pandemic

What Happened To The Flu And Other Respiratory Diseases?

A NYC based travel blogger who travels a lot used to get a respiratory infection whenever she flew. That stopped when the airline mask mandates went into effect. The mandates, of course, were designed to hinder the spread of the CoV-2 virus that causes COVID, but it makes sense that if masks and other physical (that is, non-medical) mandates worked to mitigate COVID, then we would see a decrease in other contagious respiratory diseases after the mandates were, well…mandated.

We did.

The mandates worked, despite persistent claims of some to the contrary. This particular blog subject was stimulated by a radio talk show where a couple of nonscientist talking heads announced that there was no scientific proof that the masks or other mandates prevented disease. I previously posted in these pages evidence that masks, in particular, do indeed work to retard the spread of disease (see here, here, here, and here). In this post, I present further data on how the mandates significantly reduced the incidence of other infectious respiratory diseases around the world. If the measures can reduce flu, then you can bet that they also reduced COVID-19.

Note, however, that this is not necessarily an endorsement for returning to the measures. Your humble scribe didn’t much like his glasses fogging up, or having to make two trips from the car to the store because he forgot his mask. But, let’s argue the issue based on its merits and not from false premises based on incorrect claims.

After South Korea implemented various hygiene and social distancing measures in response to COVID, they saw the 2019-20 flu season end an astounding 12 weeks earlier than the previous year. Epidemiological surveillance data bolstered by clinical diagnostic testing showed that infection from several different pathogenic respiratory viruses (including adenovirus, bocavirus, metapneumovirus, rhinovirus, flu, parainfluenza, and respiratory syncytial virus) dropped to nearly 0% just five weeks into 2020!

In the United States, the incidence of infection by influenza, respiratory adenovirus, rhinovirus, enterovirus, RSV, non-COVID coronaviruses, metapneumovirus, and parainfluenza viruses all decreased in March 2020, soon after implementation of mandates. Similar results were seen in Japan.

More dramatically, since pandemic mitigation measures were put in place, there has been a 99% global reduction of infections from both influenza types A and B compared to prior years. In particular, one of two flu B substrains has not been isolated in the world since August 2021 suggesting that this variant is now extinct. The overall genetic diversity of influenza viruses has also dramatically diminished indicating that other flu sub-types (or clades) have disappeared around the world since the pandemic mandates were put in place.

And this reduction of respiratory infectious disease does not only hold for those caused by viruses. Another study looked at surveillance data from 26 countries across 6 continents for several bacterial diseases caused by Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis, which are typically transmitted via respiratory droplets. Numbers of weekly cases in 2020 were compared with corresponding data for 2018 and 2019. Data for disease due to Streptococcus agalactiae, a non-respiratory pathogen, were also collected from nine laboratories for comparison. All countries experienced a significant and sustained reduction in respiratory bacterial diseases in early 2020 (Jan 1 to May 31), coinciding with the introduction of non-medical COVID containment measures in each country. By contrast, the incidence of disease due to S agalactiae (which is not transmitted by the respiratory route) did not differ significantly from the 2 previous years.

Clearly, the mandates significantly reduced the incidence of respiratory infections by non-COVID viruses and bacteria. They worked. So, why did we still have COVID infections after the mandates went into place? The mandates reduced, not eliminated these diseases, so infections still happened. Since we did not have historical COVID infection data from previous years to compare with, the effects of the current mandates on the incidence of COVID are not as clear cut as they are with other diseases for which we do have historical data for comparison. But, as I wrote before (see above), it is clear that places in the US and around the world that used masks and other protective measures saw reduced incidence of COVID compared to similar places that did not.

Bottom line: The studies mentioned here regarding non-COVID infectious diseases fully support data previously posted in these pages that the mandates, including masks, are effective non-medical tools for controlling infectious respiratory diseases.

Don’t let anyone tell you differently.


Still More Evidence For An Animal Origin Of The Virus

Conspiracy buffs won’t like this, but compelling new evidence presented in three papers, which include photographic and DNA data, has pretty much nailed down the origin of the SARS-CoV-2 virus. It began in a wet market animal not in the lab eight miles away as the conspiracists have conjectured. This new data comes from an international team of scientists which concluded that the coronavirus twice jumped from  caged wild animals into people at the Huanan Seafood Wholesale Market in Wuhan. These data correlate nicely with previous geo-epidemiological data showing the market, not the lab, to be the infection nidus with later infections radiating out from there.

Despite the Chinese’s government denial that live animals were sold in the Wuhan market, the new studies provide photographic evidence of wild animals sitting in stacked cages in the market in late 2019, in or near stalls where scientists found SARS-CoV-2 virus on a number of surfaces, including on cages, carts and machines that process animals after they are slaughtered at the market. This, along with a new genetic analysis pinpoints a specific stall at the market where the virus passed from an animal into people. These data also estimate the time when not just one but two zoonotic spillovers occurred, once in late November or early December and then again few weeks later. This coincides almost exactly with the timing of the outbreak of disease at and around the market.

The two initial infection events involved slightly different versions of the SARS-CoV-2 virus. The fact that they were related is evidence that the virus had spread and mutated in animals in the market before it infected humans.

A leader of two of the studies was U of Arizona professor, Michael Worobey, a viral pandemic sleuth who has been at the forefront of the search for the origins of the bug responsible for the current pandemic. His lead in the research is significant since, back in May, 2021, Worobey, along with 17 other scientists, called for investigation into the lab-leak theory. His latest research overturned that conjecture. This new evidence adds to previous evidence for an animal/market origin of the virus presented earlier in these pages here and here.

Final thought. It is sobering to think how these two simple infection events that occurred in November and December of 2019 in a Chinese market triggered something that has now caused six million deaths and untold misery around the world. And it is not finished with us.

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Another Unexpected Pandemic Consequence: Undiagnosed Cancer

In these pages, your humble bloggeur (that would be me) has written about several unusual consequences of the COVID-19 pandemic. Most of these were on the ironically funny side, such as farmed fish being too large for restaurant plates, rattlesnakes climbing in plane landing gears, and the ketchup packet shortage. But, not all of these odd aftermaths of the pandemic are humorous. The topic of this post is very unfunny.

Lungs

It seems that as healthcare providers were swamped with COVID cases, or were at reduced capacity because staff became ill, or because service slowed in order to prevent CoV-2 spread, many people have missed routine medical care for non-COVID problems. It is feared that this will create a crisis in coming years involving increased diagnosis of cancers that were caught later than usual. As we deal with the fourth wave of COVID-19 caused by the Omicron variant, we are learning that the pandemic dramatically disrupted routine health screenings for cancer and other chronic diseases. Some now predict that the next crisis that could overwhelm the US health system will be a surge in advanced chronic diseases like cancer that went undiagnosed and untreated for too long.

Screenings for several major cancers and new cancer diagnoses fell significantly during 2020, according to a study published in December 2021 in the journal Cancer. This was not because there was less cancer in the world. It was because fewer patients were seeing their doctors.

A co-author of the Cancer study, and who is a professor at the University of Maryland School of Medicine, said that we have never before seen screening rates drop so dramatically in such a short time.

In one case, a Hispanic man in his 40s first noticed rectal bleeding in early 2020 that his doctor said was probably due to hemorrhoids. The man was unable to get a timely colonoscopy to rule out cancer because the local hospitals were overwhelmed with COVID-19 patients, and he also feared catching COVID if he went to a hospital swamped with COVID patients. Eighteen months later, he finally got a colonoscopy, which revealed advanced rectal cancer. Those 18 months likely were the difference between being cured by a simple polyp removal vs dealing with a cancer that had metastasized throughout his body.

At this point, nobody knows how many cases like this are out there. We will find out.  

This patient, as thousands of others like him, had the misfortune to notice symptoms that needed followup amid the biggest disruption of medical care in US history. In 2020, while hospitals curtailed services in order to prepare for the COVID surge, the number of colonoscopies plummeted 93 percent. By the end of the year, there had been 133,231 fewer colonoscopies performed compared to 2019. There also were 62,793 fewer chest CT scans, 49,334 fewer fecal blood tests, and prostate biopsies dropped 25%.

This drop in screenings has created a huge backlog that will take months to clear. A gastroenterologist at a small community hospital in the Middle-of-No-Where, Kansas was recruited by a larger hospital in Kansas City to do nothing but colonoscopies from 7 in the morning to “whenever at night.” They had a backlog of 1000 patients—a certain percentage of whom have cancer already growing in their colons while waiting to be told they had colon cancer. And that backlog begets a fresh one of new patients who also need to be scoped because they just noticed something like rectal bleeding, but will have to wait for those who have already been waiting.

This backlog creates a subtle form of medical rationing. It forces doctors to make hard choices about which patients to prioritize. "Lucky" are the serious patients who are moved to the head of the line. Not so lucky are those whose colonoscopies or mammograms or biopsies are then further delayed.

I would rather deal with rattlesnakes in my plane's landing gear or forgo mustard on my brat (which would be pushing the limit) than delay a needed medical test or procedure. It seems that your humble bloggeur (me again) has been caught in the backlog. I am scheduled to have an enlarged parathyroid gland removed next week, but COVID can still derail that. I won’t be certain that the surgery will happen until the day before I am to be operated on and that depends, in part, on everyone, including me, being COVID-free, and the OR not being diverted for use as a COVID ICU. If it proceeds as scheduled, I will have waited several months since the initial diagnosis for the surgery. An additional routine diagnostic test I need in order to determine how the fractious organ might have affected my bone health was scheduled six months out. Six months for a routine scan?


File This Under ‘Weird Pandemic Effects’: Decreased Incidence Of Lightning

If lightning is the anger of the gods, then the gods are concerned mostly about trees.”

- Lao Tzu

Yup, since the pandemic began, it appears that trees are safer. Thanks to the lockdowns, there is less lightning to strike them.

A study presented at the fall meeting of the American Geophysical Union (AGU) analyzed atmospheric factors that may have contributed to lightning reductions of 10-20%. 

It seems that atmospheric aerosols produced by burning fossil fuels were reduced because of pandemic lockdowns. Particles in these aerosols enhance the collection of water vapor, which causes clouds to form. And the more these particles absorb water they also reduce rain and, therefore, the creation of small ice crystals that collide in the clouds and build electrostatic charges that create lightning. So, fewer aerosol particles, less bumping and rubbing, less static and fewer zaps.

I have previously noted other weird effects of the pandemic such as farmed fish being too large for restaurant plates, rattle snakes in plane landing gears, and a dearth of ketchup and mustard condiment packages to go along with less lightning. What crazy thing will happen next—the Cincinnati Bengals win a playoff game?

Oh….wait a minute……..

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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.

+++

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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