The Black Death and Later Plague Epidemics in the Scandinavian Countries: Perspectives and Controversies 9788376560472, 9788376560465

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Ole J. Benedictow The Black Death and Later Plague Epidemics in the Scandinavian Countries: Perspectives and Controversies

Ole J. Benedictow The Black Death and Later Plague Epidemics in the Scandinavian Countries: Perspectives and Controversies

Managing Editor: Katarzyna Michalak Language Editor: Michael M. Brescia

Published by De Gruyter Open Ltd, Warsaw/Berlin Part of Walter de Gruyter GmbH, Berlin/Boston

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivs 3.0 license, which means that the text may be used for non-commercial purposes, provided credit is given to the author. For details go to http://creativecommons.org/licenses/by-nc-nd/3.0/.

Copyright © 2016 Ole J. Benedictow ISBN 978-83-7656-046-5 e- ISBN 978-83-7656-047-2 The Deutsche Nationalbibliothek lists this publication in the Deutsche Nationalbibliografie; detailed bibliographic data are available in the Internet at http://dnb.dnb.de. Managing Editor: Katarzyna Michalak Language Editor: Michael M. Brescia www.degruyteropen.com Cover illustration: © „La pest.“ From Annales de Gilles le Muisit, Tournai, 1353. Ms. 13076/77 f. 24v Katalog Parler 3, S. 73. Bibliotheque Royale Albert I., Brussels, Belgium.

Contents Preface  Postscript 

 XI

Bibliography 

Glossary 

 XVIII­‌

 XX

 XXII

 1 Introduction  Perspectives and Issues   1 What is Plague? Some Basic Facts on Contagion, Transmission, and Dissemination   14 1.3 What to Look for and Keep in Mind: The Defining Features of Bubonic Plague and Some Crucial Facts    17 1.3.1 Introduction    17 1.3.2 Defining Features   18 1.3.3 Some Crucial Matters of Fact   21 Bibliography  29 1.4 Serious Plague History Under Pressure: The Twelfth Alternative Theory of Historical Plague: Comments on the Recent Paper “Climate-driven Introductions of the Black Death and Successive Plague Reintroductions into Europe”    35 1.4.1 Introduction   35 1.4.2 The Purported Functions of Caravans and the Silk Roads in the Transportation of Plague with an Overview of the History of the Golden Horde: A Brief Study in Methodological Problems of the First Degree   36 1.4.3 Patterns of Spread and Comparative Spread Rates   40 1.4.4 Absence of Evidence is not Evidence of Absence, I: On the Medievalist’s Craft and the Fallacy of Argumentum ex Silentio   47 1.4.5 Absence of Evidence is not Evidence of Absence, II: On the Presence of Rats and the Local Persistence of Plague among Them   49 1.4.6 Absence of Evidence is not Evidence of Absence, III. On the Life and Death of Rats   53 1.4.7 On the Medievalist’s Craft and more Fallacies of Reverse Circular Lines of Argument. The Functions of Scholarly Myths   55 1.4.8 The “Reintroductions” that Disappeared    60 1.4.9 The Importance of the Historian’s Craft for Understanding the Conquest of Plague and the Means and Manifestations of the Process of Combat   65 Epilogue   69 Bibliography   70 1 1.1 1.2

1.5 The Triumph of Paleobiology in Historical Plague Research   1.5.1 Introduction   73 1.5.2 The Status of Paleobiological Studies, 1998-2014    79 Bibliography   92 Bibliography to Table 1.1   96

 73

 100 The Black Death in Norway, 1348-1349  Fundamentals of Plague Epidemiology   100 Bubonic Plague and Pneumonic Plague   103 Long Distance and Short Distance Spread of Plague   105 Plague Epidemics’ Pace of Development and Spread Rates   108 The Territorial Origin of the Black Death and Its Route to Norway   113 The Arrival of the Black Death in Oslo   114 The Black Death Conquers Østlandet [the “East Country”] in 1349   124 2.8 The Black Death Arrives in Bergen    135 2.9 The Black Death Comes to Nidaros (Trondheim)   146 2.10 The Black Death Arrives in Agder and Stavanger    150 2.11 The Triumph of Death: How Many People Died in the Black Death in Norway?   151 2.11.1 Introduction   151 2.11.2 The Question of Average Household Size and the Denial of Elementary Facts: Some Consequential Analyses   153 2.11.3 Average Household Size, Numbers of Households in the Middle Ages, and Population Size and Decline   158 2.12 Life After the Black Death   163 2.13 The Powers of Spread of the Black Death   167 2.14 Contemporary Understanding of the Causation of Epidemic Disease   169 Appendix 1: Plague Epidemics in Norway 1348-1500 and Their Provenience   175 Appendix 2: Some Basic Elements of the Medieval Norwegian Agricultural System which Affect Analysis of Plague Epidemics   176 Bibliography   176 Unpublished Sources   176 Bibliography (including published sources and abbreviations)   177

2 2.1 2.2 2.3 2.4 2.5 2.6 2.7

3 3.1 3.2.

The Black Death in Norway: Arrival, Spread, Mortality. Discussions with Birger Lindanger and Hallvard Bjørkvik   183 Introduction   183 Lindanger’s Views on the Black Death’s Arrival and Spread in Norway   187

3.2.1 3.2.2 3.2.3 3.2.4

Introduction: Sources and Source-criticism   187 The Black Death in South-eastern Norway   199 The Chronicle of Hamar: A Source-critical Analysis   205 Spread Rates of the Black Death from Oslo, and the Epidemics in Stavanger and Agder   208 3.2.5 How Lindanger Relates to Problems Arising from His Theory   215 3.2.6 Social and Political Evidence on the Aftermath of the Black Death   219 3.3 Bjørkvik’s Views on the Black Death’s Routes of Spread and Mortality in Norway   223 3.3.1. The Black Death’s Spread to Norway   223 3.3.2 Medical and Clinical Problems   226 3.3.3 Mortality of the Black Death in Norway    228 3.3.4 Closing Comments on the Topics of Arrival, Spread and End of the Black Death in Norway   230 3.4 On Household Size, Population Size, and the Mortality Caused by the Black Death   234 3.4.1 Introduction   234 3.4.2 Historical Sociology and the Specificity of Medieval Demography: Some Important Perspectives and Consequences   235 3.4.3 Estimation of Population Size and the Mortality Wrought by the Black Death in Norway    244 Bibliography   250 4 4.1 4.2 4.3

4.4 4.5 4.5.1 4.5.2 4.5.3 4.5.4 4.5.5 4.5.6

The Black Death in Norway, 1348-49: Sources, Chronology, Spread. Discussion with Kåre Lunden   255 Introduction   255 Some Methodological Perspectives   256 The “Traditional Doctrine” of the Black Death’s Spread in Time and Space in Norway-and the Conventional View   259 The Chronicle of Hamar: A Brief Source-Critical Recapitulation   267 On the Time, Original Place of Arrival and Early Spread of the Black Death in Norway   271 Icelandic Annals on the Time and Spread of the Black Death in Norway   271 The Time Bishop Hallvard of Hamar Died and the Time of the Black Death in Hamar   273 The Election and Consecration of Bishop Hallvard’s Successor   275 The Time Bishop Thorstein of Bergen Died, the Time of the Black Death in Bergen and in South-eastern Norway   277 Lunden’s Assertions about King Magnus’s Circular Letter: A Closer Look   282 The Bishops: The Living and the Dead on the Morrow of the Black

Death   284 The Meeting of the Assembly of the Realm in Bergen in June 1350   286 Social Evidence on the End of Black Death   287 The Black Death in South-eastern Norway and in Sweden: The Connection   288 4.8 Donations to Religious Institutions by Will or Deed of Gift as Reflections of the Presence of the Black Death in Time and Space   290 4.8.1 Introduction: Donations to Religious Institutions in Denmark and Sweden   290 4.8.2 Donations to Norwegian Religious Institutions and the Importance of Source-criticism   291 4.8.3 Facts or Fiction: The Real History of the Time of the Black Death and its Spread in Eastern Norway   293 Bibliography   303 4.6.1 4.6.2 4.7

5

The Spread of the Black Death in Norway: Revisionists, Spread Rates, Alternative Microbiological Theories and the Role of Mutation: Discussion with Kåre Lunden and Lars Walløe   307 5.1 Introduction   307 5.2 On the Spread Rates of Plague   308 5.2.1 On the Revisionist Alternative Theories on the Spread Rates of Historical and Modern Plague   308 5.2.2 On the Spread Rates of Historical and Modern Plague   311 5.3 Did Plague Spread in the Winters?   318 5.4 The Alternative Spread Rates of Anthrax, Filoviridal Diseases, and Cohn’s Disease   324 5.5 Lunden’s Genetic Theory of the Role of Mutations and the Microbiological Identity of Plague of the Past    326 5.5.1 Part 1.   326 5.5.2 Part 2. Lunden’s Views on the Questions of Mutations and Microbiological Identity of Plague Contagion seen in the Light of Paleobiological Studies   327 Appendix 1: My Works on the Dynamics of Spread and the Spread Rates of Plague   336 Bibliography   340 6 Walløe, Juhasz and the Sociology of Plague  Bibliography   352 7 7.1 7.2

 344

 355 Lars Walløe’s Human-Flea Theory of Plague Epidemology   Introduction   355 Short History of the Human-Flea Theory on the Epidemiology of Bubonic Plague   357

7.3 7.3.1 7.3.2

Some Basic Empirical Facts Invalidating the Human-Flea Theory   365 Introduction    365 Prevalence and Levels of Human Bacteraemia (Human Plague Cases as Sources of Infection of Human Fleas)   365 7.3.3 Mechanical Transmission   369 7.3.4 Prevalence and Levels of Rat Bacteraemia (Plague Rats as Sources of Infection of Rat Fleas)   370 7.3.5 Blockage of Fleas   371 7.4 Virulence, Lethality, and Immunity: The Basis of Plague Mortality   377 7.4.1 Virulence and Lethality   377 7.4.2 Immunity   379 7.5 Defining Features of Rat-Flea-Borne Bubonic Plague   385 7.5.1 Introduction: The Concept and Uses of Defining Epidemiological Features   385 7.5.2 The Latency Period   385 7.5.3 The Inverse Correlation of Population Density and Infection Rates   386 7.6 Conclusion   388 Bibliography   389 8 8.1 8.2 8.2.1 8.2.2 8.2.3 8.2.4 8.3 8.3.1 8.3.2

8.4 8.5

Black Rats in the Nordic Scandinavian Countries. Discussion of Papers by Lars Walløe and Anne K. Hufthammer   395 Introduction: The Bombastry of Advocates of Radical Alternative Theories   395 The Ecological Habitats and Behavioural Strategies of Black Rats   398 Methodological Introduction: More about the Fallacy of Argumentum ex Silentio, that Absence of Evidence is Evidence of Absence   398 The Climate Theory of a Purported Absence of Black Rats, and the Neglect of Evolutionary Theory   399 The Denial that Black Rats Burrow   403 Did the Brown Rats Outcompete the Black Rats?   405 The Behavioural Strategy of Rats in the Face of Death. Where do Rats Die (So Where Should Archaeologists Look for their Remains)?   410 Methodological Introduction   410 “They do die in unusual [.] and inaccessible places”: The Ostensible Absence or Paucity of Black Rats in Medieval and Early Modern Rural Northern Europe   411 History and Distribution of Black Rats in Europe According to Finds of Skeletal Remains   418 Black Rats in the Nordic Countries: Skeletal Remains and Living Rats   424

8.5.1

Methodological Problems on the Presence of Black Rats in the Nordic Countries   424 8.5.2 Finds of Pre-Modern (Pre-1660) Skeletal Remains of Black Rats in Sweden and Denmark   426 8.5.3 Urban Finds of Medieval Rat Bones in Norway   430 8.5.4 Rural Finds of Skeletal Remains of Medieval and Pre-Modern Black Rats in Norway   430 8.5.5 The Plague Epidemic in Bergen 1565-1566. Without Rats?   433 8.6 The General Presence of Black Rats in Sweden and Finland and the Time and Causes of Their Decline and Disappearance   435 8.6.1 Introduction: The Functions of Disregard of Early Good Research   435 8.6.2 The Swedish Species Information Centre/ArtDatabanken on the Historical Presence of Black Rats in Sweden   439 8.7 Early-Phase Transmission? A Few Preliminary Comments    443 Bibliography   446 9

The Relevance of Recent Theories on the Microbiological Identity and Epidemiology of Plague for Scandinavian Plague History: In-Depth Studies of Two Danish Publications on Plague   452 9.1 Introduction   452 9.2 What Disease was Plague?   454 9.3 The Methodological Myth: Retrospective Diagnosis   462 9.4 The Myth That Bubonic Plague Only Spreads Contiguously   464 9.5 Three Myths: (1) The Myth of the Function of Quarantines; (2) the Myth of the Levels of Plague Mortality; and (3) the Myth of the Clustering of Plague Mortality   468 9.6 The Myth of Alternative Bubonic Plagues   470 9.7 The Myth of the Human-Flea Theory of Plague Transmission   476 9.8 The Silenced Fact: the Resurrection of Yersinia pestis from Graves of the Past   481 Bibliography   486 10

The Eight Alternative Theory on the Plague Epidemics of the Past: Discussion of Ole G. Moseng’s Composite Theory   491 10.1 Introduction   491 10.2 Some Perspectives and Methodological Considerations   492 10.3 Yersinia pestis: the Same or Different Strain or Biovar?   500 10.4 The Nosopsyllus-Fasciatus Theory   503 10.4.1 Introduction   503 10.4.2 Fur Fleas and Nest Fleas   504 10.4.3 The Significance of Distance to Human Beings for the Role of Fleas in the Epidemiology of Plague   519 10.5 Inter-Human Cross-Infection by Pulex irritans by Mechanical Transmission   534

Inter-Human Cross-Infection by Pulex irritans by Biological Transmission (Blockage)    544 10.6.1 Burroughs’s Experiments to Determine the Vector Capacity of Pulex irritans and the Significance for the Human-Flea-Borne Theory of Plague Epidemiology   544 10.6.2 Soviet Experiments Designed to Determine the Correlation Between Levels of Bacteraemia in Hosts and the Number of Bacteria Ingested by Feeding Fleas and the Formation of Blockage   545 10.6.3 Human Plague Bacteraemia: Human Plague Cases as Sources of Infection of Feeding Fleas: Epidemiological Perspectives   555 10.6.4 Cases of Human Plague and Human Plague Bacteraemia in Plague Reservoirs in USA   558 10.6.5 Some Further Comments on Moseng’s Arguments for the Theory of Transmission and Dissemination of Plague by Blocked Human Fleas   561 10.7 Epidemics of Primary Pneumonic Plague in Norway and Iceland?   565 10.8 Sailing along: From Bergen to Iceland with Primary Pneumonic Plague on Board?   579 Bibliography   585 10.6

11

On the Theories That Plague Epidemics of the Past Were Spread by CrossInfection by Human Lice or by Human Lice and Fleas. Discussion of Recent Works by Raoult and Drancourt, and by Walløe   593 11.1 Introduction   593 11.2 The Theory of Louse-Borne Plague   597 11.3 The Question of Mechanical Transmission of Plague   608 11.4 Epidemiological Manifestations of Inter-Human and Rat-Borne Transmission and Spread as Reflections of an Insect Vector   613 Bibliography   618 12 12.1 12.2 12.3 12.4 12.5 12.6 12.7 12.8

Problems with the Early-Phase Theory of the Transmission of Plague, Especially with Respect to Epidemic Plague   625 Introduction   625 The Early-Phase Theory of Plague Transmission by Fleas   627 Types of Plague Bacteraemia in Human Beings   634 The Average Size of the Ventriculus of Fleas (Stomach or Midgut)   636 What Happens with Plague Bacteria in the Ventriculus of Fleas? The Questions of Self-Purification and Bacterial Growth   638 Plague Bacteraemia in Human Beings   639 LD for Human Beings, Subinfective or Non-lethal Doses   649 Plague Bacteraemia in Black Rats: Rats and Human Beings as Sources of Infection of Feeding Fleas   652

12.9 12.10

Conclusions and Perspectives  Epilogue    655

 654

 666 General Bibliography   Unpublished Sources   666 Bibliography (including Published Sources and Abbreviations)  List of Figures  List of Tables  Index 

 694

 692  693

 666

For my sons Andreas and Tancred

Preface The work on this monograph began in November 2008. Earlier in the autumn, I had sent the huge typescript of my monograph on the alternative theories of the plague epidemics of the past to the prestigious academic Dutch publisher Brill and had received a preliminary enthusiastic reaction and the good news that it was on its way to reviewers.1 That monograph focused on the international discussion, quite briefly discussing Shrewsbury and Morris, the pioneers of alternative theories, and primarily focused on the central works of Twigg, Scott and Duncan, and Cohn. The only Nordic scholar who received comparable attention was Gunnar Karlsson, the Icelandic historian, and his theory of plague without rats in Iceland, that the alleged late medieval plague epidemics of the past in Iceland and elsewhere were primary pneumonic plague. In this case, it was shown that the two epidemics of puported plague in Iceland in the fifteenth-century could not have been plague. Otherwise, I considered the Nordic scene too peripheral to be related to in a similar thorough fashion. However, during the years spent working on this challenging project on alternative theories of plague, I noted an increasing fascination with and support of some of the alternative theories also in the Nordic countries. This was especially the case among Danish historians. In 2003, Peter Christensen published a paper with enthusiastic support of Cohn’s theory that plague was caused by a virus which had since disappeared, but had spread much like influenza.2 In her 2005 monograph on the plague epidemics of the 1650s, Lise Gerda Knudsen took great positive interest in Scott and Duncan’s theory that plague was a filoviridal disease caused by (some variant of) Ebola virus or Marburg virus, while also taking interest in Cohn’s theory, which are clearly incompatible.3 Both Knudsen and Christensen used Graham Twigg’s pioneering monograph as a mine of arguments against the conventional bubonic-plague theory without showing any interest in his anthrax theory or respect for his good judgement.4 They did not take on the arduous task of reading the primary research studies and standard works on bubonic plague, but rather passively relied on Twigg’s arguments or assertions. In 2006, Ole G. Moseng followed with his own alternative theory on the microbiological identity and epidemiological dynamics of the plague epidemics of the past, the eight according to my count. Here he argued for a composite theory if plague epidemiology. In this theory he gives substantial epidemiological roles to the rat flea Nosopsyllus fasciatus, normally associated with the brown rat (which 1  O. J. Benedictow, What disease was Plague? On the Controversy over the Microbiological Identity of Plague Epidemics of the Past. 2010. Leiden: Brill. 2  Christensen 2003: 413-50. 3  Knudsen 2005: 80, 119-21, 132-34, 146-49. 4  Twigg 1984.

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arrived after the end of the plague era), and also to the human flea as vector of interhuman cross-infection both by mass attacks with soiled mouth parts from a recent contaminated blood meal (mechanical transmission), and by blockage (biological transmission). This was combined with enthusiastic argument for a high variability of the pathogen’s properties by mutations, to the extent that he in the end could formulate his, as it may seem, self-contradictory conclusion “In time and space is plague not necessarily plague” [sic (erat scriptum)].5 This composite theory has not attracted any supporter for quite obvious reasons. It may be seen in the perspective of Hollingsworth’s characteristic of Josiah Cox Russell’s monograph on British medieval history: “Russell’s chief virtue, in fact, is that he gives others something to refute. All his figures may be altered eventually, but the debt to him will remain”.6 Nonetheless, within the Scandinavian context of plague research this theory clearly deserves a closer examination.7 Shortly later, Lars Walløe, the Norwegian professor of medicine, revived (or resurrected rather) his old full-fledged human-flea theory of the epidemiology of plague from 1982 in a leader in a Norwegian medical journal, and in 2008 he published a short paper arguing again, though more broadly, for this theory. Admittedly, my attention was so heavily concentrated on the completion of the monograph and the international discussion of alternative theories that these observations did not really sink in. However, in November 2008 I had a remarkable conversation with Lars Walløe, where it suddenly slipped out of him, as it seemed, that Kåre Lunden, the agrarian historian, would soon publish a paper on the Black Death in Norway in Historisk tidsskrift, The Journal of the Norwegian Historical Association. He would there give a comprehensive and sharp criticism of my account of the Black Death in Norway as presented in my doctoral thesis, my history of plague in Norway 1348-1654, and a long paper of 2006 (see below, Chapters 2 and 3). Because Lunden previously had published about one page on plague,8 this was unexpected. Walløe then informed me that he would also write a paper defending the human-flea theory in the light of Lunden’s criticism, and would also co-author a paper with A. K. Hufthammer, the paleoosteoologist, on the allegedly tiny and for all practical purposes urban presence of the black rat in medieval and early-modern Nordic countries. Clearly, a coordinated line of argument based on the human-flea alternative theory was underway. I realized that the basis was being established for another monograph on alternative theories; this time in relation to the Scandinavian discussion of the plague epidemics of the past. In this respect, there was more important work to be done. Shortly afterwards Lunden’s paper appeared. It is quite thoroughly commented on in Chapters 4 and 5. However, how Walløe could know beforehand that the last two unwritten and 5  Moseng 2006: 594. My translation from Norwegian. 6  Hollingsworth 1969: 58. Cf. Russell 1948. 7  See Chapter 10. 8  Lunden 2002: 41-42. See Chapter 5.2.1, p. 308, and n. 798.

XVI 

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unsubmitted papers would be published in Historisk tidsskrift remains intriguing. In 2010, these papers were published and are thoroughly commented on below in Chapters 7 and 8. By that time, my work on the present monograph was well under way. Since then, Walløe had expanded his theory with the inclusion of an important role for the human louse, a human-flea-cum-human-louse theory of the transmission and dissemination of the plague epidemics of the past. His theories on the role of human ectoparasites are comprehensively discussed below in Chapter 11. Quite a thorough presentation and discussion of the purported epidemic roles of the various species of fleas argued by several scholars are presented in Chapter 10 on “The Eighth Alternative Theory of Plague Epidemics of the Past […]”. I also was inspired by the publication of Living with the Black Death,9 a collection of papers where several of the authors, especially Christensen, Knudsen, and Moseng, argued for various alternative microbiological and epidemiological theories of plague in a Scandinavian context. Shortly later, appeared Karl-Erik Frandsen’s monograph on the last plague epidemics in the Baltic region, which is heavily concentrated on the last plague epidemic in Denmark (1710-1713).10 Bodil E. B. Perssons’s valuable monograph on the last plague epidemic in Scania (1710-1713) should also be mentioned, but it focuses on important topics other than the epidemiological. In a brief chapter, she argues though, among other things, that the epidemic was rat-flea-borne bubonic plague, but with a particular species of flea in mind, namely Nosopsyllus fasciatus, the ordinary flea of the brown rat.11 This theory is discussed quite thoroughly in Chapter 10. Sadly, summing up, I can restate the disappointment I expressed in the Preface of my previous monograph on the alternative theories on the plague epidemics of the past: “This monograph is not a work of intellectual love and joy, but of scholarly duty [.]”12 My 2010 monograph contained a chapter called “The Ethics of Scholarly Work”.13 Also this monograph could have contained a chapter with this title. It is wellsuited for the study and teaching of methodology and the ethical tenets of scholarly work. I will also encourage readers to read the first foonote to Chapter 12, the last subchapter Epilogue, and also the concluding remarks there, and consider the problems addressed in the light of the ethics of scholarly work and editorial work. Because this monograph will be published also on the Internet and it will be possible to download separate chapters, some material and arguments have had to be introduced into two or more chapters in order to make them more autonomous. This could be a source of annoyment to the readers of the monograph, but hopefully lenience comes with understanding of the reason. For the same reason, the individual 9  Bisgaard and Søndergaard (eds.). 2009. 10  Frandsen 2010. 11  Persson 2006. 12  Benedictow 2010: xv. 13  Benedictow 2010: 25-69.

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chapters have been provided with individual bibliographies. There is also a General Bibliography. Ole Jørgen Benedictow Emeritus Professor at Department of Archaeology, Conservation, and History Blindern Campus, University of Oslo

Postscript In Walløe 2010: 27-28, Walløe claims to be upset because I criticized sharply a paper he published a generation ago in Historisk tidsskrift 1982: 1-42, in contributions to newspapers where the gist of his assertions were presented, and that I also presented such criticism of it at scholarly meetings or seminars. He also considers his article unfairly discussed in a pilot project for my doctoral thesis on central topics of plague epidemiology, which was presented at the internal research seminar at the then Department of History.14 The Board of the Department considered it, on the contrary, to be so important and pioneering that they took the initiative to produce a semipublished preliminary booklet version, which is available also from the University Library. Because Walløe is unspecific, he mentions no specific piece of unfair comment, it begs the question of whether or not the criticism could have been justified and calibrated accordingly. He denounces my criticism as personal attacks, and that he for this reason cannot discuss scholarly matters with me, which I find offensive. The reason I was sharply critical at the time, can be seen in the translation of the first paper I published on plague history and on epidemiological problems more generally, can now be ascertained in Chapter 6, which is a translation of it into English. As can be seen, it addresses Walløe’s severe criticism of a paper published in 1970 by the then Oslo City Archivist L. Juhasz. This is performed by comparing the purported contents of Walløe’s references with what they actually state, all presented by citations. The pilot project of my doctoral thesis which the then Department of History published in 1984, contained much material to the same effect. However, his 2010 statements surprised me even more, because we repeatedly had discussions on plague history and epidemiology afterwards, also at a session of the Norwegian Academy of Sciences in Oslo, and in 1992, at the disputation of my doctoral thesis, a decade after my purportedly offensive personal attacks, he presented an oppositio ex auditorio. This is understandable, because this form of criticism of Walløe’s 1982 paper was now presented in expanded and a more complete form. It may not have functioned according to his intentions, because I still recall my concluding remark: “I would like to discuss this topic with him, but after he had done his homework.” The Adjudicating Committee was chaired by Professor Ottar Dahl, Professor of Historical Methodology and Philosophy at the University of Oslo, other members were Øivind Larsen, Professor of the History of Medicine ibidem, Erik Ulsig, Professor of Medieval Economic History at the University of Aarhus, Thomas Butler, Professor of Medicine and Microbiology, Chief of Section of Infectious Diseases at Texas Tech University Health Sciences Centre, School of Medicine, the world’s leading expert

14  Benedictow 1984.

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on recent plague at the time. The evaluation of the thesis by the Committee and the enclosed special evaluation by Butler were very positive. Importantly, there is not any suggestion that I should have been unfair to Walløe in any way. Dahl, Larsen, Ulsig et al., 14 May 1992. Under the circumstances, that should be a very serious matter for Walløe’s 1982 paper and could reasonably be taken to confirm that my spontaneous strongly critical reactions to the paper were justified. In November 2008, I was asked to come to a studio in the Norwegian Broadcasting Corporation to comment on the Black Death in a light entertainment program. To my surprise, it transpired that I should have a discussion with Walløe, who through his prominent connections had managed to arrange this discussion. This means, in fact, that he had made a successful effort to have a meeting with me, despite his assertion early in 2010, less than a year later, that he, since 1982, had not wished to have any discussion with me on plague history, because I allegedly should have offended him. The reason that he decided to follow another strategy or stratagem after the radio program could be that the discussion had not worked out well for him. In this connection I had an unusually interesting conversation with Walløe. Important parts of the conversation were rendered in an email of 16 December to Bjørn Bandlien, the then editor of Collegium Medievale, in order to secure it as an evidentiary document. Walløe knew that Kåre Lunden’s paper, which is commented on in Chapter 4 and Chapter 5 below, would soon appear in Historisk tidsskrift (HT), Journal of the Norwegian Historical Association. He could also (triumphantly) inform me that he would write one paper on rats together with A. K. Hufthammer, the zoologist, and that he also would write a paper advocating the human-flea theory, which subsequently would be published in HT, which are in the focus of the present Chapter 7, and Chapter 8, below. All papers would constitute a concerted attack on my account of the Black Death in my 2002 history of plague in Norway and on my 2006 paper on the Black Death, which are rendered in English translations above as Chapters 2 and 3 (Chapter 2 contains only the part on the Black Death). In 2010, the two papers Walløe mentioned appeared in Historisk tidsskrift, 2010: 13-28 and 29-43. Evidently, Walløe must be assumed to refer to a pre-arranged agreement with the editors of HT to publish these papers by Hufthammer and Walløe before they were written and had been refereed. This is the reason I have not considered it useful to respond to Lunden’s or Walløe’s papers in Historisk Tidsskrift. Instead, I began to write a collection of papers and studies in English that could relate more broadly to the discussion of alternative theories on historical plague in the Scandinavian countries, and make the essence of it more generally known, which over time evolved into the present monograph. For the same reason, some comments on the human-flea theory and Walløe’s defence of it were inserted in my 2010 monograph on alternative theories of historical plague that appeared later the same year, despite that it was peripheral to the international discussion of alternative theories, which were in the focus of this monograph. Benedictow 2010: 9-15. This constitutes the background of Chapter 7, 8 and 11.

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 Postscript

Bibliography Benedictow O. J. 1984. Pest: En epidemiologisk og historisk undersøkelse. En forstudie. [=Plague: An Epidemiological and Historical Study. A Pilot Study]. Blindern Campus, University of Oslo, Department of History. Benedictow O. J. 1992a. Plague in the Late Medieval Countries. Epidemiological Studies. Oslo: Middelalderforlaget. 11-329. Reprinted 1993 and 1996. Benedictow O. J. 2002. Svartedauen og senere pestepidemier i Norge. Pestepidemienes historie i Norge 1348-1654 [= The Black Dean and Later Plague Epidemics in Norway. The History of Plague Epidemics in Norway, 1348-1654]. Oslo: Unipub. The part on the Black Deathis published in English in Chapter 2, below. Benedictow O. J. 2004. The Black Death 1346-1353. The Complete History. Woodsbridge: Boydell & Brewer. 3 reprints, 2004 and 2006. Benedictow O. J. 2006. “Svartedauen i Norge: Ankomst, spredning, dødelighet” [= “The Black Death in Norway: Arrival, Spread, Mortality”], Collegium Medievale, 19: 83-163. In English translation in Chapter 3, below. Benedictow O. J. 2010. What Disease was Plague? On the Controversy over the Microbiological Identity of Plague Epidemics in of the Past. Leiden: Koninglijke Brill NV. Christensen P. 2003. “‘In These Perilous Times’: Plague and Plague Policies in Early Modern Denmark”, Medical History, 47: 413-450. Christensen P. 2006. “Book Review” of O. Benedictow 2004, Medical History, 50: 412. Christensen P. 2009. “Appearance and Disappearance of the Plague: still a Puzzle?” In: Living with the Black Death: 11-21. Dahl O., Larsen Ø., Ulsig E., and Butler T. 14 May 1992. Førstemanuensis Ole Jørgen Benedictows avhandling for den filosofiske doktorgrad. Innstilling fra bedømmelseskomiteen [Senior Fellow O. J. Benedictow’s thesis submitted for the degree of Doctor of Philosophy. Adjudicating Committee’s Report], [addressed to] Det Historisk-filosofiske Fakultet [Faculty of Humanities], Boks 1079, Blindern. Eisen R.J., Dennis D.T., and Gage K.L. 2015 08.19. “The Role of Early-Phase Transmission in the Spread of Yersinia pestis, Journal of Entomology (Advance Access): 1-10. DOI: 10.109.1093/jme/ tvj128. Frandsen K.-E. 2010. The Last Plague in the Baltic Region, 1709-1713, 2010. Copenhagen: Museum Tusculanum Press. Hollingsworth T.H. 1969. Historical Demography. London: The Sources of History Limited. Hufthammer A.K. and Walløe L. 2010. “Om utbredelsen av rotter i Norge i Middelalderen og tidlig nytid”, Historisk tidsskrift [Norway], 89: 29-43. Knudsen L.G. 2005. Pesten grasserer! En undersøgelse av pesten I Danmark i 1650’erne. [Kerteminde]: Landbohistorisk Selskab. Knudsen L.G. 2009. “The Course of a Mid-17th Century Plague Epidemic in Denmark.” In: Living with the Black Death: 113-134. Living with the Black Death. 2009. L. Bisgaard and L. Søndergaard (eds.). 2009. Odense: University Press of Southern Denmark. Lunden, K. 2008. “Mannedauen 1349-50 i Noreg. Kronologisk og geografisk spreiing”, Historisk tidsskrift, 87: 607-632. Lunden K. 2002. Norges Landbrukshistorie. Vol 2. Frå svartedauden til 17. Mai. Oslo: Det Norske Samlaget. Moseng O.G. 2006. Den flyktige pesten. Vilkårene for epidemier i Norge i seinmiddelalder og tidlig nytid. Thesis for the degree of Doctor of Art. Oslo: University of Oslo.

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Persson B.E. B. 2006. Gud verkar med naturliga medel. Pestens Härjingar i Skåne 1710-1713. Lund: Nordic Academic Press. Russell J.C. 1948. British Medieval Population. Albuquerque: The University of New Mexico Press. Twigg G. 1984. The Black Death: A Biological Reappraisal. London: Batsford Academic and Educational. Walløe L. 2007. “Var Yersinia pestis årsak til svartedauden?”, Tidsskrift for den norske legeforening, 127: 3193. Walløe L. 2008. “Medieval and Modern Bubonic Plague: Some Clinical Continuities”, Medical History. Supplement, 27: 59-73. Walløe L. 2010. “Var middelalderens pester og moderne pest samme sykdom?”, Historisk tidsskrift, 89: 13-28.

Glossary Abscess Local inflammation of body tissue with deep suppuration [secretion of pus] caused by bacteria that destroy the cells in the centre of the area and leave a cavity filled with pus Bacteraemia, bacteraemiae, bacteraemic Bacteraemia refers to infectious agents or toxins which have invaded the blood stream. This allows spread to almost every organ of the body. Previously, the term septicaemia was used synonymously with bacteraemia. See also Primary bacteraemic plague and Secondary bacteraemic plague Bleeding from the nose See Epitaxis Bubo, boil Hard inflamed lymph node that may suppurate, plague bubo. Boil was often used synonymously in the past Carbuncle Localized dead body tissue (gangrene) caused by plague bacteria (or staphylococci), usually by bacteria left in the site of a flea’s bite, in which case it is called a primary carbuncle Case mortality rate See Lethality rate Case fatality rate See Lethality rate Cutaneous Relating to or affecting the skin. See also Subcutaneous and Intradermal Ecchymosis The passage of blood from ruptured blood vessels into subcutaneous (see below) tissue, marked by a purple discoloration of the skin. See also petechiae Endemic Sporadic cases of an infectious disease in a human population, too few in number to be considered usefully as a designated epidemic but which show that a particular type of contagion occurs in a population, is called an endemic phase or situation. Entomology The discipline of natural science that studies insects Enzootic Sporadic incidence of contagious disease among animals, cf. endemic Epidemic Disease that spreads rapidly through a population or community for a period Epidemiology The science of epidemics, especially how epidemics are spread and transmitted Epitaxis Bleeding from the nose; in plague caused by weakening of local blood vessels by the action of plague toxins Epizootic Disease spreading among animals, i.e. a term corresponding to the term epidemic among human beings Expectoration Ejection from lung airways by coughing. In cases of pneumonic plague, bloody expectoration may contain plague bacteria from ulcers in the lungs formed by plague bacteria transported there by the blood stream. Infected droplets from expectoration can be inhaled by other persons and give rise to primary pneumonic plague. See secondary pneumonic and primary pneumonic plague. Fatality rate See Lethality rate Haemorrhage/haemorrhaging Bleeding. See also Petechiae.

Glossary 

 XXIII

Incubation period The period from infection to the outbreak of disease Infection dose A measure of virulence usually expressed as ID50, i.e., the number of microorganisms or micrograms of their toxin (see this term) with which human beings (or animals) must be infected in order to cause a morbidity rate of 50%. Cf. Lethal dose Intradermal Within or between the layers of the skin: intradermal injection of infection; for instance, by flea bite Lethality rate The proportion of those who contract a disease and die from it = fatality rate, case mortality rate Lethal dose Measure of virulence. It is usually expressed as LD50, i.e., the number of microorganisms or micrograms of its toxin (see this term) with which human beings (or animals) must be infected in order to kill 50% of them (cause a mortality rate of 50%. See Infection dose Life table Life tables are based on a series of age-specific death rates for each gender and shows, therefore, the probabilities of dying within particular age intervals according to various life expectancies at birth. Or, if focusing on the probabilities of surviving, life tables show life expectancies at each age level in societies with various life expectancies at birth Microbiology Microbiology is the science of studies of microbial organisms, i.e., bacteria, viruses, prions, fungi, etc., particularly genetic material or DNA. Because immune systems generally interact with pathogenic microorganisms, microbiology also includes the study of immune systems and their responses to infections, i.e., immunology Mixed epidemic Epidemic of bubonic plague comprising substantial proportions of cases of primary pneumonic plague; occasionally (also) of primary bacteraemic plague Morbid Diseased state or quality Morbidity rate The proportion of a population which contracts a specific disease; the rate of incidence or prevalence of a disease, the proportion of sickness of a specific disease in a specified group, locality or community Mortality The number of people who die within a particular period of time or on a particular occasion Mortality rate The proportion of a population of a locality, social class, gender, age category or occupation, which dies, no matter what the causal factors. Plague mortality is the proportion of a population which dies from this disease in an epidemic Naïve population Population without previous experience with a disease or diseases, and all members are equally susceptible. Paleobiology Study of DNA or specific proteins reclaimed from biological material of the past taken from remains of human beings or animals. See Microbiology Pandemic (1) An epidemic disease spreading over a wide geographic area or over large parts of the world and affecting an exceptionally high proportion of the

XXIV 

 Glossary

population. (2) Series of waves of epidemics with a wide spatiotemporal structure. In European history, plague has ravaged populations in three protracted series of waves of epidemics also called pandemics. The first (known) plague pandemic occurred in the period 541-767 CE; the second plague pandemic occurred in the period 1346-ab. 1690s in most of Europe, longer in the Turkish Balkans, in Russia overlapping with the third pandemic 1894-ab. 1940 (see below). The Black Death is the first gigantic, immensely disastrous and not­orious wave of plague epidemics of the second plague pandemic, spreading over almost all Europe, North Africa and the Middle East. It is therefore considered a pandemic also according to the first definition. A third plague pandemic broke out in 1894, but was stopped by countermeasures based on modern medicine and epidemiology around 1940 Pathogen Micro-organism which can cause disease Pathogenicity The ability of microorganisms to cause disease, cf. virulence Petechiae/plague spots Dark coloured spots in the skin due to invasion by plague bacteria of the capillary vessels of the skin, i.e., consequent upon the development of bacteraemia in the blood stream. Plague toxin weakens the walls of the blood vessels that tend to break and leak drops of blood (haemorrhages), which show through the skin as dark coloured spots, also called plague spots. Contemporary Englishmen often called such spots as (God’s) token, because their appearance heralded imminent and certain death. See Ecchymosis Plague focus/plague reservoir In many areas of the world where wild rodents live in great density, in colonies or otherwise, plague circulates continuously in the rodent population. Such a rodent population is called a plague focus or a plague reservoir Plague pox/plague variola Clinical feature of plague patients who have numerous pustules or vesicles which resemble smallpox Plague reservoir See plague focus Population mortality rate The mortality of an entire population (in contrast to the mortality of social subcategories like social class, gender or age, and so on). See mortality rate Primary pneumonic plague Patients with primary lung infections have been infected via the respiratory system. Droplets containing plague bacteria coughed up by persons which have plague infection in the lungs (pneumonic plague) are the source of infection (rarely also animals). See also Secondary pneumonic plague and Expectoration Primary bacteraemic plague This form of plague occurs when a flea deposits plague infection directly into a blood vessel or it is passed directly into the bloodstream without stoppage in a lymphatic node (and developing a bubo). Clinically characterized by dramatic and rapid course of illness leading to certain death without the development of bubo(es) , because the lymphatic system is not challenged. Pulmonary plague Fulminant type of primary pneumonic plague, i.e., caused by infection via the respiratory tract. Dissection of lungs of such cases do not show pneumonic foci of plague bacteria which produce a cough with bloody expectoration

Glossary 

 XXV

(sputum), but present with only hyperaemic (an excess of blood) and oedematous (accumulation of excessive fluid) changes in the lungs as well as marked bacteraemic features (see Bacteraemia). These cases are designated pulmonary plague because, even though they are anatomically similar to the bacteraemic cases of bubonic plague, they are etiologically different, because the infection enters via the respiratory tract Pure epidemics of primary pneumonic plague Concept referring to the hypothetical notion that epidemics of primary pneumonic plague can arise directly from droplet contamination from, for example, the skinning of a plague infected animal or from cats which have contracted primary pneumonic plague from the killing of plague infected rodents. This has never been observed in the field or reality. All known epidemics of primary pneumonic plague have originated in cases of bubonic plague who have developed secondary pneumonic plague, see this entry. This concept is, nonetheless, the notional basis of two alternative epidemiological theories of plague in the past maintained by C. Morris and G. Karlsson and discussed extensively in Benedictow 2010. See also Subject Index and Name Index Pustules Pustules resemble vesicles and are due to invasion of the skin by plague bacteria through the bloodstream, i.e., they are consequent upon the development of bacteraemia. See these concepts. See also petechiae/plague spots Secondary pneumonic plague In cases of bubonic plague in which plague bacteria pass into the bloodstream, they are also transported to the lungs where they often consolidate and develop ulcers. This often causes a cough with bloody expectoration, a condition that is called secondary pneumonic plague, i.e., a pneumonic condition that is secondary to the primary infection of buboes. These cases are almost invariably mortal. Such cases are the origin of primary pneumonic plague Secondary bacteraemic plague In 30-45 per cent of all cases of bubonic plague, the toxins of plague bacteria wear down the tissues of lymph nodes, so that the bacteria can make their way into the blood stream. This development causes a septicaemia that is secondary to the primary bubonic condition. See Primary bacteraemic plague and Toxin. These cases are almost invariably mortal Septicaemic, septicaemia See Bacteraemia, bacteraemic, Primary bacteraemic plague, Secondary bacteraemic plague Subcutaneous Lying or situated under the skin. See also Cutaneous and Intradermal Toxin Poison produced by micro-organisms. Each specific pathogenic microorganism produces its own toxin, which causes a particular disease when present in the system of a human or animal body Vector Carrier and transmitter of disease, especially an insect that conveys infection from one person (or animal) to another Virulence This term is closely related to pathogenicity, (i.e., the ability of microorganisms to cause disease), but introduces the con­cept of degree. See pathogen and pathogenicity. This makes it possible to differentiate between the different abilities of various pathogenic micro-organisms to produce disease and cause death in infected

XXVI 

 Glossary

persons. Virulence is measur­ed in terms of number of microorganisms or micrograms of toxin needed to cause the death in a given host, or that would kill a certain proportion of a representative host population, when administered by a certain route. This is called lethal dose (LD). The concept of infective dose (ID) denotes the number of micro-organisms or micrograms of toxin needed to cause disease without relating to mortality (rate). See these terms.

1 Introduction

Figure 1.1: The arrival and spread of the Black Death in Europe 1346-1353.

1.1 Perspectives and Issues There used to be general agreement that the plague epidemics of the past were, for all practical purposes, the same disease as modern bubonic plague. The common contagion was the bacterium Yersinia pestis, and the epidemiological basis was the common house rat in human habitats, or more specifically, black rats and their ordinary flea parasites Xenopsylla cheopis which spread the disease among rats and also to human beings. Over the last decades several new theories on the epidemiology and microbiological identity of the plague epidemics of the past have been presented and argued quite intensively. Shortly after 2000, these theories began to find favour in some quarters, and, after a few years, I considered that it would be useful to take issue with them. In 2010, appeared my 746 pages long monograph, What Disease was Plague? On the Controversy over the Microbiological Identity of the Plague Epidemics of the Past, where six of the central alternative theories in the international discussion were thoroughly analyzed. The theory that plague was spread by Pulex irritans, the so© 2016 Ole J. Benedictow, published by De Gruyter. This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License.

2 

 Introduction

called human flea, as argued by Blanc and Baltazard in the 1940s and later by Walløe, is discussed more briefly, because it seemed quite peripheral at the time. Moreover, this theory was thoroughly discussed in my 1992 doctoral thesis.15 It must be justified to conclude that the comprehensive analyses in the 2010 monograph revealed serious weaknesses in these alternative theories, establishing grounds for the invalidation of them. Some of these theories, as well as some new theories, were introduced in the Scandinavian discussion of the plague epidemics of the past. It is, as mentioned in the Preface, the objective of the present monograph to expand the perspective of the discussion of the alternative theories to include Scandinavian scholarship, which will also make my presentation and discussion of alternative theories quite complete. There are seven new alternative theories16 which increase the number of to thirteen. What these theories have in common, is that they accept that the plague 15  Benedictow 2010: 9-16; Benedictow 1992a/1993/1996: 230-37, 247-50. 16  It could possibly be said that also a different eighth new epidemiological theory should have been presented and discussed, Christakos, Oleas, Serre, et al.’s 2005 dissertation […]Epidemic Modelling: The Case of Black Death. However, this theory or model is too strange to consider. They have simply uncritically picked Scott and Duncan’s presentation and use of the so-called Reed-Frost theory of epidemiology in their 2001 monograph and used it to construct their epidemiological model. This theory is thoroughly discussed in my monograph on the alternative theories in relation to Scott and Duncan’s use of it as a base for the epidemiological model in their monograph. Benedictow 2010: 633-36. They maintained that it purportedly proved that the microbiological agent of plague of the past was a filoviridal disease, (some variant) of Ebola virus or Marburg virus, a theory that has been definitively discredited by the new paleobiological studies of biological material from plague graves as well as by conventional means of the historian’s craft. See Chapter 1.4, below, and Benedictow 2010: 610-633. L. Reed and W. Frost never published the theory themselves, for the reason that it was highly problematic and of little use. It was cautiously presented by J. Maia in Human Biology in 1968: 167-200, but also the editors found the theory so problematic that it was immediately followed in the same issue by a critical paper by H. Abbey of the Johns Hopkins University. Abbey 1968: 201-33. Christakos, Olea, Serre, et al. have in common with Scott and Duncan that they only refer to Maia’s paper, which they then are supposed to have read, but purportedly all of them have avoided to notice, when they came to the end of it, that it was followed by Abbey’s paper with devastating criticism of it. In the case of Christakos et al.’s reference to Maia, however, it is probably acquired second hand from Scott and Duncan’s presentation of the Reed-Frost theory for their special purpose. Here, only a brief crucial point shall be made, namely that the Reed-Frost theory of epidemiology is potentially usable only for the analysis of epidemic diseases spread by inter-human cross-infection and as such mainly restricted to viral diseases transmitted by droplets in closed populations, and functions poorly also in this respect. A closed population is the technical demographic term for the theoretical and quite artificial concept of a population which is not affected by immigration or emigration. It is explicitly stated and emphasized that the Reed-Frost theory cannot be used for the study of arthropod diseases. Because bubonic plague is an arthropod disease, disseminated and transmitted by fleas (the lice-borne theory is discussed below in Chapter 11), it is an obvious fallacy of methodology to test the nature of an epidemic disease that is commonly believed, also in all standard works on plague, to be spread by insects, on a model constructed according to a theory that is unable to analyze epidemic diseases spread by insects. If Christakos et al. had not been so enthusiastic about Cohn’s likewise discredited theory that historical plague epidemics was caused by an unknown viral disease spread by



Perspectives and Issues 

 3

alternatives of the past was bubonic plague caused by Yersinia pestis, albeit in the case of No. 10 with some arbitrary sweeping mutational assumptions. Because they present different alternative theories of transmission and dissemination, they are alternative epidemiological theories: (7) In 2003, F. Audoin-Rouzeau presented her alternative theory that Nosopsyllus fasciatus, the usual flea of the brown rat (Rattus Norvegicus), was the ordinary vector of bubonic plague (despite the absence of this rat from Europe before c. 1720).17 This theory is discussed at some length in Chapter No. 10 below together with Moseng’s eighth alternative theory. (8) In 2006, G. Moseng presented his thesis for the Doctor of Art degree. In it he launched the eighth alternative theory. This is a composite epidemiological theory, including the Nosposyllus-fasciatus theory, the human-flea theory, the ratborne bubonic-plague theory and, as it seems, also alternative contagions or highly mutated versions of Yersinia pestis with very different epidemiological manifestations. Unavoidably, such a composite theory may have difficulties with integration and consistency, may at times appear confusing, and requires quite a lengthy discussion to be adequately assessed in a coherent manner. It is discussed in Chapter 10. (9) Since 2006, Raoult and Drancourt have argued, with various co-authors, for a crucial role for the human louse.18 The fully-fledged louse-borne theory is the ninth alternative, it is presented and discussed mainly in Chapter 11. (10 and 11) This leads to Walløe who, in 2007-2008, revived his 1982 theory that Pulex irritans, the so-called human flea, was the crucial vector of the plague epidemics of the past. Likewise, this is an alternative theory of spread by inter-human crossinfection by a human ectoparasite.19 It has many central components and assumptions in common with the louse-borne theory with which Walløe, unsurprisingly, soon expanded his theory in papers published in 2010 and 2013, producing, thus, the eleventh theory, a composite human ectoparasite theory.20

cross-infection with droplets much like influenza, but had read Scott and Duncan’s monograph from which they took the theory for their model, they would have discovered that the terrible truth slips out on page 355: “Furthermore, typhus epidemics do not follow Reed and Frost dynamics because it is a disease with an arthropod vector” [namely lice: my insertion]. Because Cohn’s and Scott and Duncan’s theories that historical plague was viral diseases now are completely discredited, it explains the strange outcome of Christakos et al.’s model as much as it explains the peculiar aspects of Scott and Duncan’s work. Benedictow 2010: 610-63. As the great playwright Henrik Ibsen stated in Peer Gynt: “The weirder he starting point is, the more original the outcome will be.” My translation. 17  Audoin-Rouzeau 2003: 93-117, 297-346; Audoin-Rouzeau 2007: 217-29. 18  Houhamdi, Lepidi, Drancourt, Raoult 2006: 1589-596; Drancourt and Raoult 2008: 146; Ayyadurai, Sebbane, Raoult, and Drancourt 2010: 892-93; Tran, Signoli, Fozzati, Aboudharam, Raoult, Drancourt, et al. 2011: 3. 19  Walløe 2008: 59-73. 20  Walløe 2010: 13-28; Hufthammer and Walløe 2010: 29-43; Hufthammer and Walløe 2013: 1752-59. See discussion of this theory in Chapter 11, brief comments also in Chapters 7 and 8.

4 

 Introduction

(12) Quite recently the twelfth alternative theory appeared. A team of scientists including Walløe and Stenseth claimed that the Black Death and a purported rhythm of subsequent introductions of plague epidemics into Europe were imported all the way from East Asia according to a temporal rhythm of climatic variation which affected rodent plague foci in this part of the Old World. From there the plague contagion was purportedly transported by caravans for thousands of kilometres across the hostile Khanate of the Golden Horde to a besieged Kaffa on the Crimea, whence it allegedly was shipped by European merchants to Mediterranean ports: “Climatedriven introductions of the Black Death and successive plague reintroductions into Europe.” All plague epidemics should accordingly start by spreading out of some Mediterranean port, and over time at a certain rhythm decided by climatic variations in East Asia. This is a final concluding assertion, which is at variance with a great mass of evidence on the outbreaks of thousands of plague epidemics in Europe and their spatiotemporal structure, it is not and cannot be supported by evidence. This strange theory is, therefore, based on quite numerous arbitrary and erroneous assumptions and assertions, which are thoroughly presented and discussed in Chapter 1.4. They are alternative theories of plague epidemiology without black rats and their consort of fleas. In this crucial respect these theories are similar to (the majority of) the six alternative theories of plague epidemiology discussed in my 2010 monograph. In that monograph, the status of research on the presence and role of rats and their fleas is presented over 122 pages, a booklet within the book, which Walløe and Hufthammer pass over in telling silence. In this way they can avoid addressing this big corpus of facts with its powers of invalidation of their theory (theories). However, this is only the beginning of topics with powers of invalidation. Epidemics spread by inter-human cross-infection generally exhibit very different epidemiological manifestations from epidemics transmitted and disseminated to human beings by rat fleas which have left dying or dead black rats. Such differences are called distinguishing or defining features and are presented and discussed over 206 pages in Part Four of my 2010 monograph, which is also disregarded in telling silence. However, these topics are addressed again quite thoroughly below in Chapters 7, 8 and 11. What the advocates of the two human-ectoparasite theories have in common is that they refer to Blanc and Baltazard’s work for basic support, but are, as shown several times before,21 and will be seen again below,22 incompatible with them. Biraben appears, nonetheless, to assert a combined human ectoparasite theory in the introduction to the first volume of his (France-oriented) history of the second

21  See, for instance, Benedictow 1992a/1993/1996: 156-92, 227-74; Benedictow 2010: 9-16. The facts and methodological essence of the line of arguments are simply ignored, which could (and should) be seen as an expression of their strong level of validity and powers of invalidation. 22  See Chapters 7.2, 10.6, and 11.



Perspectives and Issues 

 5

plague pandemic.23 This contention is neither footnoted nor tested, although the volume contains much suitable material. Especially his comprehensive and detailed discussion of the last big European plague epidemic in southern France in 1720-1722 with instructive maps and extensive presentation of evidence is clearly incompatible with the human-ectoparasite theory.24 I have commented on this repeatedly, albeit in a purely human-flea perspective, also, as mentioned, in my 2010 monograph.25 Both theories based on human ectoparasites must therefore be commented on again and their untenability will be demonstrated again below. These alternative theories are discussed quite thoroughly from various perspectives in Chapters 7, 8 and 9, and especially in Chapters 10, 11-12. These eleven alternatives are fundamentally different and incompatible. Thus, at least ten of them must be untenable. Inevitably, at least ten of them must exhibit strong arbitrary features, and, arguably, as will be seen, all eleven. The launching of revolutionary alternative theories seems to be a rather continuous feature of recent historical plague research, also now when they are restricted to epidemiological alternatives. It implies incorrectly that there is not a huge corpus of fine medical, epidemiological, and historical research which should function restrictively on the formulation of new plausible epidemiological theories. These alternative theories seem, accordingly, to display unfamiliarity with this scholarly and scientific literature. This tends to hamper or prevent satisfactory testing of them. It is not always clear that they deserve conscientious discussion. The objective of this monograph is to present to an international audience of scholars and students engaged in historical plague studies the Nordic discussion of the Black Death and later plague epidemics in the Scandinavian countries.26 Topics include the microbiological identity of historical plague epidemics, their epidemiology as constituted by the gamut of relevant factors and issues: the presence and role of black rats, mechanisms and vectors of transmission and dissemination, seasonality, periodicity, spatial extensiveness, spread rates, and demographic effects, i.e. mortality and population change. The topic of population change leads directly to consequential analysis of economic, social, and political effects: the desertion of farmsteads, villages and local societies, changes in the pattern of settlement, effects on

23  Biraben 1975: 13. 24  Biraben 1975: 230-310. See also Benedictow 2010: 67, 107-08, 173, 190-91, 400, 405, 583-84, 586. 25  Benedictow 2010: 9-16; Benedictow 1992a/1993/1996: 229-64; Benedictow 2004/2006: 17-18. 26  The difference between Scandinavian and Nordic scholarship is found in what constitutes Scandinavia (Denmark, Sweden, and Norway), while any discussion of Nordic countries also includes Finland and Iceland. In this case, I take into account the contributions made by Finnish and Icelandic scholars. The Icelandic alternative theories have been extensively discussed in my doctoral thesis but even more so in my monograph published in 2010, and so I included these in the six theories discussed there. Benedictow 1992a/1993/1996: 207- 27; Benedictow 2010: 493-552.

6 

 Introduction

rents and taxes, and on political and administrative structures. These topics provide the basis of structural analysis, how the interaction of changed structures translated into superordinate societal effects and long-term direction of change of the social formation (social system) of the Scandinavian countries into early modern society. Of course, the Nordic discussion relates also to broader aspects of the international discussion of related topics. The discussion of these topics has long been most intense in Norway, and much less so, until quite recently, in Sweden and Denmark.27 The reason is that the severity and duration of the late medieval crisis was first discovered by Sigvald Hasund, the Norwegian agricultural historian, who in a pioneering work of 1919-1920 demonstrated the dramatic and lasting population decline in the late Middle Ages as reflected in a huge contraction of settlement, and great falls of rents and taxes.28 He also introduced the plague explanation.29 One important reason for this breakthrough was that Norwegian historical sources were better suited for this type of research than the sources available in the other Scandinavian countries. In the wake of Hasund’s astonishing findings, a number of gifted young medievalists joined this field of research and developed the so-called Norwegian school of agricultural history in the following decades, concentrating mainly on the same topics. The material developments of late medieval society were most intensely discussed by pioneering Norwegian agricultural historians. They confirmed, expanded, and deepened Hasund’s findings. They found dramatic and lasting population decline, comprehensive desertion of farmsteads and local societies, resettlement by the survivors and their descendants on the best land in the best localities, and a precipitous decline in rents and taxes with the consequent weakening of political structures in a broad sense of the term. Around 1520, the number of agricultural holdings in operation was hardly more than one-third of its pre-plague number. It was long assumed that a new, sustained net population growth started around 1500, however, this has now been shown to have occurred after the plague epidemic of 1530 at the earliest, or quite likely after the widespread plague epidemic in southern Norway of 1547-48.30

27  It must now be highly doubtful or impossible rather that plague ever reached Iceland, as often assumed. Benedictow 2010: 493-552. 28  In Norway, royal taxes were, in principle, payable on all land in operation as a proportion of the rents that were paid by tenants, or, in the case of freehold land, would be payable as if run by tenants. 29  Hasund 1919/1920. This work called Ikring mannedauen, i.e. On the Great Mortality, was first published as a long paper in 1919 and next separately as a booklet in 1920. 30  In my 2002 monograph on the plague history of Norway, which also contains a thorough demographic analysis, a somewhat different pattern appeared: although new long-term growth in settlement and population started in some parts of Norway before 1500, net long-term growth in Norway did not begin until 1530 at the earliest and, quite likely, only after the plague epidemic of 1547-1548. Benedictow 2002: 129-66, 169-79.



Perspectives and Issues 

 7

These conclusions were so amazing that Norwegian historians first assumed that this development was peculiar to Norway. Elsewhere the Black Death was a catastrophic event but transitory in its effects, a logical assumption because similar findings had not been made in other countries at the time. The basic problem, why the effects of plague should be far more disastrous and lasting in Norway than elsewhere, was not seriously addressed, although a rudimentary theory of a conjoining deteriorating climate was considered. This argument was based on the presumption that deterioration of climate would affect a population dependent on a simple medieval subsistence economy more negatively in Norway than elsewhere. For all practical purposes the Black Death and, to some extent, a few subsequent plague epidemics served as an explanatory hypothesis that was not studied and tested directly. The Black Death and later plague epidemics remained neglected in Norwegian and Nordic historiography until the topic became the focus of my doctoral thesis, Plague in the Late Medieval Nordic Countries: Epidemiological Studies (1992), which attracted much interest and subsequently had to be reprinted three times. Since then, I have, among other works, published a complete history of plague in Norway, 1348-1654, and had the opportunity to put Norwegian plague history into a broader international perspective in my 2004 monograph The Black Death 1346-1353: The Complete History, which also has been reprinted three times. In all, my publications on plague history comprise about 2500 pages, with the present monograph about 3000 pages, and my publications on Norwegian plague history taken together will then comprise over 1000 pages.31 As mentioned above, it used to be conventional wisdom that, to the extent the development of population and settlement in the late Middle Ages could be explained by epidemic disease, it was bubonic plague. Some scholars also assumed that primary pneumonic plague played a more or less important part. These views were not empirically tested. Clearly, a serious scholarly study of plague in the Nordic countries required independent identification of the disease in order to avoid the methodological pitfall of circular argument, i.e. simply assuming that historical plague was bubonic plague. The identity of the disease would have to be established as a problem and resolved by comparative methodology. This is the reason that my thesis was subtitled Epidemiological Studies. The main clinical and epidemiological features of the plague epidemics of the past, as reflected in the sources, had to be compared with modern medical knowledge of the clinical and epidemiological features of bubonic plague. Similarity would permit inference as to the identity of plague of the past and modern plague while dissimilarity would show that it was due to another disease and that its identity should be sought. Advocates of alternative theories often allege that scholars who supported the conventional bubonic-plague theory simply inferred from the

31  See Chapter 1.5, Appendix 1.

8 

 Introduction

present nature of plague to the nature of the plague epidemics of the past, the so called (conventional) retrospective diagnosis. This is an obvious methodological fallacy, and it is not true.32 The question also had to be raised whether or not plague or any other disease was characterized by a panorama of mortality-generating properties that could explain a dramatic and lasting decline of the population, contraction of settlement, and radical restructuring of peasant society. If not, this was an important conclusion which would lead to a renewed search for explanation(s). This nexus of problems seemed so overwhelming that I first wrote a pilot project on central epidemiological topics which was published by the then Department of History.33 My original working hypothesis was that no disease could have caused the dramatic late medieval developments, which I accepted were real, so there would have to be a different causation or explanation. This is emphasized by letters in bold type in my thesis’ introductory chapter,34 but is consistently overlooked (see below), an interesting fact. It was more likely, I hypothesized, that the tremendous and protracted decline in population size would be linked to a concerted effect of a nexus of multiple causes of mortality coming into play at much the same time. I recognized the rather strained character of this hypothesis, presuming a contemporaneous introduction of a cluster of mortality-generating factors. In this perspective, it appeared necessary to gather together and consider not only all relevant Nordic source material, but also to acquire good knowledge of the primary research and standard secondary works on plague and the epidemiological and clinical evidence contained in the international historical studies on plague. This proved to be a Herculean Labour that took almost a decade before I could seriously start writing my thesis. This is reflected in the Bibliography of the thesis which contains about 750 entries, all used in the running text and referred to in the footnote apparatus. This included the immensely comprehensive works (reports) of the Indian Plague Research Commission (IPRC), and important contributions by other British scientists in India and elsewhere, the numerous papers by the French research team in Madagascar, and E.R. Brygoo’s succinct monograph on their work, the work of two French researchers in Morocco, the impressive works of Wu Lien-Teh and other Chinese researchers, the important contributions of American scientists. My knowledge of Russian made possible the inclusion of important pre-revolutionary Russian and Soviet research on plague.35 This comprehensive and representative use of the research literature on modern and historical plague, has since been expanded in subsequent monographs and articles.

32  See Chapter 9.3. 33  Benedictow 1984. 34  Benedictow 1992a/1993/1996: 14. See also Benedictow 1992b: 80-81. 35  Benedictow 1992a/1993/1996: 286-329.



Perspectives and Issues 

 9

The allegation repeatedly levelled at my plague studies by Walløe and a few other scholars, that they are one-sidedly based on IPRC’s reports or another variant of bias or selection, is completely untrue, as will be evidently clear against the broad backcloth of my comprehensive publications. Readers are kindly asked to take a look in the bibliographies, and consider whether or not this allegation appears puzzling to them. Taken together, my three first monographs of 1992, 2002, and 2004, contain 2,274 footnotes, about 1,500 bibliographical entries, more than 1,000 individual studies if duplications are deducted, and 1,146 pages. The significant works of all centres of plague research are conscientiously presented. This allegation was first presented by S.K. Cohn and responded to in my subsequent long 2010 monograph on the alternative theories, with 746 pages and 1,953 footnotes.36 Similar allegations by Walløe and other scholars arguing for similarly arbitrary and misleading alternative theories are specifically responded to in the present monograph which is of about the same length and similarly meticulously footnoted with 2046 footnotes. One may wonder what it is with the present academic world which seemingly makes it necessary to make this comparison with the work of a scholar (Walløe) who have not published 100 pages on the topic and can document only a peripheral knowledge of the relevant scholarly studies, but is, nonetheless, permitted by editors of purportedly serious journals to make such offensive allegations. See, for instance, Medical History, Supplement 2008: 59, with n.3 where it is stated that I should have “invented large populations of rats in the medieval towns and countryside of northern Europe without any support from contemporary historical sources or archaeology”, referring misleading to my 1992 doctoral thesis and passing by in silence my subsequent monographs and articles. The crucial question of the presence of black rats is, therefore,(again) presented and thoroughly discussed in Benedictow 2010: 73-151, and again in Chapter 8 below.37 This allegation is always presented under the pretence that it is not a scholarly statement of fact that should be conventionally substantiated by material provided by analysis of my bibliographies and footnotes, supported by the normal use of footnotes. These allegations are always arbitrary. They are repeatedly couched in derogatory wording and serve a dire need to belittle and denigrate my work in order to pave the way for mainly arbitrary alternative theories based on few and highly selective studies. The justification for the latter characteristic has been repeatedly documented in long and thoroughly footnoted works.38 The continued use of this

36  Cohn 2002: 51-2; Benedictow 2010: 57-59. 37  In another purportedly serious journal, Past and Present, I have also been “accused” of dishonestly to have invented epidemics of the Black Death in Central Europe. This allegation will be responded to in my forthcoming second edition of the History of the Black Death (planned for 2017), and should be extraordinarily interesting reading. 38  Benedictow 1992a/1993/1996:126-274; Benedictow 2010; and comprehensively in the present monograph., see especially Chapters 6-11, where Walløe’s and Moseng’s works are thoroughly discussed.

10 

 Introduction

form of argument is, of course, a reflection of the generally weak scientific basis of all alternative theories, also after my huge monograph on them had appeared.39 Kåre Lunden’s similarly misleading assertions are commented in Chapter 4, below.40 This point will be enlarged upon in the following pages. The standard works on plague by Wu Lien Teh, J.W.H. Chun, R. Pollitzer, C.Y. Wu (1936), L. F. Hirst (1953), and R. Pollitzer (1954) are outstanding syntheses of the gigantic corpus of studies on plague. American research agrees with these standard conclusions.41 T. Butler’s monograph on Yersinia diseases appeared in 1983. Because all these outstanding scholars and scientists studied the same disease and took a strong interest in the plague epidemics of the past, they reached mainly the same conclusions (see also below). Later research has filled in the lacunae and strengthened these conclusions, removing the small margins of uncertainty which could perhaps be discerned earlier. Plague epidemics of the past and modern plague are for all practical purposes the same disease, caused by Yersinia pestis, transmitted and disseminated from diseased black rats by infective rat fleas, principally Xenopsylla cheopis. The 39  See Moseng 2007: 3272-3; Walløe 2007: 3193; Walløe 2008: 59; Lunden 2008: 610; Moseng 2009: 28; Helle 2013: 105-06, and n. 124. The scholarly basis of Helle’s misleading assertion that I only have read the work of the IPRC and uncritically apply plague epidemiology perhaps relevant to India or medieval Norway, is especially difficult to discern. In order to maintain this misleading view, he must also misleadingly maintain that there has been made no find of the skeletal remains of a black rat in a rural district of Norway. This is a denial of fact, because there have been made two such finds. Karlberg and Simonsen 2008: 135; Vretemark 2010: 8,10, 28. cf. Petterssson 2010: 31. The latter study has long been available on the Internet. These finds are presented and discussed in Chapter 8, and also in Chapter 7. Hufthammer and Walløe, and Helle have also avoided my long presentation of studies on the basic behavioural strategy of diseased or dying (black) rats springing from the fact that rats are cannibals. In order to avoid being eaten more or less alive, sick or dying rats which are unable to defend themselves hide away in inaccessible and unusual places. When urban structures crumble in the ground, skeletal rat remains in such locations are released and recoverable by archaeologists. Benedictow 2010: 85-97. See also Chapter 8.3 below. With respect to the remains of the structures of farmhouses and their immediate surroundings, this is a highly different archaeological scene. This is why Hufthammer cannot find bones of black rats in rural Norway, because she avoids the crucial question of rat behaviour and where remains of black rats for this reason should be looked for. Instead, she simply has assumed that rat bones should be found among the usual concentrations of animal bones from household consumption on the farmsteads. See Chapter 8.4, below. Another matter is the rich material on black rats in Sweden and Finland, which is also presented and discussed below in Chapters 8.4 and 8.5. Hufthammer, Walløe, and Helle, can, of course, legitimately, disagree, but that requires arguments which take into account these objections and demonstrate why they do not apply. When such elementary scholarly requirements are not met, but the counterarguments are simply passed over in silence, this can legitimately be taken as proof of the quality of my arguments and account. This is confirmed by Karlsberg and Simonsen’s and Vretemark’s finds. Importantly, these skeletal remains of black rats were found within the context of a complete excavation of the old habitation and its surroundings on a farmstead. Because Helle does not relate to any of this, his allegations must be deemed untenable and false. 40  Lunden 2008: 610; see comments in Chapter 4, below. 41  See also Benedictow 2010: 44-46.



Perspectives and Issues 

 11

study of the late medieval Nordic sources led to epidemiological inferences and conclusions in my doctoral thesis that, to my surprise, was concordant with and corroborated the standard works on plague and the quality of the primary studies on which they were based. On this crucial point, my thesis did not break new ground but ascertained the validity and empirical tenability of the established corpus of research on plague. This is still the unambiguous view of all the big and responsible health organizations, will be found on the on the home pages of the websites on plague of the World Health Organization (WHO), Centres of Disease Control and Prevention (CDC), and Yersinia Research Unit, Institut Pasteur, which are rendered and commented on below.42 In my history of plague in Norway of 2002, 1348-1654, and in my 2004 general history of The Black Death 1346-1353, this broad synthesis was tested in the strongest possible way, and, as it turned out, its tenability was corroborated. In the case of Norwegian plague history, the synthesis was the outcome of the intensive study of a complete43 material of sources and studies in the full temporal perspective of the entire second pandemic; in the case of the history of the Black Death, the synthesis was based on all available studies in 14 languages, the complete44 study of the greatest of all plague epidemics. The synthesis of the Black Death in Norway has been made available in English translation in Chapter 2, below; it was again comprehensively tested and again corroborated in a long paper of 2006, here published in English translation in Chapter 3. The complete temporal outline of plague epidemics in Norway 1348-1654 provided an entirely new opportunity for analysis of the territorial origin and periodizations of the numerous plague epidemics that broke out in this period. By comparison with similar temporal outlines and periodizations of plague epidemics in the countries with which Norway had most contact, it should be possible to identify the origin(s) of importation by temporal co-ordination of the outbreaks. Even modest pilot projects showed that the incidence and timing of plague epidemics in Norway were very different from those in neighbouring countries, Sweden and Denmark. This made it clear that this question of provenience was closely associated with trade and the contemporary plague history of Norway’s trading partners. The material on the outbreaks of plague epidemics in parts of England, the coastal commercial hubs of the Netherlands’ province of Holland, and the Hanseatic cities along the coasts of northern Germany with active commercial shipping on Norway 42  Chapter 1.2. 43  Complete in the meaning that, 13 years later, no scholar has pointed out any significant source(s) or study that have been overlooked. 44  Complete in the meaning of all studies on the spread and mortality of the Black Death, and that, a decade later, no scholar has pointed out any significant material that has been overlooked. In this case, though, I have noted a few studies of mortality on manors that were overlooked. I have also worked thoroughly through the material on seasonality, spread and the mortality among English parish priests, and gained significant new insights that will be incorporated in the second edition, which is planned to appear in 2017. Benedictow 2010: 396-488, 566-71, 595-608.

12 

 Introduction

would presumably contain the clue. Gathered together and juxtaposed in tables in columns and rows organized for comparison of time and location of outbreaks, this material uncovered a conspicuous similarity with the contemporaneous outbreaks of plague in south-eastern England, and, especially from c. 1600, to some extent with the provinces of Holland and Frisia in the north-western and northern Netherlands. It immediately became apparent that the plague was usually or mostly imported to Norway with ships from England, so that the time and rhythms of plague epidemics exhibited great similarity in these two countries. Comparison of demographic developments also showed a similar temporal outline of population decline as well as the size of the decline of the populations in the two countries.45 These findings were greatly supported by John Hatcher’s important paper on population developments in England during the period 1450-1750, which appeared shortly later.46 This also explains the finding that plague epidemics broke out more frequently in Oslo than in Bergen, the two great epicentres of the importation and spread of plague in south-eastern and western Norway. Oslo had far more vital trade connections with England than Bergen, where Hanseatic merchants from the commercial hubs of northern Germany dominated. The tables also showed that the long-term incidence of plague was significantly lower in Bergen than in England. These findings also explain why sustained population recovery began earlier in western and northern Norway than in south-eastern Norway, and that the population decline apparently was deeper and lasting longer in south-eastern Norway. The plague history of Sweden and Denmark is much less studied than Norway’s, but the incidence of importation, seasonality, and temporal rhythms of plague epidemics were clearly different, especially after 1400.47 The reason was evidently that these countries did not have such strong commercial connections with England and mostly imported plague from the Baltic region and the Hanseatic cities, and, in the later part of the plague pandemic, also from the Netherlands. This seems to imply that these countries were somewhat less exposed to plague and may have suffered less mortality and seen a smaller population decline over time. There is no evidence that plague was ever exported to Norway from Denmark or Sweden. This seems to be the real explanation for the problem that Norwegian historians identified in the 1930s and grappled with later with inadequate resources, that the plague epidemics caused a stronger and more lasting population decline in Norway than in Denmark and Sweden.48

45  Benedictow 2002:101-20, 129-66, 169-79; Benedictow 2012: 17, 33-36. 46  Hatcher 2003: 83-130. 47  See, for instance, Mansa 1873: 63-65; Ilmoni 1846: 125-304; Ilmoni 1849:18-167. 48  Hasund 1934: 148-49; Schreiner 1948: 7-10, 91-94, 120-23; Holmsen 1949: 418-22; Sandnes 1971: 205-09, 228-48; Holmsen 1977: 333-38; Sandnes 1978: 165-169; Sandnes 1981: 78-114, see especially pp. 113-14.



Perspectives and Issues 

 13

As will be clear from the chapters published below, the Nordic discussion of the nature and social effects of the late medieval plague epidemics relate in important respects to the comprehensive presentation and discussion of these issues in my 1992 doctoral thesis. My 2002 history of plague in Norway 1348-1654, and, to some extent, my 2004 monograph on the Black Death, have also become central to the Nordic discussion of the plague epidemics of the past. After this introduction, the present book therefore starts with an English translation of the relevant parts of my 2002 monograph book on the Black Death (Chapter 2). The sequence of notes are, however, affected by the deletion of textual elements that are considered peripheral in the present context, and the addition of a few notes in order to make the account updated on a few points of importance. Presumably, this discussion of my works published by the end of 2008, when Lunden’s paper appeared, will make it clear that Lunden’s assertions to the effect that my views on the microbiology and epidemiology of the plague epidemics of the past had been written a priori, as preconceived notions of a speculative or hypothetical nature, are not true.49 These allegations are comprehensible only as a reflection of unusual argumentative needs. Lunden had published only one page on the subject before his paper appeared.50 The publishability of a paper based on undocumented and undocumentable competence, and on such misleading assertions about the work against which it argues, could be seen as unusual. The support Lunden’s paper received from the Board of Editors in the Preface to the issue of Historisk tidsskrift, specifically also of central, objectively erroneous and misleading assertions, should attract attention. The first paper I published on the history of plague in 1985 was a succinct demonstration that Walløe’s “attack” in 1982 on a paper by then Oslo City archivist, Lajos Juhasz, was based on misleading references. This was definitely shown by juxtaposing Walløe’s assertions with relevant citations from the works to which he referred for support. This paper is now translated into English in Chapter 6 below, so facts can speak for themselves. For various reasons, I had to continue and broaden the critical discussion of Walløe’s article in my thesis on a number of issues. Because the thesis is in English and is, as mentioned, widely available in libraries, no part of it is represented in this monograph as one of the chapters. As has been suggested, some parts of the discussions below may appear to relate to rather unusual arguments. This was indeed the case with my monograph published in 2010. It contains also a long chapter entitled “The Ethics of Scholarly Work”, with serious methodological and factual criticism that is legitimate points for the future of historical plague research.51 I take no personal interest in the possible use of the

49  Lunden 2008: 610. See comments in Chapters 4, 5, 9 and 10 below. 50  Lunden 2002: 41-42. 51  James 2012: 1201-03.

14 

 Introduction

Chapters 2-11 of this book as a gateway to social constructions or connections within the community of scholars. Scholarly works should speak for themselves on matters of fact, theory, and understanding of social or societal developments. Most of the chapters in this monograph were originally written in English in recent years and are now published for the first time. Three of the articles have been published previously in Norwegian and are now available for the first time in English, Nos. 1-2, and 6. They are included in order to provide a better outline of the development of research on the plague epidemics of the past in the Scandinavian countries, the pool of data it has produced, and the rise of issues and debate. I have done my very best to translate as accurately as possible the original Norwegian texts into English, not verbatim, but with respect to meaning. For historical reasons, terms with the same origin have frequently acquired different meanings or are not represented in one of the two languages. This has required construction of special concepts or even neologisms in English. English and Norwegian syntaxes are different and tend to require different sentence structure. Explanatory comments for English speakers are put in brackets or in the accompanying footnotes.

1.2 What is Plague? Some Basic Facts on Contagion, Transmission, and Dissemination Alternative theories on the causal agent and epidemiology of plague are the focus of this monograph. The views of the responsible international health organization, which perform primary research on plague and monitor this disease around the world, would presumably provide useful background against which readers can consider the fundamental issues. Their views are based on long-term intensive study of plague by outstanding scientists. When bubonic plague broke out in Shanghai in the spring of 1894, causing nearly 100,000 deaths and the breakdown of the inept imperial mandarin administration, the whole world was alarmed. Shortly later, plague broke out in Hong Kong. When it started to spread around the world by steam ships, the great European colonial powers of the time became deeply concerned that it might spread to their countries. Armed by the new science of bacteriology, leading experts were organized in generously or at least well-funded large-scale research projects, especially by the British and French in India and Madagascar. Also Australian, American, and Russian scholars made important contributions, as did European-educated physicians in China. They all studied the same disease and made closely related observations and findings. For obvious reasons, they took strong interest in historical plague epidemics, comparing clinical and epidemiological features and reached much the same conclusions: 1. The plague epidemics of the past and modern plague were for all practical purposes the same disease.



What is Plague? Some Basic Facts on Contagion, Transmission, and Dissemination 

 15

2. Historical plague would have to be caused by the same pathogen as modern plague, the bacterium Yersinia pestis. 3. Plague epidemics were transmitted and disseminated from infected black rats (house rats and ship rats) to human beings. 4. The agent of transmission and spread, the vector of the disease, was rat fleas, principally the species Xenopsylla cheopis of the black rat. These are still the views of all the major international health organizations which monitor the disease and have research programs on plague; the World Health Organization (WHO), Centres of Disease Control and Protection (CDC), and Yersinia Research Unit, Institut Pasteur. This is stated unequivocally on the home pages of their websites. A few extracts illustrate the point of complete unanimity between these prestigious health organizations with respect to the pathogen, the predominant role of rat fleas as vector of epidemic transmission and dissemination, and the identity of modern and historical plague:52 Plague is a bacterial zoonosis [.] It is best known as the cause of Justinian’s Plague (middle 6th century) and the Black Death in the middle of the 14th century, two devastating pandemics that killed millions and altered the course of history. A third less-known pandemic began in China in the late 1800s [.] The Third, or Modern Pandemic prompted an intensive multinational research effort that resulted in the identification of the causative agent of plague (Yersinia pestis) [.] and conclusive evidence that rat fleas transmit the disease to humans during epidemics. Later studies indicated that smaller numbers of cases also arise as a result of persons being bitten by wild rodent fleas, handling infected animals,53 or inhaling infectious respiratory droplets coughed by persons with plague pneumonia. (WHOCC-Plague). People usually get plague from being bitten by a rodent flea that is carrying the plague bacterium or by handling an infected animal. Millions of people in Europe died from plague in the Middle Ages when human homes and places of work were inhabited by flea-infested rats. (CDC Plague) When a person has plague pneumonia, they [sic] may cough droplets containing the plague bacteria into air […] Transmission of these droplets is the only way that plague can spread between people.54

52  All bold type is mine. Readers are recommended to google WHOCC-Plague, WHO Plague (and related links), www.cdc.gov/plague, CDC Plague Home Page with various links to Natural History, Epidemiology, Fact Sheet, and Yersinia Research Unit, Institut Pasteur (accessed on 19 April 2012 and on 11 August 2013), and CDC also on 9 June 2014. See Web-links: http://www.cdc.gov/ncidod/ dvbid/plague/who_cc/; http://www.cdc.gov/ncidod/dvbid/plague/index.htm; http://www.cdc. gov/ncidod/dvbid/plague/history/htm; http://www.cdc.gov/ncidod/dvbid/plague/epi.htm; http:// www.pasteur.fr/ip/easysite/pasteur/en/research/scientific-departments/microbiology/units-andgroups/yersinia/index; http://www.cdc.gov/plague/transmission/index.html. 53  See Chapter 10.6.4. 54  See http://www.cdc.gov/plague/transmission/index.html, accessed on 9 June 2014. Cf. preceding n. My bold type.

16 

 Introduction Y. pestis is the causative agent of plague. This zoonotic disease is transmitted from animals to humans by flea bites. (Yersinia Research Unit, Institut Pasteur)

The leading international health organizations’ presentations of the status of plague research are consistent and unambiguous: modern plague and historical plague are (for all practical purposes) the same disease. It is a zoonosis, epidemic bubonic plague is spread from the black rat to human beings by their ordinary fleas, Xenopsylla cheopis. Earlier small margins of uncertainty with respect to possible slight significance of other processes of transmission and dissemination have been discarded and eliminated with (for all practical purposes) complete empirical knowledge. They do not mention or suggest that the plague epidemics of the past could conceivably have been caused by any other microbiological agent than Y. pestis. They do not mention that modern plague epidemics or historical plague epidemics should have been transmitted by inter-human cross-infection by Pulex irritans, the so-called human flea. CDC states in absolute terms that the only mode of inter-human cross-infection is by transmission of infected droplets from cases of pneumonic plague. In another way this is stated in similarly absolute terms by Yersinia Research Unit, Institut Pasteur: “Y. pestis is the causative agent of plague. This zoonotic disease is transmitted from animals to humans by flea bites.” For very good reasons, the international health organizations also do not consider plague without the presence of black rats, as strongly asserted by Walløe (2010 and 2013), and partly by Moseng (see below, Chapters 7, 8, 10,11, 12). The alternative microbiological or epidemiological theories on the plague epidemics of the past remain entirely unsupported. The reasons will be presented below as to why any considerations of this kind are no longer mentioned, even as peripheral possibilities. After 1998, the new discipline of paleobiology has provided crucial evidence on plague of the past. Paleobiology grew out of the quite recent development of biomolecular tools and techniques that enable the detection of microbial information in skeletal remains of the past. Paleobiological research includes not only studies of bacterial ancient DNA (a)DNA in skeletal remains but also of antigens, the specific proteins in the capsules of bacteria. This permits determination of the specific microbial cause of death of individual human beings in the past. In this case, it relates to the identification of aDNA and the specific F1 antigen of the protein capsule of Y. pestis obtained from skeletal remains in putative plague graves.55 This new discipline bears directly on the scholarly debate over the microbial identity of the plague epidemics of the past, which has led to a very useful early focus of paleobiology on this question. My 2010 monograph, What Disease was Plague? On the Controversy over the Microbiological Identity of Plague Epidemics of the Past, contains a chapter presenting all paleobiological studies published by the end of 2008. Below, in the 55  More accurately it is a Y. pestis-specific fraction 1-capsule antigen, which is a plasmid-expressed immunogenetic envelope glycoprotein.



What to Look for and Keep in Mind 

 17

Chapter 1.5, subsequent papers also are taken into account. By March 2014, 20 papers containing paleobiological studies of 45 skeletal materials in putative plague graves or plague pits in about 40 localities have been published. They have all identified Y. pestis, only Y. pestis. This can be seen as confirmation of the conventional view of plague researchers, physicians, historians, as well as the leading international health organizations such as WHO, CDC and Insitut Pasteur, which states that the plague epidemics of the past were indeed bubonic plague. It can also be seen as a confirmation of the conclusions I reached in my doctoral thesis, as well as in subsequent monographs and other works. The general status of research on the biology and epidemiology of plague is comprehensively presented and discussed in my 2010 monograph. The alternative theories are shown to be untenable. Because they are mutually incompatible, this would have to be the case for all of them but possibly one, however, there was no exception. This conclusion is accepted by the reviewers of the monograph: beyond reasonable doubt, the plague epidemics of the past were caused by Y. pestis and transmitted and disseminated by black-rat fleas (X. cheopis).56

1.3 What to Look for and Keep in Mind: The Defining Features of Bubonic Plague and Some Crucial Facts ... 1.3.1 Introduction The theory that historical bubonic plague epidemics and modern plague epidemics were for all practical purposes identical is based on some crucial pillars of medical, epidemiological, and entomological sciences, now including also the new science of paleobiology, see Chapter 1.4. Bubonic plague is caused by the bacterial pathogen Y. pestis. It is overwhelmingly or at least predominantly spread and transmitted from black rats to human beings by the rat flea Xenopsylla cheopis. These are unique features that should manifest themselves in unique epidemiological and clinical features called “defining features”, which distinguish bubonic plague sharply from all other epidemic diseases. The conventional theory of the identity of modern bubonic plague and historical plague is based on the observation of these features in plague epidemics of the past, now also on the more recent identification of the pathogen in biological material obtained in putative plague graves or plague pits of the past. All alternative theories, whether based on alternative pathogenic agents or alternative epidemiological theories of spread, should be able to explain these unique or distinguishing defining features. Usefully, they can be concisely preliminarily presented here as an introduction to the main body of discussion

56  See James 2012: 1201-03, and Horrox 2012: 836-37.

18 

 Introduction

in this book. They are quite exhaustively presented in my last monograph: the references to the primary studies of plague and the secondary standard works on plague will be found there together with discussion of various views. All basic data given below will be expanded in the chapters below with a full complement of references.

1.3.2 Defining Features (1) The latency period. In all cases when the time of the arrival of plague in human habitats (in the plague season) are known, it takes 19-27 days before (another) human being dies from plague. This period of latency is due to the fact that rat fleas will first seek out their natural host and trigger an epizootic in the rat colony which, according to a well-known series of stages, leads to the infection and death of a human being. This latency period is a unique feature of bubonic plague. (2) Buboes as an ordinary clinical feature. Bubonic plague is designated so because this is the only disease characterized by the usual clinical manifestation of buboes. The reason is that plague is transmitted by rat fleas which deposit contagion at an intradermal level in the catchment area of the lymphatic system. This assures that the contagion in most cases will be drained through the (afferent) lymphatic vessels to the lymph nodes, which, upon infection, will begin to swell and develop into intensely painful buboes. All alternative theories arguing for a different contagion or a different system of infection, for instance, cross-infection by droplets, should explain how the contagion would regularly be transported from the lungs to the lymph nodes. This also explains why buboes have never been observed in cases of primary pneumonic plague, where the normal plague contagion is inhaled directly into the lungs. Because bubonic plague is the only epidemic disease characterized by buboes, this clinical feature challenges directly nearly all alternative theories of plague and explains why the advocates of these alternative theories consistently refrain from addressing this crucial question and why this should not be accepted. (3) The inverse correlation of population density and infection rates. The basic rule of epidemiology is that “no matter by what method a parasite passes from host to host, an increased density of the susceptible population will facilitate its spread from infected to uninfected individuals”.57 This means that there is a consistent correlation to the effect that powers of spread will increase or decrease, co-vary with corresponding changes in population density. This is conspicuously not the case for bubonic plague and for particular reasons springing from its unique basis in black rats and their fleas. The epidemiological principle on powers of spread functions with all diseases disseminated by inter-human cross-infection, without exception; this is

57  Burnet and White 1972: 11.



What to Look for and Keep in Mind 

 19

not the case with bubonic plague, which is spread from rats to human beings by rat fleas. Then, other structural conditions forming the powers of spread come into play. This may (somewhat) inaccurately be designated the inverse correlation of powers of spread and population density. In the case of diseases spread by cross-infection, the density pattern is, so to speak, one-dimensional, comprising only human beings; the density of susceptible human beings will, accordingly, in the main decide the powers of spread. In the case of rat-based plague, the density pattern is three-dimensional, comprising the density not only of human beings but also of rats and rat fleas. The latter two density factors will tend to co-vary strongly and, therefore, to override the significance of the density of human beings. Rats are social animals living in colonies defending territories. This means that in the countryside at least one rat colony will normally co-reside with a household, whereas in urban environments several households will usually crowd together within the territory of a rat colony. Accordingly, the ratio of humans to rats and fleas will tend to be lower in urban environments than in rural areas; there would be more persons to share the dangerous rat fleas let loose from an afflicted rat colony. The systematic feature of inverse correlation reveals that the rat flea is of paramount importance for dissemination and transmission of plague among human beings. The inverse correlation invalidates all alternative theories of the epidemiology of bubonic plague, which are based on cross-infection, including the (now widely discredited) human-flea theory. I have written about this important topic in several works, first in a long paper in Population Studies in 1987, i.e. over a generation ago, again in a long chapter in my 2010 monograph on the alternative theories.58 The thundering silence these studies have been met with by all advocates of alternative theories, including Walløe, also in his recently expanded human-flea-cum-humanlouse theory,59 demonstrates their definitive powers of invalidation of this position: the invalidating arguments must be passed in silence by or the alternative theory cannot be argued at all. (4) Seasonality. The conventional principle of the correlation between increasing population density and increasing powers of spread also means that diseases spread by cross-infection “no matter by what method a parasite passes from host to host” will acquire increasing powers of spread in chilly and cold wintry weather: they gain strength from people’s intuitive and practical reactions, which are to huddle closer together, remain indoors more, and restrict living space for better and more efficient heating. The net effect is to bring people closer together, in other words to increase population density at the micro-level of human social behaviour, which means that 58  Benedictow 1987: 401-31; Benedictow 1992a/1993/1996: 177-80; Benedictow 1992b: 80-81, 83; Benedictow 2004/2006: 31-34, 284, 307, 310-13; 331; Benedictow 2010: 289-311. 59  Walløe 2010: 13-28; Hufthammer and Walløe 2010: 29-43; Hufthammer and Walløe 2013: 1752-59. See discussion of this theory in Chapters 7, 8 and 11, below.

20 

 Introduction

all interpersonally communicable diseases will gain increasing powers of spread. Bubonic plague, however, is a disease of the warmer seasons: spring, summer, and early autumn. The advent of chilly autumn weather slows it down, wintry weather makes it disappear, or only occasionally reveal its smouldering presence among the rat colonies by the odd human case, until it would reappear with warmer spring weather.60 There are two reasons for this peculiar defining feature of bubonic plague: (1) the rapidly diminishing flea population in cold weather, also indoors in old-time houses: people lived in simple house structures with beaten or packed earth floors, often so-called blackhouses (“røykstover”)61 with a central hearth on the floor for cooking and heating, and a louver, a hole in the ceiling to let out smoke and let in light, so chilly or quite cold room temperatures were prevalent in wintry conditions; (2) rats infected by plague do not develop bacteraemia, or, if they do, much lower levels of bacteraemia, which means that they are much weaker sources of infection for fleas ingesting their blood. By implication, all alternative theories based on assumptions that historical plague epidemics were spread by cross-infection are untenable. (5) The identification of Y. pestis as the contagion of the plague epidemics of the past. In the past 20 years, a new historically oriented microbiological discipline has been established, namely paleobiology. Paleobiology was developed in order to uncover the presence and identity of infectious diseases in biological remains of the past. Paleobiological plague research includes microbiological studies of (ancient)DNA and the identification of specific proteins or antigens contained in protein capsules of bacteria. In the case of paleobiological plague studies, material obtained from skeletal remains in putative plague graves are examined for remains of the aDNA or a specific antigen of a mortal disease which could be the cause of death. In the case of bubonic plague, that would be the DNA or F1 antigen of Y. pestis. Paleobiological studies can also include the study of genetic mutational change over time and the identification of various biovars or strains of various ages and locations, for instance, in Africa, Europe or Asia and their association with the three (known) plague pandemics of 541-767 (the Justinianic), 1346-1722, and 1894 c.- 1940 CE. From 1998 to March 2014, 20 articles have been published presenting the outcomes of 45 biomolecular studies of skeletal material obtained in putative plague graves or burial pits in 40 different localities and of hundreds of specimens of individual skeletal remains. They include studies of aDNA and of the F1 protein capsular antigen. They have consistently identified Y. pestis, the contagion of plague, an extremely fatal disease, which must then be considered the causative agent of disease and death. 60  Benedictow 2002: 38-40, in English translation in Chapter 2.4, pp. 111-13, and Chapter 10. See also Bendictow 2004/2006: 233-35; Benedictow 2010: 396-436. 61  Blackhouses “were simple rooms, open to the raftered roof and hand no chimney. The smoke from the hearth found its way out either through a hole in the ceiling or in the gable, or directly through the thatch in the roof. Because smoke was trapped under the ceiling, these houses could not have an upper floor.ˮ Laerum 2010: 1, 5-7.



What to Look for and Keep in Mind 

 21

This functions as the establishment of a defining feature. This topic is exhaustively presented and discussed below in Chapter 1.5: “The Triumph of Paleobiology in Historical Plague Research”. It puts in perspective all alternative theories based on alternative contagions or (arbitrary) assertions of genetic mutations, which, it is maintained, would affect the epidemiology of plague.

1.3.3 Some Crucial Matters of Fact

(1A) On rats and human beings as sources of bacteraemic blood that can make fleas infective. In order to become infective, fleas must ingest blood containing plague bacteria with sufficiently high numbers per unit of blood, i.e. bacteraemia. This raises three crucial questions that are often ignored, by Walløe with telling consistency also in his recent revival of human-flea theory, the human-louse-theory, and the expansion or fusion of these two theories into a human-flea-cum-humanlouse theory of the transmission of plague.62 The crucial empirical data that decides these questions is thoroughly presented and discussed in Chapter 12.63 1. What are the properties of plague-diseased rats and human beings as sources for infection of fleas which can make them infective? 2. What is the conversion rate between plague bacteraemia and the infection of feeding fleas? 3. How do fleas transmit plague infection? What are the prevalence and the levels of plague bacteraemia in human beings and in rats. For all practical purposes, all infected rats develop bacteraemia, while this is the case for “only” 30-45% of human plague cases.64 (1B) Statistically speaking, the levels of plague bacteraemia among infected rats are hugely higher than among human bacteraemic cases: it is nearly 1000 times higher in rats than in human beings as a comparison of rats and the human beings which develop bacteraemia. Because about all rats develop plague bacteraemia, while “only” 30-45% of human plague patiens become bateraemic, the proportion of bacteraemia among rats is much higher than among infected human beings. The levels of bacteraemia in human plague patients are also very much lower than in rats. Among rats, levels of 108‒109 (100 million to one billion) plague bacteria/mL (= millilitre or cm3) of blood are usual, they never occur among human beings by huge margins. Rats are hugely superior sources of contaminated blood for feeding

62  See Chapters 7, 8 and 11. 63  See also Chapters 8.7 and 11.3. 64  See Chapter 12, below. See also Chapters 7, 10 and 11.

22 

 Introduction

fleas compared to human beings. This is the basic reason rat fleas are the agents of transmission and dissemination of bubonic plague, not human fleas or lice. These topics are again thoroughly presented and discussed in Chapter 11 with respect to lice and in Chapter 12, with respect to fleas, see also Chapter 7. A brief introduction to the main facts can be useful intellectual luggage for the readers and is given below in 2A. (2A) When fleas ingest sufficiently contaminated blood, bacteria follow into the stomach, technically called the ventriculus or midgut. In addition to the ventriculus the stomach system of fleas consists also of a proventriculus which functions as a valve allowing fleas to make relatively speaking huge intakes of blood, because the valve prevents the blood in the strongly distended ventriculus after a feed from forcing its way back out. Therefore, after a blood meal, fleas do ‘rarely attempt to feed more frequently than once in 24 to72 hours’, this is then the minimum interval between feedings, normally ‘perhaps every 4 or 5 days’.65 Because bacteraemia does not develop in the majority of human plague cases and the levels of human bacteraemia are so low, only a few bacteria will in some cases be left on the mouth parts immediately after feeds, and general all will have disappeared after 3 hours. This means that contamination of the mouth parts with bacteria from the previous blood meal never plays an epidemic role for these two independent sufficient conditions, bacteria left on the mouth parts are too few, and they have all disappeared by the next blood meal. Fleas do not transmit plague by the bite itself.66 IPRC made the first measurement of the feeding capacity of fleas, more specifically of the rat flea X. cehopis. They concluded that the average volume of blood in the fully distended ventriculus of rat fleas (X. cheopis) is about 0.5 μL (microlitre= mm3).67 This implied that, statistically speaking, fleas (of this species) are infected with 1 bacterium per 2000 bacteria/mL in the blood they ingest. This was the infection gauge used in my 1992 doctoral thesis and also in later works. According to the data on the prevalence and levels of bacteraemia in human plague patients presented in Chapter 12, Tables 12.1 and 12.2, this meant, for instance, that 82-86% of plague patients would not infect feeding fleas at all. Recently, the findings of a new study were generously conveyed to me in a personal communication. It showed that the average blood meal of this rat flea was 0.41µL for females and 0.18µL for males.68 Clearly, IPRC had studied the feeding capacity of female X. cheopis, and the measurement was quite good. This entails that fleas of this species need to ingest blood containing on the average ~2440 and ~5560 plague bacteria in order to become infected by 1 plague bacterium, which represent the new infection-level divisors (or gauges). This slight correction implies that at least 90% of 65  Busvine 1976: 62. Cf. Eskey and Haas 1939: 1474; Eskey and Haas 1940: 46. 66  See Chapter 7.3.3. 67  IPRC, XV, 1907: 396-97. 68  Personal communication by email from B.J. Hinnebusch on 9 June 2015.



What to Look for and Keep in Mind 

 23

all plague patients will not infect feeding fleas during the course of plague disease. Clearly, human plague cases must be very poor sources of plague infection for feeding fleas. Notions of a significant role for inter-human cross-infection of plague by fleas in the epidemiology of plague are unrealistic. After a blood meal, fleas do usually feed again after 4-5 days.69 In the meantime, fleas digest the blood meal and pass it gradually into the lower digestive tract (hindgut). Only when most of the meal is digested, will fleas again feel hungry and start the search for a new feeding opportunity. This means that the digestive process takes on the character of selfpurification of infection. Seen in the light of all 326 individually human plague cases examined with respect to prevalence and levels bacteraemia, this indicates that 99.7% of all fleas would, for all practical purposes, be infection-free and non infective at the time of the next blood meal.70 This casts a sharp light over all notions of a role for human fleas or lice in the epidemiology of plague. They are dependent on neglect of basic and long known facts, certainly since the publication of my doctoral thesis in 1992.71 In the case of plague bacteraemia among rats, this is a very different matter, as will be seen below. The remaining about 0.3% has a concrete reference, one of the plague patients studied in Vietnam exhibited a level of bacteraemia of 4x107 bacteria/mL. This is about 40 times higher than a few cases with the second highest level of recorded bacteraemia,72 and thousands of times higher than in almost all other examined plague patients, clearly an extreme statistical outlier. This patient would infect both female and male fleas with doses of plague bacteria that would, if transmitted, cause the death of 50% of more of human beings. This introduces the subjects of lethality, which usually is measured as the dose of bacteria (or toxins) that would kill 50% of those infected of a specified population, i.e. LD50. Because experiments on this point cannot be performed on human beings, the cautious decision has been made to use the LD50 of a highly susceptible species of ground squirrels, namely 6,000 plague bacteria, which can be put in perspective by mentioning that an infection dose of 5,500 plague bacteria produces a mortality rate of 10% of black rats.73 In order to be infected by 6,000 plague bacteria, a flea must, according to the new infection gauge, ingest blood containing 2540x6000 = 15,240,000 or 15.24x106 plague bacteria/mL. With the exception of one human case, who exhibited a level of bacteraemia of 4x107 bacteria/mL, this is far higher, about 69  Busvine 1976: 62. 70  Chapter 12.6, pp. 646-49. 71  Benedictow 1992a/1993/1996: 227-63. 72  These are 7 human cases with a bacteraemia of ≥106, which would, according to the sex-specific gauges infect feeding fleas by ≥410-180 Y. pestis. Chapter 12.6. It is suggested there that these 8 statistical outliers, who constitute 2.45% of all plague patients examined for bacteraemia, are cases of primary bacteraemic plague, which apparently constitute around 2.45% of all cases in epidemics of bubonic plague. 73  Chapter 12.7, p. 649.

24 

 Introduction

15 times higher, than any other level of human bacteraemia recorded. These technical data represents ample hard evidence to constitute proof that human beings and human ectoparasites can only play a negligible role in the dynamics of plague epidemics. Laudisoit et al. argue that mechanical transmission of plague by human fleas was a significant element in plague’s epidemiology, that is transmission by bites with mouthparts soiled with remnants of blood containing plague bacteria from the preceding feed.74 As pointed out, the prevalence and the levels of human plague bacteraemia as recorded in Tables 12.1 and 12.2, are so low, that soiling of the mouthparts must be a rare contingency. It is a fact that human fleas can become infected, contain plague bacteria in their stomachs after a feed, like all other human ectoparasites, mosquitoes, bed bugs, ticks, or lice, it is fallacious to infer that this is evidence of transmission by contaminated mouth parts - or by any other means of transmission by any of these ectoparasites. These scholars also do not address the question of lethal dose for human beings, so that any assumption that a putative number of plague bacteria on the mouth parts of human fleas or groups of human fleas after feeding would suffice to be lethal is pure speculation x 2. These matters have been studied.75 Fleas do, as mentioned, usually take a new blood meal “every 4-5 days”.76 Bibikova and Klassovskiy performed decisive experiments relating to this question. Fleas were fed on blood containing109 or 1 billion bacteria/mL of blood, a hugely higher level of bacteraemia than ever recorded among human plague patients. Experiments carried out with a batch of 48 fleas showed that 21 or 43.75% of the fleas had contaminated mouthparts, remnants of blood containing plague bacteria, for 0-2 hours. In 15 of these cases the numbers were in single digits, in 6 cases there were more than 10 bacteria in the blood. A total number of 150-200 bacteria is suggested, or an average of 3-4 bacteria per flea immediately after having fed on extremely bacteraemic blood. In the third hour after infection, an experiment comprising 22 fleas showed that 2 had bacteria in single digits; no bacterium was left on any mouthpart after 3 hours.77 Laudisoit et al. claim that the mouthparts of fleas would still be soiled after 3 days, this must be a misunderstanding or a slip of the key.78 When fleas in nature voluntarily would like to feed again, any soiling of their mouth parts from the previous feed, would be long gone.When juxtaposed with the

74  Laudisoit, Leirs, Makundi et al. 2007. 75  See Chapters 7.3.3, 10.5 and 11.3. 76  Busvine 1976: 62. 77  Bibikova 1977: 27; Bibikova and Klassovskiy 1974: 89‒90; Benedictow 1992a/1993/1996: 239. See Chapters 10.5 and 11.3. 78  Laudisoit, Leirs, Makundi et al. 2007 : 691. They refer to item no. 21 in the Bibliography, Plague Manual: Epidemiology, Distribtution, Surveillance and Control. 1999. Geneva: WHO, in the usual manner in scientific journals, without page references, which means that ready testability of references in practice is rather impossible. I have not been able to track downs this specific reference.



What to Look for and Keep in Mind 

 25

assumed cautious LD50 for human beings of ~6000 bacteria, it becomes clear that mechanical inter-human cross-infection of plague disease does not occur. This theory should be abandoned for good. This evidence also explains that no concrete case of inter-human cross-infection of bubonic plague was observed in the huge plague epidemics in India, China, Java and Madagascar, or in the large epidemics in Egypt and Vietnam, according to the huge syntheses of plague studies in the standard works on plague, although a sprinkling of cases or sporadic rare occurrences are accepted or not excluded.79 This puts in perspective the fact that native housing and hovels swarmed with human ectoparasites.80 This evidence agrees with the fact that the notion of inter-human cross-infection of bubonic plague is incompatible with the epidemiological features which clearly emerge from the synthesis of the complete study of all data on the spread of the Black Death across Europe, the Middle East and North Africa.81 These features emerge also more generally from studies of plague epidemics, including the complete study of the history of plague epidemics in Norway 1348-1654.82 It agrees also with the general presentation of the epidemiology of bubonic plague in all standard works on plague.83 These features are generally compatible, only compatible, with the distinguishing or defining features of rat-flea-borne plague.84 (3A) Fleas do not become infective with lethal doses for human beings simply by ingesting sufficiently bacteraemic blood which makes them heavily infected. There is a pivotal difference between infected and infective fleas, only infective fleas transmit plague. Transmission requires development of blockage of the ventricular system, normally in the proventriculus, which impaires its valve function.85 Blockage occurs when fleas ingest so highly bacteraemic blood that the bacteria multiply faster in the ventricular system than they are moved into the lower digestive tract.

79  Lamb 1908: 5-93; Loghem und Swellengrebel 1914: 460-81; Liston1924: 950-54, 997-1000; Petrie, Todd, Skander, et al. 1924–25: 117-150; Wakil 1932; C.Y. Wu 1936: 261, 265, 273-74, 300-301, 304; Langen and Lichtenstein 1936: 185-86; Girard 1943: 4-43; Hirst 1953: 220-377, 459-63; Pollitzer 1954: 361, 378-81; Girard 1959: 1-11; Brygoo 1966: 39-44; Williams, Hudson, Turner, et al. 1980: 459-68: Butler 1983: 32-53. Contrary to a recurrent misunderstanding, this was also not observed in the tiny epidemic of 90 cases in Morocco in 1941. Blanc and Baltazard 1945; Girard 1943; Audoin-Rouzeau 2003: 297-344. Cf. Benedictow 2010: 167-69. 80  Girard 1943: 21-23, 25; Brygoo 1966: 36-44; Bacot, Petrie and Todd 1914: 507; Petrie Todd, Skander et al. 1924-25: 117-150; Benedictow 1992a/1993/1996: 259-63; Wu Lien-Teh 1926:187, (62-63), and 1913-14: 248-49; Pollitzer 1954: 380. 81  Benedictow 2004/2006: 50-241; Benedictow 2010: 25-484. 82  Benedictow 2002, the part on the history of the Black Death in Norway is available in English translation as Chapter 2. See also Chapters 3 - 5. 83  Wu Lien Teh, Chun, Pollitzer, and C.Y. Wu 1936; Hirst 1953; Pollitzer 1954; Brygoo 1966. 84  Benedictow 2010: 73-484. 85  R. J. Eisen, Bearden, Wilder, et al. 2006: 15380-85. In Chapter 12, this theory is shown to be empirically and technically untenable, at least in its epidemic version.

26 

 Introduction

According to quite recent research, bacterial net growth leading to blockage in the superior vector X. cheopis starts when these fleas ingest about 3,800 Y. pestis,86 a much lower figure than previously assumed, and the incidence of blockage increases with higher infection doses. The proliferation of bacteria will cause the formation of a block of gelatinous hemobacillary mass consisting of bacteria, fibrinoid-like material, and haemin, today often called a biofilm. When blood from a new feed hits a sufficiently developed blockage, it streams back taking with it not only the hugely bacteraemic blood present in the pre-blockage area of the ventricular system but also bits torn off the blockage containing thousands of plague bacteria. These regurgitants contain, according to the only study, usually roughly 24,000 plague bacteria,87 which, within wide margins of error, represent a range of lethal doses (LD) for most human beings. This corroborates the views maintained by all standard works on plague: within human environments only black rats can function as sources of sufficiently frequent and intensely bacteraemic blood to make efficient vectors infective. The basic facts on black rats and their presence and the need to understand their specific behavioural patterns are presented and discussed in over 85 pages in my 2010 monograph, which should not be easily overlooked.88 The overriding importance of recognizing and taking into account that rats are cannibals is emphasized. When rats are seriously ill and no longer able to defend themselves, they do their very best to hide away from other rats in order to avoid being eaten more or less alive. Rats die in highly unusual and inaccessible places. Dead rats are therefore rarely seen even during plague epidemics and are very hard to find also by modern specialists and plague researchers (if rats do not frequently nest in the ceilings and fall down on the floors when they become severely ill). Also these facts are found in all standard works on plague as well as in central primary studies on plague epidemics by modern researchers.89 It is true that contemporary chroniclers or physicians did not mention the observation of dead rats during plague epidemics. However, the inference that this means that rats were not present and the dynamic basis of the epidemic is a classical example of the methodological fallacy of, argumentum ex silentio, i.e. the fallacy of arguing that silence in the sources about something or someone constitutes proof that this something or someone did not exist. In other words, to argue that absence of evidence is evidence of absence. In my 2010 monograph, this problem is discussed in a separate chapter, “The Question of the Presence of Rats and the Methdological Fallacy of Inference e silentio”,90 which should also not be easily overlooked. Another typical case of this fallacy is, for instance, argued in Laudisoit et al.’s study of the fleas 86  Lorange, Race, Sebbane and Hinnebusch 2005: 1909. 87  Burroughs 1947: 381-83. 88  Benedictow 2010: 73-150. 89  Benedictow 2010: 85-116. 90  Benedictow 2010: 85-91. See also Benedictow 2004/2006: 192-93, 206-07.



What to Look for and Keep in Mind 

 27

found in human housing in an area of Africa with sporadic cases of plague. When mostly human fleas (P. irritans) were found, they concluded that this flea must be the vector of the cases of plague by inter-human cross-infection.91 The crucial point is that while human fleas will readily be found, the flea of the black rat, X. cheopis, is a fur flea which lives most of its life on the coat and will mostly be found when they leave dying92 (or dead) rats,93 which were among IPRC earliest observations.94 Laudisoit et al. acknowledge that no human plague cases were recorded in the region during their study, so few X. cheopis should be found, and would be highly unrepresentative of their real presence.95 Argumentum ex silentio is a common fallacy among the advocates of alternative theories, especially by Cohn, Scott and Duncan, Gunnar Karlsson, and Walløe.96 It is also a central and invalidating fallacy of the eleventh alternative theory of plague epidemiology recently presented by Walløe and Hufthammer. They reject that black rats and their fleas were the driving forces of the historical plague epidemics in Northern Europe, because skeletal remains of rats have not been found by archaeologists excavating late medieval or early modern settlements of detached or semi-detached farmsteads in Norway’s countryside where the vast majority of medieval people lived, but only have been found in the ground of urban centres. When the particular effects of seriously ill or dying rats’ instinctual behaviour are not taken into account and their bones are arbitrarily assumed should be found together with those of other skeletal remains from human consumption of meat,97 this is simply another blatant example of the fallacy of inference by argumentum ex silentio. When old urban structures crumble in the ground, rat bones are released from the rats’ hiding places and can be recovered by archaeologists. One could here also mention identification of the DNA or antigen F1 of Y. pestis in skeletal material from plague graves in areas where no extant written source inform that plague had raged at the time.98 Also this alternative theory is, therefore, based on a methodological fallacy. It is publishable because they are allowed by their editors to ignore central scholarly works, empirical material, and views found in the outstanding standard works on plague, and, of course, in the primary studies on plague on which they are based. This includes the broad synthetic presentation of this research given in my 2010 monograph. Another important point that is ignored or marginalized is that in Sweden and Finland, where the brown rat did not arrive until about 1800, there were

91  Laudisoit, Leirs, Makundi et al. 2007 : 687-93. 92  Brown 1995: 931; Thomas, Karstens, and Schwann 1993: 209-13. 93  On nest-dwelling and fur-dwelling fleas se below, Chapter 1.3.3; Chapters 10.4.2-3. 94  IPRC, I, Part IV, 1906: 467-82; IPRC, XVII, 1907: 436-45; IPRC, XX, 1907: 474-75. 95  Laudisoit, Leirs, Makundi et al. 2007: 691. 96  Benedictow 2010, see Index under fallacy of Argumentum ex silentio p. 722, and below. 97  Hufthammer and Walløe 2013: 1754-76; Hufthammer and Walløe 2010: 36-41. 98  See, for instance, below: Chapter 1.4.6 and Chapter 8.3.

28 

 Introduction

widespread colonies of black rats in the countryside still in the second half of the nineteenth and early decades of the twentieth century. According to central scholarly standards, counterarguments should be taken seriously. Counterarguments should be presented and discussed and assessed. It should be shown why they are not valid or untenable, or insufficiently significant to be taken (seriously) into account. If not, if the counterarguments are valid and tenable, they should be taken into account and the alternative theories rewritten or discarded. The invalidity of the theory that the plague epidemics of the past were spread by interhuman cross-infection by human fleas (and lice) has been preliminarily shown also above, and will be demonstrated again thoroughly below. It is a reason for concern that articles arguing for the human-vector theory of plague epidemiology, where serious counterarguments and invalidating facts are passed over in silence, repeatedly are publishable.99 (B) Fur Fleas and Nest fleas100 There are two main types of fleas: fur fleas, which normally ride with their hosts, and nest fleas, which normally live in the nests of their hosts. Most species of fleas are nest fleas; they live most or about their entire lives in the nests of their hosts. Their larvae feed on the blood in the droppings of the adult fleas and would succumb in the absence of adult fleas. This is, for instance, the case with the species Nopsyllus fasciatus, the ordinary flea parasite of the brown rat, Rattus norvegicus. Also Pulex irritans, the so-called human flea, is a typical nest flea which lives in the immediate surroundings of human beings, preferably in or around beds and other sleeping arrangements, which, then, constitute their nest. They come out at night, take their fills, and seek out usable places to digest their meals and, for females, to lay eggs. Nest fleas are therefore not adapted to riding with their hosts and very averse to light and avoid this contingency. Human fleas avoid riding with their human hosts. Examination of actively worn clothing did not yield many human fleas, even if human housing was greatly infested, as was the case of India, Indonesia, and North Africa. As expected, they did not find any N. fasciatus, although the brown rat was hugely present in the human environments. As a nest flea, human fleas typically move with furniture, bed linen, and suchlike, i.e. they move with the “nest”. For these reasons, human fleas will not under any circumstances be effective disseminators of plague infection, i.e. independent of the decisive points relating to the level of bacteraemia in human beings and the level needed to produce blockage. It constitutes an independent sufficient condition for rejecting a significant role in the transmission

99  Most recently, this is the case with the conspicuous absence of discussion of these facts in papers by Walløe and Hufthammer. See discussion of this theory below, in Chapters 7, 8, 10, 11. See also attached Bibliography and General Bibliography. 100  See Chapters 7-11.

Bibliography 

 29

and dissemination of plague. In sharp contrast, the properties of X. cheopis as a fur flea equip fleas of this species with behavioural features greatly suitable for the spread of plague infection. Because grain is the favourite food of black rats, their fleas have tended to be on their own in environments with grain or at least grain debris, in private grain stores, in the vicinity of querns (hand mills) where often there is grain debris on the ground, in the stores of local salesmen, in mills, bakeries, shipments of grain, and so on. These fleas have, by evolutionary selection over time, long ago developed the ability to live off grain and grain debris, being dependent on blood only for laying eggs. The rapid turnover of generations and the great fertility that characterize fleas continuously produce a correspondingly huge number of mutant specimens, and, therefore, also at some point specimens that had this special property. This meant that infected rat fleas can be transported over long distances. The humidity associated with voyages allows fleas to survive for many weeks, explaining why plague could be spread so easily by ship. Rats infected with plague will normally die in a few days. Long-distance spread of plague is closely associated with grain-eating fleas. The only bold (but imprudent) attempt at explicitly denying explicitly the importance of the distinction between fur fleas and nest fleas is addressed thoroughly below in Chapter 10.4.2.101 Otherwise, this topic has been consistently (allowed to be) passed by in silence, the only way of making alternative theories of the epidemiology of plague seemingly viable (which raises, as mentioned, questions of the quality and competence of some modern editorial work). This brief presentation of the main points of plague research after more than hundred years of studies, the overwhelming scientific basis for the positions taken by the leading international health organizations on the epidemiology of plague should be evident. The fact that alternative theories have proliferated over the last decades and attracted many scholars becomes the more curious as an academic topic of concern. It should, as suggested above, direct attention towards the competence and quality of modern academic editorial work.

Bibliography 102 Abbey H. 1968. “An Examination of the Reed-Frost Theory of Epidemics”, Human Biology. 24: 201– 233. cf. J. de Oliveira Costa Maia 1968.

101  See also Benedictow 1992a/1993/1996: 162-65; Benedictow 2010: 108, 397, 406, 682-84 102  Medieval Nordic or Norse authors are entered according to Christian names. Modern Icelandic personal names are entered according to their surnames in accordance with normal international standards. German, Nordic, and Norse personal names and place names may include letters not used in English. In the Bibliography and the index these letters are entered alphabetically according to the following rules: Å/å = AA/aa (pronounced “aw” as in “saw” in English); Ä/ä, Æ/æ = AE/ae; ü = y; Ö/ö = OE, oe; ð

30 

 Introduction

Audoin-Rouzeau F. 2003. Les chemins de la peste. Le rat, la puce et l’homme. Rennes: Presses Universitaires de Rennes. Audoin-Rouzeau F. 2007. “Le vecteur de la peste: enquête épidémiologique, archéologique et historique.” In: Peste: entre épidémies et sociétés: 217-229. Ayyadurai S., Sebbane F., Raoult D., and Drancourt M. 2010. “Body Lice, Yersinia pestis Orientalis and the Black Death”, Emerging Infectious Diseases, www.cdc.gov/eid, 16: 892-893. Bacot A., Petrie G.F., and Todd R.E. 1914. “The Fleas found on Rats and Other Rodents, living in Association with Man, and trapped in the Towns, Villages and Nile Boats of Upper Egypt”, The Journal of Hygiene, 14: 498-508. Baltazard M. 1959. “Nouvelles données sur la transmission interhumaine”, Bulletin de l’Académie nationale de médecine, October 1959: 517–525. Baltazard M. 1960. “Déclin et destin d’une maladie infectieuse: la peste,” Bulletin of WHO, 23 : 247–262. Benedictow O. J. 1984: Pest. En epidemiologisk og historisk undersøkelse. Foreløpig versjon. [Plague. An Epidemiological and Historical Study. A Pilot version. University of Oslo, Blindern: Department of History. Benedictow O. J. 1987. “Morbidity in Historical Plague Epidemics”, Population Studies. 41; 1987: 401431. Benedictow O. J. 1992a. Plague in the Late Medieval Nordic Countries. Epidemiological Studies. Oslo: Middelalderforlaget. Two reprints of 1993 and one of 1996. Benedictow O. J. 1992b. “Pestepidemiers spredningskraft i tynt befolkete landdistrikt. Kan pest forklare befolkningsnedgangen i Norge i seinmiddelalderen?” [= The Powers of Spread of Plague Epidemics in Sparsely Populated Rural Districts. Can Plague explain the Decline of the Norwegian Population in the Late Middle Ages?] In: Liv og helse i middelalderen: 80-101. Benedictow O. J. 2002. Svartedauen og senere pestepidemier i Norge. Pestepidemienes historie i Norge 1348-1654. Oslo: Unipub. The part on the Black Death is available in English translation as Chapter 2, below. Benedictow O. J. 2004. The Black Death 1346-1353. The Complete History. Woodsbridge: Boydell & Brewer. 3 reprints 2004-2006. Benedictow O. J. 2010. What Disease was Plague? On the Controversy over the Microbiological Identity of Plague Epidemics of the Past. Leiden: Koninglijke Brill NV. Benedictow O. J. 2012. “New Perspectives in Medieval Demography: The Medieval Demographic System.” In: Town and Countryside in the Age of the Black Death: 3-42. Benedictow O. J. 2015. “Problems with the Early-Phase Theory of the Transmission of Plague by Fleas”, Journal of Medical Entomology, 2015b: fortcoming. Biraben J.-N. 1975. Les hommes et la peste en France et dans les pays européens et méditerranéens. Vol. 1. Paris: Mouton. Blanc G. 1956. “Une opinion non conformiste sur le mode de transmission de la peste”, Revue d’Hygiene et de Medecine Sociale, 4, 536-562. Blanc G. 1961. “La disparition de la peste et ses causes épidémiologiques”, La Semaine des hôpitaux, 37: 105-110. Blanc G. and Baltazard M. 1941. “Recherches experimentales sur la peste. L’infection de la Puce de l’Homme, Pulex irritans L.”, Comptes rendus hebdomadaires de séances de l’Academie des sciences, 213: 813-816, 849-851. ( Their response to severe criticism by Girard ibidem: 853).

(pronounced “th” as in “the” in English) = d. Þ/þ (pronounced “th” as in “think” in English) are, in the Icelandic alphabet, placed after the letter y, an arrangement which is followed here, according to their custom (for lack of any logical alternative). Transcriptions of Russian names or titles or works written in the Cyrillic alphabet to English form are written according to standard international phonetic rules.

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Blanc G. and Baltazard M. 1942. “Rôle de ectoparasites humains dans la transmission de la peste”, Bulletin de l’Académie Nationale de Medecine. 126: 446–448. Blanc G. and Baltazard M. 1943. “Quelque remarques à propos du mémoire de G. Girard sur les ‘ectoparasites humains dans l’épidémiologie de la peste”, Bulletin de la Société de pathologie exotique. 36: 208–216. Discussions. Ibidem: 216–217. Blanc G. and Baltazard M. 1945 Recherches sur le mode de transmission naturelle de la peste bubonique et septicémique. In: Archives de l’Institut Pasteur du Maroc. 3, cahier 5: 173–354. Brown R. 1995. “Is Behavioural Thermoregulation a Factor in Flea-to-Human Transmission of Yersinia pestis?”, The Lancet, 345: 931. Brygoo E.-R. 1966. Épidemiologie de la peste à Madagascar. In: Archives l’Institut Pasteur de Madagascar, 35: 9-147. Burnet F.M and White D.O. 1972. Natural History of Infectious Disease. 4th edn. Cambridge: Cambridge University Press. Burroughs A.L. 1947. “Sylvatic Plague Studies. The Vector Efficiency of Nine Species of Fleas compared with Xenopsylla cheopis”, The Journal of Hygiene, 45: 371-396. Butler T. 1983. Plague and Other Yersinia Infections. New York: Plenum Medical Book Company. The Cambridge History of Scandinavia. 2003. Vol. 1. Cambridge: Cambridge University Press. CDC Plague, with various links to Natural History, Epidemiology, and Fact Sheet on CDC’s website, see http://www.cdc addresses below. Christensen P. 2003. “‘In these Perilous Times’: Plague and Plague Policies in Early Modern Denmark”, Medical History, 47: 413-450. Christensen P. 2009. “Appearance and Disappearance of the Plague: still a Puzzle?” In: Living with the Black Death: 11-21. Christiakaos G., Olea R.A., Serre M.L., et al. 2005. Interdisciplinary Public Health Reasoning and Epidemic Modelling: The Case of Black Death. Berlin: Springer Cohn S.K, Jr. 2002. The Black Death Transformed: Disease and Culture in Early Renaissance Europe. London: Hodder Headline Group. Cohn S.K, Jr. 2008. “Epidemiology of the Black Death and Successive Waves of Plague,” Medical History. Supplement, (27): 74–100. Desertion and Land Colonization in the Nordic Countries c. 1300–1540. 1981. Stockholm: Almqvist & Wiksell International. Drancourt M. and Raoult D. 2008. “Past Plague.” In: Paleomicrobiology. Past Human Infections: 145160. Eisen R.J., Bearden S.W., Wilder A.P., et al. 2006. “Early-phase Transmission of Yersinia pestis by Unblocked Fleas as a Mechanism explaining Rapidly Spreading Plague Epizotics”, Proceedings of the National Academy of Sciences of the United States of America, 103: 15380-15385. Girard G. 1943. “Les ectoparasites d l’homme dans l’épidemiologie de la peste”, Bulletin de la Société de pathologie exotique et de ses filiales, 36: 4-43. Girard G. 1959. “Considerations sur l’épidémiologie de la peste caractéristiques des centres endémiques asiatiques et africains”, Revue de médécine et d’hygiène d’outre-mer, No. 281; Oct. 1959: 114-120. Hasund S. 1920. Ikring Mannedauen. Ei liti sogestudie. Kristiania. Offprint in the form of a boklet of the original publication in Beretning om Norges Landbrukshøiskoles virksomhet, 1918-1919: 1-67. Hasund S. 1934. Det norske folks historie gjennem tidene, Vol. 3, Tidsrummet omkring 1280 til omkring 1500. Oslo: H. Aschehoug & Co. Hatcher J. 2003. “Understanding the Population History of England 1450-1750”, Past & Present, No. 180: 83-130.

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Helle, K. 2013. “Samfunn og rike fra vikingtiden til 1536.” In: Helle, Dyrvik., Hovland, og Grønlie. 2013. Grunnbok i norsk historie: 25-129. Helle K., Dyrvik, S., Hovland E., og Grønlie T. 2013. Grunnbok i norsk historie fra vikingtid til våre dager. Oslo: Universitetsforlaget. Hirst L.F. 1953. The Conquest of Plague. Oxford: Clarendon Press. Holmsen A. 1949. Norges historie. 1st repr. Oslo: Gyldendal Norsk Forlag. Holmsen A. 1977. Norges historie. 4th repr. Oslo: Universitetsforlaget. Horrox R. 2012. Review of O. J. Benedictow, What Disease was Plague? […], 2010, Speculum. Journal of Medieval History, 87, 836-837. Houhamdi L., Lepidi H., Drancourt M., Raoult D. 2006. “Experimental Model to Evaluate the Human Body Louse as a Vector of Plague”, Journal of Infectious Diseases, 194, 1589-1596. -http//:www.cdc.gov/plague http://www.cdc.gov/ncidod/dvbid/plague/who_cc/ http://www.cdc.gov/ncidod/dvbid/plague/index.htm http://www.cdc.gov/ncidod/dvbid/plague/history/htm http://www.cdc.gov/ncidod/dvbid/plague/epi.htm http://www.cdc.gov/plague/transmission/index.html. -http://www.pasteur.fr/ip/easysite/pasteur/en/research/scientific-departments/microbiology/ units-and-groups/yersinia/index Hufthammer A.K. and Walløe L. 2010. “Om utbredelsen av rotter i Norge i Middelalderen og tidlig nytid”, Historisk tidsskrift [Norway], 89: 29-43. Hufthammer A.K. and Walløe L. 2013. “Rats cannot have been intermediate hosts for Yersinia pestis during medieval plague epidemics in Northern Europe”, Journal of Archeological Science, 40: 1752-1759. Ilmoni I. 1846 and 1849. Bidrag til Nordens Sjukdoms-Historia. Vols. 1-2. Helsinki: J. Simelii arfvingar. Indian Plague Research Commission. 1906. Reports on Plague Investigations in India, I. “Experiments upon the Transmission of Plague by Fleas,” The Journal of Hygiene, 6: 425482, Part IV: 467-482. Indian Plague Research Commission. 1907. Reports on Plague Investigations in India, XV. “Further Observations on the Transmission of Plague by Fleas, with Special Reference to the Fate of the Plague Bacillus in the Body of the Rat Flea (P. cheopis)”, The Journal of Hygiene, 7: 395-420. Indian Plague Research Commission. 1907. Reports on Plague Investigations in India, XVII. “Experiments in Plague Houses in Bombay,” The Journal of Hygiene, 7: 436-456. Indian Plague Research Commission. 1907. Reports on Plague Investigations in India, XX. “A Note on Man as a Host of the Indian Rat Flea (P. Cheopis),” The Journal of Hygiene, 7: 472-476. IPRC, see Indian Plague Research Commission James T.B. 2102. Review of O. J. Benedictow, What Disease was Plague? […], 2010, The Economic History Review, 127: 1201-1203. Karlberg I. and Simonsen Figenschou M. 2008. Rapport: Arkeologisk utgravning. Kulturlag fra middelalder og rensessanse. Bygdøy Kongsgård, Gnr 1, bnr. 1, Oslo kommune. Vol. 1. University of Oslo, Museum of Cultual History. Karlsson G. 1996. “Plague Without Rats: The Case of Fifteenth-century Iceland,” Journal of Medieval History, 22: 263–284. Knudsen L.G. 2005. Pesten grasserer! En undersøgelse av pesten I Danmark i 1650’erne. [Kerteminde]: Landbohistorisk Selskab. Knudsen L.G. 2009. “The Course of a Mid-17th Century Plague Epidemic in Denmark.” In: Living with the Black Death: 113-134.

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Laerum [Lærum] O.D. 2010. “The Blackhouse and Røykstova: A Common North Sea Tradition”, Northern Studies. 41: 1-12. Lamb G. 1908. The Etiology and Epidemiology of Plague. A Summary of the Work of the Plague Commission. Calcutta: Superintendent of Government Printing, India. Langen de C.D. and Lichtenstein A. 1936. A Clinical Text-Book of Tropical Medicine. 1st English edn. translated from the 3rd Dutch edn. Batavia, Surabaya, Amsterdam: G. Kolff Co. Laudisoit A., Leirs H., Makundi R.H. et al. 2007. “Plague and the Human Flea, Tanzania”, Emerging Infectious diseases, www.cdc.gov/eid, 13: 687-693. Liston, W.G. 1924. “The Milroy Lectures on The Plague”, The British Medical Journal: 900-903, 950954, 997-1001. Living with the Black Death. L. Bisgaard and L. Søndergaard (eds.). 2009. Odense: University Press of Southern Denmark. Liv og helse i middelalderen. 1992. (Onsdagskvelder i Bryggens Museum, no. 6). Bergen: Bryggens Museum. Loghem van J.J. and Swellengrebel N.H. 1914. “Kontinuerliche und metastatische Pestverbreitung”, Medical Microbiology and Immunology, 77: 460-481. Lorange E.A., Race B.L., Sebbane F., Hinnebusch B.J. 2005. “Poor Vector Competence of Fleas and the Evolution of Hypervirulence in Yersinia pestis”, Journal of Infectious Diseases, 191:1907-1912. Lunden, K. 2002. Norges Landbrukshistorie. Vol 2. Frå svartedauden til 17. Mai. Oslo: Det Norske Samlaget. Lunden K. 2008. “Mannedauen 1349-50 i Noreg. Kronologisk og geografisk spreiing”, Historisk tidsskrift [Norway], 87: 607-632. Maia J. de Oliveira Costa. 1968. “Some Mathematical Developments on the Epidemic theory formulated by Reed and Frost”, Human Biology. 24: 167–200. See H. Abbey 1968. Mansa F.V. 1873. Bidrag til Folkesygdommenes og Sundhedspleiens Historie i Danmark. Copenhagen: Gyldendalske Boghandel. Mengel, D.C. 2011. “A Plague on Bohemia? Mapping the Black Death”, Past and Present, No. 211: 3-34. Moseng O.G. 2006. Den flyktige pesten. Vilkårene for epidemier i Norge i seinmiddelalder og tidlig nytid. Thesis for the degree of Doctor of Art. University of Oslo. Moseng O.G. 2007. “Den komplekse pesten ‒ revurderinger av en epidemie fra fortiden”, Tidsskrift for Den norske legeforening, 127: 3272-32775. Moseng O.G. 2009. ”Climate, Ecology and Plague: The Second and the Third Pandemic Reconsidered.” In: Living with the Black Death: 23-45. Ødegårdstid i Norge. Det nordiske ødegårdsprosjekts norske undersøkelser. 1978. Oslo: Universitetsforlaget. Peste: entre épidémies et sociétés. Plague: Epidemics and Societies. 2007. M. Signoli, D. Chevé, P. Adalin, et al. (eds.). Florence: Firenze University Press. Petrie G.F., Todd R.E., Skander R., et al. 1924–25. “A Report on Plague Investigations in Egypt”, The Journal of Hygiene, 23: 117-150. Pettersson S. 2010. Rapport : Arkeologisk undsökning Heierstadstua 2009: 1-117, with 7 Appendices. See also M. Vretemark, Bilaga [= Appendix] No. 7: 1-31. Pollitzer R. 1954. Plague. Geneva: WHO. Sandnes J. 1971. Ødetid og gjenreisning. Trøndsk busetningshistorie ca. 1200–1600. Oslo: Universitetsforlaget. Sandnes J. 1978. “Kronologi og årsaker.” In: Ødegårdstid i Norge: 154-70. See under Oe. Sandnes J. 1981. “Settlement Developments in the Late Middle Ages (approx. 1300-1540).” In: Desertion and Land Colonization in the Nordic Countries: 78-114.

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Schreiner J. 1948. Pest og prisfall i senmiddelalderen. Oslo: Det norske Videnskaps-akademi. Scott S. and Duncan C.J. 2001. Biology of Plagues: Evidence from Historical Populations. Cambridge: University Press. Thomas RE, Karstens RH, and Schwann TG. 1993. “Effect of Yersinia pestis Infection on Temperature Preference and Movement of the Oriental Rat Flea (Xenopsylla cheopis) (Siphonaptera: Pulicidae)”, Journal of Entomology. 30: 209–213. Town and Countryside in the Age of the Black Death. Essays in honour of John Hatcher. M. Bailey and S. Rigby (eds.). Turnhout: Brepols Publishers. Tran T.-N.-N., Signoli M., Fozzati L., Aboudharam G., Raoult D., Drancourt M. 2011. “High Throughput, Multiplexed Pathogen Detection authenticates Plagues Waves in Medieval Venice, Italy”, PLoS One (www.plospathogens.org), 6: 1-5. Vretemark M. 2010. “Osteologisk analys av djurben från Heierstadstua, Hof kommune i Vestfold Norge. Rapport”, Västergötlands museum, 1-31. In: Pettersson 2010, Bilaga [= Appendix] 7. Wakil AW. 1932. The Third Pandemic of Plague in Egypt. Cairo: The Egyptian University. Walløe L. 2007. “Var Yersinia pestis årasak til svartedauden?”, Tidsskrift for Den norske legeforening, 127: 3193. Walløe L. 2008. “Medieval and Modern Bubonic Plague: Some Clinical Continuities”, Medical History. Supplement, 27: 59-73. . “Var middelalderens pester og moderne pest samme sykdom?”, Historisk tidsskrift, 89: 13-28. WHO Plague, see http://www.cdc addresses above. WHOCC-Plague. The home page on plague on WHO’s website. Williams J.E., Hudson B.W., Turner R.W., et al. 1980. “Plague in Central Java, Indonesia”, Bulletin of the World Health Organization, 58: 459-467. Wu Lien-Teh. 1913-14. “First Report of the North Manchurian Plague Prevention Service”, The Journal of Hygiene, 13: 237–299. Wu Lien-Teh. 1922-23. “The Second Pneumonic Plague Epidemic in Manchuria”, The Journal of Hygiene, 21: 262-288. Wu Lien-Teh. 1926. A Treatise on Pneumonic Plague. Geneva: League of Nations, Health Organisation. Wu Lien-Teh, Chun J.W.H, Pollitzer R., Wu C.Y. 1936. Plague. A Manual for Medical and Publich Health Workers. Shanghai Station: National Quarantine Service. Wu C.Y.1936. “Insect Vectors.” In: Wu L.-T, Chun, Pollitzer, et al. Plague. A Manual for Medical and Public Health Workers: ­249-308. Yersinia Research Unit, Institut Pasteur. The home page on plague on the website of Institut Pasteur. See also http://www.pasteur address above. Ødegårdstid i Norge. See under Oe.

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1.4 Serious Plague History Under Pressure: The Twelfth Alternative Theory of Historical Plague: Comments on the Recent Paper “Climate-driven Introductions of the Black Death and Successive Plague Reintroductions into Europe” 103 1.4.1 Introduction This monograph relates in the main to alternative theories of the epidemiology and microbiology of historical plague epidemics. It is the second monograph on the subject, and another effort to defend the discipline of plague history against unwarranted, arbitrary and unserious alternative theories, at variance with the primary studies and standard works on plague. See O. J. Benedictow, What Disease was Plague? On the Controversy over the Microbiological Identity of Plague Epidemics of the Past. 2010. Leiden: Brill. 745 pp. The paper referred to in the title corroborates the importance of such efforts. One should note that none of the authors are historians. It shows, because the subject and hypotheses presented in this paper require a broad knowledge of plague history in time and space, the sources, and of the huge scholarly literature, which only the long-term dedicated historical study of the topic can give. This is the twelfth alternative theory of plague and plague epidemiology presented in recent decades with fanfares and great enthusiasm in the media as revolutionary new insights. However, because none of them is compatible with any other, so at least eleven of them will have to be basically arbitrary and entirely erroneous - and why not all twelve? One should note that this stream of revolutionary theories about the microbiological nature and epidemiological dynamics of plague, occur despite the fact that the conventional theory is based on an enormous corpus of fine medical and historical research and a number of outstanding synthetic standard works on plague. According to the authors, it is a theory to the effect that the arrival of the Black Death and subsequent or recurrent plague epidemics in Europe originated in the “mountains of the western Central Asia”, “4000 km east of the border of the Black Sea” and were climate-driven from murine reservoirs of gerbils.104 This is confusing, because 4000 km east of the Black Sea is not only east of the western Central Asia, but east of Central Asia and well into East Asia, reaching about to the Central Siberian Plateau, the western mountain ranges of Mongolia, and well into the Xinjiang province of modern China. Perhaps, for two main reasons, the authors have in mind

103  Schmid, Büntgen, Ryan Easterday, Ginzler, Walløe, Bramanti, and Stenset 2015: 1-6. Supporting information, Schmid et al. 10.1073/pnas.1412887112 2015: 1-10, is taken into account in the following examination and discussion of the theory. 104  Schmid, Büntgen, Ryan Easterday, Ginzler, Walløe, Bramanti, and Stenset 2015: 3, right col.

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Kirghizstan’s border area with China about 3500 km away: (1) because of its association with the so-called Silk Road system105 (see below), a rather grandiose name for serial caravan tracks; and (2) because this vast plague focus is and was based on gerbils all the way from this part of East Asia to about the border with the Astrakhan’ region on the coast of the Caspian Sea.106 There, susliks take over the dominant role of forming the plague focus. Although it is unusual to be 3000 km off the track, taken as a whole, the latter interpretation is preferred here. For these reasons, it will be assumed that the authors’ reference to “western Central Asia”, is a slip of the mind for western East Asia. The authors evidently presume that the Black Death started there, not in China. In reality, the distance is significantly longer on the ground when the countless bends and turns, ascents and descents of the tracks, are taken into account. The reason the authors emphasize the importance of gerbils in this process, is not clear, because they maintain that the contagion was transported by caravan, and they also claim that, in 1345-46, the Black Death spread across southern Russia, where susliks are the rodents of the plague reservoir. However, as pointed out, the part of this huge plague reservoir, which is based on gerbils, stretches all the way to the region on the north-eastern side of the Caspian Sea and to about the Astrakhan’ region. Why it is inconceivable and unmentionable that their alleged caravans could not pick up plague from gerbils in the focus along the north-eastern coast of the Caspian Sea or from susliks in regions west of it in 1346, when the presence of the Black Death can be empirically corroborated, is not explained.

1.4.2 The Purported Functions of Caravans and the Silk Roads in the Transportation of Plague with an Overview of the History of the Golden Horde: A Brief Study in Methodological Problems of the First Degree Centrally, the authors maintain that from plague reservoirs among gerbils in these (south)-western mountains of Central East Asia plague was “transported” to Europe “via the land and sea trade routes of the ancient Silk Road system”. This is assumed to be a recurrent process, which leads to “reintroductions” of plague in Europe. The description of the transportation process consists of a series of hypotheses fallaciously couched in the language of factual assertions: After a plague infection established itself in a caravan (in its animals, in the traders (?), or in fleas in its cargo, the disease could have spread to other caravans in caravanserai (caravan gathering

105  Benedictow 2013: 16-17 and ns. It is therefore also east of Issyk-Kul/Ysyk-Köl with the Nestorian graveyard, where the first appearance of the Black Death on its way from China to Kaffa has been located by several scholars, but so far on misunderstood and untenable grounds. 106  http://www.iucnredlist.org/map.html?id=19686, Rhombomys opimus (Great Gerbil), accessed 03/25.2015.

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and resting places, where goods and animals were redistributed and transported across Eurasian trade routes. Such a postulated mechanism has recently been discussed (30), and does come with several conditions that bear further investigations.

The authors do not present a single case where this process of long-distance transportation of plague contagion by caravan should have occurred. This indicates that the authors have not found such evidence, which they do not take seriously and do not address. The margins of error in each element in a chain of arguments or hypotheses are multiplicatively related. Methodologically, the argument has the character of speculation. The reference is to my 2103 paper “(30)”, where this means of transportation of plague over these distances is discussed quite thoroughly and shown to be highly problematic or implausible.107 The authors’ elegant formulation serves to conceal this fact. Here none of the problems are considered or discussed, they are passed over, which indicates lack of evidence, which is again not taken into account. The authors presuppose as a matter of course that the Silk Roads were in continuous operation throughout the period their theory relates to, “the time frame 1330-1850”.108 This is greatly erroneous, and another case of fallacy of reverse or retrogressive circular argument. In my 2013 article, which the authors know, it was shown that the Silk Road system broke down in the years 1343-1347, when the ruler of the Golden Horde went to war against the Italian trading stations, which is, then, another crucial problem the authors pass by in silence. However, the chronological limitation was due to the focus of this article and my lack of imagination to envisage than any scholars or scientists would maintain that the Silk Road system was in operation within the given time frame. This shows the use of not having a historian among the authors, but makes necessary a brief historical outline. When caravans left the Chinese stretches of the Silk Roads, they entered the territory of the Golden Horde or Kipchak Khanate, where the goods were transported, often by several caravans, over 4000 km to the Italian trading stations at the end of these routes, at Tana and Kaffa on the Sea of Azov and the Black Sea. At its peak, the Golden Horde included most of Eastern Europe from the Urals, and was extending eastwards deep into East Asia, about as far as the border between present-day Kazakhstan and Republic of Mongolia, whence it stretched along the Chinese border on the Xinjian Province, and turned westwards, running in mainly the same territorial form back to the north-eastern region on the Caspian Sea. In the south-west, the Golden Horde’s lands bordered on the Black Sea, the Caucasus mountain system and the territories of the Mongol dynasty known as the Ilkhanate, an early breakaway state of the Mongol Empire. The Ilkhanate was founded by Genghis Kahn’s grandson.

107  Benedictow 2013: 16-20. 108  Schmid, Büntgen, Ryan Easterday, Ginzler, Walløe, Bramanti, and Stenset 2015:2, 5, right cols.; “Supporting information”, Schmid et al. 10.1073/pnas.1412887112 2015: 2, 10.

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In its fullest extent, the state expanded into territories which today comprise most of Iran, Iraq, Turkmenistan, Armenia, Azerbaijan, Georgia, Turkey, western Afghanistan and south-western Pakistan, where parts of the route of the Silk Road to the Levant ran. Importantly, in this context the Ilkhanate rulers converted to Islam from 1295, an event which greatly affected the conversion to Islam in the Golden Horde from 1313, and the use of the roads. The so-called Silk Road system was dependent on the presence of a political organization over these huge distances that could by and large guarantee the safety of the caravans with their precious goods that could bear the immense transportation costs. It would have to protect the huge economic investments of the merchants, and their physical safety. It was established from the mid-1200s by the newly established vast Mongol empire. The motive is clear, the Golden Horde profited much by controlling the western section of the great overland commercial route stretching from China to the Black Sea. However, under the circumstances this was a fragile construction. The instability of this political system and the vulnerability of the Silk Roads soon emerged, beginning with the civil war of the Mongols 1260-80. In the 1290s, Nogai Kahn(† 1299), a leading military commander and a de facto ruler of the Golden Horde, came in sharp conflict with one of his subordinate commanders, Tokhta (Khan), who instigated a partial civil war. Nogai Khan was the first khan of the Golden Horde who converted to Islam. As so often, short-sighted quest for power and maximum profits, which could be the fruits of victory, trumped short-term commercial moderate incomes, but, as the result of war, intrigues and insecurity, proved elusive. As shown in my article, the Silk Roads system functioned only in brief periods, and not in the time of the Black Death or the preceding years. In 1313, the Kipchak Khan of the Golden Horde converted officially to Islam, which unleashed a process of conversion among the local Tartar populations who supported the Mongols. Eventually, in 1343 Janibeg, the then Kipchak Khan, took mili­tary action to throw the Italians out of their factories, i.e. trading stations, in Tana and Kaffa, which were the end points of the Silk Roads, and to end trade with Christians in the lands of the Golden Horde. At the same time, he severed the trade link between China and Europe along the caravan routes.109 The Ital­ian merchants were driven out of Tana in 1343, and were besieged in Kaffa in the same year, and again in the years 1345-1347. It was, in­deed, in 1346 that plague broke out in the besieging Mongol army and in some manner was passed on to the besieged Italians.110 It is excluded that the Black Death, under these circumstances, could have been transported by caravans along the Silk Roads in the Golden Horde to the Italian trading stations in the Crimea. Merchants would not risk precious goods and expensive and dangerous transportation over thousands of kilometres to the Christian Italian merchants

109  See, for instance, Norris 1977: 13; Norris 1978: 114-20. 110  Benedictow 2004/2006: 51-53.

Serious Plague History Under Pressure: The Twelfth Alternative Theory of Historical Plague 

 39

across a Muslim state which was by now in­tensely hostile to trade and contact with Christians and had gone to was in order to drive them away. Despite demonstrated access to this information, the authors assert that the Black Death moved across the territory of the Golden Horde in 1345-1346,111 a war zone, where the Kipchak Khan waged war to prevent this trade, had defeated the Italian trading station of Tana and besieged the other trading station of Kaffa. The authors have not been able to find any evidence which underpins the assertions in the main article, and in the “Supporting Information”, that plague had appeared and (was) “moved” in the lands of the Golden Horde in 1345.112 It is taken out of thin air, climate-driven, it is speculation indistinguishable from wishful thinking, inspired by the needs of their theory, the fallacy of reverse or retrogressive circular argument. The disastrous effects of the Black Death on the besieging army forced Janibeg Khan to withdraw, and the Italians succeeded in holding on to Kaffa and re-establishing themselves in Tana. However, when the Silk Roads had broken down, these towns functioned primarily as centres of local trade, with increasing difficulties, because of hostility from local authorities, and withered gradually away in the fifteenth century.113 Soon after Janibeg Khan’s assassination in 1357 followed the period of “Great Troubles” 1359-1381, when the khanate sank into prolonged internecine war, in which sometimes as many as four Khans vied for recognition by the emirs and for possession of major urban centres. After the overthrow of their nominal suzerain of the Yuan dynasty (established by Kublai Khan) with Emperor Toghan Temür († 1370) and the accession of the Ming dynasty in China, the Golden Horde lost political links with Mongolia and China. In 1381, the khanate was briefly reunited, re-establishing the Golden Horde as a dominant regional power and Muslim state. However, soon after the 1396 invasion of Tamerlane it fragmented into smaller Tatar khanates which declined steadily in power. At the start of the 15th century the Horde began to fall apart. Within its constituent territories, several Tatar khanates broke away, the Kazan’ Khanate in 1438, the Crimean Khanate in 1441, the Astrakhan’ Khanate in 1466. The remnant, which became known as the Great Horde, or just the Horde, was left with the steppe between the Dnieper and Yaik, with Sarai as its capital and with a claim to represent the tradition of the Golden Horde. These internal struggles allowed the northern vassal state of Muscovy to rid itself of the “Tartar Yoke” at the “Great stand on the River Ugra” in 1480, when the forces of the Great Horde was defeated by Ivan III of Muscovy.

111  Schmid, Büntgen, Ryan Easterday, Ginzler, Walløe, Bramanti, and Stenset 2015: 2, right col. “Supporting information”, Schmid et al. 10.1073/pnas.1412887112 2015: 10. 112  Schmid, Büntgen, Ryan Easterday, Ginzler, Walløe, Bramanti, and Stenset 2015: 2, right col. “Supporting information”, Schmid et al. 10.1073/pnas.1412887112 2015: 10. 113  See, for instance Doumerc 1987: 5-19.

40 

 Introduction

In 1475, the Ottoman Empire made the Crimean Khanate a client state and began subjugating what remained of the Great Horde. Sarai was sacked in 1502, which is considered the final fall of the Horde. Under Ottoman protection, the Khanate of Crimea continued its precarious existence until conquered by Catherine the Great it in 1783.114 The authors’ pretence that the Silk Roads were in operation during the period of the time frame of their theory of 1330-1850 (1859115), is just a sad story of a completely different kind and the debilitating effects of the overarching needs of an arbitrary and untenable theory. It is the outcome of the fallacy of the reverse circular theory, in which ostensible facts are derived by inference from the needs of the theory. The Silk Roads system in the meaning of a communication networks used by caravans transporting precious goods from China, moving across East Asia and Central Asia across the lands of the Golden Horde to European trading stations on the Black Sea, broke down for all practical purposes from the early 1340s and was never re-established as a functional transportation system. The composite caravan hypothesis and the hypothesized long term function of the Silk Road system 1330-1850(/1859) constitute three independent necessary conditions for the viability of the author’s theory: (1) that plague could be spread by caravans along the huge distances of the Silk Roads, in this case from the western mountains of East Asia; (2) that the Black Death was “transported” or “moved” by caravan from this area, began crossing the western part of the Golden Horde in 1345 and reached the Italian trading station at Kaffa in 1346; (3) plague continued to be transported along these parts of the Silk Roads and be exported for “reintroduction” to Europe until about 1850. According to the basic tenets of methodology, these propositions have here been invalidated.

1.4.3 Patterns of Spread and Comparative Spread Rates The authors explain that they have investigated the role of maritime plague import in more detail by searching for plague outbreaks in harbours that were not preceded by plague outbreaks in the 2 y prior in the city itself, in other nearby cities (104

1

0/1

>106

28

5/23

This is a noticeably higher proportion of bacteraemic cases than in the mass studies of the prevalence of bacteraemia performed at the Arthur Road, Maratha, and Modikhana Hospitals in Mumbai (see above); it is also considerably higher than found in later American studies on plague patients during the Vietnam War (and in American plague foci) (see below). The difference could reflect the much smaller group of patients (be due to chance, i.e. stochastic variation) or a high degree of selection among patients admitted within a relatively short period, which could be affected by the severity of illness. The slightly higher lethality rate (82.1%) than found in the 1961  IPRC, IX, 1906: 524‒29. 1962 Cf. Chapter 10.

642 

 Problems with the Early-Phase Theory of the Transmission of Plague ...

mass studies of 6,215 patients admitted to plague hospitals in Mumbai a few years earlier, 80.3% (see above), can also suggest that the level of the severity of illness was above the average. Arguably, these features could indicate that the prevalence and level of human bacteraemia in IPRC’s study was somewhat higher than the average represented by plague patients in Mumbai at the time. No medication was possible, so there was not any pressure to withdraw blood for bacteriological examination immediately after the patients’ admission to hospital. Because the IPRC’s group was not systematically examined for bacteraemia on arrival at hospital, these features suggest that selection on admission could or would have been affected by clinical impression of the severity of illness and slanted the group in the direction of higher prevalence of (high) bacteraemia. The temporal perspective must be inferred from Table II in the study which shows that the first sample of blood was on the average withdrawn 42.6 hours (1.75 days) before death,1963 which cannot differ much from the data on the day of illness of patients arrived at hospital given above, and that the first withdrawal was, in fact, made on admission or shortly later. Although the patients who constituted the group were individually examined for possible presence and level(s) of bacteraemia during the course of illness in the hospital, there were made only 74 withdrawals of blood, on the average 2.6 withdrawals per patient. This means that the examination was not really systematic and thorough and performed according to a regular and comparable time schedule for all patients. Importantly, however, there are no evident indications in this material of significantly increasing prevalence or levels of bacteraemia in ensuing withdrawals of blood, so the quite low number of withdrawals and bacteriological examination of blood did probably not miss out on significant developments. Taken together with all other data on the prevalence of bacteraemia among human plague cases, the IPRC’s sample is too small to affect noticeably the estimate of the general prevalence of bacteraemia among plague patients in Mumbai on admission to hospital of 43%. If we take into account that a few patients would, presumably, have developed bacteraemia during the course of illness after admission to hospital (see above), the implied general prevalence for the whole course of illness would probably be around 45%. It is, therefore. IPRC’s pioneering and quite unique systematic measurements of levels of bacteraemia in the group that is of pivotal importance. In 11 of the 16 bacteraemic cases, 68.8%, levels were slight, never exceeding 103 Y. pestis/mL of blood at any time of the illness, the majority had levels around 102 bacteria/mL, 3 cases >104 bacteria/mL. One exceptional case, a clear statistical outlier, exhibited >106 bacteria/mL. According to the infection gauge of the correlation between level of bacteraemia and the number of plague bacteria ingested by fleas established above according to sex

1963  IPRC, IX, 1906: 527.



Plague Bacteraemia in Human Beings 

 643

of fleas, female and male fleas would on the average need to ingest blood with ~2440 and ~5560 plague bacteria/mL respectively in order to ingest 1 Y. pestis. This means that 82.1-85.7% of the patients would normally not infect feeding fleas. 1 case would probably infect feeding female fleas with 1-3 bacteria, 3 cases with bacteraemia of >104 would tend to infect feeding female fleas with 4-5 bacteria, 1 case with >106 would infect female fleas with ~410 bacteria and male fleas with ~180 bacteria. The sudden leap in the level of bacteraemia in this case is remarkable, and seems exceptional, but it belongs, as will be seen below, to a small incidence of cases that can be identified with primary bacteraemic plague. This is a form of plague infection that occurs when the infective flea bites into a blood vessel and discharges the infective dose into the blood stream, which occurs in about 2.5 per cent of all cases.1964 As clearly can be seen, by huge margins, no flea would be infected by more than a miniscule fraction of the number of bacteria cautiously posited as a LD50 for human beings, namely 6,000 bacteria. Also importantly, no flea feeding on these patients would, within huge margins of uncertainty, be infected with sufficient doses to trigger the process of blockage formation, i.e. 3,800 bacteria. Thus, also the assumption that levels of human plague bacteraemia would be low was confirmed by these observations. Next, the phenomena of autopurification and bacterial growth after infected blood meals, which also were discussed above, must be considered. Evidently, fleas which feed on such plague cases and ingest so small numbers of bacteria, far below the infection dose needed to trigger net bacterial growth (around 3,800 Y. pestis), would instead undergo autopurification and be about infection-free at the time of the next blood meal. If they had not passed most of the previous blood meal into the hindgut, they would not be hungry and seek a new feeding opportunity. In the case of nest-dwelling fleas, especially P. irritans which relates to the much bigger “nests” of human habitats or sleeping arrangements, there would tend to be a significant delay from the start of search for a new blood meal and the rise of the occasion. This delay would, for these nocturnal insects, quite often include the time of daylight or use of interior light sources, and the absence or reduced presence of people who performed work elsewhere. In addition to the fact that around 70% of human fleas feeding on these human plague cases would not ingest a plague bacterium, the social context of human fleas indicates that the process of autopurification would tend to last longer and be stronger than in most species of fleas. This can explain Pollitzer’s finding1965 that human fleas had a very strong ability to free themselves of plague bacilli, also after highly bacteraemic blood meals,1966 which may contribute to explain the poor vector efficiency of this species of fleas. 1964  Choksy 1903: 30, 58. 1965  Pollitzer 1954: 344-46. The first systematic study seems to have been IPRC, XXX, 1908: 26065. 1966  Eskey and Haas 1940: 39-40; Hinnebusch, Perry, and Schwan 1996: 368.

644 

 Problems with the Early-Phase Theory of the Transmission of Plague ...

In the sample of plague patients studied by the IPRC, only fleas feeding on the statistical outlier would probably still be infected with a few bacteria at the time of the next blood meal, i.e. that 96.4-100% of all fleas feeding on them would presumably be infection-free at the time, when the hypothetical early-phase transmissions should be triggered. It is the remnants of blood meals in these hypothetically still minimally infected remaining fleas that R. J. Eisen and colleagues apparently assume would or could give P. irritans a significant or decisive role in the formation and dynamics of large-scale plague epidemics in modern and past times. In the light of these Mumbai data, this seems unrealistic also before taking into account the other data on human plague bacteremia, in order to be able to consider all such data in the light of relevant data on lethal doses of plague bacteria (LD) for human beings. These inferences are supported by the remaining individual studies of plague patients. There were, as mentioned, large plague epidemics during the Vietnam War, with about 4,500-5,600 recorded cases in the three peak years of 1965-1967.1967 American army physicians published 6 articles with studies of bacteraemia in native patients on arrival at hospitals. This tended strongly to be late in the course of illness, see Table 12.2. The 6 studies comprised 298 patients (161, 10, 40, 22, 23, 42 respectively).1968 Blood was drawn immediately on admission, just before medication with antibiotics would be administered. Among this group of patients, 79 or 26.5% exhibited bacteraemia, in the largest group 23.6%. Taking into account that some patients, if not medicated, would have developed bacteraemia after admission, the prevalence of bacteraemic cases would presumably have been around 30%. This means that about 70% would be infection free through the course of illness and would not infect a feeding flea by a bacterium. This is, however, an artificial minimum, because, as in IPRC’s study, a large proportion of the bacteraemic patients had so low levels of bacteraemia that they would not infect a feeding flea, according to the infection-level divisors. Two studies included useful data on levels of bacteraemia. Cantey studied 23 plague patients. He categorized all 7 severely ill patients at admission as “bubonicsepticemic”, i.e. according to clinical observation.1969 All of them provided positive blood cultures. Methylene-blue smears off venous blood showed that 5 of the bubonicbacteraemic patients had bacteraemia of ≥3x105 bacteria/mL of blood, 2 had ≥1.5 x106/ mL. According to his unusual choice of classification, one of the bubonic cases had bacteraemia of ≥3x105 bacteria/mL of blood. According to more usual criteria, 8 of his 23 patients, 34.8 per cent, were bacteraemic. This means that 6 cases would infect feeding female fleas with on the average ~120 plague bacteria, 2 cases would infect 1967  Marshall, Joy , Ai, et al. 1967: 604-05, 612-13; Butler, Bell, Linh, et al. 1974: S78. 1968  Marshall, Joy , Ai., et al. 1967: 604-05, 610, 612; Legters, Cottingham, and Hunter 1970: 640; Butler 1972: 269; Butler, Bell, Linh, et al. 1974: S78; Cantey 1974: 281; Butler , Levin, Linh, et al. 1976: 493‒99. 1969  According to recently agreed terminology, the category would be ‘bubonic-bacteraemic’.



Plague Bacteraemia in Human Beings 

 645

female fleas with ~600 bacteria. According to the established infection gauge, 65.2% of the patients would not infect feeding fleas with any bacterium. Because fleas which ingested ~120 plague bacteria would, in all likelihood, not contain plague bacteria in the ventriculus at the time of the subsequent feed, it seems highly likely that at least 90% would not be able to transfer any plague bacterium at the time of the next feed. At the most, fleas feeding on two of these patients, or 9% of them, would contain a few plague bacteria in their ventriculus and constitute the epidemic potential, but more likely none of them. The 42 patients group included 17 bacteraemic cases, or 40.5%: 6 had 102, which probably means that at least one of them exhibited this level of bacteraemia. 4 of them had the extreme level of >106, and 1 exceptional case had 4x107, about 40 times higher than the second highest level of bacteraemia on record. The wide range between >102‒>106 produces gross uncertainty about the 5 cases with unspecified levels of bacteraemia. This data shows that at least 7 of the bacteraemic cases would not infect feeding fleas, increasing the number of such patients to at least 32. According to the infection gauges, 5 patients would infect feeding female fleas with 0‒>~160/>410 Y. pestis, while the exceptional case would infect feeding fleas according to sex with 16,500/7,200 Y. pestis. Because bacteraemia was not determined in 5 cases, the sample size was 37 patients of whom at least 32, or 86.5%, would not infect feeding fleas before death.

Table 12.2: Prevalence of bacteraemia in human plague cases in Vietnam c. 1966-1972. Paper No.

No. of Patients

Bacilli in Blood

Bacteraemic %

1

161

38

23.6

2

10

5

50

3

40

5

12.5

4

22

6

27

5

23

8

34

6

42

17

40.5

Total

298

79

26.5

Taken together, the American material on bacteraemia from the Vietnam War comprised examination of 298 native patients of whom 79 or 26.5% exhibited some level of bacilli in the blood on admission to hospital. Although these native patients tended to arrive late in the course of illness, some of them would under normal

646 

 Problems with the Early-Phase Theory of the Transmission of Plague ...

circumstances presumably have developed bacteraemia in the remaining course of illness. It seems therefore reasonable to estimate the natural prevalence of bacteraemic cases to around 30%. A female flea feeding on the patient with a bacteraemia of 4x107 bacteria/mL would ingest ~16,400 plague bacteria, which is much higher than the cautiously indicated LD50 for human beings, and far above the bacterial dose that would engender bacterial growth (around 3,800 bacteria) and (could) make it infective by blockage. Also male fleas would, according to the selected criteria, ingest a LD50 for human beings, a dose that is twice as high as assumed necessary to engender blockage and make it infective by this ascertained mechanism. The significance of this single case is probably tiny or miniscule rather. The level of bacteremia is 40 times higher than in any other examined case of plague. This case represents 0.33 per cent of all Vietnamese plague patients examined for bacteraemia and level of bacteraemia, and 0.31 per cent of all plague cases, if the 28 plague cases examined for level of bacteraemia in Mumbai is added (see Table 12.1). This data also shows that feeding female fleas would need to ingest blood containing about 1.5x107 bacteria/µL in order be to infected by a LD50, about 6000 bacteria, and blood containing about 9.3x106 bacteria/µL in order to be infected by a minimal bacterial dose (3,800) that could trigger bacterial growth and possible blockage of the (pro)ventriculus and make it infective. This shows the potential of human plague cases as sources for infection of fleas and why inter-human crossinfection by human fleas (or lice) is completely untenable by enormous margins. Although such cases may occur, they will be exquisitely rare occurrences. So far, this problem of infection of fleas and various infectious doses have been related to quite mechanically in terms of estimates. Another important matter has so far no been mentioned, namely that various species of fleas has very different properties for development of blockage which can make them infective. The vector capacity or vector efficiency of species of fleas varies strongly and relates clearly to certain aspects of the anatomical construction of the ventricular system of fleas.1970 Taken together, this material provides substantial evidence that 90-95% of all examined Vietnamese plague cases would not infect feeding fleas, that most of those infected would ingest low numbers of Y. pestis and probably rapidly free themselves of infection, so that (nearly) 99% would be uninfected at the time of the next feed. The pathogenic significance of these infection rates need clarification in relation to questions of LD for human beings, subinfective or non-lethal doses, and will be discussed in the next chapter. The material on human plague bacteraemia contains 8 anomalous cases or statistical outliers with long leaps of levels of bacteraemia above all other measurements, 7 with >106 Y. pestis/mL of blood and 1 unique case, an extreme

1970  Pollitzer 1954: 358-64.



Plague Bacteraemia in Human Beings 

 647

outlier, with 4x107 Y. pestis/mL. These could be cases of primary bacteraemic plague, which constituted 3.3 and 2.7% of all cases in the two Indian mass studies performed in Mumbai mentioned above. IPRC recorded 1 case among 28 patients, or 3.6%, an observation that could be affected by the process of selection and small group size. It could be another bit of evidence which suggests that the prevalence and severity of bacteraemia in this group were somewhat above the average. The prevalence of this type of infection among Vietnamese cases was 7 of 298 or 2.4%. The 7 studies of levels of bacteraemia comprise 326 patients with 8 anomalous cases of this type, or 2.45%. Also four studies of bacteraemia in plague patients who had contracted the disease in sylvatic (campestral) plague foci in USA could usefully be briefly mentioned, although they in important respects are not relevant to the epidemic or epidemiological orientation of the present analysis.1971 They are based on small numbers of cases contracted singularly and over several or many years, for instance 1965-1986, mainly in New Mexico,1972 with an annual average of 2-3 cases.1973 They do not include examination of individual levels of bacteraemia, but relate only to the question whether or not the patients had developed bacteraemia. Therefore, only the general estimate of prevalence can have scientific or medical value for the central question here of human beings as potential sources of infection of feeding fleas with plague bacteria. Taken together these 4 studies comprise 144 cases of whom 58, or 40.3%, exhibited bacteraemia. Plague contracted by human beings in sylvatic plague foci in USA are linked to particular species of rodents with their special consorts of fleas, which have in common that they are unknown in all epidemic contexts. Many of these American plague cases are American Indian natives, predominantly Navajos, living in reservations in New Mexico. In the material gathered by Reed et al., and presented in their Table 3, at least 13 cases or 42% had this background. They are generally sheepherders who hunt rodents for food, especially prairie dogs and rabbits. In the process of skinning and slaughtering these animals and preparing them for consumption, they occasionally contract plague from direct contact of broken skin with infected blood or animal tissue.1974 Such cases will usually be bacteraemic by the very method of infection, which will increase the proportion of bacteraemic cases over the normal prevalence. Taking this special background into account, the prevalence of “normal” bacteraemia would seem to be around 35%. No possible case of inter-human cross-infection of bubonic plague has been observed in American plague foci. The early-phase theory of plague transmission 1971  These studies are for special reasons discussed in more detail in Chapter 10.6.4. 1972  Crook and Tempest 1992: 1253. 1973  Reed, Darwin, Palmer, et al. 1970: 468. 1974  Reed, Darwin, Palmer, et al. 1970: 468-70; Reed, Grabman, Kompare, et al. 1985: 641-42, 646; Crook and Tempest 1992: 1256. See also above WHOOC, Chapter 1.2, p. 15. See also Chapter 10.6.4, and Glossary.

648 

 Problems with the Early-Phase Theory of the Transmission of Plague ...

relates only to sylvatic plague in these plague foci and experiments with associated fleas; there is no support for this line of argument in the material from American plague foci. The insertion of this theory into the history of plague epidemics and transformation into an epidemiological theory are without empirical foundation also in this specific context. Taken together, the epidemiological implications for fleas feeding on human plague cases will be seen in the following summary of the data. The discussion of the Indian mass studies on the prevalence of bacteraemia in plague patients concluded that they clearly indicate an average of around 45% were bacteraemic, or, conversely, that 55% remained (for all practical purposes) infection-free through the course of illness. Although the small group of plague patients selected by IPRC for study of bacteraemia exhibited a significantly higher rate of bacteraemia than the contemporary Indian mass materials, 82.1-85.7% of the patients would not, according to the standard gauge of infection, infect feeding fleas, and the levels of bacteraemia of the remaining patients were so low that, taken together, 96.4-100% of fleas feeding on this group of patients probably would (for all practical purposes) be infection-free at the time of a next blood meal and hypothesized early-phase transmission. The proportion of plague cases which did not develop bacteraemia was even higher in Vietnam, around 70%. If we include in the estimate the proportion of patients with levels of bacteraemia below 2,440 bacteria m/L, who would normally not infect feeding female fleas with a single bacterium (in the case of male fleas below ~5560), it seems justified to conclude that about 90% of plague patients would normally not infect feeding fleas during the whole course of illness, and that at least or around 95% of feeding fleas would (for all practical purposes) be infection-free and non-infective at the time of the next blood meal and hypothesized early-phase transmission. Taken together, the complete data on human plague bacteraemia provides a strong case that 70-55% of human plague cases did not develop bacteraemia in developing countries with deficiently fed populations living in poverty and stressful circumstances, much like historical populations. According to the standard infection gauge that female fleas will ingest 1 bacterium from a blood titre of ~2440 Y. pestis/ mL, a high proportion of bacteraemic patients, at least 90% of all plague patients, would not infect feeding fleas at any time during the course of illness, and taking into account the process of selfpurification, at least 97.5% of feeding fleas would (for all practical purposes) be infection-free/non-infective at the time of the next blood meal and hypothesized early-phase transmission. According to the discussion above of fleas’ ability of selfpurification, it seems likely that also fleas feeding on the 7 cases with a bacteraemia of 1.5x106-106 plague bacteria/mL of blood and, according to the sex-specific infections gauges, ingest ~400-600 Y. pestis. This argument implies that 99.7% of all fleas would for all practical purposes be infection-free at the time of the next blood meal. Only the extreme outlier with a level of bacteraemia of 4x107 mL of blood, who would infect feeding fleas (X. cehopis) according to the sexed infection gauges with ~16,400/~7,200 bacteria, seems to be of clear interest in this context.



LD for Human Beings, Subinfective or Non-lethal Doses 

 649

These conclusions are based on the complete evidence of all studies on human plague bacteraemia and on the anatomical and behavioural properties of fleas that decide their vectorial potential in relation to epidemic plague. When this data is juxtaposed with data on the feeding capacity of fleas and on the development of plague infection in the ventricular system of fleas, it determines the potential of human beings as sources of plague infection of fleas and the possibility or potential of inter-human cross-infection. It constitutes a decisive empirical case, as it seems, for conclusions to the effect that inter-human cross-infection of plague by early-phase transmission of plague or by blockage cannot play a significant role in plague epidemics or does not occur. This data provides the case for rejecting any theory of plague epidemiology based on inter-human transmission by human ectoparasites. It seems also to challenge the early-phase theory of the transmission of wild-rodent plague, but this topic is not in the focus here. It has, nonetheless, uncovered a number of areas with deficient knowledge that should be clarified before definite conclusions can be drawn.

12.7 LD for Human Beings, Subinfective or Non-lethal Doses These conclusions must be assessed also in the light of data providing useful knowledge or empirical perspectives on LD of Y. pestis for human beings, i.e. the number of bacteria needed to cause mortality in ordinary human hosts who receive the subsequent flea bites. Because infection experiments cannot be performed on human beings and monkeys have proven unsuitable,1975 rodent studies must suffice, and, unfortunately, they are few. Importantly, 90% of black rats (Rattus rattus) survived primary subcutaneous inoculation with 5,550 plague bacteria (LD10);1976 the LD50 would obviously require a substantially higher infectious dose. The LD50 of California ground squirrels, Spermophilus (Citellus) beecheyi, which generally are considered highly susceptible to plague, is 6,070 bacteria1977. This data has limited relevance for the question of LD50 for human beings, except indicating the minimum infectious dose that could result this mortality rate. All discussion of this matter must be tentative in nature. One can underline the significance of the fact that the first-line of the human immune apparatus, the lymphatic system, prevents quite efficiently plague bacteria from entering the blood stream in so far as 55-70% of all human plague cases do not develop bacteraemia. Plague bacteraemia in human beings are lethal with very few exceptions, increasing prevalence of bacteraemia is closely correlated with increasing lethality rates. However, the lymphatic system is not the only defence line against plague bacteraemia. Already IPRC noted the occurrence of an apparent diminution of a weak bacteraemia in 2 (of 1975  Pollitzer 1954: 187; Meyer, Quan, McCrumb, et al. 1952: 1229. 1976  Chen and Meyer 1974: S664. 1977  Williams, Moussa, and Cavanaugh 1979: 619.

650 

 Problems with the Early-Phase Theory of the Transmission of Plague ...

28) patients who recovered, and a third patient with an “irregular or fluctuating” bacteraemia that suddenly increased a few hours before death and, thus, in the end defeated the immune defences.1978 Butler suggests, albeit without presenting adequate evidence, that “all patients probably have intermittent bacteraemia” in the early acute stages of bubonic plague.1979 Weak bacteraemia can be caused, for instance, by remains of the infection dose in the bite site(s) (also producing carbuncles) or by leakage of bacteria from buboes with walls attenuated by plague toxins. This means that anti-infection systems associated with the blood stream can, to a certain extent, cope with weak plague bacteraemia and contribute to the quite low prevalence of bacteraemia in human beings. Human beings are, apparently, quite, but not highly susceptible to plague infection. The use of ~6000 Y. pestis as LD50 for a demographically normally composed human population in developing countries or historical societies is a cautious choice of analytical tool (the infectious dose that would normally kill 50% of a representative sample of members of these human populations). The high lethality rate of around 80% in these types of societies reflects probably (also) a frequent incidence of multiple infection doses, because blocked fleas are desperately hungry and tend to bite and to transmit repeatedly. This normal level of lethality rate must reflect that epidemic plague is normally transmitted by blocked fleas. Importantly, this implies that transmission of IDs of 2‒3x103 plague bacteria would be subinfective or cause light disease, i.e. be successfully combated by the immune apparatus, and produce immunization effects that attenuate epidemic transmission.1980 Almost all fleas feeding on the registered cases of human bacteraemia presented above would be infected by numbers of bacteria that would - if transmitted to other human beings - serve to strengthen the immunity against plague infection in a population, albeit only for a brief period.1981 Only the patient with the exceptional level of bacteraemia of 4x107 Y. pestis/mL would infect feeding fleas according to sex with a number of bacteria, ~16,400/~7,200 Y. pestis, that would - if transmitted immediately - constitute a LD50 or more, according to the cautious gauge established above. This case represents 0.31% of all 326 human plague cases examined with respect to level of bacteraemia. It remains enigmatic why human fleas (or any species of flea) with a full ventriculus after a successful blood meal should immediately bite and attempt to feed again on another human being. In reality, fleas “rarely attempt”, as mentioned, “to feed more frequently than once in 24 to72 hours, and normally “perhaps every 4 or 5 days”. Instead, as pointed out, they would seek a place where they could quietly digest the meal, the females also lay eggs. Infection doses of ~16,400/~7,200 Y. pestis are much 1978  IPRC, IX, 1906: 527, 529. 1979  Butler 1983: 82. 1980  Legters, Cottingham, and Hunter 1970: 649-50. 1981  Benedictow 2010: 207-68.



LD for Human Beings, Subinfective or Non-lethal Doses 

 651

higher than the minimum of 3,800 bacteria needed to engender net bacterial growth in rat fleas and frequent development of blockage that will make them infective. Hypothetically, these fleas could transmit lethal doses by early-phase transmission, but, in contrast to transmission by blockage, this mode of transmission has not been observed and explained. All fleas which had fed on the other 325 Indian and Vietnamese cases, i.e. 99.7%, would soon begin to pass digested blood into the hindgut and more or less empty their ventriculus of possible contaminated blood, before feeling hungry and start the search for the next blood meal that, hypothetically, could or should trigger early-phase transmission. This evidence suffices to show that inter-human cross-infection of lethal doses of plague infection by the hypothesized early-phase transmission must be sporadic occurrences. The theory that early-phase transmission could play a significant or important role in plague epidemics seems unrealistic. This evidence explains also why no concrete case of inter-human cross-infection of bubonic plague was observed in the huge plague epidemics in India, China, Java and Madagascar, or in the large epidemics in Egypt and Vietnam, according to huge syntheses of plague studies represented by the standard works on plague, although a sprinkling of cases or sporadic rare occurrences are accepted or not excluded.1982 This put in perspective the fact that native housing and hovels swarmed with human ectoparasites.1983 This evidence also agrees with the fact that the notion of inter-human cross-infection of bubonic plague is incompatible with the epidemiological features which clearly emerge from the synthesis of the complete study of all data on the spread of the Black Death across Europe, the Middle East and North Africa.1984 These features emerge also more generally from studies of plague epidemics, including the complete study of the history of plague epidemics in Norway 1348-1654.1985 It also agrees with the general presentation of the epidemiology of bubonic plague in all standard works on plague.1986 These features are generally compatible with the characteristic and defining features of rat-flea-borne plague.1987 1982  Lamb 1908: 5-93; Loghem und Swellengrebel 1914: 460-81, cf. Benedictow 2010: 167-69; Liston 1924: 950-54, 997-1000; Petrie, Todd, Skander, et al. 1924–25: 117-150; Wakil 1932; C.Y. Wu 1936: 261, 265, 273-74, 300-301, 304; Langen and Lichtenstein 1936: 185-86; Girard 1943: 4-43; Hirst 1953 220-377, 459-63; Pollitzer 1954: 361, 378-81; Girard 1959: 1-11; Brygoo 1966:39-44 Williams, Hudson, Turner, et al. 1980: 459-68: Butler 1983: 32-53. Contrary to a recurrent misunderstanding, this was also not observed in the tiny epidemic of 90 cases in Morocco in 1941. Blanc and Baltazard 1945; Girard 1943; Audoin-Rouzeau 2003: 297-344. 1983  Girard 1943: 21-23, 25; Brygoo 1966: 36-44; Bacot, Petrie and Todd 1914: 507; Petrie Todd, Skander, et al. 1924-25: 117-150; Benedictow 1992/1993/1996: 259-63; Cf. 380; Wu Lien-Teh 1926:187, (62-63), and 1913-14: 248-49; Pollitzer 1954: 380. 1984  Benedictow 2004/2006: 50-241; Benedictow 2010: 25-484. 1985  Benedictow 2002, the part on the history of the Black Death in Norway is available in English translation as Chapter 2. See also Chapters 3-5 and 8. 1986  Wu Lien Teh, Chun, Pollitzer, and C.Y. Wu 1936; Hirst 1953; Pollitzer 1954; Brygoo 1966. 1987  Benedictow 2010: 73-484.

652 

 Problems with the Early-Phase Theory of the Transmission of Plague ...

12.8 Plague Bacteraemia in Black Rats: Rats and Human Beings as Sources of Infection of Feeding Fleas The preceding data brings into focus conditions for efficient transmission of high infective doses of plague bacteria to human beings. IPRC studied also plague bacteraemia in black rats.1988 Among a selection of 32 healthy rats, 23 were inoculated cutaneously with materials from fresh spleens of rats dead from acute plague, and 9 were inoculated subcutaneously with cultures of virulent plague. Of these rats, 13 and 7 respectively, were euthanized in an apparently moribund state, in the terminal or agonal phase of the disease, 2‒4 days after inoculation, on the average 3.25 days, while 10 and 2, respectively, were allowed to die naturally, which occurred, on average, 3.66 days after inoculation or 9.8 hours later. This uncovered the important fact that short periods of incubation and illness are crucial factors in the rapid development of plague epizootics in local rat populations.1989

Table 12.3: Prevalence and levels of plague bacteraemia in 32 black rats in Mumbai 1906. No. of rats

Killed/Died

Bacteria per mL

3

3/1