GUNNAR KARLSSON'S ALTERNATIVE THEORY: THAT HISTORICAL PLAGUE WAS PURE EPIDEMICS OF PRIMARY PNEUMONIC PLAGUE - Brill
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CHAPTER THIRTEEN
GUNNAR KARLSSON’S ALTERNATIVE THEORY:
THAT HISTORICAL PLAGUE WAS PURE EPIDEMICS OF
PRIMARY PNEUMONIC PLAGUE
Introduction
G. Karlsson presented his alternative theory to the international com-
munity of scholars in a paper published in Journal of Medieval History
in 1996 where he argues that two late medieval epidemics in Iceland
and more generally that plague in medieval Europe were pure epidem-
ics of primary pneumonic plague.1 For his epidemiological interpreta-
tion, Karlsson bases his alternative theory directly on Morris’s assertion
of the occurrence of pure epidemics of primary pneumonic plague,
a modality of plague disease spread by interhuman cross-infection by
droplets. The concept of a pure epidemic of primary pneumonic plague
implies that the origin of the epidemic is not a case of bubonic plague
which develops secondary pneumonia but a case in which the first vic-
tim contracted pneumonic plague directly by inhalation of infected
droplets into the lungs.
Karlsson’s paper follows quite closely and draws heavily on a paper
he published together with S. Kjartansson in an Icelandic journal in
1994 on two supposed plague epidemics in Iceland in 1402–4 and
1494–5 respectively.2 He is clear about its objective: “The present article
[as the first in Icelandic] can be seen as a defence of the late Jón
Steffensen against Benedictow’s critique of his conclusions,” namely,
that these epidemics, and also the Black Death of 1348–9 in Norway
were primary pneumonic plague.3 Thus, the central feature of Karlsson’s
(and Karlsson’s and Kjartansson’s) paper on the two supposed plague
epidemics in fifteenth-century Iceland is a comprehensive and sharp
criticism of my doctoral thesis (1993, repr. 1996). The apparent objec-
tive was to clear the way for his own theory that the epidemics were
1
Karlsson 1996: 263–84.
2
Karlsson and Kjartansson 1994: 11–74.
3
Steffensen 1973. 40–55.
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pure epidemics of primary pneumonic plague: the epithet “pure” deter-
mines that they were without any basis or origin in flea-borne plague
from rats (or other rodents) or cases of human bubonic plague.4 Thus
he thinks that the contagion was the bacterium Yersinia pestis, as in the
case of bubonic plague, but the process of dissemination was interhu-
man cross-infection by droplets and not transmission by rat fleas at any
stage of the epidemic process. This immediately presents the insur-
mountable problem of how primary pneumonic plague could arise in
the complete absence of bubonic plague and in the complete absence of
rats, a problem he surprisingly does not identify or try to explain (and
the editors and consultants of the Journal of Medieval History did not
find significant). Alternatively, he might have launched a theory of
importation, which he conspicuously fails to do and, as we shall see, for
the very good reason that this would disclose another insurmountable
problem, which is that there is no place abroad whence plague in any
form could have been imported into Iceland in these years (another
problem which the editors and consultants of the Journal of Medieval
History did not find significant).
The Icelandic epidemics exhibit such peculiar features that Karlsson,
as the first of the advocates of alternative theories, has to invent some
suitable mutations in order to defend his theory. He does not consider
that his assertion as to the occurrence of these mutations can move
from the status as arbitrary or speculative to the status as tenable
(at any level of validity) only by meeting some elementary methodo-
logical requirements, namely to explain to the scholarly community:
(1) why and how and by which process of evolutionary selection
this mutant strain or biovar came into being;
(2) when and where, in Iceland or abroad, this mutant strain of
primary pneumonic plague originated and developed;
(3) whether this mutated variant miraculously came into being twice;
and
(4) where on earth (literally) it had been in the meantime (another
problem which the editors and consultants of the Journal of
Medieval History did not find significant).
Undaunted by these formidable problems, Karlsson expands the per-
spective of his theory from its tiny and isolated Icelandic territorial
base in the middle of the North Atlantic to argue that historical
4
Karlsson 1996: 265.
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plague in Europe generally was pure epidemics of primary pneumonic
plague.
On this basis, Karlsson concludes triumphantly that by having
removed the black rat from the medieval plague he has more generally
paved the way for asserting that the medieval plague epidemics in gen-
eral, all over Europe, were primary pneumonic plague, presumably
caused by that unknown mutated variant. These assertions will be
addressed in this chapter.
The principal interrelationship between the advocates of alternative
theories is the usual one in this case: that they accept his view that there
were not rats in Iceland and that the fifteenth-century epidemics con-
sequently could not have been rat-borne, which suits their alternative
theories, but they flatly reject his theory that these epidemics or the
medieval plague epidemics generally were (pure) primary pneumonic
plague.5 The gist of these counterarguments is, thus, that there never
was a plague epidemic in Iceland, neither bubonic nor pneumonic, and
Karlsson’s assertion that there were not rats in Iceland offers an excel-
lent explanation. The obvious implication is that the severe epidemics
in Iceland were another epidemic disease or other diseases. To my
knowledge, no other scholar has supported Karlsson’s view, at least not
outside the Icelandic scholarly community where opinions apparently
differ sharply.6 One should note that there is a remarkable qualitative
difference between the way Cohn and Scott and Duncan argue their
rejections of Karlsson’s theory, and in my opinion, only Cohn makes
his case on this point in a scholarly and scientifically tenable way.7
Karlsson and Benedictow
I consider Karlsson’s reading of my thesis so bizarre and skewed that
it is, in my opinion, grossly misleading and I hope I may be excused
for considering it an expression of the weakness of his case.8 In my
5
Cohn 2002: 23, 51; Scott and Duncan 2004: 182. See also Twigg 1984: 68, 161–8.
6
Karlsson’s (and Kjartansson’s) paper’s were discussed at a conference in Iceland
and met with much criticism; papers from this conference are published in Sagnir
1997.
7
Cohn 2002: 22–3.
8
This is even more the case for the original paper in Icelandic, Karlsson and
Kjartansson 1994, but since very few read Icelandic or Icelandic scholarly journals, this
is not important in this context, only to the Icelandic scholarly community. Also the
offensive comments on my work can, therefore, be ignored.
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thesis, I presented a detailed account of the scholarly literature on pri-
mary pneumonic plague, however, to no avail so far as Karlsson was
concerned.
This highlights another feature of Karlsson’s paper: although he
argues very strongly for a theory to the effect that the Icelandic epi-
demics of 1402–4 and of 1494–5 were pure primary pneumonic plague
and ends up with a triumphant conclusion with a much wider territo-
rial sweep, linking the nature of “medieval plague” to this disease, he
has not made any attempt to acquire scholarly knowledge of primary
pneumonic plague. Not a single medical study on primary pneumonic
plague can be found in his footnotes. According to traditional academic
principles, this ought to mean that he cannot discuss the disease that
constitutes the cornerstone of his theory with the competence that only
familiarity with the primary research studies and standard works on
this disease can provide. The reason for this extraordinary approach by
a scholar is presumably that the Icelandic epidemics exhibit many epi-
demiological characteristics or features that are not compatible with
the studies on primary pneumonic plague.
This is where wishful thinking about mutations is introduced into
his arsenal of arguments. For the same reason, he cannot avail himself
of the fact that I provided a comprehensive summary of all primary
studies on primary pneumonic plague and the presentation of this dis-
ease in the standard works in my thesis. My endeavours to track down
and present the gist of these studies does not earn me any praise, it
represents, on the contrary, a significant problem that has to be man-
aged. Since Karlsson cannot use the corpus of scholarly works on pri-
mary pneumonic plague in order to form a basis for his theory and
likewise cannot use my complete presentation of it, he must find a way
out of this problem. His solution is to base his arguments on a second-
ary paper which is profoundly flawed, namely Morris’s sharply critical
review article of Shrewsbury’s monograph where Morris was the first
scholar to launch a theory that the Black Death was an epidemic of
primary pneumonic plague.
Karlsson starts in this way: “Other diseases [than bubonic plague]
are hardly considered by him [Benedictow], and all other forms of con-
tagion are excluded, mainly because they are said to be insufficient to
explain epidemics of the dimension under discussion here.”9 Firstly,
9
Karlsson 1996: 264.
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one should note the logical and factual contradiction in the opening
part of the statement, that “other diseases are hardly considered by
him” and that “all other forms of contagion are excluded:” since all
other forms of contagion unavoidably relate to many other diseases,
I cannot have excluded other forms of contagion without having dis-
cussed other diseases.10 Secondly, he fails to mention that I made a
complete presentation of the corpus of primary research on primary
pneumonic plague, and this omission allows him to present a spurious
explanation as to why I reject his theory. Thirdly, one should also note
that in the second part of the statement he sharply criticises my
approach, saying that I exclude all other forms of contagion “mainly
because they are said to be insufficient to explain epidemics of the
dimension under discussion here.”11 Thus, the truth shows through,
albeit indirectly and involuntarily, that I have discussed other alterna-
tive diseases based on other forms of contagion, but have found that
they have, inter alia, insufficient mortality-generating properties.
Notably, Karlsson acknowledges in his paper that the Icelandic annals
do not contain any clinical or diagnostic information that would per-
mit the microbiological identification of these Icelandic epidemics.
However, he contends that these chronicles provide information that
can be used for producing estimates of the population loss in both epi-
demics, and that the extreme estimated mortality level could only have
been caused by primary pneumonic plague.12 In other words, in prac-
tice he avails himself of exactly the same approach that he criticizes me
sharply for using (although I do not use it as a fundamental argument
but only as an additional argument).
Later in Karlsson’s paper, there is another sudden but indirect indi-
cation that he has read my presentation of primary pneumonic plague.
This occurs with a parenthesis within a citation from Morris’s paper to
the effect that
the great pneumonic epidemic in Manchuria would have spread much
more, “but for the heroic counter-measures taken by the great Chinese
10
Benedictow 1993/1996: 121–5, 214–27.
11
Benedictow 1993/1966: 16, 125, 266–74. As this statement is inaccurate and could
produce misconceptions about my view, I would like to point out that I have discussed
not only the size of the epidemics, as Karlsson may be taken to state, but also properties
that combine tremendous powers of spread with tremendous lethal powers, and I ar-
gue explicitly why that is a rare combination (see also above).
12
Karlsson 1996: 265, 268–84.
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doctor Wu Lien Teh [one of Benedictow’s greatest authorities on plague]
who most fortunately was put in charge.”13
However, Morris continues, unquoted by Karlsson:
Wu Lien-Teh’s classic treatise on pneumonic plague is significantly absent
from Shrewsbury’s very extensive bibliography.14
This treatise is also “significantly absent from” Karlsson’s few footnotes.
One could also note the distortion inherent in Karlsson’s combined
reference to me and “Wu Lien-Teh [one of Benedictow’s greatest
authorities on plague],” since Wu Lien-Teh is the indisputable and
uncontroverted towering expert on primary pneumonic plague, not
on “plague.” Morris’s aim was to reject Shrewbury’s theory to the effect
that the Black Death and later plague epidemics in Britain could have
caused only a minor part of the national mortality rate, about 5 per
cent, and that exanthematic typhus, smallpox and other serious epi-
demic diseases caused most of the mortality (see above). Because
Morris has insufficient knowledge of bubonic plague to effectively
counter Shrewsbury’s arguments, he launched another and appar-
ently relevant alternative theory, namely that plague in Britain was pri-
mary pneumonic plague. However, he had poor knowledge also of
primary pneumonic plague, and many of his central assertions are
unfounded. This subject is discussed below after the substance of Wu
Lien-Teh’s and other researchers’ studies on this modality of plague
have been presented, in order to perform a systematic comparison
between these studies and Morris’s and Karlsson’s assertions.
Karlsson bases his paper and theory on Morris’s ten-page review of
Shrewsbury’s monograph instead of on the primary research studies on
primary pneumonic plague because they in important respects have
the same ambition, namely to prove that the medieval plague epidem-
ics, at least in Britain and in Iceland, were pure epidemics of primary
pneumonic plague. However, Shrewsbury’s rejection of primary pneu-
monic plague as a significant causal factor of mortality is in full accord-
ance with all primary research on this modality of plague, the same
research that persuaded me to reject in my thesis the theory that the
Black Death or subsequent plague epidemics could have been pri-
mary pneumonic plague. Apart from the fact that Morris referred to
13
Karlsson 1996: 283.
14
Morris 1971: 208–9.
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Wu Lien-Teh in his text and mentioned his monograph in a footnote, it
can hardly be demonstrated that he has read his work or knows more
about primary pneumonic plague than Karlsson. Karlsson based his
case on the quotation from Morris’s paper for two crucial reasons:
(1) because it provided an impression that primary pneumonic plague
has great powers of spread, but in this case was halted by the coun-
termeasures introduced by Wu Lien-Teh;
(2) because Morris introduced the concept of pure pneumonic plague,
which Karlsson makes the cornerstone of his theory. Both asser-
tions are, as we shall see, at complete variance with Wu Lien-Teh’s
presentation of primary pneumonic plague, where it is emphasized
that epidemics of this disease arise from cases of bubonic plague
which develop secondary septicaemia with subsequent lung con-
solidation and a bloody cough spreading infected droplets. Thus,
Wu Lien-Teh maintains that epidemics of primary pneumonic
plague never are pure, never arise de novo from a first or original
case of primary pneumonic plague droplet infection.
The heart of the present monograph is the identification of epidemic
diseases of the past. This objective requires that some elementary meth-
odological rules are followed in order to ensure the validity of identifi -
cation of diseases, otherwise any mention of a severe or disastrous
epidemic in the sources can be arbitrarily taken as evidence of plague
(or any other serious communicable disease). An illustration of the
consequences of an approach unguided by methodological considera-
tions is provided by Scott and Duncan who assert that “there are said to
have been 233 outbreaks [of bubonic plague] in China between AD 37
and 1718.”15 They have used Wu Lien-Teh’s general list of epidemics in
China, for some reason leaving out the first of 224 BC.16 However, Wu
Lien-Teh does not at all suggest that all these epidemics were or could
have been bubonic plague. He emphasizes that it is possible to identify
only a couple of these 233 epidemics as bubonic plague. He has not
succeeded in finding clinical or epidemiological evidence of bubonic
plague in chronicles or literary accounts, only in three medical works.
Two of these medical works were from the first half of the seventh
century; their clinical descriptions are unambiguous but cannot be
15
Scott and Duncan 2001: 171.
16
Wu Lien-Teh 1936a: 43–51; Benedictow 2004: 40–2.
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correlated or associated with any specific epidemic(s) in China. Only
in a medical work of 1642 is a clinical description of bubonic plague
given within an epidemic context, obviously referring to the epidemic
of 1641–2.17
Identification of an epidemic disease, in this case as plague (either
bubonic or pneumonic), requires specific evidence of at least one defin-
ing epidemiological or clinical feature or a combination of features that
are unique (see above). In weak or inconclusive cases, it must be pos-
sible to demonstrate at least a possible link of dissemination from a
known epidemic of plague to the epidemic under study which may
allow formation of a hypothesis to the effect that it may have been
plague. This does not, of course, constitute any proof that it actually
was the plague; the function of a hypothesis is to legitimate research
and direct the search for corroborative evidence. This requirement is of
particular importance in the case of epidemics in a highly isolated
island like Iceland. This clarifies the basic methodological, empirical
and source-critical requirements that Karlsson should meet in order to
justify his theory of the aetiology of the purported fifteenth-century
plague epidemics in Iceland.
The Icelandic sources that provide information on these epidemics
consist mainly of brief accounts in two chronicles for each epidemic;
translations of these accounts into English are supplied in my thesis
and by Steffenson. My translation into English is provided in Appendix
2 below.18 As is most often the case with this type of source, the quality
of the information they provide is quite deficient (in the eyes of mod-
ern scholars). They have nothing to say about whence the contagion
arrived in Iceland or about defining or weaker indicative clinical fea-
tures, excepting perhaps on the typical duration of the illness. They
contain some comments on spread and mortality that are incidental
and sensational in character as would be expected from this kind of
source. Since Karlsson asserts that this “information” can be used for
17
Wu Lien-Teh 1936a: 10–3; Benedictow 2004: 35–42. This means that also McNeill’s
use of the same list is unfortunate, and his choice of a Chinese epidemic of 1331 as the
origin on the Black Death that subsequently spread all the way to the Crimea is com-
pletely unsupported by clinical or epidemiological evidence; see McNeill 1979: 152–4.
Instead, McNeill let himself be victimized as a scholar by “the overwrought imaginings
and hopelessly inaccurate quantification of the chroniclers,” to cite yet again Hatcher’s
apt description (1977/87: 21). His theory is also contrary to a number of other empiri-
cal facts, for instance, the fact that the communication lines between China and the
Crimea were severed long before the Black Death broke out in the Crimea or
Constantinople. See Benedictow 2004: 44–51.
18
Benedictow 1993/1996: 211–2; Steffensen 1974: 457, 50–1.
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estimates of mortality which are indicative of plague, this point will be
discussed below.
An intriguing question presents itself immediately and with great
urgency: how can it be possible in such evidential circumstances to
identify with a (very) high level of certainty the aetiology of the
fifteenth-century Icelandic epidemics, in this case specifically as pure
primary pneumonic plague caused by some mutant variant of the con-
tagion Yersinia pestis? This problem is exacerbated by the fact that in
his paper Karlsson does not perform source-criticism in accordance
with scholarly standards, stating only with reference to his and
Kjartansson’s paper that: “It would be tedious here to repeat all the
arguments and reservations concerning our use of Icelandic sources,
let alone all the references to sources and literature that only people
who read Icelandic could use.” Inevitably, it means that his paper, on
this crucial point, represents incomplete methodology and scholarship.
There is also another serious matter of deficient methodology of source-
criticism that will be discussed below.
Karlsson’s theory is characterized by at least three independent fatal
flaws of both empirical and methodological nature, in the sense that
each represents a sufficient condition for rejecting it as untenable or
invalid. (1) In the circumstances, when the two requirements for iden-
tification of epidemic diseases outlined by Shrewsbury cannot be met
by the Icelandic sources, it is a serious deficiency that Karlsson has
completely neglected to investigate the possible provenance, the pos-
sible territorial origin of the contagion that was introduced into Iceland
and that unleashed the purported plague epidemics there in the years
1402–4 and in 1494–5. In reality, this question is composed of two
independently decisive parts that must each be satisfactorily resolved
in order to keep the theory afloat: he must for each epidemic be able to
identify at least (1) one contemporary plague-stricken port town in
Europe which (2) was sending ships to Iceland at the time these epi-
demics arrived there. These two crucial questions or problems for the
tenability of his theory are passed by in silence. In 2002, I published a
complete Norwegian plague history from 1348–1654 which covers
more than thirty waves of plague epidemics, without finding evidence
of any epidemic of primary pneumonic plague, let alone of a pure epi-
demic of primary pneumonic plague; in fact all epidemiological evi-
dence is compatible with bubonic plague.19
19
Benedictow 2002. See also Benedictow 2006.
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Could Plague Have Come to Iceland from Anywhere?
Only a few ships came to Iceland from abroad at the beginning of the
fifteenth century, only Norwegian ships or Icelandic ships returning
from Norway, normally from Bergen. The first English fishing ship is
reported to have arrived in Icelandic waters in 1412.20 It was prohibited
by law for the Icelanders to trade with foreigners. In order to illustrate
this point one could note that in 1409, there was an intensive discus-
sion at the Icelandic all-moot (‘Alþingi’) about what to do with all the
royal incomes that had piled up in the island.21 Iceland was part of
the Norwegian kingdom, normally administered by a royal governor
(‘hirðstjóri’), and taxes were mostly paid in homespun woollens and, to
some extent, in stockfish (wind-dried cod). Evidently, the cause of the
problem was that too few ships arrived from Bergen, and that not even
the commander of the King’s Mansion22 in Bergen who was responsible
for collecting the royal incomes in Iceland, regularly sent a ship there to
collect them. In the following years the New Annals (Nyi Annáll) occa-
sionally provide telling pieces of information, for instance, under the
year 1412 we are told that “No news came from Norway to Iceland,” i.e.,
no ship arrived from Norway; next year we are told that “A ship came
from Norway,”23 a fact that the annalist finds worth mentioning. In
1419, the Icelanders wrote a letter to the king complaining that for
several years no ships had arrived from Norway according to the old
agreement with the Crown, which had been gravely detrimental to
their poor country. They therefore considered it unreasonable that the
old prohibition against trading with foreigners was still in force.24
British sources tell the same story. Ships from Britain were sailing to
20
Carus-Wilson 1966: 161.
21
Steffensen 1974: 48.
22
The ‘King’s Mansion’ is a translation of ‘Kongsgården,’ the royal administrative
centre of western Norway in Bergen. At the time, this was not a castle built in stone, but
consisted of wooden buildings surrounded by a wooden palisade and had no real de-
fensive capabilities.
23
Annales islandici posteriorum sæculorum. Annálar 1400–1800: 18–9. Also the
Icelandic Vatnsfjarðarannáll hinn elzti relates to this epidemic but it is written so long
after the event and is so infested with source-critical problems that it is not mentioned
by Gunnar Karlsson (or Jón Steffensen) who in other works shows good knowledge of
these important types of sources to Icelandic medieval and early modern history.
Annales islandici postseriorum sæcolorum, 1933–8: 22.
24
Diplomatarium Norvegicum, vol. 2, no. 651; Diplomatarium Norvegicum, vol. 4,
no. 330.
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Iceland at the time: the first English fishing ship arrived in 1412 to be
followed by many others in the subsequent years. However, throughout
the fifteenth century only English fishing ships and merchant ships
sailed to Iceland; Scottish ships do not seem to have been engaged
in fishing in Icelandic waters or trading with Iceland during this
century.25
Crucially, there is not a single account of plague in these countries in
1402. Not a single plague epidemic has been registered in England
between 1400 and 1405–7, nor was there any outbreak of plague in
Ireland or Scotland during this period,26 nor for that matter in Northern
Germany between 1396 and 1405–6, nor in the coastal commercial cit-
ies of the Netherlands between 1400–1 and 1409.27 Since the epidemic
broke out in the autumn of 1402, after the return of an Icelandic ship,28
it is also clear that the disease would have to have been imported from
a city or region where it was spreading in this year.29 In Norway, the
sources provide no certain information of plague between 1391–2 and
1452, although there are some indications that there could have been
plague in 1438–9. Norwegian sources are particularly sparse in these
decades, and it is likely that one or more plague epidemics may have
gone unnoticed. However, it is improbable that plague contagion could
have been imported into Norway and re-exported to Iceland in years
when there was no plague epidemic in the countries whence plague
was imported to Norway, and this was throughout the Late Middle
Ages mostly England, and at least once the Netherlands.30 There is no
evidence that plague was imported from Northern Germany before
25
Carus-Wilson 1966: 155–82.
26
Shrewsbury 1971: 149–50, mentions that “some time in 1402 there was ‘some
disease in Scotland that ‘caused several deaths’ in Dundee.” Evidently, he does not con-
sider it to have been plague, referring to it only as “some disease,” and since the only
concrete information on mortality is restricted to the statement that it “caused several
deaths” no impression is conveyed of a dramatic epidemic situation. And one must
keep in mind that no ships from Britain were sailing to Iceland at the time and that also
later in the century only English fishing ships and merchant ships sailed to Iceland,
Scottish ships do not appear to have been engaged in fishing near or trading with
Iceland. Carus-Wilson 1966: 155–82.
27
According to Blockmans 1980: 854, there was an outbreak of plague in Guelders,
an inland city situated in the south-eastern part of the Netherlands near the border of
Germany.
28
“Nýi Annáll,” in Annales islandici postseriorum sæcolorum, 1922–7: 9–10;
“Lögmanns-annáll” in Islandske Annaler indtil 1578: 286.
29
Benedictow 2002: 102–11.
30
Benedictow 2002: 102–11. Evidently the reason is that Denmark’s pattern of inter-
national trade was very different from Norway’s.
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1500 (or more accurately before 1628), and for the year 1402, with a
substantial margin of safety of years around it, plague is not recorded
in this area.31 According to the extant sources, plague was never
imported from Denmark in the whole plague history of Norway, and
no plague epidemic has been registered in Denmark from the end of
the fourteenth century until possibly in 1405.32
Steffensen, who recognizes that notions on provenance cannot be
dispensed with and that this question therefore cannot be ignored,
asserts that the supposed plague contagion came to Iceland with a ship
from England. His source is Sticker’s old pioneering standard work on
plague of 1908, where plague is mentioned as having occurred in
England in 1402, but without indication of his source.33 Probably
Sticker has misunderstood a reference to the epidemic in Iceland in the
Danish scholar F.V. Mansa’s proto-scientific monograph of 1875 on the
epidemic history of Denmark.34 It is a mistake or rather a slip of the pen
on the part of Sticker that Steffensen could easily have corrected by
using Shrewsbury’s recent monograph on the history of plague epi-
demics in Britain and, as we shall see, Steffensen knows the work
and has consulted it, which makes his silence on this point the more
remarkable. In fact, in another context Steffensen remarks that Sticker’s
mention of a plague epidemic in Denmark in 1402 with reference to
Mansa’s monograph is erroneous,35 apparently he knows that this pas-
sage in Sticker’s work is not correct. Furthermore, Steffensen does not
attempt to assert that ships sailed directly from Denmark to Iceland at
the time which also can be checked and corroborated in Icelandic
annals and other sources. The staple36 was in Bergen and the Iceland
trade a privilege for Norwegians. At the time of this epidemic, Icelanders
were living in isolation with only sporadic contacts abroad and, for all
practical purposes, abroad was Norway.
31
Shrewsbury 1971: 138, 141, 149–56; Ibs 1994: 206; Blockmans 1980: 836–45;
Benedictow 2002: 102–5, 354–5, see especially Table 2A showing all known plague
epidemics in Norway, England, Northern Germany and the Netherlands in the period
1348–1500 organized so as to facilitate comparison and discussion of territorial origin.
Also see the references on this subject cited just above.
32
Mansa 1873: 92–100.
33
Sticker 1908: 8; Steffensen 1974: 47–50.
34
Mansa 1873: 99.
35
Steffensen 1974: 47.
36
The Shorter Oxford English Dictionary, vol. 2, p. 2109 gives the following defini-
tion “staple:” “A town or place appointed by royal authority, in which there was a body
of merchants having the exclusive right of purchase of certain classes of goods destined
for export; also the body of merchants so privileged.”
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Thus, 1402–4 were years with unusually few outbreaks of plague in
Europe and they occurred far away from the northerly parts of Europe
and commercial centres that could serve as the point of departure for
transportation of plague by ship to Iceland. These findings permit a
secure conclusion. No doubt there was a serious or severe epidemic in
Iceland in the years 1402–4, but plague in any form based on the con-
tagion Yersinia pestis appears to be excluded: there was no plague epi-
demic in any of the countries or regions with shipping activity with
Iceland whence it could have been transported there. Another point
which excludes primary pneumonic plague is the long duration of an
epidemic which requires continuous and rapid spread in such a tiny
population (probably 30,000–40,000 inhabitants37), and this duration
would by far be the longest on the record.
At the time, Iceland was a long voyage from any port in the northerly
parts of Europe. The voyage from western Norway to Iceland would
under favourable circumstances and with suitable wind usually take
a couple weeks of sailing. However, ships from Bergen or Nidaros/
Trondheim would first sail along the coast approximately to the north-
western point of Stad, which would normally take about five days,
before they could turn and with an easterly wind sail westwards to
Iceland.38 Waiting periods for useful winds could easily take much
more time than the actual sailing.39 This would very much be the case
for ships waiting for the easterly winds necessary for sailing west-
wards to Iceland, since Norway is situated in the so-called west wind
belt which is dominated by westerly winds. In the twentieth century,
easterly winds constituted only 2.2 per cent of all wind measure-
ments in the sailing season 1 April–30 September40 in western Norway.41
Obviously, any ship with primary pneumonic plague on board among
the cramped conditions for crew and passengers after cargo had
been given strong priority would be rapidly heading for disaster.
37
See below, fn. 68.
38
Helle 1982: 68. Cf. Steen 1934: 227.
39
Steen 1942: 306.
40
The maximum sailing season is given in the important Norwegian source
Kongespeilet [The King’s Mirror] written around 1250. Here I have used the recognized
translation Kongespeilet 1947: 53, 55.
41
Since the prevailing distribution of wind direction is heavily affected by the direc-
tion of the earth’s rotation, the distribution of wind directions has probably not varied
greatly over historical time. The crude data of all wind-force measurements registered
by the wind-gauge stations in Bergen are published by the Norwegian Meteorological
Institute: www.met.no
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Since no epidemic of primary pneumonic plague has been identified
in Norwegian sources, and in the year in question (1402) not even a
plague epidemic, Steffensen’s theory is only a speculative flight of
imagination.
In the case of the supposed plague epidemic of 1494–5, the situation
is much the same. Karlsson has not attempted to identify the provenance
of the contagion and passes in silence by the problem of whence
plague contagion could have been transported to Iceland. In the mean-
time, shipping activities in northern Europe had increased greatly.
Although the small island of Iceland with its tiny population situated
in the middle of the North Atlantic Ocean on the northwestern out-
skirts of Christendom was a destination with limited attraction, it was
by now less isolated and to some extent linked to northern Europe
through trade in stockfish. At the time, English interest in fisheries in
Icelandic waters and commercial interests in the island had been
sharply reduced, due largely to strong efforts by Hanseatic cities to
drive the English away and assert their primacy and the importance of
the staple of stockfish in Bergen. By the end of the fifteenth century,
Iceland was apparently quite regularly visited by a ship sent there by the
commander of the King’s Mansion in Bergen in order to collect the
royal taxes, and stockfish may at least occasionally also have been pur-
chased in order to fill up the ship and earn some extra income. This
pattern can be discerned in a sprinkling of fifteenth-century sources
and is confirmed by the records of Bergenhus Castle, the new royal
castle in Bergen, which are extant from 1514, and where also the occa-
sional Icelandic ship is mentioned.42 The sources reveal that Iceland at
this time had some regular commercial contacts with Norway and was
now more exposed to the importation of contagion than at the begin-
ning of the century.
This puts the epidemics of 1494–5 in a somewhat different light.
However, as can be seen from Table 2A and the comprehensive com-
ments in my Norwegian plague history, there was no plague epidemic
in these years in Norway, England, Northern Germany or in the coastal
commercial cities of the Netherlands.43 In 1494, epidemics are men-
tioned in Gouda and Guelders as typical localized outbreaks and in
inland cities without shipping contacts or commercial connections
42
Norske Regnskaber og Jordebøger. See the very good index.
43
Benedictow 2002: 102–11.
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with Norway or Iceland.44 Gouda and Guelders are the only places
where there may have been outbreaks of plague this year.45
Nonetheless, Steffensen asserts again that the contagion that trig-
gered the purported Icelandic plague epidemic was imported from
England. This conclusion is seemingly the outcome of a process of
elimination. He admits that plague is not mentioned in “Scandinavia or
Denmark” in 1494. He has again consulted Sticker, who in the crucial
year of 1494 in the whole of Europe has registered plague only in
Nuremberg, and in 1495 more or less probable or possible plague epi-
demics in Landshut (Bavaria), Erfurt and in Lower Austria.46 Since
Steffensen does not specify these localities he can state rather inaccu-
rately that plague “is mentioned in many German towns.”47 Obviously,
the contagion that unleashed the Icelandic epidemic could not have
originated in any of these localities which were not Hanseatic commer-
cial cities on the North Sea or Baltic Sea. Since Sticker cannot help him
with a plague epidemic in England, not even by a slip of the pen,
Steffensen must look elsewhere for support of his theory of provenance.
He now mentions that he has consulted Shrewsbury’s recent mono-
graph, thus admitting that he knows it, but was confronted with the
fact that Shrewsbury does not consider that there has been any pesti-
lence in England in the last decade of the 15th century.48
Since he is not willing to draw the scholarly conclusion that there
was no plague epidemic either in England (or anywhere in the British
Isles) or elsewhere in northwestern or northern Europe that could
have served as an origin of the contagion which was transported to
Iceland in 1494, he looks elsewhere for support. He turns to Creighton’s
monograph of 1891, A History of Epidemics in Britain, where “minor
44
Noordergraaf and Valk 1996: 225; Blockmans 1980: 854.
45
In the following year, 1495, there appears to have been a plague epidemic in
southeastern Sweden, as the convent of Vadstena and the city of Stockholm on the
Baltic Sea is reported in contemporary chronicles as being seriously visited by pesti-
lence. Moseng 2006: 314–5. Since an outbreak of plague in Sweden in 1495 cannot be
the origin of plague in Iceland in 1494 and Sweden had no contact with Iceland by ship,
this epidemic is not significant in the present context. It is also noteworthy that eastern
Sweden was exposed to importation of plague across the Baltic Sea and had, like
Denmark, a different temporal rhythm of plague epidemics than Norway which im-
ported plague from England and northwestern Europe more generally, but never from
Sweden or Denmark.
46
Sticker 1908: 87.
47
Steffensen 1971: 53.
48
Shrewsbury 1970: 149, 155.
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epidemics are mentioned in Oxford 1486, 1491 and 1493, and it
appears that the pestilence was close to Edinburgh in March 1493.”49
Although Creighton does not use the term “plague epidemics,” but only
the unspecific term “epidemics,” this statement is taken to constitute
justification for an unqualified assertion to the effect that Shrewsbury
took no interest in minor plague epidemics and “presumably means
only large-scale epidemics.” Every reader of Shrewsbury’s highly
detailed work will know that this assumption is groundless: no epi-
demic is too small to escape his acute interest, neither can Shrewsbury’s
numerous references to and detailed knowledge of Creighton’s work
escape notice. In fact, Steffensen’s assertion in relation to Shrewsbury
work is at variance with Shrewsbury’s presentation of his research pro-
gram on fifteenth century plague epidemics: “As this work is primarily
a history of bubonic plague, an attempt must now be made to pinpoint
the possible outbreaks of that disease in the British Isles during this
century,”50 making it clear that his objective is to identify every possible
outbreak of plague. This does not exclude the possibility that he over-
looked epidemics, especially local outbreaks.51 Scrutiny of the sources
or research literature for more information is always warranted but
Steffensen did not succeed in identifying any plague epidemic and did
not accept the consequences.
The reason Shrewsbury does not mention the epidemics in Oxford
in these years is that he did not find any evidence to the effect that they
were plague. In fact, Shrewsbury has not registered a single epidemic of
plague in England “after November 1480 until an epidemic erupted at
Oxford in 1499” which he considers a “doubtful exception.” Thus,
Shrewsbury is clear in his view that in the sources there is no indication
of plague in England in the period comprising the epidemics in Oxford
and the purported Icelandic plague epidemic. It can also be shown that
he was certainly not averse to mentioning small possible outbreaks of
plague in Oxford.52
J. Hatcher and P. Slack, prominent English scholars who, in impor-
tant subsequent studies of plague in England, have fine-combed the
sources for epidemics, including the sources relating to the last two
decades of the fifteenth century, did not find any credible information
49
Creighton 1891: 283; Steffensen 1974: 53.
50
Shrewsbury 1971: 155.
51
See Gottfried 1978: 238–40.
52
See Shrewsbury 1971: 149.
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to the effect that the small epidemics in Oxford mentioned by Creighton
were plague.53 The reason may quite safely be assumed to be that there
is no such evidence. Another insurmountable problem is how conta-
gion from this small inland outbreak of an epidemic disease should
have been moved to Iceland, as the continuous lines of communication
presumed by such an event appear to be completely unknown to either
contemporaries or to modern historians. Another insurmountable
problem is that even the last mentioned epidemic in Oxford occurred
in 1493 and cannot be linked to the outbreak of an epidemic in Iceland
1494.
Steffensen appears to assume that he can brush aside Shrewsbury’s
recent work, written by a modern bacteriologist, and substitute it with
Creighton’s proto-scientific work of 1891. Creighton’s monograph is, as
noted above, written according to the spirit of an ardent protagonist
and defender of miasmatic epidemiological theory in the face of the
rise of the new science of bacteriology. This means that Creighton
denied that each epidemic disease was caused by a specific microbio-
logical agent and believed instead that miasma could take on various
forms and could develop into plague from other manifestations of
miasmatic disease (i.e., other epidemic diseases), especially from
typhus and dysentery; he also claimed that plague was due to a poison
emanating from putrescent corpses.54 According to miasmatic theory,
an outbreak of any epidemic disease could therefore be of interest to a
study of plague since it could develop into plague. This is also the rea-
son for Steffensen’s sudden use of the term “pestilence” in the citations
above. It reflects the miasmatic assumptions that have now been
inserted at the core of his argument, although nothing is explicitly said
about this extraordinary turn of his argument away from modern sci-
entific bacteriological and epidemiological premises of analysis to
untenable proto-scientific miasmatic medical theory. Besides the fact
that Creighton has not suggested that the epidemics in Oxford were
plague, it must be emphasized that Creighton does not assert that there
was an epidemic at Oxford or anywhere else in England in 1494.
Nonetheless, Steffensen sticks to his theory, although it is untrue that
Shrewsbury only took interest in major plague epidemics and ignored
minor epidemics, so that plague could have been imported from
53
Hatcher 1977/1987: 17–8; Slack 1985: 53–65.
54
See, e.g., Hirst 1953: 74–5, 87, 89, 93–4, 285; Shrewsbury 1971: 150.
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England to Iceland in 1494 in connection with some minor outbreak
of plague which Shrewsbury ignored, Creighton did not know, and
which Hatcher and Slack overlooked. According to all accumulated
scholarly knowledge on English plague history no plague contagion
could have been transported from England to Iceland in 1494.
Steffensen also mentions a possible plague epidemic “close to
Edinburgh” in 1493, referring again to Creighton as his source.
Shrewsbury takes seriously the possibility of an outbreak of plague in
Edinburgh and outlying townships in 1493 which led to the isolation of
the town, but thinks that it probably was an epidemic of typhus. He
concludes therefore his chapter on plague in Scotland in the fifteenth
century by stating: “There does not seem to be any outbreak of epi-
demic disease in Scotland that presents any circumstantial evidence
for its identification as an outbreak of bubonic plague, with the doubt-
ful exception of 1499.”55 Significantly, this epidemic did not spread to
any other place in Scotland, which makes it a very local outbreak of
whatever disease it might have been. Furthermore, an epidemic out-
break in 1493 is out of chronological co-ordination and cannot serve
even as a hypothetical origin for the Icelandic epidemic. Edinburgh
was not a commercial shipping centre, and it is rather unsurprising
that it had no known connection by ship with Norway, and certainly
not with Iceland. Again, it is not possible to construct any case for
transportation of plague contagion from Scotland to Iceland in 1494.
Thus it is not possible to adduce empirical support for the theory
that the epidemic outbreak in Iceland in 1494 was primary pneumonic
plague or bubonic plague for that matter, since there was no area or city
which was visited by plague whence plague could have been shipped to
Iceland. Undoubtedly this epidemic in Iceland was a serious outbreak
of a contagious disease or multiple contagious diseases taking a high
toll of lives. One should take note that there are numerous accounts in
the Icelandic annals of serious or severe epidemics, including accounts
that pre-date the advent of plague in Europe and also subsequent epi-
demics that typically are out of rhythm with known European plague
epidemics. Some examples may be useful: in 1292, “Came such a big
disease over all the country […] and caused great mortality”; in 1306,
“Big epidemic in Iceland and high mortality in the south of the coun-
try”; in 1309, “Big killing disease in the north of the country”; in 1310,
“Killing disease and mortality in all the Vestfjord area and the
55
Shrewsbury 1971: 151, 155.
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Southerners’ area and boil disease”; or in 1380 and 1382: “Huge boil
disease all around the country and great mortality […] disease over all
the country and huge mortality.”56
Thus, also 1494 was a year with particularly few plague epidemics
in Europe and they occurred far away from the northerly parts of
Europe and from commercial sea ports that could serve as a point of
departure for transportation of plague contagion by ship to Iceland.
Steffensen’s assertion that plague contagion came from England has
been shown to have no evidential underpinning, essentially it is an
arbitrary assertion, and likewise not a single plague epidemic was reg-
istered in these years in Norway. Again, the intensive and comprehen-
sive discussion permits a clear conclusion: no doubt there was a serious
or severe epidemic in Iceland in the years 1494–5, but it appears impos-
sible that it could have been due to plague in any form based on the
contagion Yersinia pestis.
Steffensen sees the problem of provenance clearly and appreciates
the fact that positive identification of at least one case of plague in one
sea port with at least some evidential support for possible shipping to
Iceland is crucial to instil his theory with any (level of) tenability, how-
ever low. However, he cannot come to terms with the the complete lack
of supporting evidence on both points for both epidemics.
Karlsson has chosen the option of passing the problem by in silence,
although this undermines the very foundations of his theory, quite
possibly because he recognizes that there is no supporting evidence.
This exhaustive discussion of a possible provenance of plague conta-
gion (Yersinia pestis) for the purported plague epidemics in Iceland in
the years 1402–4 and 1494–5 has been completely negative. This find-
ing constitutes a sufficient condition for characterizing the theory as
materially untenable and for the conclusion that it must be rejected.
This does not mean that there cannot be other independent and suffi-
cient conditions for rejecting the theory.
Pure Epidemics of Primary Pneumonic Plague: Fact or Fiction?
A thorough and for all practical purposes complete presentation of the
medical and epidemiological studies of primary pneumonic plague is
presented in my thesis in order to provide the broadest possible basis
56
Annales Islandici 1888: 71, 53, cf. 75, 364. My translation from Icelandic Norse.
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for my discussion of the nature of the late medieval plague epidem-
ics in the Nordic countries. It was also motivated more specifically
by my desire to provide a background for discussion of Steffensen’s
paper,57 since his theory of epidemics of primary pneumonic plague
in Iceland is not supported by a single reference to any medical or
epidemiological study of primary pneumonic plague. Karlsson who
defends his theory intensively fails to include any reference in his paper
to a primary study of pneumonic plague or to the broad summaries of
such studies provided in the standard works on plague, not even to
K. Meyer’s brief and succinct paper. However, according to the meth-
odological tenets of medical and historical science, their theory of the
nature of these Icelandic epidemics as being primary pneumonic plague
or some mutant variant of this disease can only be adequately discussed
in relation to modern medical and epidemiological knowledge on this
modality of plague, implemented in the form of a systematic compari-
son between historical data and modern data. The better and more
comprehensive the correspondence or correlation between modern
medical data and historical data, the more tenable the inference of the
identity as primary pneumonic plague.
Fruitful discussion requires a satisfactory empirical knowledge of
the medical characteristics, epidemiological structures, lethality and
demographic effects (population mortality) of primary pneumonic
plague. Since Karlsson denies that there were any rats in Iceland, he
is obliged to, launch a theory of pure epidemics of primary pneu-
monic plague, which requires that he consistently avoids the medical
literature on primary pneumonic plague and instead makes his case
depending entirely on an assertion in a review paper by Morris. This
assertion occurs in a passage where Morris scathingly and disparag-
ingly attacks Shrewsbury for denying the existence of this form of
plague:
What is the cause of Shrewsbury’s myopia?58 Perhaps it came upon him at
the moment when (on page 6) he delivered himself of the dictum “pneu-
monic plague cannot occur in the absence of the bubonic form and it
cannot persist as an independent form of plague.” This is untrue […]. The
Manchurian epidemic was indeed exclusively pneumonic, as was the
slightly less destructive outbreak of 1920–1; […] Wu Lien-Teh’s classic
57
Benedictow 1993/1996: 25–31, 214–27.
58
“Myopia” means shortsightedness in a medical sense or figuratively narrow-
mindedness.
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treatise on pneumonic plague is significantly absent from Shrewsbury’s
very extensive bibliography.59
This basic idea and crucial premise of Morris’s theory of the nature of
plague in England and Karlsson’s theory of plague in Iceland, the notion
of pure epidemics of primary pneumonic plague, can usefully be
addressed first.
Theoretically, pure epidemics of primary pneumonic plague are pos-
sible in the technical meaning that they could start de novo from an
original case of primary infection: hunters could, for instance, be
infected by droplet infection when skinning or cutting up a sick animal
with plague septicaemia; American veterinary personnel have con-
tracted primary pneumonic plague directly from pet cats which had
inhaled contaminated droplets in the process of killing rodents with
plague septicaemia. These cases relate to a rodent basis in the form of
a plague reservoir where plague circulates continuously, which is
excluded in the case of Karlsson’s Icelandic theory. Furthermore, these
very few cases have never caused spread to any other person, thus, they
have never given rise to an endemic development (with possible conse-
quent epidemic forms).60
Morris refers to Wu Lien-Teh’s monograph on primary pneumonic
plague for empirical support of the existence of pure epidemics of
primary pneumonic plague, and Karlsson does so indirectly by cit-
ing parts of the citation including the explicit reference to this work.
However, Wu Lien-Teh states the contrary unequivocally:
It is generally agreed that the pneumonic form of plague is not directly
traceable to the epizootics [i.e., does not originate by cross-infection with
plague-infected droplets from rodent to man] but arises from human
cases of bubonic plague with secondary lung involvement.61
Wu Lien-Teh states here emphatically, and repeatedly, that primary
pneumonic plague develops only from cases of secondary pneumonic
plague, i.e., human victims of bubonic plague who have developed
septicaemia. He argues that the term ‘pure epidemic of pneumonic
plague’ “should be avoided as it is misleading as far as the origin of
the outbreaks is concerned.”62 This puts Karlsson’s theory of pure
59
Morris 1971: 208.
60
Benedictow 1993/1996a: 215–9.
61
Wu Lien-Teh 1926: 162–4. Wu Lien-Teh, Chun, Pollitzer 1934: 83.
62
Wu Lien-Teh 1936b: 418–9.
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