One of the strangest things that has happened during the COVID-19 pandemic is the politicization and polarization of the American public. Instead of relying on science, people are relying on echo chambers of social media for their understanding of the disease. This breeds a lot of lies and disinformation. Instead of trying to pick apart the false arguments though, I’m simply going to show why the narrative makes a difference.
Sanche et al. reported that early on, the reproductive rate (R0) for the virus was thought to be 2.2-2.7. That is simply the number of people who get the disease from an infected individual. However, the authors calculated a R0 of 5.7 over a 6-9 day period. Just for the sake of argument though and to keep this simple, I’ll use a lower value of 3.0, which is below the 95% confidence interval in their report and 9 days for my illustration.
Under the above conditions, assume that something I say or write causes one person to behave differently and prevents them from getting infected. Over the next four generations of disease (36 days), and assuming that everyone downstream from that person doesn’t do anything to keep from becoming infected but isn’t exposed through anyone else, that would prevent 81 people from becoming infected. For arguments sake under the same conditions, let’s say I prevent that directly among 10 people. That prevents 810 infections. Assume I prevent 100 people initially from making mistakes. That would prevent 8100 infections, and if the case fatality rate was 1%, it would prevent 81 deaths.
On the flip side though, what if someone spreads messages that this is really not of any concern and to go about business as usual. No mask, no social distancing, going into crowds as one sees fit, etc. The opposite is then true under the same assumed conditions. That will spread the disease to 81, 810, or 8100 people. That’s why it’s so important to push science and facts as opposed to a laissez-faire approach fueled by anti-science and conspiracy theories. (For a recent examination of conspiracy theories in the US, there is a great episode of Frontline titled “United States of Conspiracy.”)
Set the R0 to 3, the fatality rate to 1%, the susceptibility to 100% (that’s why it’s called a “novel” virus), and see what happens with various approaches to isolation. It’s pretty stunning how quickly it spreads through 1000 people if you set that to zero.
I’ve been accused of all kinds of crazy things, such as deriving joy from watching this unfold and fear mongering. Nothing is further from the truth. I have had many sleepless nights since February as this has been unfolding.
If those assumptions were true, would I have spent much of my career working on prevention of pandemic impacts and writing here to try to get people to take it seriously? I think that a number of Americans have gone completely mad, including many I know personally.
Even then, I still want to mitigate their risk, even though I feel like I’m constantly beating my head against a wall.
A Florida high school held its graduation on July 25th. Shortly after that date, one of those in attendance tested positive for coronavirus. Almost 300 graduates and their families who were in attendance were told to quarantine by the health department.
Campers from other states (27) were not included in the analysis. 597 residents of the state were in attendance. At the time of publication, results were available for 344 (58%), and of those, 260 (76%) were positive. The age range of attendees was 6-19 years old. The authors noted that because a portion of the status of campers was not known, an even higher percentage could be infected, some transmission may have been outside of camp attendance, and it’s unknown how well prevention measures were followed at the camp.
There are a few things worth quoting verbatim from the summary:
“These findings demonstrate that SARS-CoV-2 spread efficiently in a youth-centric overnight setting, resulting in high attack rates among persons in all age groups, despite efforts by camp officials to implement most recommended strategies to prevent transmission. Asymptomatic infection was common and potentially contributed to undetected transmission.”
“Children of all ages are susceptible to SARS-CoV-2 infection and, contrary to early reports, might play an important role in transmission.”
“Physical distancing and consistent and correct use of cloth masks should be emphasized as important strategies for mitigating transmission in congregate settings.”
The results are worth noting. “The observed differences in median CT values between young children and adults approximate a 10-fold to 100-fold greater amount of SARS-CoV-2 in the upper respiratory tract of young children. We performed a sensitivity analysis and observed a similar statistical difference between groups when including those with unknown symptom duration. Additionally, we identified only a very weak correlation between symptom duration and CT in the overall cohort “
Essentially that means that among children under five years of age, there was evidence of 10-100x more virus in the upper respiratory tract than those of older children or adults, who had similar values.
They concluded “Thus, young children can potentially be important drivers of SARS-CoV-2 spread in the general population, as has been demonstrated with respiratory syncytial virus, where children with high viral loads are more likely to transmit. Behavioral habits of young children and close quarters in school and day care settings raise concern for SARS-CoV-2 amplification in this population as public health restrictions are eased.”
One particularly important finding was “individuals with viral co-infection were significantly more likely to require ICU admission, respiratory support, or inotropic support.” That does not bode well for the influenza and RSV season.
Only 93 (16%) never developed clinical symptoms. Four of the children died, two of them had no known pre-existing conditions. “Our data show that severe COVID-19 can occur both in young children and in adolescents, and that a significant proportion of those patients require ICU support, frequently including mechanical ventilation.”
Second, they state “Limited emerging evidence suggests that susceptibility to infection also generally increases with age.” and go on so state “Age-related differences in infectivity are less clear. Findings from a few contact-tracing studies suggest that children may be less infectious than adults,” although they do admit that the evidence for the second is weak For both comments, they cite research that has not yet been peer reviewed, which is unusual. The MMWR study about the outbreak at the camp in Georgia clearly provides contrary evidence against those claims.
Third, they make a case that experiences in other countries indicate that opening schools did not seem to have a big impact. The problem in drawing that comparison is that they failed to address the prevalence rate in much of the US, which is alarmingly high in many areas, so that comparison isn’t very useful.
Schools reopened on May 17th. Israel began to reopen the economy. Beaches, synagogues, and shopping malls opened on May 20th. On May 27th, restaurants, bars, nightclubs, and hotels were allowed to reopen.
Changes that increase or reduce new cases show up three weeks after they are put in place. In the epidemic curve in this graph, the green vertical bar represents three weeks after the lockdown started.
The red bar represents three weeks after schools opened. The yellow bars represent the same interval after the other economic changes were made. It’s clear that all of these three events contributed to the exponential growth that followed.
One item that is particular noteworthy happens two weeks after the impact of schools opening (indicated by dark blue bars). I had previously expected events such as protests, youth sports, and other activities that involved a population composed of individuals who were younger and thus more likely to have milder symptoms or to be asymptomatic to not be indicated in the case data. They would spread the disease to family members and others in their social circles that would be part of the 2nd or 3rd generations of disease from them 2-4 weeks after later if they themselves would have become recognized cases if tested, but didn’t.
As expected, that rise in cases is accompanied by the subsequent rise in deaths a few weeks later.
To the authors’ credit, they did state “The safest way to open schools fully is to reduce or eliminate community transmission while ramping up testing and surveillance. Adults would need to maintain social distance from each other and engage in other measures to reduce adult-to-adult transmission: for example, wearing personal protective equipment (PPE), closing school buildings to all nonstaff adults, and holding digital faculty meetings…If such measures were adopted now, transmission in many states could probably be reduced to safe levels for mid-September or early-October school reopenings.”
Unfortunately, that does not seem to have occurred in many places around the US.
The biggest omission though was a discussion around the long term impacts of infection with COVID-19, which are not known for children.
Long Term Health Impacts
There is more information about the impact of COVID-19 on other organs besides the lungs. What remains unknown is the prevalence of the clinical problems described below in those who have recovered from less severe disease, but it does seem pretty clear that ACE2 receptors are a common link in the pathological mechanism. Even less is known about the pathological findings in children and adolescents from this problems, which could hypothetically cause significant problems later in life.
Cardiac
According to UCSF, a 57-year old woman died of COVID-19. What was very unusual though was while she had mild pneumonia, the virus had ruptured her heart.
“Clinicians, too, were seeing surprising numbers of COVID-19 patients develop heart problems – muscle weakness, inflammation, arrhythmias, even heart attacks…It stands to reason that SARS-CoV-2 affects the heart. After all, heart cells are flush with ACE2 receptors, the virus’s vital port of entry.”
Hepatology published a retrospective cohort study of 1826 patients with confirmed COVID-19. “Liver test elevation has been identified as one of a growing spectrum of non-pulmonary manifestations described in COVID-19, which may potentially be attributable to hepatic expression of the primary viral entry receptor, angiotensin converting enzyme II (ACE2). Based on a large systematic review and meta-analysis (17 studies, 2711 patients), liver test abnormalities are estimated to occur in approximately 15% of patients.”
“SARS-Cov1 and SARS-CoV use Angiotensin Converting Enzyme (ACE2) as an entry point to cells. Angiotensin I and angiotensin II have been associated with inflammation, oxidative stress, and fibrosis, and ACE2 is involved in their deactivation. If overwhelming coronavirus infection, with binding to ACE2 on epithelial targets not only in the lung but in other tissues expressing these proteins, including the kidney, intestines, and brain, were to interfere with ACE2 activity, the resulting increases in angiotensin II could lead to reactive oxygen species formation and interference with antioxidant and vasodilatory signals such as NOX2 and eNOS, with further complement activation.
Ackerman et al. also described some of the vascular endothelial implications. “We found greater numbers of ACE2-positive endothelial cells and significant changes in endothelial morphology, a finding consistent with a central role of endothelial cells in the vascular phase of Covid-19. Endothelial cells in the specimens from patients with Covid-19 showed disruption of intercellular junctions, cell swelling, and a loss of contact with the basal membrane. The presence of SARS-CoV-2 virus within the endothelial cells, a finding consistent with other studies, suggests that direct viral effects as well as perivascular inflammation may contribute to the endothelial injury.
It is thought that the damage seen in blood vessels might account for MIS-C, stroke, COVID toe, and other problems.
Given how many American adults refuse to wear masks, it’s no wonder that a county education department had to create guidelines that state “If your child had a fever overnight or in the morning, please DO NOT give him/her Tylenol/Motrin and then SEND THEM TO SCHOOL!” It’s unclear how common this practice is, but it could spell problems related to notifying school districts if that data isn’t available and the parent(s) of an infected child decide to send them to school.
Conclusion
Admittedly, there are difficulties and consequences related to moving schools to a completely virtual option. The prevalence of COVID-19 in a community could be helpful in guiding those decisions, but it is imperative to think about the possible long-term impacts of this disease when making these decisions and policies. It’s a high price to pay to solve an immediate problem, especially one where there it is still unclear as to what percentage of transmission indoors is due to droplets versus aerosols, which can stay suspended for long periods of time.
It is odd to hear objections to this based on hunger, abuse, disparity, and socialization from people who have never raised these objections before the pandemic. These problems should be addressed, and should have been addressed long before this problem emerged. There is no greater need to tackle these issues than now given that it will be nearly impossible to keep children, adolescents, teachers, administrators, and support staff safe, as well as their families. It seems to be forgotten that one of the most traumatic things that can happen to a child is the death of a family member.
I don’t claim to have the right answer, but I think I know the wrong one.
