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Pearls and Pitfalls

Writing on Sports Medicine in Pandemic Times

Eichner, E. Randy MD, FACSM

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Current Sports Medicine Reports: July 2020 - Volume 19 - Issue 7 - p 245-246
doi: 10.1249/JSR.0000000000000731
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It is humbling to write on sports medicine during a raging pandemic. But as a young man, long ago, I spent 2 years as a medical epidemiologist. So I try to keep up with epidemiology, even though at this writing, in May 2020, more than 10,000 scientific or medical articles have already appeared on this novel coronavirus, SARS-CoV-2, that causes the disease COVID-19. Even more challenging is that one third of these articles are not peer-reviewed; they appear on “preprint servers” that, for a price, publish verbatim anything you send them. So, against all odds, I will start with thoughts on infections and epidemics, on our primal fear of contagion, and on quarantine or “social distancing.” Then, I will address four questions I have received that are relevant to athletes. Bear in mind the fast pace of this pandemic and our race to learn and cope. We have much more to learn about COVID-19 than we have yet learned. So when this column appears in July, part of what I write now will prove to be wrong then. But I do not know which part. Anyway, here I go.

Infections, Mankind, and History

It is said that nothing in history has killed more people than infectious disease (ID). Several stellar nonfiction or popular science books agree that ID has been a primary shaper of history. Now is the time to read John Barry's “The Great Influenza,” on the deadliest plague in history, the influenza pandemic from early 1918 to early 1920 that killed up to 100 million people worldwide. It killed more people in 1 year, 1918, than the Black Death killed in a century. It killed 650,000 Americans; during the “second wave” in 1918, as many as 200,000 Americans died in a single month, October.

Three other books come to mind. The polymath Jared Diamond wrote “Guns, Germs, and Steel” in 1996. He covers ID as a shaper of why Eurasian peoples conquered or displaced Native Americans, Australians, and Africans. But his theme is: Human history follows geography. Esteemed historian William McNeill wrote “Plagues and Peoples” in 1976. He aims to help explain human history by the ravages of ID and epidemics. He credits smallpox for helping Cortez conquer the Aztecs and Pizarro conquer the Incas. He covers epidemics from ancient to modern times, including Black Death (bubonic plague) in the 14th century and cholera in the 19th century. His book, if speculative and Eurocentric, is a novel look at history.

My favorite is “Rats, Lice and History,” by Hans Zinsser (1935). Zinsser, a Harvard microbiologist with a classical education, also traces epidemics throughout history, but he keys on typhus. He writes like none other, except maybe Kurt Vonnegut. He is cynical of humanity yet full of humanity. He shows sardonic wit and whimsical humor. He bounces all over, but it is fun to follow the bounces. He covers the sex life of the louse. He compares rats to man, saying “neither is of the slightest earthly use to any other species.” He recounts an episode in The Thirty Years' War where typhus, “single-handed,” killed so many soldiers that it “defeated both armies before they could join battle.” He also writes the best footnote ever, on the word saprophyte: “If the reader does not understand this word, it is too bad.”

Quarantine by Any Other Name

Our new quarantine is “social distancing.” The key part — to prevent spread of the virus — is physical distancing, but it also is social distancing, until the extroverts come banging on the Internet doors of the introverts via Zoom. Distancing — or quarantine — is a default measure to quell our primal fear of contagion when we lack other means to fight the dreaded ID. Early in the acquired immune deficiency syndrome panic, a Boston neurosurgeon called for Massachusetts to quarantine “irresponsible” carriers of human immunodeficiency virus on Penikese Island. Penikese, a small, barren, windswept island 14 miles off New Bedford, had a leper colony from 1905 to 1921. The Boston doctor, Frank Parker, who moved to Penikese (with his wife and a small staff) to care for the lepers — fighting for them; always reminding them of their value, humanity, and dignity — was later ostracized by the good people of Boston. He died fighting diphtheria in Montana in 1926. Frank Parker was not honored by Massachusetts until 1996 (1).

Quarantine began with leprosy, the great blight that shadowed medieval life. Medicine had nothing to offer, so the Church applied Old Testament principles to isolate lepers. The lepers wore shrouds, heard the mass for the dead, had earth thrown on them, and were led to huts outside the community. They were “quarantined” for life.

Quarantine came into its own when the Black Death exploded in Europe in the mid-14th century. Every house with a plague victim was placed under a ban. The Duke of Milan ordered all plague patients to be moved to a field outside the city to recover or die. Venice isolated incoming ships in the lagoon. Soon all travelers from plague-stricken areas were isolated for 40 d — hence the term “quarantine,” from quarantenaria, the Latin word for 40 d (2).

Today, nearly 700 years later, we face another dreaded scourge, a killing pandemic, and so far, quarantine is again our only friend. As Kurt Vonnegut would say: So it goes…

Now to the four questions I have received from sports medicine colleagues:

Question 1: Is asthma a risk factor for severe COVID-19?

The early answer is: Yes, then no, but we need more research. Health organizations cautioned that those with asthma may be at higher risk, but they based this on questionnaires with an “umbrella” box (to check or not) that included asthma, chronic obstructive pulmonary disease, or emphysema. Now, with clinical articles flooding in, asthma is “falling out.” Asthma was not named as a risk factor in a large case series from China. In New York, asthma is not even in the top 10 co-morbidities, and state officials say only 5% who died from COVID-19 had asthma. A recent comment by European researchers also notes that asthma is “underrepresented” in those with COVID-19. A study from Seattle hospitals notes that 3 (12.5%) of 24 patients with severe COVID-19 had asthma, but this is not significantly more than expected by chance. Two pediatric studies apply. Among 48 children in intensive care units (in the United States and Canada) with COVID-19, asthma was not prominent. Among 177 children and young adults in the Washington, DC area with COVID-19, although 20% had asthma, it was not more common in those critically ill, and the authors judge that although asthma commonly flares from viral infections, with COVID-19, asthma is not the primary determinant of severe disease. A laboratory study even suggests that allergic asthma may fend off severe COVID-19. So yes, we need more research.

Question 2: Are athletes with sickle cell trait prone to COVID-19 or problems therefrom?

The answer for now is no. African-Americans and other minorities are hit harder by COVID-19, but sickle cell trait (SCT) has not been singled out. Diverse clotting complications are increasingly being reported with COVID-19, not just the expected deep venous thrombosis (DVT) and pulmonary emboli (PE) in some after weeks on ventilators, or the typical disseminated intravascular coagulation in those gravely ill, but also large vessel strokes in the young and even aortic occlusion just above the iliac arteries. Some of these patients may prove to have inherited thrombophilias. Along these lines, four epidemiologic studies of adults in various populations find that, over the years, when all else is equal, SCT carriers have about a two-fold higher risk of PE, often without clearcut underlying DVT. Why this should be is unclear; here too we need more research.

Question 3: If athletes test positive for the antibody, are they immune to this Coronavirus?

Maybe. But no one yet seems to know how immune, or for how long. Let me ask a question: Say your antibody test is 99% reliable, but only 1% of your population of concern has the antibody. If a random person in that population tests positive, what is the chance he or she actually has the antibody? The intuitive answer is 99%. The correct answer is 50%. It is statistics, the Bayes theorem. Even doctors tend to answer wrong; they fall for the “base-rate neglect fallacy” (3). Even when the antibody-carrying rate rises to 5%, as it may be now in the nondense county in California where I live, 16% of the positives will be false positives. Pitfall: Antibody testing for this novel coronavirus is not yet failsafe. Do not blame me; I was an English major. Blame Bayes.

Question 4: We tell our players to sit in the front row in classrooms, to feign interest in what the teacher has to say. This fall, in light of COVID-19, should we tell them to sit in the back row?

College classrooms full of students may be risky this fall. One person infected nine others in a small restaurant in China; one person infected 96 others in a call center in South Korea; and one person infected 52 others (and two died) in a choir practice in Skagit County, Washington. A recent study finds that tiny respiratory droplets from normal speech can remain in the air for 8 minutes or longer. As the saying goes: “Hope floats.” Alas, so does this coronavirus.

Bottom line: Yes, tell them to sit in the back row, far from the teacher — and 6 ft away from all others in the room. Everyone should wear a mask. And pray that this fall is not like that of 1918.


1. Silvia J. The tragic story of Massachusetts’ leper colony and the “lights of Penikese Island,” Dr. Frank Parker and wife Marion. August 28, 2019. [cited 2020 May 18]. Available from:
2. Eichner ER. Quarantine: the once and future shield? Resid. Staff Physician. 1988; 34:66–71.
3. Fenton N, Neil M. Comparing risks of alternative medical diagnosis using Bayesian arguments. J. Biomed. Inform. 2010; 43:485–95.
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