Mysterious and Mortiferous Clouds:
The Climate Cooling and Disease Burden of Late Antiquity
Timothy P. Newfield
Abstract
What influence did climate have on disease in Late Antiquity?
Natural archives of pre-instrumental temperature indicate
significant summer cooling throughout the period. The
coolest stretch spanned the 6th and 7th c., and corresponds
startlingly to the appearance of the Justinianic Plague in the
Mediterranean region. Drawing on principles from landscape
epidemiology, this paper marries textual evidence for disease
with palaeoclimatic data, in order to understand how gradual and dramatic climatic change, the 535–50 downturn especially, may have altered the pathogenic burden carried in
Late Antiquity. Particular attention is paid to the Justinianic
Plague, but the potential impacts of a changing climate on
malaria and non-yersinial, non-plague, epidemics are not
overlooked.
A Deadly Forecast
Sometime between 688 and 692 (or was it 704?),1 on the
Hebridean island of Iona, abbot Adomnán composed a
hagiography of his cousin, the 6th c. Irish saint Columba.
Packed full of impressive miracles and prophecies, the
Vita sancti Columbae is essential reading for Ireland and
Scotland’s early Christian history. For those interested
in late antique disease and weather, one passage stands
out. Section 2.4 deals with a disease outbreak, apparently zoonotic, among people and cattle in the area of
modern-day Dublin. Adomnán recounts that Columba,
already an accomplished healer, set sail from his second
home of Iona for his native Ireland a day after the disease struck, to attend to the ‘very many’ it afflicted. The
suffering was acute: ‘awful sores full of pus’, formed on
human bodies and cow udders, causing ‘terrible sickness’ and death.2
1 The text’s date: Brüning (1917) 227–29; Anderson and Anderson
(1961) 5, 94, 96.
2 Translation quoted: Adomnán, Life of St. Columba, 2.4, in Sharpe
(1995) 156–58. The Latin that follows is from Fowler (1894) 73–75.
Somewhat peculiarly, this plague is linked to weather.
In fact, the disease is weather.3 Looking north from ‘the
low hill of Dùn Ì’ in Iona, Adomnán relates that his protagonist witnessed a ‘heavy storm cloud’ form over the
sea. Columba then informed the monk Silnán beside
him that the cloud was no ordinary cloud. Rather it was
a “morbifera nubes”, a ‘mortiferous cloud’, and it would
pass over Iona before showering people and herds
‘between the River Delvin and Dublin’ with lethal disease. After ‘a fair and fast’ voyage, the saint and his companion reached the epicentre. As forecasted, the ‘deadly
rain’ had ‘wasted’ the population. Luckily for the afflicted,
Columba and Silnán got to work right away, and their
techniques proved remarkably efficacious: once sprinkled with the water ‘in which the blessed bread had
been dipped’, people and cows alike instantaneously
convalesced.
As rich as it is, Adomnán’s report is short on specifics. This is not unusual: vague accounts of miraculous
healings are the bread and butter of saints’ lives, and
many miracles, like this one, reached hagiographers
second hand.4 Adomnán took care to identify the hill
from which Columba saw the death-dealing cloud, and
rather precisely defined the region it passed over,5 but
other details historians would now regard as important
he considered nonessential. How long did the outbreak
last? Roughly how many people and cows fell sick, and
how many of the sick died? When did all of this happen?
This is not the only late antique plague about which
little is known. In fact, our grasp of the disease burden, extreme weather, and the climate variability that
late antique peoples and animals endured is very fragmentary. The situation is improving, thanks primarily
3 Drawing on Bede’s De natura rerum, Bonser (1963) 56 sought to
explain the etiology of this morbid rain.
4 That Columba forecasted a morbifera nubes and cured people and
cattle in East-Central Ireland was related by Silnán to Iona’s fifth
abbot, Ségéne, ‘and other elders’, who presumably told Adomnán,
or so Adomnán writes. Ségéne’s abbacy spanned 623–52.
5 “… Monticulo que Latine Munitio Magna dicitur …”, ‘a little hill
which in Latin is called Munitio Magna’, and “… ab illo rivulo qui
dicitur Ailbine usque ad Vadum Clied...”, ‘from the little river which
is called Ailbine all the way to Vadum Clied’: Adomnán, Life of
St. Columba, 2.4, in Fowler (1894) 73–74.
© koninklijke brill nv, leiden, 2018 | doi:10.1163/22134522-12340068
Adam Izdebski and Michael Mulryan (eds) Environment and Society in the Long Late Antiquity
(Late Antique Archaeology 12) (Leiden 2018), pp. 89–115
90
to bioarcheological and natural sciences, but much
remains unknown. Yet, as Harper also stresses in his
chapter in this volume, it is beyond doubt that disease
and weather were sometimes linked in Late Antiquity,
via a range of intermediate factors. Although diseaseclimate linkages are not as straightforward as Columba
or Adomnán would have it, weather and climate undoubtedly influenced disease incidence and prevalence
then, as they do today.
This paper explores how the Late Antique Little Ice
Age (LALIA, see below) may have altered the pathogenic burden people, and to a lesser extent their animals,
carried in the 6th and 7th c. In an attempt to begin to
understand how dramatic and gradual temperature
change then influenced the occurrence of epidemic
and endemic disease, this contribution reads the textual
evidence for the Justinianic Plague, malaria, and nonyersinial (non-plague) disease outbreaks, against the
available paleoscientific evidence for a changing late
antique climate.6
Identified recently in temperature-sensitive treering-width series from the Alpine and Altai Mountains,
the LALIA is a long run of markedly cool summers,
which begins abruptly in 536 and peters out from about
660.7 It sits within a longer period of less extreme summer cooling known by many names, like: the Vandal
Minimum, the Late Roman Cold Period, the Migration
Period Pessimum, the Early Medieval Cold Anomaly,
and the Dark Age Cold Period. This period commenced,
depending on the climate proxies employed, in the 4th
or 5th c., and terminated in the 7th or 8th.8 Multiple
stratosphere-clouding volcanic eruptions helped keep
growing-season temperatures low during the LALIA. In
fact, this sharply defined period of cooling, unlike the
longer and more nebulous climatic regime in which it
sits, started with a bang: a cluster of large eruptions between 535 and 550. The first eruption in this sequence,
which probably generated the so-called 536 mystery
cloud, has attracted considerable attention since 1983,
and possesses a complex history. Later LALIA volcanism,
notably the eruptions of 574±2.5, 626±2.5 and 682±2.5,
are poorly understood as of yet.9
There is a sub-discipline of epidemiology (landscape
or spatial epidemiology) that addresses, in part, the
6 Plague is a generic term. Many late antique plagues, like
Adomnán’s mortiferous cloud, were not caused by Yersinia pestis,
the bacterium that causes bubonic plague.
7 Büntgen et al. (2016) 231–36. High-resolution winter temperatures
for Late Antiquity are not yet available.
8 For example: Cheyette (2008) 127–65; Büntgen et al. (2011) 581;
McCormick et al. (2012) 191–99; Helama et al. (2017).
9 Sigl et al. (2015) 543–49 dates these eruptions to “within less than
five years”.
Newfield
complex and multifactor effects climate has on disease
incidence and prevalence. Epidemiologists of this sort
tend to think temperature and precipitation variability
do not impact all pathogens (disease-causing microorganisms) uniformly. The types of pathogens a changing climate most readily influences are often said to be
arthropod-borne, zoonotic, and/or hosted primarily in
wild animals.10 These sorts of pathogens are more likely
to undergo dramatic changes in occurrence in a changing climate as their spread is dependent on insects and
wild animals, which are more directly susceptible to
climatic change than people or livestock. Indeed, the
population distribution and density of disease-carrying
arthropods and wild animal hosts, can transform swiftly in response to dramatic swings in temperature and
precipitation.11
Yet, it is not unreasonable to suggest late antique climatic change also affected the occurrence of pathogens
principally spread among people and their animals.
LALIA climate events triggered subsistence crises, which
not only resulted in malnutrition and compromised
immune function, but also led to migrations for food
and work within and beyond famine-afflicted regions.12
These movements of people, and of their possessions,
animals included, allowed for the wider transmission of
diseases spread within or between human and livestock
populations. Overcrowding in towns and cities in years
of dearth undeniably bode well for pathogens spread
within human populations too, not to mention the
gamut of water-borne diseases closely associated with
settlement congestion and poor sanitation. So, while the
focus is set here on rodent-hosted, arthropod-vectored
Yersinia pestis (‘Justinianic Plague’ section), and malaria’s mosquito-transmitted plasmodia parasites (‘Malaria’
section), attention is also given to diseases which appear to have been spread primarily among people and
livestock (‘Non-Yersinial Epidemics’ section). The hurdles historians must overcome to establish late antique
disease-climate linkages are made very apparent in this
last segment. Indeed, whether the plague studied in
10
11
12
Arthropod-borne diseases are caused by pathogens transmitted by fleas, flies, mosquitoes, lice, ticks, etc. Zoonotic diseases
can afflict animals and people. Some pathogens, like the flavivirus that causes Yellow Fever, are both arthropod-borne and
zoonotic.
Introductions to spatial epidemiology: Ostfeld et al. (2005)
328–36; Lambin et al. (2010) 1–13; Karesh et al. (2012) 1936–45;
Engering et al. (2013) 1–7; Mills et al. (2010) 1507–14; Parham
et al. (2015).
Migrating late antique famine victims: Stathakopoulos (2004)
78–80, 156, 160. On the complexity of climate-dearth linkages:
Slavin (2016) 433–47. For famine as a spreader of epidemic disease in a very different context, see Riley (2010) 466, 472.
91
Mysterious and Mortiferous Clouds
‘Non-Yersinial Epidemics’ was related to climate change
remains uncertain.
The Justinianic Plague and Mysterious Clouding
Plague and Y. pestis in Late Antiquity
Y. pestis, the pathogen behind plague, has absorbed nearly all the energy scholars have devoted to late antique
disease.13 Although we know more about ‘true plague’
than we do other diseases, several aspects of plague’s
late antique past, such as the relationship between large
plague outbreaks and climate, are still murky.
Plague is fundamentally a disease of rodents. In their
histories of pre-modern plagues, historians long fixated
on the role played (or not played) by Rattus rattus, the
black rat, and its flea, Xenopsylla cheopis.14 Recently,
there has been a greater appreciation for plague’s
versatility.15 As disease ecologists emphasise, many species of rodents, commensal and sylvatic, can host Y. pestis, and a number of fleas can transmit the bacterium,
with varying degrees of efficiency, as well as other arthropods, notably lice. It is in sylvatic rodents that the
bacterium can persist enzootically, and it is from sylvatic rodents that outbreaks ultimately emerge. People
may contract the disease if they come into contact with
Y. pestis’ wild hosts or another animal that has, but epidemics and pandemics are understood to follow the exposure of commensal rodents to the pathogen. Rodent
fleas transmit Y. pestis to people, and between people
the disease may spread via other arthropods, human
fleas and lice, or, if it comes to infect the lungs, via respiratory droplets.16 There are several clinical forms of
plague infection, including pneumonic, septicaemic
and gastrointestinal, but the focus here is on the primary
variety: rodent-hosted, flea-borne bubonic plague. This
is simply because climate most influences plague when
carried by its rodent hosts.
Many scholars in the historical and natural sciences
now hold that Y. pestis, as the Justinianic Plague, generated significant morbidity and mortality in, and well beyond, the Mediterranean region in multiple outbreaks
between about 541 and 750. In the recent past, however, both the impact and the identity of the Justinianic
Plague have been doubted.17 The latter issue is of special
importance for this paper.
Historians began to suppose some late antique
plagues were Y. pestis not long after Alexandre Yersin—
who isolated the bacterium in his Hong Kongese ‘strawhut’ laboratory in 1894—alleged the plague he captured
was analogous with ancient plagues that were bubonic
in character.18 It would be a century, however, before
historians made a good case for a bubonic Justinianic
Plague; they were responding to sceptics.19 Scholars of
diverse training questioned, on epidemiological and
symptomatological grounds, whether the initial outbreak of Justinianic Plague, and the outbreaks that followed, were ‘true plague’.20 Not long after hesitations
surfaced, however, grounds emerged on which one
could doubt the doubters. Yersinial DNA was isolated
from the remains of late antique people.
Five studies have been published that address the
discovery of Y. pestis remnants in Justinianic Plague-era
skeletons, indicating Yersin was (some genetic differences aside) correct.21 But results are so far few.22 Four of the
17
18
19
20
13
14
15
16
Some exceptions: Blondiaux et al. (1999) 519–30; Gowland
and Western (2012) 301–11; Newfield (2013) 73–113. For a nonyersinial plague in the late 400s, see Harper (this volume).
Royer (2014) 99–110.
For example: Green (2014) 27–61; Carmichael (2014); Varlık
(2015) 17–54; Campbell (2016) 5, 8, 229, 232–34, 239, 243;
Harper (this volume). Also Ziegler (2014).
Pneumonic plague is not the rapidly vast-spreading contagious disease it is sometimes said to be: Chernin (1989)
305–307; Kool (2005). It can (but does not always) spread effectively in enclosed environments, but it typically does not
spread far, in large part because of its virulence. Pechous et al.
(2016) underscore the lethality of this variant of plague, but do
not disprove the idea that its acuteness limits its spread. For
lice: Raoult (2016).
21
22
Durlait (1989) 107–19, attempted to minimise the Justinianic
Plague’s impact in the East Mediterranean, but Sarris (2002)
169–82 refuted his arguments and has been accepted by scholars since. Also Mitchell (2015) 479–91; Meier (2016) 272–74,
278–83.
For instance, Bury (1889) 399–403 attributed the Justinianic
Plague to “moral and spiritual changes,” but Bury (1923) 62–66
concluded the disease closely resembled “the terrible oriental
plague which devastated Europe in the fourteenth century”.
Bratton (1981) 174–80; Stathokopoulos (2004) 144–46; Sallares
(2007) 231–89.
For instance: Horden (2005) 134–60; Cohn (2008) 74–77.
Some doubted whether plague could be plague, in the laboratory sense, before the advent of modern medical science
and awareness of the existence of the bacterium Y. pestis:
Cunningham (1992) 209–44.
J. Krause recently observed that Y. pestis DNA has been found
in late antique skeletal material from Valencia: The Genetic
History of Plague: From the Stone Age to the 18th Century via the
Roman Empire, Science of the Human Past Lecture, Harvard
University, 16 February 2017. Known Justinianic plagues in
eastern Spain occurred in 542/43, 584, 588, 693, and 707–709:
Kulikowski (2007) 150–60.
Not all commentators, it should also be said, would be comfortable using five or 100 Y. pestis-positive teeth pulled from
late antique people to diagnosis every Justinianic plague as
bubonic plague: Twigg (2003); Horden (2005) 150; Henderson
(2014) 58.
92
Newfield
DNA studies draw on Bavarian remains, and three analysed samples derived from the same grave, two from the
same skeleton. The first study did not use, now standard,
contamination controls, and the results of the second
study (the only non-Bavarian results published so far)
have been refuted.23 Nevertheless, the yersinial residues
available since 2013 make obvious plague was a player
in Late Antiquity.24 Molecularly speaking, however,
that plague was not exactly the same as 19th c. plague
outbreaks: Justinianic-era Y. pestis seems to be extinct.25
Unlike its diagnosis, plague’s recurrence in Late
Antiquity has not been doubted. It is uncertain, however, just how long the Justinianic Plague persisted. Not all
scholars have thought the Justinianic Plague was a 200plus year affair or, in other words, that all plagues now
considered Justinianic were in fact Justinianic. Some
have wagered plague was spent by AD 600, while others
suggest it was all over by 700.26 In their seminal paper
on the so-called First Plague Pandemic, Biraben and
Le Goff proposed Y. pestis initially irrupted in the early
540s and subsequently recurred on 13 or 14 occasions
until 767.27 Stathakopolous’ wider and more critical
reading of the sources has brought the number of recurrences up to about 17.28 The last outbreak is also now
commonly dated to about 750.29 So, as it is currently
23
24
25
26
27
28
29
Wiechmann and Grupe (2005) 48–55; Drancourt et al. (2007)
332–33. The plague DNA purportedly isolated in the early medieval French graves was not early medieval.
Harbeck et al. (2013); Wagner et al. (2014) 319–26; Feldman et al.
(2016) 2911–23. Issues with the first two studies: Harbeck
et al. (2013). Continued threat of false positives: Campana
et al. (2014) 111.
Wagner et al. (2014); Feldman et al. (2016). More precisely,
Justinianic Y. pestis has not been sampled in modern reservoirs or victims of plague.
A 6th c. affair: Jones (1964) 1.288, 2.1043. Russell (1968) 178
thought plague had ended by about 700. Two centuries earlier,
Gibbon (1776) 331, had plague reoccurring for 52 years. Gibbon
undoubtedly got this figure from Evagr. 4.29: Whitby (2000)
229, though Evagrius merely noted plague had lasted 52 years
until his time, not that plague concluded in its 52nd year. Bury
(1889) 139, 353 n.3, 453–57, who wrote of a “plague of bubo”
before Yersin’s discovery, was certain plagues in the 540s and
740s were related. Sufferers also thought this plague was recurrent: Evagr. 4.29: Whitby (2000) 231.
Biraben and Le Goff (1975) 48–80.
Stathakopoulos (2004) 113–24. Note that neither Biraben and
Le Goff nor Stathakopoulos seem to have included all of the
Iberian outbreaks Kulikowski (2007) writes of, and it has been
argued recurrences continued into the 9th c. in parts of West
Asia: Morony (2007) 67–69. Not only were there likely more
recurrences than are known, but the scope of some outbreaks
has been underestimated.
The last outbreak is now rarely dated to 767, as Biraben and Le
Goff (1975) 59, 60, 71, 77, had it, but to 747: McCormick (2007)
understood, after its arrival on the Mediterranean scene,
the Justinianic Plague reappeared (or made its way into
extant sources) every 11.6 years for a little more than two
centuries.30
It appears as though Europe and West Asia were
plagued unequally. Extant sources suggest the disease was chronic in the eastern but not the western
Mediterranean.31 Correspondingly, some historians
have questioned whether plague much influenced demographic or economic trends west of the Balkans
after 600.32 Relatively few reappearances are known in
western Europe in the 7th and 8th c.—Italy in about
608, 654 (or 680), 746 (or 767), France 640 and 693,
Spain 693 and 707–709, and the British Isles 664–66 and
684–8733—but it should be stressed that sources are
then and there scarce. On the basis of the extant evidence it seems as though Justinianic Plague outbreaks
occurred primarily in Arabic, Greek, and Syriac-speaking
regions after 600. It is especially meaningful, therefore,
that the published DNA evidence for late antique Y. pestis is Bavarian, a region with no written indications of
plague. Y. pestis has been captured now multiple times
from late antique skeletons unearthed in the outskirts
of Munich.34 Like reports of plague in rural England
and France, which are thought to be Justinianic, these
German molecules prove Y. pestis was not confined to
the densely populated eastern Mediterranean, and that
it could diffuse in thinly populated transalpine Europe.
They also demonstrate true plague circulated in regions
for which there is it no written record of it.35
To be sure, much of plague’s late antique past is poorly
understood. Written sources do not tell the whole story.
For no outbreak do we have a full course or chronology,
and some outbreaks of Justinianic Plague may have escaped the textual record altogether. For instance, we do
not know from where plague washed up in Thessaloniki
30
31
32
33
34
35
292 n.7, proposed the relevant passage in John the Deacon’s
Gesta episcoporum neapolitanorum had been misinterpreted.
Others agree: Stathakopoulos (2004) 123 n.33; Little (2007) 14.
Stathakopoulos (2004) 123.
Importantly, not all late antique sources for plague are textual
(or molecular): Benovitz (2014) 487–98; Meier (2016) 267–68.
Bachrach (2007) 29–57. Others have underscored plague’s
spottiness in Europe after 600: Biraben and Le Goff (1975) 60;
Maddicott (1997) 9, 11; Devroey (2003) 47.
Biraben and Le Goff (1975) 60, 67–71, 75–77; Kulikowski (2007)
150–60. Stathakopoulos (2004) 121, has argued the 654 Italian
outbreak (Biraben and Le Goff (1975) 60, 69, 76) occurred in
680. Significantly, Morony (2007) 67–69, wagered that in West
Asia, plague persisted into the 9th c.
See nn.23 and 24.
Rural English plague: Maddicott (1997) 14, 30–39, 44.
93
Mysterious and Mortiferous Clouds
in 597, or in Canterbury in 664.36 The pathogen surely
turned up from somewhere else on both occasions. The
7th c. Justinianic outbreaks in England and Ireland were
almost certainly imported from the continent, though
our authors say nothing on the matter.37 How far plague
travelled in the years immediately prior to its initial outbreak at Pelusium, in the eastern Nile Delta in 541, is also
unsolved. As we will see, however, few scholars think the
disease emerged locally.38
The best-understood Justinianic plague is the first.
It began about mid-July 541 at Pelusium. From there, it
spread west and east, reaching Alexandria by September
541, and Constantinople by March 542. What is now
Palestine was infected in 541–42, and Israel, Syria and
mainland Turkey in 542–43. Italy, France and Spain
were hit in late 542 or 543, and Ireland likely in 544.39
Although a Mediterranean event, this plague undeniably spread far beyond that sea.40 But just how vast an
area did it affect? Almost ex silentio, some have argued
Y. pestis diffused through regions as dispersed as Finland,
Tanzania and Yemen in the 540s.41 Should the map of
the initial irruption span an area so vast as to include
these regions? These and other areas far removed from
Justinian’s Mediterranean may not have escaped late antique plague, but mapping individual outbreaks is near
impossible without written sources. Archaeologically
detected abandoned settlements and shifts in material
culture are rarely dated finely enough to tie them to specific documented plague outbreaks.42 Human remains
are likewise not easily pinned to a particular plague.43
The yersinial Bavarians are sometimes said to have died
in the initial outbreak of 541–44, but their estimated
death dates are too broad to be sure.44
What might climate have to do with this? Natural
scientists have sought an explanation for the initial irruption of the Justinianic Plague in climate since the
early 1990s.45 Journalist David Keys was the first to flesh
out a climate-plague linkage in his brazenly deterministic Catastrophe published in 1999.46 Like all those after
him, Keys focused on the 536 event, commonly known
among historians of Late Antiquity as the ‘mystery
cloud’.
Before delving into plague’s suspected connections to mysterious clouding, it is worth exploring the
scholarship on mid 6th c. climatic change to dispel any
doubts about the exceptionality, severity and vastness of
what is now understood to be a major 15-year climate
downturn.47 That paleoclimatologists have transformed
the 536 event over the last decade and historians, with
a few exceptions, have proven out-of-step with the paleoclimatological scholarship, justifies such a digression.
Problematically, Byzantinist Antti Arjava’s minimalist
45
46
36
37
38
39
40
41
42
43
44
Maddicott (1997) 12 observes Canterbury was hit very early on
in the 664 English outbreak. He thought Justinianic plagues
reached the British Isles either from Atlantic France or the
East Mediterranean directly. For Thessaloniki: Stathakopoulos
(2004) 119.
Maddicott (1997) 10.
Uniquely, Sallares (2007) 251, 285 argued the Justinianic plague
irrupted in Egypt where it is first recorded.
More on the first occurrence’s geography: Stathakopoulos
(2004) 113–16, 278–94; Stathakopoulos (2007) 101–05.
Sallares (2007) 256. Green (2014) 27–61 has challenged historians to redraw the map of the Black Death. The same must be
done for the Justinianic Plague.
Franz (1938) 404–16; Gräslund (1973) 174–93; Seger (1982) 191–
97; Robin (1992) 233–34; Gebre Selassie (2011) 42–43, 53.
Kennedy (2007) 89, 95; in regards to climatic change in the
mid 530s: McCormick (2011) 253.
Cf. McCormick (2015) 344.
Person A120, who was unearthed in Aschheim, Bavaria, and
who was instrumental in the first two late antique yersinial
DNA studies, was archaeologically dated to 525–680 and
47
radiocarbon dated to 435–631 (533±98): Harbeck et al. (2013) 6.
Some of the more recently discussed victims found in a cemetery at Altenerding, Bavaria, were archaeologically dated to
roughly 530–70 and radiocarbon dated to 426–571: Feldman
et al. (2016) 2912; see also McCormick (2015) 346.
Baillie (1991) 234; Baillie (1994) 212 vaguely connects the downturn to plague via dearth. Farquharson, (1996) 266 thought
climate facilitated the spread of plague, though he did not
attempt to tease out any causal mechanisms. Stathakopoulos
(2003) 254, observed Seibel (1857) lumped the first Justinianic
plague and the 536 mystery cloud together as though they
were causally associated. Short (1749) 64–66 loosely listed the
mystery cloud alongside earthquakes and plague, but did not
overtly connect the two.
Keys (1999) 18–22 (map on p. 17). Notably, in the same year
Stothers (1999) 720 proposed the AD 536 eruption disturbed a
plague focus in Africa or Asia, leading to the Justinianic Plague
five years later.
Historians have hesitated to accept the extent and severity of
mid 6th c. climatic change reported in the natural sciences.
Significantly, minimalist readings of the climatic events of the
530s seem to be a reaction not to the palaeoscience but to the
determinism in a pair of catastrophist books based loosely on
that science (aspects of which are now outdated), published
in 1999: Keys (1999) and Baillie (1999). His conclusions in
Exodus to Arthur aside, Baillie contributed greatly to the modern understanding of the changing climate of 536–550 (see
below). On the other hand, Keys presented unfathomable fallout from a mega 535 eruption. He managed to link the alleged
years of climatic change, which followed this trumped up
eruption, to Teotihuacan’s fall, China’s reunification, Islam’s
emergence, Charlemagne’s birth, England’s colonisation of
North America, and the rise of Japan’s modern nation state.
Unsurprisingly, historians of Late Antiquity, including those
who accepted aspects of the climate-plague linkage Keys
drew, have been disparaging of the journalist’s conclusions,
for example: Stathakopoulos (2011) 93 n.28.
94
Newfield
reading of the mystery cloud in question remains the
main channel for specialists in Late Antiquity to the ‘relevant’ science for mid 6th c. cooling.48 This is a problem
because some of the key material Arjava presented in his
2005 Dumbarton Oaks article was out-of-date by 2008.
From 18-Month Mystery Clouding to 15-Year Climate
Downturn
The June 1991 Pinatubo eruption in the Philippines is,
by most accounts, the second largest volcanic episode of
the 20th c.49 The eruption is well-documented: there are
living witnesses, a plethora of first-hand reports, newspaper articles, detailed surveys of the mountain before
and after it blew its top, photos, videos and satellite maps
of the ejecta. The 17 or 20 megatons of sulphur dioxide
it threw, at times 35 km into the sky there, turned into
fine sulphuric acid aerosol, enveloped much of the earth
within a few weeks, remained suspended for around two
years, and possibly affected the world’s climate for longer. This sun veiling (the absorbing and ‘backscattering’
of solar radiation) was observed instrumentally to have
heated the stratosphere and cooled the earth’s surface.
Like other large eruptions, Pinatubo caused a sudden,
albeit non-uniform, near-global temperature plunge in
the range of 0.5 Celsius.50
Earlier (and much larger) eruptions are more obscure.
Their size and impact on climate are still measurable,
48
49
50
Arjava (2005) penned his article in the non-volcanic interlude,
that is, when there was no evidence for eruptions about 536.
It should be noted he had a communication from Larsen,
who would soon afterwards find ice-core evidence for major
volcanism in 536 (see n.65), in which the glaciologist noted
“nothing of interest” had been found in the ice. A reading of
John Lydus’ account, one fuller and closer than that offered by
Stothers, led Arjava to conclude the event was Mediterranean
specific, more of a fog than a veil, and damp not dry. That, and
the lack of consistent evidence for poor harvests and food
shortage in the 530s (see below), suggested the cloud did not
add up to much on earth. Minimalist readings of 536 cooling post-Arjava also stem from the reluctance of historians to
engage with the paleoclimate sciences and the willingness of
historians to write nature out of history. As Arjava observed
(p.73), historians came to the science for the 536 event more
than a decade after scientists had identified it in late antique
sources. The few historians who have wrestled with the clouding since Arjava have not, as Arjava did, attempted a complete
or current synthesis of the written and scientific evidence.
Before him, Stathakopoulos (2003) 251–55, synthesised the
historical and scientific scholarship.
Alaska’s less impactful, but more voluminous, 1912 Novrupta/
Katmai event often takes the prize.
Some have estimated that summer saw temperatures fall
about 2 Celsius in the northern Hemisphere. American
Geophysical Union (1992) 3–5; Hansen et al. (1992) 215–218;
Schmincke (2004) 259–72.
however, because some effects of major volcanism
become logged in trees, ice and other environmental
archives. A recent composite, bipolar ice-core chronology of volcanic eruptions since 500 BC, identified more
than 30 eruptions that were more sulphur-rich and
climate-impacting than Pinatubo.51 Most of the culpable volcanoes are unidentified. Eyewitness accounts of
pre-modern eruptions are few and far between. More
common are cryptic observations of the atmospheric
impacts of large eruptions. The five Mediterranean reports which survive for the AD 536 mystery clouding
are no different.52 They say nothing of an eruption, but
rather describe in vague terms an unusual dimming of
the sun. Take Cassiodorus’ account of a muted moon
and a sun having lost its ‘wonted light’ and appearing
‘bluish’, as if in ‘transitory eclipse throughout the whole
year’. The 536 reports, as astonishing as they are, are so
ambiguous they leave room to doubt the phenomenon
they describe was volcanic in origin.
Scholars and armchair enthusiasts have debated what
the 536 event was, and was not, since the phenomenon
first appeared in the pages of the Journal of Geophysical
Research in 1983.53 Richard Stothers, and fellow NASA
geoscientist Michael Rampino, then announced the
discovery of the stratosphere-clouding volcanic episode
tucked away in four, but by 1988 five,54 late antique texts,
as well as in sulphates in Greenlandic ice (the Dye-3
core, as well as another core in the island’s south, drilled
and analysed in the 1970s) and pumice-lodged wood,
which they dated to 540±90, on Rabaul, the Papua New
Guinean volcano.55
Much has changed since. Rabaul is no longer part
of the story. Even before it seemed the (nearly) 12 or
(full) 18 month-long dust veil witnessed inconsistently
around the Byzantine Mediterranean was not a volcanic
dust veil, but instead some sort of ‘damp fog’,56 Rabaul
was considered an unlikely source. Early assessments
of Antarctic ice in the 1980s did not turn up major
mid 6th c. volcanism, but instead a signal from about
505, extricating from blame all southern Hemispheric
51
52
53
54
55
56
Sigl et al. (2015) 545.
Procop. Vand. 4.14, in Dewing (1916) 328–29; Cassiod. Var. 12.25,
in Hodgkin (1886) 518–20; Joh. Lydus, De Ostensis 9, in
Wachsmuth (1897) 25, cf. Arjava (2005) 80; John of Ephesus,
in Pseudo-Dionysius of Tel-Mahre, , in Witakowski (1996) 65;
Pseudo-Zachariah Rhetor, 9.19, in Phenix and Horn (2011) 370
n.305.
Stothers and Rampino (1983) 6357, 6362–62, 6367, 6369.
Rampino et al. (1988).
Stothers and Rampino (1983) 6357, 6363.
Contemporary witnesses (n.52) assign the event different
durations.
95
Mysterious and Mortiferous Clouds
volcanoes.57 Although reproposed in 2004, shortly after
cores approaching the South Pole began showing signs
of a massive event at 542±17,58 Rabaul’s eruption chronology was re-dated with greater precision twice in
11 years. It was determined the 540±90 date was, in fact,
an uncalibrated mix-up of the ages originally returned for
the pumiceous wood: 1,430±90 and 1,390±90 B.P.59 The
535/36 Rabaulian explosion actually took place sometime in the interval of 633–70 or, as of 2015, 667–99.60
Other volcanoes got their share of attention too.
Before Rabaul, the Greenlandic sulphates were associated with the great ‘White River Ash’ eruption of Alaska’s
Mount Churchill—dated roughly in 1975 to 700±100,
but in 2014 to 833–50 and in 2015 to about 85361—as
well as with, albeit very loosely, Iceland’s Eldgjá, betterknown for erupting in the 930s.62 After this, there was
the Chiapanecan El Chichón, with an eruption that was
given a 6th c. date on multiple occasions.63 There was
also Indonesia’s infamous Krakatoa (Keys speculated
this mountain erupted forcefully enough in 535 to split
Java from Sumatra),64 the now-dormant stratovolcano
Haruna, 110 km north-west of Tokyo,65 which was apparently last active in the 500s, and the El Savadorian
Ilopango. The latter received much attention in 2010
when palaeoecologist Robert Dull, more familiar than
most with the history of this lago volcánico, asserted
that its “paroxysmal” Tierra Blanca Joven event—
considered the largest Central American eruption of
the last 84,000 years, and previously given 3rd and 5th c.
dates—spawned the 536 cooling. This was after lab work
on a tree trunk, carbonised in the event, gave a death
date “consistent with” 535.66
Yet, for a while, there were no eruptions in 535/36. The
original ice dates of 540±10 and ca. 535, that Stothers and
Rampino used to explain the abnormal Byzantine veiling, were adjusted roughly at the time when Stother’s
second, and more influential article on a volcanic 536,
appeared in Science in 1984.67 This does not now seem
surprising; most 1st millennium AD eruptions have
57
58
59
60
61
62
63
64
65
66
67
Stothers (1999) 713–23, 717.
Traufetter et al. (2004) 141, 145;
McKee et al. (2015) 1–7.
McKee et al. (2011) 27–37; McKee et al. (2015) 1–7.
Hammer et al. (1980) 233, 235; Jensen et al. (2014) 875–78;
Sigl et al. (2015).
Stothers (1999) 717.
Tilling et al. (1984) 747–49; Espíndola et al. (2000) 90, 93, 102.
Keys (1999) 277–78, 86–91.
Larsen et al. (2008). Baillie (2008)’s refiguring of the ice core
chronology moves this assignment up to ca. 535.
Dull et al. (2010).
Stothers (1984) 344–45.
in recent decades shifted back or forward in time.68
Analyses of the remnants of eruptions in eruption-site
sediments, like Rabaul’s carbonised wood, can produce
dates that disagree by a half-century or more. Studies
of sulphate layers in ice cores can also vary: a couple of
years in some cases, decades in others. When the ‘536
signals’ were shuffled back to 516±4 and the well-known
GISP2 core turned up nothing of interest (the mid 6th c.
section of that international effort was lost),69 it seemed,
for more than a decade—until clear signs of ca. 536 volcanism began to re-emerge from polar ice—that the
event had other causes.
Explanations were diverse. Some held the clouding
Procopius and his peers witnessed was tropospheric
and regional, not a stratospheric phenomenon of hemispheric or global proportions. Local and remarkable,
but inconsequential volcanism was also advanced as
the cause, or some kind of ‘acid’ or ‘damp’ fog, low-hanging and malodorous.70 Others held firm: volcano or no
volcano, the event was global. Instead of a mega sundimming eruption, oceanic outgassing, an interstellar
cloud, and an impact event were proposed. The latter,
advanced in the early 1990s, did not convince everyone.
Some scholars considered an impactor a “much less
likely” explanation for 536 cooling than a major volcanic
eruption, regardless of the complete lack of evidence
then for said eruption.71 Different types of rocks and
impacts were envisioned: either a comet “air-bursted” in
the upper atmosphere and ignited one or more vast forest fires, or a “medium-sized asteroid” struck an ocean
and threw marine aerosols into the stratosphere.72 It
was even determined that the landing of a comet less
than 1 km in diameter, could have loaded the sky with
enough debris to generate multiple successive years of
cooling. So appealing was an impactor—even after the
introduction, in 2008, of a very strong basis for a volcanic
origin for the 536 clouding—it was argued that an extraterrestrial rock 640 m in diameter landed in Australia,
and together with an eruption or two, dimmed the
lights on Byzantines and carved out Australia’s Gulf of
Carpentaria.73
As persuaded as some were, the impactor theory did
not last. Even dendrochronologist Michael Baillie, who
68
69
70
71
72
73
For the recent exact dating of some early medieval eruptions,
see Büntgen et al. (2017) and Oppenheimer et al. (2017).
Hammer (1984) 51–65; Clausen et al. (1997); Zielinkski (1995)
20,949.
Grattan and Pyatt (1999) 174, 178; Arjava (2005) 79, 80, 93.
Stothers (2002) 4; D’Arrigo et al. (2003) 257.
Clube and Napier (1991) 49; Baillie (1994) 216; Rigby et al.
(2004).
Abbott et al. (2008); Abbott et al. (2014a) 421–38; Abbott
(2014b) 411–20.
96
Newfield
first advocated for a space rock in his seminal 1994 The
Holocene article (which turned 536 from a 18 month
event into a 15-year climate downturn), sided with volcanism. This was after glaciologist Lars Larsen and his
team found evidence for a major eruption in multiple
cores (Dye-3 included) at both poles.74 This big lowlatitude tropical event was affixed a date of 533/34±2, and
was said to explain why the ‘sun’s rays’, according to John
of Ephesus, ‘were visible for only two or three hours a
day’ in 536/37.75 Importantly, the Larsen paper also drew
attention momentarily to “an even larger” northern
Hemisphere deposit, given a date of 529±2. The authors
seem not to have thought this earlier event important.
There were (and still are) no indications, written or otherwise, that 529 was atmospherically or climatically unusual. Only months later, however, did Baillie draw on
an ever-growing quantity of dendroclimatological data
to suggest both of these newly recognised eruptions
were misdated: they needed to be bumped forward six
or seven years.76 This adjustment offered an explanation
for the unusual tree-ring signals Baillie had highlighted
in the early 1990s.77 It also meant the 539/40 eruption,
not that of 535/36, was tropical. The earlier of the two
occurred north of the Tropic of Cancer.
The injection of dendrochronology, and eventually
dendroclimatology, into the discussion of the 536 event,
initially with Baillie’s papers, significantly altered what
scholars thought happened in the 530s. Independently
of texts and ice, trees identify a major disturbance in
536.78 Although unknown to Stothers and Rampino in
the 1980s, trees witness the event best. With robust annual resolution, and objectivity 6th c. historians cannot
compete with, as well as a temporal and spatial awareness unmatched by ice cores or contemporary witnesses, tree-ring-width and latewood density studies
reshaped the debate about what 536 was and was not.
Mediterranean texts describe the 536 event as months
long, but the trees from Ireland, Germany, Scandinavia
and the U.S.A. which Baillie originally surveyed, signify
the event lasted more than a decade. Trees also seem
to demonstrate that 536 was not some local Byzantine
oddity; it was vast, hemispheric, even possibly global,
hence the comets and asteroids in lieu of a volcano.
Trees also reveal not one consistent low, but a marked
74
75
76
77
78
Baillie (2008) L15813; Larsen et al. (2008) L04708.
See n.52.
Baillie (2008) L15813.
Baillie (1991) 233–38; Baillie (1994) 212–17.
Some relevant studies: Briffa et al. (1990) 437 (fig. 2), 439;
Helama et al. (2002) 683 (table 3), 685 (table 4), 686; Zhang
et al. (2003) 1739 (fig. 3); Salzer and Hughes (2007) 62 (table 2),
63 (table 4), 65 (table 6), 66; Churakova et al. (2014) 145–49.
departure from normal growing conditions with acute
troughs and peaks. The first nadir sits at 536–37, the second at 540–41. A third low about 546–47, and another in
the early 550s, identified in Baillie’s original work, have
yet to receive meaningful consideration.
Over the last 20 years, dendroclimatology from across
the northern Hemisphere has confirmed, and consistently reconfirmed, that the 536 event was hemispheric
and more than a decade long. Wood from both worlds
(Old and New) and both hemispheres show it.79 Multiple
dendro-based temperature reconstructions have found
several of the coldest growing seasons, typically June–
August, of the last 2,000, or in some cases 7,500 years,
fall within the 536–50 downturn. A few examples: a 1993
paper identified that the years 536, 535, and 541 had the
second, third and fourth coldest growing seasons in a
2,000 year-long chronology from Sierra Nevada, at 3.13,
3.07, and 2.93 Celsius below the series’ instrumental
mean.80 A 2001 paper reported frost rings and other evidence for an unusually chilly 536–45 decade, with low
points at 536 and 543 (and respite at 538) in a Mongolian
series nearly as long.81 Finally, a 2015 study, using a composite northern Hemisphere chronology stretching back
to 500 BC, established the successive decades of 536–45
and 546–55 as the first and tenth coldest decades in the
series. The same trees also put six of the 13 coldest years
between 500 BC–AD 1250, within the downturn’s limits:
June-August 536 was about 2.5 Celsius and June–August
541 2.7 Celsius below the preceding 30 year average.82
Despite these advances, the mystery cloud maintains
elements of mysteriousness. It is unclear which volcanoes triggered the downturn, and there is some room to
doubt that Cassiodorus and company observed a hemispheric event. As Arjava and others have advocated,
it is not impossible they beheld a local disturbance.83
Procopius has Vesuvius bubbling, but not rupturing, in
536, but this so-called ‘extinguisher of all things green’
may have exploded then.84 Or perhaps another nearby
mountain did; an eruption at Stromboli has been dated
roughly to 550±50.85 In other words, minor volcanism in
79
80
81
82
83
84
85
At present, high-resolution palaeoclimatology for southern Hemispheric cooling in the 530s seems to come from
Patagonia alone: Lara and Villalba (1993) 1106 (fig. 3). In other
chronologies south of the equator, the 536–50 downturn does
not register.
Scuderi (1993) 1435.
D’Arrigo et al. (2001) 241–42.
Sigl et al. (2015) 547–48, extended data table 5.
In addition to Arjava (2005) and Grattan and Pyatt (1999), see
Nooren et al. (2009) 107.
Procop. Goth., 6.4, in Dewing (1919) 324–27.
Arrighi et al. (2004).
97
Mysterious and Mortiferous Clouds
the vicinity, and a major eruption in the distance, could
have coincided, one veiling Mediterranean skies, the
other marking the world’s trees.86
Much has changed since Arjava tackled the scholarship on the 536 mystery cloud. It is undeniable now
that an eruption cluster—multiple events, including
two that far outclassed Pinatubo—generated 15 years
of long-unparalleled summer cooling from 536 onward.
Nevertheless, several issues remain to be resolved. The
spatio-temporal variability of the climate forcing of
these eruptions, in particular their effects on hydrological cycles, are faintly understood. How plunging mid
6th c. temperatures affected people and environments
are other matters altogether. That summer temperatures
sank dramatically, and remained low for many years,
need not mean there was widespread famine and death.
Some regions may have suffered greatly and others far
less so. The changing climate would have impacted agroecosystems differently, and a multiplicity of strategies
were undoubtedly employed to cope. Although severe
dearth and death may have occurred in some areas, it
is important not to underestimate the resilience of contemporaries. Even in the hardest hit areas not everyone
would have come out from under the cloud worse off.87
Had the climate of the mid and late 530s had something
to do with the Justinianic plague, however, a case could
be made, whatever the evidence for famine, that climate
deterioration was instrumental in the depopulation of
the former Roman world.
first pandemic are now multiple and various, but they
may be grouped into two categories. As the following
makes clear, only one linkage has been expounded at
any length.
1.
Plague Foci Disrupted
Several scholars advocate a theory that sudden climatic change in the mid 530s disrupted a plague
reservoir. This allowed the bacterium to spread
beyond its normal range in wild rodents, and to
break out in nearby semi-commensal rodents and
people, and make its way via trade to the Mediterranean region, mingle with commensal rodents,
and irrupt as the Justinianic Plague.
1.1
Keys advanced the first of these linkages. He wagered climate forcing of the 535/36 eruption greatly perturbed a Y. pestis focus east of Lake Victoria in
Kenya and Tanzania. “Massively excessive rainfall”
on the heels of drought, or drought alone, resulted
in a “breeding explosion” and a range extension of
sylvatic plague-tolerant rodents, gerbils and multimammate mice, he suggested. In the first scenario,
unusually heavy precipitation led to unusually rich
vegetation coverage, which facilitated the population growth of gerbils and natal multimammate
mice. In the second scenario, drought killed off the
plague-harbouring gerbils and mice, leading to a
population collapse of their predators. Gerbil and
mice populations bounced back “the minute the
drought is over”, but populations of the animals
that ate them lagged behind. The “massive imbalance” between predator and prey allowed sylvatic
rodent populations to grow and expand their range
“for a few years.” In both scenarios, plague-tolerant
rodents come to mingle with more susceptible and
occasionally commensal rodent populations (the
grass rat Arvicanthis is proposed) living beyond the
plague focus. These rodents eventually mixed with
the highly susceptible and commensal black rat,
R. rattus. So, via various fleas on the backs of various rodents, the bacterium travelled outward from
its reservoir, until it penetrated human settlements
and their rodent populations. Keys proposed
settlements in coastal East Africa, possibly in
Tanzania and on Zanzibar, were afflicted first, before Y. pestis, in fleas, black rats and people, made
its way up the Red Sea, with ivory, to Egypt.88
88
Keys (1999) 17–22, 309 n.19. Several historians generally approve of Key’s climate-plague linkage, but he never received
full support: Stathakopoulos (2000) 275–76; Stathakopoulos
Volcanic Climate Forcing and the Justinianic Plague
Did aerosol-flooded stratospheres trigger the Justinianic
Plague or facilitate its arrival in the Mediterranean region? The linkages between the 535/36 eruption and the
86
87
Perhaps supporting this theory, a ‘floating’ dendro-series from
Constantinople’s hinterland recently failed to identify a major
536–50 growth departure. Of course, an impactor may have
near-simultaneously fallen from space too. Dallas Abbott and
his team described iron oxide, silicate spherules, and other
ejecta indicators in the melt-water of a portion of the ‘missing’
6th c. section of the GISP2 (dated to 533–40) in a recent paper.
A high concentration of calcium found at the once lost 536
mark was interpreted as calcium carbonate (a main component in seashells) following detection of tropical aquatic-life
microfossils (a first for Greenlandic ice), leading to the proposal that marine aerosols then also clogged the stratosphere.
While less popular among historians than collapse, more
attention is now being paid to historical resilience to natural world change among scholars of Late Antiquity and the
Middle Ages. For instance: Löwenborg (2012) 22–23; Izdebski
et al. (2016) 189–208; Preiser-Kapeller (2015) 196–97, 216–17.
See also Mordechai (in this volume), with respect to cities and
earthquakes.
98
1.2
Newfield
Before and after it became apparent that late antique plague (the Bavarian Y. pestis) originated in
Asia, some wagered climatic change in the mid
530s disrupted an enzootic plague focus in Asia,
which ultimately led to the Justinianic Plague.
Opinion has differed on precisely where the epizootic arose, some specify the Himalayan foothills in
India, others western China. Although these linkages remain undeveloped, they possess much in
common with Keys’ hypothesis. In short, climatic
change is thought to disrupt an Asian plague focus,
impelling sylvatic, plague-carrying rodents and
plague-transmitting fleas to spread beyond their
usual range and mix sooner or later with more vulnerable commensal rodents.89 How the bacterium
reached the Mediterranean region is rarely spelled
out, but different theories regarding the Asian origins of late antique plague come into play here.
1.2.1 McCormick has proposed the bacterium reached
Pelusium first, rather than the much bigger and
more connected port city of Alexandria, because
of its proximity to the Red Sea. Whether or not
Trajan’s canal, which linked the Nile and the Red
Sea, functioned in 541,90 Red Sea trade networks
may have been especially busy that year as the Sassanids invaded Syria in 540,91 disrupting overland
commercial linkages. Plague-carrying rodents may
have made their way to the Mediterranean with
goods from South Asia, brought directly to Pelusium via the canal or via caravans travelling overland
up the western coast of Arabia.92 What happened
before plague set out on the Indian Ocean is not
elucidated. Was Y. pestis already circulating among
rodent populations in India or had it recently arrived in the region?93
1.2.2 Others argue the bacterium travelled westward
overland within Asia. Long-distance treks from
East Asia have been put forward, though not
89
90
91
92
93
(2003) 253; Stathakopoulos (2004) 268; Stathakopoulos (2011)
93; Sarris (2002) 181 n.32; Horden (2005) 152–53; Sallares (2007)
285; Gebre Selassi (2011) 42–43; McCormick (2003) 20–21 n.33
notes “the chains of causality are likely more complex”.
Possible causal mechanisms have not been explored: Büntgen
et al. (2016) 231.
Power (2013) 89, suggests the canal was still operational in the
mid 6th c.
Procop. Pers. 2.5, in Dewing (1914) 294–95.
McCormick (2007) 304. Now also: Sussman (2016) 326, 347, 354
and Harper (this volume).
McCormick (2007) 303–304; cf. Allen (1979) 19; Sarris (2002)
170–72.
articulated,94 but a shorter trip, directly connected
to the climatic change of the mid 530s, has been
advanced in some detail. Stathakopoulos wagered
there might be something in the report of Marcellinus Comes’ continuator of a severe drought in
536 that ruined vast stretches of pastureland in
Sassanid Persia, and compelled 15,000 bedouins
to migrate—or, as the 6th c. chronicler alleges, the
Lakhmid ruler Alamundarus drove them—into
the Byzantine province of Euphratensis.95 Stathakopoulos suggests the drought was part and parcel
of the 535/36 event, and that the migration would
have allowed the bacterium to cover considerable
ground.96 Whether these bedouins were themselves harbouring plague, or they simply transported Y. pestis-carrying rodents or fleas, is not said. He
implies, however, that plague was active, possibly
enzootically, already in 536 somewhere, either
in or near the Sassanid empire or the Lakhmid
kingdom.97
2.
Dearth and Plague
Several scholars have wagered food shortages,
whether patchy and short or vast and severe, followed the 535/36 eruption in western Eurasia, and
were instrumental for the Justinianic Plague. Causal mechanics at work in climate-dearth-plague
linkages have yet to be explored, but it is clear
food shortages are thought to have factored in two
ways.98
2.1
Some hold famine generated widespread malnutrition, compromising the immune function of late
antique peoples, making them more vulnerable to
plague; in other words, the Justinianic Plague.99
2.2 Others venture subsistence crises caused “population disruption”, that is migration, and this facilitated the spread of plague, either in regions the
Justinianic Plague afflicted or in distant Y. pestis
foci in Africa or Asia.100
Some of these linkages can be dispensed with. The
most clearly expounded of them, linkage 1.1, is no
94
95
96
97
98
99
100
Especially since it was determined the aforementioned
Bavarian plague likely originated in or near north-western
China. This is visualised in Wagner et al. (2014) 323, fig. 4.
Marcell. com., 14.11, in Mommsen (1894) 105.
Stathakopoulos (2003) 254; Stathakopoulos (2004) 268, 269.
This runs against the argument of Sarris (2002) 171.
Among other studies, Sigl et al. (2015) 548 and Baillie (1994) 212
link plague and the climatic cooling vaguely via dearth.
McCormick et al. (2012) 198–99 n.23; McCormick (2015) 328.
Baillie (1991) 234; Baillie (1994) 212.
99
Mysterious and Mortiferous Clouds
longer tenable, at least as Keys originally presented
it. Proponents of 1.1 argue plague evolved in Africa
and emerged from its ancestral homeland in 536, or
shortly thereafter. Genomic evidence, however, refutes
the idea that plague comes from Africa. Yet, as is suggested here, this need not mean the Justinianic Plague
did not emerge in Africa. Indeed, the late antique witnesses and the DNA work are not necessarily at odds.
Although contemporaries have the Justinianic Plague
originating in East Africa,101 all remnants of ancient and
medieval plague explored genetically so far are tied to
Asia, and it appears the yersinial DNA captured from late
antique Bavaria was ultimately native to north-western
China, the Xinjiang region specifically, or someplace
nearby.102 As conflicting as this may seem, it is not out
of the question the Justinianic strain had established a
focus, of course now extinct, somewhere farther west
than the Xinjiang region, and that the plague emerged
in the 6th c. from a reservoir closer to the area we know
it devastated than north-western China or East-Central
Asia. In other words, Y. pestis did not evolve in Africa,
and late antique plague best matches strains isolated
101
102
For example: Evagr. 4.29 (Whitby (2000) 229–30) reports the
plague was thought to have originated in Ethiopia. PseudoZacharias Rhetor, 10.9, (Phenix and Horn (2011) 414–15) identifies Egypt, Sudan and Ethiopia as the region in which the
plague began. Procop. Pers. 2.22 (in Dewing (1914) 452–53), favoured, as noted, Pelusium in the Nile Delta. From Gibbon to
Sarris, historians have long favoured Africa too: Gibbon (1776)
327; Sarris (2002) 172. McCormick expressed doubts about an
African emergence before the Bavarian molecules were captured, which suggest late antique plague originated in Asia:
McCormick (2003) 21 n.33; McCormick (2007) 304.
Harbeck et al. (2013); Wagner et al. (2014) 323; Feldman
et al. (2016) 2912, 2914. That the Justinianic Plague emerged in
north-western China is not set in stone. The extant strains of
Y. pestis with which the late antique Bavarian strains compare
well have not only been isolated in Xinjiang, China but also in
Mongolia: Harbeck et al. (2013). Further, and as Spyrou et al.
(2016) 879, pointed out, Y. pestis has been sampled more often
in sylvatic rodent populations in East Asia than anywhere else;
consider that 107 of the 133 Y. pestis genomes sequenced for
the influential paper of Cui et al. (2013) 577–82 were Chinese
in origin. This means as more strains from neighbouring regions are sequenced, and made available, the origins of late
antique European Y. pestis could shift a little. For instance,
Spyrou et al. (2016) 879 suggest the yersinial DNA captured
from late medieval European skeletons compares well with
Y. pestis strains sampled recently in the Caucasus, though late
medieval Y. pestis has, like late antique Y. pestis, been tied multiple times to western China: Haensch et al. (2010); Bos et al.
(2012). Eroshenko et al. (2017), which appeared as this paper
was going to press, discusses two Y. pestis strains encountered in Kyrgyzstan that are genetically closer to the Bavarian
plague remnants than other known strains.
in north-western China and other places in the vicinity,
but the Justinianic Plague may have irrupted from one
of the regions to which late antique authors trace its origins, that is, West Asia or East Africa.
Let’s shift our attention to linkage 1.2. Problematically
for supporters of this theory, mid 6th c. plague has yet
to turn up in East or South Asian texts. At least two late
antique authors, however, suggest the plague appeared
in West Asia before arriving in the Nile Delta. Michael
the Syrian has John of Ephesus reporting that the plague
irrupted in Yemen, along with Ethiopia and Sudan
(former Himyarite and Kush lands), early on. The noncontemporary Chronicle of Séert observed that the plague
disseminated through Persia, as well as India (Sudan or
Arabia?103) and Ethiopia.104 If correct, the implication is
either that the Justinianic Plague materialised in northwestern China or someplace nearby (where late antique
yersinial DNA currently locates it) and infected parts of
South-west Asia and East Africa before irrupting in the
Mediterranean at Pelusium, or that the culpable EastCentral Asian strain of Y. pestis emerged from a now extinct West Asian or East African focus.
That Y. pestis penetrated the Mediterranean region
at multiple points is another possibility that should be
considered. Linkage 1.2.2 implies Procopius’ pinpoint
identification of the irruption of the plague at Pelusium,
and subsequent spread around the Mediterranean, a trajectory historians have followed since Gibbon, is either
incorrect or incomplete.105 To be sure, Procopius may
not tell us the whole story. Fortunately, the occurrence
and severity of the documented drought of 536, which
103
104
105
‘Byzantines’, like their Greco-Roman predecessors, often conflated or mixed up India and Ethiopia, and sometimes also
southern Arabia. That the Chronicle of Séert mentions India
and Ethiopia, implies its author or the authors its author drew
on may have mistaken southern Arabia, not Ethiopia, for
India. That said, the author may have intended to indicate the
plague afflicted both the people of the former Kush region of
Sudan and the Aksum kingdom of Ethiopia. Mayerson (1993)
169–74; Schneider (2015) 184–202. Wood (2014) 124–25 n.67
notes the Chronicle of Séert’s account of the plague is dependent partially on John of Ephesus’ writings and the lost work
of 8th c. historian Bar Sahde.
Michael the Syrian, Chronicle, 9.28 (Chabot (1901) 235);
Chronicle of Séert, 32 (Scher (1911) 182–83). Others, as noted
(n.101), put the plague in Ethiopia. Yemen and Sudan are not
encountered in John of Ephesus’ account of the plague, preserved in the work of Pseudo-Dionysius of Tel-Mahre. That
compiler excluded the earliest bits of John’s plague passage:
Pseudo-Dionysius of Tel-Mahre, in Witakowski (1996) 77
n.356. The easternmost region John mentions, in the portions
of his text extant in Pseudo-Dionysius, is Mesopotamia (see
below).
Gibbon (1776) 327–28.
100
Newfield
is central to linkage 1.2.2, can be tested, as moisture-sensitive proxies exist for the region,106 but there are issues
with this linkage nonetheless. It is doubtful plague could
have irrupted in Syria in the late 530s and escaped the
written record. Further, if the bedouins were diseaseridden and dying, presumably Marcellinus’ continuator would have said so. Perhaps, instead, they somehow
introduced Y. pestis to a suitable environment in Syria,
from which it irrupted in 541 or later.107 But, was plague
already present in Sassanid Persia (somewhere from
modern-day Pakistan to Iraq) or in Arabia in the 530s?
Plague infiltrated a Sassanid army in 543 in Atropatene,
and Procopius notes the disease had not by then broke
out in Assyria,108 but were Sassanids earlier exposed
elsewhere? Perhaps plague was spreading among rodent
populations in Sassanid lands. As noted, the Chronicle of
Séert has the Justinianic Plague circulating in the region
seemingly before summer 541, when it struck Pelusium.109
That John of Ephesus has Yemen infected early, and
plague in Palestine before Mesopotamia, suggests the
Justinianic Plague landed or irrupted in the Arabian
Peninsula’s south-west, and spread up the Red Sea.110 At
the same time, it may have spread west into East Africa.
Linkages 1.1 and 1.2 seek to explain the arrival of
plague in the Mediterranean world in 541. Linkage 2.1
ties the 535/36 eruption not to the occurrence, but to
the mortality, of the first pandemic. Like 1.1, linkage 2.1
is doubtful, though it is not so easily dismissed. Famine
and malnutrition, or the threat of them, cannot outright explain the plague’s occurrence or high mortality. In short, there is no plague without the bacterium,
a sizeable rodent population to host it and efficient
flea vectors, and people need not be severely malnourished or immunologically compromised to die from Y.
pestis.111 Detailed bioarchaeological analysis on plague
victims from a Black Death mass grave has concluded
that the frailer and the older were more likely to die.112
But it is clear that late antique people, like people today,
106
107
108
109
110
111
112
Textual and palaeoclimatic evidence for early 6th c. West
Asian drought, is considered in McCormick et al. (2012) 197
n.22. Cook et al. (2015) identifies significant drought conditions across parts of Europe in AD 534–36.
This could explain the problem of the five-year gap
Stathakopoulos refers to: Stathakopoulos (2004) 269.
Procop. Pers. 2.24, in Dewing (1914) 474–77.
The presence of plague in India, Persia and Ethiopia seems
to be dated in the text to the tenth year of Husraw I’s reign
(540–41): Chronicle of Séert, 32 (Scher (1911) 182, cf. 182 n.5).
Pseudo-Dionysius of Tel-Mahre, in Witakowski (1996) 80.
While Y. pestis does not struggle to kill the young or healthy,
the most detailed palaeopathological studies of a plague mass
grave to date have the oldest and frailest dying often, see below.
DeWitte (2014) 98–123.
whether or not immunologically feeble and physiologically stressed, were very likely to die from plague in lieu
of prompt antibiotic treatment.113 Aggregate mortality
might have been slightly greater in a population that recently suffered famine, but Justinianic outbreaks would
have claimed many lives either way. If dearth was a factor, it is likely because of the non-dietary consequences
characteristic of severe subsistence crises: linkage 2.2.
But what is the evidence for famine in the early years of
the downturn?
Many families and communities may have been able
to absorb one bad harvest in the 6th c., but few could
absorb two or three in succession. Consecutive years
of poor growing conditions were certain to take a toll.
Nevertheless, evidence for vast crop-failures and starvation is not as forthcoming as one might expect. A few
contemporary reports of despair and devastation are
motific or hyperbolic, like the Milanese gossip about
Ligurian mothers eating their young, reported in the
Liber Pontificalis, and the claim made in the same text
of a great dearth ‘throughout the entire world’. However,
neither they, nor less-sensational accounts of suffering,
such as the terse ‘failure of bread’ jotted into the Irish
annals, or John the Lydian’s ‘the produce was destroyed’,
should be written off as lacking any grounding in an
immediate post-eruption reality.114 In 537 Cassiodorus
wrote of a general food shortage, failed harvests in
Liguria, and ‘starving people’ in Lombardy. Yet, in the
same year, he also reported rich Istrian crops of grapes,
olives, and grains. In 538, he refers to growing-season
frost and a drought damaging grain, fruit, and grape harvests, as well as general food scarcity, but his letters also
mention ‘an exceptionally abundant’ previous harvest,
one good enough to stave off famine. In 538, he mentions another good grape crop in Istria, but Friulians and
Venetians suffering a dearth of millet, wheat, and wine
crops.115 Although it is unclear whether crop failures occurred at all in many areas—such as most of the western Mediterranean and trans-alpine Europe, or even
North Africa—Cassiodorus’ references to crop health
imply the occurrence of dearth was patchy.
Is the dendroclimatological evidence from central
and northern Europe, for truly exceptional 536–37
growing-season temperatures, evidence enough for
famine? One recent paper that modelled the forcing of
113
114
115
Perry and Fetherston (1997) 36, 58. As the WHO notes, “untreated plague can be rapidly fatal”: who.int/csr/disease/
plague/en/ (accessed 20 July 2017).
Lib. Pont. 1.291; Annals of Ulster in Hennessy (1887) 46–49;
Charles-Edwards (2006) 94–95; Annales Cambriae in Williams
(1965) 4.
Hodgkin (1886) 519–20; Cassiod. Var. 12.22, 12.27, 12.28, 12.26, in
Hodgkin (1886) 513–14, 521, 523–24, 520–21.
101
Mysterious and Mortiferous Clouds
the downturn’s largest eruptions, found it was precisely
where written evidence is especially thin, north of the
Alps, that the 535/36 eruption would have most significantly impacted temperature. Dense aerosol loads for
both this and the 539/40 eruption occurred north of 30°,
but north of 50° the veiling was much thicker.116 Had
crops failed in northern Europe for successive years,
triggering famines, the movement of people and goods
associated with severe dearth could have helped the initial plague occurrence along. Migrations, like that which
Marcellinus’ continuator reported, could spread plague,
pneumonically or gastrointestinally, or possibly between rodent populations. If the worst hit areas lay far
north of Mediterranean shores, however, dearth is not
so easily tied to any northward spread of disease.
Another aspect of shortage-related “population disruption” merits notice. Crop failures also inspire hoarding, and hoarding is associated with a noticeable uptick
in commensal rat numbers. Populations of R. rattus
may have fared well, as such, during any mid 6th c.
famine.117 Again, however, this might not have factored
into any northern European experience of plague in
Late Antiquity, as these commensal creatures are considered non-instrumental in the spread of plague there.118
Still, it should be stressed that evidence for major
subsistence crises in the immediate context of the
Justinianic Plague is not known.119 The latest of the
aforementioned reports of dearth dates to 538, and
there is no known evidence for general famine in the
Mediterranean world following the 539/40 eruption,
though temperatures then plummeted too.120 Famine or
no famine, perhaps the sudden cooling triggered by the
539/40 eruption disrupted plague-susceptible rodent
populations in the Mediterranean region just as the bacterium arrived.121 Whether or not cooling or reported
116
117
118
119
120
121
Toohey et al. (2016) 401, 405, 406, 410, fig. 2.
Silver (1982) 107–20; Silver (2012) 214–17, 225.
Hufthammer and Walløe (2013).
Stathakopoulos (2004) 270–77, 289, 294–96 observes multiple
siege-related shortages in the late 530s and 540s. Cheyette
(2008) 156 refers to “major famines” triggered by the 535/36
event in Europe “perhaps continuing as late as 541”, but does
not provide a reference. Harper (this volume) also downplays
the role of famine.
The Irish annals document a ‘failure of bread’ in 536 and 539,
but the latter is possibly a doublet. In any case, plague did not
make its way to Ireland until 544. The Chronicle of Séert has a
famine following the Justinianic Plague, Chronicle of Séert 32
(Scher (1911) 186).
In his popular history of the pandemic, publisher W. Rosen,
who also favoured an East African emergence, suggests low
temperatures in 536 drove a rapid expansion of commensal rodent populations, which facilitated the plague’s rapid
spread and high mortality around the Mediterranean in
(and unreported) dearth, contributed to Mediterranean
and European plague mortality and dissemination in
541–44, to account for the arrival of Y. pestis at Pelusium,
or elsewhere, we must turn to linkage 1.2 (more distant
foci of Y. pestis) and the relationship of the bacterium’s
sylvatic rodent hosts in those foci with climate.
The role of climatic change in late antique plague
recurrences, a subject yet to be broached, also warrants consideration.122 Recent multidisciplinary work
has sought to connect the Black Death, and 15 of its
recurrences in the Mediterranean and Europe, to climate variability in Central Asia. This work has been
specifically focused on the influence of changing temperature and precipitation on the long-tailed ground
squirrel and Altai marmot, the primary Y. pestis-carrying
rodents in the region, from which yersinial DNA captured from late medieval Europeans is thought to have
derived.123 The study concluded that unfavourable climatic events, which triggered the collapse of sylvatic rodent populations—causing their fleas to search out new
hosts and allowing the bacterium to spread outward
from its Asian foci—“consistently preceded” plague
reintroductions by 15±1 years. Once unleashed in Asia,
plague was then transmitted westward, in ways yet to be
determined, until it reached the Mediterranean, and irrupted in commensal rodent and human populations.
Did climate events also trigger yersinial epizootics, which might be tied to multiple irruptions of the
Justinianic Plague? The matter requires serious attention, and it may be more complicated than the abovementioned (and already quite complex) study, published
in 2015, indicates. Indeed, it is no longer commonplace
to think plague was never native to, or enzootic in, western Eurasia. Three genomic analyses of Y. pestis captured
from late medieval and early modern casualties, appeared in 2016.124 Each suggests, on molecular grounds,
that plague was not continually reintroduced to Europe
after the Black Death, but rather it became endemic
or enzootic in or nearby Europe. Exactly where, and
in what, Y. pestis set up shop is unclear. Some propose
plague became enzootic in wild rodents; others wager it
persisted by continually cycling through urban rats and
people. Either way, reintroductions of the bacterium do
not account for all Black Death recurrences.125
122
123
124
125
541–43: Rosen (2007) 189, 193, 200, 201–03. If correct, dramatic
cooling again in 540–41 would have further assisted the expansion of R. rattus populations.
As McCormick et al. (2012) 198 and Haldon et al. (2014) 123.
Schmid et al. (2015). See also: Stenseth et al. (2006) 13,113–14;
Kausrud et al. (2010) 112.
Seifert et al. (2016); Bos (2016); Spyrou et al. (2016).
Historians have also got involved: Carmichael (2014) 157–91;
Pribyl (2017) 215–23. Earlier: Panzac (1985) 82–91.
102
Newfield
Relevant here are text-based studies on Byzantine
reappearances of the Justinianic plague, which argue
Y. pestis became endemic or enzootic in West Asia,
south-western Syria specifically, in the late 6th c.126 From
the East Mediterranean, plague is thought to have often
diffused widely following local Levantine earthquakes,
which disturbed the nascent plague focus. Although
seismic events can disrupt sylvatic rodent populations,
and recent plague outbreaks have been tied to earthquakes (such as the 1907 epidemic in San Francisco,
USA, and the 1994 epidemic in Beed and Surat, India),127
there is room to doubt the claim Y. pestis anchored itself
in Syria. The finding is rooted in the assumption that the
late antique record of plague is complete. That there is
more evidence for plague in the Levant then than there
is elsewhere need not mean plague became enzootic or
endemic there. Likewise, plague was not necessarily absent where and when there is no evidence for it.128 Still,
that a non-extant plague focus came into being in 6th c.
Syria, possibly with the assistance of bedouins, or elsewhere in West Asia or East Africa, from which (some)
plague recurrences irrupted, is a real possibility worth
further consideration. Plague may have spread up the
Red Sea to Trajan’s canal from Yemen, landed at Berenice
before making it to the Nile, or travelled overland along
Arabia’s western coast to reach the Nile Delta, but it may
not have arrived in Yemen direct from India. It may have
previously focalised in Arabia or East Africa.129
126
127
128
129
Tsiamis et al. (2011) 36–41; Tsiamis et al. (2013) 55–64.
Stathakopoulos (2007) 105 earlier hinted plague may have become “endemic” in Syria from the 13th to the 18th occurrence.
Earthquakes in plague foci are considered potential triggers
of plague epidemics: Duplantier (2012) 195; Catanach (2001)
146. Horden (2005) 152 dismissed an earthquake connection
in Late Antiquity, but he focused on tremors and plagues in
Constantinople only. He considered climate, the 536 event
in particular, a more likely trigger of the Justinianic Plague.
McCormick (2007) 308 thought tremors warranted further
consideration.
Tsiamis et al. (2011) 38 attempts to identify late antique
“plague-free” periods. Cf. Stathakopoulos (2007) 103–105;
Maddicott (1997) 9. Also see Mitchell (2015) 372–401.
Stathakopoulos (2007) 104 suggests plague may have
“never ceased to be present” in late antique Iraq, Syria and
Mesopotamia. Green (2015) xiv–xv implies an early, pre 541,
arrival in East Africa. The evolutionary distance (63 Single
Nucleotide Polymorphisms) between the Bavarian Y. pestis and the plague strains to which it is most closely related,
raise the possibility, as Green argues, of a “time-gap” between
plague’s departure from north-western China, or someplace
nearby, and its arrival on the Mediterranean scene. For the
SNP count: Feldman et al. (2016) 2918 and ‘Supplementary
Materials’ S9–S11.
On the supposed link between antique plague and
climate there is clearly much work to do. Collaborative
multidisciplinary analyses will better determine if and
how Justinianic Plague outbreaks were linked to climate. Both distant and local temperature and precipitation pulses require consideration, as the establishment
of enzootic foci within or near the Mediterranean region cannot be ruled out, on the basis of the evidence
currently available. Some recurrences could have been
truly Mediterranean, and the consequence of local climate anomalies or earthquakes perturbing new or now
extinct plague foci, and others may have been imported
from afar.
A dizzying number of other matters call for consideration too. Focus so far has been on climatic changes
precipitating yersinial outbreaks, but might sudden
and dramatic changes in temperature and precipitation
not also have served to curb the diffusion of Justinianic
outbreaks in certain regions of the Mediterranean and
Europe, via their effects on the bacterium’s hosts and
vectors?130 LALIA episodes of climate forcing, for instance, might have complicated Y. pestis’ flea transmission. Perhaps plunging temperatures came to the aid
of plague sufferers in the 570s. The third (?) outbreak of
Justinianic Plague, a pan-Mediterranean event between
about 571 and 573,131 seems to have abated about the
time of the third major stratosphere-clouding eruption
of the LALIA (574±2.5). Other known outbreaks of the
Justinianic Plague also possibly occurred in the context
of the large LALIA eruptions of 626±2.5 and 682±2.5.
The alleged seventh recurrence is visible in West Asia
in 626–27, the tenth in Italy in 680, and the eleventh
in West Asia and North Africa in 687–90. Did climatic
change promote or foil these outbreaks? This raises another question: could a single episode of climate forcing have initiated a plague outbreak in one region and
drawn an earlier outbreak in another region to a close?
Yet more issues warrant attention. Most pertinently,
was climate a factor in the retreat of plague from the
Mediterranean region in the 8th c. after the LALIA petered out?132 Whether or not Y. pestis established itself
somewhere near the Mediterranean in the 6th c., it is
only logical to also query whether changing environmental conditions also had something to do with the
bacterium’s decline in the region in the 8th c. If it did,
might climate have played a role in the multi-century
130
131
132
Cf. McCormick (2007) 308.
Stathakopoulos (2004) 118 fixes Biraben and Le Goff’s reading
of the sources (1975) 58, 59, 65, 74.
Again, not everyone is convinced plague ceased to affect West
Asians in 750: n.28 above.
103
Mysterious and Mortiferous Clouds
absence of plague from the regions known to have been
devastated by the disease in Late Antiquity?
To overcome any lingering suspicion that late antique
plague-climate connections are simply coincidental, it
will be essential to establish the various mechanisms
through which climate could have influenced plaguecarrying rodents and plague-transmitting arthropods to
spur or hinder plague outbreaks in people.133 What effect did dramatic summer cooling have on populations
of sylvatic plague-harbouring rodents, or on the survival
rate and transmission efficiency of plague-communicating arthropods? Naturally, these sorts of questions
are more easily answered for Y. pestis foci which still
exist, than they are for the extinct foci of the Justinianic
Plague.
Lastly, and most obviously, if the climate forcing of
the 535/36 and 539/40 eruptions contributed to the
arrival of the Justinianic Plague in the Mediterranean
region, or the irruption of plague from a historical West
Asian focus, similar forcing could not have so assisted
successive outbreaks, as no recurrence was proceeded
by such pronounced climatic change. Support for the
claim that climate triggered the initial outbreak would
be had if climate events similar to, albeit weaker than,
that which preceded the initial outbreak precipitated
yersinial recurrences. It is a bit puzzling, however, if the
critical climate here is East-Central Asia’s, as plague outbreaks in late medieval Europe have been deemed to lag
15±1-years behind the changes in climate in Asia, which
triggered them. The Justinianic Plague irrupted in about
a third of the time, five or so years after the dramatic
climatic change of 536. Although Y. pestis can travel in a
number of ways and it is not impossible that late antique
plague shuttled more rapidly across Asia than did its late
medieval cousin,134 this might mean Y. pestis began its
westward trip before 536, as described in 1.2.2. It is also
possible that the climate downturn triggered the emergence of a plague strain, native to north-western China
or someplace nearby, from a focus in West Asia or East
Africa.
about malaria’s late antique or medieval victims, plasmodia parasites or anopheles transmitters, historians
have long assigned malarial disease an important role in
their histories of ancient and early modern demography
and economy.135
Like plague, malaria is an etiologically complex and
ecologically sensitive disease.136 Multiple species of
plasmodia parasites can cause human malaria. Six are
currently known to medical science—Plasmodium
falciparum, P. vivax, P. malariae, P. ovale (x2) and
P. knowlesi—but only three—P. falciparum, P. vivax and
P. malariae—are thought to have a deep Mediterranean
and European history.137 These parasites are transmitted
strictly to and between humans via mosquitoes, specifically female mosquitoes of the Anopheles genus. Over
40 anopheles species are capable of transmitting human
malarias, though not all of these arthropods are equally
accomplished or efficient vectors (about 20 are significant) and some are refractory to certain plasmodia. Four
are commonplace in histories of Mediterranean and
European malaria on the basis of their role in the transmission of plasmodia in the 19th and 20th c.: Anopheles
atroparvus, An. labranchia, An. sacharovus and An. messea. Mosquitoes are, in a sense, both vectors and hosts
of plasmodia parasites. This distinguishes them from
other impactful mosquito-borne diseases, like Yellow
Fever. The life cycle of plasmodia parasites partly takes
place in the anopheline vector and partly in the human
victim. In very basic terms: female anopheles deposit
malaria parasites, as sporozoites, into a human victim’s
135
136
Malaria in Late Antiquity’s Changing Climate
Let’s leave yersinial rodents and fleas behind for a moment. Other pathogens burdened late antique populations too and some, most notably malaria, were also
arthropod-borne. Although not much has been written
133
134
Consider the findings of Stenseth et al. (2006); Ben-Ari et al.
(2012).
Possibly not overland, as in the 14th c., but by sea: as in linkage
1.2.1, from the Indian Ocean to Arabia or the Red Sea.
137
Ancient and early modern: Scheidel (2001) 75–91, 175, 250;
Sallares (2002); Dobson (1997) 287–367. Late antique and
medieval: Franklin (1983); Hoffmann (2010) 138–143; Ziegler
(2016); Newfield (2017).
The literature on malaria is vast. For what follows: Kreier and
Baker (1987) 159–77; López-Antuñano and Schmunis (1993)
135–266; Brown and Nelson (1993) 267–87; Mayxay et al.
(2004) 233–40; Baton and Ranford-Cartwright (2005) 573–80;
Collins and Jeffery (2007) 579–92; Becker (2008) 19–28; White
(2008) 172–73; Becker et al. (2010) 170–80; Sinka et al. (2010);
Sutherland et al. (2010); Imwong et al. (2011); Zeibig (2013)
136–51; Singh and Daneshvar (2013) 165–84; and the WHO’s oftupdated fact sheet on malaria: www.who.int/mediacentre/
factsheets/fs094/en/ (accessed August 2017).
Identified as a cause of human malaria in 2008, P. knowlesi
seems to be confined to south-east Asia. P. ovale, considered
new in 1922, is rarely seen outside Sub-Saharan Africa and
the western Pacific, though P. knowlesi and both P. ovales, like
other plasmodia, are occasionally imported into ‘post-malaria’
Europe. However, this does not necessarily mean they are a
recent phenomenon (Rutledge et al. (2017) 101–104) or they
were never a component of western Eurasia’s disease burden.
A Europe without P. ovale: Sallares (1991) 273. Dobson (1997)
311 considers P. ovale “relatively rare in European populations”.
104
Newfield
bloodstream. The parasites journey to the liver and attack its cells. Having matured and multiplied there, they
re-enter the bloodstream as merozoites. These invade
red blood cells, which they, after 24 to 72 hours, erupt,
causing malarial disease. Not all merozoite-infused red
blood cells break down, however. Some produce gametocytes, cells which mosquitoes can pick up when feeding. In the anopheline gut, these eventually develop into
sporozoites, which can then be deposited into another
human victim.138 That mosquitoes are fundamental to
the transmission of malaria parasites, as well as the lifecycle of plasmodia, underlines the simple fact that in
endemic zones the more people there are, and the more
effective anopheles transmitters there are, the more malaria there will be.
It is partly because mosquitoes are vectors and hosts
that climate must factor in histories of malaria. Diverse
matters must be taken into account to understand malaria’s occurrence, but temperature and precipitation are
among the most important. Like plague’s fleas, malaria’s
mosquitoes are sensitive to these things. Indeed, warming
accelerates mosquito development and also facilitates
the proliferation of mosquito populations, lengthens
adult anopheles’ average lifespan and shortens the interval between blood meals. It also speeds up the parasite’s
life cycle.139 Indeed, each plasmodia has its own temperature requirements to develop in the mosquito gut.
P. falciparum demands at least 19–20 Celsius through
the ‘sporogonic phase’, and P. vivax and P. malariae
15–16 Celsius. At these temperatures, P. falciparum will
take as many as 23 days to develop, P. vivax 30 days and
P. malariae 35 to 45. Yet, in the right conditions, these
parasites develop at a quicker pace. P. falciparum and
P. vivax sporozoites may be primed in ten days at 26
Celsius. Because of these dependencies, malaria was
principally an estivo-autumnal disease in Europe, and
few think P. falciparum, which causes the most virulent
variety of malaria, was ever endemic north of the Alps.140
Mariologists and historians of disease generally hold
that P. falciparum, P. vivax and P. malariae were relatively
stable in Europe until their 20th c. elimination. Exactly
when these plasmodia arrived in Europe, however, is a
matter of debate. The prevailing opinion seems to be
they were introduced to the Mediterranean region and
southern Europe in particular before the Common Era.141
138
139
140
141
For malaria’s life cycle, see the scholarship in n.136.
Becker et al. (2010) 29; Krovats et al. (2000) 42–43. For warming
and Roman malaria: Sallares (2002) 101–103.
Histories of pre-modern malaria which have taken climate seriously, include: Knottnerus (2002) 339–53; Reiter (2000) 1–11;
Harper (this volume).
Tuscany’s Maremma is said to have been malarial as early as
300 BC, parts of Sicily by 400 BC, and stretches of the Greek
If they were not all then present, heterogeneous sources
indicate strongly all three were known along stretches
of the Mediterranean basin in the Roman imperial
period.142 A reference in the work of Pliny the Elder suggests P. vivax was active also in what is now Belgium in
the 1st c. AD.143
Historians have not considered in depth which plasmodia, if any, were flourishing in Late Antiquity and
the Middle Ages, or where. Although scholars of ancient and early modern malaria have alleged malaria
was more-or-less a constant feature of the pre-modern
pathogenic load,144 some historians have wagered the
distribution, incidence and prevalence of plasmodia underwent significant changes in the 5th through
7th c.145 Many scholars believe the late antique Mediterranean, for example, was vastly more malarial than it had
been earlier. A volatile 6th c. Italian climate, the alluviation of Mediterranean river valleys, effective anopheline
vectors colonising Italian marshlands, a 6th c. adoption
of the moldboard plough in northern Europe, and the
appearance of risiculture in a few Mediterranean places,
have been blamed for an expanding occurrence of malaria in Late Antiquity.146
Malaria certainly did not go dormant in Late
Antiquity, as Grmek suggested,147 but did its occurrence
really change much? It is quite reasonable to suppose
rates of exposure to plasmodia evolved considerably
in the past in the wake of climatic, demographic and
landscape change, but can the evolution in the occurrence of a quintessentially endemic disease more than a
millennium ago really be grasped today? Expansionists
have argued depopulation, land abandonment, declining investment in water infrastructure, and wetland regeneration facilitated malaria’s spread in Late
Antiquity, but they have offered little evidential support for their claims. The most detailed studies to date
142
143
144
145
146
147
coastline by 500 BC: Jones (1907) 53, 69; Jones (1909) 131;
Sallares (1991) 275, 277 [not in biblio].
Sallares (2002) 13–22; Scheidel (1994) 157; Marciniak et al.
(2016).
Plin. HN 31.8.12 (Jones (1975) 384–85).
For instance, Braudel (1995) 64 claimed malaria was “permanently installed” around the Mediterranean.
Biraben bet P. vivax and P. malariae migrated into transalpine Europe after Late Antiquity with the help of the Vikings:
Biraben (1998) 324, 345. Knotternus proposed P. vivax made its
way north in Late Antiquity and P. malariae joined it by 1100:
Knotternus (2002) 339, 342–45. The following suggests both
were incorrect.
Braudel (1995) 65, 81; Duby (1974) 13, 262; Skinner (1997) 65;
Romer (1999) 473; McCormick (2001) 38–39; Devroey (2003)
46; Devroey (2009) 154; Christie (2006) 489.
Grmek (1963) 1093; Grmek (1983) 380–402; Grmek (1989)
275–77.
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Mysterious and Mortiferous Clouds
have turned not to clinical descriptions of the disease,
but to inscriptions and bones. Scheidel surveyed Late
Roman epigraphs, and identified in them a strong late
summer-early autumn peak, which he associated with
P. falciparum and malaria co-infections.148 Gowland
and Western focused on bone lesions, specifically rates
of etiologically non-specific cribra orbitalia in 5,802
individuals from 46 Anglo-Saxon sites. The distribution of this spongy cranial growth correlated well with
An. atroparvus’ 19th c. geography, and with what were
low-lying wet regions in the Anglo-Saxon period. A
similar association was not established with enamel
hypoplasia, another indicator of poor health. For these
scholars, this suggested P. vivax was long present in many
regions of Anglo-Saxon England.149 Naturally, Gowland
and Western, and Scheidel, posit, as do other historians
of malaria, that populations of sufficiently efficient vectors were long stable too. Their data suggest stability, but
where there are not continuous runs of evidence for malaria anopheles, stability can only be assumed.
Other scholars have drawn attention to written accounts of disease that seem to have been malarial.150
Plasmodia cause febrile diseases with characteristic
cycles. Importantly, not all malarias are the same: the
severity of pathology varies between plasmodia and
the intermittency between paroxysms differ according
to the development of parasites in the human victim.151
P. falciparum and P. vivax have a cycle of 48 hours (possibly 36 for the former), meaning they produce a marked
fever on days one and three. This makes them tertian
fever (tertiana febris). P. malariae generates a fever every
72 hours or on days one and four, making it quartan
fever (quartana febris). This distinctive intermittency
means malaria can be confidently retrospectively diagnosed. Yet, P. falciparum cannot be counted on to exhibit
feverous spikes every 36/48 hours. It tends to provoke a
continuous (quotidiana) fever, with peaks on days one
and three. P. vivax and P. malariae can present as well
with a daily fever at first. Naturally, other pathogens,
dual and triple plasmodial infectious, and parallel exposures to the same malaria, can obscure clear patterns of
malarial fever as well. Nevertheless, many P. falciparum
148
149
150
151
To the determinant of malaria’s victims, plasmodia often interact deleteriously with other pathogens: Scheidel (1994)
152–53, 159–62, 167. On malaria’s interactions with other
pathogens: Faure (2014).
Gowland and Western (2012) 301.
Most notable is the work of Handley (2003) 108; also Horden
(1992) 70–71; Wood (2004) 211–12. Knotternus (2002) 344, 345,
and others have seen malaria in cryptic references, to either
regions being insalubrious in a typically plasmodial season, or
months being unhealthy in a plausibly malarial area.
See n.136.
infections express as daily fevers, P. vivax infections as
tertian fevers, and P. malariae as quartans.
The cyclical fevers of the weaker, albeit still violent
and debilitating, malarias were easily identified in the
past, and are visible today in premodern sources. A recent, but not exhaustive, search for plasmodial paroxysms (clinical expressions of malaria-like disease) in the
extant textual evidence of Frankish Europe, has turned
up 64 references to malaria, 42 of which are quartans,
or P. malariae, the most cold-tolerant form of the disease.152 The majority (52) of these plasmodial fevers are
Merovingian in date. In fact, 50% of all Frankish references to malaria are encountered in the late 6th c. writings of Gregory of Tours.153 P. vivax and P. malariae were
found across 6th c. Merovingian France, but P. malariae
appears to have been the most prevalent variety, as far as
the written evidence indicates.154 Whether this was the
case in the 7th c. we do not know: there are 44 references
to malaria in the 6th c., but only five in the 7th.
Multiple factors might explain the dominance of
P. malariae in Merovingian Europe. Most malarial
Franks are encountered in hagiographical texts, which
focus on cures. That P. malariae is the weakest of the
malarias, and an unlikely killer, may explain why nearly
66% of identified Frankish intermittents are quartanarii. The fact that P. vivax is often more common where
it and P. malariae are present, and quartans are found
in nearly all Frankish regions marked by tertians, supports this theory. In other words, P. vivax may have
been more common than it appears to have been, and
tertains may figure less often in Frankish sources than
quartans because P. vivax kills more of its victims. This
said, P. malariae requires a smaller host population than
P. falciparum or P. vivax to sustain itself, and it is more
capable of inhabiting areas that are thinly populated. If
dearth and plague eroded human numbers in mid 6th c.
France, quartans may have come to dominate the malarial landscape. Depopulation does not fare well for
P. falciparum or P. vivax.
Then there is climate. As a long run of markedly cool
summers, the Late Antique Little Ice Age stands to have
negatively impacted the incidence and prevalence rates
of arthropod-borne diseases, like P. falciparum and
P. vivax, that struggle in cool climates. Of all malarial
fevers, quartans may have been least affected by estivoautumnal cooling just when Frankish sources imply
P. malariae was most common. A complex of factors might explain the high number of Merovingian
152
153
154
Newfield (2017) 251–300.
Newfield (2017) 271 n.52 for references.
Of course, is it hard to say whether quartans were more common in Frankish texts than in Franks themselves.
106
Newfield
quartanarii, but a multidisciplinary analysis is needed
of the influence of the cooling evident for Late Antiquity
on malaria, specifically on the lifecycles of the plasmodia, and of the breeding and feeding habits of the anopheles, thought to have been instrumental for plasmodial
disease then.
Malaria continued to cause illness and to kill during
the LALIA, and in this there is agreement with two earlier sketches of malaria’s history during the early modern
Little Ice Age. These studies argued a cooling climate
was then of little consequence for the disease. The most
recent of them wagers malaria’s “high-days” correspond
precisely to the LIA.155 Indeed, the issue is not whether
malaria continued to contribute to morbidity and mortality, but whether Little Ice Age climates, late antique or
early modern, altered the landscape of plasmodial disease. Malaria persisted, but what types were dominant
and were plasmodia as common as they were in warmer
climate regimes? This has implications for our estimation of historical disease burdens. Although some scholars are adamant that human factors drive malaria’s ebbs
and flows, malaria may have nonetheless experienced
a decline in both little ice ages. Pre-modern sources
are hardly numerous enough to say otherwise. Indeed,
the early modern malarial uptick identified previously
might simply reflect an increase in written indications
of the disease.
Non-Yersinial Epidemics and Late Antique Cooling
Not all late antique diseases were arthropod-borne.
Throughout Late Antiquity there is sporadic evidence
for non-yersinial epidemics, some of which are associated with food shortages. Connections between climate
cooling and these epidemics hinge primarily on the effects of temperature on crops. The downward trend in
late antique summer temperatures would have exacerbated the risk of dearth, but whether subsistence crises
occurred more often during the LALIA than earlier, or
later, is impossible to tell, as the pre-modern record of
food shortages, like that of epidemics, is incomplete.156
Subsistence crises warrant attention as they could set off
migrations for food and work, and movements of peo-
155
156
Reiter (2000) 1–11; Knottnerus (2002) 339, 340, 351; also Reiter
(2001) 141–61; cf. Lindsay and Joyce (2000) 185–87.
Stathakopoulos (2004) 32–33 finds there were more famines
in the 6th c. than the 4th, 5th or 7th c. in the Byzantine world,
but, as he observes, there are multiple reasons for this. The archaeological record of mass graves might better reflect trends
in the occurrence of mortality crises. McCormick (2015) 353,
identifies “a tremendous surge” in mass death events in the
6th and 7th c.
ple, and possibly of their livestock, could disseminate
diseases spread person-to-person or domesticate-to-domesticate. Crowding in towns and cities in years of dearth
also assisted the transmission of pathogens spread directly between people. Moreover, malnutrition compromises immune function, making the victims of food
shortages in some, but not all, instances more likely to
suffer severe disease.
Climate-dearth-epidemic linkages are not easily
pulled from textual and scientific archives. At the moment, establishing coincidence is a difficult task in and
of itself. This is partly because written evidence for
non-yersinial epidemics and food shortages has yet to
be treated in depth. Stathakopoulos’ catalogue of late
Roman and early Byzantine plagues and subsistence crises is exemplary,157 but a similar study is needed for the
western Mediterranean and Europe. At the same time,
the late antique evidence for dearth needs to be read
against the climate proxies which have emerged since
Stathakopoulos published, and within which the LALIA
has been identified. Case studies of non-yersinial epidemics, like those devoted to Justinianic outbreaks, are
required as well. The challenges entailed in doing this
sort of work are made apparent here in a case study of
one plague, potentially connected with dearth triggered
by dramatic climatic change. The outbreak in question
was almost certainly not Justinianic or bubonic plague.158
Let us return to Adomnán’s mortiferous cloud and
the large eruption of 574±2.5. There are grounds to argue
Columba’s pestilential rain was more widespread than
the saint or his biographer would have their followers
believe, and that it took place about the time of the
unidentified 574 volcanic event. Columba left for Iona
in 563 and died there in 597. The plague Adomnán recounts occurred between those dates. Only one epidemic is reported in the Irish annals during Columba’s
Hebridean residence. The Irish record of disease outbreaks, of course, is fragmentary, but it is feasible the
epidemic reported in the annals in the mid 570s is the
same plague Adomnán wrote about.
Different sets of Irish annals give different years for
the plague in question, but all accounts of it stem from
a single passage in a non-extant text very likely written, like the saint’s vita, at Iona.159 At 574 the Annals of
157
158
159
Stathakopoulos (2004) 177–386.
Such is the state of the written evidence that some consider
the Irish irruption of the disease outbreak sketched here to be
bubonic plague: Woods (2004) 500–501; Dooley (2007) 219.
It is thought the non-extant ‘Iona Chronicle’ or ‘Iona Annals’,
written at the monastery of Iona, was a significant source before 740 for the section of the so-called ‘Chronicle of Ireland’.
This was (another) non-extant work which informs pre 912 entries in the surviving Irish annals, but not everything included
107
Mysterious and Mortiferous Clouds
Tigernach (AT) record “scintilla leprae et abundantia
nucum inaudita”, ‘a glimmer of lepra and an unheard
of abundance of nuts’. The Annals of Ulster (AU) date
the same passage to 576. In that year the Annals of
Inisfallen (AI) has “cnómes imda”, ‘a plentiful crop of
nuts’, and, in 577, “bolggach for doenib”, ‘people afflicted
with bolggach’.160 Scholars of these texts hold the correct date for this mortality and bountiful nut harvest
is 574.161 Whether the original entry on which these surviving passages are based was jotted down as, or soon
after, people were dying, is debated. Some hold that the
lost text was kept current at the monastery of Iona from
just about the time Columba founded it in the 560s,162
but others argue the text only provides a contemporary
witness from the late 7th c.163 Either way, the annals provide a glimpse of a disease outbreak not reported in any
other insular source, unless, of course, this annalistic
plague was Adomnán’s pestilential rain.
There is no consensus on the diagnosis of the plague
encountered in the annals. Editors and translators of the
surviving texts have advanced various identities, some
rather dubious. The AT and AU’s lepra is unlikely to
have been leprosy, a slowly progressing and faintly contagious disease, as some have it, and whether bolggach
was medieval Irish for smallpox, as several historians
have proposed, is difficult to say.164 This is not the only
160
161
162
163
164
in the Iona Chronicle was written in Iona. It is not impossible
the 574 mortality was an item included from another text.
Bannerman (1974) 9–26; Evans (2011) 23; Evans (2010) 2–3,
12–14.
The translations presented here are those available on CELT:
www.ucc.ie/celt (accessed August 2017). Note the dates given
to these passages have varied in different editions and translations of these texts. For example, in the Annals of Tigernach
(Stokes (1896) 151) the AT passage is assigned to AD 575, as is
the AU passage in the Annals of Ulster (Hennessy (1887) 64–
67). The AT and AU passages are near identical, though the
former has abundantia and the latter habundantia. A similar
passage does not appear in the Chronicon Scotorum.
McCarthy (2005); Ludlow (2010) 23.
Smyth (1972) 9–12; Charles-Edwards (2006) 8–9.
Hughes (1972) 99–115, 142.
MacArthur thought that the identification of this lepra and
other epidemics recorded in the Irish annals with leprosy
“absurd”, but he pushed the idea that bolggach was smallpox: MacArthur (1949) 183, 184. Other authorities agreed:
Shrewsbury (1949) 25, 38–39; Bonser (1963) 60, 63, 66–70.
MacArthur posits (p.184) whether leprosy-like disease and
smallpox could have been confused on account of the “extensive scabbing which accompanies the drying of [smallpox] pustules”. The Dictionary of the Irish Language (www.
dil.ie (accessed August 2017)) defines bolggach as a “name
of disease(s) characterized by eruptive spots or pustules on
the skin, smallpox”. This is problematic for several reasons. To
begin, the definition is made partially on the basis of modern
appearance of the term, or a variant thereof, in Ireland’s
annals, and it is apparent at least some medieval Irish
thought lepra and bolggach were interchangeable.165
Like the former, the latter term implies the disease
manifested cutaneously, possibly causing blisters, a pronounced rash, lesions or swellings on a victim’s skin.166
This could be smallpox, but it could also be a number
of other infections, including measles. Alternatively, the
disease might have been gastrointestinal, as bolg can
mean both blister and belly.167 This said, the association
with lepra indicates bolggach often affected the skin.168
Although the annals do not mention dead cows,169
both the outbreak of 574 and the mortality Columba
presaged, seem to have afflicted many people, to have
come and went, and to have altered the appearance of
their victims. Adomnán writes of ulcera (sores or ulcers), painful, purulent and possibly raised, and lepra
certainly refers to a serious disease that affected the look
165
166
167
168
169
translations of medieval annals. It is important to point out
for this paper, that the 574 mortality is the earliest plague to
be identified as bolggach, and that the AI annalist made no attempt to define the disease clinically. The earliest extant copy
of any set of Irish annals, the AI, is late 11th c. in date. It is
almost certain that the compiler translated the Latin encountered in the text also used by the AT and AU into Irish, and
that he equated lepra with bolggach, as did others (see n.165).
Nevertheless, lepra and bolggach likely referred to a host of
different diseases. Indeed, it should not be assumed medievals used bolggach, or other disease terms, systematically. It is
hardly clear that the same pathogen, whatever it was, caused
disease outbreaks centuries apart that non-contemporary
annalists identified as bolggach.
Consider the passage encountered, with minor variances, in
the AU, AT and CS at 680: lepra grauisima in Hibernia que vocatur bolgacach, ‘a most severe lepra in Ireland which is called
bolgacach’ (AU); lepra grauissima in Hiberniam quae uocatur
Bolgach (AT); lepra grauissima quae uocatur bolgach (CS).
Other appearances: at 743 the AU has … & in bolgach …, ‘the
bolgach was rampant’, and at 779 … in bolggach for Erinn huile ..., ‘the bolggach throughout Ireland’; at 1061 the AT has
… teidm mor a Laignib .i. in bolgach & treghaid, cor’ladh ár
daíne sechnón Laighen …, ‘a great pestilence in Leinster, to wit,
the ‘smallpox’ and colic, so that there was a great destruction
of people throughout Leinster’.
See n.164.
Notably, … bolggach for doenib … is translated as … fluxus ventris in populo … in Annales Inisfalenses (1825) 8.
Some additional support for the idea bolggach affected the
skin, comes via Mageoghagan’s Book, an early 17th c. English
translation of an earlier Clonmacnoise-based Irish text: “diseases of the leaprosie did abound and knobbes this year”:
Annals of Clonmacnoise, in Murphy (1896) 89. The entry is not
precisely dated, but falls between notices assigned dates of AD
569 and 579.
The annals do not record another epizootic mortality of cattle
for more than 100 years.
108
Newfield
and feel of one’s skin, perhaps making it “scabby, scaly or
crusted”,170 as could bolggach. There may be something
with the nuts too. It has been proposed these nuces were
not nuts at all, but a corruption of an earlier, perhaps
contemporary, description of the disease’s symptoms:
nut-sized buboes, carbuncles, pustules or ulcers.171 If so,
the plague was unknown to the Irish people (the nuts
are said to have been inaudita) or at least the contemporary generation.172
Were the plague Columba put out and the bolggach
one and the same, it seems unlikely that the community
at Iona would have escaped the disease, or that the outbreak would only have infected Dubliners, as reported
in the vita. According to Adomnán, Columba saw the
deathly cloud pass quietly over the monastery he founded (and where Adomnán was an abbot when the vita
was composed) before it devastated the people of the
Dublin area. Kept as it was within the territory of Dál
Riata, the lost set of Iona annals possesses an outlook
that is both Irish and North British. It very well may, as
such, contain references to epidemics in various regions
of the insular north-west. At the same time, the lost
text was clearly concerned with events in the vicinity of
Iona. Most likely, the text sheds light on an epidemic in
574 that spread in north-western insular Europe and afflicted Iona.
Notably, there are multiple accounts of outbreaks of
virulent and appearance-altering diseases on the continent about this time. Best known is the aforementioned
third recurrence of the Justinianic Plague of 571–73/74.173
Whether a disease characterised as ulcera, lepra, bolggach or nut-like bumps (possibly the size of acorns174)
could be plague, as it is presently known, is doubtful.175
170
171
172
173
174
175
Shrewsbury (1949) 25.
Woods (2004), who advanced this theory, very much thought
the 574 plague was Justinianic and yersinial. He suggests
… habundantia nucum inaudita … is a misreading for … magna
pestis glandularia ... “Etymologically”, he points out, “the noun
glandula does mean ‘little nuts’” (pp.498–99). A copyist may
have mistaken a description of the disease to mean there was
a good nut crop, but might the original entry not simply have
indicated that little acorn-size marks or bumps characterised
the disease?
Were this ‘true plague’ it would have likely been known, considering plague is thought to have arrived in Ireland in 544,
where it is described as ‘the first mortality, which is called blefed’: Annals of Ulster, in Hennessy (1887) 48–49.
Stathakopoulos (2004) 118, 314–16 corrects Biraben and Le Goff
(1975) 58, 59, 65, 74.
The annals do not identify the species of nut, but oak mast
(acorns) was common, and prized for pigs.
Where the nut-sized lesions were located is not known, and
most acorns (if the nuts were acorns) seem on the small size
for plague buboes.
Were bovines a victim, the 574 plague was certainly not
yersinial. But not all 6th c. epidemics were Justinianic or
bubonic. In another disease outbreak, which Marius of
Avenches labelled variola—and which can be traced in
what is now Italy, Switzerland and France about 570—
people and cows seem to have died alongside one another.176 Did Columba confront this plague in Ireland
in 574?
On the basis of historical sources and molecular clock
studies,177 it has been proposed that the continental
plague of about 570 was a morbillivirus, one ancestral
to modern rinderpest and measles.178 The human-bovine mortality Adomnán wrote of, on the other hand,
has been identified, in editions and translations of the
text, as well as scholarship on early medieval insular epidemics, as an extinct smallpox-cowpox orthopoxvirus.179
There are reasons to doubt this designation, not least
because it seems smallpox evolved from taterapox or
camelpox, or emerged with these poxes from an ancestral orthopoxvirus.180 In any case, it is notable that contagious and acute febrile diseases, which marked their
victim’s skin, were often documented in the second half
of the 6th c. on the continent.181
One may conjecture the 574 bolggach and morbifera
nubes spread in Ireland and northern Britain after washing up in the British Isles from the continent, where
the disease was recorded as variola. Strengthening the
connection, bovines were susceptible to the mortiferous cloud and the variola. Indeed, Marius has the latter killing off beef animals throughout Italy and France.182
The evidence is slight,183 but a case can be made for a
human-bovine plague spreading in multiple regions between 570 and 574, concurrent to the third occurrence of
the Justinianic plague.184
176
177
178
179
180
181
182
183
184
Marius of Avenches, Chronica, in Mommsen (1894) 238;
Agnellus, Lib. Pont. Eccl. Rav. 28.94 (Holder-Egger (1878) 337).
Furuse et al. (2010) 1–4; Wertheim and Kosakovsky Pond (2011).
Newfield (2015) 8–9.
Adomnán, Life of St. Columba, 2.4, in Fowler (1894) 74 n.4;
Adomnán, Life of St. Columba, 2.4, in Sharpe (1995) n.217;
Shrewsbury (1949) 39.
Li et al. (2007); Hughes et al. (2010) 50–59; Babkin and Babkina
(2015). For discussion and a possible relationship with the
Antonine Plague and the plague of 494, see Harper (this
volume).
For instance: De Vita Sanctae Radegundis 2.17 (Krusch (1888)
390).
Marius of Avenches, Chronica, in Mommsen (1894) 238.
Justinianic plagues have been strung together with less.
Consider Biraben and Le Goff’s “thirteenth wave” of Justinianic
plague: Biraben and Le Goff (1975) 59, 60, 70, 76.
Was this plague also the plague reportedly brought to Arabia
from Ethiopia in 569, and often retrospectively diagnosed as
109
Mysterious and Mortiferous Clouds
Did the emergence or spread of this variola-bolggach
have anything to do with climate? The Irish flare-up of
the disease seems to have coincided temporally with
food shortages reported some distance away along
Mediterranean shores. The Liber Pontificalis mentions
an ‘extreme famine’ in central and northern Italy during
Benedict I’s pontificate (June 575–July 579), but seemingly also in the context of the Lombard advance into
the peninsula (568–72). The 7th c. Alexandrian chronicler John of Nikiu also observes starkly ‘a pestilence in
all places, and a great famine’ just before or about the
time when the eastern Roman Emperor Justin II abdicated his throne (December 574).185
As in the mid 530s, surviving sources may reveal
only part of a larger subsistence crisis in the mid 570s.
Naturally, that known Central and East Mediterranean
food shortages cannot be dated with precision, complicates attempts to link them to each other, and to the climate forcing of the 574 eruption. The current standard
ice core chronology of volcanism puts that eruption in
the Tropics, and dates it to within 2.5 years. Northern
hemispheric tree-ring chronologies, telling of summer
temperatures, register a sudden and dramatic worsening of conditions in 574—the June-July-August of 574
was the twelfth coldest June-July-August north of the
equator since 500 BC—indicating the eruption likely
took place in late 573 or early 574.186 Might we use this
dendroclimatology to link the aforementioned famines,
date them to late 574–75 and, in doing so, associate them
with Late Antiquity’s Little Ice Age? If so, it is still quite
uncertain how this dearth contributed to the spread of
the bolggach, if it did at all. There is no evidence for unusual movements of people in 574, though if there was
severe dearth in parts of western Europe, it is possible
some would have been. That said, if the bolggach and
variola were the same disease, that disease was clearly
doing well without any swing in temperature before 574.
Towards Consilient Histories of Late Antique Climate
and Disease
Understanding what effects the LALIA as a whole, and
episodes of dramatic climate variability within it, may
185
186
measles or smallpox? Paulet (1768) 77–78; Moore (1815) 46–55;
Hopkins (1983) 25, 165–66.
Lib. Pont. 1.308; John of Nikiu, Chronicle 94.18 (Charles (1916)
150). John places the famine after a Samaritan uprising, certainly that of 572–73, and before the retirement of Justin II.
Other sources put the pestilence, if this is the third Justinianic
plague, in Constantinople in 572–73: Stathakopoulos (2004)
118.
Sigl et al. (2015) extended data figure 5.
have had on the pathogenic burden endured by late antique people and animals, is no easy task. It is not impossible, as suggested here, that the changing climate of the
Late Antique Little Ice Age, through manifold factors,
facilitated and impeded outbreaks of the Justinianic
Plague, altered the plasmodial disease landscape and
lessened the malaria burden, and, through subsistence
crises, led to the coalescence of disparate disease environments, not previously or often intertwined. Yet, satisfying causal linkages between climate and disease in
Late Antiquity remain elusive. Multidisciplinary collaborative efforts are required to explore the issues raised
here.
Predictably, we need more of everything. In particular,
more text-based work is required to better identify the
spatio-temporal parameters of late antique epidemics,
epizootics, endemics and subsistence crises, and more
high-resolution climate data are required to better capture the variability of climatic change in Late Antiquity.
To some extent this is more about synthesising already
existing evidence, and interweaving the methods and
results of different fields of study, than it is about generating new evidence. For the Justinianic Plague and early
Byzantine dearth, for example, there is a generation of
scholarship to build on. Regarding climate proxies, several covering the period and region of interest have already been constructed; the late antique runs of those
series only need now to be given detailed consideration.
It should be stressed that precipitation data must be
brought to bear on the questions raised here as well, as
should winter temperature and hydroclimate data when
they become available. It may be that the effects of the
6th c. volcanic cluster on precipitation exercised more
influence on Y. pestis than did the dramatic decline in
temperature. Non-volcanic, internal climate forcing is
yet another issue worthy of attention. The focus in this
paper has been on the effects of large eruptions, but
some of the coldest stretches of the LALIA are not tied
to volcanism.187
Finally, we might consider how climate’s influence
on plague might have impacted the occurrence of malaria and vice versa. For instance, if dramatic climatic
change facilitated the establishment of Y. pestis in the
Mediterranean region, might the mortality resulting
from recurrent plague account, together with summer
cooling, for the apparent dominance of P. malariae?
Population thinning would have made things difficult
for P. falciparum and possibly P. vivax. Further, how
might the effects of climate on plague and malaria have
altered the occurrence of other diseases? Establishing
187
In Europe, in the mid 560s and very early 600s: Büntgen et al.
(2016) fig. 4.
110
Newfield
how these diseases interacted is yet another matter.
Did P. malariae and P. vivax offer protection against
Y. pestis (as has been proposed for P. falciparum), or did
they interact deleteriously with plague?188 If the former,
might a wide prevalence of P. malariae in Frankish lands
partially account for the patchiness of plague epidemics
from the late 6th c.? Perhaps Y. pestis simply took a greater demographic toll in regions rife with P. falciparum.
Questions are rapidly outstripping answers. Of
course, in looking for answers we must be careful not
to make too much out of too little. The more sparse
and cryptic the evidence, the easier it is to erroneously
construct impactful events, or meaningful trends, and
to link them causally with potentially unconnected
phenomena.189 The plague of 570–74, and the link very
tentatively drawn between it and the 574 eruption, may
be a case in point. While establishing correlation is essential, and clearly difficult in Late Antiquity, we must
remember that correlation is not enough.190 That climate influenced disease occurrence in the 6th and 7th c.
is certain, but teasing out the nitty gritty, the mechanics
of the linkages, is a challenge we must overcome going
forward. After all, in correlation we might find causation, or we might not.
Acknowledgements
The author thanks the referees for their comments and
corrections, Monica Green for reading and improving the sections on plague, Kyle Harper for fruitful exchanges on several topics addressed herein, and Francis
Ludlow and Dan McCarthy for entertaining questions
about the dating of the lepra and bolggach.
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