Medieval Globe

THE MEDIEVAL GLOBE Volume 1 | 2014 INAUGURAL DOUBLE ISSUE PANDEMIC DISEASE IN THE MEDIEVAL WORLD RETHINKING THE BLACK DEATH Edited by MONICA H. GREEN Immediate Open Access publication of this special issue was made possible by the generous support of the World History Center at the University of Pittsburgh. Copyeditor Shannon Cunningham Editorial Assistant PageAnn Hubert design and typesetting Martine Maguire-Weltecke Library of Congress Cataloging in Publication Data ©A catalog2014 Arc record Medieval for this Press, book Kalamazoois available from and Bradfordthe Library of Congress This work is licensed under a Creative Commons Attribution- NonCommercial-NoDerivatives 4.0 International Licence. ThePermission authors to assert use brief their excerpts moral right from to thisbe identified work in scholarly as the authors and educational of their part works of this is work. hereby granted pro vided that the source is acknowledged. Any use of material in this work that is an exception or limitation covered by Article 5 of the European Union's Copyright Directive (2001/29/EC) or would be determined notto be require “fair use” the Publisher’sunder Section permission. 107 of the U.S. Copyright Act September 2010 Page 2 or that satisfies the conditions specified in Section 108 of the U.S. Copyright Act (17 USC §108, as revised by P.L. 94-553) does ISBNwww.arc-humanities.org 978-1-942401-04-9 CONTENTS .....................................................................vii List of Illustrations The Medieval Globe Carol Symes ............................................................................. Introducing 1 Pandemic Disease in the Medieval World: Rethinking the Black Death Editor’sMonica Introduction H. Green ........................................................................ to 9 Taking “Pandemic” Seriously: Making the Black Death Global Monica H. Green ...................................................................... 27 TheAnna Black Colet, Death Josep and Xavier Its Consequences Muntané i Santiveri, for the Jordi Jewish Ruíz Ventura, CommunityOriol Saula, in M. Tàrrega: Eulàlia SubiràLessons de fromGaldàcano, History and and Clara Archeology Jáuregui ............. 63 TheSharon Anthropology N. DeWitte of .................................................................... Plague: Insights from Bioarcheological Analyses of Epidemic Cemeteries 97 Stuart Borsch ........................................................................ Plague Depopulation and Irrigation Decay in Medieval Egypt 125 Ann G. Carmichael .................................................................. Plague Persistence in Western Europe: A Hypothesis 157 New Science and Old Sources: Nükhet Varlık. Why the Ottoman Experience of Plague Matters 193 vi CONTENTS Heterogeneous Immunological Landscapes and MedievalFabian CrespoPlague: and An Matthew Invitation B. Lawrenzto a New ....................................... Dialogue between Historians and Immunologists 229 The Black Death and the Future of the Plague Michelle Ziegler ..................................................................... 259 Beginnings of the Yersinia pestis Polytomy Epilogue:Robert HymesA Hypothesis ....................................................................... on the East Asian 285 featured source Monica H. Green, Kathleen Walker-Meikle, and Wolfgang P. Müller. Diagnosis of a “Plague” Image: A Digital Cautionary Tale 309 PLAGUE PERSISTENCE IN WESTERN EUROPE: A HYPOTHESIS ANN G. CARMICHAEL Yersinia pestis HuMan PlaGue outbreakS occur after fleas infected with can find no other preferred hosts. Thus, plague is similar to the- vector-borne infectious diseases that have been described as “spillovers,” because humans are not directly involved in the primary ecological pro cesses that govern pathogen persistence (McMichael 2010; Ostfeld 2011; Quammen 2012). Plague persists via transmissions within a population of reservoir hosts, such as Eurasian great gerbils and marmots. This hidden, silent stage1 of plague transmission is now called “maintenance phase” plague, and involves only burrowing rodents and their fleas. Burrows provide protected microenvironments for temporary survival of both bacteria and flea larvae (Anisimov, Lindler, and Pier 2014; Wimsatt and- Biggens 2009). The precise mechanisms and ecological triggers that cause a wider, explosive “amplification phase” of plague, when highly sus ceptible animals begin to die, are not yet fully understood (Gage 2012). Intensive laboratory and field research projects focus on events early in a “transmission shift”: from ongoing flea-borne transmission within a maintenance host population to rapidly widening rodent die-offs, spread- by many flea species (Buhnerkempe et al. 2011). Today, several low-tech, early-alert surveillance systems teach peo ple living near plague hotspots how to notice deaths among the rodents involved in plague amplification. Should the warning signs escape notice,- laboratory and/or autopsy investigation of sudden human deaths in a plague-endemic region become the next-best alert that it is time to inter I owe an incalculable debt to Monica Green and Carol Symes, for their editorial inter- ventions; to Fabian Crespo, Nükhet Varlık, and Michelle Ziegler for detailed feedback on various points of my argument; and to George Sussman for his very helpful suggestions and edits. During the earliest formulations of this paper, my colleague Ellen Dwyer provided critique crucial to my eventual argument; her comments at that 1 inchoate stage proved invaluable. The terms “sylvatic” or “enzootic” are still used to refer to plague transmission exclusively among animals. More uncommonly, maintenance phase plague is called “primary plague,” and amplification (the spread to highly susceptible animal hosts), “secondary plague.” On the shifting scientific terminology, see Gage and Kosoy (2005). – the Medieval Globe 1 (2014) pp. 157 191 158 ann g. CarmiChael rupt plague’s spread. The remedy in both cases is the same: using pes- ticides Yersiniato kill the pestis fleas and flea larvae in areas near human habitation or worksites (Dennis and Staples 2009; Duplantier 2012; Stenseth et al. 2008). persists because it can infect a wide range of fleas, many of which do not feed on humans (Hinnebusch 2010). Environmental conditions that favor flea activity and replication are Yersinialinked to pestisplague amplification (Wimsatt andYersinia Biggins 2009;pseudotuberculosis Adjemian et al. 2007; Davis, Calvet, and Leirs 2005; Keeling and Gilligan 2000). Indeed, Y. pseudotuberculosisevolved from its ancestor, , through the acquisition of DNA permitting the infection of fleas. Because isYersinia able to live pestis and replicate freely, typically in water, it needs genes that allow it to utilize environmental resourcesY. pestis as nutri - ents. The new species lacks such capacity: it is an obli- gate pathogen. Instead, flea-borne transmission permits ’s survival, as well as its capacity to survive at the body temperature of fleas (26°C/79°F), a capacity which is conferred by two unique plasmids (i.e., DNA molecules within the bacterium, but separate from the DNA chro- mosome of the organism). Even though slightlyYersinia over pestis 90% of the DNA is the same in both organisms, the “extra-chromosomal” or plasmid DNA is essential to the extraordinaryY. pestis virulence of 2 (Hinnebusch 2005; Keim and Wagner 2009; Eisen and Gage 2009). Because most fleas are able to clear infection from their gastrointestinal system relatively quickly, evolutionary pressure selects for strains of plague that overwhelm mammalian immune defenses, ensuring high concentrations of bacteria in the bloodstream. When fleas feed on an infected mammal, most of these insects can become transiently infected, able to transmit the organismYersinia to a new pestis mammalian host (Perry and Fetherston 1997; Stenseth et al. 2008; Suntsov 2012). In sum, knowing that the evolution and survival of depends upon conditions favoring flea replication and dispersal changes how we historians can approach the problem of plague’s four-hundred-year persistence in Western Europe. 2 Y. pestis Y. pseudotuberculosis Y. pestis Many of the genes which shares with became “pseudo- genes” serving no known purpose. Some of the novel virulence genes that develops after the flea bite are genes that block many of the systemic immuneY. pestis defenses that warm-blooded mammals deploy. These genes are turned on (“upregulated”) at a temperature of 37°C/98.6°F. Similar to other emergent pathogens, lost or scrambled key components of the chromosomal DNA of theY. pestis ancestor organism, and it acquired the two additional plasmids unique to the killer bacterium, possibly in separate stages (Hinnebusch 2005). Many of the functions new to related to flea-borne transmission, but some included virulence factors in mammals, particularly the ability to cause an overwhelming pulmonary infection (Price, Jin, and Goldman 2012). 159 plague persistenCe in Western europe: a hypothesis Bio-historical interest in European plagues typically concentrates on the origins and nature of the disease that appeared in 1347. Second- arily, interdisciplinary interest once centered on the possible reasons for plague’s eventual disappearance from Western Europe: a region that, for the purposes of this historical study, I will limit to medieval Christendom. Nicely summarized a generation ago by Stephen Ell (1984), plague’s disappearance subsequently became a relatively less interesting locus of interdisciplinary

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