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Volume 16, Number 10—October 2010
Letter

Body Lice, Yersinia pestis Orientalis, and Black Death

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To the Editor: A scientific debate with public health implications wages: What caused the medieval European plague epidemics known as Black Death? Recent articles note inconsistencies between a rat flea–borne pandemic of Yersinia pestis (the bacterium that causes bubonic plague) and the documented characteristics of Black Death (1, among others). Ayyadurai et al. (2) acknowledge that a rat flea–only hypothesis does not fit Black Death observations, but they resolve theoretical transmission inconsistencies through a louse-borne hypothesis. Ayyadurai et al. base their surety of fact—that medieval “plagues” were caused by Y. pestis infection—on a 2007 study (3) in which 5 of 36 teeth of “plague” victims, none of which were dated to the Black Death era (1347–1351), contained biological evidence of Y. pestis. The 3 locations in that study were all port cities: 2 on the Mediterranean Sea and 1 on the Rhone River. As Duncan and Scott (4) note, bubonic plague most likely existed endemically near ship-borne trade, unlike the fast-moving epidemic fronts exhibited by medieval “plagues.” Moreover, Gilbert et al. (5) found no Y. pestis DNA in 61 skeletons from primarily nonport locations in England, France, and Denmark.

We do not dispute the authors’ claim that Y. pestis might have been present in some skeletons from port cities in France, or that body lice might, under certain circumstances, transmit the Orientalis biotype of Y. pestis; their work appears careful and considered. However, given the differences mentioned above and improved knowledge on the rapidity of virus mutation and worldwide transmission potential, we merely argue that the simplest explanation for medieval plagues has yet to be ruled out: that they may have resulted from a human-to-human transmitted virus. Adding complexity to an already complicated etiologic theory, and stating such as historical fact based on limited geography and sample size, does not seem congruent with Occam’s razor.

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Mark Welford and Brian Bossak
Author affiliations: Author affiliation: Georgia Southern University, Statesboro, Georgia, USA

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References

  1. Welford  MR, Bossak  BH. Validation of inverse seasonal peak mortality in medieval plagues, including the Black Death, in comparison to modern Yersinia pestis–variant diseases. PLoS ONE. 2009;4:e8401. DOIPubMedGoogle Scholar
  2. Ayyadurai  S, Sebbane  F, Raoult  D, Drancourt  M. Body lice, Yersinia pestis Orientalis, and Black Death. Emerg Infect Dis. 2010;16:8923.PubMedGoogle Scholar
  3. Drancourt  M, Signoli  M, Vu Dang  L, Bizot  B, Roux  V, Tzortzis  S, Yersinia pestis Orientalis in remains of ancient plague patients. Emerg Infect Dis. 2007;13:3323. DOIPubMedGoogle Scholar
  4. Duncan  CJ, Scott  S. What caused the Black Death? Postgrad Med J. 2005;81:31520. DOIPubMedGoogle Scholar
  5. Gilbert  MT, Cuccui  J, White  W, Lynnerup  N, Titball  RW, Cooper  A, Absence of Yersinia pestis–specific DNA in human teeth from five European excavations of putative plague victims. Microbiology. 2004;150:34154. DOIPubMedGoogle Scholar

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DOI: 10.3201/eid1610.100683

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To the Editor: The letter of Ayyadurai et al. (1) reminded us of a little-known paper (2) on rats and Black Death by our colleague and mentor David E. Davis. He researched and wrote in his retirement after years of research and reflection on rat ecology and rodent-borne diseases (3,4). Rattus rattus is commonly recognized as the vertebrate host of flea-borne plague that swept through Europe in the 1300s, killing >50% of the population. Davis believed this explanation did not fit what he knew of the ecologic requirements of fleas and black rats. He studied reports of archeologic excavations and reviewed poems, medieval bestiaries, and paintings and concluded that these rats were scarce during the Black Death era.

His theory, based on historical information and investigative trips to Europe, was that invasive rats, if present, mostly occurred in low densities in port areas, not in rural inland areas. He noted that the expected rodent die-offs with bubonic plague were not associated with human epidemics and that rodent fleas would not have been active during winter to transmit plague. Flea-borne transmission from rodents usually causes a few deaths per household, but deaths of entire households commonly occurred in the medieval epidemics. Human-to-human transmission of pneumonic plague must have occurred, but as described by Ayyadurai et al., there was evidence of human bubonic plague, suggesting vector involvement. Davis did not present a viable reservoir/vector hypothesis for plague transmission; this and the later, well-known association of R. rattus and other rodents with plague throughout the world, may partially explain why his ideas received little attention. The finding that human body lice can be bubonic plague vectors suggests a mechanism for human-to-human transmission continuing during winter in inland areas and, as suggested by the authors, could also explain total deaths in households.

References

  1. Ayyadurai  S, Sebbane  F, Raoult  D, Drancourt  M. Body lice, Yersinia pestis, and Black Death. Emerg Infect Dis. 2010;16:8923.PubMedGoogle Scholar
  2. Davis  DE. The scarcity of rats and the Black Death: an ecological history. J Interdiscip Hist. 1986;16:45570. DOIGoogle Scholar
  3. Anonymous . Profiles of previous Wildlife Disease Association leaders: David E. Davis 1913–1994. J Wildl Dis. 1995;31(suppl):15.PubMedGoogle Scholar
  4. Davis  DE. The characteristics of rat populations. Q Rev Biol. 1953;28:373401. DOIPubMedGoogle Scholar
  5. Ayyadurai  S, Sebbane  F, Raoult  D, Drancourt  M. Body lice, Yersinia pestis Orientalis, and Black Death. Emerg Infect Dis. 2010;16:8923.PubMedGoogle Scholar
  6. Welford  M, Bossak  B. Body lice, Yersinia pestis Orientalis, and Black Death [letter]. Emerg Infect Dis. 2010;16:1651.PubMedGoogle Scholar
  7. Welford  MR, Bossak  BH. Validation of inverse seasonal peak mortality in medieval plagues, including the Black Death, in comparison to modern Yersinia pestis–variant diseases. PLoS ONE. 2009;4:e8401. DOIPubMedGoogle Scholar
  8. Drancourt  M, Roux  V, Dang  LV, Tran-Hung  L, Castex  D, Chenal-Francisque  V, Genotyping, Orientalis-like Yersinia pestis, and plague pandemics. Emerg Infect Dis. 2004;10:158592.PubMedGoogle Scholar
  9. Pusch  CM, Rahalison  L, Blin  N, Nicholson  GJ, Czarnetzki  A. Yersinial F1 antigen and the cause of Black Death. Lancet Infect Dis. 2004;4:4845. DOIPubMedGoogle Scholar
  10. Bianucci  R, Rahalison  L, Massa  ER, Peluso  A, Ferroglio  E, Signoli  M. Technical note: a rapid diagnostic test detects plague in ancient human remains: an example of the interaction between archeological and biological approaches (southeastern France, 16th–18th centuries). Am J Phys Anthropol. 2008;136:3617. DOIPubMedGoogle Scholar
  11. Wiechmann  I, Grupe  G. Detection of Yersinia pestis DNA in two early medieval skeletal finds from Aschheim (Upper Bavaria, 6th century AD). Am J Phys Anthropol. 2005;126:4855. DOIPubMedGoogle Scholar
  12. McLean  RG, Fall  MW. Body lice, Yersinia pestis Orientalis, and Black Death [letter]. Emerg Infect Dis. 2010;16:16512.PubMedGoogle Scholar
  13. Blanc  G, Baltazard  M. Recherches expérimentales sur la peste. L’infection du pou de l’homme: Pediculus corporis de Geer. CR Acad Sci. 1941;213:84951.
  14. Raoult  D, Dutour  O, Houhamdi  L, Jankauskas  R, Fournier  PE, Ardagna  Y, Evidence for louse-transmitted diseases in soldiers of Napoleon’s Grand Army in Vilnius. J Infect Dis. 2006;193:11220. DOIPubMedGoogle Scholar
  15. Raoult  D, Roux  V. The body louse as a vector of reemerging human diseases. Clin Infect Dis. 1999;29:888911. DOIPubMedGoogle Scholar

Table of Contents – Volume 16, Number 10—October 2010

Page created: September 08, 2011
Page updated: September 08, 2011
Page reviewed: September 08, 2011
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.
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