Previous month:
October 2021
Next month:
December 2021

November 2021

The Long Haul, Part 3: Long Neurological COVID

As I have noted before in this series, acute COVID-19 often appears with neurological symptoms ranging from loss of smell to severe depression to stuttering to brain fog, mania and psychosis. It sometimes has been linked to suicidal ideation. In addition, long haulers often have cognitive symptoms and structural brain changes similar to those seen in aging brains and in those with Alzheimer’s disease. An early survey of 153 COVID-19 patients in the UK and a more recent study of people hospitalized with the acute disease in Italy both found that about a third had neurological symptoms of some kind ranging from sensory problems, motor impairment, and cognitive issues that persist after clearing the acute infection. Other estimates of neuro involvement in long COVID have trended even higher. Many people who survived earlier coronavirus infections such as SARS and MERS also experienced neurological impairments up to 3.5 years after acute infection. Obviously many of these symptoms of long COVID are very serious while others are more annoyances. So, what is going on? Researchers have pretty well cataloged the unusual range of long COVID’s neurological symptoms and now are at the very early stages of understanding their causes and how to treat the problems. Here, I label long COVID that primarily manifests itself with neurological symptoms as “long neuro COVID” in order to distinguish it from other long COVID problems that primarily involve the lungs, heart, or other organs.

What is long neuro COVID like? In the early days of the pandemic, a newly minted English MD worked on the front lines in a COVID ward and soon became a patient herself. Being 35 and healthy she expected to quickly recover but underwent the long haul, which she has written about. The acute phase of the disease lasted about two weeks, but by 4-5 weeks, she was experiencing new persistent problems including tachycardia with a resting heart rate of 140 bpm (normal is 60-100) that would increase to 170 after minimal exertion such as getting a glass of water. She also was breathless with a resting respiratory rate of 20-24 (12-16 is normal), saying it felt like her “body forgot to breath.” She described cyclic bouts of pins and needles in all four extremities, and whole-body shaking as violent as if she were having a seizure. There were feelings of impending doom, and, despite extreme mental and physical exhaustion, she was unable to sleep, which eventually led to hallucinations. Those symptoms slowly subsided over a few months only to be replaced by intense pain very deep in one ear. This ultimately led to tinnitus and some hearing loss and a diagnosis of encephalitis. Ten months later, she wrote that  she was recovering but was far from normal. She suspected that these symptoms were driven by a dysfunctional autonomic nervous system, a condition called dysautonomia. The autonomic nervous system is what regulates your organs and allows you to breath, your heart to beat, your gut to move food through it, and controls your blood pressure without you having to think about it all. Since her experience in early 2020, it has been confirmed that long neuro COVID can wreak havoc with both the peripheral and central nervous systems.

 

After two years of long COVID, we now know that long neuro COVID symptoms are wide ranging; some are devastating, like stroke, encephalitis, and even psychosis or mania, or even suicide. Other neuro symptoms are more subtle such as cognitive decline, loss of smell, hearing loss, balance problems, fatigue, memory problems, and difficulty concentrating or brain fog. Others are bizarre, such as stuttering. This seemingly unrelated range of symptoms suggests that there might be several different subtypes of long neuro COVID, possibly arising from distinct pathologies.

Back in July 2020, one of the first studies was published describing neurological symptoms that appeared long after the initial COVID disease. This since has been followed by several other reports of neurological or neuropsychiatric problems long after recovering from acute COVID disease. One study by Oxford scientists published last February, found that about 33% of post-COVID patients are left with long term mental health or neurological symptoms including brain fog, headaches, dizziness, and cognitive problems such as difficulty doing simple math. Some studies have shown an elevated incidence of PTSD, and seizures or movement disorders  long after COVID recovery. Other post-COVID patients have new-onset depression, psychosis, and suicidal behavior as reported in JAMA Psychiatry by a Columbia University research team this past spring. In this large study investigators examined electronic health records of more than 236,000 COVID-19 patients, mostly in the US. The researchers compared their records with records from those who experienced non-COVID respiratory tract infections during the same time frame and found an increased incidence in anxiety and mood disorders in post-COVID patients. More than three months after diagnosis, these common psychiatric diagnoses were found in about 34% of COVID survivors. Other studies confirmed that having the disease led to doubled risk for anxiety, depression and sleep disorders.

Importantly, researchers did not see an increased incidence of other neurological problems such as Parkinson’s disease or Guillain-Barré syndrome in long COVID patients, both of which sometimes follow viral infection. This suggests that long neuro COVID involves a select subset of neurological problems rather than an indiscriminate neurological malady.

Similarities between long COVID and Alzheimer’s disease. The cognitive issues seen in many long neuro COVID patients share intriguing similarities with Alzheimer’s disease (AD) and normal aging. Thus, an international group of researchers found that more than half of patients 60 or older who had been infected with the CoV-2 virus showed acceleration of Alzheimer’s-like symptoms such as cognitive decline. Other researchers at the University of Texas Health Science Center, San Antonio studied more than 200 older adults from Argentina who had COVID-19. Those who had a persistent loss of smell were more likely to experience AD-like cognitive issues. Importantly, the area of the brain affected in AD overlaps with the area that processes smell. It also might be relevant that the sense of smell, which is often lost in COVID patients, is also often reduced in AD patients.

Three to six months after they were infected, more than half of these patients still struggled with AD-like cognitive challenges including persistent forgetfulness, difficulty sequencing tasks, and forgetting words and phrases. How sick a patient was with acute COVID-19 was not an indicator of whether they would experience this cognitive decline. In other words, AD-like symptoms also occurred in people who only had mild COVID.

COVID-19, of course begins as a respiratory disease and investigators have long been tuned in to the potential links between respiratory diseases and the brain. For example, AD-like changes in cognition and behavior were also observed in people with Severe Acute Respiratory Syndrome (SARS) and with Middle East Respiratory Syndrome (MERS). Infection with other respiratory viruses can also increase the risk of Alzheimer’s.

Together, these findings suggest that some patients with long neuro COVID might have an acceleration of Alzheimer’s-related symptoms and pathology, but it is too soon to conclude that long neuro COVID causes AD, or even that AD and COVID-related cognitive dysfunction are even related. A major distinction between classical AD and AD-like long COVID is that the latter do not show the amyloid brain plaques which are pathognomonic of AD, which suggests that these could be distinct cognitive maladies with overlapping symptoms. Furthermore, other studies showed that worse cognitive scores in long COVID patients correlated with patients who had lower oxygen saturation during a 6-minute walk test. This makes it possible that persistent oxygen deprivation in the brain due to lung compromise during COVID could cause cognitive difficulties in these patients.

At this point, these observations simply raise many unanswered questions on whether there is a real overlap with COVID and Alzheimer's disease. But, it is too soon to say that COVID-19 increases a person's risk for Alzheimer's vs causes a different neurological problem symptomatically related to AD.

What causes long neuro COVID? Long COVID represents a broad category of over 200, often unrelated symptoms encompassing 10 organ systems. It likely consists of multiple different maladies with manifold causes, of which long neuro COVID is at least one broad category. Based on its biology and range of symptoms, long neuro COVID also likely entails more than one specific problem. It makes sense then that the many different manifestations of long neuro COVID would arise from different causes. Such seems to be the case. Researchers have cataloged several genetic, structural, inflammatory, and infectious correlates to the various symptoms, painting a complicated picture. Then things get really confusing since viral infection of neurological tissues and/or the attendant inflammatory responses could cause the observed structural changes and all this could be predisposed or mitigated by genetics. In other words, things are as clear as mud right now about what causes long neuro COVID. Investigators are just now making basic observational correlates between the neurological changes and long neuro COVID symptoms, and these correlations will be followed by the harder studies to learn just how these changes might cause the plethora of symptoms that have been documented.

On the genetic front, a Stanford U team found that long neuro patients manifest widespread changes in gene expression in the region of the brain involved in complex processing of human thought. These genetic changes affected genetic pathways that play a role in mental illnesses such as schizophrenia and depression. Although these results were made in the brains of patients who died of acute COVID disease, such fundamental changes in gene expression in the brains of patients with acute COVID would plausibly lead to long-lasting post-COVID effects. Similar changes in gene expression were not found in the brains of people who died from flu or from nonviral causes, which strengthens a possible cause and effect relationship of gene expression changes to some long neuro COVID symptoms.

But, what causes changes in brain gene expression? Is it directly due to viral infection in the brain or secondarily due to the immune inflammatory response to the virus? Maybe both? Or is something else involved? Evidence exists for all these possibilities.

One report on 111 unvaccinated patients from the Chicago area showed that 56 who had long neuro COVID cognitive problems showed a particular immunological signature that was not found in people who cleared the acute infection without long term problems. The severity of cognitive deficits correlated with reduced memory T cell responses to certain parts of the virus, and with enhanced antibody (or B cell) responses to one of the viral proteins. Furthermore, it has been observed that females are more prone to devleop long neuro COVID. Since women also are more likely to get autoimmune disease, some have put these observations together to suggest that there might be an autoimmune component to some long neuro COVID symptoms.

The above study assessed the anti-CoV-2 immune responses of T and B cells from the peripheral blood but not from the brains of the patients. In other words, it did not address whether the immune response in the body affects brain function or whether an antiviral immune response directly occurs in the brain affecting cognitive function. Other researchers have shown that the virus can indeed enter the brain via the nose and spread from the olfactory lobe to the frontal and temporal lobes of the brain. Other confirmatory studies have found viral protein expression in cortical neurons of autopsied brain tissues, and have directly shown that the virus can infect neurons in tissue culture. While these findings are consistent with direct infection of the brain and the possibility of immunological damage to the organ, they do not settle the question of whether viral infection itself might directly damage the central nervous system, or whether it is the immune reaction to the virus that causes the problems.

Perhaps confounding all of this are the results of a large study on gross brain structure conducted by researchers at the University of Oxford and at the NIH. In this study, researchers used the UK Biobank, an existing database, which contains brain imaging data from >45,000 people in the UK going back to 2014. This means that there was pre-COVID baseline imaging data the researchers could compare to post-COVID brain images. New images were collected from 394 of these patients who caught COVID and compared to their pre-COVID images and to 388 controls who did not catch COVID-19. The groups were otherwise matched based on age, sex, common disease risk factors, etc. The results showed that those who caught COVID suffered significant loss of gray matter in the frontal and temporal lobes on the left side of the brain. This brain loss was found regardless of COVID disease severity. Those who were COVID-free had no brain tissue loss. Interestingly, these regions of the brain are responsible for smell, taste, memory, and emotion, all of which can be affected in long neuro COVID patients. We also often talk about the left temporal lobe in the context of aging and Alzheimer’s disease because that is where the hippocampus is located, which plays a key role in memory and other cognitive processes associated with aging and AD. While it is normal to see reduction in gray matter with age, the COVID-linked changes were greater than that typically seen during normal aging. All of this raises questions about how COVID might affect the natural aging process in the brain.

In addition to these genetic, immunological, and structural changes in the central nervous system of COVID patients, autopsies also have revealed clotting in multiple organs including the brains of many patients. About one in 50 COVID brains showed evidence for an ischemic stroke, which is when a blood clot interrupts blood flow to a region of the brain downstream from the clot. Ischemic strokes in COVID patients tended to be more severe and more likely to result in severe disability or death than stroke in non-COVID individuals. Again, while these findings were made on autopsies of patients suffering from acute COVID, these ischemic strokes would have caused long term manifestations presenting as long neuro COVID.

There are other, very specific and very peculiar neurological symptoms that might arise from more specific neurological abnormalities. For example, some long COVID patients display hearing loss and or balance problems which suggest vestibular involvement that could be due to CoV-2 infection of the inner ear. Scientists at MIT and Stanford found that the ACE2 protein, which is the cell receptor for the CoV-2 virus, is expressed on certain inner ear cells obtained from surgery patients. Since inner ear tissue is difficult to obtain, the researchers directed stem cells to develop into inner ear cell precursors or that could assemble into primitive inner ear  organoids in tissue culture and showed that the CoV-2 virus could infect them. Together, these observations support, but do not prove, that infection of the inner ear is a cause of hearing and balance issues in some long neuro COVID patients. It is relevant to note that it is not unusual for hearing loss and balance disorders to be caused by other viral infections of the inner ear.

Then there also are the rare long COVID patients who develop an odd stuttering problem. Typically, stuttering originates in the complex circuity of the brain that controls speech and this speech disruption usually appears when children are learning to talk. However, “neurogenic stuttering” can arise in adults after brain trauma. Since only a few researchers are investigating long COVID-associated stutter, the cause is not well understood, but, the link between neurogenic stuttering and brain injury raises the possibility that inflammation and/or micro-clotting caused by the virus or by the immune response to the virus in the brain microvasculature could lead to the neurological damage that causes stuttering.

Bottom line. These many new findings, while provocative, do not yet fully tell us how long neuro COVID arises, or how to treat it. But, they raise many new questions: What do these COVID-related brain changes mean for the process and pace of brain aging in long COVID patients? Over time does the brain recover? How do we medically deal with these patients? Can we prevent long neuro COVID? Etc.

Stay tuned, we will see.

Note: In order to have blog updates delivered to your email, see the simple Subscription Instructions here. Remember, you can easily unsubscribe when you want.


Lessons for COVID Vaccinations And Herd Immunity From Influenza And Rubella

Note: The following is modified from the blog post, “Rubella: We vaccinate for far less,” by Katelyn Jetelina, MPS, PhD who is an “epidemiologist, biostatistian, professor, researcher, wife, and mom of two little girls.” She writes a blog entitled, “Your Local Epidemiologist.”

 “Those who cannot learn from history are doomed to repeat it.”

 George Santayana

 

In the US, more than 300,000 kids aged 5-11 have been vaccinated with the Pfizer COVID-19 vaccine, which has proven that the vaccine is safe and can benefit some kids. It prevents infection, COVID-19 disease, death, long COVID-19, and keeps kids in school. Admittedly, only a few kids develop serious COVID disease and fewer have died from it. Most infected kids only have mild, if any, symptoms. Vaccine skeptics use this fact to stridently argue against childhood COVID vaccines. So, why are we pushing to vaccinate children who rarely get seriously ill?

There are two reasons why we vaccinate anyone. The first reason is to protect the vax recipient from the disease; this is an individual-level benefit of the vaccine. The second is to protect a larger population by trying to retard disease spread; this is a population-level benefit of vaccines that is better known as herd immunity.

But, anti-vaxers only focus on the fact that childhood vaccines provide little individual-level benefit to children and wholly ignore the larger population-level benefit of the vaccines. As I have written before, vaccinating children who are at low risk for serious disease is still very important for reducing viral spread in order to  prevent more dangerous viral mutants from emerging. It also is important for reducing infection and disease in more vulnerable people in the population. It is these population-level benefits that are the most important reason to vaccinate low-risk children. Vaccinating children for a population-level benefit, rather than for individual-level benefit, is not at all new and is a very acceptable practice. Here are a couple of examples.

Influenza: A few decades ago, Japan mandated flu vaccines for all school kids. That vaccine slowed the spread of flu in schools leading to many fewer student illnesses and absences. More significantly, vaccinating all school kids also caused a sharp drop in flu deaths in older people like school teachers and staff, parents, and grandparents who have close contact with the kids.

Kids are walking incubators for respiratory viruses and readily spread their germs to others. Infected children essentially are virus vectors much like mosquitoes are vectors for malaria and yellow fever. Therefore, in Japan, the flu vaccine effectively shut down a major vector of influenza infection for at-risk older people. That is an undeniable and important population-level benefit of vaccinating school kids against the flu.

Rubella: Now, let us take a deeper dive into rubella, or German measles, and its vaccine, which is the “R” in the MMR shot. It is especially enlightening to compare the natural history of rubella to what we are learning about COVID-19.

Both COVID and rubella are caused by airborne viruses that spread when infected people cough, sneeze, or even talk. As with COVID, rubella symptoms in children are quite mild. They include its tell-tale measles-like rash, sore throat, low grade fever, mild pink eye, and general discomfort. But, about 25 to 50% of infected children will not experience any symptoms. Likewise, many CoV-2 infected kids also do not develop symptoms. But, asymptomatic kids infected with either rubella or CoV-2 readily spread their viruses to friends and family; hence, they can be significant vectors delivering both viruses to people at-risk for serious disease.

Over the last two years, we have learned that COVID mostly (with significant exceptions) causes serious illness and death in older people or for those with certain other health conditions. Similarly, while rubella only causes mild disease in most children, it is incredibly dangerous for developing fetuses. A woman infected with rubella during the first 3 months of pregnancy has a 90% chance that the fetus either will not survive or will develop Congenital Rubella Syndrome (CRS), characterized by deafness, blindness, heart defects, and/or severe brain damage. In the early 1960s, a rubella outbreak began in Europe and spread to the US. In 1964-65 ~12.5 million total cases were reported in America affecting nearly 50,000 pregnancies. More than 11,000 of the infected mothers miscarried, or delivered still-born babies. Of the >20,000 infants born alive to infected mothers, the majority had severe illnesses: 2,100 died shortly after birth, 12,000 were deaf, 3,580 were blind, and 1,800 had permanent mental disabilities.

The rubella outbreak proved hard to contain because, as with COVID, infected asymptomatic people make it hard to know when someone is spreading the virus. Rubella also is just as contagious as COVID. Both viruses have an R0 = 6-7 meaning that each infected person will infect, on average, 6-7 other people. For comparison, flu’s R0 = 2-3, which means it is about half as contagious as the other two viruses. It, therefore, is not surprising that like rubella, the COVID outbreak is proving hard to contain.

Soon after the 1960s rubella pandemic began, a safe and effective vaccine was quickly developed and approved for use in Europe and North America (this is reminiscent of the quick development of the COVID vaccines). Early on, there was a robust international debate on who should get the rubella vaccine. There were two schools of thought:

  1. Despite the fact that rubella only caused mild problems in kids, some proposed vaccinating all children hoping to provide indirect population-level protection for pregnant women and their at-risk fetuses.
  2. Others argued that because children were only minimally affected they should not be subjected to the vaccine and that only women of childbearing age should be vaccinated. This, proponents argued, would more specifically protect those most at risk.

Ultimately, it was found that countries that chose #2 were not able to sufficiently reduce the virus, because it still spread unfettered among children. This strategy did not reduce the rates of CRS. Eventually, option #1, vaccinating low-risk children (like what we are moving toward with the COVID vaccine) was adopted world-wide. Vaccination rates of school kids reached ~85% in the US, which last experienced a serious rubella outbreak in 1995. In 2004, transmission of rubella was eliminated in the United States and in 2015, it was eliminated in all the countries of North and South America.

Soon, the MMR vaccination was mandated for children in all 50 states. It is important to realize that these mandates were not to protect kids from the mild disease but to protect the at-risk population, or fetuses. In other words, we vaccinate kids against rubella not so much to protect them, but to provide a significant population-level benefit to others.

Today, because of broad rubella vaccination of low-risk children, we see an annual average of just 10-15 cases of CRS in the US that are traced back to international travel to countries with poor rubella vaccination rates. In contrast, in countries with low vaccination rates, about 120,000 children are born each year with severe CRS birth defects and even more die in utero.

Bottom Line: This country, and indeed all of the Americas and most of Europe came together to eliminate endemic rubella through broad population-level vaccination programs targeting low-risk groups responsible for spreading the virus to the high risk population. Japan saw the same effect with influenza. They focused on broadly vaccinating a low-risk population (school kids) and saw great benefits in the high-risk older population. As we approach a broad COVID vaccination strategy that includes giving the shot to low-risk children, it very likely will have a population-level benefit and help protect those most at-risk for serious disease.

It is important to note that the population-benefit conferred by the COVID vaccine also applies to all of us and not just to children. When we are vaccinated, not only does it protect us, it also provides significant protection to at-risk people around us. That, in fact, is called “herd immunity.”

Note: In order to have blog updates delivered to your email, see the simple Subscription Instructions here. Remember, you can easily unsubscribe when you want.


The History Of Vaccine Mandates In The US

Note: In order to have blog updates delivered to your email, see the simple Subscription Instructions here. Remember, you can easily unsubscribe when you want.

As employers and the President are pushing vaccine mandates because too many have refused them, voices are crying out for their perceived rights saying “my body my choice.” They do not like their bosses or the government telling them to get vaccinated. This is a clash between individual rights and public health measures designed to save lives and to protect the larger community. Who gets to make the key decisions? How far can the government and employers go? Do individual rights trump community safety?

On Sept. 9, Biden announced the most sweeping vaccine requirements in American history, ordering that businesses with 100 or more employees ensure that all their workers are either vaccinated or get tested weekly for the coronavirus. The new rules also require vaccinations for federal workers and for federal contractors, as well as for workers at healthcare facilities that receive funding from Medicare and Medicaid. This will affect about 100 million people.

The authority for these government mandates, claims Biden, is a 1970 federal statute that gives the Secretary of Labor authority to issue a six month Emergency Temporary Standard (ETS) to protect workers from “grave danger from exposure to substances or agents determined to be toxic or physically harmful.” His move has triggered a political and legal battle, with many Republican governors vowing to fight the mandates in court. The mandates raise several new questions regarding this vague statute: Is a virus a “…toxic or physically harmful substance?” Does COVID-19 present a “grave danger?” Has the executive branch exceeded its authority in offering a solution to a problem previously reserved to the states? Do these mandates violate the 14th Amendment by depriving workers of their personal liberties? It is important to note that Biden’s mandates do not actually make vaccines compulsory: The government may levy a fine or forbid a child from attending school, but no American will be forced to get an unwanted jab. This has not always been the case.

There are historical precedents for vaccine mandates and even for forced vaccination.

In February 1991, five Philadelphia children died from measles, a disease that was mostly eradicated in the US, due to vaccination. Measles once sickened millions of kids, each year hospitalizing ~50,000 and killing close to 500 before a successful vaccine was developed in 1963. After that, cases dropped dramatically as all states mandated measles shots for school children. Vaccine hesitancy and resistance were rare because people saw the tangible success of the measles vaccine.

But, in Philadelphia that winter of 1991, the serious cases of measles came from a single source, a church cult that rejected “…all means of healing apart from God’s way.” Church members took no medicines, owned no thermometers, and saw no doctors. Rejecting all birth control, they raised large families in close quarters, a recipe for the measles epidemic, which they cooked. Trying to contain the threat to the rest of the city, officials worked through the courts to gain access to the homes of the congregants and received the authority to vaccinate the children against the wishes of their parents. In this public health emergency, defending the parents’ anti-vax actions was close to impossible. Even the ACLU took a pass.

Vaccine mandates even appeared during the Revolutionary War. George Washington mandated that all his troops be immunized against smallpox, even against their will. He described smallpox to Virginia’s Governor Patrick Henry as “more destructive to an Army in a Natural Way, than the Enemy’s Sword.” As I wrote earlier in these pages, smallpox had doomed the Colonial Army’s assault on Quebec in 1775, and it threatened Washington’s main force. Washington’s mandate proved a brilliant gambit and smallpox largely disappeared from the ranks. Some historians point to the mandate as a major factor in winning the war against the Brits.

During that war, smallpox vaccination entailed a primitive vaccination procedure known as variolation. That involved opening a lesion from an infected person and scraping its contents into the arm of a recipient. It was effective, but the vaccinated person became quite ill for a couple of weeks, and about 3% of them died from the pox. Later, in 1796, the English scientist Edward Jenner discovered a much safer method of immunization using cowpox, a virus similar to smallpox that did not cause significant disease in people. But the new smallpox vaccine got a mixed reception in the US as some resisted it for reasons of personal safety based on the variolation experience. They rationalized, “what good could possibly come from polluting the body with dangerous foreign matter?” Or, “Why challenge the plans of the Creator?” Still, Jenner’s vaccine was a clear improvement over variolation and drove a steady decline in smallpox outbreaks throughout the 19th century. States began passing laws mandating smallpox vaccinations for school children, and some forcibly vaccinated prisoners, paupers, and orphans.

In 1905, the issue of vaccine mandates reached the Supreme Court in the seminal case of Jacobson v. Massachusetts. Henning Jacobson, a Lutheran pastor in Cambridge had defied a city ordinance requiring smallpox vaccinations during an outbreak. He refused to pay a $5 fine so he was arrested. Jacobson posited that “healthy and law-abiding” people like himself (even though he was disobeying the law at the time) posed a minimal danger to the community. He argued that even if his refusal to be vaccinated led to him spreading the smallpox virus, the only victims would be others “who failed or refused to be vaccinated.” In other words, he reasoned that it would be ok to not get the vax because the vaxed would be safe, but wholly ignored the rights to safety of those who were not vaxed. 

It is an argument that is repeated today about the CoV-2 vax. Using modern science that was not available in the early 20th century, experts have repeatedly refuted this argument, explaining that many people who want the vax cannot be fully vaccinated because they are immunocompromised, or allergic to the vaccine’s contents, or do not have access to the vaccine. Also, we now know that the more RNA viruses, like the coronavirus, are allowed to spread, the greater the chance more deadly variants can appear. Jacobson’s contention that the decision to vaccinate solely belongs to the individual, not to the state, employers, or to medical authorities remains a central tenant of today's anti-vaxers.

The Supreme Court disagreed with Jacobson. The majority opinion, written by Justice John Marshall Harlan, asserted that “the liberty secured by the Constitution does not import an absolute right in each person to be at all times, and in all circumstances, wholly freed from restraint.” Rather, he argued, the Constitution rests upon “the fundamental principle of the social compact…that all shall be governed by certain laws for the protection, safety, prosperity and happiness of the people, and not for the profit, honor or private interests of any one man, family or class of men.” Jacobson had not only broken the law, the court suggested he also had violated the principle upon which a well-ordered society depends. We are not wholly independent the court ruled. The greater good of the community can trump individual rights.

Using Jacobson as precedent, the Supreme Court in 1922, upheld a local ordinance in San Antonio requiring proof of smallpox vaccination for people entering “public schools or other places of education.”  

Later, during World War II, the US military made vaccines mandatory for a host of diseases, such as typhoid, yellow fever and tetanus, and it still mandates certain vaccines for troops in certain deployments. Soon after the war very successful vaccines were developed against several childhood diseases like polio, measles, mumps and chickenpox. Guided by the Supreme Court’s ruling in Jacobson, all 50 states put laws on the books mandating many of these vaccinations for school children. Even today, many school districts and colleges mandate certain vaccines for students and staff. Hospitals, too, often mandate certain vaccines for their staff. Until lately, vaccine mandates have not generated much angst and anger.

Why is this? Perhaps vaccines have done their job too well: Many of them have erased the tragic evidence of why they were needed in the first place. The world no longer deals with small pox, thanks to the vaccine. Almost no one in this country has seen someone ravaged by polio, or a child hospitalized with measles, or who lost his hearing due to chicken pox, all thanks to vaccines. Yet, now with COVID-19, anti-vaccine anxieties have found their way into the political mainstream, especially among conservatives. An estimated 80 million American adults remain unvaccinated against COVID and represent potential factories for producing the next deadly coronavirus variant, which is very preventable.

As I have addressed before in these pages, many factors fuel resistance to the life-saving shots, including doubts about their quick development and their possible long-term effects. But a growing distrust of professional expertise, including medical science, has also played a role, which is unwarranted. Who are you going to believe, a medical scientist like me with nothing to gain in the debate (except the safety of my friends, family, and self), or someone who read a web post from folks who are selling nostrums they claim will protect you, like Dr. Steve Hotze, or from one of America’s Frontline Doctors whose web site claimed that gynecological problems were caused by having sex with demons? Do you jump on the side of those who tout that their individual freedoms have been abridged, but who do not consider the freedoms from disease of the greater community, and whom the courts already have decided against?

Almost 300 years ago, Benjamin Franklin struggled over whether to have his sons variolated against smallpox. In his “Autobiography,” he worried that well-meaning people were tragically misjudging the calculus between the risks and benefits of the procedure, as he had once done, with a tragic result. He wrote, “In 1736, I lost one of my sons, a fine boy of four years old, by the smallpox….I long regretted bitterly and still regret that I had not given it to him by inoculation. This I mention for the sake of the parents who omit that operation, on the supposition that they should never forgive themselves if a child died under it; my example showing that the regret may be the same either way, and that, therefore, the safer should be chosen.”