Journal of Interdisciplinary History, XLVI:1 (Summer, 2015), 1–38.

Timothy P. Newﬁeld
Human–Bovine Plagues in the Early Middle
Ages This article combines written and plausible physical evi-
dence for the human–bovine plagues (large outbreaks of acute dis-
ease) in 569–570 and 986–988 C.E. with evidence from two recent
and independent molecular clock analyses (MCAs) that establish the
divergence of measles (MV) from rinderpest (RPV) c. 1000 C.E. It
proposes that the plagues of 569–570 and 986–988 testify to the
outbreak of an MV–RPV ancestor that caused mass mortality in
cattle and people. In other words, when spreading among cattle,
a now-extinct morbillivirus episodically colonized and spread in
human populations during the early Middle Ages.1

The diseases that afﬂicted early medieval Europeans have
attracted considerable attention during the last ﬁfteen years. Yet,
most of the scholars involved, historians and bioarchaeologists
alike, have rarely discussed pathogens other than Yersinia pestis or
the occurrence and effects of diseases other than such episodic epi-
demics as the Justinianic Plague (otherwise known as the Early
Medieval Pandemic). Economic, medical, and social historians of
the early Middle Ages have occasionally devoted a few words to
the nonbubonic epidemic of 569–570, the spread (or dormancy) of
malaria, and the supposedly non-Yersinial plagues reported in

Timothy P. Newﬁeld is Postdoctoral Research Fellow, Department of History, Princeton
University. He is the author of “Early Medieval Epizootics and Landscapes of Disease: The
Origins and Triggers of European Livestock Pestilences, 400–1000 CE,” in Sunhild Kleingärtner,
Newﬁeld et al. (eds.), Landscapes and Societies in Medieval Europe East of the Elbe (Toronto,
2013), 73–113; “The Contours, Frequency and Causation of Subsistence Crises in Carolingian
Europe (750–950),” in Benito I. Monclús (ed.), Crisis Alimentarias en la Edad Media: Modelos,
Explicaciones y Representaciones (Lleida, 2013), 117–172.

The author thanks the Social Sciences and Humanities Research Council of Canada for
its support of the research and writing of this article. The author also thanks Philippe Lemey
for explaining the workings of molecular clocks, Joel Wertheim for answering questions about
the morbillivirus molecular clock analyses, Olivier Putelat for proofreading the section about
mass bovine burials, and an anonymous reader for helpful comments and direction. All errors
are the author’s.

© 2015 by the Massachusetts Institute of Technology and The Journal of Interdisciplinary
History, Inc., doi:10.1162/JINH_a_00794

For the idea that an MV–RPV predecessor was zoonotic in historical time, see Yuki Furuse,
1
Akira Suzuki, and Hitoshi Oshitani, “Origin of Measles Virus: Divergence from Rinderpest
Virus Between the 11th and 12th Centuries,” Virology Journal, VII (2010), 3.

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TIM OTHY P. NEW FIELD

early Irish annals. Similarly, palaeomicrobiologists and palaeo-
pathologists have drawn sporadic attention to some chronic, often
nonlethal but endemic early medieval infections—such as leprosy,
malaria, and tuberculosis. But, for the most part, non-Justinianic
plagues, not to mention endemic diseases and epizootic diseases,
have received little attention.2

For recent work on the Justinianic Plague, see Dionysios Stathakopoulos, “The Justinianic
2
Plague Revisited,” Byzantine and Modern Greek Studies, XXIV (2000), 256–276; Michael C.
McCormick, “Rats, Communications, and Plague: Toward an Ecological History,” Journal of
Interdisciplinary History, XXXIV (2003), 1–25; Stathakopoulos, Famine and Pestilence in the
Late Roman and Early Byzantine Empire: A Systematic Survey of Subsistence Crises and Epidemics
(Aldershot, 2004), 110–154; Peregrine Horden, “Mediterranean Plague in the Age of Justinian,”
in Michael Maas (ed.), The Cambridge Companion to the Age of Justinian (New York, 2005),
134–160; Stathakopoulos, “La peste de Justinien (541–750): questions médicales et réponses
sociales,” in Anna-Marie Flambard Héricher and Yannick Marec (eds.), Médecine et société de
l’Antiquité à nos jours (Harve, 2005), 31–48; idem, “Invisible Protagonists: The Justinianic Plague
from a Zoocentric Point of View,” in Ilias Anagnostakis et al. (eds.), Animals and Environment in
Byzantium (7th–12th c.) (Athens, 2011), 87–95; Lester K. Little, “Plague Historians in Lab Coats,”
Past & Present, 213 (2011), 267–290; the twelve chapters in idem (ed.), Plague and the End of
Antiquity: The Pandemic of 541–750 (New York, 2007).

For comments on non-Justinianic early medieval disease, see Joel-Noël Biraben, “Disease in
Europe: Equilibrium and Breakdown of the Pathocenosis,” in Mirko Grmek (ed.), Western
Medical Thought from Antiquity to the Middle Ages (Cambridge, Mass., 1998), 324, 345; McCormick,
“The Imperial Edge: Italo-Byzantine Identity: Movement and Integration, A.D. 650–950,” in
Hélène Ahrweiler and Angeliki E. Laiou (eds.), Studies on the Internal Diaspora of the Byzantine
Empire ( Washington, D.C., 1998), 25–31; Otto S. Knotternus, “Malaria Around the North
Sea: A Survey,” in Gerold Wefer et al. (eds.), Climate Development and History of the North Atlantic
Realm (Berlin, 2002), 339, 342–345; Jean-Pierre Devroey, Economie rurale et société dan l’Europe
franque ( Vie-IXe siècles) (Paris, 2003), 46; idem, “Catastrophe, crise et changement social: à propos
des paradigmes d’interprétation du développement médiéval (500–1100),” in Luc Buchet et al.
(eds.), Actes des 9e journées anthropologiques de Valbonne ( Valbonne, 2009), 154; Donnchadh Ó
Corráin, “Ireland c.800: Aspects of Society,” in Dáibhí Ó Cróinín (ed.), A New History of Ireland.
I. Prehistoric and Early Ireland (New York, 2005), 578–583. For more complete studies, though out
of date, see Wilfrid Bonser, “Epidemics during the Anglo-Saxon Period,” Journal of the British
Archaeological Association, IX (1944), 48–71; idem, “Epidemics,” in idem, The Medical Background
of Anglo-Saxon England: A Study in History, Psychology, and Folklore (London, 1963), 51–97;
William P. MacArthur, “The Identiﬁcation of Some Pestilences Recorded in the Irish Annals,”
Irish Historical Society, XXIII (1949), 169–188.

For some palaeopathology, see Joel Blondiaux et al., “Epidemiology of Tuberculosis: A 4th
to 12th c. AD Picture in a 2498-Skeleton Series from Northern France,” in Gyorgy Pakﬁ et al.
(eds.), Tuberculosis: Past and Present (Budapest, 1999), 519–30; G. Baggieri and F. Mallegni,
“Morphopathology of Some Osseous Alterations of Thalassic Nature,” Palaeopathology Newsletter,
CXVI (2001), 10–16; Blondiaux et al., “Microscopic Study and X-Ray Analysis of Two
5th Century Cases of Leprosy: Palaeoepidemiological Inferences,” in Charlotte A. Roberts
et al. (eds.), The Past and Present of Leprosy: Archaeological, Historical, Palaeopathological and Clinical
Approaches (New York, 2002), 105–110; M. G. Belcastro et al., “Leprosy in a Skeleton from the
7th Century Necropolis of Vicenne-Campochiaro,” International Journal of Osteoarchaeology, XV
(2005), 431–448; Jesper L. Boldsen, “Leprosy in the Early Medieval Lauchheim Community,”
American Journal of Physical Anthropology, CXXXV (2008), 301–310.

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H UM A N –B OVI N E PL AGU E S

| 3

Specialists of periods richer in written sources than the early
Middle Ages advise that it is a serious mistake to dismiss the baseline
of endemic disease. They argue that the constant pressure of non-
killing pathogens inhibited demographic and economic growth
over the long term far more than most epidemics. Nonkilling dis-
eases also contributed signiﬁcantly to excess mortality via mal-
nutrition and secondary infections, aggravating the death toll
during periods of dearth and epidemic. A growing body of work,
some of it centered on the early Middle Ages, also ﬁnds that epi-
zootic disease, of domestic bovines especially, carried considerable
repercussions for human health and economy in organic agrarian
economies like those of early medieval Europe, which were largely
dependent on cattle for traction and fertilizer and, to a lesser extent,
for dairy and meat.3

Additionally, the Justinianic Plague west of the Balkans after
600 may well be ill-deserving of the attention that historians and
scientists have given it. In a 2007 study, Bachrach argued that the
Justinianic Plague, which is now held to have occurred from four-
teen to eighteen times between 541 and 750 (or 767), did not have
the dramatic, long-term negative effect on Merovingian France’s
demographic curve that most scholars suppose; outbreaks were
“too infrequent and widely dispersed.” A similar argument could
be advanced for neighboring European regions, as the series of
charts and maps that Biraben and LeGoff attached to their seminal
article about the “ﬁrst bubonic plague pandemic” appears to sug-
gest. Their essay demonstrates clearly that most seventh- and
eighth-century Justinianic re-occurrences did not much affect
Central, Northern, or Western Europe. Moreover, subsequent
research conﬁrms that Justinianic plagues after 600 were largely re-
stricted to Greek-, Syriac-, and Arabic-speaking lands, and eruptions

3 Walter Scheidel, Death on the Nile: Disease and the Demography of Roman Egypt (Leiden,
2001), xxi; Andrew Cunningham, “Disease: Crisis or Transformation?” in Troels Dahlerup
and Per Ingesman (eds.), New Approaches to the History of Late Medieval and Early Modern Europe
(Copenhagen, 2009), 407; Carroll Gillmor, “The 791 Equine Pestilence and its Impact on
Charlemagne’s Army,” Journal of Medieval Military History, III (2005), 23–45; Newﬁeld, “A
Great Carolingian Panzootic: The Probable Extent, Diagnosis and Impact of an Early
Ninth-Century Cattle Pestilence,” Argos: Bulletin van het Veterinair Historisch Genootschap,
XLVI (2012), 200–210; idem, “Early Medieval Epizootics and Landscapes of Disease: the
Origins and Triggers of European Livestock Pestilences, 400–1000 CE,” in Sunhild Kleingärtner
et al. (eds.), Landscapes and Societies in Medieval Europe East of the Elbe: Interactions Between Envi-
ronmental Settings and Cultural Transformations (Toronto, 2013), 73–113.

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TIM OTHY P. NEW FIELD

4 |
further west were rare and regional—in England and Ireland (664–
666 and 684–687), in France (c.640 and 693), and in Italy (608, 654,
746, and possibly 767).4

Conceivably, seventh-century northwestern insular Justinianic
outbreaks could imply corresponding continental disseminations,
and physical evidence for Y. pestis in places where written evidence
for the Justinianic Plague is lacking (sixth-century Aschheim,
Germany, and seventh-/ninth-century Vienne, France) might well
suggest that written sources do not tell the whole story. It remains
uncertain, however, whether seventh- and early eighth-century
outbreaks in the West were vast and numerous enough to inhibit
demographic growth until 750. Extant sources signal regular and
signiﬁcant population pruning in Europe only before 600, and
principally in the south.5

THE PROMISE OF AN INTERDISCIPLINARY METHODOLOGY This article
looks at a range of issues, both new and not so new, but all of them
wholly non-Justinianic. Like other recent studies in the history of
disease, it combines the sources, methods, and results of usually
isolated disciplines—in this case, history, evolutionary biology,
and zooarchaeology—offering insights unattainable otherwise.
The results herein are necessarily more speculative than deﬁnitive.
The temporal parameters of the written evidence and the spatial
parameters of the zooarchaeological evidence are precise (at least

4 Bernard S. Bachrach, “Plague, Population, and Economy in Merovingian Gaul,” Journal of
the Australian Early Medieval Association, III (2007), 29–57 (Bachrach argues that damage before
600 was minimal, a position not supported herein); Devroey, Economie rurale, 47; Jean-Nöel
Biraben and Jacques LeGoff, “La peste dans de haut moyen âge,” Annales: Économies, Sociétiés,
Civilisations, XXIV (1969), 1484–1510.
For Y. pestis in early medieval bones, see Ingrid Wiechmann and Gisela Grupe, “Detection of
5
Yersinia pestis DNA in Two Early Medieval Skeletal Finds from Aschheim (Upper Bavaria,
6th Century A.D.),” American Journal of Physical Anthropology, CXXVI (2005), 48–55; Michel
Drancourt et al., “Yersinia pestis Orientalis in Remains of Ancient Plague Patients,” Emerging
Infectious Diseases, XIII (2007), 332–333; M. Harbeck et al., “Yersinia pestis DNA from Skeletal
Remains from the 6th Century AD Reveals Insights into Justinianic Plague,” PLOS Pathogens, IX
(2013), 1–8. Regardless of the validity of his ﬁnal conclusion, Samuel Cohn’s observations about
the epidemiological (and, to a lesser extent, symptomological) mismatch of (modern) bubonic
plague with the Justinianic Plague demonstrate that the popular diagnosis of the sixth- through
eighth-century plague is not uncomplicated. See Cohn, “Epidemiology of the Black Death and
Successive Waves of Plague,” in Vivian Nutton (ed.), Pestilential Complexities: Understanding
Medieval Plague (London, 2008), 74–77.

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H UM A N –B OVI N E PL AGU E S

| 5

to the year in the texts), but the reverse is not true. The impreci-
sion in the temporal and spatial parameters of the molecular data
also create difﬁculty in marrying the different datasets. That the
zooarchaeological material presented below is evidence of epi-
zootic disease is also a matter of some dispute.6

The present study is also an exercise in retrospective diagnos-
ing, a tool as much debated as practiced, which yields satisfying
results only when a preliminary diagnosis, usually based on written
reports of symptoms, is conﬁrmed via the isolation of the suspected
pathogen in skeletal remains. No one appears to have successfully
applied the palaeomicrobiological techniques that have been em-
ployed in studies of past bubonic plague, leprosy, and tuberculosis
to the diseases studied herein—the closely related morbilliviruses
MV and RPV. A speciﬁc issue for this analysis, which is central to
the debate about retrospective diagnosing, concerns the intended
meaning and possible inconsistency of certain “medical” terminol-
ogy, such as variola, over time and place.7

Notwithstanding these caveats, the collaboration between
early medieval textual accounts of plagues, MCAs of the divergence
time of measles and rinderpest, and recently uncovered bovine
graves, allows for strong, albeit tentative, retrospective diagnoses
of two non-Justinianic, early medieval mortalities. The utilization
of different data helps to explain otherwise difﬁcult-to-interpret
early medieval accounts of simultaneous plague-scale deaths in
people and cattle, and it allows for speculative disease identiﬁca-
tions sturdy enough to support an assessment of the extent and
consequences of two postclassical human–bovine disease events

For a recent interdisciplinary study in the history of disease, see Sharon DeWitte and
6
Philip Slavin, “Between Famine and Death: England on the Eve of the Black Death—Evidence
from Palaeoepidemiology and Manorial Accounts,” Journal of Interdisciplinary History, XLIV
(2013), 37–60.
For the retrospective diagnosis debate, see Jon Arrizabalaga, “Problematizing Retrospective
7
Diagnosis in the History of Disease,” Asclepio, LIV (2002), 51–70; Andrew Cunningham,
“Identifying Disease in the Past: Cutting the Gordian Knot,” idid., 13–34; Piers D. Mitchell,
“Retrospective Diagnosis and the Use of Historical Texts for Investigating Disease in the Past,”
International Journal of Paleopathology, I (2011), 81–88. Current biomolecular techniques may be
unable to identify remains of viruses in archaeological specimens and therefore MV and RPV. For
cattle remains from a major French burial sent for laboratory study (discussed below), see Sylvain
Renou, Cédric Beauval, and Marie Maury, “Un bilan des connaissances sur les epizooties au
Moyen Âge et un episode de mort extraordinaire de bovines à Luxé (Charente) durant l’époque
mérovingienne,” in Ginette Auxiette and Patrice Meniel (eds.), Les dépots d’ossements d’animaux en
France, de la fouille à l’interprétation (Montagnac, 2013), 140.

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TIM OTHY P. NEW FIELD

that would be impossible on the basis of the written evidence
or physical evidence alone. In drawing on MCAs and advancing
tentative MV–RPV diagnoses, this article not only adds ﬂesh to
theory-based molecular studies and the deep past of two pathogens
of major public-health importance; it also broadens the under-
standing of early medieval mortality crises and the demography
of mid sixth- and late tenth-century Europe.

The study provides palaeomicrobiologists with a new direc-
tion, should techniques become available for the study of viruses
in archaeological specimens and heretofore overlooked farm-
animal and zoonotic pathogens of the past (zoonotic pathogens
being capable of causing disease in both humans and other ani-
mals). More generally, the diverse datasets expand the focus of
medieval disease studies to include human-domesticate disease as
well as extinct pathogens. The plagues of 569–570 and 986–988
studied below are the oldest antecedents to such present-day acute
and highly infectious diseases of livestock as avian or swine inﬂu-
enza, capable of jumping species and colonizing human popula-
tions. The attention to extinct disease is particularly noteworthy:
Retrospective diagnosing and the historiography of disease often
function on the assumption that the diseases in the historical record
still exist and work in familiar ways. This article, at least the
molecular part of it—highlights errors in that manner of thinking.
To make use of an extinct morbillivirus diagnosis, however, the
paper is forced to presume that an ancestral MV–RPV would have
behaved in humans like MV does and in bovines like RPV did until
its 2011 eradication.8

EARLY MEDIEVAL HUMAN–BOVINE MORTALITY EVENTS A recent
survey of early medieval written sources for epizootic disease turned
up eighty-three passages, to which four others now may be added,
pertaining to between thirty-two and ﬁfty-four individual European
(and some Western Asian) animal plagues. The passages are sufﬁ-
ciently short and vague that efforts made to match and separate them
were not always successful, leading to uncertainty in the number
of plagues recorded. That said, forty-four passages clearly refer to

8 On May 25, 2011, the Organisation mondiale de la santé animale declared the world free
of RPV, as did the Food and Agricultural Organization on June 28, 2011. See David M.
Morens et al., “Global Rinderpest Eradication: Lessons Learned and Why Humans Should
Celebrate Too,” Journal of Infectious Diseases, CCIV (2011), 1–4.

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seven vast outbreaks of epizootic disease, and another fourteen
passages seem to refer to an additional three major livestock mortality
events. Of the total passages, twenty-nine, or 33 percent, refer to
zoonotic outbreaks in humans and farm animals. Of that 33 percent,
at least 86 percent identify cattle as the sick domesticate. Seemingly,
acute infectious diseases common to people and cattle, though rare
in the modern era, were not unusual in early medieval Europe.9

It is unlikely, but not impossible, that non-bovine livestock
died in some early medieval bovine and human–bovine plagues.
Cattle are mentioned far more often than other domesticates as
suffering virulent widespread disease in the early Middle Ages,
possibly because, at least in part, their deaths mattered more: In
many regions, they were the most socioeconomically important
species on the farm. Early medieval written sources suggest that
horses and sheep may have been next-most affected by disease
outbreaks; pigs sustained only rare, localized epizootics. The ques-
tion of whether these animals were healthier than bovines or simply
of less interest when dead to early medieval writers is uncertain, and
hence signiﬁcant for retrospective diagnosing. That few pathogens
are known to cause large outbreaks of acute disease in multiple
domesticated species, however, suggests that non-bovines were
indeed less exposed to highly infectious, acute diseases.10

At least three of a possible nineteen early medieval human–
bovine plagues were major events, spreading across parts of continen-
tal Europe and northwestern insular Europe c. 569–570, 868–870,
and 986–988. There is also some indication that the vast cattle pan-
zootic of 809–810 was zoonotic; one of the sources for it refers to
concurrent mortalities in humans. Textual and potential physical

For the recent survey, see Newﬁeld, “Early Medieval Epizootics,” 79–88, 112. The four
9
animal plagues not included therein are (1) the “lethal plague” c.401 that Ruﬁnus of Aquileia
describes as spreading “far and wide,” carried by Alaric and the Goths “to the ruin of ﬁelds,
herds and men” (Ruﬁnus of Aquileia [trans. Philip R. Amidon], The Church History of Ruﬁnus
of Aquileia: Books 10 and 11 [New York, 1997], 3); (2) the pestilential cloud that affected mid-
sixth-century humans and bovines in Ireland (Adomnán of Iona [ed. J. T. Fowler], Vita sancti
Columbae [Oxford, 1894], II.4, 73–75); (3) the “great food shortage and mortality of people
and pestilence affecting beasts” of 869 (Byrhtferth [ed. Cyril Hart], East Anglian Chronicle
[Lewiston, 2006], 89); and (4) the cattle plague in the Saltair na Rann, discussed herein.
10
For early medieval diseased horses, sheep, and pigs, see Annales qui dicuntur Einhardi, in
Friedrich Kurze (ed.), Monumenta Germaniae Historica Scriptores rerum Germanicarum (Hanover,
1895), VI, 89, 91; Annales Fuldenses, in ibid. (1891), VII, 105, 127; Annales Quedlinburgenses, in
Martin Guise (ed.), ibid. (2004), LXXII, 484, 489.

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TIM OTHY P. NEW FIELD

evidence for these plagues provides grounds for fairly good disease
identiﬁcations, since multiple epidemiological (epizootiological, in
the case of animal disease) properties can be teased from them. For
instance, the sources indicate, signiﬁcantly, that among domesticates,
only bovines died in these plagues. More robust, but still tentative,
text-based diagnoses, founded on knowledge of epidemiology/
epizootiology and symptoms, are harder to ﬁnd; only two of the
eighty-seven references to animal disease unambiguously mention
symptoms. Those passages pertain to the 569–570 and 986–988
plagues.11

THE PLAGUES OF 569–570 AND 986–988
Sometime during the late
500s (c.585?), Marius, bishop of Avenches, wrote in his chronicle,
“Virulent disease greatly afﬂicted Italy and France with a ﬂow of
the bowels and variola, and beef animals died especially through
the aforementioned places.” Marius dates the passage to 570, but
from the mid-560s, he is a year ahead. The second and last source
for the 569–570 plague is much later, composed c.835 to 840 by
Agnellus of Ravenna in his Liber Pontiﬁcalis Ecclesiae Ravennatis: “In
the ﬁfth year of Emperor Justin II [570] there was a pestilence of
oxen and a destruction everywhere.” Marius and Agnellus’ accounts
of die-offs in 569–570 are almost certainly independent of one
another but probably refer to the same mortality, given the unlike-
lihood that multiple large plagues affecting cattle would erupt in
successive years in roughly the same region (Marius places the out-
break in France and Italy; Agnellus addressed events primarily in
northern Italy). Agnellus’ known sources do not refer to the plague,
and although it is unclear whether Agnellus consulted Marius’
Chroncia, his writing shows no verbal parallels with it. Agnellus cited
two nonextant works—the Chronicon by Maximian of Ravenna,
which may have extended into the 570s, and an unknown “annalistic
source” thought to have continued until 573. He may have derived
his account from one of these texts.12

For a zoonotic 809–810 panzootic, see Annales Laurissenses Minores, in Georg Heinrich
11
Pertz (ed.), Monumenta Germaniae Historica Scriptores (Hanover, 1826), I, 121; for this cattle
plague, Newﬁeld, “Carolingian Panzootic,” 200–210.
12 Marius of Avenches, Chronica, in Theodor Mommsen (ed.), Monumenta Germaniae
Historica Auctores Antiquissimi (Berlin, 1894), XI, 238; Agnellus of Ravenna, Liber Pontiﬁcalis
Ecclesiae Ravennatis, in Oswald Holder-Egger (ed.), Monumenta Germaniae Historica Scriptores
rerum Langobardicarum et Italicarum (Hanover, 1878), 337; Deborah Mauskopf Deliyannis
(trans.), The Book of Pontiffs of the Church of Ravenna ( Washington, D.C., 2004), 49, 205.

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| 9

Agnellus assigned no spatial parameters to the epizootic, and
those of Marius are general. The plague appears to have affected a
wide region, however, as both authors claim independently.
Whether the disease was prevalent throughout what is now France
and Italy is less certain. Marius tended to focus on Burgundy, the
region where he lived; the mortalities that he reported may have
concentrated there and in neighboring northern Italy. Agnellus
may have been referring to mortalities in the same area. Yet on
the basis of the evidence available, it would be unwise to limit
the 569–570 plague to Burgundy and the northern Italian penin-
sula, considering the emphasis that both authors placed on the
number of deaths and the improbability of so acute and wide-
occurring a disease being endemic (enzootic, in the case of animal
disease) to the area in which it erupted. The plague was almost
certainly introduced from another region or disease pool, possibly
some distance away, where it was native. The temporal parameters,
triggers, geographical origins, and paths of dissemination of the
plague are all hazy, though the Lombard migration from western
Hungary into Italy and brieﬂy to parts of France in 568 might
have introduced the plague to those regions.13

The species involved are much clearer. Although some
scholars have read Marius’ passage as evidence of an exclusively
human epidemic and others a bovine epizootic, both authors might
have been referring to people and cattle. Marius and Agnellus
wrote explicitly of cattle dying (animalia bubula and boves) and
implied—in Marius’ case, anyway—concurrent deaths in humans.
Indeed, Marius’ reference to dead beef animals appears as an inser-
tion in his report of a human disease also spreading in Italy and
France. The interitus that Angellus mentioned, following his note
about the cattle pestilence, could be read as additional emphasis
on the magnitude of the cattle die-off or as a separate mortality
of another species, in all likelihood human, unrelated in Angellus’
mind to the pestilentia bovum.

13
RPV was a mild disease with low rates of morbidity and mortality in enzootic zones but a
severe disease with high rates of morbidity and mortality in epizootic zones. See, J. Anderson,
Thomas Barrett, and G. R. Scott, Manual on the Diagnosis of Rinderpest (Rome, 1996), 6–7;
Anonymous, “Rinderpest,” in Susan E. Aiello and Asa Mays (eds.), The Merck Veterinary
Manual 8th Edition (Toronto, 1998), 543. Sixth-century Burgundy was centered in Geneva,
spanning nearly from Arles in the south to Sens in the north and from Bourges in the west
to Basle in the east. For the Lombard migration and introductions of ecdemic epizootic disease
into early medieval Europe, see Newﬁeld, “Early Medieval Epizootics,” 75, 88–99, 111.

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10 | T I M OT H Y P . N E W F I E L D

The sources for the plague from 986 to 988 are more numerous
and explicit, though also brief. The Anglo-Saxon Chronicle observes
that “the great cattle plague ﬁrst came to England” in 986, and
three versions of the Welsh Brut y Tywysogion have an animal die-
off occurring in that year or in 987. The most reliable and complete
rendering, the Peniarth MS 20, records that “a mortality took place
upon the cattle in all the island of Britain.” A longer account is
encountered in the Chronicon ex Chronicis, slotted into the year
987: “Two plagues unknown to English people in past generations,
namely, a fever of humans and a plague of animals, which in English
is called ‘shit’ but in Latin can be called the ‘ﬂux of the bowels,’ have
thoroughly afﬂicted all England, and raged indescribably in all parts
of England, affecting people with a great destruction and widely
consuming the animals.”14

The “plague and mortality, cattle plague, and disease” that
Wulfstan II includes in his list of England’s recent difﬁculties in
Sermo Lupi ad Anglos may also be this 986–988 mortality, since
he composed his homily in 1014, and no other English bovine
die-off is known between the 890s and the 1040s. Wulfstan was
probably alluding to the 986–988 plague in another homily com-
monly attributed to him (Napier 35) and written around the same
time as the Sermo Lupi ad Anglos, which beseeches God’s help
against (among other disasters) “cattle plagues or human plagues
through sudden diseases.”15

Across the Irish Sea, the Annals of Tigernach, Annals of Ulster,
and Chronicon Scotorum record pestilential deaths of people and
cows in 987. Following notice of “a colic in the east of Ireland”
and subsequent human mortality, the Tigernach observes that “the
beginning of a great murrain, to wit, the unknown máelgarb, came
for the ﬁrst time”; the Chronicon notes “a sickness . . . in the east of
Ireland which caused death among the people” and “the beginning
of the cattle-plague, the máelgarb, such as had not occurred before”;

14 Margaret Ashdown (trans.), “The Anglo-Saxon Chronicle (C), Annals 978–1017,” in
English and Norse Documents Relating to the Reign of Ethelred the Unready (Cambridge, 1930),
40–41; for the Chronicon ex Chronicis, Jennifer Bray and P. McGurk (trans.), Chronicle of John
of Worcester II (Oxford, 1995), 436–437; for Brut y Tywysogyon: Peniarth MS. 20, Thomas Jones
(trans.), Brut y Tywysogyon, or Chronicle of Princes: Peniarth MS. 20 Version (Cardiff, 1952), 10.
For Wulfstan’s passages, see Dorothy Whitelock (ed.), Sermo Lupi ad Anglos (London,
15
1952), 39–40, 57–59; Arthur Napier (ed.), Wulfstan: Sammlung der ihm zugeschriebenen homilien
nebst untersuchungen über ihre echtheit (Berlin, 1883), XXXV, 170; Joyce Tally Lionarons, The
Homiletic Writings of Archbishop Wulfstan ( Woodbridge, 2010), 30–32.

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H UM A N –B OVI N E PL AGU E S
and Ulster tells of “a sudden great mortality which caused a slaugh-
ter of people and cattle in England, Wales and Ireland.”16

| 11

The Saltair na Rann is thought to refer to this plague as well.
In fact, the cattle mortality has long been used to date this Irish
versing of biblical history to the late tenth century, unsurprisingly
given the way in which the poet (or an interpolator) describes the
passage of time to the present: “From Adam of the bright singing
orders” to “the great slaughter of cattle” and the period “From the
birth of Christ . . . ” until “the hundred-fold destruction of the
cattle” (which leads to a 988 dating). He then proceeds to list
the kings reigning “when the pitiful vengeance came on the cattle
of many countries.” The Irish, Welsh, and Scottish kings men-
tioned were indeed ruling when the disease was spreading, but
those from farther aﬁeld either may not have been (like Lothar
of France d. March 986) or, to the best of our knowledge, were
not (like Otto II of Germany d. 983) in power when the disease
passed through their, or what were their, realms. Another king,
England’s Edgar I, had been dead for a decade (975). The Saltair
na Rann clearly does not supply reliable evidence for the mortality
in England or on continental soil from 986 to 988. That the ﬁrst
king in the list is Scottish (Cináed mac Maíl Choluim) and in
power during the outbreak, however, raises the possibility that
Scotland was affected.17

For the Irish annals, see The Corpus of Electronic Texts (CELT), available at http://celt.
16
ucc.ie/publishd.html (accessed March 14–15, 2011). William M. Hennessy (trans.), Chronicon
Scotorum (London, 1866), 231, dates the pestilence to 985, which was changed to 986 in CELT.
Idem (trans.), Annals of Ulster (Dublin, 1887), 497), is preferable to Mac Airt’s translation in
CELT, though Hennessy dates the passage one year early. Dan McCarthy conﬁrmed the date of
987 to be correct in a private correspondence of July 22, 2011.
17 Whitley Stokes (ed.), Saltair na Rann (Oxford, 1883), I.XII.2337–2372, i, v, 34 (errone-
ously dating the plague to 985); Benjamin T. Hudson, Vikings Pirates and Christian Princes:
Dynasty, Religion, and Empire in the North Atlantic (New York, 2005), 62, 69, 220, n. 46. Some
scholars have interpreted this entire dating passage as an interpolation, others only the kingly
section. Gearóid S. Mac Eoin noted and accepted the common “plague dating” of 988 but
argued that the regal part was inserted later, possibly by a Scotsman. He also proposed the
Saltair na Rann’s Corkonian connection, although Airbertach mac Cosse of Rosscarbery is
not universally accepted as having written the text: Gearóid S. Mac Eoin, “The Date and
Authorship of Saltair na Rann,” Zeitschrift für celtische Philologie, XXVIII (1960/61), 51–67;
idem, “Observations on Saltair na Rann,” ibid., XXXIX (1982), 2, 11, 20–21. The 988 plague
date implies that the Saltair na Rann was not composed in central Ireland, where Irish annals
document the outbreak a year earlier, unless the disease persisted there for a year and the poet/
interpolator chose not to date the mortality according to its initial appearance. A composition
at a distance, perhaps the far southwest, as Mac Eoin proposed, may account for the date. The

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12 | T I M OT H Y P . N E W F I E L D

Like that of the seventh- and eighth-century Western European
Justinianic plagues, knowledge of the spatial and temporal parameters
of this plague, as well as the plague of 569–570, is limited. The
sources indicate that the pestilence that began in 986 appeared ﬁrst
(among the regions known to have suffered from it) in England
before spreading westward to Wales in 986 or 987 and Ireland
in 987. The entry in the Anglo-Saxon Chronicle that it “came to
England” suggests that the disease was ecdemic or foreign to north-
western insular Europe and brought to England from the continent,
as does its apparent westward trajectory and alleged, or implied, wide
prevalence and high mortality. Reference in the Annals of Tigernach
and Chronicon Scotorum to the massive losses in Ireland, the dating of
the plague in Irish texts to 987 and 988, and the implication in the
Annals of Ulster that the disease appeared in England and Wales
before Ireland reveal that this plague did not originate in Ireland.
The labeling of the disease as new or unknown in England and
Ireland may be a trope; such qualifying of plagues was not then
atypical. Nevertheless, the plague was almost certainly imported
from another disease pool, likely by living cows or people but pos-
sibly by other means as well. Although there is no record of wide-
spread livestock disease on the continent in the late tenth century
prior to 986, large concurrent human and bovine mortalities are
reported in central-north Germany in 989–990 and 993. These events
may be interpreted as either the continued circulation of the dis-
ease on the continent after its insular introduction or as unrelated
plagues.18

Five independent and contemporary texts emphasize the vast-
ness of the mortality among people and cattle. That several of
these passages were composed originally at a distance from each
other (in all probability Abingdon for Anglo-Saxon Chronicle;
Worcester for the Chronicon ex Chronicis; St. David’s for the Welsh Brut;

translation in this paragraph is from David Greene, which was unﬁnished at his death but
available on the website of the Dublin Institute for Advanced Studies—www.dias.ie (accessed
March 10, 2014).
18 The plague is dated in Brut’s Peniarth MS. 20 to 986 (no dates are given in the Red Book
or Brenhinedd y Saesson versions of the Brut). Based on a comparison of passages in Peniarth,
the Annals of Ulster, and Chronicon Scotorum, however, Jones, the editor of the Brut texts,
proposes that the dates given in the Peniarth from 974 to 1003 are a year behind. For
continental human–bovine plagues in 989–990 and 993, see Annales Quedlinburgenses, 447; Annales
Hildesheimenses, in Georg Heinrich Pertz (ed.), Monumenta Germaniae Historica Scriptores (Hanover,
1839), III, 68, 70.

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| 13

Clonard or Clonmacnoise for the Annals of Tigernach and Chronicon
Scotorum; Clonard, Clonmacnoise, or Armagh for the Annals of Ulster;
and possibly Rosscarbery for the Saltair na Rann) supports the sources’
claim of a general, rapidly developing outbreak (the Annals of Ulster
describe the plague as “sudden,” as Wulfstan II seems to do), pre-
suming animals died not far from where the texts were composed,
and manuscripts did not circulate widely during the plague years.
The Saltair na Rann’s poetic treatment of the cattle mortality as a
memorable event and Wulfstan’s inclusion of people’s and cattle’s
deaths in his homilies (assuming that he refers to the plague of
986–988) suggests that the event was by no means triﬂing. People
and cattle in south-central England, the West Midlands, south-
western Wales, and central (and possibly northeast) Ireland seem to
have been afﬂicted within about a year. Such a fast and wide dis-
semination implies that the pathogen was not principally arthropod-
or soil-borne but transmissible between susceptible species, like the
569–570 plague—yet another indicator that animals south of the
English Channel were affected.19

The pestilence’s trigger, geographical origin, and duration,
however, remain opaque. The outbreak does not, for instance, appear
to correspond spatially or temporally to a subsistence crisis, climatic
anomaly, or major conﬂict that could have fostered its introduction
into Britain or continental Europe. That Danes brought it with them
to the Hebrides and Irish Sea region in 986 seems unlikely considering
the dating and progression of the outbreak, as traced above. Follow-
ing the methods of dissemination common to infectious airborne
diseases, including MV and RPV, these plagues likely spread within
and between both urban and rural communities along local and
regional routes of travel and trade. Although exceptional events
may have driven the causative pathogen from a distant region, once

19
RPV and MV are typically introduced to regions via the travel of their victims, either
before, during, or after the incipient stages of severe disease. See T. U. Obi, P. L. Roeder,
and W. A. Geering, Manual on the Preparation of Rinderpest Contingency Plans (Rome, 1999), 5;
Anderson, Barrett, and Scott, Diagnosis of Rinderpest, 7; Robert T. Perry and Neal A. Halsey,
“The Clinical Signiﬁcance of Measles: A Review,” Journal of Infectious Diseases, CLXXXIX
(2004), S4; Gregory Hussey, “Measles,” in Richard David Semba and Martin W. Bloem
(eds.), Nutrition and Health in Developing Countries (Totowa, 2008), 216; Centers for Disease
Control and Prevention, “Measles,” in W. Atkinson, J. Hamborsky, and S. Wolfe (eds.),
Epidemiology and Prevention of Vaccine-Preventable Diseases ( Washington, D.C., 2012), 178.
For the 989–990 and 993 mortalities, see Georg Waitz (ed.), Annales Hildesheimenses (Hanover,
1878), VIII, 25, 26; Guise (ed.), Annales Quedlinburgenses, 477.

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14 | T I M OT H Y P . N E W F I E L D

it was introduced elsewhere the normal movements of people and
cattle were likely sufﬁcient to cause the mortalities reported. Major
events, such as the Lombards’ arrival in Italy, which may have itself
introduced the pathogen of the 569–570 plague to Western Europe,
no doubt helped, but they were not, as the 986–988 plague testiﬁes,
always necessary.20

The Chronicon ex Chronicis’ dating suggests that the disease
persisted for a year at least in some regions, as does the assigning
of the plague to 988 in the Saltair na Rann. Areas especially cattle-
rich may have suffered longer. The Annals of Ulster’s account of a
“great mortality of people, cattle, and bees throughout Ireland”
in 993 may signify the outbreak’s persistence there for many
years, similar to Ireland’s experience with the 1314/25 panzootic.
While the Anglo-Saxon Chronicle, Brut, and Saltair na Rann refer
solely to the bovine mortality, the Chronicon ex Chronicis and Irish
annals (and possibly Wulfstan) make it clear that humans died
concurrently.21

MASS BOVINE GRAVES Until recently, the evidence for large early
medieval plagues of livestock derived strictly from written sources.
The dearth of identiﬁed mass burial sites appears to have had little
to do with the once-popular interpretation of intact or largely
intact animal skeletons that showed no traces of butchery as rem-
nants of ritual or offering but to an actual absence of known
animal “plague pits.” The abandonment of animals that were vic-
tims of disease, extreme weather, or famine in ﬁelds, forests, and
water may account for the lack of known mass burials, as would
their interment away from excavated human sites. Early medieval

For the Danes, see T. M. Charles-Edwards, Wales and the Britons, 350–1064 (New York,
20
2014), 541. That the Airgíalla managed to steal 2,000 head of cattle from Armagh in 996
(Ó Corráin, “Ireland c.800,” 569) suggests, but does not conﬁrm, that the 986–988 mortality
spared Armagh and that this Annals of Ulster passage derived from the other Irish sources (a
Clonmacnoise-group text). Lesser conﬂicts in northern Wales and on Mann in 986 and 987—
involving Hiberno-Scandinavians, Welsh, and Danes—and the capture and presumed sale of a
reported 2,000 Anglesey inhabitants in 987 (Charles-Edwards, Wales and the Britons, 549–550),
may have fostered the plague’s development in Britain. The Danes’ ability to pillage a handful
of southern Welsh monasteries with Guthfrith Haraldsson in 988 and exact a tribute from
Maredudd ab Owain in 989, however, implies that they did not fall sick in large number in
986–988 but that the southern Welsh did. Hudson speculates that the Danes and Haraldsson
attacked peoples “weakened” by the plague in the Hebrides, Mann, and Wales (Vikings Pirates, 62).
For the 993 mortality, see Annals of Ulster and Chronicon Scotorum in CELT (n.16). The
21
Chronicon Scotorum limits the death toll to Clonmacnoise.

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| 15

animal-bone assemblages thought to demonstrate large cattle
mortalities, however, have now been unearthed in England,
France, and Switzerland, and, like recently discovered mass animal
burials from earlier and later periods, linked to epizootic disease.
Such sites give some credence to the textual reports of large
bovine mortalities. Indeed, these English, French, and Swiss graves
lend conﬁdence, though not conﬁrmation, to reports of sudden
and severe cattle die-offs in early medieval Europe—the plagues
of 569–570 and 986–988 in particular—in much the same way
that the more common human plague pits do for Justinianic
plagues. The mass graves may also expand the known geographical
bounds of the 569–570 and 986–988 plagues, underscoring obser-
vations made about the causative pathogens’ principal mode of
transmission, and probable high communicability, morbidity, and
mortality.22

The number of animal skeletons necessary to indicate a large
mortality event has been set at about four. These animals need not
be buried in a single pit; multiple individual burials sufﬁce. But
individually interred creatures must be contemporaneous and,
when carbon-14 tested, show homogenous dates. Preferably, the
animals should be articulated, though bulky creatures could have
been chopped into large pieces for transport. But so far as researchers
are concerned, signs of a quick and deep burial; the covering of
carcasses with lime (a traditional agricultural disinfectant); no or little
recovery of meat, hides, hooves, or horns; and interment at an age
otherwise optimal for draught, milk, and meat all serve to indicate
an epizootic. Mass burials of a single species may be considered

For cattle abandoned in ﬁelds following the 809–910 and 878 disease outbreaks, see
22
Poeta Saxo (ed. Paul de Winterfeld), Annalium de Gestis Caroli Magni Imperatoris Monumenta
Germaniae Historica Poetarum Latinorum (Berlin, 1899), IV, 236–253, 51–52; Kurze (ed.),
Annales Fuldenses, 92. Various ancient and late antique authors, perhaps reﬂecting common
practice, recommended the isolation of sick animals. Drawing on Columella in the late fourth
or early ﬁfth century, Vegetius, for instance, stated that the graves of dead animals should be
placed deep and far from human settlements. See E. Lommatzsch (ed.), Digestorum Artis
Mulomedicinae Libri (Leipzig, 1903), I.1.3, 16; I.17.3, 34; IV.2.15, 283–284. No known mass
burial dated to the early Middle Ages suggests a human–bovine plague. Domesticates were
buried separately from humans; the animals (notably horses) occasionally found in human burials
are generally considered to be ritual sacriﬁces or grave goods, see Bonnie Effros, Merovingian
Mortuary Archaeology and the Making of the Early Middle Ages (Berkeley, 2003), 164–165; Howard
Williams, Death and Memory in Early Medieval Britain (New York, 2006), 82, 175, 177; Pamela J.
Cross, “Horse Burial in First Millennium AD Britain: Issues of Deposition,” European Journal of
Archaeology, XIV (2011), 190–209.

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16 | T I M OT H Y P . N E W F I E L D

additional proof of a disease event, since most known virulent
livestock diseases affect only one species. The English, French, and
Swiss burials ﬁt most of these criteria, though they cannot be con-
sidered deﬁnitive evidence for epizootic disease without further
laboratory study for causative pathogens. These cattle might have
died as a consequence of extreme weather or famine.23

The ﬁrst of the large early medieval bovine burials was un-
covered in Shapwick, England, about a 75 miles southwest of
Abingdon, 80 miles south of Worcester, and 120 miles east of
St. David’s, across the Bristol Channel; seven intact animals were
found in a limekiln, which was not fully excavated. All of the
cattle were adult males, likely draft animals, articulated and devoid
of skeletal stigmata, suggesting that they were healthy and died a
sudden death in a disease outbreak of a “national” scale. Researchers
have posited the early eleventh century as a probable date, but the
radiocarbon-dated tibiae permit a wider range of 980 to 1160, mean-
ing that these animals could have succumbed to the 986–988 plague.
The grave’s proximity to the location of the English and Welsh
written reports for that pestilence would support this notion,
though other bovine epizootics are reported for southern England
within the 980 to 1160 window.24

The second of the multi-specimen graves was uncovered in
Luxé, France, 340 miles west of Avenches, 600 miles west of
Ravenna, and about 140 miles west of the western edge of early
medieval Burgundy—ten largely intact bovine skeletons in close
singular pits with an early medieval dating around the early seventh
century, though some carbon-14 dates are as early as 570. Like the
Shapwick animals, these were in the prime of their life (most of
them between one and six years old), showing no signs of chronic
infection or malnourishment and no or little evidence of having

Sophie Lefebvre, “Inhumations de bovines sur le site medieval et moderne d’Auby ‘I’Îlot
23
Béguinage’ (Nord),” in Auxiette and Meniel (eds.), Les dépots d’ossements d’animaux, 150, 152;
Annelise Binois, “Approche méthodologique des mortalités de masse ovines en archéologie,”
ibid., 278, 279–280; Renou, Beauval, and Maury, “Un bilan des connaissances,” 136, 140;
Olivier Putelat, “Archéologie des depots animaux et mortalité extradinaire du cheptel bovin
au premier Moyen Âge: Plaidoyer pour une redynamisation et une mise en perspective de la
recherché,” in Auxiette and Meniel (eds.), Les dépots d’ossements d’animaux, 249, 252, 253, 259–262.
Louisa J. Gidney, “Murrain or Starvation? Catastrophic Cattle Mortality Events in
24
Medieval and Ports Medieval England and Their Repercussions,” in Richard Thomas and
Theodore G. Antikas (eds.), Animal Disease in Past Human Societies: Proceedings of the Fourth
ICAZ Animal Palaeopathology Working Group (Atlanta, forthcoming).

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| 17

been used for meat or raw materials. The burials were deep and
rapidly completed.25

Five bovines found at a third site at Bure, Switzerland, are
dated to the late ninth through early eleventh century. The one
bovine that was carbon-14 dated appeared to be buried slightly
before the others, in the mid-tenth century. The others were
interred simultaneously or near simultaneously, some of them
covered with limestone blocks. It has been suggested that the
animals at Bure may have died from the same cause as the seven
bovines uncovered at nearby Bourogne (3) and Vellechevreux
(4) in France. Regardless of whether the physical evidence in this
case is sufﬁcient to conﬁrm a general mortality event, these ani-
mals, unlike those found at Shapwick and Luxé, died a consider-
able distance from the known parameters of the 986–988 plague,
to which they may be associated; they very well may have died in
another epizootic.26

HUMAN–BOVINE PLAGUE DIAGNOSING AND MORBILLIVIRUS MOLECULAR
It is advantageous for the purposes of diagnosing both the
CLOCKS
569–570 and 986–988 plagues that symptoms and epidemiology/
epizootiology can be identiﬁed. Indeed, written and possible phys-
ical evidence for these mortalities provides good grounds for estab-
lishing their causative agents. Traditionally, historians have diagnosed
pre-laboratory outbreaks of disease symptomologically, but a
symptoms-based approach is not necessarily the best approach; nor
is it in every case applicable. As Cohn argued forcefully in his rejec-
tion of the bubonic plague diagnosis of the Black Death, a better
method, leading to a stronger, though still tentative, disease identi-
ﬁcation entails consideration of both symptoms and epidemiology/
epizootiology. Although early medieval authors rarely commented
directly on epizootiology, key properties are often apparent enough.
A general understanding of morbidity and mortality, the species sus-
ceptible to the pathogen, the relevance of environmental conditions,
and the underlying health of victims is often obvious. Rarely evident
are the previous pathogen exposures (acquired immunity) or second-
ary infections (antagonistic or symbiotic disease interactions).27

Putelat, “Archéologie des depots animaux,” 250–257.

25 Renou, Beauval, and Maury, “Un bilan des connaissances,” 135–141.
26
27 Cohn, The Black Death Transformed: Disease and Culture in Early Renaissance Europe (New York,
2002).

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18 | T I M OT H Y P . N E W F I E L D

Epizootiology has proved pivotal for the diagnosing of pre-
laboratory epizootics. The tentative RPV identiﬁcations of the
809–910 and 1314–1325 bovine plagues hinged on determining
the ability of their pathogens to spread rapidly and indiscriminately
with regard to seasonal changes or the health of their victims, to
achieve high rates of morbidity and mortality, and to attack cattle
alone (or predominantly, in the case of the ninth-century out-
break). Existing comments on the 569–570 and 986–988 bovine
mortalities, which played down or ignored their zoonotic nature,
lean toward RPV on account of the references to diarrhea. But,
excusing for a moment concurrent human mortality, the epi-
zootiological properties of these plagues also support an RPV diag-
nosis: high rates of morbidity and mortality; the targeting of cattle;
an ability to disseminate quickly and plausibly without regard for
seasonality or environment; and, assuming the Shapwick and Luxé
bovines to have died in these events, lethality among even healthy,
mature animals. Had people succumbed to a different disease than
did cows in 569–570 and 986–988, RPV diagnoses for these plagues
would be sturdier than for those of the 809–810 and 1314–1325
panzootics, or the supposed 376–386 pan-European cattle mortal-
ity, since fourth-, ninth-, and fourteenth-century sources contain
references only to RPV-like symptoms (cows with upset stomachs
or cows suffering emaciation).28

RPV is always a good candidate for fast-moving, large-scale
bovine epizootics of the past that have been attributed with the
deaths of many animals. When explicit reference is made to loose
bowels in such outbreaks, RPV is the only option known to modern
science. Were contagious bovine pleuropneumonia more conta-
gious and mortal, it would be a candidate for those major medieval
epizootics for which diarrhea was not an explicit symptom. So
would highly infectious and fast-spreading foot-and-mouth dis-

For the supposed late fourth-century panzootic, see A. Barton, “Plagues and Contagions
28
in Antiquity,” Journal of the American Veterinary Medical Association, CXXIX (1965), 505; Clive
A. Spinage, Cattle Plague: A History (New York, 2003), 47, 82, 88; for a reappraisal, Newﬁeld,
“Epizootic Disease in Medieval Europe: Seven Cattle Pestilences and Directions for Future
Research,” in Thomas and Antikas (eds.), Animal Disease in Past Human Societies (forthcoming);
for the eighth- and fourteenth-century panzootics, idem “Carolingian Panzootic,” 200–210;
Slavin, “The Great Bovine Pestilence and Its Economic and Environmental Consequences in
England and Wales, 1318–50,” Economic History Review, LXV (2012), 1239–1266; Newﬁeld,
“A Cattle Panzootic in Early Fourteenth-Century Europe,” Agricultural History Review, LVII
(2009), 155–190.

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| 19

ease, were it far more acute then than it is now, though its ability to
infect sheep, goats, and pigs—animals rarely identiﬁed as victims of
epizootics in the early Middle Ages—would have to be
acknowledged.29

That the 569–570 and 986–988 pathogens were common to
people and cattle complicates RPV identiﬁcations considerably,
since RPV is unique to bovines. The usual diagnosis for a disease
that affected both humans and farm animals is anthrax, but it is a
highly problematical identiﬁcation for large disease outbreaks in
people and cattle. Although anthrax spores cause acute disease,
they are soil- and sometimes arthropod-borne and, as such, depen-
dent on particular environmental and seasonal conditions and
incapable of spreading easily between herds and regions. Nor is
anthrax particular to humans and cattle: All animals are susceptible
to it, though grazers like cows and sheep are the most common
victims. With no real pathogenic alternative, it is not surprising
that the two plagues assessed herein have been interpreted as both
epidemics and epizootics. Treated separately, the bovine deaths are
easier to explain. Like the pathogens killing cows, those killing
people must have been highly communicable and virulent consid-
ering the short time in which they covered so much ground. They
also must have been transmitted between like species; pathogens
passed easily between humans account best for large rapidly devel-
oping epidemics.30

Several diseases ﬁt this epidemiology; reported symptoms do
little to narrow down the candidates. The 986–988 human victims
had fevers, but many pathogens cause a fever. If fever were the
most salient symptom, inﬂuenza might be suspected. Assuming

29 The pestivirus Bovine Viral Diarrhea Virus, as known to modern science, is a fairly con-
tagious but not especially mortal disease with a 4 to 8% fatality rate. Although its victims suffer
diarrhea, it is considered a new virus (emerging in the 1940s), which does “not behave like
rinderpest.” See Dirk Deregt, “Introduction and History,” in Sagar M. Goyal and Julia F.
Ridpath (eds.), Bovine Viral Diarrhea Virus: Diagnosis, Management and Control (Ames, 2005),
3–34. Foot-and-mouth strains known to modern science kill fewer than 5% of their victims.
See William A. Geering and Juan Lubroth, Preparation of Foot-and-Mouth Disease Contingency
Plans (Rome, 2002), 1, 7, 10–15. For pleuropneumonia, see Geering and William Amanfu,
Preparation of Bovine Pleuropneumonia Plans (Rome, 2002), 5–9.
30
For anthrax, see World Organisation for Animal Health, Anthrax in Humans and Animals
(Geneva, 2008), 1–5, 8–17; Spinage, Cattle Plague, 85 (though Spinage interprets the 987 Irish
mortalities as anthrax [90]); Newﬁeld, “Early Medieval Epizootics,” 91–92. Bovine tubercu-
losis (Mycobacterium bovis), another well-known disease of cattle, can infect and kill cows and

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20 | T I M OT H Y P . N E W F I E L D

that early medieval authors did not universally report every phys-
ical expression of a pathogen or even necessarily the principal sign,
other diseases causing fever might be considered, such as MV and
smallpox. Fever from MV can be in the range of 103 to 105 degrees
Fahrenheit, a couple degrees higher than smallpox.31

Little else is certain about the disease expression in humans.
Indeed, another factor complicating the identiﬁcation of the
569–570 and 986–988 plagues’ causative agents is establishing
who suffered what. Did humans have diarrhea along with cows
in 569–570 and 986–988? Was variola common to both species
in 569–570? Marius is unclear about loose bowels and variola in
the sixth century. The Annals of Tigernach mentions people suffer-
ing colic in 987, though the Chronicon ex Chronicis reserves scitta for
cows. Tentative diagnoses of these plagues founded on the aspects

people, but it is as poor a diagnosis as anthrax. It is a chronic, debilitating disease primarily of
cattle but capable of sickening humans and a number of other species, domesticated and wild.
In cattle, M. bovis is associated principally with production losses (milk and meat), not mor-
tality. Although it can involve the digestive tract and cause “intermittent diarrhea” in both
cows and people, this disease expression is rare. The principal symptoms in humans are weight
loss and fatigue. Although spread between cattle via the respiratory tract, M. bovis reaches hu-
mans via the consumption of contaminated dairy products and then spreads from person to
person, if pulmonary. But bovine tuberculosis is slow-moving: About 5% of people develop it
within two years of exposure; another 5% may develop it later. See Charles O. Thoen et al.,
“Tuberculosis in Animals and Humans: An Introduction,” in idem, James H, Steele, and John
B. Kaneene (eds.), Zoonotic Tuberculosis: Mycobacterium Bovis and Other Pathogenic Mycobacteria
(Ames, 2014), 3–5; Anna Rovid Spickler et al. (eds.), Emerging and Exotic Diseases of Animals
(Ames, 2010), 107–110.

In eighteenth- and nineteenth-century catalogs of ancient and medieval disease outbreaks,
the 569–570 and 986–988 plagues, however vaguely understood, were divided commonly into
epidemics of people and epizootics of cattle. This tradition persisted into the twentieth century, as
is especially evident with regard to the 569–570 plague and works on smallpox. Thomas Short, A
General Chronological History of the Air I (London, 1749), treated the 986–988 human and bovine
mortalities separately, choosing not to diagnosis (91). Jean-Jacques Paulet twice separated the
569–570 deaths of people and cattle. He mentions both of them but discusses only the former
in his early study of past epizootics, Recherches historiques and physiques sur les maladies épizootiques
(Paris, 1775), 73. He overlooks the sick cattle entirely in his treatise on the history of petite vérole—
Historie de la petite vérole I (Paris, 1768), 78, 85, 87, 93. Robert Willan, An Inquiry into the Antiquity
of the Small-Pox, Measles and Scarlet Fever (London, 1821), mentions but does not address the
569–570 bovine mortalities in his early study of smallpox (96). Wilhelm Dieckerhoff, Geschichte
der rinderpest und ihrer literatur (Berlin, 1890), 25, 28, assigns the human and bovine deaths of both
569–570 and 986–988 to different causes. More recently, Stathakopolous, Famine and Pestilence,
313–314, considers the 569–570 deaths of cattle and people together but does not advance a
diagnosis.
31
and Prevention, “Measles,” 174.

Perry and Halsey, “Clinical Signiﬁcance of Measles,” S4; Centers for Disease Control

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H UM A N –B OVI N E PL AGU E S
of their symptoms and epidemiology/epizootiology not in doubt—
the bovine diarrhea and the plagues’ ability to disseminate widely
and kill people and cattle rapidly—and molecular clocks recently
run on the morbilliviruses MV and RPV indicate a possible solution
to the problem. A joint MV–RPV diagnosis of these plagues can
untangle Marius’ ambiguity, accounting for both people and cows
being diarrheal. First-time victims of MV are likely to have a severe
reaction to the pathogen, especially if they are undernourished by
modern standards (as many early medieval Europeans likely were);
under these conditions, diarrhea can be acute enough to cause
death. More than 63 percent of MV victims in developing countries
before the introduction of the vaccine suffered diarrhea.32

On this point, the work of physician Abu Bakr Muhammad
ibn-Zakariya Razi (Rhazes) may be signiﬁcant. Rhazes penned
multiple treatises c. 900 that clinically differentiated between judari
and hasbah, diseases read respectively and retrospectively as small-
pox and MV before and since the crystallization of either in the
laboratory. Assuming the accuracy of these identiﬁcations—and
a variety of MV was present in postclassical Western Asia—Rhazes’
work would illuminate MV’s symptoms in the early Middle Ages (a
couple decades on either side of 900, and even earlier, given his
debt to descriptions of judari and hasbah in the work of seventh-
century Aaron of Alexandria).33

Though Rhazes wrote mainly about endemic judari and
hasbah, observations of diarrhea form a not unimportant part of

For diarrhea, malnutrition, and measles in unexposed populations, see Hussey, “Measles,”
32
218, 219, 220; Perry and Halsey, “Clinical Signiﬁcance of Measles,” S6–S7; Centers for Disease
Control and Prevention, “Measles,” 174; for undernourished early medieval people, Kathy
Pearson, “Nutrition and the Early-Medieval Diet,” Speculum, LXXII (1997), 1–32.
33 Richard Mead and Thomas Stack, who provided the ﬁrst English translation of
Rhazes’ Arabic text—A Discourse on the Smallpox and Measles (London, 1748), xi–xii, 3, 100,
113–204—understood judari and hasbah to refer to smallpox and measles. So did Paulet, who ﬁrst
translated Rhazes’ text from Latin into French—Historie de la petite vérole (Paris, 1768), II, 1–102—
and several other eighteenth- and nineteenth-century editions of Rhazes’ text (in various
languages), such as William Alexander Greenhill, A Treatise on the Small-Pox and Measles (London,
1858), 5–9, 22–75. Many later studies agree: Willan, Inquiry, 1–2; Moore, Small Pox, 4, 56, 113;
Hirsch, Historical Pathology, 123, 154; Edward J. Edwardes, A Concise History of Small-Pox and
Vaccination in Europe (London, 1902), 3; Cyril William Dixon, Smallpox (London, 1962), 187–
188; Hopkins, Greatest Killer, 27; Tucker, Scourge, 14; Wilkinson, “Virus Concept,” 2–3; Ann
G. Carmichael and Arthur Silverstein, “Smallpox in Europe before the Seventeenth Century:
Virulent Killer or Benign Disease?” Journal of the History of Medicine and Allied Sciences, XLII
(1987), 147, 151–152.

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22 | T I M OT H Y P . N E W F I E L D

his work on these diseases, suggesting that loose bowels may have
been common to MV during the early Middle Ages regardless of a
population’s familiarity with the disease. In his treatise on judari
and hasbah, Rhazes reports victims of both diseases to have ex-
perienced a loosening of the bowels, identifying the diarrhea of
hasbah sufferers as far more severe and debilitating than that of
judari sufferers. In his Liber ad Almansorem, Constinens and Divisio
Morborum, Rhazes repeats that hasbah diarrhea is worse, and in
the Constinens, he observes that it could cause death. A combined
MV–RPV diagnosis can also explain the tagging of the 986–988 plague
with máelgarb, “bald-rough,” in the Irish sources. The focus in Irish
texts on this description of afﬂicted animal hides implies either
that diarrhea was not understood there as the primary sign of the
disease or that the annalist was concerned principally with the ﬁnan-
cial repercussions of damaged hides. Like ﬂuxus intraneorum, a rough
hair coat is typical of RPV, though it is not a classic or distinguishing
symptom of the disease.34

What is known about variola? The accepted assumption is
that the Avenchene bishop understood variola as affecting humans
and that his variola was smallpox (Variola major). As far as can be
told from extant sources, Marius coined the term variola, and
although Constantinus Africanus, who wrote in the eleventh-
century, is considered the ﬁrst author to use variola in speciﬁc ref-
erence to smallpox, Marius’ usage has led many authors since at
least 1768 to diagnose a 569–570 epidemic as smallpox. Variola has
been held to derive from the Latin adjective varius—“changing,”
“varying,” or “different.” In histories of smallpox, however, the
translation is usually “blotchy” or “spotted.” It can also derive from
the noun varus, meaning “spot,” “pimple,” and, in histories of small-
pox, “pustule.” The extent to which variola was used in reference to
a single disease in the early Middle Ages is uncertain. It may have
referred to a number of acute and fast-acting illnesses that affected
victims’ appearance, as lepra is held to have been an umbrella term

For Rhazes and diarrhea, see Rhazes, Kitab ﬁ al-jadari wa-al-hasbah, in Greenhill (trans.),
34
A Treatise on the Small-Pox and Measles (London, 1858), XIII, 67–70; idem, Liber ad Almansorem,
ibid., X.18.8, 86; idem, Constinens, ibid., XVIII.8.49, 114; idem, Divisio Morborum, ibid., CIL.3
and .7, 92, 94. Attention is also drawn to hasbah-associated diarrhea in two case reports at-
tributed to Rhazes: Max Meyerhof, “Thirty-Three Clinical Observations by Rhazes (circa
900 A.D.),” Isis, XXIII (1935), 321–356; XXIV (1936), 343–344; XXVII (1939), 344–345.
For RPV and rough hair coats, see Wohlsein and Salik, “Rinderpest,” 73.

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H UM A N –B OVI N E PL AGU E S
referring to chronic disﬁguring diseases like leprosy and psoriasis.
Variola does appear, however, to have been a disease of humans.35
As early commentators on the history of smallpox observed,
several references to variola occur within a century or two of
Constantinus Africanus. Most of these variola sufferers were un-
known to the authors who diagnosed them, but all of them were
human. The likely mid-twelfth-century Genealogia comitum
Flandriae depicts Baldwin III dying in 962 of a morbo variolorum, and
Ekkehard IV of St. Gall in his early eleventh-century Casus sancti
Galli refers to a variolam morbus that attacked the Bavarian bishop
Kaminold and was treated by Notker Physicus also in the third
quarter of the tenth century. Bishop Ludger (742–809) was reputed
to cure two cases of variola, one in Bramsche, north Germany, and
the other in ‘Ballova,’ mentioned in the so-called “second vita” of
the saintly Utrechter written in the second half of the ninth century
in Werden. In his Gesta Abbatum Sancti Bertini Sithiensium of the
early 960s, Folcuin reports a young noble’s release from a disease that
“doctors call variola” in 938 in St. Bertin, northern France. Addition-
ally, the early eleventh-century Frulandus Murbacensis, in his Passio
Leudegarii Episcopi III, refers to the mid-seventh-century Bishop
Leodegar curing the son of a Neustrian Palace Mayor of variola in
the eastern French town of Autun. Frulandus implied that variola was
well known, though it is uncertain whether he meant in Leodegar’s
era or in his own.36

35
Paulet, Historie de la petite vérole I, I, 78, 85, 87, 93; Willan, An Inquiry into the Antiquity of
the Small-Pox, Measles and Scarlet Fever (London, 1821), 86–105; James Moore, The History of the
Small Pox (London, 1815), 6–8, 19, 81, 88, 146–147; August Hirsch (trans. Charles Creighton),
Handbook of Geographical and Historical Pathology (London, 1883), 126; Jon. Hermann Baas (trans
H. E. Handerson), Outlines of the History of Medicine and the Medical Profession (New York, 1971;
orig. pub. 1889), 240; Edwardes, Concise History, 3; Dixon, Smallpox, 187; Biraben and LeGoff,
“La peste,” 1493–1494; Jonathan B. Tucker, Scourge: The Once and Future Threat of Smallpox
(New York, 2001), 2; Donald R. Hopkins, The Greatest Killer: Smallpox in History (Chicago,
2002), 25; Devroey, Economie rurale, 46; Jennifer Lee Carrell, The Speckled Monster: A Historical
Tale of Battling Smallpox (New York, 2004), xv; S. L. Kotar and J. E. Gessler, Smallpox: A
History ( Jefferson, 2013), 3–4. Constantinus Africanus’ description—De Omnium Morborum
in Constantini Africani post Hippocratem et Galenum (1536), VII.8, 152–153—may fail to con-
vince everyone.
36 D. L. C. Bethmann (ed.), Genealogia comitum Flandriae, MGH SS IX (Hanover, 1851),
304, 306. Jean de Langhe refers to this work in the largely derivative early portions of his
fourteenth-century Chronicon Sancti Bertini, but he adds that the disease is called variola and
pocca. See Holder-Egger (ed.), MGH SS XXV (Hanover, 1880), XXVIII, 776. Ekkehard
IV, Casus sancti Galli continuatio I, in G. H. Pertz (ed.), MGH SS II (Hanover, 1829), 136;

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24 | T I M OT H Y P . N E W F I E L D

Other than associating variola with people, these iterations do
little to explicate Marius’ meaning. Nor is it clear whether these
later authors are referring to one disease, let alone V. major or
V. minor. Though Murbacensis, Ekkehard, and the author of
the Ex Vita Sancti Liudgeri associate variola with pustulas (pustules
or blisters), bodily ulcera (ulcers or sores), inﬂatio (swelling), and
pustulas-related blindness, all of which may indicate smallpox, only
the Genealogia comitum Flandriae describes variola as lethal. Since
none of these texts suggests that variola was wide-ranging, as Marius’
does, variola may have signiﬁed diseases with different degrees of
virulence and communicability, in much the same way that the
term lepra was not reserved for slow-moving, milder diseases but
on occasion applied to plagues that modern historians associate with
smallpox.37

Unsurprisingly, a few scholars have drifted far from a ﬁrm
identiﬁcation of Marius’ variola as smallpox. Moore proposed it
to be bubonic plague, given the timing of 569–570 plague, which
occurred in the midst of several supposed outbreaks of Y. pestis and
variola’s absence from European texts for at least three centuries
after Marius. Moore’s singular position was that Marius’ original
manuscript, which, in Moore’s view, must have been difﬁcult to
decipher and nearly illegible, was probably reworked with a later
transcriber’s interpolations. More recently, Dixon soberly observed
that Marius’ variola is simply unidentiﬁable in lieu of a clinical de-
scription of the disease. Wilkinson maintained that neither Marius’
variola nor that of other writers before Rhazes can be identiﬁed as
smallpox for lack of a good clinical description. Assuming that
Marius’ variola refers to a skin eruption or other visible effect, as
the Latin suggests, smallpox remains a possibility, but MV is also a
candidate for it.38

Ex Vita Sancti Liudgeri II, ibid., II.29, 424, II.33, 423–424; Folcuin, Gesta Abbatum Sancti Bertini
Sithiensium, in Holder-Egger (ed.), MGH SS XIII (Hanover, 1881), CVI, 628. Frulandus Mur-
bacensis, Passio Leudegarii Episcopi III, in B. Krusch (ed.) MGH SrM V (Hanover, 1910),
XXXI, 360. This variola may not, in fact, belong to the second vita, written c.850, but to
the third, written c.890. Altfrid’s vita of Ludger, written c.840, the saint’s so-called “ﬁrst vita,”
does not mention it. Paulet diagnosed Marius’ variola as petite vérole in 1768 (see n. 35).
37
38 Moore, Small Pox, 6–8, 19, 81, 88, 146–147; Dixon, Smallpox, 190; Hirsch, Historical
Pathology, 126–127; Lise Wilkinson, “The Development of the Virus Concept as Reﬂected
in Corpora of Studies on Individual Pathogens: 5. Smallpox and the Evolution of Ideas on
Acute ( Viral) Infections,” Medical History, XXIII (1979), 2, n. 6.

For smallpox as lepra, see Donnchadh Ó Corráin, “Ireland c.800,” 581.

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| 25

If Rhazes’ judari and hasbah are smallpox and measles, respec-
tively, his guidelines for differentiating between the two may be
important. For Rhazes, the difference lay in the severity of nausea
(worse in hasbah) and back pain (worse in judari), not the color,
degree, or location of any blotchiness, rash, or other skin eruption.
In his treatise on the diseases, he addressed judari pustules fre-
quently and depicted hasbah sufferers as pustular (contrary to mod-
ern experience with MV), and in his Liber ad Almansorem, he
identiﬁed victims of both diseases as appearing reddish and pustu-
lar. In his Divisio Morborum, he echoed that judari and hasbah
cause pustules but, in accord with modern knowledge, he also
noted that hasbah’s fever is more severe. This observation occurs
again in Rhazes’ largely derivative Constinens, in which he wrote
that that the skin of those who suffered from these diseases turned
red, except that the hasbah pustules came “out all at once,” “on
the surface of the skin,” whereas those of judari emerged “gradually”
in the form of round eminences. These distinctions concerning the
skin are compatible with what is known about smallpox and MV.
Though Rhazes thought that physicians could differentiate be-
tween the two through the careful study of symptoms, his work
portrays these diseases as more similar than distinct. Familiarity
with the nuances was clearly required to distinguish between
them. Non-professionals, like Marius, with or without previous
experience may have confused them, employing a single term
for both.39

39 Rhazes, Kitab ﬁ al-jadari wa-al-hasbah, III.1–2, 34–35; VIII.1–2, 56; IX.1–2, 57–58;
XIV.2–4; .7, 7–10, 71–73; idem, Constinens, XVIII.8.6, 102–103; XVIII.8.19, 105; XVIII.8.47,
113; XVIII.8.62, 119; XVIII.8.65, 119–120; XVIII.8.71, 121; XVIII.8.80, 126; XVIII.8.81,
127; XVIII.8.82, 127; idem, Liber ad Almansorem, X.18.1, 84; X.18.7, .9, 86; idem, Divisio Mor-
borum, CIL.1, 90. The distinctions that Rhazes makes concerning the effects of hasbah and
judari on the skin seem compatible with smallpox and measles in that their rashes are red
and appear facially before spreading out over the body, but a smallpox rash gradually blisters
and becomes pustular whereas a measles rash remains ﬂat. That said, measles’ rash is often
characterized as maculopapular, and the papules emanating from the macules are very occa-
sionally referred to as pustules. See, for example, Alpay Azap and Filiz Pehlivanoglu, “Mea-
sles,” in Onger Ergonul et al. (eds.), Emerging Infectious Diseases (London, 2014), 347, 351, 353;
Ludvig Hektoen, “Experimental Measles,” Journal of Infectious Disease, II (1905), 239, 241.
Some have had no difﬁcultly accommodating Rhazes’ description of hasbah (measles) as pus-
tular. See S. C. Ashtiyani and A. Amoozandeh, “Rhazes Diagnostic Differentiation of Small-
pox and Measles,” Iranian Red Crescent Medical Journal, XII (2010), 481. Closer attention may
be required regarding Rhazes’ pustule terminology in the original Arabic.

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26 | T I M OT H Y P . N E W F I E L D

Neither measles nor smallpox are zoonotic. The relationship
between smallpox and cowpox, closely related orthopoxviruses,
was essential to Edward Jenner’s late eighteenth-century smallpox
vaccine, but cowpox, though zoonotic and transferable between
humans and cattle, is neither a rapidly spreading disease nor an acute
disease in humans or cattle. Cowpox also affects numerous other
animals, from rats to rabbits, cats, and horses. A joint smallpox–
cowpox ancestor is therefore a bad ﬁt with the epidemiology/
epizootiology of the 569–570 and 986–988 plagues. In any case,
recent molecular clocks determined that smallpox colonized humans
many thousands of years ago, and comparisons made between gene
sequences in several studies now show that smallpox has little in
common with cowpox. Its similarity to taterapox and camelpox
indicates that it evolved from one of those viruses or emerged
independently from an ancestral poxvirus with them. Had an ances-
tral cowpox–smallpox orthopoxvirus ever existed—a proposi-
tion that is highly unlikely on ﬁrm biological grounds—it would
have been a bad ﬁt for the 569–570 and 986–988 plagues symptomo-
logically as well. The only orthopoxvirus known to cause diarrhea
in its victims is monkeypox, diarrhea being a secondary complica-
tion of that mild and rare disease, which also afﬂicts rodents and
humans.40

Like smallpox, MV spreads between humans and requires a
minimum population in the hundreds of thousands to become
endemic and survive. Contact between a human population with
the disease and another without it (in other words, between dis-
ease pools) results in an epidemic and, in a sufﬁciently large new
population, a new endemic focus. Scholars have long surmised

40
Sergei N. Shchelkunov et al., Orthopoxviruses Pathogenic for Humans (New York, 2005), 2,
160, 162, 193–248; Yu Li et al., “On the Origins of Smallpox: Correlating Variola Phylogenics
with Historical Smallpox Records,” Proceedings of the National Academy of Sciences, CIV (2007),
15787–15792; Austin L. Hughes et al., “The Evolutionary Biology of Poxviruses,” Infection,
Genetics and Evolution, X (2010), 50–59; Jessica M.C. Pearce-Duvet, “The Origin of Human
Pathogens: Evaluating the Role of Agriculture and Domestic Animals in the Evolution of
Disease,” Biology Review, LXXXI (2006), 371–373. William H. McNeill, Plagues and Peoples
(New York, 1976), 45, and Jared Diamond, Guns, Germs, and Steele: The Fates of Human
Societies (New York, 1997), 204–207, among others, speculated that smallpox diverged
from cowpox. Although smallpox is the notable exception, many poxviruses exhibit “highly
diverse host ranges” and “infect a broad spectrum of animals.” See Sherry L. Haller et al.,
“Poxviruses and the Evolution of Host Range and Virulence,” Infection, Genetics and Evolution,
XXI (2014), 15.

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| 27

that MV and its morbillivirus cousin RPV diverged in antiquity c.
3000 B.C.E. on the western steppes and that post-divergence MV
established an endemic focus in Western Asia (ancient Sumer),
where a human population could support its survival. The sup-
posed morbillivirus “archaevirus” RPV was thought to have
evolved c. 8,000 to 10,000 years ago on the central or eastern
steppes in large herds of bovines. MCAs run recently on MV and
RPV, however, dispute this theory.41

That a diagnosis of a MV–RPV predecessor can be considered
for the 569–570 and 986–988 plagues is based on two independent
morbillivirus MCAs conducted in Sendai and San Diego to deter-
mine when measles diverged from rinderpest. Divergence dates
refer to the time of the most recent common ancestor, the latest
point at which, in this case, the current genetic diversity of MV
and of RPV were united as one genotype. The morbillivirus MCAs
employed the rate of MV and RPV’s recent evolutions, their known
molecular distancing, to estimate their date of separation, pro-
ceeding on the assumption, following from the neutrality theory
of molecular evolution, that the rate of evolution is constant.
Because rates of evolution vary, however, relaxed clock models,
used in both morbillivirus studies, have been developed, allowing
varying rates of evolutionary progression along different phylo-
genetic branches. Nonetheless, these analyses provide only rough
diversiﬁcation times, since they are restricted to modeling recent
evolutionary history that may not be entirely applicable to the
distant past in the case of rapidly evolving viruses. The ﬁrst MCA
assigned MV and RPV’s most recent common ancestor to the eleventh

For the old paradigm, see Barrett and Paul B. Rossiter, “Rinderpest: Impact on Humans
41
and Animals,” Advances in Virus Research, LIII (1999), 93–94; Barrett, “Rinderpest and Dis-
temper Viruses (Paramyxoviridae),” in Allan Granoff and Robert G. Webster (eds.), Encyclopedia
of Virology (San Diego, 1999), III, 1559, 1563–1564; Diane E. Grifﬁn, “Measles Virus,” in
David M. Knipe et al. (eds.), Fields Virology (Philadelphia, 2001), 1401; Peter L. Roeder
and William P. Taylor, “Rinderpest,” Veterinary Clinics of North America: Food Animal Practice,
XVIII (2002), 516; Andrew Cliff, Peter Haggett, and Matthew Smallman-Raynor, World Atlas of
Epidemic Diseases (Boca Raton, 2004), 42–43 (with maps); Ashley C. Banyard, Bertus K. Rima,
and Barrett, “The Morbilliviruses,” in Barrett, Paul-Pierre Pastoret, and Taylor (eds.), Rinderpest
and Peste des Petits Ruminants: Virus Plagues of Large and Small Ruminants (Amsterdam, 2006), 23;
Stephen C. Stearns and Jacob C. Koella, Evolution in Health and Disease (New York, 2008), 169;
Peter Roeder, Jeffrey Mariner, and Richard Kock, “Rinderpest: The Veterinary Perspective on
Eradication,” Philosophical Transactions of the Royal Society, CCCLXVIII (2013), 1; Azap and
Pehlivanoglu, “Measles,” 348.

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28 | T I M OT H Y P . N E W F I E L D

and twelfth centuries C.E. The second one pushed it back to the
ninth or tenth centuries C.E., estimating the morbilliviruses’ rate of
evolution to be faster.42

This difference of a century or two in ancestry may be notable
on historical grounds, but the general agreement between the two
independent studies that MV and RPV separated postclassically is
more signiﬁcant. Without the independent conﬁrmation of
the second MCA, however, this conclusion, which contradicts the
ﬁrmly held theory that MV ﬁrst appeared millennia before the
Common Era, might have been suspect. This article, which pro-
poses that the 986–988 plague was an outbreak of an MV–RPV fore-
runner, prefers a separation no earlier than the late tenth century,
roughly in agreement with both molecular studies, though it does
not suppose that historical evidence for disease be given precedence
over molecular data.

It is not known where the divergence occurred. The ﬁrst
molecular study stipulates only that MV evolved from RPV “in an
environment where cattle and humans lived in close proximity.”
Were the 569–570 and 986–988 plagues an MV-RPV ancestor, the
separation probably would not have happened in Europe, since
these plagues caused considerable mortality in European cattle
populations; before divergence, the ancestral morbillivirus was
ﬁrst conﬁned to bovines; and pathogens do not typically cause
large sudden die-offs in the same population within which they
evolved, spent considerable time, and were endemic/enzootic.
This article holds the origins of the 569–570 and 986–988 plagues,
and the divergence, to have been extra-European. Considering the
sizable human and bovine populations required for endemic MV

For MV–RPV MCAs, see Furuse, Suzuki, and Oshitani, “Origin of Measles Virus,” 1–4; Joel O.
42
Wertheim and Sergei L. Kosakovsky Pond, “Purifying Selection Can Obscure the Ancient
Age of Viral Lineages,” Molecular Biology and Evolution, XXVIII (2011), 3355–3365; for
molecular clocks, Francisco Rodriguez-Trelles, Rosa Tarrio, and Francisco Ayala, “Molecular
Clocks: Whence and Whither?” in Philip C. J. Donoghue and M. Paul Smith (eds.), Telling the
Evolutionary Time: Molecular Clocks and the Fossil Record (London, 2005), 5–26; Philippe Lemey
and David Posada, “Molecular Clock Analysis,” in Lemey, Marco Salemi, and Anne-Mieke
Vandamme (eds.), The Phylogenetic Handbook: A Practical Approach to Phylogenetic Analysis and
Hypothesis Testing (2009), 362–372. If the second morbillivirus MCA underestimated evolutionary
rates, and the divergence were pushed slightly deeper in time, the 986–988 plague may be
evidence of the temporary co-existence of an ancestral morbillivirus with distinct measles
and rinderpest viruses.

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and enzootic RPV, respectively, the separation probably took place
in Asia, as has long been suspected.43

POSSIBLE CONSEQUENCES OF THE PLAGUES Like most of the early
medieval accounts of epidemics and epizootics in Europe, the
sources for the 569–570 and 986–988 plagues say nothing about
short- or long-term consequences beyond a brief mention of
inﬂated dairy prices after 987 in what is likely a late version of
the Welsh Brut. There are also no means, direct or indirect, to
measure sudden or short-term changes in human or bovine pop-
ulation levels across the areas affected. Nonetheless, the vast spatial
parameters, high mortality, and concurrent attack on people and
cattle of the 569–570 and 986–988 outbreaks probably translated
into considerable short-term, and weaker long-term, demographic
and economic consequences.44

If an ancestor to MV and RPV were indeed to blame, outbreak
parameters larger than those that the written sources and bovine
graves suggest would be likely, due not only to the highly conta-
gious nature of these viruses (75 to 90 percent of those in contact
with MV victims become infected) and the possibility of an ances-
tral virus passing between species (therefore more easily dissemi-
nated) but also to the pathogen’s extra-European origin. MV and
RPV are density-dependent diseases requiring large numbers for
endemicity/enzooticity. MV demands an urban population of at
least 250,000 or a series of well-connected smaller centers to become
endemic. It could have become established in Rhazes’ populous
Western Asia, rather than in early medieval Europe, which was pre-
dominantly rural, with few towns surpassing a population of 10,000.

Furuse, Suzuki, and Oshitani, “Origin of Measles Virus,” 1. Grifﬁn, “Measles Virus,” pre-
43
viously located the MV–RPV divergence “where cattle and humans lived in close proximity”
(1401). For an Asiatic divergence, see “old paradigm” works cited in n. 41. That the
eighteenth-century bovine panzootics, thought to be RPV, spread westward into Europe also
indicates that MV and RPV did not separate in Western Europe. For the comparatively vast
scholarship on these cattle plagues, see Spinage, Cattle Plague, 103–150, 241–262. The Shapwick
and Luxé bovines may provide further evidence for an extra-European origin, since in enzootic
zones, RPV typically affects young cattle after their maternal immunity dissipates, not mature
cattle. See Anderson, Barrett, and Scott, Diagnosis of Rinderpest, 6–7, 10; Anonymous, “Rinderpest,”
543.
44 Brut y Tywysogion in Cambrian Archaeological Association, Archaeologia Cambrensis
(London, 1864), X, 36–37.

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Foci of the ancestral virus may be suspected on the steppes or possibly
in Western Asia but not further west.45

A zoonotic ancestor to MV and RPV, given what is known
about each of them now, would also have caused signiﬁcant pop-
ulation loss in naïve or unexposed human and bovine populations;
20 to 30 percent of infected people and 80 to 95 percent of infected
cattle may have died. Marius’ particular emphasis on the magnitude
of the bovine losses in 569–570 may be interpreted as evidence of
such uneven mortality between the species. The qualiﬁcation of
the 986–988 cattle mortality but not the corresponding human
mortality as “great” in the Annals of Tigernach also suggests that
bovine losses surpassed human losses at that time, as does the silence
in the Anglo-Saxon Chronicle, Brut, and Saltair na Rann regarding
human deaths. The simultaneous loss of people and cattle would
have had signiﬁcant repercussions—deaths in one population com-
pounding the demographic and economic effects of deaths in the
other. Though human fatalities might have diminished the impact
of concurrent bovine fatalities (reducing apace the demand for the
products and services that cattle provided), the unequal mortality of
a combined morbillivirus might have offset any collapse in demand
for draft, fertilizer, milk, meat, and hides.46

45
Populations of 250,000, 300,000, and 500,000 are commonly cited for endemic measles.
See Andrew D. Cliff and Peter Haggett, “Global Trends in Communicable Disease Control,”
in Norman Noah and Mary O’Mahony (eds.), Communicable Disease Epidemiology and Control
(Chichester, 1998), 24; Lauren Sompayrac, How Pathogenic Viruses Work (Mississauga, 2002) 31;
Cliff and Matthew Smallman-Raynor, Oxford Textbook of Infectious Disease Control: A Geo-
graphical Analysis from Medieval Quarantine to Global Eradication (New York, 2013), 14. In the
early Middle Ages, Rome, Europe’s largest city, possessed c. 25,000 people. See Adriaan
Verhulst, The Carolingian Economy (New York, 2002), 106.
For measles’ communicability, see Perry and Halsey, “Clinical Signiﬁcance of Measles,”
46
S4; Hussey, “Measles,” 216; for mortality rates, D. Nanche, “Immunology of Measles Virus
Infection,” in Grifﬁn and Michael B. A. Oldstone (eds.), Measles: Pathogenesis and Control
(Berlin, 2009), 153, 163; Peter Wohlsein and Jeremiah Salik, “Rinderpest and Peste des Petits
Ruminants—The Disease: Clinical Signs and Pathology,” in Barrett, Pastoret, and Taylor
(eds.), Rinderpest and Peste des Petits Ruminants, 69. Endemicity and vaccination programs have
made measles a childhood disease. As Robert Sallares, The Ecology of the Ancient Greek World
(Ithaca, 1991), 249–252, pointed out, without endemic foci, severe attacks of MV would not
have been restricted to children in postclassical Europe. Large mortalities have been attributed
to the introduction of measles into previously unexposed populations. For example, in 1875
the virus killed 25 to 30% of Fiji’s 150,000 inhabitants within six months. See R. A. Derrick,
“Fiji’s Darkest Hour: An Account of the Measles Epidemic of 1875,” Transactions and Proceed-
ings of the Fiji Society, VI (1959), 3–16; Cliff, Haggett, and Smallman-Raynor, Measles: An
Historical Geography of a Major Human Viral Disease from Global Expansion to Local Retreat,
1840–1990 (New York, 1993). Since pathogen virulence is not ﬁxed, an ancestral RPV could

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Outbreaks of disease common to people and cattle on this
scale could have affected early medieval populations and their
organic agricultural economies for a generation, especially in more
densely populated areas. The 569–570 plague, alongside the mid-
sixth-century Justinianic plagues, would have contributed to the
contraction of southern European settlement and arable land
already then underway. The 986–988 event, like other ninth-
and tenth-century mortality crises, would have temporarily undone
or stalled settlement and arable expansion initiated in many north-
western European regions long before the 980s. Compared to
bubonic plague, which can kill more than 50 percent of its victims,
a MV–RPV predecessor may have been mild in humans, with a
mortality rate like that of MV alone. Yet more people would have
contracted it than any rodent-based Y. pestis had it been, like MV or
RPV, airborne, easily spread between species, and infectious days
before severe disease expression.47

High human morbidity may be expected in small but con-
gested early medieval settlements. A rough idea of the possible
mortality in affected towns is obtainable by superimposing measles’
virulence on virgin populations. If 25 percent of a settlement with
a population of 5,000, roughly the size of mid-sixth-century
Ravenna and mid-tenth-century London, were to come into con-
tact with a pathogen as virulent as that proposed herein, 250 to 375
deaths would ensue. If 75 percent were infected, the number of
fatalities would be in the range of 750 to 1,125. Considering the
high infectivity of MV and RPV, morbidity rates less than 50 percent
seem unlikely for a pathogen that disseminated efﬁciently among
people.48

have been more acute in human populations than measles is in pristine populations now.
Increases in virulence are known to accompany the spread to new species. See Andrew D.
Morgan and Britt Koskella, “Coevolution of Host and Pathogen,” in Michel Tibayrenc (ed.),
Genetics and Evolution of Infectious Diseases (London, 2011) 149. A source for the continental
989–990 human–bovine plague reported that the bovine mortality was greater than the hu-
man mortality, further implying that this die-off was tied to the insular plague of 986–988. See
Annales Quedlinburgenses, 447.
47 World Health Organization, “Plague,” Fact Sheet, 267, available at www.who.int/
mediacentre/factsheets/fs267/en/ (accessed November 1, 2014).
For Ravenna and London’s postclassical populations, see Deborah M. Deliyannis, Ravenna
48
in Late Antiquity (New York, 2010), 322, n. 42; John McDonald, Production Efﬁciency in Domesday
England, 1086 (London, 1998), 52.

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32 | T I M OT H Y P . N E W F I E L D

Using the same incident percentages and mortality rates,
smaller, more representative towns of 1,000 may have seen be-
tween 50 deaths (25 percent infected, 20 percent killed) and 225
deaths (75 percent infected, 30 percent killed). If 90 percent were
exposed, 270 deaths might be expected. Town industries and mar-
kets would have suffered correspondingly. Lower morbidity rates
and fewer deaths in humans would have accrued in the country-
side, though a decline in agricultural activity in the wake of a
combined human–bovine plague is nevertheless certain. Labor-
intensive sectors, such as arable farming, possibly would have suf-
fered considerably in the short-term. Since ﬁxed inputs of human
and animal labor were required to keep agrarian systems running,
mortality could have depleted such inputs sufﬁciently to disrupt
production. At least in some areas hit by the 569–570 pestilence,
viticulture, with its heavy labor requirements, would also have been
susceptible. Additionally, an ancestral morbillivirus may have
blinded some human survivors. Severe keratitis and corneal scarring
from MV is a common source of blindness in untreated and mal-
nourished populations.49

Because animal rearing was more prominent than arable agri-
culture during the sixth century than during the tenth, even in
Ireland where cattle raising very much dominated before the ninth
century, the 569–570 and 986–988 cattle mortalities did not affect
food supplies uniformly. Specialized, large-scale, late Roman cattle
rearing, primarily north of the Alps (in areas of northern France,
Belgium, Germany, the Netherlands, and Britain), as well as in
some cisalpine and southerly transalpine regions (see, for example,
Cassiodorus’ remarks on the Calabri peculiosi and his mentions of
cattle droves emanating from Italy’s south, and some late Roman
bovine-dominated Provençal animal-bone assemblages), generally
gave away in the sixth and seventh centuries to mixed animal
husbandry. But bovines, although smaller, remained prominent
in most early medieval agrarian regimes, essential as they were
for draft power and fertilizer. Zooarchaeology suggests that the
number of cattle increased in late rather than early Anglo-Saxon

For measles and blindness, see Perry and Halsey, “Clinical Signiﬁcance of Measles,” S7–S8;
49
for the Justinianic plague of 571, see Gregory of Tours, Liber de passione et virtutibus sancti Iuliani
martyris, in Bruno Krusch (ed.), Monumenta Germaniae Historica Scriptores rerum Merovingicarum
(Hanover, 1885), I.2,XLVIa, 131–132; Marius, Chronica, 238.

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England in part because of an extension of cultivation and greater
demand for traction as the amount of arable land multiplied.50

Some regions were more bovine-centric than others, but the
569–570 and 986–988 plagues seem to have spread whether or not
a region was primarily given to animal rearing or to arable land.
Severity of impact, however, would have ﬂuctuated regionally,
even locally, corresponding to the degree of reliance on cattle
for traction (arable agriculture, transportation, and warfare); for
fertilizer (arable agriculture); for milk and meat (diet, trade, and
warfare); and for bone, hide, and horn (industry and trade); as well
as on the ability to replace or replenish cattle via the market. In
general, bovine fatalities likely had worse repercussions for human
health in the ninth century because of a generally less varied diet
and a greater reliance on cattle for draft and fertilizer. Where animal
rearing was dominant and diversiﬁed, cattle losses were easier to
repair and stocks of sheep and pigs easier to augment as compen-
sation for lost bovine milk and meat, despite presumably higher
morbidity and mortality rates. DeWitte and Slavin argued that
dramatic declines in milk, meat, and grain following the 1314–1325

For Roman and early medieval cattle, see Anthony King, “Diet in the Roman World: A
50
Regional Inter-Site Comparison of the Mammal Bones,” Journal of Roman Archaeology, XII
(1999), 169–171, 174, 176–180, 182, 190; Geoffrey Kron, “Archaeozoological Evidence for
the Productivity of Roman Livestock Farming,” Münstersche Beiträge zur Antiken Handelsgeschichte,
XXI (2002), 55, 57, 59–64; Annie Grant, “Domestic Animals and Their Uses,” in Malcolm Todd
(ed.), A Companion to Roman Britain (London, 2004), 374–377, 381, 382, 384, 387; Timothy
Howe, “Domestication and Breeding of Livestock: Horses, Mules, Asses, Cattle, Sheep, Goats,
and Swine,” in Gordon Lindsay Campbell (ed.), The Oxford Handbook of Animals in Classical
Thought and Life (New York, 2014), 104; Vianney Forest and Isabelle Rodet-Belarbi, “À propos
de la corpulence des bovines en France Durant les périodes historiques,” Gallia, LIX (2002),
291–295, 298; Tamara Lewit, “Pigs, Presses and Pastoralism: Farming in the Fifth to Sixth
Centuries AD,” Early Medieval Europe, XVII (2009), 79, 80; Benoît Clavel and Jean-Hervé Yvinec,
“L’archéozoologie du moyen âge au début de la période moderne dans la moitié nord de la
France,” in Jean Chapelot (ed.), Trente ans d’archéologie médiévale en France: Un bilan pour l’avenir
(Caen, 2010), 76–77, 80; N. J. Sykes, “From Cu to Sceap to Beffe and Motton: The Management,
Distribution, and Consumption of Cattle and Sheep in Medieval England,” in Christopher M.
Woolgar, Dale Serjeantson, and Tony Waldron (eds.), Food in Medieval England: Diet and Nutrition
(New York, 2006), 57–58; Terry O’Connor, “Livestock and Deadstock in Early Medieval Europe
from the North Sea to the Baltic,” Environmental Archaeology, XV (2010), 1, 2, 6–11, 13; idem,
“Livestock and Animal Husbandry in Early Medieval England,” Quaternary International,
CCCXLVI (2014), 109–115, 109–118; Finbar McCormick, “The Decline of the Cow: Agricultural
and Settlement Change in Early Medieval Ireland,” Peritia, XX (2008), 210, 214–217, 219–221;
idem, “Agriculture, Settlement and Society in Early Medieval Ireland,” Quaternary International,
CCCXLVI (2014), 119–130; Ó Corráin, “Ireland c.800,” 568–574; Cassiodorus (trans. Thomas
Hodgkin), Variae (London, 1886), III.50, 225; VIII.33, 382; XI.39, 484; XII.12, 499.

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34 | T I M OT H Y P . N E W F I E L D

panzootic resulted in shortages of calcium, protein, and vitamin
B12, heightening the vulnerability of people to disease for more
than a decade. A similar situation may have prevailed after 569
and 986.51

In arable areas, the loss of grain must have been severe. Slavin’s
assessment of fourteenth-century English manorial data reveals that
equine-rich landlords were able to maintain their arable acreage
after the 1314–1325 panzootic by increasing the number of horses
employed as draft animals by about 40 percent. Other land owners
were less fortunate. Winchester’s estates, for example, tilled about
18,000 acres before that bovine plague crossed the Channel in 1319
but only 9,000 in 1321 after it had claimed roughly 62 percent of
the national herd (more than 1 million cattle). Oxen were the draft
animals of choice in the areas hit by the 569–570 and 986–988
plagues. The relative unavailability of equines as a traction sub-
stitute implies arable contractions more severe and long-lasting
than in the 1300s.52

The evidence does not indicate that early medieval bovine
mortalities triggered severe food shortages by themselves. Cattle
plagues contributed most often to production failures and famines
generated by extreme weather and short-term climatic anomalies.
In lieu of additional environmental shocks, the threat of wide-
spread food shortage that the loss of draft animals and fertilizer,
and the corresponding contraction of arable land, posed does
not appear to have materialized in 569–570 or 986–988. Only
Wales recorded a subsistence crisis that could correspond to the
tenth-century pestilence. The simultaneous deaths of people and
cattle in many early medieval plagues is another probable explana-
tion. Indeed, the excess human mortalty may have curbed demand
for grain enough to prevent famine, even though bovines were
possibly 75 percent less likely than humans to survive infection.

51 DeWitte and Slavin, “Between Famine and Death,” 37–60.
For the consequences of the 1314–1325 panzootic, see Slavin, “Great Bovine Pestilence,”
52
1241–1266; idem, “The Fifth Rider of the Apocalypse: The Great Cattle Plague in England and
Wales and Its Economic Consequences, 1319–1350,” in Simonetta Cavaciocchi (ed.), Le
interazioni fra economia e ambiente biologico nell’Europa preindustriale, secc. XIII–XVIII: Proceedings of
the 41st Study Week of the Fondazione Istituto Internazionale di Storia Economica “F. Datini” (Florence,
2010), 171–181; for the importance of oxen in early medieval agrarian regimes, Verhulst,
Carolingian Economy, 67; Banham and Faith, Anglo-Saxon Farms, 86, 108–110.

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Nevertheless, the loss of essential human and animal labor would
have heightened vulnerability to dearth in arable regions.53

The value of milk, meat, and hides surely inﬂated after the
569–570 and 986–988 plagues, as the possibly corrupt version of
the Brut reports and as they did in the early fourteenth century.
Meat and hides of diseased animals might have been salvaged,
although we do not know for sure. The Irish annals suggest that
hides were damaged, and the available zooarchaeology implies that
hides and meat were not taken from plague cattle. If they were,
they may have served to spread the disease while fresh. The recov-
ery of urban and rural communities, agricultural production, and
especially bovine stocks would have taken considerable time. As
Gregory of Tours noted in his account of a bovine mortality in
591, cattle plagues severely impeded breeding and replenishment.
Five years after the 1314–1325 panzootic, only 9 percent of English
manors had restocked. Not until the Black Death was the seigniorial
herd in England restored, largely via farm transfers, markets (which
were less numerous and interconnected in most regions affected in
569–570 and 986–988), and natural regeneration.54

For cattle plagues and food shortage in the early Middle Ages, see Newﬁeld, “The
53
Contours, Frequency and Causation of Subsistence Crises in Carolingian Europe (750–950),”
in Benito I. Monclús, Crisis Alimentarias en la Edad Media: Modelos, Explicaciones y Representaciones
(Lleida, 2013), 133, 166. Subsistence crises reported in Wales in 988/89 and 993/94 may attest to
heightened susceptibility to shortage following the 986–988 plague (Brut y Tywysogyon: Peniarth
MS. 20, 10), though the pestilence may have caused the ﬁrst of these two crises.
54 Meat was plentiful after plagues for those willing to eat it. Early medieval annalists and
chroniclers are quiet on the consumption of plague cattle, but the zooarchaeology addressed
above suggests that sick animals were not always eaten. For biblical restrictions on eating car-
rion in the early Middle Ages, possibly indicating that people ate diseased domesticates, see
Rob Meens, “Pollution in the Early Middle Ages: The Case of Food Regulations in Peni-
tentials,” Early Medieval Europe IV (1995), 3–19. High medieval sources suggest that the meat
of bovine victims of acute disease was often salvaged. See Newﬁeld, “Epizootics and the
Consumption of Diseased Meat in the Middle Ages,” in Francesco Ammannati (ed.), Religione
e istituzioni religiose nell’economia Europea, 1000–1800: Proceedings of the 43rd Study Week of the
Fondazione Istituto Internazionale di Storia Economica “F. Datini” (Florence, 2012), 619–639, n. 11;
also see Putelat, “Archéologie des depots animaux,” 266. RPV could spread for a few days post-
mortem via trade in fresh hides (untreated and undried) and fresh meat. The movement of these
goods is considered to possess considerably less potential for virus dissemination than the move-
ment of live cattle. See Spinage, Cattle Plague, 16–17; Obi, Roeder, and Geering, Rinderpest
Contingency Plans, 5; Anderson, Barrett, and Scott, Diagnosis of Rinderpest, 7; R. G. Bengis, “Animal
Health Risks Associated with the Transportation and Utilisation of Wildlife Products,” Revue
scientiﬁque et technique de l’OIE, XVI (1997), 104, 106. For Gregory of Tours’ remarks, see his
Libri Historiarum X, in Krusch (ed.), Monumenta Germaniae Historica Scriptores rerum Merovingicarum
(Hanover, 1937), I, X.30, 525.

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Natural regeneration was the most common and the most
prolonged method of herd replenishment during the early Middle
Ages. Heifers gestate for nine-and-a-half months and rarely deliver
multiple births; sexual maturation takes at least fourteen months.
The wait for optimum milk production is about twenty-four
months, and raising an ox and training it to plow can take years.
Moreover, cattle surviving acute disease would have been weak,
malnourished, and, in the short run, unlikely to become pregnant.
Pregnant heifers with an ancestral MV–RPV may have aborted, as
those suffering RPV often do. Subsequent mortality events would
have slowed recovery further, especially in the sixth century, for
bovine and human populations (during the cattle plagues of
583–584 and 591 in France and with the Justinianic plague of
571 in France and Italy, among later sixth-century visitations). Sur-
vivors of the 569–570 and 986–988 plagues possibly beneﬁted from
immunity to re-infection, however, as morbilliviruses are known
to confer life-long protection. A low level of temporary immuni-
zation against MV and RPV is passed maternally as well. Yet, without
endemic foci or regular exposure to the ancestral virus, populations
would have been left vulnerable to re-infection and similar deadly
events caused by the same disease within two generations.55

REMAINING QUESTIONS There are molecular, textual, and possibly
zooarchaeological grounds for suspecting that a now-extinct MV-RPV
morbillivirus occasionally erupted in early medieval Europe, taking a
considerable demographic toll in the human and bovine populations
before burning out. The plagues of 569–570 and 986–988 may pro-
vide historical substance to the laboratory-detected postclassical di-
vergence of MV and RPV, but many questions remain regarding the
occurrence and epidemiology/epizootiology of that virus before di-
vergence. Whether the virus was spread directly and easily among
people and among cows, as well as across species, matters a great deal
for the estimation of its plausible impact, as does the virus’ mortality
rate in humans and bovines. Does the emphasis in the sources for the

For RPV and aborted pregnancies, see Wohlsein and Salik, “Rinderpest,” 71; for MV, RPV,
55
and immunity, Nanche, “Immunology of Measles,” 151, 160, 162–164; S. Louise Crosby,
Chieko Kai, and Kazuya Yamanouchi, “Immunology of Rinderpest—An Immunosuppression
but a Lifelong Vaccine Protection,” in Barrett, Pastoret, and Taylor (eds.), Rinderpest and Peste des
Petits Ruminants, 196–197; Wohlsein and Salik, “Rinderpest,” 69.

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| 37

H UM A N –B OVI N E PL AGU E S
569–570 and 986–988 events on bovine deaths indicate that the
pathogen was neither as virulent nor as widespread in people as it
was in cattle? If the virus were much more lethal for cattle than
people, as proposed herein, we would have an explanation for
why certain early medieval plagues, like those discussed herein and
that of 809–810, appear in some sources as zoonotic but in most
sources as epizootic.

A virus capable of jumping species would explain why some
early medieval bovine plagues—that of 809–810 especially—could
disseminate over a large area of Europe more quickly than could the
fourteenth- and eighteenth-century (post-divergence) European
cattle panzootics thought to be RPV. That the best candidate for
the 809–810 panzootic is RPV raises another crucial issue—the tem-
porary co-existence of an ancestral MV–RPV with distinct MV and RPV
varieties. Does a c.1000 C.E. MV–RPV divergence negate MV diagnoses
of ancient Anthenian, Antonine, and Cyprian plagues (however
unpopular those disease identiﬁcations may now be), the reading
of Rhazes’ hasbah as MV, or interpretation of early medieval Japanese
epidemics as MV? Was a distinct MV virus endemic in postclassical
Western Asia, as historians have long argued, and was an MV–RPV
forerunner located somewhere else from where it erupted into
Europe? Could MV have diverged before 1000, spread into Europe,
but failed to establish endemicity there or elsewhere?56

56
Possibly of note, Orosius (trans. A. T. Fear), Seven Books of History against the Pagans
(Liverpool, 2010), VII.27.10, 367, reports that the Cyprian plague claimed people and cows
( jumenta and pecuda); Carl Zangemeister (ed.), Historiarum adversus Paganos Libri VII (Leipzig,
1889), VII.27.10, 269. An earlier passage of interest comes from the Roman historian Livy. In
the context of a drought in Italy in 428 B.C.E, which was purportedly severe enough that cattle
died of thirst, diseases—in particular, one identiﬁed as scabies—began in bovines and spread to
humans via interspecies contact (volgatique contactu in homines morbi). “Country people and
slaves” were infected ﬁrst, but the disease eventually spread to “the city.” See Livy (trans.
B. O. Foster), Ab Urbe Condita Libri II (Cambridge, Mass., 1967), IV.30.7, 354–355. Dionysus
of Halicarnassus’ account differs slightly. He reported cattle and sheep dying on account of the
drought, but he connects the mortality in domesticates to the mortality in humans less explic-
itly. He speciﬁes that the disease in humans caused “dreadful pains in the skin with its itchings
and in case of any ulcerations raged more violently than ever, a most pitiable afﬂiction and the
cause of the speediest of deaths.” See Dionysus of Halicarnassus (trans Earnest Cary), Roman
Antiquities VII (London, 1950), XII.6, 216–217. In light of the morbillivirus MCAs, Jennifer
Manley, “Measles and Ancient Plagues: A Note on New Scientiﬁc Evidence,” Classical World
107 (2014), proposes that measles can no longer be considered the cause of the Athenian or
Antonine plagues (393–397), though she does not speculate about what the new scientiﬁc
evidence could mean for the history of pre-divergence zoonotic plagues.

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38 | T I M OT H Y P . N E W F I E L D

Many intricacies in MV and RPV’s history still need to be
untangled. As scientists attempt to unravel the molecular history,
they would do well to work with historians when suspected diver-
gences are set in historical time. Overlooked written sources for
disease or re-appraisals of well-known ones can lend support to
estimated divergence dates, as they do in this article. For their part,
historians of postclassical and earlier Europe would do well to
engage scientiﬁc studies to understand the pathological realities
underlying the written accounts and the archaeology of acute
disease. Such interdisciplinary work will lead to a better under-
standing of the evolution and geography of pathogens. Integral
to all this activity, and so far missing, is palaeomicrobiology for
the ancestral species of modern pathogens. Extracting and analyzing
the necessary material from potential specimens in archaeological
contexts may require the further development of biomolecular
techniques. However, without palaeomicrobiological study, con-
nections made between molecular clocks and written and archae-
ological evidence for acute disease remain speculative.

The tentative connections advanced in this article represent a new
approach to the history of disease and the impact of disease on
people and their animals. For periods not endowed with copious
written sources, like the early Middle Ages, molecular clocks are
particularly useful, providing grounds for more detailed assess-
ments of the origins, parameters, and consequences of plagues.
MCAs allow for dynamic histories of disease and for the inclusion
of past inter-species disease outbreaks—events of special interest
given today’s “emerging diseases.” Indeed, this article suggests that
an ancestral MV–RPV morbillivirus episodically colonized and
spread in human populations, as have the SARS Coronavirus and
Ebola Disease Virus in recent years. MCAs not only reveal that
people and animals in the distant past faced a different assortment
of pathogens than people and animals do now, such as an MV–RPV
ancestor, but also that people long ago were confronted by new
diseases, such as MV, that are now familiar.57

57 The emergence of the ebola disease virus may have been early medieval. See Y. H. Li
and S. P. Chen, “Evolutionary History of Ebola Virus,” Epidemiology and Infection, CXLII
(2014), 1140, 1142.

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