Hektoen International

A Journal of Medical Humanities

Quarantining souls: The impact of plague village

Anahita Dua
Wisconsin, United States

Eyam church and graveyard where plague victims are buried.
Eyam church and graveyard where
plague victims are buried.

Infectious diseases have debilitated or ended more lives in history than any other illness. Quarantine, from the Italian quaranta, has been implemented since the fourteenth century as the cornerstone of a coordinated effort to control the spread of disease.1 Isolation is the crux of a successful quarantine, and was used by a rural British village to save the lives of its people in 1665.1

Since the 6th century the plague occurred in three major pandemics and has caused millions of deaths.2 It likely originated in central Asia and then spread westward along the major trade routes into Italy, then France, and finally the United Kingdom.2 As medicine was ineffective against it, the only way to prevent death was to avoid contact with infected persons. Hence, in 17th century Britain, when villagers discovered that an inhabitant had died of the plague in their town, their immediate reaction was to flee to a neighboring village. Unfortunately, they would often bring with their belongings the fleas that harbored the dreaded Yersinia pestis, the organism that caused the plague or “black death.”1-4

In September of 1665, the plague reached Eyam, a small British village. George Viccars, a tailor, imported flea infested cloth from London, contracted bubonic plague, and died. The citizens of Eyam knew they had been exposed to the disease and turned to their church leader, Reverend William Mompesson, for advice. Reverend Mompesson, with the support of Puritan minister Thomas Stanley, persuaded the people of Eyam to self-quarantine. This would make a death sentence a near certainty but would also prevent the spread of plague to surrounding areas in England. The ministers implemented precautions to prevent infection amongst villagers by insisting that families bury their own dead and by relocating church services outside. In keeping with the policies of isolation, infective spread was minimized by having donated food and supplies left outside the village boundaries for locals to retrieve. The Earl of Devonshire freely donated food, but any goods or money used as payment for other items were “purified” with running water from the well or left in vinegar soaked holes for the outside world.4-6

After fourteen months of self-quarantine the 350 population of Eyam had dwindled to just 83 (Fig 1).4-6 Interestingly, survival was not correlated with exposure: Elizabeth Hancock, who lost her husband and six children to the plague, survived even though she lived close to infected people and had to handle their dead bodies. Other unexpected survivors were Marshall Howe, the grave digger who survived despite handling dead bodies, and Reverend Mompesson, who lost his wife Catherine.

Genetics is the basis of a medical theory explaining why some persons survived and others perished. In 1996 researchers found 14% of direct descendants of the citizens of Eyam had the CCR5-delta 32 mutation. This mutation had previously been studied because those with one copy of the CCR5-delta 32 mutation are resistant to HIV and those with two copies are immune to HIV. While there has been no direct evidence linking CCR5-delta 32 mutations to plague immunity, the high percentage of carriers is significant in Northern European populations and may be attributable to another pandemic: smallpox. People with the CCR5-delta 32 mutation may have been resistant to smallpox, hence the high propagation of the mutation in this population. Therefore, the increased prevalence of this genetic mutation in Eyam community descendants may simply be incidental.7,8 

With an almost 80% mortality rate the decision to self-quarantine was undoubtedly heroic. But was it the right thing to do? A recent study noted that in the first nine months the transmission of plague was predominantly from fleas to humans, but after that point a sudden peak in mortality (as indicated by church records) may have resulted due to a more aggressive transmission pathway (human to human because of proximity).4 Researchers have hypothesized that this mode of transmission was more consistent with inhalation of Yersinia pestis causing pneumonic plague, a highly lethal syndrome. A mathematical model for plague dynamics was designed that incorporated both indirect (fleas-rats-humans) and direct (human-to-human) transmissions; results from historical data from Eyam and this mathematical model correlated suggesting that confinement facilitated the spread of the infection by increasing contact rates.4 Another study concluded that the policy of quarantine was likely misguided and resulted in substantial death for Eyam’s citizens because of the increased contact with infected persons.6

Regardless of the academic controversy, the decision of the people of Eyam to self-quarantine in order to save the lives of their compatriots is indisputably heroic. While the exact number of lives Eyam’s residents saved by their valiant decision will never been known, their courageous decision to save those lives at their own expense will be remembered as a genuine act of humanity.


  1. Matovinovic J. A short history of quarantine (Victor C. Vaughan). Univ Mich Med Cent J. 1969 Oct-Dec;35(4):224-8.
  2. Zietz BP, Dunkelberg H. The history of the plague and the research on the causative agent Yersinia pestis. Int J Hyg Environ Health. 2004 Feb;207(2):165-78.
  3. Tognotti E. Lessons from the history of quarantine, from plague to influenza A. Emerg Infect Dis. 2013 Feb;19(2):254-9. doi: 10.3201/eid1902.120312.
  4. Massad E, Coutinho FA, Burattini MN, Lopez LF. The Eyam plague revisited: did the village isolation change transmission from fleas to pulmonary? Med Hypotheses. 2004;63(5):911-5.
  5. Eyam and the Great Plague of 1665. http://www.historylearningsite.co.uk/eyam_and_the_great_plague_of_166.htm Accessed Nov. 7th, 2013
  6. Coleman MP. A plague epidemic in voluntary quarantine. Int J Epidemiol. 1986 Sep;15(3):379-85.
  7. Cohn SK Jr, Weaver LT. The Black Death and AIDS: CCR5-Delta32 in genetics and history. QJM. 2006 Aug;99(8):497-503.
  8. Duncan CJ, Scott S. What caused the Black Death? Postgrad Med J. 2005 May;81(955):315-20.

ANAHITA DUA, MD, MBA, MS, is a general surgery trainee with a trauma and vascular focus. She graduated from the University of Aberdeen Medical School and is currently in surgical residency training at the Medical College of Wisconsin. She has a Masters of Science in Trauma Sciences from Queen Mary University of London and is in her 2nd year of post-doctoral research training at the University of Houston, Texas. Dr. Dua travels extensively doing humanitarian medical mission work and has volunteered in a medical capacity in Afghanistan, Palestine, India, Kenya, Peru, Haiti, Chad, and the Democratic Republic of the Congo.

Highlighted in Frontispiece Summer 2015 – Volume 7, Issue 3
Summer 2015  |  Sections  |  Infectious Diseases

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