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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 first scholar to reject any role for
the plague pathogen of Yersinia pestis, whether disseminated by rats
and fleas 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. Thus, 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. The 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 first advocate of an alternative theory of historical plague
epidemics who has chosen not to fulfil 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. This 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 fulfil the scholarly requirement
of systematic and complete testability, the difference in the number of
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footnotes between these three works reflecting differences in size and
scope and the significant 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
reflect 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
1
Scott and Duncan 2001: xiii; Scott and Duncan 2004: viii.
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The Alternative Theory 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 scientific 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 sufficient levels of mortality to have explan-
atory potential for the demographic effects 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
2
Twigg 1983: 211–22.
3
Twigg 1984: 214, 217.
4
Twigg 1984: 217.
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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 affected only rarely.”7 There 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. The 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 often acquire anthrax through ingestion of spores and spread of
organisms from the intestinal tract, this is exceedingly rare in humans.
Thus, 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 confirmed 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. This is explained by the mass consumption of “raw or
5
Brachman 1990: 880.
6
This 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.
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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, “The mortality
rate is low and the great majority recover in a few days.”10 This 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 often 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.
The 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 often cited Irish chronicler John Clyn? This 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
10
Manson’s Tropical Diseases 1982: 393.
11
Jawetz, Melnick, Adelberg 1982: 207.
12
On plague pustules, see above: 364, 368–78.
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is about 20 per cent.13 In contrast, the lethality rate of bubonic plague is
80 per cent.14
Importantly: “There are no documented cases of person to person
transmission”15 of anthrax. Anthrax has only one genuinely epidemic
form, namely gastrointestinal tract anthrax.
Thus there are several independent sufficient 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. This 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.” Thus, 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 justified in losing interest in
mortality rates in possible historical cases of anthrax among human
beings in the present context. The 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
efforts 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
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.
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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
affected 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
effective 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 lethali-
ty (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.
Thus, Twigg’s anthrax theory has no significant historical founda-
tion. It is medically and epidemiologically untenable and cannot
16
Twigg 1984: 214.
17
Jawetz, Melnick, Adelberg 1982: 206.
18
Benedictow 1993/1996: 146–9.
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explain the mortality rates caused by the Black Death—something that
Shrewsbury’s theory also fails to do.
The Historical Basis: The 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. This is particularly the case in the final 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. The case for anthrax” (pages 200–22). In this chapter, J.F.K.
Hecker’s (1795–1850) monograph on The Epidemics of the Middle Ages
which was first 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 superficial and deficient 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.
The 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. This
work was originally prepared in the 1880s23 and first published in 1893;
the edition of 1908 used here by me and by Twigg is a reprint “with one
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.
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or two minor corrections, and a few additions.” The text of Gasquet’s
monograph represents pre-scientific miasmatic notions of the cause of
epidemic disease, and all medical and historical works he refers to rep-
resent this miasmatic view and pre-scientific 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. This 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 quantification of the chroniclers.”25 There will be occa-
sion below to address this point more specifically. 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 quantification” are, thus, passed
on and given a new lease of life long after 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 first
published in 1842 and also for one point of importance on the ninth
reprint of 1744 of Mead’s monograph.26 L. Bradley’s fine modern family-
reconstitution-based demographic study of 1977 on the epidemic at
Eyam27 is mentioned only indirectly in a comment to the effect that
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.
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Bradley disagrees with Wood’s analysis, without indicating why, which
might have revealed very good reasons. However, it shows that Twigg
knows Bradley’s fine demographic study, but like Cohn and Scott and
Duncan, does not take its findings 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 prolific use of
obsolete pre-scientific 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? The 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 final chapter, it becomes obvious that a theory to the effect 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 flesh of obviously sick, moribund or dead ani-
mals was simply untenable and impossible to take seriously.
The Telluric-Miasmatic Theory 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
offered 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 specific meteorological conditions relating to or
inspired by an outbreak of foot-and-mouth disease in livestock in
1967–8. This mechanism of spread is not mentioned in later standard
works on medical microbiology, for instance, by Jawetz, Melnick and
28
Shrewsbury 1971: 522–9.
29
Bradley 1977a and 1977b.
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Adelberg.30 Airborne contagion connected with specific 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 identified with
pneumonic plague.31
These 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 scientific 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 scientific methodology,
but that was over two thousand years ago. According to the tenets of
modern scientific methodology, Twigg must first 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 scientific literature on anthrax, Twigg restricted pul-
monary anthrax to the episodic and largely individual occurrence
among woolsorters, which has no epidemic form. There is no spread
30
Jawetz, Melnick and Adelberg 1982: 395–6.
31
Twigg 1984: 220–1.
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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.
There is always, as a matter of principle, at least a tiny element of doubt
or uncertainty associated with scholarly or scientific statements. The
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 scientific meth-
odological parlance means not based on facts, only on logical infer-
ence. Twigg apparently does not know that analogies, like definitions
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 after 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
32
See Hirst’s excellent presentation of these aspects of miasmatic theory in Hirst
1953: 22–72.
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It is tempting to speculate yet further and to suggest that the sequence of
earthquakes and floods 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 prolific 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
scientific and unscientific 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 offers 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 scientific 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 differentiate 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.
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.
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The 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 significant 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. The 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 unscientific miasmatic-telluric theory in order to
defend his theory. This can only be taken to reflect 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.
The Pace of Spread of Plague
There is another reason for Twigg’s attraction to miasmatic theory. This
is the distant thunder of the works of modern scientific 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 scientific 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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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 scientific 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 first but necessarily “immature” modern
scientific 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 diffusive 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 This 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
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 five 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.
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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 chiefly 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 fine 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 difficulty 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, reflects the fun-
damental weakness of his theory.
It is important to recognize that the diffusive 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
41
Above: 153.
42
Simpson 1905: 62.
43
Simpson 1905: 65.
44
Simpson 1905: 71.
45
See Bell 1951.
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civilization which offered 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:
The extent of the contagious power of the Black Death has been almost
mystifying. The 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 often 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. This 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.
The 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 flour. These 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
The point is that epidemiology is a subdiscipline of sociology in that it
focuses on the study of the effects of social interaction, and that the
powers of spread of epidemic diseases vary greatly with different types
of social formations and must be seen within a societal framework of
analysis. The 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 offered new mechanisms and much stronger opportunities
for dynamic spread, as was the case also for other microbiological
46
Benedictow 2005: 46–7.
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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
effort 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.
The 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 scientific 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
47
Cf. Benedictow 2004: 387–9.
48
See above: 194–204.
49
Twigg 1984: 212.
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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.
These 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
The 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 This is unacceptable for
several reasons. Firstly, Gasquet, to whom he first turns,56 makes it
entirely clear that the name Black Death is not contemporary with this
epidemic or subsequent plague epidemics but appears sometime after
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
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.
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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 craftsmen or labourers working with hides
and has a lethality rate of about 20 per cent (in unmedicated cases).
This 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.
Thirdly, by focusing on Gasquet’s obsolete account, Twigg can neglect
S. D’Irsay’s paper of 1926 on “The 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.” This 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 first registered in Sweden
in 1555 and about fifty 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. This happened much later: according to Hirst
and Shrewsbury, the term the “Black Death” is used in history-oriented
literature59 in England for the first time in 1823, and was, according to
Shrewsbury, for the first time introduced in English medical literature
in 1837 with the translation of Hecker’s monograph The Black Death in
the Fifteenth 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
59
Hirst 1953: 32.
60
Shrewsbury 1971: 37.
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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 Thus, 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 after he has discussed the origin and meaning of the term
the “Black Death” and despite much effort 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 find and potentially
important contribution to the history of the Black Death, because there
is none. This is also the reason neither French historians nor German
historians have picked up Leclainche’s assertion. In modern French
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.
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scholarly work on the Black Death, the epidemic is unequivocally iden-
tified 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 flawed 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
The 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. The 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 The 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
first volume (1908).70 So could Twigg, who must be assumed to know
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. They have missed the
spread to England by some of the epidemics. See for instance Maddicot 2007:
171–214.
70
Sticker 1908: 26–35.
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