twigg's alternative theory - Brill

CHAPTER FOURTEEN

TWIGG’S ALTERNATIVE THEORY

Introduction

Twigg is the central scholar in the brief modern history of alternative theories of the microbiological identity of historical plague epidemics. In his monograph of 1984, he was the fi rst scholar to reject any role for the plague pathogen of Yersinia pestis, whether disseminated by rats and fl eas or by droplets, and who introduces a microbiological alterna-tive. In order to clear the way for their own alternatives, the subsequent advocates of alternative theories to a very large extent base their rejec-tions of any role for Yersinia pestis on Twigg’s arguments. Th us, Twigg’s arguments for complete rejection of the Yersinia pestis theory of his-torical plague epidemics must be central in the critical discussion of the alternative theories in this monograph. Several of his main argu-ments have been thoroughly discussed above and shown to be unten-able, namely the arguments relating to the presence and role of rats, the comparative implications of the mortality rates in the Indian plague epidemics of the late nineteenth and early twentieth centuries, and his confusing discussion of metastatic spread of bubonic plague, which at least implies the denial of the importance of this phenomenon in the epidemiology of bubonic plague. Th e time has come to consider his microbiological theory and his historical line of arguments, the main arguments which have so far not been the subject of intensive discussion.

Twigg is the fi rst advocate of an alternative theory of historical plague epidemics who has chosen not to fulfi l one of the central requirements for scholarly work, namely that of systematically providing footnotes for all facts and for all data or ideas from the works of other scholars in the text. Th is contrasts unfavourably with the three monographs he has used most for his account of the Black Death, namely F.A. Gasquet’s of 1908, P. Ziegler’s of 1969, and Shrewsbury’s of 1971, which contain 375, 532, 466, footnotes respectively; Shrewsbury’s monograph contains in all 3290 footnotes for the whole plague history of the British Isles until 1666. All three scholars conscientiously fulfi l the scholarly requirement of systematic and complete testability, the diff erence in the number of

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554 chapter fourteen

1 Scott and Duncan 2001: xiii; Scott and Duncan 2004: viii.

footnotes between these three works refl ecting diff erences in size and scope and the signifi cant number of relevant studies which had appeared in the sixty years that divide them, and also Ziegler’s longish introduction on the Black Death in Europe until the landing in England. In all, Twigg’s monograph contains just twenty-one footnotes, but he mainly provides indications of author and work in the running text, and for each chapter a list of bibliographical references of works pur-portedly used in writing it, without indication of the relevant pages. In addition, at the end of the monograph comes a brief curious list called “Major Works on Plague and Disease,” and an even briefer and more peculiar list called “Secondary Works Not Mentioned in Text,” which refl ect the fact that he has refrained from providing more than episodic footnotes or references. Certainly, this is at variance with a basic neces-sary condition or requirement for producing scholarly work, namely to assure ready testability. It is not practicable to read the whole length of a number of the large monographs and papers mentioned in the text or in the bibliographical list associated with a chapter in order to check or test the numerous points in his text which occasion disbelief or sur-prise. When Twigg refers to, for instance, “Wu Lien-Teh et al. (1936),” this is a standard work of 530 pages; “Sticker (1908)” is over 500 pages; “Hirst (1953)” comprises 467 pages; “Pollitzer (1954)” contains almost 700 pages, and so on. I have repeatedly given up trying to identify ref-erences that I consider desirable to check. Twigg mentions, for instance, that Simpson (1905) states that the “Great Plague of London took six months to travel from St Giles’ to Stepney,” but since neither St Giles nor Stepney is mentioned in the Index, even under London, I had to give up identifying the reference, but luckily eventually found it by chance while looking for something else.

It is useful to compare Twigg’s assertions with the texts of his refer-ences for critical examination. Although I have the great advantage of having over many years endeavoured to read all relevant medical, his-torical and demographic studies on plague, I must throw in the towel and admit that Twigg’s monograph is not really testable for me, at least not within the boundaries of reasonably hard work. Unfortunately, the same practice has been picked up by Scott and Duncan, his close schol-arly friends and associates and producers of another alternative theory of the nature of historical plague which is based on his arguments for rejecting the bubonic-plague theory (see below).1


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twigg’s alternative theory 555

2 Twigg 1983: 211–22.3 Twigg 1984: 214, 217.4 Twigg 1984: 217.

Th e Alternative Th eory of Anthrax

Twigg’s theory is that the plague epidemics of the past were caused by anthrax.2 His alternative theory is a known disease with known properties that lends itself to scientifi c discussion and for this pre-cise reason can be easily rejected, and to my knowledge has been generally rejected. Twigg’s anthrax theory contains three central assumptions:

(1) that anthrax can cause suffi cient levels of mortality to have explan-atory potential for the demographic eff ects of the Black Death;

(2) that the Black Death’s pattern of spread can be correlated with the spread of epizootics which can be shown with reasonable proba-bility to be caused by anthrax;

(3) that the clinical descriptions of human plague cases are similar to human anthrax and not bubonic plague.

Twigg comments on the decisive question of human mortality twice, both times basing his argument on arbitrary assertions and assump-tions,3 for instance (my enumeration):

It [anthrax] is, though, [1] probably equally fatal to man [as to cattle and sheep] and this, coupled with its [2] symptoms and its [3] high mortality rates, means that [4] it must be a prime contender for the alternative position [as the cause of plague/Black Death]. Furthermore it needs no vectors, [5] the spores being the agent of infection and [6] easily carried in the air or on skins, furs and wool and it is for this reason that anthrax has been known as “wool sorters disease.”4

As can readily be seen, this crucial passage is completely unsupported by footnotes or references to demographic and medical evidence or scholarly literature. It is, of course, true that anthrax is spread by spores, as stated in point 5; however, it is also true that anthrax is mainly spread to human beings in the form of anthrax bacteria, especially in the case of people who have ingested contaminated meat, and it is also true that this is by far the most common way human beings contract anthrax (see below). Twigg is attempting here to strengthen his case by making an implicit case for the importance of cross-infection which is errone-ous and may be one of the reasons for the absence of supporting


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5 Brachman 1990: 880.6 Th is discussion of anthrax is based on the following works: Jawetz, Melnick,

Adelberg 1982: 207–8; Manson’s Tropical Diseases 1982: 393; Brachman 1980: 83–93; Sternbach 2003: 463–7; WHO, Media centre, Fact sheet no. 264, October 2001: 1–2. www.who.int/inf-fs/en; Centers of Disease Control, www.cdc.gov./ncidod, FAQ’s – Medical Facts About Anthrax 1–2.

7 Jawetz, Melnick, Adelberg 1982: 207.8 www.cdc.gov./ncidod FAQ’s – Medical Facts About Anthrax 1–2.9 Jawetz, Melnick, Adelberg 1982: 208.

footnotes or references. As stated by Brachman: “Human-to-human or insect transmission has not been proven.”5

As a basis for discussion of this alternative theory, a brief summary will be given of recent medical discussions of anthrax in relation to human beings.6 Anthrax is “primarily a disease of sheep, cattle, horses, and many other animals; humans are aff ected only rarely.”7 Th ere are three forms of anthrax: (1) gastrointestinal tract anthrax, (2) pulmo-nary or inhalational anthrax, and (3) cutaneous anthrax. Gastroin-testinal tract anthrax is the only form of anthrax that can take on an epidemic character, as the other two forms occur only individually or endemically, that is episodically or incidentally and dispersedly.

Gastrointestinal tract anthrax “usually follows the consumption of raw or undercooked contaminated meat.”8 Importantly, this epidemic form of anthrax is quite rare. Th e main reason for this is that human beings do not graze: “In animals the portal of entry is the mouth and intestinal tract by the ingestion of spores on vegetation.” “While ani-mals oft en acquire anthrax through ingestion of spores and spread of organisms from the intestinal tract, this is exceedingly rare in humans. Th us, abdominal pain, vomiting, and bloody diarrhoea are rare clinical signs.”9 In other words, whilst animals ingest anthrax spores, human beings usually ingest anthrax bacteria with meat. For obvious meth-odological reasons, it is not permitted to infer that mortality rates among human beings and farm animals from ingestion of anthrax contagion are the same; it must be formed as a hypothesis that can be tested and confi rmed by corroborative evidence, if possible, which Twigg does not do.

However, according to Manson’s Tropical Diseases, gastrointestinal tract anthrax commonly occurs in epidemics when cattle which have died from anthrax in heavily infected areas are eaten by large numbers of people. Such epidemics are apparently associated with parts of Africa. Th is is explained by the mass consumption of “raw or


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10 Manson’s Tropical Diseases 1982: 393.11 Jawetz, Melnick, Adelberg 1982: 207.12 On plague pustules, see above: 364, 368–78.

undercooked contaminated meat,” especially among pastoral nomads who suddenly are confronted with mass death of their cattle and wish to use as much as possible of these animals as food before the meat spoils. Importantly, this book provides data on lethality rates (= case fatality rates). According to this standard medical work, “Th e mortality rate is low and the great majority recover in a few days.”10 Th is conclu-sion of low mortality among human beings from gastrointestinal tract anthrax, the only form of anthrax that can take on an epidemic form, is incompatible with Twigg’s assertion of population mortality or level of lethality for past plague epidemics. It can, therefore, serve as evidence of why he does not support his assertion on this point by evidence readily obtainable in the scholarly literature.

Both cutaneous and pulmonary anthrax are strongly associated with individual occupational exposure to contaminated hides or wool, while the pulmonary form is oft en called “woolsorter’s disease,” as also men-tioned by Twigg (see above). However, pulmonary anthrax, which is caused by inhalation of contagion into the lungs, occurs only rarely,11 which contrasts sharply with Twigg’s undocumented assertion above of easy dissemination by cross-infection and considerable numbers of cases. Pulmonary anthrax is characterized by high mortality, however, high mortality among a tiny incidence of cases among woolsorters entails negligible population mortality.

Th e cutaneous form of anthrax, caused by the entry of contagion through a cut or an abrasion in the skin (cutis), accounts for 95 per cent or more of human cases globally. When Twigg argues that (the English) Galfrid le Baker’s mention of a highly mortal form of plague “charac-terized by small black pustules on the skin” refers to cutaneous anthrax, he implies arbitrarily that it was usual or normal at the time that per-sons had numerous abrasions and cuts which were contaminated by anthrax contagion. Why does he not consider the possibility that this description refers to bubonic-plague pustules, a feature also men-tioned by the oft en cited Irish chronicler John Clyn? Th is is a clinical feature that will be discussed comprehensively below.12 Twigg again ignores the question of mortality, however, this is not unknown: the lethality (case fatality) rate of untreated cases of cutaneous anthrax


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13 www.cdc.gov./ncidod FAQ’s – Medical Facts About Anthrax 1.14 I believe all useful data on lethality rates in historical bubonic plague epidemics

still can be found in Benedictow 1993/1996: 146–9.15 WHO, Media centre, Fact sheet no. 264, October 2001: 1. www.who.int/inf-fs/

en,fact.

is about 20 per cent.13 In contrast, the lethality rate of bubonic plague is 80 per cent.14

Importantly: “Th ere are no documented cases of person to person transmission”15 of anthrax. Anthrax has only one genuinely epidemic form, namely gastrointestinal tract anthrax.

Th us there are several independent suffi cient conditions for reject-ing the anthrax theory on epidemiological and medical grounds alone. To my knowledge, historical sources do not provide believable descrip-tions of any epidemic of gastrointestinal tract anthrax among human beings, which is the only form that possibly could take on an epidemic character. Th is corresponds to the concluding statement on mecha-nisms of spread in the standard work on microbiology by Jawetz, Melnick and Adelberg: “Contact with infected animals or with their hides, hair, and bristles is the source of infection in humans.” Th us, in an historical perspective, sources of incidence of the disease would only include tanners’ risk of contracting this disease from work with hides and possibly the risk to people from wearing clothing made from contaminated hides, which will occasion episodic cases of cutaneous antrax, and the sporadic individual incidence of “woolsorters’ disease” in export centres of wool like London, or in the proto-industrial cen-tres of wool cloth production like Florence, Ghent, and so on. Taking into account the lethality rate of 20 per cent associated with untreated cases of cutaneous anthrax, one seems justifi ed in losing interest in mortality rates in possible historical cases of anthrax among human beings in the present context. Th e enormous mortality caused by the Black Death and the dramatic population decline it caused are incom-patible with the incidence and mortality of human anthrax.

One of the most conspicuous features of Twigg’s monograph is his eff orts to play down the level of mortality caused by the Black Death (see below) and to play up the level of mortality causable by anthrax. He does not discuss in a serious way the relative rarity of this disease among human beings and the fact that the vast majority of anthrax cases have the cutaneous form with a relatively moderate lethality level. He makes no attempt to adduce an evidential platform that would allow


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16 Twigg 1984: 214.17 Jawetz, Melnick, Adelberg 1982: 206.18 Benedictow 1993/1996: 146–9.

him to argue that the rare type of epidemic gastrointestinal anthrax ever caused large human population mortality rates at a regional or national level in medieval Europe and continued to ravage Europe for 300 years.

Instead, Twigg makes the following three misleading assertions which will be commented on in the order 2, 3, 1:

[1] the introduction of antibiotics has reduced the death rate from cutaneous anthrax to a very low level but [2] visceral anthrax is little aff ected by antibiotic treatment and [3] the death rate may be as high as 90 per cent.16

(2) Twigg’s assertion that the mortality rate of “visceral anthrax,” a curi-ously expanded term that presumably corresponds closely to the con-cept of gastrointestinal tract anthrax, “may be as high as 90 per cent” is not supported by reference(s) to scholarly work(s) in the text or an accompanying footnote, it must be rejected as arbitrary. His assertion on this important point is incompatible with the level of normal lethality given in Manson’s Tropical Diseases (cited above), namely that the “mortality rate is low and the great majority recover in a few days.”

(3) According to standard works on microbiology, antibiotics are eff ective against gastrointestinal tract anthrax,17 thus Twigg’s undocu-mented assertion to the contrary is disappointing.

(1) When Twigg states that antibiotics have today reduced the lethality (case fatality) rate of cutaneous anthrax to a very low level without informing his readers about the normal mortality rate of untreated and unmedicated cases, he leaves his readers with the impression of a very high normal lethality rate in cases of cutaneous anthrax in the past. However, although a lethality rate of about 20 per cent in untreated cases of cutaneous anthrax is moderately high, it compares unimpressively with bubonic plague’s normal lethality rate of around 80 per cent.18

Certainly much can be said about contemporary chroniclers’ clinical descriptions of the Black Death, but they never mention as symptoms of the disease the “abdominal pain, vomiting, and bloody diarrhoea” that characterize gastrointestinal tract anthrax.

Th us, Twigg’s anthrax theory has no signifi cant historical founda-tion. It is medically and epidemiologically untenable and cannot


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19 Twigg 1984: 204–7, 211. See also pages 46–7, 60–1.20 Twigg 1984: 202–3. See Gasquet 1908: 8–9.21 Creighton 1891: 144, fn. 1. Here Creighton refers to the English translation of

1837 of Hecker’s work on the Black Death of 1832, but Hecker had not improved his knowledge of the Black Death in England between 1832 and 1837.

22 Creighton 1891: 144, fn. 1, 200.23 Gasquet 1908: xxi.

explain the mortality rates caused by the Black Death—something that Shrewsbury’s theory also fails to do.

Th e Historical Basis: Th e Use of Obsolete and Peripheral Studies

A curious feature of Twigg’s monograph is his predilection for obsolete works based on miasmatic and astrological theories of epidemic dis-ease. Th is is particularly the case in the fi nal and crucial Chapter 11 where he summarizes his evidence and argues the case for his anthrax theory: “Clinical symptoms in the Black Death and in some other dis-eases. Th e case for anthrax” (pages 200–22). In this chapter, J.F.K. Hecker’s (1795–1850) monograph on Th e Epidemics of the Middle Ages which was fi rst translated into English in 1837 and reprinted in 1844 and posthumously in 1859, is referred to eleven times (and repeatedly elsewhere).19 Hecker is also referred to indirectly through Twigg’s use of Gasquet’s references to Hecker’s work, for example on the clinical features of the Black Death.20 Hecker is even cited on an important point of the Black Death’s epidemiology in England, although Creighton has made it clear that Hecker’s superfi cial and defi cient knowledge on the Black Death in England is taken from J. Barnes’s monograph the History of Edward III of 1688.21 Creighton refers disparagingly also to Hecker’s “a priori habit of mind” for making assertions of fact without support from sources.22 It would be surprising if Twigg has not noticed these relevant comments, since the main work of Creighton, the last champion in England of the miasmatic theory of epidemic causation, predictably is frequently cited in support of his argument, for example three times in Chapter 11.

Th e skilful ecclesiastic amateur historian F.A. Gasquet (Abbot President of the English Benedictines) and his pioneering work on the Black Death in England is referred to ten times in Chapter 11. Th is work was originally prepared in the 1880s23 and fi rst published in 1893; the edition of 1908 used here by me and by Twigg is a reprint “with one


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24 Twigg 1984: 214–5. Another of Twigg’s pervasive inaccuracies crops up here: the title of the work cited in the references on page 245 under Mead’s name was not written by him but rather by Joseph Browne (whose book was also published 1720). Browne, like Mead, had never seen a plague case in his life, so the comments are irrelevant in both cases.

25 Hatcher 1977: 21.26 Twigg 1984: 192–5.27 Bradley 1977a: 63–94.

or two minor corrections, and a few additions.” Th e text of Gasquet’s monograph represents pre-scientifi c miasmatic notions of the cause of epidemic disease, and all medical and historical works he refers to rep-resent this miasmatic view and pre-scientifi c epidemiology and medi-cine more generally.

In addition R. Mead’s view on the clinical symptoms of plague pub-lished in 1720 is taken seriously by Twigg;24 although Mead was born in 1673, he had never seen a case of plague in his life. Th is does not end the list of miasmatic and obsolete works Twigg refers to in chapter 11, which include W. Wood’s monograph of 1842/1865, H. Harrod’s paper of 1867, and so on.

Within this framework which mainly is of interest and relevance for the history of medicine, a number of contemporary chroniclers are cited and referred to on the clinical features of the Black Death without any attempt at explaining their social, cultural or medical framework. Source-criticism is not mentioned or applied. Without the source-critical training of medieval historians, Twigg inevitably becomes a victim of what Hatcher calls “the overwrought imaginings and hope-lessly inaccurate quantifi cation of the chroniclers.”25 Th ere will be occa-sion below to address this point more specifi cally. Twigg, who apparently neither likes source-criticism nor medieval demography, inevitably subjects himself to this process of scholarly victimization at the hands of medieval chroniclers whose assorted utterances of “overwrought imaginings and hopelessly inaccurate quantifi cation” are, thus, passed on and given a new lease of life long aft er most of them should have been laid gracefully to rest.

In his discussion of the last plague epidemic in the village of Eyam in Derbyshire in 1665–6, Twigg relies on W. Wood’s monograph fi rst published in 1842 and also for one point of importance on the ninth reprint of 1744 of Mead’s monograph.26 L. Bradley’s fi ne modern family- reconstitution-based demographic study of 1977 on the epidemic at Eyam27 is mentioned only indirectly in a comment to the eff ect that


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28 Shrewsbury 1971: 522–9.29 Bradley 1977a and 1977b.

Bradley disagrees with Wood’s analysis, without indicating why, which might have revealed very good reasons. However, it shows that Twigg knows Bradley’s fi ne demographic study, but like Cohn and Scott and Duncan, does not take its fi ndings into account. Shrewsbury’s useful 1971 demographic discussion of the same material28 is passed by in silence. Bradley and Shrewsbury agree on the basis of modern medical, epidemiological and demographic analysis that the epidemic at Eyam was indeed bubonic plague.29

Twigg’s monograph abounds in such examples. His prolifi c use of obsolete pre-scientifi c studies is obviously contrary to central tenets of scholarly work and unavoidably raises the question: why does Twigg to such an extent build his case on long obsolete studies, scholarly antiques based on miasmatic epidemiological theory with characteristic astro-logical and telluric aspects? Th e reason can hardly be any other than because he needs them, because in the end Twigg has to resort to mias-matic theory himself, albeit in a slightly modernized version, in the futile hope that it can save the last vestiges of credibility of his theory. In his fi nal chapter, it becomes obvious that a theory to the eff ect that the European populations should have been eating the Black Death both on the Continent and in England or that herds of sheep and cattle should have been transported by galleys from Constantinople to Mediterranean ports and been driven across the Continent whilst peo-ple eagerly devoured the fl esh of obviously sick, moribund or dead ani-mals was simply untenable and impossible to take seriously.

Th e Telluric-Miasmatic Th eory of Anthrax

Eventually, it becomes clear to Twigg that there had to be another very dynamic mechanism of the spread of anthrax. At this point, central aspects of the miasmatic theory of epidemiology seemingly off ered him a solution. He takes as his point of departure experimen-tal studies on the possible airborne passage of the foot-and-mouth virus under some specifi c meteorological conditions relating to or inspired by an outbreak of foot-and-mouth disease in livestock in 1967–8. Th is mechanism of spread is not mentioned in later standard works on medical microbiology, for instance, by Jawetz, Melnick and


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30 Jawetz, Melnick and Adelberg 1982: 395–6.31 Twigg 1984: 220–1.

Adelberg.30 Airborne contagion connected with specifi c meteorologi-cal conditions accords completely with classical Greek miasmatic the-ory of the causation of epidemic disease and miasmatic epidemiology’s central tenets on the dissemination of epidemic disease.

Against this background, Twigg argues that the

extraordinarily rapid dissemination of the Black Death suggests pulmo-nary anthrax moving in a similar way […] this form of the disease could very likely have been the illness which has hitherto been identifi ed with pneumonic plague.31

Th ese few words contain a number of fallacies of methodology and neglect of facts. Firstly, Twigg uses a hypothetical mechanism of aerial spread of foot-and-mouth disease to suggest by analogy that this could also be the case with pulmonary anthrax, which he arbitrarily com-pares with pneumonic plague, and goes on to build on these analogies as if they were materially established by empirical evidence. According to modern scientifi c methodology, analogies can only be used for con-struction of working hypotheses, all use of analogies for inference to fact or reality is fallacious. It is true that classical Greek scholars and physicians used analogies for evidentiary purposes in this way, in accordance with their incompletely developed scientifi c methodology, but that was over two thousand years ago. According to the tenets of modern scientifi c methodology, Twigg must fi rst adduce good evi-dence showing that pulmonary anthrax can spread by air in epidemic form according to the pattern of the viral foot-and-mouth-disease and the bacterial primary pneumonic-plague disease. If he were able to do this, he would also be obliged to document that pulmonary anthrax can spread with extraordinary rapidity, faster than any other epidemic disease which is dependent on interhuman transmission, before he could single it out as a possible candidate for the epidemic disease in question. However, Twigg does not attempt to satisfy these premises or basic conditions, and his inference from rapidity of spread to pulmo-nary plague is, therefore, a circular type of argument based on a purely hypothetical analogy. Indeed, earlier in his monograph, in accordance with the modern scientifi c literature on anthrax, Twigg restricted pul-monary anthrax to the episodic and largely individual occurrence among woolsorters, which has no epidemic form. Th ere is no spread


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32 See Hirst’s excellent presentation of these aspects of miasmatic theory in Hirst 1953: 22–72.

rate characteristic of the Black Death that can “suggest” that it was (pri-mary) pneumonic plague; this conclusion is literally taken out of thin air. For the same methodological reason, an analogy cannot be used to “suggest” a factual condition, since use of the term “suggest” indicates a level of tenability, albeit low. Conspicuously, Twigg transforms the level of tenability associated with the concept of “suggest” into the level of tenability of “very likely” without the mediation of evidence. Scholarly work is associated with the principle of fallibility, which dic-tates that on principle no scholarly statement can be absolutely true. Th ere is always, as a matter of principle, at least a tiny element of doubt or uncertainty associated with scholarly or scientifi c statements. Th e level of tenability of “very likely” is therefore about as certain as a schol-arly statement can be and is correspondingly demanding with respect to its evidential basis, presupposing a solid empirical material. In this case, Twigg has not adduced any evidence, so not only is the asserted level of tenability of “very likely” untenable, it is also methodologically invalid and can be characterized as fallacious. Twigg goes on to use term “speculate” to describe his reasoning, which in scientifi c meth-odological parlance means not based on facts, only on logical infer-ence. Twigg apparently does not know that analogies, like defi nitions and concepts, cannot be used for evidential purposes or for inference to fact or reality, and consequently cannot be associated with tenability, but can only be discussed in methodological terms of usefulness as intellectual tools for analysis. He treats levels of tenability along the whole register from the very lowest level of speculation, via suggestion up to almost the highest level of very likely as if they are interchangea-ble and independent of evidence. Also this part of Twigg’s work is methodologically confused and comprehensively at variance with the basic tenets of (social) science.

To my knowledge, Twigg is the only modern scholar who has been inspired by miasmatic epidemiological theory to a degree that he also cites telluric aspects of this theory, that is, the idea that mias-matic contagion is let out from the ground aft er it has been disturbed by volcanic activities, earthquakes or astrological constellations, to be spread by the wind and cause epidemics when it reaches human settlements:32


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33 Twigg 1984: 221.34 Hirst 1953: 41.35 Twigg 1984: 46–7, 60–1, 204–7, 211.36 Twigg 1984: 45–7, 56–7, 60–1, 70, 103, 202–4, 207.37 Twigg 1984: 221.

It is tempting to speculate yet further and to suggest that the sequence of earthquakes and fl oods in the East before the Black Death might have disturbed anthrax in the soil and the spores were then carried by air cur-rents to the Mediterranean and Europe.33

Telluric-miasmatic explanations for outbreaks of serious epidemic dis-ease are a clear feature of Hecker’s epidemiological thinking in his works of the 1830’s,34 which Twigg refers to eighteen times,35 and of Gasquet’s monograph, which he refers to twenty-three times.36 Seen against the background of Twigg’s prolifi c use of these works and other miasmatic works (see above) in support of his anthrax theory, it can be legitimately assumed that this is his source of inspiration. By accepting long-discarded explanations of a serious epidemic outbreak, in this case the principle of telluric explanation of the origin of airborne miasma for the Black Death, Twigg has crossed a crucial line between scientifi c and unscientifi c work.

He goes on to state that:

Anthrax is widely known in African mammals, however, and air currents bearing spores of anthrax could easily reach northern Europe, as shown by the deposition of Saharan dust in England in recent years.37

Again Twigg uses an analogy, in this case based on the relatively rare instances of air transport of Saharan sand to England, which does occur, to assert that this easily could be the case for anthrax spores, an assertion for which he off ers no evidence. How can he know that air-borne anthrax spores from Africa “could easily reach northern Europe” when he is unable to provide any evidence for the factual occurrence of such transport at all? In ordinary scholarly or scientifi c discourse, the phrase “could easily reach northern Europe” should imply substantial empirical evidence for this phenomenon, quite a lot actually, in order to be able to diff erentiate between the rare occurrence, the sporadic occurrence and the quite regular occurrence that alone can prove that this could easily be the case. Instead, the fact is that he has no evidence to show in support of his assertion: it is based on the implication, the methodological fallacy, that an analogy can provide or constitute empirical evidence allowing inference to fact or reality.


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Th e analogy is false for several reasons:

(1) the assertion that sand and anthrax spores have much the same properties in relation to airborne transport requires evidentiary support, without which it is an arbitrary assertion.

(2) the assertion that Saharan animals could be the source of anthrax spores that could be transported by wind to northern Europe in the same way as Saharan sand requires evidentiary support. When it is maintained without evidence that this can, in fact, occur, also this assertion takes on the character of an arbitrary argument.

(3) anthrax epizootics among cattle are not uncommon in parts of Africa (see above), and it is well known that Sahara is full of sand, but cattle are not common in the sand oceans of the Sahara, and large, numerous herds of contaminated cattle are required to cre-ate signifi cant amounts of spores. It is the parts of Africa south of the Sahara that are inhabited by more or less nomadic pastoral people with large herds moving through large areas which are at the heart of the matter, and it is the question of whether or not air currents could transport anthrax spores from these areas which is the real problem Twigg should have addressed with energy and dedication. Th e conclusion he would have reached can be stated: that there is no historical evidence that air currents with spores from these areas have reached the northerly parts of Europe.

Twigg resorts to unscientifi c miasmatic-telluric theory in order to defend his theory. Th is can only be taken to refl ect the obvious unten-ability of his theory and the length to which he is willing to go in order to construct a basis for it.

Th e Pace of Spread of Plague

Th ere is another reason for Twigg’s attraction to miasmatic theory. Th is is the distant thunder of the works of modern scientifi c plague resear-chers with excellent medical education from Cambridge and Oxford in England as well as leading universities in France and the U.S.A. who made such tremendous progress in the scientifi c study of bubonic plague in India, China, Madagascar, Vietnam, and elsewhere in the twentieth century. Many of them put great emphasis on the history of plague and comparison between the old clinical and epidemiological descriptions and accounts of plague and their modern observations of


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38 Simpson 1905: 23.39 Twigg 1984: 135. He does not identify where in Simpson’s work he has found this

instance; see, however, Simpson 1905: 70. Similarly, plague took over fi ve weeks to move from Westminster to the city parish of St Olave, Hart Street. Cox 1910: 153.

40 IPRC 1907h: 827, cf, Map IV; Lamb 1908: 19.

thousands of plague patients and plague’s epidemiology. On this basis and without exception they reached the conclusion that the disease they studied and the historical plague epidemics were the same. If Twigg had wished in earnest to learn from modern scientifi c discus-sions of this topic, he could have studied the works of Simpson of 1905, Sticker of 1908 and 1910, Wu Lien-Teh of 1926, Wu Lien-Teh, J.W.H. Chun, R. Pollitzer, C.Y. Wu of 1936, Hirst of 1953, Pollitzer of 1954, and papers by other leading plague researchers like Greenwood and Liston of the IPRC, just to name the most important in this context.

Twigg mentions most of them in his text, but not on central points of epidemiology or clinical features, only on points that do not bear seriously on his theory. As shown above, his assertions on the mecha-nisms and patterns of spread of bubonic plague are untenable and are based on highly selective references and peculiar interpretations. Simpson’s monograph, the fi rst but necessarily “immature” modern scientifi c work to emerge from the studies of British physicians and epidemiologists in India, is, for instance, referred to twice. Twigg cor-rectly points out Simpson’s view that the Black Death, in relation to earlier plague epidemics, “was distinguished by its rapid spread and destructiveness,” “Never before had it shown such diff usive qualities.”38 Twigg takes this in support of (1) his view that the Black Death could not have been bubonic plague and (2) compares it with a purported slow pace of spread in India and cites again Simpson who points out that (3) the “Great Plague of London [of 1665] took six months to travel from St Giles’ to Stepney.”39 What Twigg describes here is, of course, contiguous spread of plague by contact between rat colonies, and the example from London 1665 is similar to the observation of IPRC that “the infection in the rats took six weeks to travel 300 feet” in a section of Sion village outside Mumbai.40 Th is means, of course, that the plague in London 1665 and in India of the early 1900s had a very important feature in common, namely that they could spread very slowly in a contiguous way. However, given this comparison I do not understand why a structural similarity of pace of spread of bubonic plague in India


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41 Above: 153.42 Simpson 1905: 62.43 Simpson 1905: 65.44 Simpson 1905: 71.45 See Bell 1951.

and the Great Plague of London does not constitute evidence that the Great Plague in London was the same disease as in India, namely bubonic plague. Twigg overlooks the fact that if his point was correct, there would not have been any Great Plague in London; only a few small patches of the great city would have been ravaged.

Since Twigg has used Simpson’s monograph, another important question remains unanswered: why Twigg ignores Simpson’s informa-tion on the great importance of metastatic spread by leaps,41 for instance, that “in Canton, many persons, especially the well-to-do, removed to the country, thus forming fresh foci for its dissemination; and in the same way the outbreak in Hongkong no doubt arose from persons hav-ing migrated from Canton to Hongkong.”42 In China as well “the infec-tion on land has followed chiefl y the routes of busiest intercourse.”43 Simpson also provides much information on spread by leaps in India, for instance, in connection with the mass exodus out of Mumbai when the plague epidemic suddenly blazed up: “Fugitives from Bombay and the Bombay Presidency were not long in carrying infection to the other provinces of India.”44

Twigg also passes by in silence the conspicuous phenomenon of metastatic leaps in the Great Plague of London, as can bee seen from Bell’s fi ne study of it, for instance: the spread of the disease by leaps in the city and in the outparishes and liberties, establishing numerous new centres of spread in the rat colonies more or less according to a geometrical progression of incidence. Bell has no diffi culty in showing that the epidemiological and clinical features of this epidemic in London correspond very closely to those of bubonic plague.45 Twigg’s obligation to ignore the typical metastatic patterns of spread of bubonic plague in clothing or luggage or goods that lent the Black Death and subsequent plague epidemics dynamic powers of spread and was also such a conspicuous feature of bubonic plague in India, refl ects the fun-damental weakness of his theory.

It is important to recognize that the diff usive powers of the Black Death were so strong in Europe in the middle of the fourteenth century because it arrived in a territorially interconnected and integrated


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46 Benedictow 2005: 46–7.

civilization which off ered epidemic disease in general entirely new powers of spread. My brief introduction to this aspect of medieval soci-ety in a journal of popular history runs like this:

Th e extent of the contagious power of the Black Death has been almost mystifying. Th e central explanation lies within characteristic features of medieval society in a dynamic phase of modernization heralding the transformation from a medieval to Early Modern European society. Early industrial, market-economic and capitalistic developments had advanced more than is oft en assumed, especially in northern Italy and Flanders. New, larger types of ships carried great quantities of goods over extensive trade networks that linked Venice and Genoa with Constantinople and the Crimea, Alexandria and Tunis, London and Bruges. In London and Bruges the Italian trading system was linked to the busy shipping lines of the German Hanseatic League in the Nordic countries and the Baltic area, with large broad-bellied ships called cogs. Th is system for long-dis-tance trade was supplemented by a web of lively short and medium-distance trade that bound together populations all over the Old World.

Th e strong increase in population in Europe in the High Middle Ages (1050–1300) meant that the prevailing agricultural technology was inad-equate for further expansion. To accommodate the growth, forests were cleared and mountain villages settled wherever it was possible for people to eke out a living. People had to opt for a more one-sided husbandry, particularly in animals, to create a surplus that could be traded for staples such as salt and iron, grain or fl our. Th ese settlements operated within a busy trading network running from coasts to mountain villages. And with tradesmen and goods, contagious diseases reached even the most remote and isolated hamlets.

In this early phase of modernization, Europe was also on the way to “the golden age of bacteria” when there was a great increase in epidemic diseases caused by strong increase in population density and in trade and transport while knowledge of the nature of epidemics, and therefore countermeasures to them, was still minimal.46

Th e point is that epidemiology is a subdiscipline of sociology in that it focuses on the study of the eff ects of social interaction, and that the powers of spread of epidemic diseases vary greatly with diff erent types of social formations and must be seen within a societal framework of analysis. Th e powers of spread of the Black Death in the form of bubonic plague were much stronger than before because it reached a European society that off ered new mechanisms and much stronger opportunities for dynamic spread, as was the case also for other microbiological


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47 Cf. Benedictow 2004: 387–9.48 See above: 194–204.49 Twigg 1984: 212.

pathogenic agents.47 While Simpson can be excused for not placing his correct observation in this historical societal perspective, since the development of medieval economic history was only in its infancy at the time, there is no such excuse for Twigg.

Twigg again produces a fallacy of methodology by not comparing like with like, but comparing things that are not in pari materia to infer from dissimilarity of (epidemiological) manifestations to dissimilarity of (microbiological) causation. He compares plague’s pattern of spread in the form of the Black Death in a helpless medieval Europe around 1350 with plague developments around 1900 in the Indian subconti-nent governed by British colonial authorities “armed” with European historical experience, modern organizational abilities and modern medical science, albeit in an early stage of development. As shown also above, Twigg ignores, among other things, the fact that the British colonial administration in haste built the largest anti-epidemic organi-sation the world has ever seen on the basis of a long and largely suc-cessful tradition of epidemic countermeasures that had successfully defeated bubonic plague in Europe as early as in the seventeenth cen-tury and also on the basis of the new bacteriological understanding of disease and increasingly on a real understanding of the mechanisms of dissemination of plague.48 Given that European authorities succeeded in stamping out plague at the middle of the seventeenth century, it is a strange notion that they, with a gigantic well-organized anti-epidemic eff ort based on superior medical and epidemiological knowledge at their disposal, should not have succeeded in keeping spread and mor-tality of bubonic plague to a minimum around 1900 and in the early twentieth century.

Th e second time Twigg refers to Simpson’s work concerns a minor point regarding which animals may contract plague.49 As can now be readily seen, Twigg avoids discussing Simpson’s quite large historical section where historical plague is compared with bubonic plague in India and identity is concluded.

Sticker’s work on historical plague and modern scientifi c counter-measures is treated in the same manner: these two volumes are referred to only once, for a peripheral speculative assertion of the mortality rate


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50 Twigg 1984: 46–7. See Sticker 1908: 106. Sticker is the only of these scholars who contracted plague in India and, fortunately, survived.

51 Twigg 1984: 20.52 Twigg 1984: 39. 45. Cf. Benedictow 12004: 48–9.53 Twigg 1984: 77–8, 81–2, 85.54 Twigg 1084: 202–13.55 Twigg 1984: 213.56 Twigg 1984: 202–3.57 Gasquet 1908: 7–8.58 See Manson’s Tropical Diseases 1982: 393 with picture.

in the plague epidemic in Cairo 1574.50 Chun, who has written very usefully on the presentation of the clinical features of bubonic plague, is also mentioned once, in relation to the average duration of the course of illness in cases of primary pneumonic plague.51 Twigg refers to Pollitzer’s monograph in connection with questions relating to the his-torical origin of the Black Death and the understanding of the head-stones in the Nestorian graveyard at Issyk-Kul.52 Hirst is mentioned in connection with a discussion of the history of the black rat in England,53 but his broad historical discussion of epidemiological and clinical fea-tures characteristic of bubonic plague, which represents a fatal threat to Twigg’s theory, remains unused.

Th ese are representative examples of how restrictively and selectively Twigg discusses the modern standard works on plague in contrast to his predilection for obsolete miasmatic works and his problematic rela-tionship with methodology.

Anthrax and the Name Black Death

Twigg maintains that in order to determine the microbiological nature of the Black Death a “good starting point is the name Black Death.”54 Th e intention is to link the term Black Death with anthrax, a Greek word that means coal and conveys connotations of black, because this would signify that the use of the word black had a concrete clinical descriptive purpose associated with anthrax.55 Th is is unacceptable for several reasons. Firstly, Gasquet, to whom he fi rst turns,56 makes it entirely clear that the name Black Death is not contemporary with this epidemic or subsequent plague epidemics but appears sometime aft er the last outbreak of plague in Britain.57 Secondly, the characteristic black associated with the name anthrax refers to the anthrax pustules of cutaneous anthrax which usually develop a black colouring.58 It has


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59 Hirst 1953: 32.60 Shrewsbury 1971: 37.

nothing to do with the only epidemic form of anthrax, namely gas-trointestinal tract anthrax, on which Twigg’s theory in reality relies or with the only form with high lethality rates, namely the rare pulmonary or inhalational anthrax, although Twigg refrains from mentioning it. Cutaneous anthrax is, as mentioned earlier, ordinarily an occupational disease of tanners and other craft smen or labourers working with hides and has a lethality rate of about 20 per cent (in unmedicated cases). Th is form of anthrax disease, which is the only one that is associated with black pustules, can at most cause population mortality of some tiny fraction of 1 per cent. It does not have explanatory potential for the mortality rates caused by the Black Death of 1346–53.

Th irdly, by focusing on Gasquet’s obsolete account, Twigg can neglect S. D’Irsay’s paper of 1926 on “Th e Origin of the Expression: Atra Mors” in which he convincingly shows that the term “Black Death” is a mis-translation of the term “atra mors” where atra can mean both “terrible” and “black,” thus, the “terrible death” by mistranslation was changed into the even more graphic term the “Black Death.” Th is explanation appears otherwise to be generally accepted and to have been so for quite a long time. D’Irsay argues also convincingly that this mistransla-tion originated in Scandinavia, where it was fi rst registered in Sweden in 1555 and about fi ft y years later in Denmark. It may seem that this was a mistranslation that was quite likely to occur, especially for per-sons without a good Latin education, and it may have occurred repeat-edly and independently before the sinister and frightening connotations caught the imagination. Th is happened much later: according to Hirst and Shrewsbury, the term the “Black Death” is used in history-oriented literature59 in England for the fi rst time in 1823, and was, according to Shrewsbury, for the fi rst time introduced in English medical literature in 1837 with the translation of Hecker’s monograph Th e Black Death in the Fift eenth Century.60 Clearly, the term the “Black Death” was intro-duced into English by persons and adopted by a population who had never seen a case of plague or its clinical manifestations. In normal scholarly discourse, this would be taken as decisive proof that plague does not have a clinical feature characterized by the colour black and that the origin of the adjective “black” must have a non-clinical origin. Twigg knows well and refers repeatedly to Ziegler’s monograph where


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61 Ziegler 1970: 18.62 Twigg 1984: 245.63 Twigg 1984: 204–7.64 Twigg 1984: 211. My translation from French.65 Jawetz, Melnick, Adelberg 1982: 437.66 Twigg’s italics.

this mistranslation of atra mors is underlined as “the most likely expla-nation,” its Scandinavian origin is mentioned, and where all alternative explanations of the term the “Black Death” are rejected because they are later than the plague period.61 Twigg refers to D’Irsay’s paper in the bibliographical list at the end of this Chapter 11,62 but ignores it in the text. Twigg’s attempt to link the (misnomer) “Black Death” with the black colour of (cutaneous) anthrax pustules is unsuccessful and misguided.63

Surprisingly, in support of his view on this point Twigg cites the French veterinarian E. Leclainche’s work on veterinary medicine of 1936: “In the terrible epidemic of smallpox of 1345–50 (la mort noire, der Schwarze Tod), the horses, the sheep and the goats died in thou-sands.”64 Th us, highly unusually, Leclainche asserts that the Black Death was an epidemic of smallpox that also caused high mortality among domestic animals. However, according to modern standard works on microbiology, “variola [= smallpox] infects only humans and mon-keys,”65 consequently, the concomitant epizootic must have been another disease. One could have expected that this rather far-fetched and microbiologically untenable view which also runs contrary to Twigg’s anthrax-theory, would have induced him to take a rather scep-tical attitude toward the competence and quality of Leclainche’s work. Instead, he states enthusiastically: “Variole is smallpox (Latin variola) and not only did this great outbreak kill domestic animals but it was referred to as the black death.”66 He has a motive for doing so: suddenly, many pages aft er he has discussed the origin and meaning of the term the “Black Death” and despite much eff ort had not succeeded in adduc-ing evidence that the name was contemporary, he triumphantly quotes Leclainche’s assertion that the epidemic at the time was called the Black Death, “la mort noire, der Schwarze Tod.” However, he cannot provide his readers Leclainche’s source for this sensational fi nd and potentially important contribution to the history of the Black Death, because there is none. Th is is also the reason neither French historians nor German historians have picked up Leclainche’s assertion. In modern French


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67 Biraben 1975: 7–18; Dubois 1988: 313–6. My translation from French.68 Little 2007: 14; Sallares 2007: 288; McCormick 2007: 292.69 Biraben and Le Goff 1969: 1484–510; Biraben 1975: 26–48. Th ey have missed the

spread to England by some of the epidemics. See for instance Maddicot 2007: 171–214.

70 Sticker 1908: 26–35.

scholarly work on the Black Death, the epidemic is unequivocally iden-tifi ed as bubonic plague. In the words of Dubois in the most recent summary of French research on the Black Death: “almost everywhere in France, the plague has assumed the bubonic form with secondary manifestations” (the small reservation relates to primary pneumonic plague).67 Leclainche was a veterinarian without training in the craft of the historian and the historical aspects of his work are fatally fl awed by his lack of historical knowledge of medieval society and of training in historical source-criticism and the application of historical methodol-ogy more generally.

Anthrax’s Historical Association with Other Epizootics among Domestic Animals and Plague

Th e same fundamental problems can also be readily seen in Twigg’s use of Leclainche’s supposed information that “in 801 there was plague in Charlemagne’s empire which took men and animals alike and in 840 there was plague in men and horses.” Anyone who has taken a serious interest in the history of plague will know that there were no plague epidemics at the time of Charlemagne. Th e last possible outbreak of plague in the Justinianic plague pandemic was in 766 in Rome or per-haps in Naples and Sicily in 750.68 Th e last epidemic within the area of present-day France may have occurred in 694, and the last quite certain French epidemic of plague in this pandemic took place in Southern France in 655. All epidemics of this pandemic with their geographical extension are presented in a paper by Biraben and Le Goff of 1969; they are presented systematically over twenty-two pages which include a table with geographical information and individualized maps in Biraben’s monograph of 1975 which Twigg has entered in his bibliogra-phy.69 Twigg could easily have determined that Leclainche’s assertions were unhistorical and left his work aside. Leclainche could have used Sticker’s valuable presentation of the Justinianic pandemic in his fi rst volume (1908).70 So could Twigg, who must be assumed to know


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71 Twigg 1984: 210.72 Trow-Smith 1957: 153–7, 240–1; Dyer 1988: 29; Grant 1988: 154, 185; Astill and

Grant 1988: 216–7.73 See, for instance, Manson’s Tropical Diseases 1982: 348–55, 191–4.

Sticker 1908 since he refers to it once, albeit on a peripheral point of mortality in the plague epidemic in Cairo of 1574–6 (above).

Serious or severe epidemic diseases among human beings were usual in the Middle Ages. As Twigg correctly states: it “is very likely that the people of the Middle Ages suff ered from a wide variety of diseases.”71 However, contagious diseases among cattle and sheep and other domes-tic animals were also a general feature of life and these animals suff ered from a variety of diseases, anthrax and foot-and-mouth disease, which are commented on by Twigg, but also sheep scab, sheep pox (variola ovina), brucellosis and trichinosis. Leading English agricultural histo-rians agree that epizootics frequently took a serious toll of English live-stock in medieval England: “Major epidemics of disease caused serious losses to the sheep population in England in the late thirteenth and early fourteenth centuries. Some fl ocks were reduced by as much as two-thirds.”72 Th is means that it was quite usual that epidemics among human beings and epizootics among domestic animals took place more or less concomitantly and that there was no pathogenic or dissemina-tive connection between them. Contemporaneousness of events does not constitute proof that they are causally related, it justifi es only the establishment of a working hypothesis to the eff ect that this could have been the case, with the function to induce the scholar to look for cor-roborative evidence. Consequently, it is a fallacy of methodology to conclude without further specifi c investigation that livestock and human population were hit by the same disease, as Twigg usually infers. Specifi c corroborative evidence must be adduced. And anthrax is not the only disease that can aff ect both farm animals and local popula-tions in quite close epizootic and epidemic developments; this is also the case with brucellosis and trichinosis.73 Also for this reason it would be a fallacy of methodology to conclude that concomitant epizootic and epidemic developments must refl ect anthrax—specifi c evidence would need to be adduced. If specifi c evidence cannot be produced, Twigg must admit that he has raised a working hypothesis that he is not able to prove and thus has no case.

Twigg enthusiastically writes repeatedly about the numerous epiz-ootics among domestic animals reported in the chronicles and other


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74 Twigg 1984: 200–1, 211, 217.75 Sternbach 2003: 1–3; Brachman 1990: 877.76 Grant 1988: 185; Smith 1988: 208.77 Twigg 1984: 217.

sources from the Early Middle Ages into the Late Middle Ages.74 Th e readers must be excused for assuming that Twigg considers this to be evidence of anthrax, since the accounts on this point cannot serve any substantial purpose for his project if they refl ected a considerable number of other epizootic diseases. However, eventually a major prob-lem confronts Twigg: if anthrax had been around for many centuries before the Black Death, it becomes impossible to explain the excep-tional mortality caused by the Black Death. So, he must introduce a new disease into Europe, namely anthrax in the form of the Black Death. Th is fl ies in the face of what is known about the history of anthrax, which is usually assumed to be mentioned in the Bible and in sources from Antiquity,75 and English agricultural historians are cer-tain that it was present in pre-plague England.76 It also fl ies in the face of what is known about the level of mortality rates caused by the Black Death (see below). Actually, Twigg’s line of argument turns out to be circular: “Although recorded on many occasions before 1348, murrains had never been accompanied by such an unprecedented human epi-demic and this leads me to think that the Great Pestilence was caused by an organism not only common to man and animals, but because of its severity, perhaps new to both of them.”77 Th us, anthrax must be a new disease to fulfi l Twigg’s preconceived idea that the Black Death could be anthrax.

Twigg does not make a serious attempt to demonstrate the tenability of his second central assumption, namely that the Black Death’s pattern of spread could, even by the most creative exercise of imagination, have resulted from the fact that from Spain to Norway, from England to Russia, European populations were consuming “raw or undercooked” meat contaminated by anthrax and according to a temporal and spatial pattern co-ordinated with and compatible with the spread of plague. At the time, livestock was not a usual cargo, certainly not over considera-ble distances, and because the epidemic outbreaks in seaports were normally not preceded by epizootics among cattle and sheep, the cru-cial role played by ship transportation of the Black Death at long or intermediate distances is incompatible with the spread of anthrax. Nor was meat such a major part of diet (see below).


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78 Twigg 217–8.79 Benedictow 2004: 262–6, 368, 375–7.80 Campbell 1985: 314. Cf. Smith 1988: 208.81 Twigg 1984: 211.

Twigg’s assumptions take on an increasingly hypothetical and speculative character: “Th e route by which plague is reputed to have reached Europe could be the very same one that anthrax used.” “If anthrax had come from the East it could have been swift ly spread across Europe from Marseilles and other ports.”78 Th us, it is a fantastic sce-nario Twigg outlines for his readers of big herds of cattle being trans-ported by galleys fi rst from Kaff a to Constantinople, from Constantinople to Mediterranean ports, especially Marseilles, from whence they were driven across Europe, disseminating spores and contagion and produc-ing instant mass mortality everywhere. Everywhere people gladly devoured contaminated meat from slaughtered sick animals or animals having died from “murrain” without ever or anywhere coming to sus-pect that it could be dangerous, although they saw people dying every-where in droves, people that only had in common the fact that they had eaten meat from animals killed by “murrain.” Inexplicably, poor people who usually could not aff ord meat but had to do with porridge and coarse bread had even higher mortality than the affl uent and rich.79

In fact, Twigg is unable to show that concomitant epizootics and epi-demics were usual even in England. For this reason, B.M.S. Campbell points out in his review of Twigg’s monograph that Twigg’s theory is undermined by the absence of detectable abnormal mortality among demesne livestock during the Black Death.80 Campbell is not impressed by Twigg’s attempts at documenting the contrary by basing his account on Hecker’s pre-scientifi c work of 1837 which for plague is based on Barnes’s monograph on the History of Edward III of 1688 (see above): “Hecker says that the plague in England was soon accompanied by a fatal murrain among the cattle, which, left without herdsmen, fell in their thousands.”81 Why does Twigg base his theory on a long obsolete work, and why does he not provide Hecker’s source, since it is of such vital importance to the viability of his theory?

Instead, Twigg goes on to cite a small part of a chronicle-based sen-tence by Rees about the Black Death in London in 1348 to the eff ect “that animals as well as men were aff ected.” However, Twigg refrains from citing the following part where Rees applies source-criticism and


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82 Rees 1923: 29.83 Ibid.84 Ziegler 1970: 135; Benedictow 2004: 134–7.85 Islandske Annaler 1888: 275–6.86 Twigg 1984: 217–8. Nothing negative is meant by my characterization of Veale’s

monograph as narrowly England-oriented (its title is Th e English Fur Trade in the Later Middle Ages), only that its focus or perspective poorly serves Twigg’s sweeping Europe-wide line of argument. Th e same goes for its temporal perspective which, as the title shows, is strongly oriented towards the post-Black Death period.

87 Veal 1966.

adds cautiously: “but accurate evidence is not easily obtained,”82 which, in my view, makes the statement practically valueless. Medieval chron-iclers must be used with great caution even when their accounts or information are not obviously incredible or unreliable. Th eir informa-tion must be testable by similarity of independent accounts or other forms of source material. Th is point can be further demonstrated by citing the fi rst part of Rees’s chronicle-based statement left out by Twigg: “scarcely one-tenth survived [in London],”83 which should be impossible even for bubonic plague with a lethality rate of 80 per cent of those infected. Are the views of a chronicler who makes such an evidently hopelessly exaggerated assertion really credible? Is it true that Rees’s account on this point can serve to support a case for a concomi-tant epizootic and epidemic in London? How can it be made compati-ble with Ziegler’s correct observation that the Black Death broke out in London earlier than in the surrounding districts, actually by a margin of several months?84 Th is can only serve to illustrate the great caution with which medieval chroniclers should be treated. Icelandic chroni-clers assert that only fourteen people survived in London.85

Twigg’s attempt to take refuge in the international trade of hides, furs and wool on the basis of E.M. Veale’s fi ne, but quite narrowly England-oriented monograph, is unconvincing.86 Nothing is said in this study about skins or furs as vehicles of the spread of zoonoses to human populations at the time, nor about anthrax, nor about any other animal disease,87 which shows that Twigg is forced to proceed by spec-ulation. Assuming speculatively that anthrax was actually spread by this trade, this scenario would only result in the sporadic incidence of cutaneous anthrax with a lethality rate of about 20 per cent and rare cases of pulmonary anthrax, two forms of contagious disease that, taken together, can cause population mortality rates of fractions of 1 per cent (see above). It cannot be accepted as a serious proposition that


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88 Twigg 1984: 215.89 Trow-Smith 1957: 153–7, 240–1; Astill and Grant 1988: 216.

these forms of anthrax could have spread in large waves over the conti-nent and across England, causing havoc everywhere. Th is is why it has not been possible to adduce evidence to this eff ect.

Since Twigg is not able to provide evidence demonstrating the con-comitant spread of mortal epizootic disease among manorial herds during the Black Death, he is lead to emphasize his speculative approach. A few pages later he resorts to another pre-scientifi c work, this time by H. Harrod of 1867, which also speaks clearly for itself: “On the Manor of Heacham, Norfolk, there was murrain from 1346 to 1411 without pause and it attacked horses, cattle, sheep, pigs, chickens, ducks, geese, swans, pea-hens and even hives of bees.” It is, of course, impossible that the same zoonose should be the cause of an epizootic among all these animals. At the basis of this statement lies the mias-matic theory which is mono-causal and also can explain why birds and bees are severely hit, since miasma is spread by contaminated air. Finally, Twigg refers to E.L. Sabine’s paper on “Butchering in Medieval London” in which it is stated that the “periods of 1314–20 and 1346–89 were times of murrain among domestic animals,” in the second period also among poultry and wild birds, and specifi cally among sparrows in 1366.88 Th is should make it clear that “murrain” is a word used to des-ignate any or at least a large number of diseases among animals and that murrains in this more general meaning of zoonoses were an ordinary part of medieval life, before the Black Death and aft er the Black Death. Murrain is the contemporary concept of epizootic, equiv-alent to the contemporary concept of pestilence for epidemic; in the case of pestilence bleeding of human victims was usual, and in the case of murrain bleeding of livestock was usual.89 Importantly, Harrod and Sabine do not maintain that there was concomitant spread in time and space of murrains among domestic animals and mortality among peo-ple in the Black Death. Twigg has not produced evidence to the eff ect that anthrax spread concomitantly with the Black Death in England, as Campbell correctly points out.

Th e scholarly literature on the Black Death and subsequent plague epidemics typically consists of studies of outbreaks that are not pre-ceded by any epizootic among cattle and sheep. One important reason that epizootics among livestock did not usually develop on a grand


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90 Astill and Grant 1988: 216–7.91 Twigg 1984: 43–4.

scale comparable with the Black Death is that medieval people were not so helpless as Twigg must assume. Th ey had learned from long experience and made strong eff orts to contain the spread of murrain. “For example, animals that died of murrain were burnt, and their heads placed on stakes to tell travellers to avoid the area.”90 Th us, medieval people employed some of the main methods used today to eradicate epidemics of anthrax, foot-and-mouth-disease and scrapy. For the same important reason, medieval people did normally not eat domes-tic animals which had died from outbreaks of murrain, i.e., from dan-gerous epizootic diseases.

Th e Black Death’s Origin and Spread and the Anthrax Th eory

Twigg puts much emphasis on an account of the Black Death’s spread, especially the early phase, and he has an important reason or objective for doing so: “It is essential to examine the biological logistics of the Black Death in order to attempt to determine whether this particular epidemic could have been bubonic plague.” In his third chapter, titled “Th e Black Death – Origins and Spread to Europe” he says that his goal is “to examine the origin of the Black Death and the way it reached Europe, in the light of modern knowledge of plague biology.”91 Twigg wishes to use the history of the Black Death’s origin and spread to show that it is incompatible with bubonic plague but compatible with anthrax. Th is is a legitimate and potentially useful way to address the question of the microbiological identity of the Black Death and to con-sider possible alternatives. However, Twigg’s quite poor knowledge of medieval history and source-criticism and limited reading of the avail-able modern accounts of the history of the Black Death combine to result in various assertions and discussions which are out of line with reason and reality. Because so much of his account is factually wrong, for practical reasons only a small representative sample of data and arguments with relevance for his objective can be discussed.

Several contemporary chroniclers assert that the Black Death started in the lands of the Golden Horde in south-eastern Russia, in a region containing a large plague reservoir where people still contract bubonic plague today. Th ey also assert that it was spread by galleys from the


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92 Benedictow 2004: 44–73.93 Benedictow 2004: 50–2.94 Scott and Duncan 2004: 231, 242.95 Scott and Duncan 2004: 241–2.96 Twigg 1984: 47–55; Benedictow 2004: 17–21, 51–73. See also above chapter 4.

Italian trading station at Kaff a in the Crimea to Constantinople and seaports on the Mediterranean littoral. Th is outline of the origin of the Black Death can be safely confi rmed by the early history of outbreaks.92 It is correctly recognized as a serious threat to several of the alternative theories, because it establishes a continuous line from an area of a known plague reservoir to the introduction of plague in Constantinople and in important commercial hubs of the Mediterranean littoral. Th e threat to Twigg’s theory is especially great, since the chroniclers have nothing to say about epizootics among livestock spreading concomi-tantly with the Black Death in the regions where it broke out in the spring of 1346 and until it reached the camp of the army besieging Kaff a.93 Twigg and Scott and Duncan endeavour on erroneous grounds to claim that the Black Death could as well have come to Mediterranean Europe from Alexandria or Syria, and Scott and Duncan have pro-duced a map showing as established fact that the Black Death spread from Alexandria to Messina in Sicily.94 For Scott and Duncan it is cru-cially important to link the origin of the Black Death to Africa, since the haemorrhagic diseases of Ebola and Marburg are closely associated with Western Africa; the fact that these diseases have no known history in north-eastern Africa or the Middle East is ignored. Th ey also present a completely outdated and misleading map of the spread of the Black Death that does not show the origin in south-eastern Russia and the spread out of Kaff a (see below).

A central aspect of this topic is obviously the issue of the spread of plague over long distances. To his credit, Twigg is the only advocate of an alternative plague theory who attempts to do this explicitly in rela-tion to the Black Death’s fi rst phase of spread: most of the other advocates of alternative theories ignore the problem or accept unques-tioningly Twigg’s discussion of the problem as Scott and Duncan do.95

Twigg rejects the possibility of long-distance transportation of bubonic plague by ship from Kaff a by agency of the nexus of rats and fl eas on untenable grounds.96 However, a hundred pages later Twigg asserts that when bubonic plague was raging in India a hundred years ago, it was repeatedly transported from there by steamship all the long


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97 Twigg 1984: 47–54, 147.98 X. = Xenopsylla.99 Twigg 1984: 85.

100 Hirst 1953: 324, 330–1.101 Hirst 1953: 330–1.102 Pollitzer 1954: 387.

and time-consuming way to England. In this connection he states cor-rectly that “Ships represent the greatest danger of introducing plague, mainly by means of rats and fl eas in the cargo,” and goes on to mention a number of occasions when this occurred.97 In this passage, Twigg reveals that he is fully aware of the fact that bubonic plague spreads easily by ship over long distances, i.e., by metastatic leaps (per saltum), although he systematically refrains from taking it into account in his epidemiological analyses of the Black Death.

Th e reality of metastatic leaps refl ects the fact that rat fl eas can sur-vive away from their rat hosts for quite a number of weeks in humid and moderately warm climate typical of much transportation by ship, much longer than Twigg asserts, again without a substantiating foot-note: “although in ideal conditions X.98 cheopis may live for a month without its host it is doubtful if at the end of that time it could transmit plague.”99 Th is is strongly at variance with Hirst’s statement that in favourable circumstances, “at temperatures below 15° C. the chief vec-tor of bubonic plague, X. cheopis, can certainly survive in a very heavily infected state for at least fi ft y days,” and this is not the limit: “it is highly improbable, however, that the maximum longevity of unfed, infected rodent fl eas is known.”100 It can be usefully added that this rat fl ea sur-vives unfed in a very heavily infected state for 23 days at 27 °C. In Madagascar, researchers discovered that this rat fl ea could survive for months on grain debris,101 which demonstrates the signifi cance for the spread of plague of the transportation of corn and farina, which were the most common goods in medieval transportation.

Th e length of time dangerous rat fl eas can survive a voyage is further extended by the period of the epizootic among the ship’s rats that even-tually leads to the release of infected fl eas from dead rats in a situation where many of these fl eas do not fi nd new rat hosts. In this perspective, the number of rat colonies on board large ships such as galleys (and cogs) and also the relative localization of their territories in the ship take on signifi cant interest,102 since the strong reduction of a rat colony to this point takes ten to fourteen days (see above). Th is is at the


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103 Twigg 1984: 51.104 Twigg 1984: 45–7, 60–1. On these few pages, Hecker and Gasquet are referred to

fi ve and seven times respectively (and many more times elsewhere). Cf. Above: 565, fns. 35, 36.

105 Biraben 1975–1: 48–92; Biraben 1979: 30–40.

heart of the matter when Twigg correctly writes that the “galleys could therefore presumably support many rats,”103 because the presence of two or more rat colonies that were successively attacked by plague would readily add four or more weeks to the time preceding the point when rat fl eas would be on their own. Th e point is the following: rats defend their territories and the food resources within them and they respect the boundaries of adjacent rat territories in order to avoid being attacked, which means that another rat territory will not be invaded until its rat colony is severely reduced and unable to defend it. When the rats of an unaff ected rat colony invaded the territory of such a defenceless rat colony, they would pick up their fl eas, and thus the process would be repeated and the time horizon of the epizootic would be further extended and potential epidemic developments would be correspondingly postponed. Th us, there is a clear potential for a sub-stantially expanded time horizon before plague epidemics break out on galleys. For the same reason the long-term survival of infected rat fl eas will tend to be much longer than Twigg assumes.

If Twigg’s objective was to give a tenable, updated account of the early phase of the Black Death’s spread on the basis of best possible facts, it is diffi cult to understand the scholarly grounds for his prolifi c use of Hecker’s pre-scientifi c work on medieval epidemics of 1837 (posthumous reprint of 1859) and of Gasquet’s account written around 1890,104 and for his neglect of M.W. Dols’s fi ne monograph on the Black Death in the Middle East of 1977, or Biraben’s monograph on plague of 1975 or his paper of 1979,105 and several other excellent works that were available at the time he was writing his monograph. Th e vast majority of works on the Black Death were written not only aft er Hecker’s work but also aft er Gasquet’s, and this is the case for all works written aft er modern medicine, epidemiology and bacteriology were established.

Inevitably, Twigg’s temporal outline of the Black Death’s spread from the Crimea to the Mediterranean coasts is wrong, as is his outline of its further spread over Europe, even for his native England. Inexplicably, he provides a map of the Black Death’s spread across Europe that he informs his readers is taken from a small paper on the Black Death by


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106 Ziegler 1970: 106–7.107 Twigg 1984: 48–2, 49, 54, 55–3, 62, 78, 79–2, 82, 85, 90, 175, 189–4, 220.108 Carpentier 1962: 1062–92.109 Benedictow 2004: 1–2. See also the map in Benedictow 2005: 44.110 Benedictow 2004: 44–224.111 Scott and Duncan 2004: 29.112 Biraben 1975: 88–9.113 Biraben 1979: 30–40, map on p. 34.

W.L. Langer in Scientifi c American of 1964. However, Langer has not drawn it. It is also published in Ziegler’s monograph106 which he has used extensively, referring to him by name twenty times in his text.107 Th is map is taken from a general paper on famines and epidemics in the fourteenth century by É. Carpentier published in 1962, two years before Langer’s paper.108 In this paper, she makes a pioneering attempt at sketching an outline of the spread of the Black Death at an early stage of plague research based on quite a small sample of studies, which was due to her limited access to studies in other languages. Th e result was seriously fl awed, and it does not show the spread from the Crimea, which should have been important to Twigg given his point of depar-ture, but starts in Southern Europe. It is so inaccurate or erroneous for the spread of the Black Death in the British Isles that it is diffi cult to understand how a British scholar was not struck by it. How profoundly fl awed the map is can be easily ascertained by comparison with the map I provide in my monograph on the Black Death109 and is reprinted on page 2 above which is based on a detailed description of its spread over almost 200 pages taking into account the national research from all countries that were ravaged by it.110 Scott and Duncan also chose to republish Carpentier’s map, but since they too have chosen to ignore the standard requirement for scholarly monographs to provide foot-notes, nothing is said of the map’s origin or background, and they let their readers believe that it could be of their own making.111

Ten years before Twigg published his monograph, Biraben had pub-lished a much improved, although still defi cient, map of the Black Death’s spread across Europe.112 Twigg mentions this work in the two lines preceding Carpentier’s map, but on a point regarding the Black Death’s arrival in Bordeaux. Biraben’s very diff erent and much improved map shows the Black Death’s origin in the Crimea. In 1979, Biraben published a much improved map on the spread of the Black Death in the Middle East which should have been of particular interest to Twigg at the time he wrote his monograph, but it remains unmentioned.113


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114 Dols 1977: 36–7.115 Although Twigg has used the posthumous edition of 1859, 1837 is the real histo-

riographic age of the work.116 Twigg 1984: 46.117 Benedictow 2004: 63–4.118 Dols 1977: 182.

Also Dols renders a much better map than Carpentier’s in his fi ne monograph on the Black Death in the Middle East of 1977.114

What makes Carpentier’s map so attractive? Is it that it shows the spread of the Black Death at six-monthly intervals in long curved lines without refl ecting the important part that ship transportation played in the process of dissemination and thus “conceals” the role of metastatic leaps. Th e numerous indications of metastatic leaps by ship are exactly the conspicuous aspect of the map I have drawn, fully supported by evidence in my text.

Carpentier’s map does not show the Black Death’s spread out of south-eastern Russia from Kaff a on the Crimea by ship. Twigg can therefore indicate a theory of the Black Death’s geographical origin and route of spread to Europe very diff erent from the established view that it broke out in southern Russia and was spread from Kaff a by Italian galleys. Instead, he cites Hecker’s pre-scientifi c work of 1837115 where it is stated that “before the plague reached Europe it had killed daily, in Cairo, between 10,000 and 15,000 people.”116 Th is is wrong. In Egypt, the Black Death fi rst reached Alexandria in the early autumn of 1347 by a major metastatic leap from Constantinople, and this was the deci-sive epidemic event in this part of the world, which established the great epicentre of spread in the Middle East and North Africa. Th e Black Death’s spread out of this great and bustling city did not start until the late autumn, and by normal spread rates it did not reach Cairo until, as it seems, the summer of 1348,117 since the epidemic raged at its worst there in October–December.118 Th is also means that the Black Death had reached southern England and north-western France shortly before or at about the same time it reached Cairo, and had already rav-aged a large part of Europe. Mortality rates by plague cannot be dis-cussed on the basis of the type of information provided by Hecker. Dols’s careful specialist discussion of mortality rates is valuable. All this is uncritically taken over by Scott and Duncan.

Twigg’s assertion that the Black Death could have been shipped to Europe from Syria at the same time it was shipped from Kaff a is


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119 Twigg 1984: 46–7.120 Biraben 1979.121 Dols 1977: 57–60.122 Twigg 1984: 51, 54.

unfounded and untenable. Scott and Duncan accept this view, since it somewhat shortens the distance to West Africa which is the only known region where Ebola disease and Marburg disease occur. Th us, the Crimea is an impossible origin for their alternative contagion for ship-ment to Constantinople and the Mediterranean littoral. Th e fact is that the Black Death spread from Alexandria to Syria, was raging in Gaza in April and May of 1348 and in Damascus in July, a year aft er the out-break in Constantinople, and at the time when the Black Death had ravaged large parts of Southern Europe and had even begun spreading in England out of Melcombe Regis (Weymouth) and was closing in on Paris from Rouen. Twigg’s extensive use of Hecker’s pre-scientifi c work of 1837 for his account of the early spread of the Black Death is intrigu-ing.119 At the time he was writing his monograph, Twigg should have used Dols’s excellent study of 1977, also Biraben’s monograph of 1975 and his paper of 1979120 which have much valuable information to off er on this topic. However, Dols and Biraben are able to write their mono-graphs on the assumption that the Black Death was bubonic plague without landing in any obvious epidemiological diffi culties. Metastatic leaps of bubonic plague by ship play a central role, in the words of Dols, for instance: “Al-Maqrizi informs us that the Black Death reached Egypt in the early autumn of 748/1347—about the same time that it arrived in Sicily. It may have been spread simultaneously to Asia Minor and the Levant by merchant ships.” “Th e fact that the Black Death arrived in Egypt at approximately the same time that it reached Sicily would strongly suggest its transmission by the brisk Christian mari-time trade from the Black Sea and Constantinople.”121

Twigg’s eff orts to prove that the Black Death cannot have been bubonic plague are undermined by other serious weaknesses of facts and assumptions. Twigg states that the “Genoese would, at the earliest, have left Kaff a during October and at the latest by December,” and assumes arbitrarily that the Genoese galleys which he claims arrived in their home city in January had been sailing directly from Kaff a.122 Th is is wrong: in Constantinople the outbreak was recognized in early July, which in the case of bubonic plague means that the contamination was introduced in early May. Actually, chroniclers mention that Genoese


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123 Benedictow 2004: 60–5, 69–73; Dols 1977: 53.124 Twigg 1984: 46.125 Benedictow 2004: 53, 63–4, 69–73, 96–101.126 Twigg 1984: 55.127 Dols 1977: 53–61.128 Twigg 1984: 54.129 Twigg 2984: 47.130 Benedictow 2004: 127.131 Benedictow 2004: 61.

galleys fl ed from Kaff a in the spring of 1347 and contaminated the metropolis, which as can easily be seen fi ts the facts.123 It can be shown that Twigg knows these accounts.124 Th e temporal progression of these accounts also fi ts with the central facts of the further spread: the out-breaks in Alexandria in early autumn 1347, in Messina on Sicily at the end of September and in Marseille by 1 November,125 not in February, as Twigg asserts.126 Th ese facts are related in considerable detail in Dols’s monograph.127 In this way, Twigg clears the ground for an argu-ment to the eff ect that “Flea breeding must have been very low at that time both on ship and ashore.”128 On the contrary, many of these events took place at the height of the fl ea-breeding season.

Twigg is very reluctant to take into account the fact that Constanti-nople was contaminated in the Black Death’s fi rst phase of spread by galleys that had fl ed from Kaff a, making only an off -hand comment that Gasquet (1908) thinks that plague was “probably carried” from Kaff a to Constantinople.129 Twigg attempts to avoid or downplay the point that Constantinople could function as an intermediary base for further dissemination into the Mediterranean littoral by other ships contaminated in the harbours of the metropolis, and that they could even have been contaminated before the outbreak by exchange of goods, in a similar way to what was reported to have occurred in the harbour of Melcombe Regis (Weymouth) in England.130

Twigg needs to adduce evidence to the eff ect that long voyages are incompatible with plague biology and argues his case on the assump-tion that all ships from Kaff a sailed directly to their Mediterranean des-tinations, mainly Venice and Genoa, which makes the continuous voyage at sea (i.e., without stops for trade or to acquire supplies) as long as possible. It enables him also to ignore the notion that many of the ships which spread plague along the Mediterranean coasts in the autumn of 1347 could have been contaminated in Constantinople.131 Crucially, Twigg does not mention that the Genoese and Venetians


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132 Th e ancient Greek colony of Tyras, later called Akkerman, from 1946 with the Slavic name of Belgorod(-Dnestrovskiy), in Romanian Cetatea Alba.

133 Pounds 1974: 360–7.134 Lopez 1976: 109.135 Bratianu 1929; Pounds 1974: 360–8.136 Byrne 1930/1970: 36–7, 44, 52.

along the shipping lanes had quite number of other minor trading sta-tions and ports that they used for rest and provisioning. In the words of N.J.G. Pounds, there was “a ring of trading stations along its [the Black Sea’s] coastline,” for instance, Mauro Castro on the estuary of the Dnestr and Trebizond,132 and aft er having left Constantinople, for instance, Chios, Nauplion, Coron, Modon and Monemvasia, Corfú (Kerkyra) on the shores of Greece, and on the last stretch homewards up the Adriatic the Venetians used the ports of Ragusa (Dubrovnik), Spalato (Split) and Zara (Zadar), whilst the Genoese especially used the ports of Messina and Naples for their last stretch homewards.133 Th is also means that they had the opportunity to halt the voyage for shorter or longer periods of time and to hire additional sailors. Even an elementary introduction to the commercial history of the Middle Ages like R.S. Lopez’s fi ne little monograph Th e Commercial Revolution of the Middle Ages, 950–1300 mentions that “the Genoese established a cluster of colonial outposts all around the Black Sea.”134 Th us, Twigg’s presump-tion that returning Venetian and Genoese galleys would have to sail directly to their patriae is without basis in elementary facts of medieval trade history. In this way, Twigg has construed an artifi cial argument against bubonic plague being shipped out of a region where there is a permanent plague reservoir in order to clear the ground for his own theory, although no concomitant epidemic of anthrax is mentioned in the lands of the Golden Horde by the chroniclers (see above).135

For his presentation of the routes of the Italian galleys homewards from their easternmost trading station at Kaff a Twigg refers to E.H. Byrne’s small monograph on Genoese shipping in the High Middle Ages. However, this work is oriented towards their western trade routes, towards Barcelona, Málaga, Tunisia and Ceuta, and towards the Levant. It focuses on topics relating to shipping and business and relates rather peripherally to actual sailing and the system of sea lanes and ports used along the routes. Nonetheless, Byrne gives some pieces of information on ports of call along the sailing routes.136 As can be seen, much more useful information on this topic can be found in modern standard


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137 Twigg 1984: 52, 54.138 See above: 78–82, 219–24.139 Creighton 1894: 144–9.140 Twigg 1984: 52, cf. 54. Twigg’s italics; Creighton 1891: 148–9.141 Benedictow 2004: 52–3.142 Cited aft er Gasquet 1908: 19–20.

works on medieval economy like Pound’s still very useful monograph of 1974 which has also a rich standard apparatus of footnotes as well as fi ne bibliographical entries at the end of each chapter—as scholarly books should.137

Medieval chroniclers’ rhetorical exaggerations and loose relation-ship with facts are some of their most obvious features. What medieval chroniclers assert and what they do not mention are a rich source of great surprises to modern scholars.138 For this reason, assertions of the pace of spread that cannot be tested against independent sources, and in cases of data relating to cities, against local population records, can-not be accepted. Twigg considers it appropriate, on the contrary, to cite the chronicler Gabriele de Mussis, but he cites him indirectly, accord-ing to Creighton’s summary,139 who was, as pointed out above, the last champion of miasmatic theory in England. Twigg cites Creighton to the eff ect that,

there were no cases of plague on board ships, although the very atmos-phere or smell of the new arrival seemed suffi cient to taint the whole air of Genoa and to carry death to every part of the city within a couple of days.140

Firstly, as already pointed out by Gasquet, it is not true, as Creighton repeatedly asserts, that Gabriele de Mussis had himself been in Kaff a and left with a Genoese galley for his home town and that his account therefore is based on personal observation. In fact, de Mussis stayed in his home town of Piacenza and pieced together his account on the basis of what he heard from sailors or merchants and other sources of hear-say. His account can readily be shown to be based on misinformation and misconceptions and miasmatic notions.141 It is also not true that there were no cases of plague on board: “It so happened that when the ships left Caff a—some bound for Genoa, some for Venice, and some to other parts of the Christian world—a few of the sailors were already infected.”142 Obviously, Creighton shapes his summary of de Mussis’s account in a way that serves his campaign for miasmatic theory against the rise of the new science of bacteriology or microbiology and puts


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143 Benedictow 2004: 52–3.144 Twigg 1984: 45–7, 56–7, 60–1, 70, 103, 202–4, 207.145 I have assumed that Twigg did not believe that the galleys arrived from Kaff a full

of contaminated wool that was immediately spread all over the city and that the great majority of Genoa’s inhabitants were woolsorters who en mass contracted anthrax by inhalation, and even this fl ight of fancy would be insuffi cient for explanation, since we also must assume that the woolsorters did not early detect that work with wool at the

special emphasis on the theory that the ships carried merchandise con-taminated with miasma. And in fact de Mussis’s account is formed according to contemporary miasmatic notions of epidemic disease.143 Creighton’s presentation of this material is therefore doubly imbued by miasmatic notions. Twigg neglects the basic approach of the historian’s craft , namely to identify the original source and start source-critical work from there, or he would have noted Gasquet’s correct rendering of de Mussis account, a work he knows well and refers to by the author’s name twenty-three times in his running text.144 Miasmatic notions can imply extreme contagiousness by touch and extreme spread rates since spread is not dependent on contact but is eff ected by wind. On this basis, Twigg can conclude that the disease introduced from Kaff a to Genoa could not have been bubonic plague. However, would any epi-demic disease known to modern medical science spread across Genoa in a couple of days, even intensely infectious diseases like smallpox or infl uenza, since they are dependent on interpersonal contact for trans-mission? Is it not only miasmatically contaminated air that can spread an epidemic disease in this way, because people will inhale it as it blows down their streets and in through their windows? Is it really a medi-cally and epidemiologically qualitative diff erence between de Mussis’s, Creighton’s and Twigg’s accounts? Are they not all based on miasmatic assumptions?

Scott and Duncan take great interest in much the same events, namely the Genoese galleys’ arrival in Messina on Sicily, and subse-quently in their home town. Th ey take over wholesale Twigg’s argu-ments which can seemingly serve to undermine the bubonic-plague theory and as such clear the ground for their own alternative theory.

De Mussis’s account is in fact yet another defi nite proof that the dis-ease was not anthrax. It cannot be accepted that the galleys arrived in Genoa from Kaff a with herds of cattle or sheep on board which were seriously sick from or had recently died from anthrax and that the pop-ulation of Genoa eagerly consumed the fl esh of these animals all across the city with extraordinary epidemic speed, actually in two days.145


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time was extremely dangerous. Of course, signifi cant epidemic outbreaks of pulmo-nary anthrax have so far not been discovered.

146 Benedictow 2004: 285–91.147 Benedictow 2004: 71; Twigg 1984: 55.148 Twigg 1984: 55.149 Anglada 1869.150 Ziegler 1969: 64, 293, 312.

According to elementary scientifi c principles, Twigg should be obliged to demonstrate in concrete detail how this could have been possible and on this basis form a realistic and tenable explanatory model; the fact that he has declined to do so means that his assertion is unfounded and can be taken as evidence that such modelling is impossible. Even if every inhabitant of Genoa were infected, the lethality rate would only have been about 20 per cent, only a fraction of Italian mortality rates in the Black Death estimated on the basis of population records and other types of demographic sources, for instance one-third of the mortality rate in Florence.146 Also Scott’s and Duncan’s alternative theory of a fi loviridal disease is excluded, since these diseases spread only by direct physical contact and transmission of living contaminated cells, which makes for an exceedingly slow spread and tiny outbreaks (see below).

Th e outbreak in Genoa appears to have been recognized at the end of 1347, not in January, as Twigg states.147 Assuming that it was bubonic plague, the contamination would have been introduced into the city about seven weeks earlier and would have had much time to prepare the ground for an outbreak in January aft er having developed for at least a couple of months, provided that the temperature was moder-ately chilly for the season. However, there is no source material availa-ble which can provide an empirical basis for a spatio-temporal outline of the Black Death’s spread across the city. Th e inherent dangers of accepting the “overwrought imaginings” and “hopelessly inaccurate quantifi cations” of medieval chroniclers can be further illustrated.

Twigg’s monograph exhibits no trace of the scepticism of medieval sources and the great importance of source-criticism that is uppermost in the minds of all medievalists worth their salt. Twigg claims, for instance, that 56,000 persons died from the Black Death in Marseilles.148 Th is fi gure is taken from Ziegler’s monograph, and since Ziegler, according to the ordinary standards of scholarly work, provides a supporting footnote it can be ascertained that it comes from a pre- scientifi c149 study of 1869,150 which allows identifi cation of the original source as a contemporary chronicle. However, Ziegler took this fi gure


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151 Gasquet 1908: 39.152 Baratier 1961: 66–7.153 Normal demographic adjustments with respect to the population growth in the

time between the end of the epidemic and the writing of the registers indicates rather a mortality among the householders of 54–55 per cent.

154 Benedictow 2004: 308–15.155 Twigg 1984: 55–62; Benedictow 2004: 126–45.

and its footnote from Gasquet’s monograph who more accurately informs his readers that the fi gure is 57,000, represents the death toll for a month and, therefore, constituted only a small part of the total mortality which according to the implied information must in the end have numbered hundreds of thousands of victims.151 Th us, this is a case of serial uncritical and careless copying of information in which only the fi rst author has read the original study and none has read the origi-nal source or applied source-criticism. Th is type of serial dependence characterizes Twigg’s historical account as a whole (far more than Gasquet’s and Ziegler’s monographs).

Th e demographic history of Provence has been written, although Twigg has not taken account of this. According to E. Baratier, the expert on Provence’s medieval and early modern demography, the city of Marseilles contained only about 15,000 inhabitants in 1315, and pre-sumably also on the eve of the Black Death,152 a piece of information that at the time Twigg wrote his theory had been available for almost a generation, and was also available to Ziegler. Th us, Twigg is prepared to accept and to convey to his readers the suggestion that fi ve times as many people died in the Black Death in Marseilles in one month of the epidemic as actually lived there. According to Baratier’s study, 52–3 per cent of the householders in Provence died in the Black Death, both in the urban centres and in the countryside,153 which corresponds to a population mortality rate of about 60 per cent.154 Th is means that Twigg by ignoring Baratier’s work avoids citing this order of population mor-tality for a large region and explaining how it can be compatible with the mortality rates of anthrax. He has also failed to fi nd empirical data showing or at least suggesting the concomitant raging of an anthrax epidemic among cattle and sheep and to demonstrate that there is close contemporaneity between the spread of the Black Death among human beings and the spread of an anthrax epizootic.

Twigg’s account of the Black Death’s spread out of Marseilles, a mile-stone in its history, and its extension into a much broader picture of its spread across large parts of Europe is also wrong.155 Th e crucial point is


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156 Benedictow 2004: 107–8; Dubois 1988: 316.157 Benedictow 2004: 97–9, 101–8. Cf. Dubois 1988: 314–6.158 Twigg states that the source for his (misleading) presentation of the Black Death’s

spread out of Paris is Gasquet’s monograph of 1908, however his text is very close, al-most a verbatim, rendering of Ziegler’s account which is largely but not entirely based on Gasquet’s account. Twigg 1984: 56–7; Ziegler 1969: 64–5. Cf. Gasquet 1908: 39–53.

159 Benedictow 2004: 126–8.

his untenable assumption that bubonic plague spreads only by contact between contiguous rat colonies: “If it is assumed that rat populations were contiguous throughout the region—and they would need have been—the rate of spread across France is as follows […].” It is this false premise, the denial that bubonic plague spreads over distances by met-astatic leaps by rat fl eas in clothing, luggage or merchandise, which permits Twigg to construct obviously untenable spread rates from Marseilles to Carcassone or from Carcassone to Bordeaux or from Marseilles to Avignon or from Avignon to Lyon, or from Marseilles to Paris, thus producing phoney proof that the Black Death cannot have been bubonic plague. All his indications of the Black Death’s time of arrival at these locations are systematically erroneous and his spread rates correspondingly misleading. According to Twigg’s account, the Black Death spreading northwards from Lyon should have broken out in Burgundy in July and August and inexplicably have reached Paris in time to break out there in June. However, the Black Death did not break out in Paris in June, but towards the end of the third week of August.156 Th is highlights the important fact that the Black Death did not spread from Marseilles to Paris, but from Rouen to Paris,157 because it arrived in Rouen with a ship from Bordeaux by an instance of a metastatic leap, and produced an outbreak which began 24 June.158

Twigg’s rejection of the notion that bubonic plague spreads by leaps and acceptance of obsolete miasmatic and erroneous information on the spatio-temporal progression of the Black Death across Europe combine to make his discussion of the events in his own country quite absurd. He seems to accept that the Black Death broke out fi rst in the southern seaport of Melcombe Regis (Weymouth), shortly before 24 June, referring indirectly to the Grey Friars Chronicle which provides this information, but then all reason evaporates. “Th ere can only be speculation about where it came from,” he asserts, although it is une-quivocally stated in the Chronicle with some concrete detail that it came with a ship from Gascony.159 Th is is normally and reasonably taken to mean that the Black Death was brought to England by a ship from


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160 Benedictow 2004: 101–4,161 Biraben 1975: 74; Dubois 1988: 316; Benedictow 2004: 108.162 According to the information provided by the chroniclers, plague broke out in

Melcombe Regis shortly before 24 June, in Rouen about 24 June, a small diff erence in time which probably refl ects the fact that Rouen was a considerably larger urban cen-tre, a city of some 30,000 inhabitants; quite likely these two urban centres were con-taminated at the same time.

163 Ziegler 1970: 125.164 Benedictow 2004: 126–34, 137–40.

Bordeaux where the Black Death had been raging for several months.160 Rouen was infected by a ship from Bordeaux which caused an outbreak there almost simultaneously with the outbreak in Melcombe Regis (Weymouth). However, Twigg speculates that the contagion could have been shipped from Calais to Melcombe Regis, although the Black Death broke out in Calais in December, half a year later than in Melcombe Regis.161 He also speculates that the Black Death could have arrived in Melcombe Regis from northern French ports or the Channel Islands. Th e earliest outbreak in a northern French port is the outbreak in Rouen which does not precede but is about simultaneous with the out-break in Melcombe Regis, which could suggest that these two seaports were contaminated by ships sailing from Bordeaux in the same convoy, as merchant ships oft en did at the time.162 Th e suggestion of an origin in the Channel Islands is not based on a dateable source and cannot be used for determining the Black Death’s time of arrival.163 Twigg assumes also that the Black Death could have been on board ships sailing directly from the Mediterranean. Th is implies that at a time of unique disaster and immense diffi culties for organizing great trade expeditions, galleys should have left Genoa or Venice unusually early for a voyage of roughly 4500 km for the Genoese with a duration of roughly three to four months and substantially longer for the Venetians. If the disease they brought with them had been anthrax, the voyage would have taken place with contaminated herds of live cattle or sheep on board which immediately on arrival alongside the quay of the harbour of Melcombe Regis would have to be driven through England. I cannot imagine how this disease could function on board among animals and men for such a long journey, but the burden of proof is on Twigg. Twigg goes on to cite other chroniclers with later datings of the original outbreak in England and other ports of arrival, although none of these alternatives are compatible with the known pattern of early spread in England which is based on the sources.164


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165 Twigg 1984: 57–68; Benedictow 2004: 126–45.166 Twigg 1984: 58; Benedictow 2004: 142, cf. 229–31.167 Twigg 1984: 72.

Twigg’s account of the spread of the Black Death in England is unten-able, as shown also above in the chapter on seasonality.165 Th e main reason is that Twigg bases his account of the Black Death’s spread across England on the false assumption that spread over land was dependent on rat-to-rat contact, according to the scholarly myth he pioneered that bubonic plague spreads only between contiguous rat colonies. Th is enables him to assert correctly that this mechanism of spread could not produce the observed pace of spread, “not even one and a half miles per day.” Actually the average pace of spread on the ground of the Black Death in England was substantially slower, about 1–1.5 km a day, which still is much faster than the spread rate between conterminous rat colo-nies.166 Twigg denies that human beings perform the central role in the spread of plague by transporting infected rat fl eas in clothing, luggage or goods, by ship or by land, bringing about metastatic spread. His con-clusion is therefore based on the denial of fact. Th is argument is taken over by Scott and Duncan: they accept unconditionally his account of the spread of the Black Death in England.

Twigg’s Demographic Argument

It is important for Twigg to argue for the lowest possible level of mor-tality in the Black Death in the hope that it will not be obviously incom-patible with his highly exaggerated and speculative assertions of mortality causable by anthrax (see above). In his view, the “mortality in the years 1348–9 has frequently been exaggerated and treated as though no other epidemic periods could be compared to it.”167 For this view he provides no reference. At the time Twigg was writing his monograph, there was a broad consensus on the level of mortality caused by the Black Death, namely Hatcher’s estimate of 1977 in a small but outstand-ing book on the interaction of economic, demographic and plague-related developments in late medieval England. Highly conscious of the fact that the vast majority of the population was constituted by peas-ants in the broadest sense of the term Hatcher based his estimate mainly on manorial and other types of local mortality data. However, due to a certain paucity of data he also underlines the signifi cance of the


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168 Hatcher 1977: 21–6.169 Titow 1978: 466.170 Hollingsworth 1969: 58.171 Hatcher 1977: 13.172 Postan 1966: 561–2; Ohlin 1966: 78–80; Hatcher 1977: 23–4.

mortality rates for the benefi ced clergy who had much the same territorial distribution but highly diff erent characteristics as a social category. He concludes that this material bears “testimony, with a lack of precision but a compelling force, to a death rate of at least 30–5 per cent,” and that the “most judicious estimate of the national death-rate in 1348–9 in the present state of knowledge: 30–45 per cent.”168 In Hatcher’s view, the minimum mortality level was thus about a third of the population, the average apparently nearly 40 per cent. One should note that Hatcher in the gentlemanly tradition of Oxbridge academics seeks a cautious balance of the facts with respect to the mortality esti-mate, which makes J. Titow, the highly regarded English agricultural historian, remark in his review of the book that “it is diffi cult to see on the evidence here assembled, how it could have possibly been any lower.”169 Obviously, this level of mortality was much too high to be compatible with Twigg’s theory.

Presumably, this is the reason Twigg turns instead to Russell’s pio-neering monograph British Medieval Population of 1948 for his mortal-ity data. Th is means that he must pass in silence by the comprehensive and sharp criticism of this work and also much fi ne new research that had been published in the following thirty-six years. Russell engages in little source-criticism and he makes a number of assumptions with respect to central demographic structures and developments that have been quite generally rejected in the discussion following the mono-graph’s publication. In 1969, T.H. Hollingsworth generously concluded that “Russell’s chief virtue, in fact, is that he gives others something to refute. All his fi gures may be altered eventually, but the debt to him will remain.”170 Or as Hatcher also elegantly formulates his view: “One of the major sources of nonconformist beliefs is the work of J.C. Russell.”171 For quite a number of solid scholarly reasons, the mortality fi gures have been subjected to particularly damaging criticism, for instance by M. Postan, G. Ohlin, and Hatcher.172

In this context, the very special nature of Russell’s material on mortality in the Black Death must be strongly emphasized. It relates to the mortality among tenants-in-chief, the supreme and extremely


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173 Russell 1948: 214–8.174 Russell 1948: 216.175 See, for instance, Hatcher 1977: 24. Cf. above: 421–2; Benedictow 2004: 342.176 Hatcher 1977: 23–4.177 Coale and Demeny 1983: 43. See, also, Benedictow 2004: 249, 350.

exclusive class of feudal nobles who held land directly from the king, the barons of the realm; he based his research on a category of docu-ments called inquisitions post mortem which eff ectuated the transfer of such feudal land following the death of the possessor (in the epidemic).173 Th e social unrepresentativeness for inference to general mortality and distribution of mortality according to age, gender and social class more generally is overwhelming. It contrasts sharply with Hatcher’s endeav-ours, in accordance with the basic tenets of sociology and demography, to base his general mortality estimate as much as possible on data rep-resentative of the social classes constituting the vast majority of the population.

Technically, Russell used a population of tenants-in-chief of 505 per-sons of whom 138 or just over 27 per cent died, but this fi gure is beset by severe problems.174 Th e mortality of 138 tenants-in-chief is much too small to constitute a base for reliable statistical inferences and too unrepresentative both with respect to social class and with respect to age to be of any use for generalizations with respect to general mortal-ity or mortality according to age or gender.175 Conspicuously, 23 per cent of the population of tenants-in-chief died in the following plague epidemic of 1361–2, despite general agreement that this was a much smaller epidemic: Hatcher is obviously right in his conclusion that this refl ects the fact that the samples are too small to provide useful statistics.176

With respect to the younger age categories, this material is so tiny that estimates of mortality based on it or including it must be rejected as useless. It comprises no infants who, in the case of males according to Model West life table, level 4 (life expectancy at birth of 25 years), are liable to a normal mortality rate of 32 per cent,177 but according to these statistics astonishingly suff ered no case of mortality in the year of the Black Death. Ages 1–5 are represented by three children of whom one died making for a mortality rate of 33 per cent for these fi ve age catego-ries, which is, of course, a valueless exercise in statistics. Only one of thirteen children of ages 6–10 died, producing an incredibly low mortality rate of 7 per cent in the Black Death, whilst, according to the


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178 See Benedictow 2004: 350.179 Benedictow 2004: 342, 350.180 Hatcher 1977: 24.181 Razi 1980: 104.182 Rusell 1948: 231.183 Russell 1948: 262. “Th e information from the table (10.13) suff ers from being a

relatively small sample.”184 Twigg 1984: 63.185 Twigg 1984: 63.

life table, normal mortality in these ages would be 19.5 per cent.178 According to Russell’s material, children of these ages had the luck to have only a small fraction of their normal mortality in the year of the Black Death. Th is is the reason I have previously rejected using the material gathered by Russell for mortality estimates.179 Hatcher points out that, according to evidence from the chronicles, the Black Death “struck mainly at people in the prime of life” but underlines carefully the great uncertainty associated with this type of evidence.180 However, a few years later Z. Razi’s study of the manor of Halesowen appeared, which Twigg could have put to good use. Here Razi concludes that “the child mortality in the Black Death was very heavy,” that, in fact, “child mortality in the plague must have been catastrophic.”181 Quite a number of pages away from his table, Russell points out that the “chroniclers have to tell of very heavy mortality of children.”182 However, using a wording echoing Russell’s own endeavours to minimize the impression of seriously fl awed material183 and ignoring the severe criticism of it, Twigg notes with considerable understatement that this material con-stitutes “an unfortunately small sample,”184 (unfortunately) without specifying the methodological and source-critical implications of the characteristic “unfortunately.” Th is permits Twigg to proceed to use Russell’s material as if the sample is not “unfortunately small,” as if it is not too small and mortally fl awed for almost any demographic use.

Undaunted, Twigg goes on to use Russell’s estimates both of general mortality and age-distribution of mortality in the Black Death. He starts with age-distribution which, according to demographic science, is particularly demanding with respect to the quality of material. His point of departure is the valid argument that diseases vary in the mor-tality rates they infl ict on specifi c age classes and “if this information is available and is accurate it can be of some assistance in helping to nar-row the fi eld in the identifi cation of past epidemics.”185 Surprisingly,


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186 Russell 1948: 216–7.187 Ohlin 1966: 78–80.188 Since Twigg does not provide a footnote to this comprehensive material pub-

lished by the Commission this year (which may suggest a secondary source of informa-tion), I will give it: IPRC 1907g: 763.

189 Twigg 1984: 63–4.

Twigg pretends that such information is “available” and “accurate” in the form of Russell’s fi gures, which is at variance with all comments by other scholars. Russell concluded that the plague fell more heavily on older men than on the young.186 G. Ohlin, the demographer, challenged this conclusion, and demonstrated that Russell’s source-critical and statistical approaches were fl awed and that age, according to this source material, made no diff erence to this particular risk of death in this social class,187 a piece of important information that was available to Twigg but is ignored or overlooked. Th is means that Twigg’s age-specifi c premise is untenable.

However, this is only a disappointing beginning. Twigg goes on to argue that the Black Death and bubonic plague in India around 1900 were diff erent diseases. He asserts that this can be demonstrated by comparing Russell’s table showing the age-distribution of the mortality in the countryside among the English baronial class in the Black Death in 1348–9 and a table produced by the IPRC in 1907 showing mortality in bubonic plague in Mumbai City among a caste-structured popula-tion consisting mainly of poor and destitute social classes.188 On this basis, he concludes that it is “clear without any elaboration that there is considerable diff erence between these two disease mortality patterns”189 and that this constitutes evidence that the Black Death could not have been bubonic plague, but must have been some other disease. Ignoring for the moment the devastating criticism of Russell’s material, this rep-resents neglect of basic sociology and social science as integral parts of demography and epidemiology. It would have been sensational at least or rather inexplicable if these two tables had showed similar distribu-tion of age-related mortality. Th e only acceptable usage of such a com-parison is to demonstrate the diff erentiation of mortality pattern caused by great disparity in social, economic, political and cultural circum-stances. It is exactly the absence of “elaboration” according to social science that permits Twigg to make this inference. On the same page, the IPRC gives mortality fi gures distributed according to religion showing strong diff erentiation of mortality according to this criterion


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190 IPRC 1907g: 763–4.191 Scott and Duncan 2001: 111–2.192 See, for instance, Benedictow 2004: 249.193 See. e.g., Titow 1969: 68; Hatcher 1977: 22–4; Razi 1980: 100; Benedictow 2004:

342.194 Russell 1948: 216, 230.195 Postan 1966: 561–2; Hatcher 1977: 13–4; Titow 1969: 67–8, 84–5; Benedictow

2004: 259–60.

alone.190 Th is use of Russell’s data is uncritically taken over and pre-sented by Scott and Duncan as proof that the Black Death could not have been bubonic plague because in comparison to the epidemic real-ities in India “the overall mortality of bubonic plague is much lower” and “killed predominantly those in the 6–40 year age group.”191 If Scott and Duncan had taken interest in English medieval demography which is at the heart of the matter here, they would have known that in a population with an average life expectancy at birth of around 25 years the “6–40 year age group” constituted the predominant proportion of the population.192

Next, Twigg turns to the question of general population mortality. Russell dares to claim that the mortality of the nobility is representative of general population mortality. Th is assertion must be dismissed out of hand, which has been emphatically done by several scholars.193 Inference to general population mortality on the basis of this material is an obvious fallacy of the methodology of social science. Th e assertion fl ies in the face of one of the central fi ndings of demography, namely that mortality across European society in time and space tends to be strongly skewed according to age, gender and social class. Th e general predilection of the Grim Reaper for infants, young children, poor and destitute people, and his relative lenience with the upper classes, are documented beyond all reasonable doubt or dispute. Russell argues, also erroneously, on the basis of the skewed age-structure of his data that real mortality must have been lower than the 27 per cent shown by his material (138 deaths among 505 tenants-in-chief).194 Using in addi-tion the Poll-Tax registers of 1377 for retrospective analysis, in a way that has also been severely criticized,195 he concludes with a mortality rate for tenants-in-chief of 20 per cent, which is directly transformed into an estimate of general population mortality. Th is estimate is enthu-siastically accepted by Twigg as the point of departure for his own discussion of the level of mortality, disregarding Hatcher’s serious


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196 Hatcher 1977: 13.197 Hatcher 1977: 68; Hatcher and Miller 1978: 29; Smith 1988: 191. Cf. Miller and

Hatcher 1995: 393; Hatcher and Bailey 2001: 31.198 Hallam 1988: 536–7; Smith 1991: 48–9.199 Hatcher and Bailey 2001: 31.200 Russell 1948: 263.

warning: “there are strong reasons for believing that Russell’s estimates of English population in 1348 and 1377 are gross understatements.”196

Russell’s estimate can be dismantled in various ways, not only on the basis of the small size of the material and of its lack of social diversity and representativeness. Twigg must be the only scholar in the last sixty years who accepted Russell’s contention that average household size in medieval England was 3.5 persons, and not 4.5, which alone makes for a diff erence of almost 30 per cent in population size. On this basis, Russell estimates England’s population on the eve of the Black Death at 3,757,000 inhabitants. Th is estimate diff ers sharply from Hatcher’s esti-mate in his widely admired account of 1977, a generation later, of “4.5–6 million, with the balance of possibilities pointing to the higher reaches of this range.” Already the following year, in a study therefore also available to Twigg, the minimum side of this estimate was revised upwards by E. Miller and Hatcher to 5–6 million people, an estimate with which R.M. Smith agreed a decade later.197 Th is development regarding pre-plague population estimates casts sharp light on the weakness inherent in Russell’s pre-plague population estimate. Th is is also the case with later estimates of late medieval English population size. In 1988, Hallam revised the population estimate further upwards to about six million inhabitants on the eve of the Black Death, with which again Smith agreed a few years later,198 and this is the present status of research on which there is broad agreement among British scholars in the fi eld of medieval demography; Hatcher and Bailey also appear close to accepting this fi gure in 2001.199 On the ground of popu-lation estimates alone, mortality in the Black Death must have been very much higher than Russell claimed. According to Russell, the English population was around 2.25 million immediately following the Black Death,200 an estimate which is quite close to prevailing scholarly opinion. Th is means that, at the time Twigg wrote his monograph, combining the prevailing scholarly opinion on pre-plague population size and Russell’s post-plague population estimate, the mortality caused by the Black Death had reduced the population from 5–6 million to


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201 Benedictow 2004: 360–7.202 Benedictow 2004: 362–77.203 Russell 1948: 221–2, 230.204 Twigg 1984: 59.205 Gasquet 1908: 86.206 Th e concept of plurality refers to the quite frequent occurrence that the incum-

bent also held (an)other benefi ce(s) and was represented in the parish by his vicar.

2.25 million, or by 46–62.5 per cent. Shortly aft erwards, the population estimate of about six million on the eve of the Black Death was confi rmed and accepted, meaning that the fi gure of 62.5 per cent was confi rmed according to the premises laid down here. Th is is exactly the fi gure at which I arrived on the basis of my analysis of seventy-nine manorial studies,201 most of which were available to Twigg at the time he wrote his monograph. Why did Twigg not collect the data on mano-rial mortality rates as I did, providing a broad picture of mortality among the peasant classes who constituted the vast majority of the English population? As my data unequivocally show, the mortality rate among the customary tenants who represent the upper classes of peas-ant society must have been in the order of 55 per cent. Supermortality among the rural proletariat, the all-but-landless classes and among children and women means that the real population mortality rate must have been signifi cantly higher.202

In addition, at the time Russell and Twigg wrote their monographs the mortality rates of the benefi ced parish clergy was known to be at least or close to 40 per cent, which Russell in reality gives up on explain-ing.203 Twigg makes considerable eff orts to undermine the mortality studies based on institutions of the benefi ced clergy during the Black Death. He starts by asserting erroneously: “It is generally accepted that the vacation of a benefi ce automatically implies the death of the incum-bent and some writers have assumed that all vacations during 1348–9 were due to death from plague.”204 Th is has, as mentioned, certainly not been true since Seebohm’s work of 1865 and possibly until Gasquet’s monograph appeared in 1893 where it is made clear that vacancies were due not only to death but also to “exchange, or resignation” and that such cases must be deducted.205 Twigg’s statement is fol-lowed by a reference to Th ompson’s work of 1947 on the organization of the English clergy in the Late Middle Ages. However, the point that vacancies were due also to resignations, exchanges of livings, plurali-ties206 and absenteeism is strongly emphasized by Th ompson in his


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207 Th ompson 1911: 303–4, 315–6; Th ompson 1914: 97–102.208 Hatcher 1977: 25.209 Benedictow 2004: 354–7.210 Hatcher 1977: 25.211 Benedictow 2004: 356.

pioneering studies of 1911 and 1914 of the registers of institutions of the dioceses of Lincoln and York.207 Th is has since been generally taken into account by scholars; Hatcher for example states that “one has to be especially careful to eliminate all vacancies excepting those arising from death.”208 However, if Twigg had mentioned Th ompson’s two excellent studies, it would be diffi cult for him to avoid mentioning that aft er having taken these problems of resignations of vacancies into account and deducted them from the material, Th ompson still found mortality rates of 40.2 and 44.2 per cent respectively, without taking into account institutions in vacancies caused by the Black Death per-formed in the following couple of years, which would have added sub-stantially to the mortality rates (see above). Lunn’s study of the diocese of Coventry and Lichfi eld’s bishop’s register where also all resignations are noted have produced a mortality rate of 40.1 per cent, likewise without taking into account Black Death-related institutions in vacan-cies which were fi lled in the following couple of years. Pickard found a mortality rate among parish priests in the diocese of Exeter of 51.5 per cent in the period of the Black Death, but when surplus institutions aft er deduction of normal mortality in the following years are taken into account, the real mortality rate appears to have been about ten percentage points higher. Resignations have been found in the diocese of Ely’s bishop’s register and the two studies performed on them have reached mortality rates of 57 and 60 per cent respectively, which should make mortality at around at least the same level certain whatever the possible inaccuracy of the registration of resignations and other causes of vacancies.209 In sharp contrast to Twigg’s account, Hatcher concluded in 1977 that “great weight must be attached to a revised average death-rate of around 35–40 per cent for benefi ced clergy.”210 None of these mortality fi gures for the benefi ced clergy in various dioceses is below 40 per cent and the average must be something like 45 per cent. Th orough source-critical and epidemiological discus-sion of the mortality among the benefi ced clergy in my monograph on the Black Death led me to conclude that the available data summa-rized in Table 31211 should be considered “minima or more likely


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212 Benedictow 2004: 343–58.213 Hatcher 1977: 22.214 Twigg 1984: 72; Hatcher 1977: 25.215 Hatcher 1977: 21–5.

underestimations,”212 with the implied suggestion that the real mortal-ity rate was on the order of 50 per cent. Aft er having gone thoroughly over the studies and evidence cited above a second time, above I con-clude that the mortality rate probably was even higher when Black-Death-related vacancies which were fi lled in the following years are consistently taken into account. Th e discrepancy between these esti-mates and Hatcher’s is not the important point here, which is what Twigg should have known and taken into serious consideration at the time he was writing his monograph, and the fact that the available esti-mates of mortality among the parish clergy would have had damaging consequences for his theory. How could it be that the mortality of ten-ants-in-chief in the Black Death should be under half of the average mortality among the regular clergy of a dozen monastic houses built of stone like the castles of the lay lords, namely 45 per cent?213

Twigg mentions Hatcher’s population mortality estimate of 1977 of 30–45 per cent, especially his central estimate of 35–40 per cent but neglects to take it into account.214 Th e way this is justifi ed should be considered: Twigg asserts that “Hatcher considered that the estimate produced by the E.A. Kosminsky (1955) of a national death rate of 30–45 per cent is the most reasonable one.” Th is is not correct, the estimate is entirely Hatcher’s own based on an independent, cogent and thorough discussion of sources, studies, data and problems.215 Kosminsky, the Soviet historian of the Academy of Sciences in Moscow, does not make any population estimate for any time in the High Middle Ages or in the Late Middle Ages. On the contrary, Kosminsky rejects the notion that there was a long-term late medieval sharp population reduction. He acknowledges that there was a “decrease in population in the 14th and 15th centuries,” however, he maintains that it was not “directly related to the Black Death of 1348–9 and the epidemics of the 1360s” since “the decline in population began earlier than the Black Death, and that it continued longer than could be accounted for by the results of the plague.” Instead, Kosminsky launches his own doctrinaire Marxist explanation of a population decline based on the evolution of feudal rent, class struggle, a crisis of feudalism, the development of


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216 Kosminsky 1955: 14, 22, 32. He repeats this analysis a few years later, see Kosminsky 1957.

217 Hatcher 1977: 12–3.218 Smith 1988: 208–9. Cf. Benedictow 2004: 342–77.

“the labour service system,” and “especially burdensome forms of exploitation,” “a further intensifi cation of serfdom,” “the most intense feudal exploitation of the English peasantry” and, fi nally, the conclu-sion: “Th e growth of feudal exploitation began to exhaust peasant agri-culture and at the same time to whittle down the productive forces of feudal society, destroying the conditions for reproduction of the labour force.”216 Th us, according to Kosminsky, the real reason for the late medieval population decline, in the modest form which he accepts, was caused by the intense exploitation of the peasantry within the frame-work of feudal society and its detrimental eff ects on reproduction among the peasant classes. Does Twigg cite this misleading assertion about the source of Hatcher’s mortality estimate because he needs to discredit Hatcher’s estimate, since it is incompatible with his anthrax theory? Why does he associate Hatcher’s estimate with Kosminsky’s dogmatic Marxist analysis which Hatcher, in fact, dismisses out of hand?217

Only four years aft er Twigg’s monograph was published, Smith increased the estimate of mortality in the Black Death to around 50 per cent on the basis of much the same data that were available to Twigg.218 It was just a question of taking a serious and unprejudiced interest in the subject. Without going into the matter in further detail, we can be certain that the available data at the time Twigg wrote his monograph had made it clear that the level of mortality, the generalized mortality rate in the Black Death, was very much higher than Russell had claimed.

Th is explains Twigg’s curious emergency landing in Russell’s unten-able and obsolete mortality fi gures: all other current and reliable data and discussions of the subject at the time he was writing his mono-graph showed such high mortality rates in the Black Death that they would directly invalidate his anthrax theory. Only this can explain Twigg’s statement that

Earlier estimates of a death rate of one- to two-thirds of the population through plague (Seebohm, 1865; Gasquet 1908) have been reviewed and modern work shows that the population had begun to decline before


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219 Twigg 1984: 70–1.220 Hollingsworth 1969: 264; Gasquet 1908: 225–7, 237–8.221 Twigg 1984: 72.

1348 and that the plague losses in 1348–50 were perhaps nearer 20 per cent of the population (Russell, 1948).219

In order to save his theory, Twigg must compare Russell’s fi gures, which at the time he wrote his book were more than a generation old, and throughout this period had been generally rejected, with studies published in 1865 and 1908, passing by all relevant later scholarly works, and all scholarly work on the topic between 1948 and 1984. Instead, it should have been clear to Twigg for quite a number of years that Seebohm’s and Gasquet’s estimates were still respectable, even had gained in respectability, especially if it is taken into account that they both tended to give priority to a mortality rate of around 50 per cent, the magnitude of the population loss in the Black Death which Smith arrived at in 1988.220 Th e pre-plague population estimate of fi ve million used by Gasquet is also much closer to modern population estimates than Russell’s and the post-plague estimate of something like 2.5 mil-lion corresponds quite closely to modern estimates.

However, Russell’s untenable and generally rejected estimate was still too high for Twigg and could still serve as grounds for falsifi cation of his theory or at least for rendering it highly improbable. Taking into account the normal lethality rate of anthrax, a population mortality rate of 20 per cent would imply quite unrealistically that every person in England of whatever social class, gender or age, had eaten anthrax-contaminated meat. Th is is the reason Twigg needs arguments for fur-ther reductions of the estimate of the specifi c mortality caused by the Black Death. He argues that one must also take into account “the pres-ence of a variety of infectious and other diseases, the twenty per cent reduction of the population must include these and cannot be attrib-uted to plague alone.”221 Twigg wisely does not attempt to indicate how many percentage points he would like to deduct on the basis of this argument but leaves it to the reader to make a substantial further deduction on the impression of a plethora of serious infectious diseases and other diseases that aff ected population mortality. According to demographic science, Twigg’s argument here really concerns normal mortality in the period which should be deducted in order to produce an estimate of the net mortality eff ect of plague in the period of the


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222 In England, the Black Death broke out shortly before 24 June 1348 and lasted into the late autumn of 1349 that is, somewhat less than a year and a half.

223 Russell 1948: 367.224 Russell 1948: 216. Distributed on three years, Russell’s deduction for normal

mortality implies a notion of normal yearly mortality at the time of c. 1.2 per cent, a fi gure I fi nd diffi cult to understand, although it presumably relates to the untenably low normal mortality rates, also according to Russell’s own reactions, emerging from his material on tenants-in-chief. Russell 1948: 210–1. A normal annual mortality rate of 3.6 per cent is quite usual for the early modern period, especially the eighteenth cen-tury, in Western and Northern Europe. In an epoch-making paper for medieval demo-graphic research, Hatcher has shown beyond any doubt that late-medieval normal or average mortality rates were much higher than corresponding early-modern mortality rates. Hatcher 2003. His views correspond closely to my own views, Benedictow 1996b: 29–91, 189–91. Benedictow 1996c: 156–74; Benedictow 2003: 238–44; Benedictow 2004: 250–6. Russell’s deduction for normal yearly mortality and Twigg’s should have been signifi cantly higher.

225 Twigg 1984: 72.

Black Death. However, Russell has already deducted normal mortality! Assuming (erroneously) that the Black Death lasted for three years, 1348–50222 he states: “Th e reduction of the initial loss to 20 per cent proceeds from better calculation of plague losses, which could take into account age specifi c mortality […], discounting of ordinary mortality of the three years and avoidance of other statistical diffi cul-ties.”223 Th us, in order to produce as low a mortality rate as possible, Twigg deducts twice the normal mortality in the period of the Black Death. Th e mortality rate of 20 per cent and the information on deduc-tions stand on the same page and in direct connection as qualifying explanations of the concluding mortality rate.

Correcting for age-related bias in his original material, Russell reduced his original estimate of mortality among tenants-in chief from 27.3 per cent to 23.6, which shows that Russell made a deduction for ordinary mortality in the three plague years of 3.6 per cent.224 Russell reduced this mortality estimate further, as mentioned, to 20 per cent by using the Poll-Tax registers of 1377 for retrospective analysis. Th is means that Twigg would like to arrive at a net plague mortality fi gure of 16.4 per cent. However, fearing that this is not a suffi ciently low mor-tality rate to be suitable for making a convincing case for anthrax, Twigg presents the following speculative argument: “It is not beyond the bounds of possibility that more than one new and exceptionally virulent disease organism invaded Europe during this period.”225 One may legitimately wonder what Twigg thinks he can gain for the defence


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226 Scott and Duncan 1996: 18.227 Scott and Duncan 1996: 19.228 Karlsson 1996: 281.229 See, for instance, Islandske Annaler 1888: 324, 383.

of his theory by forwarding this arbitrary idea without any empirical or evidentiary support.

Concluding Remarks

In a paper published in 1996, Scott and Duncan supported or were at least attracted to Twigg’s anthrax theory with respect to their discussion of an epidemic in Penrith and the surrounding region in the 1590s which contemporaries called plague. In their discussion of this theory, the diffi culties remain unresolved in incompatible statements on the characteristic or defi ning features of anthrax. Th ey start by asserting that anthrax “can be spread easily from person to person”226 and make on this basis a number of quite strange speculative eff orts in order to produce an epidemiological theory to this eff ect. However, on the next page they point out that “human infection is almost invariably from animal sources.”227 Clearly, Scott and Duncan eventually recon-sidered their support for Twigg’s anthrax theory and invented their own theory.

All the other advocates of alternative theories reject Twigg’s theory (as they all reject each other’s theories). Karlsson rejects it on the ground that “no mortality of any kind of animals is ever mentioned in the [Icelandic] annals.”228 Th is is not correct: serious epizootics causing great mortality among the cattle and the sheep respectively in the island are mentioned in the annals, in fact they were so serious that they caused widespread starvation and also considerable mortality among the human population since “many farmsteads were deserted.” As it is said that this occurred when “no ship arrived from Norway,” the source of the infections must have been internal in the island.229

Twigg has presented an alternative theory of the microbiological nature of historical plague with such signifi cant epidemiological and historical fl aws that it has been generally rejected as an obviously untenable theory. Nonetheless, Karlsson, Scott and Duncan, and Cohn credit him with the great epidemiological erudition and insight to have shown in a defi nite way that the Black Death could not have been


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230 Cohn asserts that I, like some other named scholars, “cite Twigg in their bibliog-raphies but in their texts give his arguments no hearing at all.” Cohn 2002: 53. Th is is not true, as all other of his comments on my thesis. At the time I wrote my thesis, Twigg’s theory had not received any favourable comments from other scholars, which constituted a case for not focusing on it in a thesis aimed at clarifying the microbiologi-cal identity of medieval plague in the Nordic countries. In this situation, it appeared appropriate to focus on what disease medieval plague could have been and not on what was agreed that it could not have been. However, I have not passed Twigg’s theory by in silence as Cohn asserts. I point out that the “suggestion of anthrax has not attracted any support for obvious reasons” and assume in good faith that it is a good argument that, “according to the standard works on microbiology, ‘the mortality rate is low and the great majority recover in a few days’ .”230 At the time, I could not foresee the necessity or potential usefulness of detailing my views on Twigg’s monograph. Nunc factum est.

rat-borne bubonic plague. Th e reason is that Twigg’s rejection of his-torical plagues as being bubonic plague functions as a justifi cation for the construction of their alternative theories.230


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