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My First Blog Post

What is this blog, who should read it and what will you get?

Be yourself; Everyone else is already taken.

— Oscar Wilde.

This is the first post on my new blog. I’m just getting this new blog going, so stay tuned for more. Subscribe below to get notified when I post new updates.

What is this blog about?

I cover important current national and state-level issues in health care – particularly health care policy and health care law. Because of the nature of the topics I cover, they are at the intersection of health care and politics.

Why is this blog important?

Unfortunately, sources of information about these important issues are often biased, come with a particular political point of view or are written or sponsored by industry interests. Of course, I have biases of my own, but I also have the ability to present an issue objectively and discuss the pros and cons of all sides of the issue so that readers can make an educated opinion on the issue for themselves. I believe that if you give readers balanced and complete information, they will be able to engage in the discussion productively and come to well-informed opinions and solutions.

Of course, there are few issues in health care that I do not have an opinion about, and there are many who, because of my background and experience, want to know how I come out on a particular issue. I will share those opinions with you on the blog, but I will be clear and explicit with you when I am expressing my own view. You can then take it for what its worth.

Who is this blog for?

Really, any one with an interest in topical health care policy and legal issues. However, there are some who may have a particular interest in this blog:

  1. Health care CEOs. Health care leaders are very busy and barraged with information. They simply cannot read everything, and much of what they get is not completely objective. This is a site where CEOs can get up-to-date, important information on topics of importance to health care leaders that they can trust. As a recently retired health system CEO, I know what information CEOs need, and there are few other sources of information written by a CEO for CEOs. This is also a source of information that CEOs can use to provide important updates to their teams and their boards.
  2. Board members of hospitals, health systems, insurance companies and other health care organizations. Health care is complicated. It is particularly challenging for board members who come from other industries to understand the complexities of health care. This blog can serve to keep board members informed about important issues that their companies are likely dealing with, as well as to keep them informed as friends, family, neighbors and colleagues ask them about these topical issues since they are likely aware that they serve on a health care board.
  3. Students and other health care leaders. Students of health care will appreciate how complex issues are presented in an easy to understand blog. Current and future health care leaders need a good source of current information, but also a source that may challenge their thinking or help them think about current health care challenges in a fresh and new way.
  4. Journalists. Health care reporters and journalists can at times be challenged to get the information and background that will really help them understand a complex issue that they must digest in very little time in order to hit deadlines and to ask interviewees the “right” questions. This blog will help them do just that.
  5. Legislators. Legislators have a tough job. They have to make law about complex issues in areas of industry that they may not be expert in. To make matters worse, they are often inundated by parties and lobbyists that are interested in what is best for their business, not necessarily what is best for that state or our country. This is an unbiased source of information to help legislators understand these complex issues and the pros and cons of various positions.

Who am I and why should you trust what I have to write?

I am a physician, board certified in Internal Medicine. I practiced for ten years. I am also a health care attorney. I have taught a course titled Regulation of Health Care Professionals for about 13 years, first at the University of Houston Law Center and most recently at the University of Idaho College of Law. I have also written a text book by the same title.

I was the CEO of a large teaching hospital in the Texas Medical Center for almost four years and most recently, I was the President and CEO of a health system for a little over ten years. That health system was recognized for being a national leader in quality and for its transformation of its business model from fee for service to value (full risk arrangements).

While a health system CEO, I had a blog for about 8 years – Dr. Pate’s Prescription for Change.

How often will I post new information?

I am going to try to write something weekly. I am not going to commit to a specific day. There may be times that I miss a week. There will be others will I will post something more frequently, especially when there is breaking news. So, be sure that you are subscribed to the blog so that you receive notice when I have a new blog post. You can also follow me on twitter. I will tweet my new blog posts. My current twitter handle is @drpatestlukes, but I will be creating a new twitter handle soon given my impending retirement from St. Luke’s Health System. I will let you know as soon as that new twitter account is set up.

Is it Safe to Fly on Commercial Airlines?

I have been asked this more than once. And, I don’t actually know the answer, because I don’t know of any good studies that address this question. There is little debate that in some cases, there do appear to be infections that can be traced back to flights. But, I have no idea how many and exactly what any particular person’s risk is. However, this doesn’t help people who have to make decisions about travel in the next couple of months, so I will at least share with you what my own decision is and why.

Personally, I will not be flying for at least the next six months. Why?

  1. Cases of new COVID infections are increasing in the majority of the US states and in many of the countries that I might be attracted to as tourist destinations and that others might be likely to travel to for business.
  2. I believe that cases are going to continue to increase over this fall and winter, and in fact, may be worse than anything we have seen so far. Why? We are seeing a confluence of new epidemiologic risk factors – more K-12 schools opening every week with in-person classes, colleges and universities holding classes in-person, the resumption of sports, the re-opening of bars, more and more examples of large gatherings in defiance of public health recommendations (and many infections from extended family get togethers, neighborhood bbqs, weddings, etc.), the movement of gatherings indoors due to air quality in the western US or due to colder weather, the upcoming cold and flu season, the projections that at least 90 percent of Americans remain vulnerable to infection and the increasing evidence that the D614G mutation, which is more contagious, is likely the predominant SARS-CoV-2 strain in the US and Europe.
  3. The reason that 1 and 2 above are so important to my analysis is that the greater the number of cases in the community, the greater the odds that you will encounter one or more infected persons during your travel – the taxi or ride-sharing service to the airport or from the airport to your final destination, the shuttle bus or train between terminals or to or from parking lots, the hotel you will be staying at, etc.
  4. In my personal observations, it seems that people may be more likely to stay home from work sick than they are to cancel travel plans. I recall vividly a flight last year where the person across the aisle and one row back was coughing incessantly during the flight. Two days later, guess what? Yes, I had a nasty cold with an annoying and persistent cough!
  5. While airplanes do generally seem to have excellent air circulation, air exchanges and filtration, that is during flight. Probably all of us can remember boarding flights when it was hot outside and desperately fiddling with the air flow control valve above your head trying to get some cold air only to find out that the engines are not on fully and the air conditioning system will not turn fully on until beginning the take-off process.
  6. When up in the air, people will be taking their masks off to drink, snack and eat meals. There is also the issue of someone taking their mask off and then falling asleep or someone taking it off and refusing to put it back on. Are the flight attendants going to awaken the passenger in order to have them put their mask back on? Are flight attendants going to insist that a passenger wear their mask if they refuse? Certainly, we have seen many businesses that require the wearing of masks, but do not enforce it in the store.
  7. One must consider all the associated activities with any event. So, while the actual flight may or may not be safe, does the airport require everyone to wear masks at all times? Is there physical distancing at security? At baggage claim? At the taxi or ride-sharing stand? At the gate? During the boarding process?
  8. During the time I practiced medicine, I had patients get ill while out of state. Arranging care under those circumstances can be less than optimal, but generally doable. On the other hand, I have had patients get ill over seas and this is far more complicated.
  9. Lastly, given my concerns about significant increases in cases this fall and winter, one does have to consider the actions various states may take (travel restrictions or quarantining requirements) and restrictions the US or other countries might put in place that might require you to quarantine or might interfere with your ability to travel.

So, for all these reasons, I do not intend to travel for at least the next six months. Others might come to different conclusions, and of course, that is their prerogative. It is merely my hope that these factors may be helpful to you as you think through the risk/benefits of travel for you and your loved ones and make your own decisions in the next few months. If you do decide to travel, be extra careful about your adherence to all the safety precautions we have been promoting to reduce your chance of being infected. And, if you do become ill before your flight, please do everyone a favor and stay home!

Reopening Schools Safely

I have been an outspoken critic of school boards making decisions to reopen schools for in-person classes in areas with high degrees of community spread of COVID without giving due consideration to public health advice and medical input and without articulating their reasoning when choosing not to follow this advice.

I do appreciate that the decision about whether to reopen schools entails more considerations than only medical ones. That is the reason that I have stated publicly that doctors should not be the ones to make these decisions.

But, if the board’s decision is to open schools for in-person classes against the public health advice, then, as Dr. Jim Souza, Chief Medical Officer for St. Luke’s Health System told a number of the boards, the likelihood of success will be directly related to the strength of their schools’ operating plans.

I totally agree. I believe that the schools with very well-thought-out operational plans with clear responsibilities and accountabilities will be the ones with the best shot of keeping infections under control and preventing an outbreak. Because if there is significant community spread, these schools will have cases, almost certainly during the very first week of school, and very possibly the first day.

While this is great advice, the few operational plans I have seen at the school board level have not qualified as the kind of well-thought-out, detailed operational plans that I think about, nor what I suspect Dr. Souza had in mind. I realized that the boards were likely expecting the individual schools to come up with more detailed plans, but I felt very sorry for those principals and teachers, few of whom, if any, have public health, infection control, or virology expertise.

Certainly, the schools have access to the excellent guidance put out by the CDC and the state public health departments, but seldom is that guidance understandable to these education professionals in terms of the application to the specific circumstances and challenges they face in operating a school.

So, in an effort to help, I have volunteered my assistance to schools that want a review of their operational plans and suggestions as to how to improve them, and then further offered to do walk-throughs to identify issues that you really can’t be aware of until you see the facility and hear what normally happens from the principal and teachers who work there. In addition, it gives me an opportunity to answer the many questions teachers have. I should point out that this blog piece is about K-12 schools. Colleges and universities have many more and, in many cases, different issues and concerns.

The following may be of interest to schools that have not yet re-opened. My hope is that what I have advised the schools that have taken me up on my offer may be of help to you in strengthening your own plans and that my framework for doing the walk-throughs might enable you to do think about issues that I raise on those walk-throughs.

So, the first step when a school does ask for my help is to ask them to send me a copy of their operational plan. This allows me to look through, identify elements that are not up to date or correct and identify missing elements. I then mark the plan up, return it to them for their review and they can accept whichever of my changes and suggestions they like.

What I often find is that the plans usually offer very little detail. The plans often include guidance from public health authorities, but the plans seldom indicate how that guidance will be applied in the setting of school, how often it will be done, whose responsibility it is to do it, and how it will be accomplished in settings outside of the classroom. (I’ll provide examples below in my discussion of the walk-throughs). The detail is important, because this is likely to be the biggest factor in whether you have contained, isolated infections or an outbreak in the school.

I also find that the plans generally have little information on informing teachers, students and parents on necessary preparations before they show up for the first day of class; education of teachers, staff, parents and students about COVID and their responsibilities under the operational plan; a detailed communications plan; and the safety precautions that need to be implemented on the school grounds before a student even enters the door of the school.

Finally, I seldom see the amount of detail necessary to address non-classroom activities safely – physical education, choir, band, cheerleading, athletics, cafeteria, etc.

With this said, let me state that I think the schools that I have reviewed did a really amazing job at putting these plans together. They are educators and not public health experts, and to have done what they did shows a tremendous amount of thought and care. But, the critiques I have made are a reflection that to create a really good plan requires the partnership of educators who know how things happen in the school and the issues they face everyday with public health or medical experts who can offer fresh eyes and identify areas of risk that are less likely to occur to non-medical experts.

So then, with my comments in hand, the school can decide if they want to do a walk-through. If so, I generally ask the principal, a note-taker, the building maintenance expert, a classroom teacher and each of the teachers of the non-classroom areas – PE, music, coaching staff, etc. – to meet with me outside the front door to the school.

We start off with a discussion of what is going to undermine the success of the plan? For example, if the plan has not been well communicated to everyone who has a role in the plan, then there is little chance the plan will be successful. Has the plan been circulated? Is the plan easily available? Does everyone understand it? Do teachers have incentives to come to school sick – e.g., loss of pay, lack of availability of substitute teachers? Do parents have incentives to send their children to school sick – e.g., consequences under the attendance policy, inability for the student to keep up on their school work from home, challenges accessing or paying for a doctor’s visit and note to return to school?

Then we move on to what are the issues and concerns on school day, before students even enter the front door. How early can students arrive? If there is a significant amount of time students could be on campus without oversight, we could have problems. This could result in congregating outside in close proximity without masks on and children seeing their friends that they may not have seen in six months. There may be hugging, high-fiving, and all kinds of high-risk interactions. As I told one school, you have a great plan for when students are in the classroom, but they may end up being infected in the parking lot before they even walk through the front door.

We then need to discuss how students arrive. Will they come by bus or by car? Buses pose threats of their own. Buses generally do not have as good of air circulation as we would like, so we need all students and the driver in masks, extra distancing and the windows open when weather permits.

There is also the question as to whether the school is going to do temperature checks and/or symptom screening. Some argue against this because only a minority of children have fevers and/or symptoms when infected with COVID. Thier concern is that teachers and others may develop a false sense of security or complacency if they know the children have passed the temperature screening and/or symptom screening. My position is different. First, even if we only identify a few cases this way, it is worth it to keep them out of the school building. Second, with cold and flu season coming, we are not just screening for COVID, but also colds and influenza. We don’t want any of that in the school because all are contagious and we seldom can tell these conditions apart without testing, so I would argue we should do everything we can to keep everyone who is ill, including those who may not realize it yet, out of the school and from contact with others. Finally, I think it is easy enough to educate teachers that they should assume that every person they interact with at school is potentially contagious, and temperature and symptom screening has only identified some of those who pose a risk.

Here is what the largest study to date of signs and symptoms of COVID in children showed us:

  • 30% will have a temp >100.4
    • 39% will have a temp 99.5 – 100.4%
    • 22% of kids will be truly asymptomatic
    • 8.5% will be symptomatic with characteristic symptoms.
    • 66.2% have symptoms, but not those that are commonly recognized as COVID.
    • 25.4% of kids developed symptoms after diagnosis.
    • Kids that were symptomatic were symptomatic from 1 – 36 days. (61% still symptomatic at 1 week; 38% at 14 days; 10% at 21 days)
      • 60% had respiratory symptoms – cough, rhinorrhea
      • 18% had gastrointestinal symptoms – abdominal pain, diarrhea
      • 16% had loss of taste or smell

So, the reason I go into this at this point is that ideally, we want to screen children if we are going to screen them before they get on the bus and before they get out of the parent’s car. Obviously, once the kid is handed off to the school, it could be some time before we get a parent back to the school to pick their child up and we really don’t want a potentially infectious child hanging out at the school. So, can someone go on the bus to screen temperatures and symptoms before the child gets on the bus? Can we have staff screen children in their parents’ cars in the parking lot before the child gets out of the car? And, if they are going to do the temperature check, what are they going to use for the temperature cut off? Guidance commonly states 100.4, but in light of the above, and to keep it simple for screeners, I recommend just using 100.

The other thing we need to do is ensure that before the child gets in the bus or out of the parent’s car, they have an acceptable mask on and are wearing it correctly. If they don’t have a mask or forgot it, we need to have masks there and available to give the child. It is important to note that face shields are not an acceptable alternative.

At one school, as we were doing this review outside the school building, I noticed a half dozen building contractors going in and out of the school without masks on. It was a great opportunity for me to remind them that everyone who goes in the school building must wear a mask, even contractors and visitors. In fact, I calculated the incubation period for them to demonstrate that if one of the teachers was infected by a construction worker, they would likely be at their peak infectiousness on the first day of school!

We are ready to begin the walk-through. I turn to the building maintenance staff. We discuss the difference between droplet and airborne transmission and discuss strategies to increase air circulation and ensure that air is exhausted to the outside rather than being recirculated. In addition, in cases where we cannot get a sufficient number of air exchanges per hour, we discuss options of opening windows, opening doors and having classes outdoors.

While on the subject of airborne transmission, we check the bathrooms out. Many of the newer restrooms do not have lids on the toilets. I discuss the aerosolization that occurs with flushing toilets, the benefit of closing the lid of the toilet before flushing if there is one, and the need to restrict the number of students using the restroom if there are not lids. Further, we discuss the implications for virus to contaminate all surfaces in the restroom – the floor, the stall doors, the counters, the faucets, the paper towel dispenser, the door to exit the bathroom, etc. Therefore, in addition to washing their hands, I recommend placing a sanitizer just outside the bathroom for a final hand-sanitizing after exiting the restroom.

That leads to the next point. Sanitizers. Schools have done a good job of placing sanitizers near the classrooms, however, many of the ones I have seen do not give a visual cue that the sanitizer is empty. Therefore, I stress that it is important that someone has it in their workflow to make periodic rounds to fill sanitizers. Unfortunately, when empty, rather than finding another, kids will often just forego sanitizing their hands.

I then look at classrooms and ask the teacher to tell me all the movements in the classroom a child might be expected to make. It turns out that while they do a great job of distancing desks, there are places in the room where books or other resources are kept and where many students may go at once to get or return something. That then compromises our distancing. So, we talk about other ways to accomplish it by the teacher handing them out or staggering the students as they go to the area.

Speaking of airborne transmission, an important feature to look at in the classroom is the air return. Sometimes it is over the door at the entry way, but on other occasions, I have seen them right over the teacher’s desk (this is the worst possible location) or sometimes over a student’s desk. Given that aerosols will follow the airstreams, the virus will travel in a directed manner right over the teacher’s or student’s head. I always suggest that the teacher’s desk be moved if that is the case, or if it is over a student’s desk, then I advise moving the desk as much as possible (to reduce the risk of airborne transmission) while still maintaining distancing (to reduce the risk of droplet transmission), but if it is going to have to be near that airstream then keep that in mind and don’t put a vulnerable student under it or a student who for some reason is unable to wear a mask or unlikely to be compliant with mask wearing.

I also take this opportunity to discuss the need for cleaning – desks, chairs, keyboards, etc. I advise them to be clear in their plan who is responsible for cleaning what and how often. In addition, we discuss whether there are special education teachers or teachers or interpreters for the hearing impaired. These teachers often want to use face shields. I explain the limitations of face shields and the need for even greater than 6 feet of distancing when they are going to be used, but pointing out the likelihood that they provide little, if any, protection to the teacher or student for airborne transmission. Therefore, I suggest that they at least try to use face masks that have a clear area over the mouth.

Then we discuss movements of students in hallways between classes, for recess, lunch, or fire drills. I recommend that they stagger hallway movements (other than for fire drills, or obviously, a real fire) to minimize contacts that one class has with any other class. This will help contain isolated infections from becoming outbreaks. Teachers often express that they have no idea how to maintain distancing during these hallway movements. My suggestion is for teachers to assign students an order in which they will walk single-file out of the room, down the hallway and to their destination. For example, Jimmy is to follow Susie. Then, tell each student (except the first one) to extend their arm out in front of them, but not to touch the person in front of them. While not six feet, this distance will be sufficient for people while walking to ensure adequate distance to minimize the risk of exposure. Of course, all students should be wearing their masks, as well.

We then finish up with special risks – those not in a traditional classroom. Many schools are having students eat outside or in their classroom. This is great. However, for those who will be having students eat in the cafeteria, we discuss the need to stagger lunch periods so that we reduce crowding in the cafeteria, the need for distancing being even more important because masks come off to eat and drink, the risks of the meal time not being structured and supervised (students sharing food/drink, visiting friends and getting too close with their masks off, or yelling, shouting or cheering which expels greater amounts of virus in respiratory droplets and transmits them further than six feet.

Another activity with increased risk is choir, for the same reasons that students may not be wearing masks, and singing expels greater amounts of virus in respiratory droplets further than six feet. There is also risks of airborne transmission with singing. So, we discuss options for choir to convene outside or if indoors, with good air exchanges or alternatively doors and windows open, and with double the physical distancing. The same thing goes for cheerleading. Yelling and cheering will increase the amount of virus in respiratory droplets and spread them further.

Band has similar issues as a number of band members cannot play their instruments with masks on. Worse, all of the brass instruments I can think of have spit valves and players have traditionally emptied their spit valves by blowing hard into the instrument with the valve open and allowing the spit to fall to the ground. This could be problematic if a player is infected. Obviously, the best solution is to practice outside. Marching bands will be used to this. This can be more of a challenge for concert bands or orchestras. If the practice is going to be indoors, everyone who can wear a mask should. While all band members should be spread six feet apart, brass instrument players may need to have this distance doubled. In addition, it may be best to use a pee pad or similar floor covering below the player for emptying their spit valves. The pads should generally be picked up and disposed at the end of the practice by someone who knows how to handle potentially contaminated materials and dispose of them and that person should wear gloves. If students are going to dispose of them, then there is a need for careful hand washing or sanitizing afterwards. Since we don’t know whether emptying a spit valve may be an aerosolizing event, it may be best to have a trash receptacle, tissues and hand sanitizer at each brass instrument player’s seat so that as they open the spit valve, they can put tissues up to the opening and collect saliva into the tissue rather than allowing it to fall to the ground.

Physical education presents some additional concerns. Like singing, yelling, shouting, and cheering, heavy and fast breathing associated with exercise will potentially spread more virus in respiratory droplets and for a further distance than six feet. Physical distancing at all times will be important. Also, it is likely that equipment will be shared among students, so there needs to be extra attention to cleaning balls, ropes, and gym equipment in between uses. Certainly, activities involving close contact (e.g., wrestling) or frequent passing of a ball (e.g., basketball) should be avoided if possible. Special consideration to physical distancing must be given to locker rooms and showers. Locker rooms tend not to have high efficiency air circulation. One quick test – if you can smell the odors of sweaty kids in the locker room, then you are breathing enough stagnant air that you could also be breathing in the virus.

Finally, I often get asked about sports. Each sport needs to be examined with particularity, and I will not go through every sport here, but let me take one sport and give you an example. Swimming. Swimming should be a relatively safe sport from a COVID point of view. A swimmer swimming in a lane is going to be distanced and we are not aware of any risk that a swimmer could contract this virus from the pool water. However, while the act of swimming might be very safe, associated activities could be very dangerous. For example, swimmers obviously shouldn’t wear masks while swimming. But, if the teammates who are not swimming are congregating on the side of the indoor pool, without masks and are cheering their teammate on, this may be a very high-risk situation. Similarly, for all sports, we have to know how all the associated activities are going to be handled. Are there going to be in-person team meetings? Will distancing be possible? Will everyone be required to wear a mask? What about away games? Will students carpool? This would be risky given the close proximity students would be in in a car and likely without masks. Will they be travelling by bus? (See the concerns I mentioned above about school buses).

Well, this is how I am trying to help schools have detailed operational plans and be the best prepared they can be for the beginning of in-person classes. I hope that this can be of use to other schools that have not yet opened and that you might consider some of these risk points and questions as you do your own assessment of your plan, and hopefully a walk-through. But, I encourage you to engage someone who is knowledgeable about this virus, but not an educator to do your review and walk-through. Fresh eyes are very important. Good luck. I am hoping that we can keep students, their families, teachers and your staff safe.

Myocarditis Due to COVID

I have long been frustrated that people tend to lump the effects of COVID into two buckets – (1) infections in young persons that tend to be asymptomatic or mild and (2) infections in the elderly that may land them in the hospital or even result in death. Both extremes certainly exist and are common outcomes, but there is so much more in the middle. There are children and young adults who die and there are young adults who develop very severe illness and may suffer disabling complications including heart attacks, strokes and residual lung disease, deconditioning and PTSD following prolonged mechanical ventilation. Further, there is another set of people with an average age in their late thirties or early forties that develop long-term, disabling effects long after they appear to have recovered from their COVID infection called “long-haulers,” who I have previously written about. We need to change he discussion of COVID from one of full recovery or death to one of a spectrum of disease outcomes, including many outcomes that we simply do not understand yet, nor have we had sufficient time to know the long-term effects. One complication of COVID on this spectrum is myocarditis.

The subject of today’s article is myocarditis, a complication of COVID that has been recognized since April, but has recently attained attention due, in part, to the occurrence of this condition in college and pro athletes and some attention-getting decisions about whether college teams would play football this season, in no small part due to concerns about myocarditis.

What is myocarditis?

Myocarditis is inflammation of heart muscle – the myocardium. It may be caused by many different things, but viral infections are among the most common. Among the most common viruses to cause myocarditis are adenoviruses (a group of viruses that cause cold-like illness, pneumonia, diarrhea and pink eye in people of all ages), coxsackievirus (the cause of hand, foot and mouth disease in children) and other enteroviruses (viruses that enter the body through the intestine and generally cause cold symptoms).

How does myocarditis present?

The classic presentation of viral myocarditis is a report of a viral-like illness with fever, muscle aches and upper respiratory symptoms followed by the onset shortness of breath, chest pain and/or palpitations, and fast and/or irregular heart-beats. Not everyone recounts a preceding viral-like illness, but in those that do, the symptoms of heart failure may present over a few days to a few weeks after the viral illness.

When these patients are evaluated, they may have abnormal electrocardiograms, an echocardiogram may be normal or may show a reduction in the heart’s pumping effectiveness, or a cardiac MRI may show areas of swelling or inflammation in the wall of the heart, or even scarring. In addition, a blood test for troponin, a protein in heart muscle, may be elevated indicating that the heart muscle cells have been damaged.

How does a viral illness cause myocarditis?

We haven’t been sure whether the virus actually attacks or invades the heart muscle cells or whether the inflammation associated with the virus or the immune response to the virus is what harms the heart muscle, or possibly both mechanisms could be at play. A recent study (Lindner et al, JAMA Cardiology, July 27) in patients with myocarditis from COVID who died showed that the causative virus, SARS-CoV-2 could be detected attacking and invading heart muscle cells.

What happens to patients with viral myocarditis?

We don’t yet know for patients with myocarditis from COVID. Before COVID, patients with viral myocarditis often recover on their own or with anti-inflammatory medications in a matter of months. Most will recover their full heart function. However, some patients can experience life-threatening arrhythmias and some patients go on to develop serious heart failure. A weakness in pumping of both sides of the heart is one of the main predictors of death in patients with severe myocarditis.

So, what do we know about myocarditis in COVID patients?

The first case of COVID-19 infection in a patient that resulted in fulminant myocarditis as a complication was reported on April 10 in a 63-year-old man with no history of heart disease or underlying hypertension. This patient had elevated levels of the heart muscle protein, troponin, in his blood, enlargement of part of his heart, low pumping movement of his heart muscle and the pumping effectiveness of his heart was reduced by 40 – 50 percent (LVEF 32%). In this particular case, the patient’s heart function largely recovered, however he died of secondary infection on the 33rd day of hospitalization.

Since then, we have seen heart muscle involvement in many cases of patients sick enough to have required hospitalization. But, myocarditis is not the only manifestation of heart disease from COVID. COVID actually produces a pro-thrombotic state, i.e., a greatly increased tendency of the blood to clot abnormally. This has resulted in some patients experiencing significant pulmonary embolism (blood clots to the lungs), which if severe can impair the functioning of the right side of the heart; myocardial infarction, i.e., heart attacks due to blood clotting in the arteries that provide the blood supply to the heart muscle; and clotting of stents in coronary arteries producing heart attacks in those who previously had angina, underwent a cardiac catheterization and were found to have a blockage in their coronary artery for which a metal strut of a sort is placed in the artery to open up the blood flow through that artery. In addition, some patients with COVID develop a shock-like state, and we know that the imbalance between the oxygen and metabolic requirements during shock and the lower supply can cause abnormalities in the heart muscle and a release of troponin into the blood, thereby making this condition difficult, if not impossible, to distinguish from myocarditis.

More recently, patients who recovered from COVID have been evaluated with cardiac MRI looking for signs of myocardial involvement. It should be noted that we have not generally screened asymptomatic patients recovering from other viruses to look for evidence of myocarditis, so we don’t know if asymptomatic myocarditis is a common occurrence with other viruses.

These recent studies showed that a significant percentage of persons who recovered from COVID, including those who experienced relatively mild illness were found to have cardiac MRI evidence of myocarditis, including athletes.

The long-term impact of COVID-19 myocarditis, including the majority of mild cases, remains unknown. In symptomatic patients, especially those with significant involvement of their heart and impairment to their heart’s pumping effectiveness, there is a risk of arrhythmia as well as progression to fulminant heart failure and cardiogenic shock. But, for those who are asymptomatic, whose myocarditis is being picked up incidentally on cardiac imaging, we simply do not know yet why they developed this complication, what the risks are, whether some will go on to develop significant cardiac problems, or whether all of these individuals will recover with time.

Perhaps it is not surprising that myocarditis can result from infection by the SARS-CoV-2 virus since its target, the ACE2 receptor protein, can be found in the cell membranes of heart muscle cells. But, a report in July garnered a lot of attention.

In a study in JAMA Cardiology published on July 27, Puntmann et al reported that in a cohort of 100 patients recently recovered from COVID-19, “cardiac magnetic resonance imaging revealed cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%), which was independent of preexisting conditions, severity and overall course of the acute illness, and the time from the original diagnosis.”

53% of the patients were male and the mean age was 49 years. The median time interval between COVID-19 diagnosis and the cardiac MRI study was 71 (range 64-92) days. 67% of the patients were considered to have had mild illness and recovered at home, while 33% required hospitalization. At the time of the cardiac MRI study, 76% of the patients had elevated levels of the heart muscle protein, troponin, in their blood signifying heart muscle injury.

As of the time of the cardiac MRI study, 17% of patients reported atypical chest pain, 20% reported palpitations, 36% reported ongoing shortness of breath and general exhaustion, of whom 25 noted symptoms during less-than-ordinary daily activities, such as a household chore. The authors conclude their paper by stating, “although the long-term health effects of these findings cannot yet be determined, several of the abnormalities described have been previously related to worse outcome in inflammatory cardiomyopathies.”

Also recently, cases of post-COVID myocarditis have been reported in college and professional athletes. We are awaiting a medical publication that is rumored to show that approximately 15 percent of Big Ten football players who were infected with COVID demonstrated evidence of myocarditis in follow-up evaluations. However, until this paper is peer-reviewed and published, we don’t have any of the details we need to draw conclusions from this.

From everything we know thus far, the clinical presentation of SARS-CoV-2 myocarditis varies among cases. Some patients may present with no symptoms and the myocarditis is detected only because of a screening protocol for athletes, some may present with relatively mild symptoms, such as fatigue and mild shortness of breath, whereas others report chest pain or chest tightness on exertion. Some patients do deteriorate, showing symptoms of tachycardia (fast heart beat) and acute-onset heart failure with cardiogenic shock. In these severe cases, patients may also present with signs of right-sided heart failure. The most emergent presentation is fulminant myocarditis, defined as ventricular dysfunction and heart failure generally within 2–3 weeks of contracting the virus. This complication occurred in a beloved nurse practitioner who was in her 40s and cared for children at St. Luke’s.  

While the acute inflammation and injury to the heart are the current focus receiving attention, the long-term effects of healed myocarditis are completely unknown. We have seen in patients with other forms of myocarditis that in the process of healing, scarring of the heart muscle can disrupt the normal electrical pathways of the heart and result in life-threatening arrhythmias, even when the acute inflammation has resolved.

Post-COVID myocarditis in Idaho

I spoke to two experts here in the Treasure Valley to see what they were seeing and what their thoughts about this complication are. I interviewed Dr. Andy Chai, a cardiologist at St. Luke’s Health System who specializes in advanced heart failure and transplant cardiology and who serves as the medical director of St. Luke’s Clinic-Heart Failure and Dr. Nathan Green, an interventional cardiologist with St. Luke’s Health System who serves as the medical director of the Heart and Vascular Service Line at St. Luke’s.

Both doctors indicated that they are seeing cases of myocarditis related to COVID here in Idaho and while these patients have most often ranged in age from their thirties to their fifties, they have also had disease ranging from mild to severe, including patients who have died from their myocarditis.

Both doctors lament how little we know about this condition at this time. They certainly expect that those with myocarditis who have well-preserved heart function, limited areas of involvement of myocardium and low levels of troponin elevation are likely to do well. For others, who have more significant inflammation, we don’t yet know what to expect, but we are managing these cases much like other cases of viral myocarditis and following up with serial evaluations to monitor their progress.

I did ask both doctors about sports this fall and winter given the amount of disease transmission we have in the communities we serve, as well as this yet poorly understood risk of myocarditis in athletes who might become infected. Neither doctor felt that the threat of myocarditis should be the determining factor of whether sports are played. The risk of transmission of COVID among those who participate in sports and to their families, teachers and others is certainly worth consideration of whether middle schools and high schools hold sports events this fall. However, perhaps more important if a school is going to have athletic programs this fall is how strong the operational plans of each school are.

As for an athlete who has seemingly recovered from COVID and now has an abnormal result on a cardiac MRI screening, as to whether that athlete should sit out for the season was a much more difficult decision. One doctor pointed out that we simply do not have good guidelines as to how safe a significant amount of exercise is for someone with myocarditis. Pre-COVID, we were generally only seeing symptomatic patients with viral myocarditis, and we tend to recommend limited exercise such as walking until we see the myocarditis resolve. One doctor suggested that if the athlete’s participation is especially compelling – a professional athlete whose family’s income is at risk, especially when you consider the much more robust safety protocols they have in place and resources available to protect these athletes or a collegiate athlete with aspirations of going pro- it makes it more difficult to tell that athlete they must sit out the season if the myocarditis appears to be subclinical or very mild. However, for student athletes in middle and high school, it seems prudent to exercise more restraint until we know more about this condition.

I then brought up the long-haulers who have significant symptoms and/or disabilities months after supposedly recovering from COVID, some of whom have reported chest pains, palpitations, and/or shortness of breath with relatively mild exertion. I asked whether these individuals need to be evaluated for possible myocarditis and both doctors indicated yes, without any hesitation.

Finally, I asked the doctors a question sure to make any cardiologist cringe. I asked whether in light of the not infrequent occurrence of myocarditis following COVID and the potential for impairment of heart function and certain EKG findings known to place patients at risk, might this be one more reason why people should not take hydroxychloroquine or hydroxychloroquine plus azithromycin for COVID, and both immediately and emphatically agreed that these medications might be even more likely to cause harm in the setting of a COVID patient who has developed myocarditis.

So, I have told you most of what we know at this time about myocarditis in the setting of or following COVID infection. Perhaps it is equally important to tell you what we don’t know.

  1. We don’t know the prevalence of this complication. In other words, we don’t know what percent of people who are infected with COVID go on to develop myocarditis.
  2. We don’t know who is at risk for developing myocarditis and what determines who will develop myocarditis and who won’t.
  3. We don’t yet know the long-term effects of myocarditis. Do most of the people who develop myocarditis recover on their own in a matter of months? Do some have long term heart problems?
  4. Should we be screening everyone who recovers from COVID for this condition or are there certain individuals who should be screened? If so, when and how often should they be screened?
  5. For those who have mild myocarditis, is it safe for them to exercise? How much, how often and at what intensity?
  6. If someone with myocarditis following COVID gets re-infected with COVID, will they develop a recurrence or a worsening of their myocarditis?

No doubt, we will learn more about this condition with time. As we get important new information, I will be sure to share it with you.

The Long Term Effects of COVID

The most common misinformation that I hear about COVID is not “this is a hoax” or “masks don’t work” or “kids don’t get sick” or “kids don’t transmit COVID” or “this is no worse than the flu.” It is a statement that goes like this, “Opening schools must be based on decisions that balance the risks – we know that kids generally don’t get sick with this virus, but we know the risks of abuse, suicide and food insecurity if we don’t open schools.”

The problem is that while we do have a long history of understanding risks to some kids when they are not in school, school boards often convey that they have weighed these risks against the risks of COVID. They have not. I have not even heard very much discussion about COVID risks at school board meetings, and frankly, school board members don’t know what the risks of COVID are, because no one yet knows what all the risks of COVID are.

The risks of COVID are often presented as two potential outcomes – (1) you get infected and may either be asymptomatic or have a mild illness or (2) a few may get severe illness and have to be hospitalized, and some of them may die. This ignores a vast array of complications (including strokes) and long-term effects, which may be life-altering for those who get them. This group of patients is not being considered in our decision-making, our policy-making or our assessment of the costs of this pandemic relative to the impact on employers of absenteeism and loss of worker productivity, the incremental costs to their health plans or the costs related to long-term disability. And, with loss of employment, I have not seen any projections of the impact of this to state Medicaid plans or in the event of a decision by the U.S. Supreme Court to strike down the Affordable Care Act early next year (more about this at the end).

So, in this group in the middle that doesn’t get talked about, we are finding many young, previously healthy and active individuals who are describing disabling long-term effects of their COVID infection, often even though they described the infections as mild and certainly not requiring hospitalization, lasting for months, and in many cases, that have continued to persist to this point. There is even a name given to these individuals – “long-haulers.”

These patients have not yet been systematically studied, and there are challenges to understanding what is going on because not everyone had confirmed infection, many likely having been infected during the initial surge in cases when testing was difficult to obtain or when they had symptoms that were not on our early symptom lists having only been recognized later. Further, many of these patients do not have positive antibody tests either, which we know happens in some cases of infection, and perhaps has some relationship to the symptoms these patients are experiencing. Interestingly, in a study of 1,400 long-haulers, two-thirds of those who underwent antibody testing had negative antibody tests, including some who had previously documented positive PCR tests.

The symptoms being experienced by these patients are wide-ranging, and it seems as though no two patients are alike. However, what is common to many of these patients is what they describe as a marked change compared to their “pre-COVID” status, and oftentimes quite disabling symptoms. These have included:

  • Extreme fatigue, one patient describing it too exhausting to take showers. Some describe being unable to stand for long periods of time.
  • Awakening with shortness of breath
  • Burning sensations in the tips of their fingers and/or toes
  • Diarrhea
  • Discomfort with taking a deep breath
  • Hair loss
  • Hand tremors
  • Headaches – often throbbing
  • Heavy menstrual periods or loss of menstrual periods
  • Insomnia
  • Memory loss – “brain fog”- a combination of short-term memory loss and inability to focus
  • Nausea
  • Night sweats
  • Palpitations, tachycardia
  • Persistent fevers
  • Seizures
  • Sensitivity to light and/or sound
  • Shortness of breath, getting winded walking up stairs
  • Tendency towards bruising

Some patients have reported that their symptoms are resolving, while others continue to be plagued by them. It is hard to know exactly how many people have been affected by these “post-COVID” symptoms because there is no standard definition for their condition and no central repository for reporting of these conditions, but it is believed that this disorder affects more than 90,000 people in almost 100 countries, including the US, UK, India, France, Finland, Senegal, and South Africa. Some suggest about ten percent of those infected with COVID will develop long-term effects.

Interestingly, while most people consider those in their 30s and 40s to be of “low risk” for severe COVID and death, the average age of these long-haulers has been 38, and while men tend to have worse outcomes and more severe illness with COVID infection, these long-haulers have been mostly women.

NYC’s Mount Sinai Hospital is one of the first hospitals in the country to establish a post-COVID clinic. They have reported seeing this predominance in women and the average age of their patients was reported as 44. Dr. Putrino, who runs this clinic, has indicated that many long-haulers have symptoms that resemble dysautonomia, an umbrella term for disorders that disturb the autonomic nervous system, which controls bodily functions such as breathing, blood pressure, heart rate and digestion. It remains unclear whether the virus itself causes damage that results in these long-term effects, or whether these long-term consequences are a result of an over-active or exaggerated immune response, despite the failure to develop an antibody response or the loss of antibodies once produced.

More than 90 percent of long-haulers whom Putrino has worked withalso have “post-exertional malaise,” in which even mild bouts of physical or mental exertion can trigger a severe physiological crash. “We’re talking about walking up a flight of stairs and being out of commission for two days,” Putrino said. This is the defining symptom of myalgic encephalomyelitis, or chronic fatigue syndrome. 

The CDC has had little to say on this subject, but it acknowledges that 35% of COVID patients, even those with mild illness, do not recover even after 3 weeks.

Studies

There are few clinical studies on these patients. Here are results of some of the few studies that have been done.

  1. One report is from patients themselves. A patient-led research team of 640 patients  reported their own characteristics at  https://static1.squarespace.com/static/5e8b5f63562c031c16e36a93/t/5f25b5bfb3f4f86b1bf4d5f5/1596306894541/2020+Survivor+Corps+COVID-19+%27Long+Hauler%27+Symptoms+Survey+Report+%28revised+July+25.1%29.pdf

The most common symptoms reported were (in descending order) fatigue, muscle or body aches, shortness of breath or difficulty breathing, difficulty concentrating or focusing, inability to exercise or be active and headaches.

2. Study out of Germany   https://jamanetwork.com/journals/jamacardiology/fullarticle/2768916

This study examined the cardiac MRIs of 100 people who had recovered from Covid-19 and compared them to heart images from 100 people who were similar but not infected with the virus. The average age of the study group was 49 and two-thirds of the patients had mild illness and recovered at home, while 33 percent were hospitalized. More than two months later (median time interval from diagnosis with infection to the MRI evaluation was 79 days), infected patients were more likely to have troubling cardiac signs than people in the control group: 78 patients showed structural changes to their hearts, 76 had evidence of a substance in their blood signaling cardiac injury typically found after a heart attack, and 60 had signs of ongoing inflammation of their heart muscle.

3. Italian study  https://jamanetwork.com/journals/jama/fullarticle/2768351

87.4% of hospitalized patients (mean age 56.5 years) still had at least one symptom, and often a variety of symptoms, after two months since the onset of their initial symptoms of infection. The most common symptoms were fatigue and shortness of breath.

4. A researcher from the Indiana University School of Medicine in July surveyed 1,500 long-haulers from Survivor Corps, an online COVID-19 support group. They reported almost 100 distinct symptoms, from anxiety and fatigue to muscle cramps and breathing problems.

5. Cases of type 1 diabetes among children in a small UK study almost doubled during the peak of Britain’s COVID-19 epidemic, suggesting a possible link between the two diseases that needs more investigation. Thirty children in hospitals across north-west London presented with new-onset type 1 diabetes during the peak of the pandemic, approximately double the number of cases typically seen in this period in previous years, with clusters of cases in two of these hospitals. Twenty-one children were tested for Cobid-19 or had antibody tests to see whether they had previously been exposed to the virus.  In total, five children tested positive, either for active Covid-19 infection or previous exposure to the virus. However, antibody testing was not routine, and fourteen children were not tested for previous exposure to Covid-19. At the height of the outbreak in the UK, testing was not widely available and many of the children were not able to be tested during the time they may have been infected.

Karen Logan at Imperial College Healthcare NHS Trust and supervising author of the study, said: “It appears that children are at low risk of developing serious cases of Covid-19.  However, we do need to consider potential health complications following exposure to the virus in children. Our analysis shows that during the peak of the pandemic the number of new cases of type 1 diabetes in children was unusually high in two of the hospitals in north west London compared to previous years, and when we investigated further, some of these children had active coronavirus or had previously been exposed to the virus.”

Other studies/information:

There are several points that I want to close with.

  1. We have only begun to understand the long-term effects of COVID infection. In some, they may be annoying, in others they are debilitating, and in others, they may be life-threatening (e.g., insulin-dependent diabetes, if this is proven to indeed be a consequence of COVID infection). Some people appear to recover over a few months, others continue to be plagued by these effects nearly half a year since their likely infection. There is much we don’t know. Why do some people recover quickly, yet others have lingering symptoms? Who is at risk for developing prolonged effects from their COVID infection? Do these symptoms eventually resolve, or will there be some who are plagued by these symptoms or disabilities for the remainder of their lives? Are there treatments that can improve their wellbeing? What happens to these individuals if they were to become re-infected? Do they have more or less risk than others of becoming re-infected?
  2. School boards and public health boards have, for the most part, not paid enough attention to these long-term effects of COVID as risks when they balance the risks of opening vs. not reopening schools for in-person classes, and even more importantly in decisions as to whether to hold athletic events or not.
  3. We have not yet begun to contemplate the implications of these long-term sequelae on society. Will long-haulers impact workplace absenteeism and productivity? Given that some long-haulers are reporting changes to their menstrual cycles, will this impact the ability to conceive? Will long-term disability result in an increase in behavioral health issues such as anxiety, depression or even suicide? What will be the costs of caring for these individuals over the long-term? And, as I have said on many occasions and written on others, this is particularly concerning at a time when the Affordable Care Act is being challenged in the U.S. Supreme Court this fall with the request that the Court strike the law down. As far as we know, Republicans have no back-up health plan that they believe can be passed by Congress and enacted into law if the ACA is struck down.

A decision by the Court to strike the ACA down (see my earlier blog posts for a full discussion of this legal challenge) would eliminate guaranteed issue, community rating, Medicaid expansion and the public insurance exchanges, along with the advance premium tax credits and subsidies. So, if a person lost their job and with it their health insurance, they would have two possible alternatives to get insurance – Medicaid and the public insurance exchanges with the assistance of financial assistance from the government. However, if the ACA is struck down, there is no Medicaid expansion and the public insurance exchanges will be gone. If the person is able to purchase insurance on their own, without the restrictions of the ACA, an insurer could deny coverage for someone who has been infected with COVID as a preexisting condition, or if they were to offer coverage, they could do so by increasing the premium significantly.

There are many implications of post-COVID effects, and we don’t understand what most of them are yet. This is an area that requires much more time to see what develops and what the answers are to the questions I posed above, more research, and is just one of the reasons we all need to pay attention to the Supreme Court decision that likely will come out in the first part of next year.

School Boards Should Not Get Blanket Liability Protections for Reopening Decisions

The following is an opinion piece I wrote that was published in the Idaho Press Tribune.

It has long been established in every jurisdiction of our country, that those who provide certain products or services to the public and consumers can be held liable for providing those products or services without the exercise of reasonable care. As a practicing physician, I knew that if I provided a service or procedure to a patient and it did not meet the standard of what an ordinary and prudent physician in my specialty would have provided, and as a result, a patient was harmed, I could be held to account. No physician likes this, and being sued is professionally devastating, but I think we would all admit that we practice better medicine and document our care better because of this potential liability.

There are many things that Sen. Thayn and I do not agree with each other on. There is one thing that we are in agreement on – physicians should not be making policy decisions, e.g., whether to implement stay at home orders and whether and when to open schools. Physicians approach problems differently – we are all trained to do our very best for every single patient and to not harm any patient. Policy decisions necessarily weigh many risks – public health, the economy, social needs, employment, etc. Physicians without public policy and political expertise are poorly prepared to make these decisions.

While physicians should not make these policy decisions, where I strongly disagree with Sen. Thayn is the notion that medical or public health advice should be disregarded or discounted. The Governor, legislators and school boards should not be bound by medical or public health advice for the decisions they need to make, but on the other hand, it is irresponsible to not even consider it. My guess is that if Sen. Thayn needed tax advice, he would solicit that advice from a tax expert. Obviously, he doesn’t have to take that advice, but there is some peril in disregarding that advice. Similarly, my guess is that if he had a painful tooth, he would not take a pair of pliers to his neighbor and ask that the neighbor remedy his tooth problem. At a visit to his dentist, the dentist would diagnose the problem and then present Sen. Thayn with the options and the benefits and risks of each option. Again, the senator need not take that advice, or is free to get a second opinion, but it may be unwise to completely disregard or ignore that advice when doing so can lead to more serious oral health consequences.

So it is with our school boards. These boards are entrusted with the safety of our teachers and students. We are facing a pandemic with a novel virus. We are beginning to see consequences of COVID infections that we have previously been unaware. School openings are a difficult issue. Opening (or not) a school for in-person education requires the weighing of many considerations – financial; health and wellbeing of teachers, students and their families; risks to children of not opening schools, the impact on the economy and workforce, etc. These are not decisions for doctors, but for these boards.

There are times that a physician determines that the standard treatment is not the best option for a specific patient. But, when that is the case, we explain the basis for not using the standard treatment to the patient, and we document it. This should not result in liability if there is a good basis for this deviation. But, if we choose to ignore the accepted and best treatment available without informing our patient as to why, we may be held liable when the patient is harmed, if that harm is the result of our decision. As the legislature considers liability protections for school boards and businesses, I encourage us to require of those we are extending the protections to do the same. Explain to the public and document in their public records the basis for determining that non-medical reasons trump the medical and public health concerns, so that we can hold boards to account and a jury can determine whether that decision was negligent.

What We Think We Know about Immunity for SARS-CoV-2 – How I would explain it to a Fifth Grader

Some physicians have been pushing for people to get antibody tests for COVID in ways that I believe have been irresponsible. Recently, I commented on twitter (@drpatesblog) on yet another case, in which a patient with documented COVID infection was tested for antibodies 40 days following the resolution of his illness, and antibodies were not detectable. One of my followers, an elementary school teacher, asked if I could explain immunity to SARS-CoV-2, the virus that causes COVID, as if she was a kindergartner. I thought about how difficult that would be, but how many people this would help understand these complex concepts if I could. I decided that I couldn’t get it down to a kindergartner level, but perhaps I could explain it at a 5th or 6th grade level. Here is how I did.

The immune system is actually very complex. Most often, people equate antibodies with immunity to something, but antibodies are just one part of a very complicated system, and having antibodies to something doesn’t always mean you are immune to it. So, hear is what we know about the immune response to SARS-CoV-2 for a 5th or 6th grader:

If a bacteria or virus invades your body, and you have never been exposed to that invader before, the first response of your body is to send in ground troops that will try to stop these invaders at your border (your skin or just under your skin if you get cut, or your nose and throat if it is trying to invade your body there, or your gut, if it is trying to make entry there).

The ground troops with their rifles are called white blood cells (or white cells), and they don’t care who the enemy is, they just attack and try to shoot anyone (in this case a bacteria or virus) who doesn’t have the same uniform as the rest of the body (in this case, features that these white cells recognize as being your own body as opposed to an invader).

Just like we have different military forces (Army, Marines, Navy, Air Force, National Guard, etc.) and they all have slightly different roles and tactics to attack an enemy, we have many different types of white cells in our blood, and they each conduct different kinds of warfare against these bacteria and viruses.

Just like our ground troops can throw a hand grenade or fire a cannon and blow up our enemies as well as things around them that we might otherwise not want blown up (like innocent bystanders or buildings, etc.), our white cells start releasing chemical warfare against these invaders of our bodies and they cause some indiscriminate inflammation and surrounding tissue damage, as well, but as an attempt to kill these invaders or at least slow them down.

What our ground troops (white cells) are trying to do is prevent these invaders, in this case a virus, from crossing that boarder (our nasal passages and throat in the case of SARS-CoV-2) and entering into our towns and cities (in this case our cells), where they an take over our food supplies and manufacturing plants that will allow them to make more invaders (viruses) that can then increase their attack on us.

This chemical attack is what makes us feel bad – fever, aches, cough, runny nose, etc.

Now, all this time that our ground troops (white cells) are fighting the invaders (virus) off at our borders with their rifles, hand grenades and cannons, they have already sent the message back to headquarters that we have invaders, a sample of what they look like, and a request that we need some weapons that will specifically target these invaders to stop them before they get into our towns and cities (cells) where they will make more invaders (virus). These weapons will be very specifically targeted to this invader so that they only kill the invader and don’t cause all the collateral damage (destruction of property and injury or death to our own body’s cells and tissues as friendly fire).

HQ then revs up the manufacturing plant and starts making these highly targeted bombs (antibodies) that recognize something that is different that makes up these invaders that is not present in our normal body cells and tissues. This different thing is called an antigen and HQ manufactures these special bombs (antibodies) that only blow up anything that has that particular antigen and leaves everything else alone. It ordinarily takes HQ 7-14 days to make these specialized bombs (antibodies).

In the meantime, our ground troops (white cells) have to hold off the invaders. Sometimes they do, but often times, some of the invaders get into our towns and take over the food supply and start manufacturing new viruses.

Now, if you get an antibody test while you are sick but before HQ has had time to make antibodies, the test will be negative, even though you are infected. This is called a false negative. It is also possible that you had some left over antibodies from a prior invader, but you already defeated that invader, but the antibody test identifies those antibodies as antibodies to this virus because they look a lot alike, even though the antibodies it is recognizing don’t work against this new invader, or don’t work very well. This is called a false positive – the test is telling you that you have the antibodies when these are not the antibodies we are looking for. Unfortunately, that can make someone hang out with someone in close contact who has these invaders because the person thinks they are protected, but these invaders move from the infected person to you and now you become infected.

Now, these bombs (antibodies) come in a number of different kinds. Antibodies do often defeat invaders, but not always. We have examples of other virus invaders where HQ makes plenty of antibodies, but the invaders march on and take over our cities and don’t seem to be slowed down by the antibodies. In the case of this coronavirus, we think antibodies are important, but we don’t know yet. This is a reason to save your money and don’t get an antibody test.

Now, back to the types of bombs (antibodies). It turns out that you need one kind of antibody if the invader is crossing the skin (IgG) and you likely need a different antibody (IgA) if the invader is crossing a mucosal border (your nose or gut). Polio was a gut invader. We developed two different vaccines – a shot and a sugar cube, and it turned out that the sugar cube worked the best, because it caused HQ to make IgA better than the shot did. Everyone talks about IgG and that is what the antibody tests check for, but it may be that IgA is equally or more important – we don’t know. The good news is that in one of the first vaccine trials to be reported, it appears that the vaccine does stimulate a robust response of both IgG and IgA.

Okay, back to the types of bombs HQ is making. In addition to different types of antibodies like IgG and IgA (and there are others), some of these bombs are really powerful killer bombs called neutralizing antibodies, because in a test tube, they keep the enemy from entering into our towns and cities (cells), and if the invaders can’t get into our cells, they can’t make more invaders, so, when we shoot or bomb all of the invaders at our borders, its over because there are no more invaders.

In this regard, recent studies have been disappointing. Of those who have been infected, it appears that only 1 – 10 percent of these people make neutralizing antibodies in levels that based on other infections, we would guess that these would be clearly effective against this virus. Let me add that we don’t know that an antibody is truly a neutralizing antibody in someone’s body just because it is in a test tube. And, we don’t know how important neutralizing antibodies are in the immune response to SARS-CoV-2 (there are other examples of viruses that induce lots of neutralizing antibodies to be produced, yet they don’t slow or stop the infection).

So, if not everyone is making neutralizing antibodies or enough neutralizing antibodies, then what are they making? Well, it turns out that some of these other bombs (antibodies) are like paint balls/pellets, where you shoot the invader and it doesn’t kill them, but they are now marked. Marking these invaders can help other parts of our immune system go after them. This other part of the immune system is called the cellular immune system.

In this case, HQ is not only making highly specific bombs (antibodies – for extra credit, this part of the immune system is called humoral immunity and for credit to skip a grade, that part of the immune system with our troops on the ground at our borders is called innate immunity. It is innate because we are born with it and it does not require ever having been exposed to something to fight it. It is ready to fire on sight), but also highly specialized tanks (T-cells).

Remember, the humoral immunity – antibodies – takes time if you have never been exposed to that invader before. We have to get the body part to HQ, HQ has to design a blueprint for the bombs, and then we have to manufacture the bombs (antibodies) and that all takes about 7 – 14 days.

A recent report showed that a patient who was infected and recovered, but even 40 days after recovering still had not made measurable levels of bombs (antibodies). And, we have seen that in various studies, anywhere from 2 – 16 percent of people who were invaded (infected) did not make bombs (antibodies) that were targeted to this invader (coronavirus), at least not in levels we could measure. So, these people would be said to have a false negative test – in other words, they were infected, but have a negative antibody test. Now, if that was not disappointing enough, we also found in recent studies that if you did make bombs (antibodies), which the vast majority of those who were invaded do, HQ appears to decrease production in much shorter period of time than we had hoped. We would like HQ to keep making the bombs in case, once defeated by our body, the virus is planning to attack us again this fall or next winter. Unfortunately, in 13 percent of those who were symptomatic and 40 percent of those who were asymptomatic, bomb levels dropped to a level that most of our tests could not detect after just 2 – 3 months.

So, what does this all mean? First, we don’t know how important antibodies are in the fight against coronavirus and to our immunity against reinfection. If they are important, then these studies are bad news.

But, since most people are getting over the virus without measurable antibody or with low levels of antibodies, my guess is that another branch of the immune response (cellular immunity) may turn out to be far more important. Before I turn to cellular immunity, let me conclude on antibodies.

Don’t waste your money on an antibody test. Whether it is positive or negative, we have little idea of what either means. And, even if positive, you cannot assume you are immune. You must continue to use precautions. These antibody studies give us little confidence that you will be immune this fall/winter if you did get infected during the first spike of cases back in March/April, if antibodies are important to the immune response.

So, now, lets get to the good news – cellular immunity and vaccines. So, while HQ is mass producing bombs (antibodies), they have also been producing highly specialized tanks (T-cells).

These specialized tanks (T-cells) also come in several types. As, I mentioned previously, the goals of our innate immune system (our troops at the border) is to kill the invaders, or at least hold the invaders from getting to our towns and cities (our cells, where they can take over our manufacturing plants and make more invaders) until HQ has time to produce the specialized bombs (antibodies). Once an invader gets into a city, our innate immune system is not very effective and our specialized bombs (antibodies) generally can’t get inside to capture the invaders. It’s like ISIS getting into a town or city where they can create a stronghold and many barriers of protection as opposed to being out in the open in the unoccupied land by our borders.

So, HQ makes these T-cell tanks while they are making the antibodies. One of these tanks has the ability to find pieces of the invaders and it amplifies the attack in those areas (helper T-cells). Another type of tank can identify which towns or cities (our cells) have been invaded, and while our antibodies can’t penetrate the invader’s hold on the towns, these tanks just blow up the cell and kills all the invaders who are occupying the town (our cells) (these are called cytotoxic or killer T-cells). And, thinking ahead, HQ makes tanks with advanced radar, infrared detection capabilities and other abilities to quickly detect these same invaders again should they ever try to cross our border again once we have defeated them (memory T-cells). The long-lasting antibodies and the helper and memory T-cells are useful, because while the first time we face an invader, the entire range of our arsenal (humoral- antibodies- and cellular – T-cells) takes 7 – 14 days to mount our full response, the next time we see the invader, all of these parts of our immune response can be called to duty almost immediately, so much so, that we often will not get sick or have any symptoms, or if we do, with some unusual exceptions (like Dengue fever), we will only have a mild case.

What we also found out in these recent studies, is that while the antibody response to SARS-Co-V-2 was not particularly encouraging, the cellular response in nearly everyone was. Not only did those who did not mount a very good antibody response develop a good cellular response, but even family members who lived with someone who was infected, but to the best of our knowledge, did not get infected themselves, still developed a good cellular immune response! And, for many viruses, we know that the cellular immune response tends to be more important for viruses, because there are diseases that you don’t produce antibodies, and these patients tend to get serious bacterial infections, but not severe viral illnesses; while there are other diseases for which patients have problems with their T-cells and they tend to get bad and prolonged viral infections, like shingles that will occur in multiple locations (whereas shingles tends to occur only in a single area in those with otherwise healthy immune systems).

Vaccines can often be engineered to trigger specific antibody responses that we want (like neutralizing antibodies against a specific part of the virus that appear to be especially protective against viruses getting into cells), but they also often trigger the cellular immune response. Even if the antibody response declines over a few months, we have many examples (e.g., measles) where the memory cells specific for that virus can persist for many decades, if not the remainder of your life.

So, to sum up:

  1. Don’t get an antibody test – we have little idea what it means (and avoid those who push these tests or claim to be able to tell you what it means).
  2. If you think you had COVID earlier in the year, but didn’t get tested, you probably didn’t (only about 8 percent of such individuals appeared to have actually had COVID), and even if you did, we don’t know whether you could get infected again this fall, so take all precautions.
  3. While results from antibody studies have been disappointing, results of cellular immunity are quite good and we have very good reason to be hopeful and optimistic about current vaccines under development and testing.
  4. In the meantime, the key to slowing the transmission of this virus is putting distance between those who are infected with and shedding the virus and those who are susceptible (and everyone should assume that they are susceptible).
  5. Since we don’t know who is infected and may be shedding the virus (because they may not feel sick yet), if you have to be in proximity to other people, the best option to reduce your chances of getting infected is for EVERYONE to wear a mask. The added benefit is that the same infection control practices for coronavirus are likely to slow down or prevent the spread of other respiratory and influenza viruses that we are likely to encounter this fall.

This is now the point where I apologize to all the fifth and sixth grade teachers for thinking I could teach something as well as they do and to all the immunologists out there for the liberties I took in trying to explain this very complicated matter.

Herd Immunity for SARS-CoV-2

I frequently get asked about herd immunity, what is it; how long will it take us to get to it for this new SARS-CoV-2 virus that causes COVID; and why don’t we just throw caution to the wind, lock up granny and throw COVID parties until we have enough people infected (no one has actually phrased it this way, but you know you were thinking it!) that we now have herd immunity and can go on with our lives?

What is herd immunity?

The concept of herd immunity is used in the context of contagious, infectious diseases (most often viruses) and usually vaccine-induced immunity. The idea is that there are some in our population who may not be able to be vaccinated (e.g., newborns or those who have significant immunocompromise, especially when all we have is a live virus vaccine), those who can be vaccinated but may not develop a robust immune response (in some cases due to limitations of the available vaccine and in some cases the elderly who may not generate the same level of immune response as someone younger) and those who simply refuse to get vaccinated.

Herd immunity describes the point at which enough people in that population are immune (it could be through natural infection, but more often as a consequence of vaccination) that the virus cannot efficiently transmit within that population, so while a single of small group of people may be able to be infected for any of the reasons I stated above, generally you don’t see large outbreaks as we currently are for COVID.

Herd immunity helps protect those who remain susceptible to infection in the population because the large number of immune persons means that these vulnerable individuals are far less likely to be exposed to someone who can transmit the virus to them.

What determines the level of immunity a population needs to have so that we have herd immunity?

It is important to understand a few principles. First, the more contagious a virus is, the higher the level of immunity required in a population to provide herd immunity. For example, measles is one of the most contagious viruses. To avoid outbreaks of measles, we believe at least 94% of the population needs to have immunity.

Second, this was much simpler before we became a global society. Just to illustrate the point, let me make up a scenario. So, my best executive assistant ever just had a baby this month. Let’s say that in Boise, we have great herd immunity for measles. But, let’s say that she decides to go to a resort town in Idaho for the holidays later this year to be with family and to go out shopping for gifts in this resort town. However, this resort town is comprised of antivaccers, and the level of immunity is only in the low eighties. There are other visitors to this resort town and one family brings a child who develops measles while visiting. Measles begins to spread like wildfire (just to put things into perspective, measles is probably about 6 – 7 times more contagious than COVID). While my assistant’s child was not yet at the age to be vaccinated and thus remains susceptible, but was reasonably well protected in Boise, this beautiful little girl is now highly vulnerable in this community they have traveled to. So, when we speak of herd immunity, we are talking about the percentage of immunity within populations, but it is important to know that the virus can continue to spread in populations that have not achieved herd immunity, and susceptible persons may benefit from the protections of herd immunity in one population, but if they move or travel to an area with a population without herd immunity, they will have to take many more precautions since they will no longer have the benefit of protection within the herd.

Third, even within a population with herd immunity, we have examples such as religious and communal living communities within those populations with herd immunity that did not believe in vaccinations and were relatively isolated anyway because those communities were closed and not being exposed to the contagion, but later had significant outbreaks when persons form those communities made an international trip and then returned to their communal setting, bringing the infection with them.

What is the level of immunity in the population needed to protect the vulnerable from COVID?

Short answer, we don’t know. I have seen or heard projections anywhere from 10 – 90%. That doesn’t help us much.

So, most of us have most commonly heard the projection of 60% of the population with immunity to protect the vulnerable from continued outbreaks of COVID. Where did that number come from?

Well, there are mathematical models to predict the levels of immunity required for herd immunity. The simplest is the equation 1 – 1/R0, where R0 (R naught) is the number of people that an infected person will infect when at the beginning of an outbreak, at which time no mitigation strategies have yet been implemented. That number for SARS-CoV-2 is believed to be between 2.2 and 2.7. So, if we plug in R0 = 2.5, we get 1 – 1/2.5 = 0.6, i.e., the projection that herd immunity will require 60% of the population to be immune.

Now, while this is a convenient little equation, you may not be surprised to know that life is more complicated than this and that while this mathematical projection may be directionally correct, as I alluded to above, there are many factors that may contribute to what level of immunity will be required for herd immunity in different settings. For example, differing susceptibility levels in different populations could alter the level of immunity required for herd immunity. If young people are less susceptible to infection, a developing country with a much lower average age might require a lower level of immunity for herd immunity than a more advanced nation with a higher life expectancy. Social interactions can also impact this. In populations living in high density housing, significant crowding, or where people must show up to work sick in order to avoid losing employment, then higher levels might be necessary.

So, let’s go back to our equation, realizing it is not precise, it may not project the level of immunity required for populations that vary significantly from others in terms of their susceptibility, social interactions and risks for exposure, but with that said, let’s see if we can make sense of the range of 10 -90% that you can find out there, depending on whose projections you are taking.

One more thing about R0 before we begin. If a person who is infected infects less than one person on average, the virus is not transmitting efficiently and is unlikely to produce outbreaks and community spread of the infection. In other words, with an R0 of <1, we don’t have a lot of concern about the need for herd immunity. So, if R0 was 1.1 for this virus (which I don’t know anyone who believes that), then the level of immunity for herd immunity would be projected to be 1 – 1/1.1 = 0.1 or 10%. This is why I don’t currently believe that these low-end projections for herd immunity for this virus of 10 – 20%. In addition, while we still don’t know the percentage of Americans who have been infected, if you assume that 40% of all the infections have been asymptomatic (this is a reasonable assumption) and if you look at the confirmed cases of COVID in the country and if you assume that everyone who was infected is now immune (another fact that we doubt is the case), you can end up with an estimate that about 10.8% of the US population has been infected so far. Obviously, we have not achieved herd immunity as COVID cases are soaring around many parts of our country, so projections as low as 10% certainly don’t seem likely.

If you use the range that is commonly believed to be the R0 for this virus of 2.2 to 2.7, then you get a range of projections for the percent of the population with immunity needed to get herd immunity of 0.55 – 0.63, or 55 – 63%. That seems right to me, but as I said, we just don’t know. To the extent that these numbers are somewhere close to the levels of immunity required for herd immunity, we are a long ways off from achieving herd immunity, and given the impact on our economy, health care costs, the burdens on hospitals, the complications that some people appear to be developing post-COVID and the lives lost with just getting to 10 – 11% of Americans infected, there simply isn’t a reasonable basis to support the lock granny up, throw caution to the wind and get back to life as normal proposals to accelerate us getting to herd immunity, if that is even possible.

What do I mean, “if that is even possible?”

Well, herd immunity is based upon durable immunity in the herd. We still don’t know whether people who have been infected with SARS-CoV-2 are immune, and if so, for how long? There has been a lot of talk about antibodies, as if that was the entire basis for immunity (which it is not). But, studies on patients who have recovered from COVID are not particularly reassuring regarding the antibody response. Studies have suggested that not everyone makes antibodies following infection, oftentimes the antibodies produced are not the desirable types of antibodies that we would guess would be protective, even those who do make these best kinds of antibodies often do not produce them at high levels and a significant proportion of those who do develop antibodies experience a significant decline in their antibody levels in as little as two to three months. If antibodies are critical to the immune response against this virus (and I am not sure they are), and if these studies have accurately described the antibody response, then we would likely never have herd immunity through natural infection.

Now, don’t get too discouraged. First of all, our experience, though early, is that we have not seen a lot of cases where we believe a person previously infected with COVID has become re-infected. I don’t rule this possibility out, but if it does occur, it does not seem to be common. And, it may be because we have been chasing the wrong thing – antibodies. Oftentimes, with viruses, we find that the cellular immune response (see my prior blog post about this, as well as a soon upcoming one) is actually the most important. It may be that there are much higher levels of immune protection in our population than we think, since tests for cellular immunity are far more complicated, less available and not able to be performed in other than highly specialized laboratories. Regardless of this, it is very possible that the vaccines will stimulate a strong cellular immune response and a better antibody response than natural infection does, and in fact, with two vaccines for which we have data from early trials, that appears likely to be the case. The next challenge – get enough people vaccinated when a safe and effective vaccine is available that we can get somewhere around 60% of our population with durable immunity to this virus.

Questions for School Boards and School Principals

School leaders and decision-makers all across the country are trying to make decisions about whether to open schools for in-person education, when to open schools, and how to open schools safely both for students and their faculty and staff. These decisions are all the more difficult because unfortunately, for many parts of the country, there is significant community spread of the virus, school boards and leaders for the most part are not public health experts, there are significant political pressures and there are liability risks.

There certainly is guidance available from the CDC and the American Academy of Pediatrics. Obviously, complying with that guidance will be of significant help in defending a liability lawsuit, whereas decisions to depart from that guidance will create greater risk. Further, a decision to depart from the guidance may create job security risks for those leaders who are employed or political risks for those who are elected if we have the kinds of outbreaks and illness that has occurred at summer camps or that ends up contributing to strained hospital capacity. But, even with the guidance, there will be many unanswered questions, and boards and leaders would be well-advised to seek additional guidance from local public health agencies and medical experts.

Even a decision to follow the guidance may be challenging, especially with the fact that face masks and face coverings (for ease, I will subsequently refer to both as “face masks” or “masks”) have unfortunately become a political, emotional, and philosophical issue that strongly divides us, despite wide-spread agreement among medical experts, scientists and public health organizations that face masks, if worn correctly and by a sufficiently large enough percentage of the population, will significantly reduce the transmission of the SARS-CoV-2 virus when it is not possible to physically distance. The challenges for school boards and leaders who cave to the pressure not to mandate masks are that they will potentially be under pressure from teachers’ unions or associations concerned about protecting teachers’ health and lives, and potentially significant liability risks as rules of evidence will generally not allow for experts to introduce these political, emotional and philosophical arguments that are not supported by science or the expert community at large to be introduced in court as a defense.

My best advice to school boards and leaders is to undertake your due diligence, examine the guidance from the CDC, AAP and other reputable public health and medical organizations and then ask the following questions of the medical and public health experts who are advising you on your reopening policies, as a key element of coming to the best policy for your particular school or school district is to be fully informed of the risks and benefits, and a key element of defense in a liability action is to show that you were diligent in asking and considering the advice of experts. It may be helpful to ask and have these questions answered on the record both to demonstrate to the public your diligence, but also to create a record for your potential defense.

  1. Does the degree of community spread that we are seeing in our communities significantly increase the risk of exposure and transmission of the virus in our classrooms and school buildings that would then be likely to increase illness among our school children and staff?
  2. While there is evidence that children, if infected, tend to experience less serious illness, have there been children of the ages of our school children who have experienced severe enough illness to require hospitalization?
  3. If so, is there any effective way that we can identify which of our students could potentially develop serious illness so that we can take additional precautions to protect those students? If so, what would those additional precautions be?
  4. Studies suggest that the majority of children who are infected remain asymptomatic. If so, will symptom checkers or temperature screenings be able to identify those students who might then pose a risk of attending classes and transmitting the virus?
  5. If we cannot identify these students and parents are not aware that their child is sick and therefore know to keep their child home from school, what are the most effective means to prevent an infected, but asymptomatic (or pre-symptomatic) child from transmitting the virus to staff and students?
  6. What lessons can we learn from the outbreaks at summer camps that are applicable to our school reopening?
  7. This fall and winter, like every school year before the coronavirus, children will be exposed to a number of respiratory viruses and we know that many of these will be transmitted among students. Plus, we fully expect to have another influenza epidemic in the US. So, at points in time, the school is likely to have a number of children with fevers, coughs and runny noses. Because of the high disease activity of coronavirus across many parts of the country and disruptions in the supply chain, current testing for coronavirus is quite commonly delayed and often taking as much as 1 – 2 weeks for test results to come back. Since the Trump Administration has not announced any new strategies to address this testing logjam, we might assume that testing will continue to be a challenge this fall. If we have children who are ill, but we have these delays in testing, how are we going to know whether one or more of these children has infection with the SARS-CoV-2 virus and whether classmates and their teacher may have been exposed? I assume that we cannot close the school or quarantine teachers and classmates every time a student has a cold until we can get test results back a week later to confirm that is the case. What would our action be?
  8. One of the concerns about school reopening is that children may be exposed to the virus and while they are likely not to suffer severe illness, they may take the virus home with them. Do we know what percentage of our school’s children live with or stay with a vulnerable adult? Are there additional precautions we need to take for these children?

What You Should Know About Immunity to Severe Acute Respiratory Syndrome Coronavirus Variant 2 (SARS-CoV-2), the virus that causes COVID

Those that follow my blog, follow me on Twitter, listen to me answering listener questions about the coronavirus on radio or watch me on local television news programming will know that I have been an outspoken critic of offering SARS-CoV-2 antibody testing to the general public dating back to March. I still am, and as it turns out, many of the reasons I provided for objecting to the testing are turning out to be supported by recently released research studies. So, with this blog post, I am going to try to help you understand what little we know about the immune response and potential immunity to the SARS-CoV-2 virus, and some of the implications. There is both good news and bad news. If you are not interested in all the background and discussion of the research, you can skip to the bottom for my summary take-away points.

But first, a few disclaimers.

  1. These early studies are fascinating and informative, but not definitive. In other words, they do provide us with insights, but every research study is limited in what information it can provide and how broadly applicable the implications can be. For example, the findings of a study that looks at the response in a laboratory or in an animal may or may not be the exact way the immune system works in a human being. The findings of a study testing adults may or may not be applicable to children. The findings of a study testing persons who were hospitalized may not be the same findings that would have been found in individuals who were less severely ill and did not require hospitalization. You get the idea. So, before we conclude that the research we are going to review is broadly applicable, we need to see this replicated in other studies and in various populations of persons tested to see whether these findings are validated for everyone, or whether there may be important differences in different groups of people.
  2. The field of immunology is extremely complicated, and because this is a summary for lay persons without any particular knowledge of immunology, I will of necessity be oversimplifying my explanations below (my apologies in advance to laboratory scientists and immunologists) and will make no attempt to provide a comprehensive discussion of the immune response.
  3. We must readily admit that there is much that we don’t know and still don’t understand about the immune response to this virus. While it is amazing how much we have learned in just six months about this novel virus, nevertheless, we have only scratched the surface. As more research is conducted, we may learn that things we thought were true today are no longer true in the future.
  4. Finally, the SARS-CoV-2 virus, like all RNA viruses, is rapidly mutating. The overwhelming number of mutations will be inconsequential and will not impact the discussion below. However, there has already been one significant mutation, and there very well be more in the future. When there is a significant enough mutation or mutations to actually constitute a new strain, that new form of the virus can be more or less virulent (the significant mutation I mentioned above resulted in the virus being more infectious [more transmissible], but surprisingly, does not appear to be causing more severe illness), and if the mutations are of extreme significance, it could affect how well our current antibody tests work, how effective our immune response is and how well a vaccine (when we have one) will work.

Okay, here we go.

The first thing we need to do to understand possible immunity to the SARS-CoV-2 virus is understand the parts of the immune system. One of my criticisms of those who have been publicly promoting antibody testing is that they have not been clear with the public and likely contributing to further misleading the public because they tend to place all of the emphasis only on antibodies and seem to imply that having antibodies is to some degree synonymous with immunity. While people are probably most familiar with antibodies when they think of the immune system and immunity, I would make a wager that most people are under the misconception that antibodies = immunity. They do in some cases, but we have many examples where they do not.

First of all, antibodies come in various kinds. The kind most people are aware of is IgG and this has been the target of the current antibody tests. But, IgG has limitations. It cannot attach to a virus that has already gotten into a cell. It also is not present in mucosal tissues, like the gut, which happens to be a huge source of the receptor that the SARS-CoV-2 virus attaches to. To combat SARS-CoV-2 in the lining of the gut, you need IgA, not IgG. None of the current antibody tests check for the presence of SARS-CoV-2-specific IgA antibody.

Even within IgG, there will be many different specific IgG antibodies that target different proteins on the coronavirus – some are specific for the spike protein, some are specific for protein in the envelope of the virus, and so on. In other words, different IgG molecules will attack different parts of the virus. Some of these will be more effective than others, and not all, or even most, will accomplish the end-goal of preventing the virus from entering into a cell where it can replicate and perpetuate itself. Antibodies that do this are called neutralizing antibodies. The currently, widely available antibody tests just test for IgG and are unable, in most cases, to tell us how much antibody someone has and how protective those antibodies are.

The antibody response is just one part of a complicated and interrelated immune response. Antibodies take time to be produced. If you have not been exposed to SARS-CoV-2, then you will have no SARS-CoV-2-specific IgG antibodies in your blood. Once infected, it will take you a week or even more to develop and produce IgG antibodies. In the meantime, your immune system does not just let the virus have its way with your body. We have what is called an innate immune system, which is actually quite robust and complicated, but it recognizes that this virus is not part of you and will begin to attack it. The attack is a general response, not a targeted, specific one, so it can result in the mobilization of many types of white blood cells and chemicals whose role is to produce inflammation and an environment hostile to the virus, including cells that try to swallow the virus and destroy it inside these white cells before the virus can get into other cells that don’t have this capability and instead the virus can hijack its cellular machinery to mass produce new virus. Basically, there is a race between the virus and the immune system with the virus trying to invade the body and enter into cells, where it will be relatively safe (at least from the innate immune system and antibodies (which are called the humoral immune system) long enough to produce large amounts of new virus. Meanwhile, the innate immune response is racing to capture and destroy the virus before it can get into cells to replicate, and if the innate immune response cannot thwart the virus infection, at least buy time for the next part of the immune response called the adaptive immune response, which is a targeted and specific attack against this particular virus both with humoral immunity (antibodies) and cellular immunity (specialized immune cells that can enhance the antibody response and, unlike antibodies, can identify the cells that the virus has entered and kill those cells to stop production of new virus). This innate immune system response can be so intense that it produces wide ranging nonspecific symptoms, such as fever, fatigue, and a sense of feeling ill or unwell.

So, what is wrong with someone who thinks that they had an illness getting a SARS-CoV-2 antibody test to see if they had COVID? Well, it turns out there are plenty of reasons this may not be a good idea.

  1. If you just have an overwhelming sense of curiosity, a hundred bucks to spare, you understand all the limitations of this test and you are committed to continue to practice all of the recommended infection control measures (frequent hand washing, physically distance, wear a mask when you cannot physically distance, etc.), then I actually don’t have an objection to you getting the test.
  2. There is wide variation in the quality of antibody tests. Some are more reliable than others. It is challenging for a non-expert to be able to differentiate the better tests from the ones that are far less accurate. Further, none of these tests have been validated by the FDA. We often have to rely on the manufacturer’s own representations without much information about how they did their own testing and with the realization that they have a tremendous financial conflict of interest with an incentive to make a determination that the test is accurate, and it may not be. As a case in point, one test produced by a very reputable manufacturer and commonly used self-reported the sensitivity of the test as being 97.2 percent, which is considered very good. However, when independently tested, the sensitivity was determined to be only 82.1 percent, which would not be considered to be a good test.
  3. Even with an accurate test, if you test a population that has a low prevalence of infection, a positive test can be more likely to be a false positive test than a true positive test. In other words, the test may indicate the presence of antibodies, but you actually don’t have the antibodies to the SARS-CoV-2 virus. Obviously, it would be dangerous for someone to think that the positive test means they were infected and now are immune and then not take precautions that might now put the person at greater risk for infection. As an example, the pregnancy test is a pretty good test. But, if you test people who are unlikely to be pregnant, for example, a woman who is in her fifties or a woman who has had a hysterectomy, a positive test is more likely to be a false positive than a true positive. To take it even further, imagine that you take one thousand biological men and administer a pregnancy test. You might end up with a handful of positive tests. Obviously, they are not pregnant. It could be a problem in processing the test or a cross-rection with something else that is causing the test to appear positive, but there actually could be a few men who are producing the same pregnancy hormone that pregnant women produce, but it is because the men have a tumor that produces that same hormone, even though they obviously are not pregnant. So, we have to be very cautious in interpreting antibody tests when used on people in Idaho, where it is estimated that perhaps only two percent of the population has been infected.

A significant part of my argument against this testing has been we really don’t know how accurate it is, we don’t know if everyone produces antibodies to infection (e.g., it has been the case with other infections that mild or asymptomatic infections may not result in a significant antibody response, and in fact, many people with COVID have had mild illness or no symptoms), we have the risk to have false positive and false negative tests, and even if someone does make antibodies, we don’t know how much or how good the antibodies are and whether they will confer immunity, and even if so, for how long. Further, one large provider here in Idaho was pushing performing antibody testing on employees and reporting the results to their employer. For the life of me, I cannot imagine why I would want my employer to know my antibody test results. What would they do with that? If I was positive, would they put me in situations where I was more likely to be exposed to SARS-CoV-2 than other employees thinking that I could not catch COVID again? Would the employer decide I didn’t need to have all the expensive and limited PPE that is made available to other employees? I can think of a situation where an employer might want to know if certain areas of its business created high risk and infections, but in my opinion, employers should only receive aggregate rates of positivity and not individual employee’s test results.

It turns out that these recent studies confirm my concerns. While most people who have recovered from COVID do produce some antibodies, the amount and type of antibodies vary widely from person to person. It does appear that those with more severe infections produce higher levels of antibodies, and this is not unique to SARS-CoV-2 infections. However, the studies suggest that 2 – 8.5 percent of those who were infected do not seroconvert (in other words, have a positive antibody test) even weeks following infection. One study of individuals who were infected (confirmed with a PCR test) showed that 10 – 11 percent did not have a positive antibody test after 14 days, and another study of persons who were infected, but remained asymptomatic, showed that at 3 – 4 weeks following infection, about 19 percent of these individuals did not have a positive antibody test for IgG. Similarly and surprisingly, almost 16 percent of those who were symptomatic that they compared this study group to, also did not develop a positive antibody test. Further disappointing was the fact that over 2 – 3 months, 40 percent of the asymptomatic individuals who did initially produce antibodies, no longer produced them in amounts that could be detected by the antibody tests. Similarly, almost 13 percent of those who were symptomatic and initially produced antibody became negative on antibody testing after 2 – 3 months.

While a recent study shows that almost everyone makes some neutralizing antibody, a third of patients make them in very low titers, and only one percent of patients made these types of antibodies in very high levels that would likely be associated with immunity if neutralizing antibodies can confer immunity (which we do not know at this time). Another study of convalescent plasma donors from New York City showed that about 10 percent of donors had very high levels of neutralizing antibodies, but around 16 percent of donors had undetectable levels. Interestingly, this study also showed that antibody levels declined after 3 weeks.

To the extent that antibodies following natural infection are critical to immunity (and, we do not know that they are), the news is discouraging and suggests that most people may have limited protection and for a much shorter duration than we had contemplated. On the other hand, several of the neutralizing antibodies that nearly all persons made following infection were extremely potent, even though most people made them in very small amounts. This is very good news for our vaccine efforts, because if the vaccine can be designed to trigger the production of these particular neutralizing antibodies, then the vaccine may be highly effective.

All the discussion about antibodies and antibody testing ignores the fact that for most viral infections, cellular immunity generally plays an even more important role in fighting and preventing the infection than antibodies do. And, the good news from recent studies is that a very strong cellular immunity response was noted in everyone who has recovered from COVID, even those who had mild illness or who were asymptomatic, including family members who were exposed by a confirmed case in their family, but never determined to have become infected themselves.

Two key parts of the cellular immunity response are the development of helper and memory cells and cytotoxic or killer cells, all of which are specific to this virus. It turned out that everyone tested in this recent study developed specific memory/helper T cells. These cells can cause antibodies to be produced quickly upon exposure to the virus instead of the week or more delay that occurs when the person is exposed the first time to the virus and they can amplify the antibody production against the virus. Seventy percent of all those tested developed killer cells, which are the cells that detect the body’s cells that have been infected by the virus and kill those cells to terminate the replication of the virus. The helper cell response to the spike protein of the SARS-CoV-2 virus was very strong and robust. The good news about these findings is the suggestion that, as opposed to the case if antibody response is critical to immunity, if cellular immunity plays a key or the key role in immunity, many more persons previously infected could be likely to be immune and the duration of immunity may be considerably longer since the antibody levels declined rapidly and significantly with time, but the cellular immunity would likely be much more durable.

So, there remains much more to be learned about the immune response to SARS-CoV-2 and what is required for immunity, and if there is immunity, how long-lasting it will be. However, we certainly have interesting research studies from which we can make some inferences:

  1. A significant number of people appear not to develop antibodies in sufficient amounts that can be detected by the commercially available antibody tests, especially if they had very mild or an asymptomatic infection. This will result in false negative tests.
  2. Even if persons who were infected initially developed antibodies, a significant percentage of people stopped making sufficient levels of antibodies that could be detected after several months. This will result in false negative tests.
  3. We still do not know whether the presence of antibodies means that the person is likely to have immunity, but if it does, it appears that a very small percentage of people are likely to have strong protection.
  4. Even if antibodies do confer immunity, there is reason from these studies to be concerned that this immunity is short-lived, perhaps only lasting for months.
  5. Based upon all of these findings, a positive antibody test has the real potential to create a false sense of security for the person who tests positive, and potentially for their employer, which could cause the individual to take less precautions than he or she otherwise would, but yet the person may not be protected or fully protected, and if it has been months, the person may have lost their immunity.
  6. On a different note, the cellular immunity response (compared to the humoral immunity or antibody response) is far more encouraging, and this leads me to speculate as to whether this could explain why we are seeing relatively low levels of disease activity in some of the earlier hotspots in our country, at a time when many other places in the country are seeing marked increases in cases.
  7. Finally, these recent studies provide encouraging news for our developing vaccine options.

Here are the key take-a-ways:

  1. 2 – 16 percent of people don’t develop a positive antibody test after infection. These people will have false negative tests.
  2. Even if people do develop a positive antibody test after infection, in 2-3 months, 13 – 40 percent of those will have declining antibody levels to the point that they may no longer be detectable on the commonly used antibody tests.
  3. If antibodies are critical to immunity, it appears that only 1 – 10 percent of those infected make the kind of antibodies that we would predict would confer immunity. And, these antibodies, too, appear to decline in just a matter of weeks to months.
  4. While these antibody studies are discouraging, the other branch of immunity (cellular immunity) is very encouraging and studies showed that everyone infected (and even those who had significant exposures to infected individuals) developed a robust cellular immunity response even if they did not develop antibodies, and we have reason to believe that this immunity might be far more lasting than what is likely if antibodies are key to immunity.

So, for now, stay at home and work from home when you can. When you have to go out, physically distance. When you are unable to physically distance, wear a mask or face covering. And, instead of shelling out a hundred bucks for an antibody test that tells you little and provides no actionable results, consider donating that hundred bucks to a COVID relief effort.

COVID-19 Vaccine -Many Questions Remain

We all remain hopeful that a safe and effective vaccine to protect us from infection by the SARS-CoV-2 virus will be available within a year. This is far from certain, however, there reportedly have been promising results in early trials (we know little more than what has been in press releases because results of these studies have not been published in peer-reviewed medical literature yet). It is also promising that more than 150 vaccines, using different components of the virus to stimulate the immune response and different adjuvants that may enhance the immune response and prolong the immunity are being investigated. With so many variations undergoing trials, it offers hope that we may even have a variety of vaccines to choose from for our patients that can be tailored to their particular circumstances (e.g., we cannot use live vaccines in patients who are immunocompromised, and sometimes we find certain vaccines are more effective than others in children or in the elderly).

There remain many questions about these potential vaccines:

  1. When will we have a vaccine?

There has been speculation that we could have a vaccine this fall, perhaps as early as October. That would be wonderful, but very hard to believe. And, when people talk about a date that a vaccine may be available, we really need to be clear about what that means. Is that the date clinical studies conclude that the vaccine is safe and effective? Is it the date when the FDA approves the vaccine? Is it the date when manufacturing of the vaccine begins? Is it the date the vaccine is ready for distribution? Is it the date that the vaccine will be in pharmacies and doctors’ offices? The time over which these events transpire can very well be many months.

2. Will there be a sufficient supply of vaccine?

Given that the entire world will need the vaccine, it is widely believed that there will be limited amounts of vaccine available for some time until enough can be produced. The type of vaccine impacts how difficult it is to produce the vaccine and how long it will take. Given this, the state of Idaho is already beginning to determine priority levels for the vaccine. It is anticipated that vaccine will be prioritized to first responders, health care workers and high-risk individuals. So, when we asked above when the vaccine will be available, another question is when will it be broadly available to the public, as opposed to limited in supply such that it must be prioritized and rationed?

3. How many doses of vaccine will be required?

We don’t yet know. It appears that there is one vaccine that may only require a single dose, but it seems likely that most of the others will require a series of two injections a month apart. This has important implications. First of all, compliance with a two-vaccine series would be anticipated to be less than that of a single vaccination. Secondly, a two-series vaccine would generally be more expensive than a single dose vaccine, and cost may create a barrier to immunization. Finally, given the few manufacturers of vaccine syringes and needles and the anticipated increased demand for influenza vaccine, as well routine vaccinations for children, we might encounter shortages, particularly if the coronavirus vaccine requires a two-injection series.

4. How often will vaccination be required?

Unfortunately, recent studies suggest that the antibody response to natural infection with SARS-CoV-2 virus is very short-lived and that it is very possible that as many as 79 percent of those infected do not generate protective antibodies. There certainly is the potential to produce vaccines that will stimulate an improved immune response with the production of neutralizing antibodies, in addition to other immune enhancing effects, and it is possible that we may be able to promote more durability of the immune response with the right adjuvant. Nevertheless, it is very likely that we are looking at the potential of people needing an annual vaccination or perhaps a booster every two to three years.

5. Will the vaccine be effective in the elderly and immunocompromised patients?

There is a senescence of the immune response with increasing age. We will have to determine whether vaccines generate a sufficient immune response in the elderly, whether they require a stronger dose or perhaps more doses more frequently. Immunocompromised patients generally are not able to be given attenuated live vaccines, so we will need other options, and in fact, there are quite a number of other types of vaccines being studied. How effective those other vaccines are will likely depend upon the nature of the underlying immune deficiency.

6. How critical is IgA to the immune response and protection from SARS-CoV-2, and will the vaccine provoke an IgA response?

What we hear about in the press and media about “antibody tests” are tests that detect the presence of IgG, a type of antibody that is available to attack virus in the blood. However, IgG has two important limitations. It is ineffective at attacking viruses once they enter into a cell, and it is ineffective at attacking virus in tissues, especially the lining of the gut. IgA fulfills the latter role.

This is an important issue because the SARS-CoV-2 virus attaches to a receptor called ACE-2. That protein receptor is in the lining of the nasopharynx, the lungs and the gut. Currently, we believe that the target of the initial infection is the nasopharynx, but can the entryway for infection be the gut? Is IgA important in the defense from infection with this virus, as it is for certain other viruses, like polio? Will the vaccine trigger a sufficient IgA response?

The vaccine development for protection from the SARS-CoV-2 virus is encouraging, but far from certain. There remain many questions. No doubt we will get answers to many of these questions soon.