think we are far from the end results that we will watch unfold over the upcoming months and years.

This is a difficult blog post for me to write because by nature, I am an eternal optimist, and that trait is aided and abetted by another trait in that I have a great propensity for being naïve. During the first couple of years of the COVID-19 pandemic, I optimistically and naively believed that (1) the pandemic would be our wake-up call to take infectious disease threats more seriously, and as a result invest more in research and preparedness (the exact opposite is occurring); (2) the clear and mounting evidence would persuade the citizenry and our elected leaders of the value of vaccines and the need to think about treating the circulating air in public buildings as a public health measure in much the way we thought about the need to treat water for public health back in the early 1900s (it didn’t); and (3) those doctors who promoted disinformation would be held accountable or at least fade away from the public light in shame (that largely did not happen).

As of April 17, 2025, the CDC has reported 800 confirmed cases of measles in the U.S. in 25 states: Alaska, Arkansas, California, Colorado, Florida, Georgia, Hawaii, Indiana, Kansas, Kentucky, Maryland, Michigan, Minnesota, New Jersey, New Mexico, New York City, New York State, Ohio, Oklahoma, Pennsylvania, Rhode Island, Tennessee, Texas, Vermont, and Washington. The number of actual cases is likely orders of magnitude higher as there are time delays in confirming and reporting cases, not all cases have sought medical care, and there have been reported to be some efforts among some communities to keep cases from being disclosed. Not only are the actual numbers almost certainly far higher, this outbreak is likely far from over. I will be surprised if this outbreak ends before the end of this calendar year and before extending to every state.

There are some interesting demographic data about these confirmed cases:

Under 5 years: 249 (31%)
5-19 years: 304 (38%)
20+ years: 231 (29%)

Percent of Age Group Hospitalized

Under 5 years: 19% (47 of 249)
5-19 years: 7% (21 of 304)
20+ years: 6% (15 of 231)

Many people have the idea that measles would just be an issue for toddlers and preschoolers. But, as one can see, the outbreak is impacting children at all ages, including nursery, pre-school, elementary, middle school, high school, and even college. Some will be surprised by the number of cases in persons over 20 years of age. However, this is easily explained. The U.S. mounted a campaign to eliminate measles through immunization that resulted in measles cases precipitously dropping by 1991 and a certification that measles in the U.S. had been eliminated by 2000. Thus, persons born after 1990 (i.e., 35 years old and younger) who were not vaccinated, would have a fairly good chance of not having been exposed to measles and therefore susceptible to infection now. Further, I would suspect that a fair number of those that are over 20 years of age are also parents. If they were not vaccinated as children, there would be a good chance that they would not vaccinate their children and that many of these parents may have been infected by their children.

Another surprise to some may be that 15 of those over age 20 were hospitalized for measles. I actually am surprised that the number was not higher. Typically, those that are under 5 and those who are adults are the ones at highest risk for severe complications of measles such as pneumonia.

Further, as I have written before, this will not be the end of the health consequences from this outbreak of measles even once it does end. We know that those recovered will experience varying degrees of immune amnesia, meaning that they will lose some degree of their immune protection to other viruses as well as bacteria that they accumulated over the years, and as a consequence, their health risks and mortality rates are higher than the general population for the next few years until that immunity is reconstituted. Further, there is an absolutely dreadful and universally fatal neurological condition (subacute sclerosing panencephalitis) that, though fortunately rare, we are almost certain to see, probably in the next 3 – 7 years, due to the large number of people infected.

Much of what I wrote about above has been discussed with the public about the scale of this outbreak and the health consequences. However, what I have not heard is a discussion about is what other implications this outbreak has for us and our children and grandchildren.

While our focus has been on measles, it is important to realize that this same population of measles-susceptible individuals is also susceptible to rubella (German measles) and mumps since the vaccines for all three viral diseases has been included in a single vaccine – MMR – for their entire lifetime. Infection with measles provides no protection against rubella or mumps. It would not be surprising that measles would be among the first of these viral illnesses to emerge due to its high transmissibility and infectiousness, and the high levels of population immunity required to provide herd immunity (~95%).

I expect that we will see outbreaks of rubella and mumps in the months and years to come for a number of reasons. First, the wide-spread measles outbreak (over 800 reported cases as this time, however, I suspect that the actual number is in the thousands) is a good indicator of the number of children and young adults likely also susceptible to rubella and mumps. Measles is more highly contagious than rubella or mumps, and whereas the head immunity threshold is ~95% for measles (meaning that if a population has less than that number of its members protected against measles by virtue of vaccination or prior infection, then the potential for outbreaks increases significantly), that threshold for rubella is ~85% and for mumps is 85 – 90%. Thus, we expect measles to be the bellwether for disease outbreaks due to lack of herd immunity, but mumps and then rubella are certainly concerns to follow, unless high numbers of those not protected receive the MMR vaccine in response to efforts to contain the measles outbreak. Unfortunately, our federal response to the measles outbreak has not sufficiently focused on MMR vaccination, but rather confusing messages that tout various alternative approaches that we know do not prevent infection by the measles, German measles or mumps viruses.

So, let’s discuss these two other diseases and explain the concerns about their reemergence, if I am correct in my prediction.

Rubella (German measles)

As stated above, measles is the most contagious virus we know. Its reproduction number (R0), meaning the number of susceptible persons who are likely to be infected by one person with infection ranges between 12 – 18. German measles (rubella) is also transmitted by air and quite contagious, but much less so that measles. The R0 for rubella has been difficult to quantify and far ranging in various settings, but commonly believed to be < 5.

Rubella is caused by the rubella virus. Illness is characterized by fever, rash and swelling of the lymph nodes. Rubella is, in most people, a milder illness than measles, however, rubella has been a more common cause of birth defects than measles, and frequently, more severe defects. In fact, rubella has been the most frequent infectious disease cause of birth defects.

Rubella is a vaccine-preventable illness and the vaccine was approved in the U.S. in 1969. It was administered as a single dose vaccine until it was incorporated into the MMR vaccine in 1971 as a two-dose series. Through vaccination efforts, rubella was eliminated in the United States in 2004.

One of the feared conditions occurs when a pregnant mom is infected with the rubella virus, which can then pass to and infect the unborn child. That condition is referred to as congenital rubella syndrome. My fear is that many of the young girls and women who are infected in the current measles outbreak, will not seek vaccination against rubella, and that this will potentially give rise to an increase in congenital rubella syndrome in their future children.

Congenital rubella syndrome (“CRS”) is a constellation of possible manifestations that can include stillbirth, premature labor, brain structural abnormalities, liver involvement and enlargement, jaundice, growth retardation, cataracts, heart disease, and hearing loss. The risk of the fetus developing CRS is estimated to be 80% if the mother is infected with rubella during the first trimester, and this drops to a bit over 50% in the first part of the second trimester and then to 25% if the maternal infection occurs in the last part of the second trimester. CRS is a range of mild defects to severe, with severe occurring in roughly 10-20% of cases of CRS. The infants born to mothers infected in the third trimester can have congenital abnormalities, but they typically are milder and fewer and don’t present as the constellation of abnormalities characterized by CRS.

The last major rubella epidemic in the United States was from 1964 to 1965, and the toll was very significant. An estimated:

  • 12.5 million people got rubella
  • 11,000 pregnant women lost their babies
  • 2,100 newborns died
  • 20,000 babies were born with congenital rubella syndrome 

In recent years, we typically have 10 or fewer cases of rubella infections per year and no cases of CRS. Most of these resulted from exposure during international travel or living abroad.

Mumps

The mumps virus is of similar contagiousness to the rubella virus with a R0 of just under 5 (about 4.8).

The mumps vaccine is very effective, however, unlike the measle vaccine which generally results in lifetime protection, the protection from the mumps vaccine does wane after 16 – 51 years, with an average of 27 years. So long as we continue to have high rates of vaccination such that 85 – 90% of the population is protected, older adults should remain at low risk even with waning immunity.

Mumps is generally a mild, though miserable, illness in children in which they experience fever and swelling of the parotid glands (these are salivary glands located over the cheeks just in front of the ears and extending down to the bottom of the jaw giving rise to a chipmunk appearance in children with infection), however, in rare cases, those infected can develop a serious inflammation of the brain requiring hospitalization that can cause death or permanent disability. However, as many as 10% of mumps infections acquired after puberty may cause severe complications including orchitis (swelling of the testicles), meningitis (inflammation of the lining around the brain), and deafness that can be transient or permanent. Orchitis can result in shrinking of the testicle or testicles and at least temporary loss of or decrease in fertility. Girls and women who are infected may develop oophoritis (an inflammation and swelling of the ovaries) and/or mastitis (an inflammation and swelling of the breasts).

In the case of measles and rubella, our concern in future outbreaks would be for those who are unvaccinated or those who are immunocompromised. However, if we do experience outbreaks of mumps in the future, we would be concerned that some young to middle-aged adults, as well as older individuals might be susceptible even though previously vaccinated due to waning immunity. If that happens, I suspect we would institute a third booster of mumps vaccine.

These would be truly sad developments given our previous success and knowledge accumulated over the years.

A Comprehensive Review and Update on Avian Influenza (Bird Flu) in the U.S.

I have been writing about avian influenza since April 1st a year ago in a large number of blog posts.

To understand why I have written so much about this virus and why it remains a concern to me, let’s first review information I have previously provided and then let’s discuss an update and why there is growing concern.

Many of my long-term followers of the blog will recall that Dr. Epperly and I wrote a book entitled: Preparing for the Next Global Outbreak: Lessons from the Schoolhouse to the White House https://press.jhu.edu/books/title/12896/preparing-next-global-outbreak that was published by the Johns Hopkins University Press and released in April of 2023. In that book, we point out why we are at risk of future pandemics, why we need to prepare for them, and the lessons learned (117 of them, specifically) that should influence our preparedness and future responses to a pandemic. I also explained that pandemics are not 100-year events as commonly believed among the public, and why it would not be surprising for us to have another pandemic as soon as a decade from our last (recall that COVID-19 was declared a pandemic in March of 2020.)

Part of pandemic preparedness is surveillance of viruses with pandemic potential. (By the way, a pandemic does not have to be caused by a virus, and prior pandemics have been caused by bacteria, however, advances in science and medicine and the difference in transmission modes among viruses, bacteria, and fungi make viruses the strongest candidates for causing future pandemics.)

When I pick viruses for my list of those with the greatest pandemic potential, the criteria I use are:

1st level selection:  Viruses with airborne transmission, i.e., the virus is emitted from the mouth and nose of the infected person in small enough particles that it can be carried large distances in an area with common ventilation (e.g., a home, classrooms, an airplane, public spaces) and can hang suspended in the air for some period of time. (examples are SARS-CoV-2, influenza viruses, and the measles virus).

2nd level selection: Of those viruses with airborne transmission, then I rank highest on the list those viruses that have the suspected or demonstrated ability for sustained human-to-human transmission and those that are novel viruses or known viruses with novel mutations, recombinations or reassortments for which there is expected to be little population-level immunity. (A novel virus is one that has not previously circulated in the current human population, and as a consequence, there is no or little existing immunity in humans and all or most all people would be considered susceptible to infection.)

(Levels 1 and 2 select for viruses with pandemic potential, then level 3 selects for the likely severity of the pandemic were it to materialize, which means not only would the virus be considered to have pandemic potential, but the pandemic would likely cause severe disease manifesting as the need for medical care and potentially hospitalization, be disruptive to society and its normal functioning, and have the potential for overwhelming our health care system.)

3rd level selection: Then, of those viruses that satisfy the first and second levels of selection, I rank those viruses with any of the following traits higher up the priority list, and even higher up the list based upon the number of these traits that they have:

  1. Relatively high levels of morbidity (illness, but not death) and mortality (death) across all age groups, or at least many age groups;
  2. Significant presymptomatic or asymptomatic spread of infectious virus;
  3. School-aged children able to transmit the virus efficiently;
  4. High infectious load of virus (the amount of virus in the nose and throat) in infected persons;
  5. Low infectious dose required for transmission (the amount of virus that you must breathe in to become infected);
  6. The virus is not particularly vulnerable to environmental factors (temperature, humidity, UV light) and is able to remain infectious in the air and on surfaces for an extended period of time;
  7. No existing test or the only available tests are high complexity tests that can only be conducted in certain specialized laboratories (meaning that we will have trouble knowing the full extent of transmission of the virus in real time and we will not have the ability to quickly screen persons to determine whether they are infected with the virus);
  8. Widespread zoonotic and reverse zoonotic spread (the virus can transmit among humans, to our pets and farm animals, and back to humans);
  9. Non-durable immunity from infection and vaccination (meaning that reinfections will further increase the amount of disease transmission and illness, and the potential exists, as with COVID-19, that repeated infections will lead to long-term health conseequences);
  10. No existing vaccine that is effective or that could quickly be modified to be effective in preventing severe disease;
  11. No known existing medications with antiviral effect against the virus;
  12. High degree of viral fitness and rapid evolution to increase transmissibility; and
  13. Significant levels of infection among health care workers and nosocomial spread (this refers to patients infecting other patients and health care staff allowing for continued transmission chains among the most vulnerable people and the work force needed to care for patients) in health care facilities.

Using my criteria, avian influenza viruses and novel coronaviruses certainly have to be at the top of the list.

HPAI A(H5N1), an influenza A virus [HPAI is the abbreviation for “highly pathogenic avian influenza.” When referring to an avian influenza virus as being highly pathogenic we are indicating that it is a virus that causes death to all or the vast majority of birds (often chickens) that it infects as opposed to low pathogenic avian influenza viruses (LPAI) that do not typically cause severe illness or death in birds].  

Let me take a moment and explain some of the nomenclature I am using. The A in “A(H5N1)” is an abbreviation for an influenza A virus (as opposed to influenza B, C or D viruses. A (other than the avian influenza viruses) and B viruses circulate across the globe in humans and generally cause seasonal epidemics annually. Influenza C generally causes very mild illness, and therefore, is not seen as a public health threat, nor is its activity tracked. Influenza D viruses circulate primarily in cattle, and we have not identified spillovers into humans.). The H5 refers to hemagglutinin subtype 5). The influenza virus has an envelope (not all viruses do), and hemagglutinin is the major protein found within the envelope. It is both involved as a site for binding to cells to cause infection, but also a target for neutralizing antibodies. There are 18 antigenically distinct (meaning that our immune responses to one form of hemagglutinin may provide little, if any, cross-reactive protection against another) subtypes of hemagglutinin protein – (H1 – H18).

The designation N1 refers to the fact that the other major protein of the virus is neuraminidase type 1. The neuraminidase is another envelope protein that plays a number of roles in the transmissibility of the virus, the infectivity of the virus and in the release of viral progeny once reproduced in an infected cell. There are 11 antigenically distinct subtypes of neuraminidase proteins – (N1 – N11).

A(H5N1) viruses are avian influenza viruses adapted to infect and transmit among birds because the cell receptor the virus attaches to that allows the virus to enter the cells of birds and replicate has an α-2,3 sialic acid sugar attached to the protein receptor whereas human influenza viruses utilize receptors on the cells of the human lung with α-2,6 sialic acid sugars that allows them to infect humans and transmit forward from humans.

The first identified outbreak of H5N1 was among poultry in Scotland in 1959. The first known transmission of this virus to a human was in 1997 in Hong Kong. In that year, a total of 18 persons were infected, and six of them died- i.e., a case fatality rate of 33%.

The predecessor virus to the one now spreading in North America has circulated in birds since at least 1996 (the first infection of the H5N1 virus that we are currently dealing with was detected in 1996 in China in a domestic goose) when it caused an epidemic among birds. The good news was that from 1997 until 2024, only a total of 902 sporadic human A(H5N1) cases had been reported from 23 countries, caused by different HPAI A(H5N1) virus clades.

Avian influenza viruses are of the N5 or N7 type. There are three avian influenza types that have been responsible for large disease outbreaks- H5N1, H5N8 and H7N9. Of these three, H5N1 is considered to be the most pathogenic and severe.

The first recognized transmission of the virus to non-human mammals was in 2021 to foxes. However, from late 2021 on, there have been concerning spread of the virus to an ever-expanding range of animal species and increasing numbers of infections within those species. Unfortunately, the wider geographic range of infections and the involvement of new species create opportunities for the emergence of new and potentially more dangerous variants of the virus. Further, the easy transmission observed between certain mammalian species, such as Spanish minks and Peruvian sea lions, raises concern about the potential for the virus to establish reservoirs in different animal populations and pose ongoing risks to both animal and human health.

Influenza A viruses are carried by wild birds in their intestinal tract and can be shed by these birds through various means, such as saliva, feces and nasal secretions. Transmission of HPAI H5N1 resulting in human infection primarily occurs through direct contact with infected birds. 

The introduction of H5N1 into North America was not known to have occurred until late 2021, and this resulted from migratory birds. The bad news is that with ongoing transmission in animals, the virus does evolve and there is always the chance that it could mutate or reassort in a manner that would increase transmission to humans. In fact, the reference to different HPAI A(H5N1) virus clades is a reference to significant genetic changes to the virus warranting assignment to a new clade (for influenza viruses, we call these clades, but you can think of them as strains). The other bad news is that from 1997 to 2024, there is a cumulative case fatality rate of greater than 50% in humans.

In the last century, there have been four occasions when influenza viruses with genes that originated from swine (pig) or avian (bird) reservoirs entered the human population with wide-spread, efficient and sustained human-to-human transmission causing pandemics [1918 Spanish flu A(H1N1), 1957 Asian flu A(H2N2), 1968 Hong Kong flu A(H3N2), and 2009 swine flu A (H1N1)]. (Recall that I mentioned above that there is a common belief that pandemics are 100-year events, but obviously, this is not the case, and here I am only listing pandemics caused by influenza viruses.)

Thus far, while the H5N1 virus has infected humans, it has not shown the ability for efficient human-to-human transmission, and unless and until that happens, it will not produce a pandemic. Most of the infections have been in people with close contact with infected animals, and we have not seen much forward transmission, even to family members.

Then, why all the concern? The concern is that the virus is spreading globally, even to remote areas (including Antarctica), with an alarming expanded range of hosts, including occasional spillovers to humans, all of these events increasing the potential for mutations or reassortments that would all the virus to efficiently transmit to and among humans.

Waterfowl are natural hosts for low pathogenic influenza viruses. These wild and migratory birds then move to new locations and carry the virus with them. They congregate with domesticated ducks and geese to which they can transmit the viruses. Influenza viruses mutate frequently and while the virus started out as a low pathogenic virus (promoting its spread by these migratory birds that are not too sick to relocate geographically and find new domestic birds to transmit the virus to), there is the potential for the virus to evolve to a highly pathogenic form of virus that can result in loss of many domestic birds (some involved in our food chain) as it is transmitted among these birds and then potentially back again to migratory birds that can carry the virus to new areas of the state, country or world further infecting more domestic poultry before these birds die as appears to be happening with this current H5N1 epizootic.

What has been alarming during the past two years is that this particular HPAI A(H5N1) has been increasingly identified in mammals that generally have not been impacted by previous avian influenza viruses and we have seen the evidence that this particular virus can be highly pathogenic in many of these species of animals, as well, including ocean animals.

Human transmission of avian influenza viruses has historically been rare, as opposed to swine influenza viruses, which are much more suited for human transmission (while avian influenza viruses utilize only the α-2, 3 sialic acid receptors, swine have both α- 2, 3 and α- 2, 6 sialic acid receptors (the latter being the receptor type in the human lower airways), but still relatively uncommon (for example, we had three documented cases in 2023 (two in Michigan and one in Montana – all from direct exposure to pigs at fairs).

Swine flu is endemic to pigs. But pigs can be the intersection between birds (poultry on farms or even wild birds that transiently stop on land shared with pigs, or in the case of HPAI, where the bird carcasses remain following their death) and humans (farmers, visitors at fairs, live markets, etc.) and pigs can serve as a “mixing bowl” for human, swine and avian viruses when co-infected with both types of virus.  “Mixing bowl” is a reference to the fact that coinfections of pigs with these different strains of influenza virus can result in the influenza viruses swapping segments of their genetic material, a process referred to as reassortment, in which the resulting virus has an increased ability to transmit from the pig to humans, and the most worrisome case being when the resulting reassorted virus also has the ability to transmit efficiently from humans to other humans. In fact, this is exactly what happened with the influenza A virus that caused the 2009 pandemic [A(H1N1)pdm09]. Genetic sequencing of this virus revealed that the eight gene segments of the virus were from a mix of avian, human and swine origins.

We have been experiencing an epizootic (an epidemic in animals) of avian influenza in dairy cattle in the U.S. for more than a year now, and we still have demonstrated little ability to contain the spread of this virus. The earliest detected cases were in Texas. This is also where we had the first detected spillover into a dairy worker.

We know where this virus came from: it’s a reassortment between Eurasian highly pathogenic avian influenza and low pathogenic North American avian influenza strains that were circulating naturally in wild birds.

While we have known for some time that cows could be infected with influenza D viruses, we previously had not observed avian influenza virus infections of cattle to any significant degree. And while we knew experimentally that virus could infect the mammary tissue of cows, mastitis was the common and prevailing manifestation of avian influenza infection in cattle, resulting in very high levels of virus in the milk of infected cows. An additional concern arose when it was reported by at least one laboratory that cow utters have both α- 2, 3 and α- 2, 6 sialic acid receptors giving rise to the theoretical risk that cows’ utters could serve as “mixing bowls” for different influenza viruses in addition to pigs.

Further, farmers started reporting deaths of domestic and peridomestic (wild animals that surround and come into frequent contact with domestic animals) on their farms, particularly grackles and pigeons and outdoor domestic cats who we believe contracted infection from drinking infected raw milk from the cows. Disturbingly, the cats known to be infected showed rapid and drastic neurological deterioration and death in the majority of cases.

We have now identified at least 70 human infections, with 1 reported death. However, more concerning are cases of bird flu of a different clade that are in migratory birds and have spilled over to humans. Most recently (April 8, 2025), a previously healthy, 3-year-old Mexican girl died from respiratory manifestations (respiratory failure) after a month’s long illness of avian influenza from a clade (D.1.1 transmitted by wild birds, compared to the B.1.1 and B.1.3 clades that have been transmitted by cows) of virus that is related to the case of a man in Louisiana who died from bird flu in January of this year (he was an older man and did have underlying medical conditions) from this clade of the virus. A person in Wyoming and a poultry worker in Ohio also were infected with this clade and experienced severe disease requiring hospitalization. A 13-year-old girl was also infected with this same clade and hospitalized in Canada with very severe disease requiring extraordinary care for a protracted period of time in the intensive care unit to save her life. Though these deaths are tragic, it might not be as concerning had these occurred in persons who had prolonged and close contact with cattle or poultry. However, most had no obvious source of contact with animals or exposure to account for their disease.

A case report in the New England Journal of Medicine provided us with important details about this first known transmission of H5N1 from a dairy cow to a human.

In late March of 2024, the farm worker developed redness and discomfort in his right eye. The worker denied having any fever, chills, cough, shortness of breath or loss or distortion of vision.

The worker denied any contact with dead or diseased birds or poultry. He did report close contact with cows, including cows that were showing signs of possible infection with avian influenza manifested by lethargy, fever, decreased appetite, dehydration, and/or decreased milk production. He did routinely wear gloves, but no other PPE including masks or eye protection.

On physical examination, the patient did not appear severely ill. His lungs were clear.

His eye examination revealed the following:

We are looking at the patient facing us, so the eye on the left side of this photo is actually his right eye, and the eye to our right is actually his left eye. Looking at his left eye, he has conjunctivitis (inflammation of the conjunctiva, which is the superficial lining of the eye and eye lids). We can see that it is red and injected, meaning that we see the blood vessels much more prominently than in someone with a normal-appearing eye. His right eye demonstrates a subconjunctival hemorrhage, in other words, there is bleeding directly under the conjunctiva. We can tell that there is a hemorrhage (bleeding) because the redness is confluent and obscures the blood vessels, whereas in his left eye, we can see the blood vessels much more clearly.

The examiner swabbed the patient’s nose and right eye to test for influenza virus. The test (which looks for genetic traces of virus) of both samples was positive for influenza A and for the H5 protein, which is indicative of avian influenza. That test also suggested that the amount of virus in the eye sample was very high. The CDC performed additional testing that confirmed that the virus was A(H5N1) and genetically the same as the virus detected to be circulating among dairy cows.

The patient was instructed to isolate at home and was started on an oral antiviral medication (oseltamivir). Over the ensuing days, the patient’s conjunctivitis resolved and no family members developed signs or symptoms of infection.

Additional testing of the virus genetic material revealed that it had not mutated in a way that would change the receptor-binding protein from the avian form (α- 2, 3-linked sialic acid [we do have this form or receptors in our eyes]) to the human form (α- 2, 6-linked sialic acid [this is the receptor type in the human respiratory tract]). On the other hand, the virus retrieved from the infected farm worker had acquired a mutation in the PB2 protein that has been associated with adaptation of the bird virus to mammals, including humans. Fortunately, the virus did not have the mutations that we associate with developing resistance to our usual influenza A virus antiviral agents.

This is good news/bad news. The bad news is that cows can transmit the virus to humans who are in close and prolonged contact with infected cows, though we still don’t know how transmission occurred – respiratory droplets from infected cows? Contact with virus in the milk of infected cows and then touching or rubbing one’s eyes? Aerosolization of virus from the milk when cleaning floors or equipment used in milking the cows?

The good news is that the patient did well and appeared to recover well, the virus did not show worrisome changes that would suggest that the virus can now efficiently transmit to and among humans, and the patient did not appear to infect anyone in his household, though we were not provided with any information as to what precautions were used in the home and how many persons were in the home. I suspect that the disease was relatively mild and mostly caused conjunctivitis is that the avian influenza virus involved had not acquired the ability to bind to α- 2, 6 sialic acid receptors and therefore, was unable to infect the person’s lungs.

There remain many questions. One question is whether the antiviral treatment prevented him from becoming more ill and/or did it shorten his course of illness? I also hope that they will carefully follow this farm worker over time. We know that in other mammals, this virus has seemed to produce significant neurological disease. The eyes can be a route for viruses to access the brain. It would be good to follow this patient to ensure he does not develop any signs of neurological disease in the future.

The continued transmission of A(H5N1) in cattle and in wild birds with spillovers to humans and domestic and peridomestic animals continues to concern me in that we are rolling the dice and giving this virus more chances to mutate and reassort. As I mentioned, this is an RNA virus and RNA viruses are more prone to acquire mutations because they often do not have the same proof-reading systems in place to catch errors when the RNA is being transcribed to produce viral proteins.

Many mutations are of no significance, some are detrimental to the virus and those viruses will generally lose in competition to more fit forms of the virus, so they disappear over time, and then some may be advantageous to the virus (increase viral fitness through increasing transmissibility, receptor binding or evading immune defenses).

The viruses that infected the cows and the humans that are generally causing conjunctivitis and mild illness are the same version of virus (B.1.1 or B.1.3). The viruses that have infected wild birds and then transmitted to humans causing much more severe disease are a different one that has infected cows (D.1.1).

We can look at the phylogenetic trees for this virus (you probably have seen these, but not known what they are called or what they mean, if you have followed the developments with SARS-CoV-2 over the past five years. These are diagrams that plot out the various versions of the virus starting (usually at the left side of the diagram) with the original form (wild-type) or at least the first discovered form of the virus and then those new versions of the virus with the fewest mutations will be closer and those with the most mutations will be further away from the original form of the virus. When the collection of mutations has been found to be significant, then the SARS-CoV-2 virus was assigned a new variant name (and appears on a new branch of the phylogenetic tree) or in the case of this A(H5N1) virus, it is assigned to a new clade.

We can look at a phylogenic tree for the changes in each of the viruses’ major proteins that we are interested in. We previously discussed the H or HA (hemagglutinin) protein and its role (especially in virus attachment to the host cell and fusion with the host cell’s membrane in order to allow the virus to enter the cell). This virus has the H5 subtype protein, and the phylogenic tree shows that there have been relatively minor mutations to this protein (that is good, because this protein is a vaccine target due to the fact that neutralizing antibodies are made to this protein as a result of infection). We can look at the tree for the N or NA (neuraminidase) protein (important in facilitating the release of newly formed viral progeny from the cell), in this case, the N1 protein, and see that it too, has relatively minor mutations, though certainly more than have occurred within the H protein (again, good news, because the H1 subtype is also a target for vaccines, but also of some of the antivirals we use).

There is a mutation required to the PB2 protein (not a vaccine target) that is necessary for transmission to mammals, though not sufficient in and of itself to allow for transmission to humans, and we see that has occurred, but only in the samples taken from infected humans, suggesting that this was an “in-host” mutation (occurred in the human after infection during translation and replication within human cells rather than in any of the cattle or prior bird samples). However, there are many more mutations to this protein and far more “divergence” (distance away from the prior forms – due to the large number of mutations), and I would not be surprised to find that it is developing in wild birds, and we are just not detecting it because we are not doing enough testing, as we did detect the mutation in a dead mammal. Perhaps one of these mutations explains the increased transmission in mammals.

Of course, this discussion just addresses mutations. As mentioned above, influenza viruses are known for reassortments with other influenza viruses, where they can exchange gene segments. This would potentially result in far more drastic change in the nature of the virus than simple mutations.

We fast forward to a year later and we now have concerning news coming from Texas dairy cattle. An article published in Nature Scientific Reports from March 14, 2025 titled “Superior replication, pathogenicity, and immune evasion of a Texas dairy cattle H5N1 virus compared to a historical avian isolate” reports on the development of a concern that I warned about last year. That is to say, if we allow certain viruses (especially RNA viruses, of which avian influenza is such a virus) to continue to spread, we risk the virus evolving and developing traits that can increase viral fitness, and potentially even develop changes that would allow it to evolve to infect humans.

The article reports that after spreading to nearly 900 dairy farms (including Idaho) and resulting in at least 39 (at the time of this study) known human infections, the avian influenza virus that has been spreading among cows has developed superior growth capability and rapid replication kinetics when studies in human lung cells in vitro (meaning in a laboratory setting as opposed to in the human body).

Worrisome for us, when the more recent isolates of the virus were tested in laboratory mice, the virus demonstrated more pathogenicity than earlier forms of the virus did, and infection in mice was accompanied by high virus titers in the brain and high mortality in the mice. Further, the virus had acquired new capabilities to thwart innate immune responses (these are our immune defenses that occur most immediately (as opposed to antibodies that take time to develop, don’t require prior exposure to the invading pathogen, and are far less specific and targeted than our antibody or cellular immune responses.)

A quick word on virologic studies. Information we gain from studies varies in its application to real-life human bodies and disease. For example, at the low end, during COVID-19 and future pandemics, we do studies referred to as in silico, which means that the study was done by computer modelling. For example, when we know the protein of a new virus that we want to target for antivirals or vaccines, the computer can generate a 3D model of the protein, as well as the medication of interest or the vaccine candidate to give us an idea as to whether the medication or vaccine might be likely to be effective. This is good for helping us prioritize our drug and vaccine candidates, but it only provides a low degree of confidence that the drug or vaccine will actually work in real life human bodies and in disease. For example, there were indications from in silico modeling that ivermectin might be a drug candidate because ivermectin appeared likely to bind an amino acid on the spike protein and an amino acid on the ACE-2 protein receptor. Further, it even seemed to be effective in the next step up of evidence, in vitro experiments, where we take a sample of the virus, a sample of human cells that the virus is known to infect and mix in the drug, in this case, ivermectin, in the laboratory to determine whether it impedes the virus from entering the cells, and it did. But, plenty of in silico and in vitro experiments that appear promising fail to pan out when taken to the next steps of clinical investigation.

When we have a promising drug or vaccine candidate, it is common to next move to studies in animals, particularly mice, because they are abundant, easy to manage, and cheap. The advantage of mice over laboratory experiments is that mice are living creatures, and unlike experiments in test tubes and cell cultures in a laboratory, they have circulatory systems, respiratory systems, immune systems, and actual functioning organs. This will often give us more indication as to whether the medication or vaccine that seemed to work in a test tube does work in a living being, however, mice still are much different than humans, and success in mice does not necessarily mean that it will work in humans leading to a common saying among scientists – “mice lie and monkeys exaggerate.”

However, different human diseases are often better suited to different animal models. For example, ferrets more closely resemble the anatomy and functioning of the human lung than mice do. On the other hand, mice develop cancers years faster than humans do, and so they can be very helpful in testing substances for carcinogenicity (the ability to induce cancer) such as has been done with food dyes. Again, mice are different than humans. When the substance does not cause cancer in the mice, that is reassuring, but not conclusive evidence that the same substance will not do so in humans, and conversely, if the substance does cause cancer in mice, that is concerning and calls for close observational studies in humans, but we often do not see cancer develop in humans.

When studies in common laboratory animals tend to further support the effectiveness of a drug or vaccine, it is common for us to then study it in larger animals that are more biologically related to us, especially mammals, and even better primates. These animals are much more expensive and it is harder to do studies in as large a group of these animals as it would be to do in mice. Studies in these animals are far more predictive of success or failure in humans and give us additional insights as to dosing and potential safety issues.

Now returning to the study referenced above, these findings related to increase in pathogenicity, severity of disease and antagonism of the innate immune response are important and concerning, but we have to keep in mind that they are results in mice, which may not be exactly the same in humans.

I’ll conclude with this. Whatever we think we know about this avian influenza outbreak in North America, particularly, the United States, it is an incomplete picture. Our government is not doing enough testing, surveillance and research into potential therapies and vaccines. The past administration did make an effort, but it was delayed and inadequate. Unfortunately, unconfirmed reports from people inside the CDC indicate that they are being told not to test dairy and poultry workers (recall the President’s comments in his first term when dealing with the COVID-19 pandemic – we wouldn’t have so many cases if we weren’t testing) and not to publicly report their symptoms. Many of the experts that were investigating and tracking this outbreak were fired in the government layoffs until someone realized this. Efforts were made to rehire them, but I don’t know how many were successfully retained. The NIH has made drastic cuts to research at a time when we need more influenza research. We are already suffering the loss of scientists from the government and universities due to personnel cuts and cuts to funding. Further, the Secretary of HHS is distracted and causing distraction by directing attention away from these real-time threats and to revisiting settled issues such as whether vaccines are associated with the development of autism, promoting elimination of fluoride from drinking water, and stoking the flames of a measles epidemic.

Again, I don’t know whether this will become a pandemic, but I can pretty much assure you that given all these changes, if it does, we will be delayed in recognizing it and we will be unprepared to deal with it. There is good reason to believe that this virus would be at least 20 times more fatal than SARS-CoV-2, and would kill many more children and possibly disproportionately so relative to older persons.

A mystery may have been solved

Long-time followers of my blog may remember the perplexing occurrence and significant number of cases of hepatitis (liver infection/inflammation) in 2022, first noted in the U.K. occurring in COVID-19-unvaccinated children under the age of 16 years that we have since referred to as acute hepatitis of unknown origin (AHUO) at a time when fewer mitigation measures were being taken to protect children in schools against airborne transmission of viruses. Clinically significant hepatitis is not a predominant feature of most cases of COVID-19, yet, many of these children were quite ill with the liver disease, some critically ill and still some requiring liver transplantation. Tests for the usual suspects (e.g., hepatitis A, B, C, D and E viruses) were all negative. After all the testing and review of cases, the major remaining differential diagnoses were narrowed down to adeno-associated virus co-infection with adenovirus or autoimmune hepatitis. We may now have a different answer.

We have known since the early days of the pandemic that SARS-Co-V-2 RNA can be detected in the stool of patients with acute COVID-19. Subsequent investigation and a publication by Zuo et al demonstrated that SARS-CoV-2 RNA can continue to be detected in some COVID-19 patients in the convalescent phase of the infection (when symptoms are resolving or have resolved).

Given mounting evidence of viral persistence in some people following SARS-CoV-2 infection and the fact that detection of viral RNA after the infection has supposedly resolved can be an indication of viral persistence, a group of investigators began to search for evidence of the virus in other organs of the gastrointestinal tract Residual SARS-CoV-2 viral antigens detected in GI and hepatic tissues from five recovered patients with COVID-19 | Gut. Using conventional immunohistochemistry (this is a process by which investigators create antibodies that are specific to the protein they wish to search for, tag these antibodies with a substance that will show up under the microscope, inject the antibodies into the tissues, then cut up the tissue into sections that can be stained and examined under a microscope), these investigators examined the tissues obtained from five patients who seemed to have recovered from COVID-19.

The protein they targeted was the nucleocapsid protein (NP) of the virus, as this protein is not present in any of the vaccines used in the U.S. or most other countries, only being an issue in the few countries that utilized whole inactivated virus in their vaccines, such as China. Thus, in those who have not received inactivated whole virus vaccine, the presence of NP (and by extension antibodies to NP) is a consequence and indicator of prior infection regardless of vaccine status.

These researchers detected SARS-CoV-2 NP in the colon, appendix (this is a finger-like projection extending from the colon very close to the location where the small intestine connects to the large intestine), ileum (this is the last part of the small intestine just before it connects to the large intestine (or colon), hemorrhoid tissue, liver, gallbladder and lymph nodes from these five patients who recovered from COVID-19, ranging from 9 to 180 days after testing negative for SARS-CoV-2 by nasal swabs. In fact, two of the five had NP detected in each of these locations, an indicator of how far and extensively the virus spreads within the body even in “mild” cases. The findings were validated by confirmatory identification of SARS-CoV-2 spike (S) protein and in some cases the presence of SARS-CoV-2 RNA.

Building on these two studies, with good evidence for viral persistence that can involve the liver as long as six months after even what appeared to be a “mild” infection, in an environment of a rapidly evolving virus with increasing immune escape capabilities, and especially at the time (2022) when we were seeing new Omicron variants as often as every several months, the case for autoimmune hepatitis has become strengthened.

Given the persistence of nucleocapsid protein embedded within liver cells following a prior infection, the potential for hepatitis due to cell-mediated killing of the liver cells as a consequence of efforts to clear the virus or autoimmune hepatitis upon subsequent reinfection with a similar, but distinct antigenic variant of SARS-CoV-2 are reasonable hypotheses.

This leads us to a new study published this year, Characteristic immune cell interactions in livers of children with acute hepatitis revealed by spatial single-cell analysis identify a possible postacute sequel of COVID-19.

These researchers examined the liver biopsies obtained from 12 patients (mean age 9.5 years) who were hospitalized between February 2022 and December 2022 in European countries who tested negative for acute adenoviral or SARS-CoV-2 infection and who met the WHO criteria for AHUO. Three of the 12 showed serological evidence of past adenoviral infection and 10 of the 12 had a history or serological evidence of past COVID-19. Eight of the 12 were known to have had a recent bout of COVID-19 with a median onset of 2 months prior to the hospitalization for AHUO. Unlike the original cohort noted in the U.K., a third of these children had a history of past COVID-19 vaccination.

Imaging mass cytometry (my apologies in advance to laboratory scientists who might be reading this as I have no expertise in this area – this is a technique that utilizes metal tags of antibodies designed for up to 40 antigens found in different types of cells that is applied to a tissue specimen. A machine then scans the tissue with a laser that generates signals from the metal tags that create detailed pictures of the cells in the tissue. The pictures reveal the location of the antigens targeted within the cells to allow identification of their intracellular locations as well as to help us understand how they are interacting with the cell) identified significant infiltration of the liver tissue with CD8+T- cells, which are cytotoxic T-cells (the cellular part of the immune response that identifies infected cells and kills them in order to rid the body of the virus within). The degree of infiltration and immune activation correlated with the severity of the hepatitis.

Further, the investigators detected SARS-CoV-2 antigens in ACE2- expressing cells in the areas of the liver with significant pathology in 11/12 samples using several different detection methods (we have known for some time that not everyone who has had COVID-19 will test positive on serological testing (measurement of antibodies in the blood).

The identification of immune-mediated liver injury associated with the detection of SARS-CoV- 2 antigens suggests a possible association of AHUO with prior SARS-CoV- 2 infection, further suggesting that the hepatic disease could have manifested as a part of Long COVID or post-acute sequelae of COVID-19.

PCR testing for adenovirus in liver specimens was negative in all of the subjects. Conversely, detection of SARS-CoV-2 proteins occurred in 11 of the 12 subjects. Notable was the extent of immune-cell infiltration in all subjects, and the degree of infiltration correlated with the clinical severity of each child’s course of illness. Further, the colocation of infiltrating cytotoxic T-cells in areas where SARS-CoV-2 proteins were detected suggests an antigen-mediated pathology.

The fact that the SARS-CoV-2 virus itself was not detected in the liver tissues and cells raises the concern that has already been raised as a possible underlying explanation for Long COVID, that virus is persisting and residing in areas of the body that are more difficult for the immune system to surveil and remove virus from (one candidate in these patients was already identified in the earlier studies I referenced above – the small and large intestines). In this instance, the thought would be that the persisting virus is replicating, although likely far less than in an acute infection, and shedding viral proteins that are entering the venous system that returns blood from the bowels that passes through the liver where the proteins can be deposited prior to the blood returning to the right side of the heart. Support for this theory is the fact that a biomarker for a disturbance of the gut integrity with subsequent leak into the vascular system (zonulin) has been detected in plasma along with spike protein. As a result, in at least some cases, immunopathology results and hepatitis may be the presenting illness as a result of liver cell injury due to the infiltration of immune cell infiltration targeting cells for destruction due to the presence of viral protein.

Of interest, this same situation of persistent SARS-CoV-2 virus in the GI tract with SARS-CoV-2 RNA detected in stool weeks after initial infection at a time when nasal swab testing for SARS-CoV-2 had long since turned negative has been postulated as the mechanism behind MIS-C (multi-system inflammatory syndrome in children) that we often saw present weeks to months following acute infection.

Of course, nothing from this study rules out the possibility that adeno-associated virus 2 (AAV2) contributes to the development or increases the risk for AHUO, but clearly, prior or co-infection with AAV2 does not appear to be necessary for the development of AHUO.

In conclusion, it appears that AHUO may be a post-COVID-19 immune-mediated hepatitis, another potential part of the spectrum of illnesses that may occur as part of the post-acute sequelae of COVID-19.

Idaho Legislature Votes to Make Ivermectin an Over-the-counter Medication

Kyle Pfannenstiel has excellent reporting in yesterday’s issue of the Idaho Capital Sun Idaho Legislature approves ivermectin deregulation, sending bill to governor • Idaho Capital Sun about the Idaho Legislature approving a measure to overrule federal law that requires ivermectin to be dispensed to humans pursuant to a prescription, which these Legislators believe will allow ivermectin to be sold over-the-counter in Idaho pharmacies and stores.

Here is the pertinent section of the bill that was just approved by the Idaho House and Senate:

“Notwithstanding any law to the contrary, ivermectin suitable for human use may be sold or purchased as an over-the-counter medication in this state without a prescription or consultation with a health care professional.”

The clause, “Notwithstanding any law to the contrary” might have been glossed over by those who don’t love legal jargon as much as I do or know what laws might be to the contrary, but there is an important law to the contrary – The Food, Drug, and Cosmetic Act that was enacted by the U.S. Congress.

The Durham-Humphrey Amendment divided drugs and medications into two categories: those that can only be sold and dispensed pursuant to a prescription and over the counter (OTC) medications that may be sold for self-administered use without the clinical oversight of a physician. The FDA has been delegated the authority to make the assignment of these two categories to those medications that can be legally sold in the U.S.

The Food, Drug, and Cosmetic Act has long been considered to be the supreme law of the land (that means overriding any state laws that are in conflict with the statute) and to displace states from this area of regulation that would otherwise lead to a patchwork of laws across the country. It has made sense to most of us that this would be the case as it allows for a concentration of expertise in a federal agency (the FDA) to undertake the lengthy and complicated issue of reviewing the basic science, animal and subsequent human studies of safety and efficacy for the myriad classes of medications to determine whether they are safe and effective, the appropriate indications for their use, the proper dosing and what side effects and adverse effects must be listed for health care professionals and for patients. I know of no states that would have this degree of expertise and infrastructure to both conduct the initial applications of medications and the post-marketing surveillance.

On the other hand, I did not fall out of my chair when I learned that the Idaho Legislature was considering this bill given what appears to me to be growing anti-science sentiment and a growing appetite to challenge federal laws by enacting state laws that are in conflict – a legal strategy that previously would have been sure to fail and considered a waste of taxpayer dollars, but more recently seems increasingly more plausible after EMTALA (the Emergency Medical Treatment and Active Labor Act) was found not to mean what its plain text says and what those of us who have studied it for almost 40 years always thought it meant.

Frankly, I fully expect one (or both) of two things to happen that will make the issue of Idaho law (assuming the governor does not veto the bill) in this instance being struck down a purely academic question and not one that sees the light of day in our hallowed halls of justice. First, I fully expect Dr. Martin Makary, the newly confirmed head of the FDA, who infamously pronounced that the U.S. would achieve herd immunity to SARS-CoV-2 and the pandemic would be over in just over one year (April of 2021), under the leadership of RFK, Jr., Secretary of HHS, will pronounce a recategorization of ivermectin to over-the-counter status. Second, even if I am wrong in my prediction, I cannot imagine a scenario where the current administration would attempt to enforce federal law and prevent Idaho from implementing this law. Without legal action by the federal government, there would be no case to be challenged in the courts.

Putting legal analysis to the side, there are so many disturbing issues about this latest action of the Idaho Legislature. These are not serious legislators and I will explain why below.

  1. It would seem plain and obvious that if the legislature had never before entered into the field of regulating (rather deregulating) prescription medications and decided that this was now an area ripe for state regulation that it might want to hold some hearings, listen to some expert opinions, consider the implications of doing so (process, precedent-setting, legal, etc.), but that apparently didn’t happen. So, is the legislature going to embark on a review of all medications and make their own determinations as to whether they should be prescription or over-the-counter? If not, what will be the criteria for selecting which medications they will review? What criteria will they use? What expertise will they rely on? Personally, I have not felt that we need more government, more cost to taxpayers, and a legislature that needs to find more things with which to consume itself continuing its inching towards being a full-time job.
  2. It would also seem plain and obvious that if the legislature is now going to undertake classifying medications, that it might want to hear from experts on the specific medications in question, let’s say maybe the board of pharmacy or maybe, in the case of ivermectin, some infectious disease experts? But as Mr. Pfannenstiel reported, “Idaho lawmakers didn’t hear public feedback on the bill from doctors, pharmacists or health care professionals.” That kind of makes me think that perhaps they merely want to pass something to score political points, but don’t want to be inconvenienced by hearing all the reasons that this might be a really bad idea or harm Idahoans. In fact, one only needed to listen in to the discussion to be aghast at all the misinformation and baseless claims made that would lead one to believe that ivermectin is nearly a cure-all, despite the very limited role for this medication in the evidence-based treatment of illness.
  3. Of course, to the extent that the legislature is intending this to be their one and only foray into regulating medications, this is a problem of their own making. It was appalling to the medical community that the legislature actually promoted disinformation early on in the pandemic in giving unprecedented access to anti-vaccine messaging and late in the pandemic by introducing bills that would likely impair our response to future pandemics. (As an aside, the legislature is now recognizing the serious physician shortage such that it is contemplating the need to purchase a medical school while at the same time failing to have any insight that these anti-science/anti-medicine actions are undermining their stated objective of recruiting and retaining more physicians in Idaho).

It is a common strategy of antivax organizations to promote unproven preventatives and treatments to people to give them more confidence in refusing vaccination. Ivermectin was promoted on the flimsiest of data as a preventative against COVID-19 in the same way that vitamin A is now being touted as a preventative against measles. The problem is that well-designed, high-quality studies show that neither works. In the case of ivermectin, Idaho emergency room and critical care physicians often dealt with families who brought in a family member critically ill with COVID-19 only to learn that the assurances they received from a coordinated network of doctors touting their telehealth services for patients to receive ivermectin at a hefty cost were baseless. And, now Texas parents of children hospitalized for severe measles are learning that vitamin A not only did not prevent their unvaccinated child from getting measles, but that doctors are now having to address the harms the children have suffered as a result of vitamin A overdoses as well.

As Mr. Pfannenstiel points out in his article, “The U.S. Food and Drug and Administration, or FDA, hasn’t approved ivermectin to treat or prevent COVID-19, saying the federal agency finds existing clinical trial data don’t show “ivermectin is effective against COVID 19 in humans.” There are multiple high-quality studies that all support this conclusion, and I have previously provided and written about many of them on this blog.

  • The Legislature has pursued a number of bills that limit, restrict or even prohibit the use of a number of the tools that are available to address a future pandemic. There certainly are reasons to rethink a number of the approaches undertaken in the course of combating the COVID-19 pandemic. But, can anyone point to a committee or work group that has undertaken a review of our pandemic response and assimilated a list of lessons learned? Can anyone point to one bill that the legislature has introduced, held hearings on, and passed into law that would strengthen our pandemic preparedness? Please let me know if so, because I am not aware of anything as to either of these strategies that would seem to be the work of a serious legislature that wants to use real life lessons to help protect our state and its citizens.

How strong were the arguments of lay persons in favor of this bill? Let’s look at a couple:

  1. According to Mr. Pfannenstiel, “Supporters argue making ivermectin more widely available for human use would avoid people buying versions of the drug intended for animals, and it would make human use safer by providing more information on appropriate doses.” This is illogical. First, the legislature didn’t buy analogous arguments for marijuana (and, by the way, I personally believe rightly so), so there is a problem of internal inconsistency. Second, the reason people were buying animal versions of ivermectin is because the state stood back and allowed certain physicians to promote disinformation that ivermectin would work and reputable physicians wouldn’t prescribe it because it was not safe and effective for the prevention or treatment of COVID-19.

Human use of a medication at appropriate doses does not make it safer if there is no benefit from taking the medication at any dose. Deceiving the public as to the benefits of ivermectin and then making it more available by making it over-the-counter does not protect Idahoans nor does it serve public health. In fact, given the implied claims of these disinformation doctors and appallingly some public health board members that ivermectin was essentially 100 percent effective in preventing SARS-CoV-2 infection and severe disease not only promoted the use of a medication that has potential adverse effects, while offering no benefit, but also gave many of these deceived Idahoans a sense of invincibility that actually increased their exposures and risks of infection mistakenly thinking that they couldn’t be infected while taking the medication.

  • In one example provided by Mr. Pfannenstiel, “Rep. Faye Thompson, R-McCall, said she recently went to a local feed store hoping to buy ivermectin for herself and her family to use, but stopped out of confusion over the appropriate dose.” This touches on the other issue that terrifies me about making ivermectin over-the-counter. I do believe that competent adults should be able to make foolish and irresponsible decisions if that is what they want and it won’t harm someone else. But, I fear that the fact that these same adults are already thinking that it is a brilliant idea to buy medications intended for animals for their children from a local feed store will mean they will give these over-the-counter medications to their children for inappropriate uses. Given that ivermectin is being already being touted by some of the disinformation doctors as a treatment for bird flu (a potentially lethal infection in children), a preventative and treatment for cancer, and God knows what all else, I fear that parents will resort to ivermectin rather than seeking medical care for a prompt diagnosis and effective treatment for potentially dangerous threats to the health of Idaho children. This would be a travesty.

Lest the reader of this blog post believe that this bill was just some fringe element of the Republican party, Mr. Pfannenstiel reported that this bill received bipartisan support, including only one vote against it in the House. One Democratic Representative that I had the impression was thoughtful offered his support of the bill on the basis that there are people who think ivermectin works comparing it to medical marijuana for the treatment of pain. I don’t know a single reputable physician or pharmacist that believes we should make all medications that people think works for something over-the-counter when the evidence clearly shows they are wrong.

I could go on much longer, but let me close with one horrifying thought. Mr. Pfannenstiel reported about one Idaho Senator giving credence to the notion that ivermectin is close to being a cure-all stating that “Some people will use it like taking vitamins.”

Measles

What is measles?

Measles is a highly contagious virus that causes infection (also called measles). Because it is so contagious, most people who have not yet been infected or vaccinated who are exposed to someone infected with the virus will develop measles.

How is measles transmitted?

Measles is spread by direct contact with respiratory droplets (spit/saliva/secretions emitted when someone who is infected talks, coughs or sneezes) and also by airborne routes (meaning that the virus can be suspended in the air and can expose people who are in the same room even if not close by or even by entering the room after the infected person has left until there has been enough air exchanges to remove all the virus).

What is the typical case of measles like?

Often a person who is infected will begin to feel very tired and easily fatigued, lose their appetite, begin to experience fever, will develop a runny nose and cough and pinkeye. Several days later, a red rash erupts, usually on the face, but gradually spreading down the body over the chest and abdomen, the arms and legs. The rash will often involve the palms of the hands and the soles of the feet. Patients often feel the worst during the first couple of days of the rash. In uncomplicated cases, patients tend to start to feel better and have resolution of the fever several days after the rash begins. The cough is usually the last symptom to resolve.

Why try to prevent cases of measles?

While many people recover uneventfully from measles, there are many alarming potential complications of measles and other than knowing that older individuals and those that are immunocompromised are more likely to develop severe disease and complications, we cannot predict which children will develop potentially life-threatening complications.

Prior to the availability of a vaccine, there would be as many as half a million cases of measles each year in the U.S. After vaccines were widely available, cases of measles in the U.S. were as low as 100 in a year. In the early 1960s, prior to the availability of the measles vaccine, roughly 8 million children world-wide would die of measles complications every year.

What are the complications that can occur after measles infection?

One of the most common and also unique complications of measles infection is what is referred to as “immune amnesia,” meaning that there is a loss of some of the immune protection the person had already built up prior to getting infected with measles either due to vaccination or due to prior infection. Researchers had noted that in the few years following measles infection, children seemed to have higher rates of infection and even more severe outcomes. When looking into why, they discovered that the measles virus is able to use a receptor on certain immune cells of the body to infect the very cells that produce antibodies and are meant to protect us from infection. Following measles, the researchers found that persons could lose anywhere from 11 to 73 percent of their preexisting antibodies to both viral and bacterial infections and that this loss of immune protection could last as long as three years. If you want more details, see https://www.science.org/doi/10.1126/science.aay6485.

The most common acute complications involve the lungs and the brain. Pneumonia accounts for about 60 percent of the deaths in infants with measles. Pneumonia can be caused directly by the measles virus or can be a result of a superimposed bacterial infection due to the damage caused by the measles virus that can facilitate bacteria invading the damaged lungs.

The brain complications most often manifest as a condition referred to as encephalitis (meaning an inflammation of the brain), and can take one of two forms. Acute (meaning occurring during the measles illness rather than after it) encephalitis is often recognized by a recurrence of the fever or fever that doesn’t resolve in the normal timeframe, along with headaches, seizures, and a change to the level of consciousness (less alert, confused, etc.). While most people survive this complication, prior to vaccines, some individuals would be left with deafness, blindness or other permanent brain dysfunction.

An even more dreaded, but fortunately rare, complication of measles is subacute sclerosing panencephalitis (SSPE), the other form of encephalitis, but unlike the acute encephalitis above, this encephalitis does not have its onset until years after the person has seemed to have fully recovered and it is uniformly fatal. Typically, others will note personality changes, the patient’s handwriting begins to clearly deteriorate, and they become forgetful. As the condition progresses, the patient becomes progressively less able to walk, stand, and even talk. The patient may become combative, begin to have seizures and eventually lapses into a coma.

Is the measles vaccine safe and effective?

Getting the measles vaccine to prevent measles infection is generally safer than getting the measles infection itself. The measles vaccine is highly effective and like the infection itself, confers life-long protection for most people. However, one of the ways this is achieved is by using the actual measles virus but pre-treating it so that it is in a weakened (attenuated) form. For healthy children and adults, the vaccine will not cause the measles disease and therefore will prevent the various complications from occurring. However, because the virus is not killed, the vaccine is generally not advised for people whose immune systems are weakened or otherwise compromised.

The vaccine is highly effective. A single dose is 93 percent effective on average at preventing measles and a second dose increases effectiveness to 97 percent on average.

The following graph depicts the cases of measles in the U.S. before and after the measles vaccine was made available (1963):

For details on the safety of the measles vaccine, see https://www.cdc.gov/vaccine-safety/vaccines/mmr.html.