pandemic

The Long Haul, Part 4: The Cost of Long COVID In Terms Of Individual Health And Quality Of Life

Surviving COVID-19 is one thing, recovering is another.

My frustration with those who would minimize the impact of COVID-19 is reaching an apex. I constantly have to deal with their baseless rationalizations that “it is just a cold,” or “it only kills 0.01% of people” (actually the number is 2% around the world), etc. And I constantly reply to these iconoclasts that COVID has become, by far, the leading killer in the US. I also explain over and over that treating simple mortality percentage as the only relevant statistic to consider is falderal. For example, the Spanish flu also killed “only” 2% of those infected, but in just 24 weeks, that virus killed more people around the world than were killed in WWI AND WWII together! The percent figure is meaningless without considering the percent of what. Why do they continue to ignore the devisor and, hence, the total number of deaths?

A small percentage of a very large number is, in fact, another large number.

Those who wish to downplay the significance of the pandemic only focus on this mortality percent, but mortality is NEVER the whole story for any pandemic. A serious person will also consider the morbidity caused by the disease. In fact, the major CDC publication on health in the US is called the Morbidity and Mortality Weekly Report. Notice that it considers both morbidity and mortality, and further notice that morbidity is listed first in the title. I have made three prior posts in this series on Long COVID, about the significant lasting morbidity of COVID-19. You can see these posts here, here, and here. In those posts, I shared data showing that some ~10-30% of COVID survivors suffer serious health problems that last months.

In those posts, I mentioned the cases of a young, healthy MD, and of a young, healthy journalist, both of whom struggled with long COVID, and how it affected their careers and cost them thousands of dollars in out-of-pocket expenses for the dozens of tests and doctors they needed. In an article in Maclean’s magazine, a reporter interviewed many Canadian long COVID patients and heard how their lives have been turned upside down. They reported that they are unable to live like they used to and care for their families, do anything mildly strenuous, or even cook their meals. They spend long stretches of time in bed. Many of those interviewed had not returned to work several weeks after recovering from the acute disease.

Anecdotes like these have been repeated millions of times around a world that, according to the Johns Hopkins University COVID tracker, has seen more than 330 million cases of COVID (and this is a significant undercount since many countries do not record these data well). Research has corroborated these anecdotes.

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Common long-term symptoms include debilitating fatigue; respiratory problems; and “brain fog.”  Other common symptoms include compromised function of the heart, and kidneys, which sometimes require transplantation. Wide-spread clotting problems can cause significant illness and even limb amputation. There also are frequent neurological and neuropsychiatric symptoms as highlighted in Part 3 of this series. Surprising manifestations continue to emerge, such as new-onset diabetes.

Lung scarring often occurs in patients who experienced COVID-caused acute respiratory distress syndrome (ARDS), a common problem seen in acute COVID patients who required ICU care. ARDS is a serious respiratory problem that can be caused by different respiratory viruses and other things. About a third of patients with ARDS arising from any cause were unemployed 5-years later because of their lung damage. It is fully expected that patients with COVID-related ARDS will be found to fare similarly.

There also is the dysfunctional immune response common in many moderate to severe COVID cases that can cause long-term multi-organ damage, particularly in the liver and kidneys. It can also disrupt coagulation control of the blood, sometimes leading to amputations, mostly in patients in their 30s and 40s. It was reported that amputations due to vascular problems have doubled since the CoV-2 virus arrived. Compromised coagulation control in COVID patients can also precipitate adverse cardiovascular events such as heart failure, or hemiplegia due to strokes. Data from the COVID Infection Survey on long-COVID suggest that the risk of major adverse cardiovascular events and long-term illness is about ten times higher in COVID patients (even after mild COVID) compared to non-COVID matched controls. A Dutch study found that 31% of COVID ICU patients suffered thrombotic complications. These problems can unexpectedly pop up in people who had completely recovered from COVID.

A global survey tallied 205 different symptoms across 10 different organ systems that can persist after COVID infection has cleared. Typically, these manifold long COVID symptoms do not appear in isolation, but in multi-symptom clusters. A long hauler typically has several of these problems at a time.

While it is estimated that overall, 10-30% of COVID patients become long haulers, reports on the number of people suffering long COVID vary widely. Depending on the report, anywhere from 30-90% of COVID survivors suffer long term health problems. And even at the lower end of that range, 30% of over 330 million people world-wide who have been infected is a very large number. It represents an enormous personal toll in terms of lost health and diminished quality of life. Some of these reports are summarized below.

  • Half of 70,000 hospitalized UK COVID-19 patients experienced long-term complications, according to a study published in July. Complications occurred regardless of age group: For instance, 25% of adults aged 19-29 developed complications, as did 33% of those aged 30-39. Complications affecting the kidneys and respiratory system, liver injury, anemia, and arrhythmia were the most common.
  • Many COVID-19 survivors require extensive and prolonged rehabilitation. An European study found about one-third of 1,837 non-hospitalized COVID patients (i.e., those with mild disease) needed a caregiver three months after their symptoms started.
  • In April the CDC reported in its Morbidity and Mortality Weekly Report that 69 percent of nonhospitalized adult COVID patients in Georgia required
  • one or more outpatient visits 28 to 180 days after their diagnosis.
  • A study published last February in the Journal of the American Medical Association found that roughly one-third of 177 people who had mild COVID disease not requiring hospitalization reported persistent symptoms and a decline in quality of life up to nine months after illness.
  • 70% of people hospitalized for COVID-19 in the UK had not fully recovered five months after hospital discharge. They averaged nine long COVID symptoms requiring continued medical care.
  • A study in South Korea found that 90% of patients who recovered from acute COVID experienced long-term side effects.
  • According to a report in the journal, Lancet, 75% of people hospitalized with COVID-19 in Wuhan early in the pandemic, reported continued problems with fatigue, weakness, sleep problems, anxiety and depression six months after being diagnosed with the disease. More than half also had persistent lung abnormalities.

Data like these have been commonly reported around the world, pointing to a more chronic and expensive health problem than seen with the flu or common cold, which often is caused by different coronaviruses. A July 2021 article in Scientific American talked about how all of this indicates that long COVID will cause a “tsunami of disability” that will affect individual lives as well as create enormous strain on the health system. Consider the numbers: More than 60 million Americans (this is an underestimate since many COVID cases are not reported) have been infected with the CoV-2 virus. Therefore, if only 30% of these suffer long COVID, we are talking about 20 million long haulers and counting.

The related health care and disability costs of all of this are also still being calculated. How many “long haulers” will not be able to return to work for months, or at all? How many will need short-term disability payments, and how many will become permanently dependent on disability programs? As increasing numbers of younger people become infected, will we see a generation of chronically ill? This then moves us to consider the economic and financial cost of long COVID, which will be the topic of the next installation in this series.

Stay tuned.

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Lions And Tigers And…Deer? Oh My!

First it was bats and humans, then domestic cats and dogs, farmed mink, and big zoo cats; now gorillas, hippos, and wild deer that have been infected by the SARS-CoV-2 (CoV-2 for short) virus. Many of these animals have become ill and several have died of COVID-19, most recently three snow leopards in South Dakota and Nebraska zoos. This is quite a wanton virus.

Of course, before CoV-2 and COVID-19 were known to the world, we knew that bats, humans and a few other animals, notably civets and even camels, were ready hosts of several different strains of “‘rona” viruses. We also knew that domesticated animals are also susceptible to their own coronavirus diseases—in fact veterinary coronavirus vaccines have been in use for years. Humans are known hosts for several coronaviruses, including those that cause the common cold, as well as the viruses that cause SARS, MERS, and now COVID-19. And we know that humans often catch these germs from bats and other intermediate hosts as diverse as civets and camels. After we genetically identified CoV-2 and were able to follow its spread, we quickly noticed that domestic pets also could be infected. This was closely followed with news that seven big cats at the Bronx zoo had become infected, and that mink farms across Europe were hotbeds for CoV-2 spread between humans and the animals and back. In fact, mink farms became such a hotbed of CoV-2 zoonotic spread that a couple of European countries completely shut down mink farming and culled all their animals. Several US states have also sharply curtailed mink farming. PETA probably applauds.

More recently two snow leopards at the Lincoln, NE children’s zoo and one in a zoo in South Dakota died from COVID. The Lincoln zoo also had two infected Sumatran tigers who recovered after being treated with steroids and antibiotics to prevent secondary infections and pneumonia. How the animals were infected is uncertain, but the most likely scenario is that they caught the virus from a caretaker. The problem is, none of the caretakers tested positive for the virus. Bats? Something else?

Since April 2020, when a tiger tested positive at the Bronx Zoo, dozens of other animals in zoos around the world have caught COVID. This month, the Denver Zoo reported the first coronavirus cases in hyenas, and the St. Louis Zoo found eight positive cases among its big cats, including two snow leopards. Abroad, the virus has killed a lion in India and two tiger cubs in Pakistan. Big cats seem especially susceptible since three other snow leopards at the Louisville Zoo were infected last December, and another snow leopard tested positive at the San Diego Zoo in July. The virus doesn’t just infect our fuzzy friends either; two hippos, named Imani and Hermien, at a zoo in Antwerp recently tested positive for COVID-19. Zoo keepers were first alerted to a potential problem when they noticed that the colossi had “runny noses.”  One reckons that a runny nose for a hippo is a big deal. One also wonders who gets to dab that nasal maw in order to test for the virus.

In fact, zoo and domestic animal infections have become so prevalent that an animal COVID vaccine developed by Zoetis, a NJ-based veterinary pharma company and former Pfizer subsidiary, has been authorized by the USDA for experimental use. The Cincinnati Zoo, for one, has vaccinated  80 animals, from giraffes to apes, against COVID.

Deer too. Oh my! It is one thing for zoo animals to acquire COVID—their captivity makes it easy to limit their interaction with other animals and humans to prevent spread of contagions, and they seldom complain that their rights are being infringed when they are quarantined. However, COVID in wild animals is a different story, as we have seen with bats and how easily they transmit the virus to humans. Scientists now have evidence that CoV-2 also readily propagates in white-tailed deer. In fact, the virus is already widespread in cervids across the US, which likely has significant implications for the long-term course of this pandemic.

In September of last year, genetic analysis of the gene that encodes the ACE2 protein (i.e., the viral receptors expressed on many cells in the body) in many different animal species suggested that CoV-2 could easily infect deer (and several other animals too). A survey of white-tailed deer in the Northeast and Midwest found that 40% had antibodies against the CoV-2 virus, indicating prior exposure. Between April and December 2020, veterinarians at Penn State found active CoV-2 infections in ~30% of deer tested across Iowa. Then during the winter COVID surge in humans from Nov. 23, 2020, to Jan. 10 of this year, ~80% of the tested deer were infected. The prevalence of the virus in deer was 50 to 100 times greater than in Iowa residents at the time (and the deer reportedly did not wear face masks). The study, published about two months ago, indicates that white-tailed deer have become a permanent reservoir for CoV-2. While it is not fully understood how the virus entered the deer population, genetic sequence analysis of nearly 100 viral samples found that the variants circulating in deer matched the variants circulating in people. This suggests that deer caught the virus from people multiple times in Iowa alone. How that happens is not known since people usually do not have close contact with live deer. More concerning is whether viral variants arising in deer readily pass back to people.

Bottom line. Clearly, a lot of different animal species can catch Cov-2 and spread it. It is clear that people can spread coronaviruses to pets and other animals, but the FDA says that the reverse, animal-to-human virus transmission, is not common. But, it clearly happens as we have seen with this pandemic, and with many other viruses that cause SARS, MERS, AIDS, Ebola, flu, etc., that spread from animals to humans. The prevalence of CoV-2 infection in so many species of mammals, especially in animals that have close contact with humans, suggests that several animal species, not just bats, can serve as permanent reservoirs for the virus and the jump to humans is something that can happen over and over. This is not unprecedented. It is what we see with influenza, which is carried back and forth between the Northern and Southern hemispheres with migratory birds, in which different flu viruses shuffle their genomes to create the new strains of flu for which we have to vaccinate against each year. This animal reservoir for flu makes it next to impossible to eliminate influenza, and similar animal hosts for CoV-2 likely would make it nigh impossible to eliminate COVID too. I raised this specter some months ago in these pages when reporting that pet dogs and cats can carry the virus. Our furry friends represent a viral reservoir that is in even closer contact with people than bats, deer, and fortunately, hippos and leopards.

We also have to be worried about the CoV-2 virus mutating in the different animal species that harbor and spread it. We know that happens in bats, which makes it almost certain that new strains of the virus will arise in deer and dogs too. We have already seen this on mink farms in the Netherlands and Poland. Farmworkers passed the virus to captive animals where it spread, mutated, and then spilled back into humans. In fact, zoonotic transmission from animals to humans probably happens thousands of times a year. Researchers from the EcoHealth Alliance and from Duke-NUS Medical School in Singapore, estimate that each year many people are newly infected with SARS-related coronaviruses. Many may get sick, but there are many reasons why most of these infections never grow into noticeable outbreaks (for example see my earlier blog post about unusual respiratory infection clusters in China and Los Angeles just before COVID). The researchers also created a detailed map of Asian habitats of 23 bat species known to harbor SARS-related coronaviruses then overlaid it with data on where humans live to create a map of potential infection hot spots. They found that close to 500 million people live in areas where bat-to-human transfer is likely, and this risk is highest in southern China, Vietnam, Cambodia, and Indonesia. Other surveys done before COVID-19 showed that many people in Southeast Asia harbor antibodies against other SARS-related coronaviruses. Blending these data with data on how often people encounter bats and how long antibodies remain in the blood, the researchers calculated that ~400,000 undetected human infections with these viruses occur each year across the region.

That is just for bat-to-human transfer in Southern Asia. It now looks like we will have to also concern ourselves with zoonotic coronavirus transfer from Buddy and Bambi too.

For this reason, researchers are working to develop a universal coronavirus vaccine that will be effective against most viral strains and variants. I will write about this soon. Stay tuned.

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Clue: Dr Mustard In The Parlor With A Hypodermic

In earlier posts, I noted odd and unexpected effects of the pandemic. These included farmed fish growing too large for restaurant plates, Denmark culling all its mink from mink farms, a shortage of individual condiment packets, and a problem with rattlesnakes in the landing gear of mothballed commercial planes.

And now this.

The Associated Press just reported that there has been a surge in in-home pet euthanasia services because of the pandemic. Companies, such as Pet Loss at Home, or Lap of Love, offer home pet euthanasia services because the pandemic has led to restrictions on people inside vet clinics and hospitals, meaning that pets would have to be put down without their human companions present. By offering house-call euthanasia, the pet’s family members can be present for the depressing deed and say goodbye to their furry friend. In non-pandemic times, the animals would be put to sleep in a vet clinic with family members present. But, these are pandemic times.

Although it has been well documented that house pets can catch CoV-2, viral infection is not what is driving the calls for home euthanasia. Rather, these home pet deaths are being driven by normal pet maladies such as cancer, lymphoma, kidney disease, etc. The owners just want some way to be with their chums at the end.

Who can blame them?


The Long Haul, Part 2: What Is Long COVID?

In the 1890s one of the biggest pandemics in recorded history, known then as the “Russian flu”, swept the world and killed one million people (for perspective, that is out of a world population about ¼ of today’s population). That “flu” is now thought to have been a novel coronavirus. Like the current coronavirus, SARS-CoV-2, the Russian “flu” was a new human pathogen so few people had any natural immunity to it and it was quite lethal. Not only that, but as the pandemic waned, it left in its wake a global wave of long-lasting neurological problems in the survivors. A similar long-lasting post-acute disease wave followed the next big pandemic, the “Spanish” flu of 1918 (which really was due to the influenza virus). The common symptom following the Spanish flu was lethargy so bad that in Tanganyika (modern-day Tanzania), for example, it caused a famine because people were too debilitated to pick the harvest. Other viral outbreaks, including SARS, MERS, and Ebola, also have been associated with long-term sequelae in survivors. However, today’s long COVID complications are far more common and far more variable than the persistent symptoms following these other viral pandemics. The variety of unrelated long COVID symptoms has flummoxed doctors hard pressed to diagnose and, hence, treat the constellation of chronic problems that appear in each patient.

As I wrote in Part 1 of this series, a wave of what has become known as “long COVID” is emerging in many people who have recovered from the acute disease. A recent review chronicling the effects of long COVID reported that “long haulers” commonly experience fatigue, sleep problems, and joint and muscle pain long after their bodies cleared the virus. Other symptoms range from the mundane to the bizarre: brain fog, shortness of breath, fatigue, tremors, tooth loss, racing heart, glaucoma, and diabetes among others. Long haulers are also at a significantly increased risk of dying months after infection. A large study found that after surviving acute COVID-19, patients had a 59% increased risk of dying within six months after their initial diagnosis. This translates into an extra eight deaths per 1000 patients. Thus, the consequences of the acute disease itself are just the tip of the iceberg.

Because the official definition of the chronic problem is fluid, we are still learning what this new malady is. A UK study published last December simply defined the syndrome as a collection of symptoms lasting for more than 28 days after initial diagnosis. However, another British study as well as Britain’s National Institute for Health and Care Excellence vaguely and broadly define long COVID as “signs and symptoms that develop during or after an infection consistent with COVID-19, and that continue for more than 12 weeks and are not explained by an alternative diagnosis”. It does not specify a list of what the symptoms are.

But, there are many. A global survey tallied 205 different symptoms across 10 different organ systems that can persist after COVID infection has cleared, including those affecting the heart, lungs, gastrointestinal system, muscles, and joints. There also are frequent neurological and neuropsychiatric symptoms as highlighted in Part 1 of this series. A sufferer typically has several of these problems at a time (14 different symptoms on average), with the most debilitating usually being one of three: severe breathlessness, fatigue, or “brain fog”. Other common symptoms included compromised function of the lungs, heart, and kidneys sometimes requiring transplantation. There also have been skin rashes, and newly diagnosed diabetes.

What exactly is long COVID? About the only thing we can say with any certitude at this time is that long COVID exists but is not easy to describe, possibly because it really is more than one malady. The only constant between different long COVID patients with different symptoms is that the conditions are a collection of varied symptoms that persist long after the acute disease subsides, which sounds as vague as the British definitions described above. Long COVID clearly represents a new health malady or maladies since it is not generally found in uninfected people, but is common in COVID survivors; yet not all COVID patients experience it. Long COVID can affect any post-COVID patient at any age, but it mostly presents in middle-aged people and seems to slightly prefer women. Even people with asymptomatic CoV-2 infection can have late arising effects that fit the profile of long COVID.  Multiple studies have shown that infected people who do not get acutely ill can still show irregular lung scans, for example. One such study found that nearly 60% of people with asymptomatic infection showed some lung inflammation in CT scans. Other studies have shown that young people with asymptomatic or mild infections can have long lasting cardiac issues, while others show signs of small blood vessel damage.

Some of these symptoms can be similar to other recognized, if not fully understood chronic problems, such as chronic fatigue syndrome (CFS), which is one of the most common complaints that long haulers have. CFS remains a mystery malady with an unknown cause, but it often follows a viral or bacterial infection. It is, therefore, possible that long-COVID CFS-like problems might be no different from classic CFS. It also is possible that CFS-like long COVID symptoms are not at all related to what is recognized as classic CFS, and they are simply different illnesses with similar symptoms. Time and research will tell.

Broadly speaking, there are three types of long COVID patients, according to one NIH scientist. The first are generally characterized by “exercise intolerance”, meaning they feel out of breath and exhausted from even mild physical activity. The second are characterized by cognitive complaints like brain fog and/or memory problems. The third type experiences problems with the autonomic nervous system, which controls things like heartbeat, breathing and digestion. Patients in this group suffer from symptoms such as heart palpitations and dizziness. Impairments of the autonomic nervous system are known as dysautonomia, which is an umbrella term for a variety of syndromes. Physicians treating long-COVID patients say there has been a marked increase in dysautonomia since the pandemic began. A rehabilitation doctor at Mount Sinai Hospital, in New York, says that roughly 80% of people who show up at his long COVID clinic have dysautonomia of one type or another.

Not only do long COVID patients suffer chronic debilitation, they also are at increased risk of dying. One of the largest studies of Covid-19 “long haulers” found that COVID survivors had a 59% increased risk of dying within six months after contracting the SARS-CoV-2 virus. The excess mortality translates into about 8 extra deaths per 1,000 patients. Thus, the pandemic’s hidden toll is that many patients require readmission, and some die, weeks after the viral infection abates.

What causes long COVID? What causes the myriad of symptoms lumped under the long COVID umbrella are being studied, but it seems that not all are actually caused by the CoV-2 virus. Based on what we have gleaned from observations of a few million long COVID patients around the world, the focus is on three possible biological explanations. One is that long COVID is due to a persistent viral infection. A second possible cause could be an autoimmune disorder. The third possibility is that it is a lingering consequence of tissue damage caused by inflammation during the initial, acute infection.

Supporting the first hypothesis that the infection persists even after COVID disease has passed is that some patients very slowly clear the virus completely. The virus or its remnants persist along with the long lasting symptoms. These patients are not infectious so it could be that they harbor some altered form or fragment of the bug which does not replicate, but is nevertheless making some viral product that their bodies are responding to. This is known to occur with other viruses, including measles, dengue and Ebola. RNA viruses are particularly prone to this phenomenon, and CoV-2 is an RNA virus. Direct proof of this hypothesis is lacking, but pertinent clues abound. A study published recently in Nature showed that some people had traces of CoV-2 proteins in their intestines four months after they had recovered from acute COVID-19. Viral products from CoV-2 have also been found in people’s urine several months after their recovery. All this is circumstantial evidence, to be sure, but viral persistence is consistent with long COVID in certain patients.

The second hypothesis, that long COVID is an autoimmune disease, holds that the virus causes something to go awry with the immune system inciting it to attack some of the body’s own tissues. Some evidence backs this idea, too. The immune system is a complex, tightly regulated machine designed to discriminate between your own cells and foreign entities such as viruses. Sometimes this ability to distinguish self from non-self fails and an immune response is generated to one’s own tissues. Some patients suffering from long COVID have badly behaving macrophages, which are immune cells responsible for gobbling up foreign invaders and displaying them to immune cells inciting them to make antibodies or to kill infected cells. Other long COVID patients exhibit abnormal activation of their B-cells, which churn out antibodies against the pathogen that can sometimes cross-react with the body’s own cells causing complications. Since antibodies circulate for several months after an infection, it makes sense that this could cause problems months after recovery from the disease. Again, this evidence is circumstantial, but consistent with the observations in some long haulers.

The third hypothesis about the cause of long COVID holds that the body’s inflammatory response during the acute illness causes long-term damage to cells and tissues leading to chronic inflammation. This sometimes happens with other viral diseases, but it could be particularly likely with COVID-19 since out-of-control inflammation, caused by a cytokine “storm” is a common hallmark of severe cases of acute illness. One guess is that the inflammation damages parts of the autonomic nervous system, or that the virus might damage the cells that line blood vessels, either by infecting them directly and/or via inflammation from the immune response. This could change the way blood flows to the brain and other organs, and may thus explain the brain fog and other organ failure that is sometimes seen. This too remains circumstantial, but consistent with current observations in certain patients.

Bottom line: Long COVID probably embraces several different chronic conditions with different causes. Studies to investigate each of these possibilities are under way.

We will see.


Delta: It is always better to prevent than to treat!

Previously in these pages I wrote that it was important to vaccinate kids as well as all adults, even though kids generally do not get very sick from CoV-2 infection. I also opined that it was important to get vaccines to third-world Asian and African countries that lack them. I further lamented the inability of one of the world’s leading vaccine manufacturing countries, India, to vaccinate its own population. The common reason for these exhortations in separate blog posts was the need to suppress the spread of the virus as much as possible, which I submit is just as important as protecting people from COVID-19 disease. We need to try to suppress the emergence of new viral variants since they could be more deadly and even cause significant disease in younger, healthier people. Such variants could also learn to ignore vaccine immunity and set us back to square one fighting the pandemic. As viruses replicate, they make random genetic mistakes in copying themselves. By chance, some of those mistakes can potentially make the virus more infectious or deadly. It is crucial to slow virus spread as much as possible with vaccines and social distancing measures in order to reduce the chance of such new, more deadly variants developing.

At this juncture, let me introduce the Delta variant and say, “I told you.”

Delta is more infectious. The Delta variant was first detected in October 2020 in India during that country’s long, strict shutdown. As I earlier reported, it then exploded across the country after those restrictions were lifted the following March in time for huge national  election rallies and a major religious holiday that brought hordes of Hindu worshippers to the banks of the Ganges. Delta quickly overtook previous iterations of the virus in India and has now spread to more than 100 countries, meaning that it has a significant advantage over other variants in the race to infect people. Delta was first detected in the U.S. in March and by mid-July accounted for 83% of all U.S. cases. As of the end of July, the Delta variant had caused at least 92% of the new infections in the United States, according to covariants.org, a research firm in Bern, Switzerland. The Johns Hopkins University tracker reported that daily US COVID-19 cases rose from just over 13,000 at the end of June to almost 131,000 in mid-August. almost all of which are due to Delta.

Delta has kept some of the most successful mutations found in earlier variants that first appeared in England and South Africa, but it also contains new genetic changes that, together, enable it to spread faster. In an earlier blog post, I talked about the R0 value, or the measure of a virus’s ability to spread. For seasonal flu, R0 is about 2, meaning that on average, an infected person will infect two others. For the original SARS-CoV-2, R0 was ~4, which means that on average, an infected person infected four others. Now, according to the CDC, the Delta variant has an R0 of 8-9 meaning that an infected person will, on average, pass the virus to 8-9 others. Therefore, Delta is about 4-times as contagious as the virus first identified in Wuhan. Clearly, viral variants are trending toward increased ability to spread. We can expect that the virus is not finished evolving and could become even more contagious.

How do the mutations make Delta more infectious? Research now shows that Delta has an incubation period of four days, which is the time it takes to begin spreading after infection. The original virus incubated for six days. Thus, people are becoming contagious sooner. Also, people infected with Delta are found to carry >1200-times the viral load compared to prior virus iterations. People carrying more virus pump more virus into their environment making them more infectious. With earlier variants, conventional wisdom held that you needed to be around an infected person for about 15 minutes in order to catch an infectious load of the virus. That wisdom now holds that one only needs to be in the presence of a Delta-infected person for 1-5 minutes before becoming infected. 

Some vaccinated people can also be infected and spread Delta. With any viral vaccine, the hope is that the vax will not only prevent disease, but also retard the spread of the virus, ideally reducing its R0 value to <1. When an infected person only spreads the virus to fewer than one other person, the epidemic/pandemic would be nipped in the bud. So far, the vaccines have done a pretty good job reducing the spread of the virus; however, the Washington Post recently obtained an internal CDC document  citing a combination of recently obtained data from outbreak investigations and other studies showing that vaccinated individuals can sometimes be infected with Delta and transmit the virus as easily as those who are unvaccinated.

The data showed that vaccinated people infected with Delta sometimes had viral loads similar to infected and unvaccinated people. These data came from a July 4 outbreak in Provincetown, MA where 127 vaccinated people were infected with the Delta variant in the superspreader outbreak and they appeared to carry as much virus as unvaccinated people who also became infected. Vaccinated people with breakthrough infections only showed mild symptoms including cough, headache, sore throat, or fever. Four were hospitalized and no deaths were reported. On July 3, the day before the event, the Massachusetts Department of Public Health reported a two-week average of zero COVID-19 cases per 100,000 residents. By July 17, after the superspreader event, that number rose to 177 daily cases per 100,000. The ability of Delta to infect some vaccinated people and spread from them has been further confirmed by research published by Public Health England.

This is the reason why the CDC just recommended that all people, including vaccinated people, again don face masks when in public indoor spaces. Fortunately, the virus does not cause significant disease in this population meaning that the vaccines still protect from serious disease.

So far.

Vaccine efficacy. The CDC reports that even though the current vaccines do not fully protect against breakthrough infections, such infections only occur in about 0.1% of the 140 million vaccinated people and they still reduce the risk of severe disease 10-fold and they still reduce the risk of breakthrough infection three-fold. That is the good news.

The disappointing news is that real-world studies of vaccine efficacy indicates that the current vaccines have become somewhat less effective at preventing infection from the Delta variant than they were against earlier versions of the virus. One way to measure a virus’s ability to evade vaccines is to take antibodies from vaccinated patients and combine them with the virus in the lab, then measure how much of the virus is neutralized, or prevented from infecting cultured human cells. Dr. Akiko Iwasaki, an immunologist at Yale University, and colleagues used this technique to compare how well different coronavirus variants can withstand vaccine immunity. Iwasaki found that Delta was better at evading neutralization than earlier versions of the virus. More concerning, however, is that they also found that two other variants, Beta, first found in South Africa, and Gamma, from Brazil, were even more adept at avoiding antibody neutralization. It appears that viral mutations are being gradually selected for their ability to bypass the immunity conferred by the current vaccines. That trend is worrisome.

Other reports coming in now indicate that the early vaccine efficacy of ~95% has dropped to 70-80%. This value represents the protection a vaccinated person can expect when exposed to the virus. The increase in the number of vaccinated people who become infected suggests either that that their immunity is fading over time, or that, as mentioned above, Delta is learning how to avoid vaccine immunity. Or both. As I wrote earlier, the initial antibody response to a vaccine naturally decays over time but immunity is usually sustained via memory immune cells which serve as quick-response sentinels to subsequent exposure to the pathogen. Memory immune cells were found in another study to be robust six months following mRNA vaccination and able to efficiently respond to the known viral variants. This indicates that long-term immunity remains strong and suggests that Delta has begun to learn how to avoid vaccine immunity.

Stay tuned.

Severity of Delta disease. In India, the Delta variant caused more severe and faster illness than earlier variants, and now in the US, Delta also seems to more readily cause significant disease and do so in younger people. Currently, teens 16-17 years old are now seeing the highest rate of COVID-19 cases among all age groups in the US. That is up from a rate of 48 per 100,000 on July 10, to 200 per 100,000 people on August 14. As Delta now accounts for >95% of new COVID-19 infections and hospitalizations in the US, doctors on the front lines are reporting anecdotally that unvaccinated people in their 20s and 30s are becoming more critically ill, and faster than they did before Delta arrived. Studies in a handful of other countries confirm that Delta causes more severe disease in younger people. For example, a study in Scotland reported that patients infected with Delta ran twice the risk of needing hospitalization. Researchers in Canada confirmed this and reported that young people infected with Delta had a 4-fold increased risk of requiring ICU care and double the risk of death. Other studies out of Singapore and India further corroborated these observations.

The emergence and rise of a viral variant with enhanced infectability and increased morbidity in younger, healthier patients is a prediction I and others have made in the face of the continuing global spread of this virus.

I told you so.

What does it all mean? Breakthrough infections we are now seeing in vaccinated people could be especially worrisome. The immunity conferred by vaccination usually retards viral spread and reduced viral replication scales down the development of new, more virulent viral variants. But, when immunized people do get infected and the virus grows in their bodies, the virus has to fight the vaccine immunity to eventually develop new mutations that allow the virus to simply brush off vaccine immunity. With Delta, we might be seeing the early stage of this viral evolution in vaxed people.

Vaccine resistance by the virus can be prevented by a rapid and robust vaccination effort as a team of European scientists recently reported in the journal Nature. It is imperative to get vaccines to countries that remain largely unvaccinated, and we need to get the naysayers in countries with more robust vaccine efforts to understand how their actions perpetuate the pandemic and promote the development of dangerous variants. There is no rational reason for the vast majority of people to refuse vaccination. The ongoing pandemic is totally preventable.

Vaccines have eradicated small pox in the world and polio from most developed countries. Measles is now extremely rare in the US thanks to vaccines. Go to an old cemetery and count the number of headstones belonging to children who died before 1950, then compare that to the number of kids who died after 1950. That striking difference is a powerful testimony to the effectiveness of vaccines as preventive medicine.

It is always better to prevent than to treat!

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A Critical Federal Vaccine Mandate

In response to the viral pandemic, the military ordered all service personnel to receive a controversial vaccine against the virus. The edict also prohibits military families and other civilians who live in high virus transmission areas from entering military bases. Furthermore, military personnel suspected of having contact with infected people are ordered to quarantine. All this was met with stiff opposition from many troops, from certain States, and even from Congress.

COVID-19 in 2021? 

No. Smallpox in 1777.

In 1777 facing an outbreak of smallpox that threatened his troops’ combat readiness, General George Washington ordered that all troops in the Continental Army be inoculated against smallpox. At the time, vaccination against smallpox was quite rare and not widely known. It involved a procedure known as variolation, where a small amount of pus from an active smallpox blister was scratched into the arm of a recipient. The low dose of the smallpox “pathogen” (the world did not know about viruses at that time) would, hopefully, just make the person sick and not kill him while conferring resistance to future smallpox exposure. Variolation was quite controversial and was even prohibited in Washington’s home state, Virginia. Variolation, in fact, did kill a relative of the King George of England. The relative was given too high a dose of pus and developed a full blown case of lethal smallpox. Many others also died from the procedure, hence the controversy.

When the revolution began, the Continentals faced not only the British military, but also the highly contagious smallpox virus carried by European troops coming from England and Germany. Europeans were well exposed to the disease where many survived and had protective immunity. Smallpox was relatively unknown in the Colonies so the colonists did not have that level of protection, and part of Washington’s genius was to realize that. As European troops arrived in Boston and New York, the virus spread through those cities and as the troops deployed, the disease threatened to run rampant through the colonies, potentially decimating the country and the Continental Army.

Washington, who survived smallpox as a child, was somewhat familiar with the rare practice of variolation, which was brought to England from Constantinople in 1721 by Lady Mary Wortley Montagu. By ordering it for his troops, despite stiff opposition from the Continental Congress, he acted as perhaps the country’s first public health advocate and averted a potentially disastrous epidemic among his troops.

After the battles of Lexington and Concord, the Continental Army encamped across the Charles River from Boston, which was stricken with smallpox from the arriving British soldiers. Washington prohibited anyone from Boston from entering his camps. He also swiftly quarantined anyone suspected of being infected, which was perhaps the first example of contact tracing. Washington’s actions were very heady stuff for the pre-epidemiology, pre-infectious disease era.

Washington did not immediately order variolation since he knew that the significant side effects of the procedure would temporarily incapacitate the troops who would take a few weeks to recover. Instead, he waited until the fighting subsided and both sides took a breather. Then he ordered the vaccinations against the wishes of the Continental Congress which initially forbade army surgeons from performing variolation.  Washington first ordered that all new recruits undergo the procedure believing that they would be healthy by the time they were battle ready and when the war was battle was ready for them.

Washington’s prescience was soon proven. Several thousand Continental troops marched on Quebec under Major General John Thomas who refused to follow Washington’s vaccination orders. He, and one-third of his 10,000 soldiers died from the pox and the force was soundly defeated.

Washington then moved to inoculate his main army and by 1777, 40,000 soldiers had been vaccinated in defiance of Congress. Infection rates in the Continental Army dropped from 20% to 1% and, after seeing these results, lawmakers soon repealed bans on variolation across the Colonies. One historian claims that Washington’s decision to inoculate his troops “…was the most important strategic decision of his military career.”

That radical decision could be a big reason why we do not today have the Union Jack flying over these 50 colonies. I find all of this to be an amazing, but little known fact about the American Revolution. Variolation might have been as important to the Colonists’ victory as was the French Navy finally showing up at Yorktown.

Immunology rocks as much as French naval cannons!

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Snakes On A Plane: Another Weird Pandemic Effect

In these pages, I have commented on some unexpected consequences of the pandemic, to wit: With reduced restaurant business, farmed fish are not selling and the fish are getting too big for the restaurants to buy--a vicious circle. And with the switch from sit-down dining to take-out, there has been a run on ketchup packets, creating an expensive secondary market for the packets on ebay. Now we learn that as a result of the pandemic, planes are having a problem with snakes—rattlesnakes to be precise.

Since the start of the pandemic, thousands of planes from airlines around the world have been grounded in hot, arid deserts, which are ideal for long-term aircraft storage. Australian airline, Qantas, stored about a dozen of its A380 superjumbos in an airfield near Victorville, in California's Mojave Desert. It is an area well known for feisty rattlers who love to curl up around the warm rubber tires and in the aircraft wheels and brakes. The maintenance workers use a low-tech solution, giving each plane its own designated 'wheel whacker' as part of the engineering kit, complete with the aircraft's registration number written on it. The whacker is a repurposed broom handle.

Prior to any landing gear inspections, the workers walk around the plane whacking the wheels and landing gear with the broom stick to scare off any slumbering snakes. Some scorpions have also been rousted.

It takes more than 100 man-hours to make a wide-body aircraft airworthy after storage—now they have to add a few more minutes for “whacking” the tires and landing gear.

It puts a new meaning on “check your luggage.”


What Caused India’s Devastating Second Wave?

Understanding what contributed to a second, more intense COVID-19 surge in India can inform the rest of the world on how to avoid a similar surge for this and future pathogens. This outbreak threatens to extend the pandemic itself and drive world-wide infections to new highs, creating an enormous a breeding ground for new and potentially more dangerous viral variants. If variants emerge that are not touched by the current vaccines, the world will be at square one with the pandemic. What a depressing thought.

It appears that the second wave arose due to a combination of three things: 1) India’s relaxing quarantine measures back in January, 2) the emergence of more rapidly spreading viral variants, including one that first appeared in India, and 3) a very poor rollout of vaccines to protect India’s population from spread of the virus. These are further discussed below.

  1. Relaxed safety measures. India’s second surge came after loosening restrictions, which let public complacency set in, which, in turn, was exacerbated by government officials like Prime Minister Modi and Health Minister Harsh Vardhan declaring that the pandemic was defeated. Life returned to normal. Masks went away, as did social-distancing. Weddings and parties resumed, which usually are large events in India. A new season of state-level elections ushered in big political rallies and street parades. A massive religious festival known as the Kumbh Mela took place, bringing an estimated 5 million Hindu pilgrims to the banks of the river Ganges in April. By mid-March, cases started gradually climbing again—then suddenly accelerated, becoming a vertical line rather than an upward sloping curve. The government was slow to respond. It was not until late April that Modi finally acknowledged the urgency of the situation. Local containment measures are beginning to be enacted, including shutting down the capitol of Dehli, and a few Indian states. However, Modi remains reluctant to enact country-wide restrictions like he did during the first wave. Without a more aggressive vaccine campaign, that could be a bad decision.

The more the virus spreads throughout India, and even into its neighboring countries of Nepal, Pakistan, and Bangladesh, the greater the risk that it will generate more infectious and dangerous viral variants that will not be affected by the current vaccines. If that happens, well vaccinated countries will have to start over. That is not a pleasant prospect, and is further discussed below.

  1. More infectious viral variants. India’s more deadly second wave of the CoV-2 virus can also be attributed to more infectious and more persistent viral variants. In this second wave, India, like many other countries, has been inundated with viral variants first identified in the UK and South Africa that were recently discussed in these pages. The UK variant has a mutation in its spike protein that makes it more infectious than its parent virus. The South African variant has a different mutation in its spike protein that makes the virus more resistant to some vaccines.

India’s second surge also has introduced the world to a unique viral variant dubbed the "double mutant," which was first identified in October. It is now the dominant strain in the state of Maharashtra, home to India’s financial center, Mumbai.

“Double mutant” is actually a misnomer for this variant since it has 13 mutations throughout its genome. However, it acquired that sobriquet because it has joined the UK and South African spike protein mutations in the same virus. It is a double whammy.

While scientists are still learning about the double mutant variant, India is seeing people who were previously infected become re-infected with this new variant. Also, younger and healthier people are being hospitalized in greater numbers. These observations are concerning. Similar observations of re-infection have also been seen in Brazil with yet another viral variant that was first identified there (more about Brazil in a future post). The ability of viral variants to re-infect people can be an important driver of future pandemic waves even in countries where the population is well vaccinated, but where isolation measures have been lifted or ignored.

For the country overall, the double mutant virus made up 70.4% of the samples collected during the week ending March 25, and that is compared with 16.1% just three weeks earlier, according to Covid CG, a tracking tool from the Broad Institute of MIT and Harvard. The tool mines data from the GISAID Initiative, a global database for coronavirus genomes. These data also show that the double mutant virus has already hopped to at least 21 countries including the US. In Australia viral genome sequencing showed that the double mutant made up 40% of the samples collected over the week ending April 15, compared with 16.7% a month earlier. It accounted for 66.7% of samples from New Zealand for the week that ended April 8, up from 20% a month ago. It also has been detected in California, according to Dr. Benjamin Pinsky, director of the Clinical Virology Laboratory at Stanford University. Clearly, where the double mutant virus appears, it quickly achieves dominance.

  1. Poor vaccine distribution. As of 4/30, India had only administered 15 million vaccinations, a tiny proportion of its population of 1.4 billion people. The country is the primary producer of the AstraZeneca vaccine that has run into supply chain problems causing delays in vaccine delivery. In February, Biden signed the Defense Production Act to boost U.S. COVID-19 vaccine production but that decision cut off US exports of raw materials that India needs in order to maintain its vaccine production capabilities. Thus, vaccine makers around the world, including the Serum Institute of India (SII), the largest vaccine manufacturer in the world, face a shortage of materials to make COVID-19 vaccines. The ban has garnered much criticism as resource hoarding that threatens global vaccine production. On April 16, SII appealed directly to Biden to lift the embargo of raw material exports so that vaccine production could continue. Several days later, the White House announced it would partially lift the ban for materials the Indian company needed to manufacture the AstraZeneca vaccine, specifically.

The US also inexplicably has a large stockpile of millions of doses of the AstraZeneca vaccine, that were made here, even though it is not approved for use in the US. If we are not using it, why not release the stores to the world? The Biden administration also has faced criticism for hoarding these doses that could help India and other countries around the world that also are experiencing a new surge in infections. On Friday, April 30th, the U.S. Chamber of Commerce called on Biden release the AstraZeneca vaccines to India and other hard-hit countries.

There is some irony in all of this since India is a huge manufacturer of vaccines and pharmaceuticals for the world, and likes to bill itself as the “pharmacy of the world.” India produces 60 percent of the world’s vaccines, but cannot supply its own country, partly because of reduced production due to the supply chain problems, but also because it failed to order sufficient vaccine doses. India almost completely halted vaccine exports last month in order to divert supplies to its domestic population, which is affecting supply in the rest of the world. Rather than rely on its own manufacturers for vaccines, India approved Russia’s Sputnik vaccine, and has fast-tracked the approval process for other vaccines manufactured in foreign countries. That means that while the industrialized world was being vaccinated with vaccines produced in India, the country was still looking at approving foreign-made vaccines for use in its country.

Bottom line. The combination of relaxed safety protocols, the appearance of deadlier viral variants, and poor distribution of vaccines to its people has left the country as the world’s epicenter for the pandemic. As the virus races through its huge population, all of this provides an enormous breeding ground for new variants to arise, which is worrisome even for countries that have had successful vaccine rollouts and have begun to see reduced viral spread. Let us hope this is not a perfect storm for restarting the pandemic with vaccine-resistant variants.

And India is not the only problem. In Africa, vaccination is also off to a slow start. Just 6m doses have been administered in sub-Saharan Africa, fewer than in New Jersey. Just 1% of African adults have received a first jab, versus a global average of 13%. Prepare for Africa to become the next hot-spot and breeding ground for troublesome variants, if Brazil and South America do not beat them to the punch.

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The Coronavirus Condiment Conundrum

The vexing thing about a novel pathogen and its attendant disease is that we expect it to behave like earlier pathogens and maladies we have experienced. But, sometimes historic diseases poorly predict the new problems that novel pathogens can raise. One such unexpected fallout from the current coronavirus pandemic was that farmed fish were getting too big for restaurant plates as discussed earlier in these pages. Now, the current pandemic has us facing another unpredicted conundrum, a critical shortage of ketchup packets!

CNN recently reported that restaurants have descended into a mad search for ketchup packets. One Denver tavern owner admitted to purloining ketchup packets from nearby McDonald’s and Wendy’s fast food franchises in order to meet his customers’ needs. Adding to his emergency, the tavern is across from Coors Field, to which the baseball All Star Game has been moved, thanks to Georgia’s new voter reform laws. As a 30+ year Wisconsinite (or “Sconnie” for short) and, thereby somewhat expert in brats, and hot dogs, I offer a suggestion to reduce this ketchup shortage--never, ever put ketchup on brats or hot dogs. Mustard is the proper condiment for these tubes of tasty processed meat. Admittedly, if everyone took this advice it could cause a deficit of that tangy yellow or brown topping and add to our COVID misery. There is nothing sadder than a bare brat, unless it is one slathered with ketchup. Folks in Chicago likely agree. Have you ever seen a Chicago dog with ketchup? It will have a luminescent green relish, but never ketchup.

This shortage of ketchup packets began last summer when the CDC began discouraging dine-in service at sit-down restaurants and encouraging delivery and takeout instead. Sit-down restaurants coast-to-coast began packing food for people who expected condiment packages with their meals. Suddenly, this packet packing by formerly traditional restaurants competed with fast food places for ketchup packets. As a result, demand went up, prices increased, and supply went down for those little 1/3 ounce packets. That is called economics.

In response, Heinz, the biggest ketchup producer in the country, just days ago announced it was increasing production of ketchup packets to 12 billion a year. A condiment Warp Speed?

This ketchup shortage also has fueled an underground market for the old packets you might have hoarded in a kitchen or desk drawer, or baked in your car’s glove box or under the seats. Entrepreneurial diners with a cache of ketchup packets are selling their treasures on eBay and Facebook Marketplace. One Indianapolis entrepreneur sold 20 Heinz ketchup packets for $8 shortly after the Wall Street Journal reported on the ketchup shortage. This too is called economics.

While all this reflects entrepreneurial principles, it is not exactly an efficient market. The prices in dozens of ketchup-packet listings posted online ranged from a quarter to $5 per packet. The latter was offered in a lot of 20 packets for $100. On eBay a week ago, an acupuncturist from NY posted “Assorted Ketchup packets for Apocalypse Survival,” with a starting bid of 99 cents for three packets. They soon were up to $11.50. Who knew ketchup was essential during an apocalypse?

What is next--a shortage of relish, mayo, and mustard packets? Maybe sugar and fake-sugar packages? It might not be too late to begin stocking up on condiments in case of an apocalypse. Make sure to store your bounty in a secure place, maybe along with your toilet paper and hand sanitizer.

Amazingly, people fret about vaccine safety during this ketchup shortage. Who ever heard of a vaccine protecting anyone from an apocalypse?

Is it time for lunch?


Paying The Piper

In the face of a pandemic caused by a new and deadly virus, states and local governments enact social-distancing measures, bans on crowds, closure orders, and mask mandates in an effort to flatten the curve and prevent health care systems from being overwhelmed with critically infected people. Initially, people are fairly compliant with the order, but, as the days of restriction turn into weeks, then months, compliance wanes. Theater owners complain about financial losses. Clergy bemoan church closures. People argue whether children are safer in classrooms or at home, and many rebel at having to wear face masks in public, complaining that the government has no right to infringe on their civil liberties. Sound familiar?

But this is not about the 2020-21 coronavirus pandemic; these are descriptions of the US response to the deadly Spanish flu pandemic between 1918 and 1920. In many ways our current pandemic mirrors the one that occurred a century ago, and that is presciently described in the book, The Great Influenza, by John M. Barry. Like CoV-2, the H1N1 “Spanish” flu killed less than 1% of the people it infected, but during a third wave of infection with a more virulent strain, that flu killed more people around the world in just 24 weeks than were killed in the 10 years of WWI and WWII combined! In remote areas with little access to health care, the flu wiped out entire villages.

Like COVID-19, the Spanish flu pandemic hit hard and fast, going from a handful of reported cases in a few cities to a nationwide outbreak within a few weeks, then with increased mobility due to WWI, it quickly spread around the world, from America to Europe and back. Many communities, responding to the ebbs and flows of the epidemic waves, issued several rounds of closure in an attempt to keep the disease in check. These social-distancing orders worked to reduce cases and deaths. However, just as today, they often proved difficult to maintain. By the late autumn of 1918, just weeks after wide-spread social-distancing orders went into effect, the pandemic seemed to be coming to an end as the number of new infections declined. People clamored to return to their normal lives. Businesses pressed officials to be allowed to reopen. Believing the pandemic was waning, some state and local authorities began rescinding public health edicts. Sound familiar?

Americans hurried to return to their pre-pandemic routines. In some cities, they packed into movie theaters and dance halls, crowded into stores and shops, and gathered with friends and family for holidays and celebrations. Meanwhile, officials warned the nation that cases and deaths likely would continue for months to come, but the warnings fell on increasingly deaf ears, as people enjoyed a return to normalcy. The nation carried on, inured to the toll the pandemic was taking. But as health officials warned, the pandemic wore on, stretching into a third deadly wave that lasted through the spring of 1919, with a fourth wave hitting in the winter of 1920. Some blamed those world-wide resurgences on careless Americans.

The different responses and experiences of two large American cities are noteworthy here. In Denver, local business interests lobbied heavily to get rid of the quarantine measures that had shut down schools, churches, libraries, pool halls, businesses, and theaters. The city capitulated. The city opened up and was hammered by the deadly third wave of the flu. On Armistice Day, November 11, 1918, residents poured out of their homes to celebrate the end of World War I. A few days later, many were dead, victims of the pandemic flu. Two weeks later, a headline in the Denver Post captured the devastation: “All Flu Records Smashed in Denver in Last 24 Hours.”  An editorial in the Denver Monthly Magazine said, “For some reason, even the most enlightened citizens will not take the influenza epidemic seriously. They know that it is the most widespread epidemic that has ever visited America. They know the disease is a deadly menace and snuffs out life almost before the victim realizes he is ill. Yet when health officers try to impress upon people the necessity of following essential rules and regulations, the average citizen simply refuses to heed these admonitions.”

In contrast to Denver, St. Louis enacted and maintained strong social distancing measures, including in-home quarantines for infected people. They experienced a fraction of the deaths that Denver saw. The quarantine measures worked there.

The similarities in our responses to the 1919-20 flu and 2020-? coronavirus pandemics are noteworthy. But, there is one big, hopefully defining difference between the two pandemics that might make the outcomes quite different. Vaccines. There were no flu vaccines to rescue the world from the ravages of the Spanish flu. In fact, the influenza virus would not even be discovered for another 15 years, and a vaccine was not available until 1945. For the first 12 or so months of the current coronavirus pandemic, we were in the same boat—we faced a novel virus with no vaccine or effective medicine. When there is no available medical response to a pathogen, we must rely on protective public health measures to provide a buffer against the pathogen while we learn how to respond to it.

Today, we have significant advantages with a much better understanding of virology and epidemiology then we did in 1918. We know that both social distancing and masking work to help save lives. Most critically, we now have multiple safe and effective anti-CoV-2 vaccines that are being deployed, with the pace of vaccinations increasingly weekly.

Still, the deadly third wave of influenza shows what can happen when people prematurely relax their guard against viruses that can mutate and become more deadly. That is why we must remain vigilant while the coronavirus vaccines roll out. We are still learning about this virus and are only beginning to learn about the variants spawned by the virus. We still need a public health buffer from the virus to keep us safe until we better understand its full capabilities and can vaccinate more people.

Be smart. Stay safe. Get the vaccine.