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Home , First plague pandemic, History of malaria, Late Antiquity, Plague of Cyprian

Invisible Environmental History: Infectious Disease in

Kyle Harper

Abstract became puffed up and filled with pus, making a fearful sight. Some had sores or pustules over their whole body, This study argues that the biological environment is prop- even to the palms of their hands and the soles of their erly a part of environmental history. The — feet’.2 The receded, but the ‘marks of the afflic- bacteria, viruses, —that cause infectious disease tions’ remained visible upon the victims. Retrospective were the principal cause of mortality in ancient , but diagnosis is a notoriously hazardous exercise, particular- the particular array of pathogens was both locally specific ly in the case of texts written by non-medical personnel and unstable over time. Pathogenic microbes are ecologically some 1500 years in the past. We will not delve into the sensitive, so the background of local , and the influ- methodological issues here, but suffice it to say that ence of climate variability and climate change, determined the Chronicle’s brief report of this pestilence is, despite patterns of disease and mortality. The connections between the inherent uncertainties, exceptionally important. It is climate variability and climate change, on the one hand, and hard to imagine that a pustular rash covering the entire the disease profile of a population, on the other, are complex, body, including the face, palms, and soles, could be any- and this paper traces some of the main pathways of influence, thing other than epidemic , caused by the virus with specific reference to a few of the best known diseases Variola major. The details of the described— and epidemic events in the later Roman period. especially the incidence of lesions on the palms and soles—are among the most important diagnostic symp- toms that differentiate smallpox from other diseases.3 Introduction: Disease and Environment Even worse lay in store for the eastern . The Chronicle reports that in March of AD 500, there was a The Chronicle of Pseudo-Joshua the is an account of locusts upon the fields. In April, scarcity set in, of the history of and environs in the years AD and price of grain rose. In June and July, millet (a panic 494–506.1 While its author is unknown, the text is the crop) was sown, but it faltered. Now there was misery work of an eyewitness who had experienced the dra- and true famine; subsistence migrants poured into the matic convulsions that shook the eastern edges of the city. The poor turned to eating inedible plants and scraps in these years. The first half of the text of refuse. In the winter, mortality spiked, as disease car- describes a sequence of natural disasters, while the sec- ried off the exposed and starving refugees. The limited ond narrates the war between the and Romans capacities of the municipal authorities and the Church that occurred during the reign of Anastasius I. The au- were overwhelmed by the sick and the dead. The toll thor’s viewpoint is coloured by his religious perspec- continued to rise for months, as pestilence—perhaps tive; he sees the events of his age through the lens of the caused by the same pathogen as before, although we people’s sin and God’s chastisement. While the text has cannot say—erupted again across the region, carry- often been mined for details about the early 6th c. con- ing off rich and poor indiscriminately. The crisis had flict with Persia, its description of the natural calamities overwhelmed the buffers—better nutrition, preferable in Edessa are an unusually vivid and detailed record of housing—that offered the wealthier classes modest pro- sudden environmental turbulence in one corner of the tection from epidemic disease.4 late antique world. The Chronicle of Pseudo-Joshua the Stylite is remark- The environmental crisis started in AD 494/95, when able by any measure. It was featured in Peter Garnsey’s a plague befell ‘all’ the people. God sent a pestilence that would make the body ‘like a mirror’, revealing the state of the soul on the exterior of the body. ‘Swellings and tu- mours appeared on all our citizens, and the faces of many 2 Pseudo-Joshua, Chron. 26 (edd. and transl. Trombley and Watt (2000) 23). 3 Stathakouplos (2004) 248–49, on the outbreak, identifying it as smallpox. I have offered further reflections on this source and 1 The text is edited by Chabot (1927) 235–317. On the text, see others for smallpox at: http://www.kyleharper.net/smallpox-re- Debié (2015) 10–14; Wiemer (2006); Brock (1979–80) 11. A modern sources-and-thoughts/ (last accessed March 2017). English translation is available: Trombley and Watt (2000). 4 Pseudo-Joshua, Chron. 38–44.

© koninklijke brill nv, leiden, 2019 | doi:10.1163/9789004392083_019 Izdebski and Michael Mulryan (eds) Environment and in the Long Late Antiquity (Late Antique Archaeology 11–12) (Leiden 2018), pp. 298–313 Kyle Harper - 9789004392083 Downloaded from Brill.com10/01/2021 05:10:18AM via free access Invisible Environmental History: Infectious Disease in Late Antiquity 299 classic study of famines in antiquity, precisely because has been a powerful and volatile force in . the kind of true food crisis it portrays was relatively un- The human story has been intertwined with the rise of common.5 Normally, ancient societies had layers of re- new and evolving pathogens, and as we have come to dundancy and batteries of stored energy to make them realise the importance of ‘emerging infectious diseases’ resilient in the face of environmental fluctuation. But in in our own world, we are sensitised to appreciate their this case, one by one, these strategies—storage, safety importance in the distant past. crops, political patronage, connectivity—all failed. The The ecological, environmental, and evolutionary threshold of endurance was crossed, and the social order background of disease history matters enormously for experienced a truly catastrophic sequence of disasters. the study of Late Antiquity, not least because the arrival The Chronicle reports these events with an eye for detail, of Yersinia pestis in AD 541 has a claim to be the most for example the price of grain at various stages of the consequential event in the entire period. The ongoing crisis, the daily death tolls, and so on. This kind of social study of this bacterium’s genome and microbiology has meltdown was the exception rather than the rule in an- helped us to understand that its advent was the result tiquity, but it was always a real possibility in an agrarian of exquisitely complex environmental and historical society exposed to the vagaries of the environment. contingencies. The sheer destructiveness of this single The Chronicle of Pseudo-Joshua the Stylite offers pathogen is an example of the overwhelming power another lesson, though, for the student of ancient of nature. But the story of the first plague is environmental history. As reflected in its pages, the phe- a paradigmatic example of how human societies have nomenon of infectious disease was both environmental shaped nature, preparing the way for nature in turn to and historical. Infectious diseases are caused by micro- redirect the course of human societies. bial agents, such as bacteria, viruses, and protozoa, that are pathogenic to humans. These germs are ecologically specific and environmentally sensitive. They are the Two Big Ideas: Malthus and McNeill product of evolution, and the force of constantly operates on them. Thus, the disease environ- Thomas Malthus might be considered the father of envi- ment changes over time, as humans transform ecologies, ronmental studies, and his basic model emphasising the as climate variability and climate change reshape local ecological constraints of human society remains (with ecologies, and as pathogens evolve. If environmental qualification) a fruitful way to approach environmental history is the study of humanity’s changing relationship history. Starting with the first edition of his Essay on the to nature over time, including both the physical and bio- Principle of Population, published anonymously in 1798, logical contexts of life, then disease history is properly a Malthus developed a theory of development with two part of environmental history. variables: human population and the food supply. Since The purpose of this chapter is to lay out some of the human populations could grow faster than output in ag- relationships between the physical environment and riculture, which was strongly constrained by the avail- the disease environment, with a focus on the late an- ability and quality of land, population growth would tique world. Throughout, we will emphasise three dy- eventually be slowed or reversed by one of two mecha- namics: the importance of local ecologies, the role of nisms. This was either by the “preventative check”, such the physical climate as a cause of biological instability, as cultural brakes on fertility, like late marriage, or more and the predominance of evolution as a source of dra- violently by the “positive check”, by which is meant matic change. It is inevitably challenging to reconstruct spikes in mortality via war, famine, or pestilence. In ancient disease history, but, increasingly, traditional neo-classical Malthusian theory, the mortality rate is en- written and documentary sources are complemented by dogenously determined by the wage level, and popula- bioarchaeological and paleo-molecular evidence.6 The tion levels should fluctuate homeostatically around the history of disease is being revolutionised by the study subsistence wage.8 of skeletal remains and DNA, and in the process, a new The theories of Malthus, ironically, proved to be the paradigm is beginning to take shape, one which puts most spectacularly wrong in the case of his own country. disease evolution in the foreground.7 Disease evolution England was in the vanguard of the , which was first and foremost a transformation in the en- ergy basis of society. In the formulation of John McNeill, 5 Garnsey (1988) 3–6. 6 See Green (2014), for an example of consilience in practice. 7 See e.g. Harkins and Stone (2015). 8 See the helpful discussion of Landers (1993).

Kyle Harper - 9789004392083 Downloaded from Brill.com10/01/2021 05:10:18AM via free access 300 Harper the transition from plant energy to fossil energy made us mechanistically to regulate mortality in response to modern.9 But Malthus’ model works much better in the wage levels. The specific biology of microbial pathogens conditions of pre-modern economies, where the hard matters, and so the history of disease must take into ac- constraints of plant energy held. In the ancient world, count a broader set of ecological factors. The first history energy was forbiddingly scarce, and in the long run, as of disease to do so was William McNeill’s Plagues and his theory would predict, economic development, in the Peoples, which, in 1976, offered what might be consid- form of technical advance, was turned into population ered the classic model of disease history.14 With little growth rather than higher incomes.10 Crudely, in the more than some core principles of (how millennia between the invention of agriculture and the diseases behave at the population level) and remark- Industrial Revolution, populations grew, but wages did able intuition, McNeill offered a global history of dis- not. Life near subsistence was the common lot in the age ease that foregrounded change over time in response of agriculture. When Malthus published the Essay, aver- to the altered circumstances of human societies. In the age global income was not significantly higher than it classic model, humans were afflicted by a set of very old had been for the first farmers,11 but by 1800, there were infectious pathogens from our primate days, and we a billion humans alive.12 At large scales, Malthusian pre- picked up others during our dispersal around the globe. dictions seem to hold. But the ‘Big Bang’ of disease history was the Neolithic However, as Keynes said, in the long run we are all Revolution. Sedentary habitation and close proximity to dead. Even when considerable allowances are made for domesticated animals were decisive, allowing zoonotic the complexity of the “positive check,” the study of his- pathogens to leap to humans. Diseases evolved in the torical demography has shown that mortality rates do various centres of civilisation, and over the course of not neatly obey the predictions of Malthusian theory.13 time, trade and greater connectivity brought the disease In other words, wage levels are not a very good predictor pools of the together with explosive effect, as of mortality rates, which are often (though not always) germs found virgin populations. The colonisation of the found to be weakly endogenous, or strictly exogenous, that followed was an even more devastating to the economic status of a population. Mortality has microbial migration.15 been a wild force throughout human history, rising and Given that it was formed in an age without molecu- falling without a clear relationship to wage levels. The lar evidence, it is impressive that the essentials of the main reason for this flaw in Malthusian theory is close- ‘classic model’ have held up so well, but the intervening ly related to the biology of infectious diseases. In pre- decades have brought new evidence and new perspec- modern societies, infectious diseases were the main tives. The 1970s were the peak of a triumphal phase in cause of death, and the mechanisms that determined the , as one by one the old scourges the impact of infectious disease were only partially me- of the past were subdued by greater , vac- diated by factors under the control of the wage level. It is cines, and . The eradication of smallpox was true that lower wages meant poorer nutrition, and that the pinnacle of achievement for global ; poor nutrition inhibited the body’s immune response to optimism reigned.16 But the victory over infectious dis- invasion, thereby exacerbating morbidity and mortality. ease has now stalled, and in some cases reversed. The But, the range of factors at play in the determination of terrifying roster of emerging infectious diseases—Zika, mortality rates by infectious disease was much wider. , AIDS, avian , SARS, MERS, and so on— Hence, mortality rates moved in ways that were not syn- has reminded us that the ‘creative destruction’ of na- chronous with changes in income levels. ture is not spent. Evolution remains a volatile source of In short, mortality has not been endogenous in the new enemies and new tools for old enemies. In all, the way Malthus’ theory would predict, because germs importance of Old World ‘crowd diseases’, supposedly are not a generic and interchangeable array that act contracted from domesticated animals, looms smaller than when the classic model of disease history was con- structed. The sheer density of city life is only one factor 9 McNeill (2015). that can sustain the threat of pathogenic microbes, as 10 Clark (2007) 32: “in the preindustrial world sporadic techno- the worst infectious diseases leapt to humans not from logical advance produced people, not wealth.” 11 Maddison (2001). Few studies venture earlier than ca. AD 1000, but see Scheidel (2010) and more generally Morris (2013) and (2010). For a recent conspectus of wage divergence in the long 14 McNeill (1976). Anticipated by some of the work of the run, see Fouquet and Broadberry (2015). Annales school, e.g. Le Roy Ladurie (1973). 12 McNeill (2015); Livi-Bacci (2012); Klein Goldewijk, Beusen, and 15 McNeill (1976); Crosby (1986); Diamond (1997). Janssen (2010). 16 Garrett (1994) 30–52, is a brilliant overview of this triumpha- 13 See e.g. Brooke (2014); Hatcher (2003); Landers (1993). list moment in global public health.

Kyle Harper - 9789004392083 Downloaded from Brill.com10/01/2021 05:10:18AM via free access Invisible Environmental History: Infectious Disease in Late Antiquity 301 farm animals, but from wild animals. Wild animal res- mortally dangerous.21 These parasites (pathogenic bac- ervoirs now seem of greater importance than the classic teria, viruses, protozoa, fungi) have evolved particular model ever envisioned.17 molecular tools, known as virulence factors, that allow The Neolithic Revolution, then, may have been less them to cause disease in humans. Pathogens are, in fact, than the ‘Big Bang’ in the history of disease. It was not highly exceptional beings. a greater proximity to farm animals that has been de- A pathogen’s biology determines how it operates: cisive, but rather the combination of growing human how it is transmitted, how it invades the body, how it populations and greater connectivity, interacting with a evades the innate and adaptive immune response, and background of ongoing disease evolution, very often in so on. These particularities shape the ecological needs the wild. Here, genetic evidence is rapidly filling in the and preferences of individual germs. Consider just a picture. ‘Molecular clocks’ are a way of mathematically few examples. The smallpox virus, for instance, was a estimating the date of evolutionary events based on the directly-transmitted obligate human parasite and re- rate at which a given microbe is thought to evolve. In quired a chain of continuous to survive.22 recent years, it has become clear that some of the most Plague is a rodent disease transmitted principally by flea notorious pathogens in human history—such as tuber- bite; it is permanently present in colonies of burrowing culosis, , smallpox and bubonic plague—are as- rodents in various parts of the globe, and only to tonishingly young.18 A basically stable set of diseases has humans under peculiar circumstances.23 Yellow is not existed since time immemorial; rather, the last few spread by bite, and generally confined to trop- millennia have witnessed dramatic changes in the over- ical and sub-tropical where its vector thrives.24 all landscape of pathogenic enemies faced by humanity. Some parasites take advantage of dense populations to The history of disease, then, is a complex part of the spread directly between humans, and thus flourish in human story. Sometimes the disease regime is shaped overcrowded urban environments. Others are transmit- by endogenous factors: the impulse-response between ted via the faecal-oral route, and find opportunity in un- population pressure and higher mortality. More often, sanitary conditions; and so on. the patterns of disease history are shaped by the spe- Weather and climate exert strong controls over the cific biology—the tools as well as the constraints—of ecology, and therefore the prevalence, of infectious dis- individual pathogens. These microbes are ecologically eases of humans at particular times and places (fig. 1). and environmentally sensitive, and they have a volatile The mechanisms by which weather and climate control evolutionary history. Ecological transformation, climate infectious diseases are many and complex. The physical change, and random genetic mutation are all sources of environment can influence the pathogen itself, as well instability and change, on various timescales, in the long as intermediate species such as hosts or vectors, and/or and tumultuous history of our relationship with the in- the human victim. Ambient temperature, for instance, visible companions who share the earth with us. might alter microbial physiology. Disease vectors and hosts, like , rodents, or bats, have breeding cycles that are controlled by heat and humidity. Human Ecology, Environment, Evolution physiology and behaviour are influenced by temperature and precipitation, and the effects of these parameters on We can appreciate the particularity of pathogenic mi- agricultural subsistence. The physical environment can crobes by reflecting on how rare they are. Microbial life affect human physiology, nutritional status (critically is roughly three and a half trillion years old, and Earth important for immune function), social behaviour (such is home to maybe a trillion different microbial species.19 as crowding, migration, or violence), and the effective- The individual human is home to an average of 40 trillion ness of environmental controls (e.g. sanitation). All of bacterial cells alone,20 and yet most of this microbial life these mechanisms can operate on multiple timescales, is indifferent to us. There are only around 1400 microbes from short-term ecological changes, such as a rainy year known to be pathogenic to humans, even fewer are obli- leading to a malaria outbreak, to long-term evolutionary gate human parasites, specific to humans; fewer still are ones. The latter could include the strong geographic pat- terning of many diseases, even today, or the prevalence throughout historical times of the most deadly form of

17 Harkins and Stone (2015); Barrett and Armelagos (2013). 18 TB: Bos et al. (2014); Comas et al. (2013). Malaria: Loy et al. (2017). Smallpox: Duggan et al. (2016). Plague: Rasmussen et al. 21 Woolhouse and Gaunt (2007). (2015); Cui et al. (2013). 22 The classic study of smallpox is Fenner (1988). 19 Locey and Lennon (2016). 23 Benedictow (2004). 20 Sender, Fuchs, and Milo (2016). 24 McNeill (2010).

Kyle Harper - 9789004392083 Downloaded from Brill.com10/01/2021 05:10:18AM via free access 302 Harper

figure 1 How climate controls infectious diseases (author). malaria (P. falciparum) in much of southern , as The seasonal mortality patterns from ancient Newfield describes in his chapter of this volume. have revealed a strong amplitude of variation, with a As has been understood since at least the time of huge wave of deaths in the late summer to early autumn. , cyclical changes in temperature and pre- When the data are controlled by age group, it is nota- cipitation throughout the year have complex effects on ble that the elderly (and only the elderly) experienced the incidence of disease. Ancient lack the a small, secondary wave in the winter, likely due to re- ‘cause of death’ records that, while often crude, allow spiratory infections that commonly prey on those with historians of the later and Early Modern weaker immune systems in the cold months. Even by period to trace patterns of mortality in past societies.25 the standards of pre-modern societies, the Roman pop- But an empirical and methodological breakthrough was ulation seems to have experienced an unusual degree of accomplished by Brent Shaw and Walter Scheidel, who seasonal variation in mortality. The pattern is even more realised that the abundant evidence for the seasonality striking given that the Roman sample is biased toward of death offered indirect clues about disease ecologies young adults, who generally comprise the hardiest sub- in the Roman world.26 Tens of thousands of Christian population. The sheer amplitude of variation makes a tombstones from the later Roman empire record the prima facie case that infectious disease was an excep- date when the deceased passed into the afterlife. In the tionally strong mortality factor in .27 modern world, where infectious disease has receded as a The dominance of high summer and early autumn in cause of death, seasonal variation in mortality has been the mortality regime at Rome suggests two kinds of cul- strongly (though not completely) suppressed: death prit at work. First, it has been reasonably hypothesised comes more or less equally in all seasons. However, in that the ‘dog days’ of summer exacerbated mortality environments where infectious disease is a predomi- from gastro-enteric diseases, caused by bacteria such as nant factor, mortality rates fluctuate across the year in Salmonella and Shigella. In a city with an extraordinari- patterns that reflect the specific habits of the pathogenic ly large and densely packed population, the challenge microbes that cause death. Maybe the most notable fact of environmental sanitation overwhelmed even the to emerge from these studies was the reality of strong re- Romans’ engineering prowess. These diseases are spread gional differences in patterns of death within the Roman via the faecal-oral route, ingested in contaminated food provinces. looked different from Rome, northern and water. They cause fever and diarrhoea and, particu- different from ; local ecological fac- larly in a world without pharmaceuticals, can tors clearly exerted influence on the seasonal rhythms cause severe morbidity and mortality, especially among of dying in the Roman empire. frail sub-populations. The Roman habit of early wean- ing meant that infants were perilously exposed to these

25 E.g. Carmichael (1986). 26 Harper (2015a); Scheidel (2001) and (1996); Shaw (1996). 27 Harper (2015a).

Kyle Harper - 9789004392083 Downloaded from Brill.com10/01/2021 05:10:18AM via free access Invisible Environmental History: Infectious Disease in Late Antiquity 303 pathogens, although infant mortality remains some- typical in other places, this evil abounds in this thing of a ‘black box’ in the case of the ancient Romans.28 city.32 Second, the surge of deaths in the autumn has been taken as a signature of malaria. The seasonal mortality Now there is also firm evidence from archaeological profile is only one indication among many that malaria genomes that malaria was a presence in the Roman was an especially heavy burden on the Romans. Thanks empire.33 above all to the work of Robert Sallares, we have a de- The name malaria comes from the Italian for ‘bad air’, tailed and reliable understanding of the role of malaria and it is the quintessential ecological disease. It was not in Roman antiquity.29 Malaria is a disease caused by uniformly distributed across the empire, but rather con- protozoa. These are single-cell parasites centrated in areas that supported the breeding of the with complex life-cycles, transmitted between humans mosquito vector. Malaria is above all a problem; via the mosquito. There are different spe- it flourishes in marshy and wet places. The specific con- cies of malaria-causing Plasmodium protozoa, includ- figurations of Roman economy and society may have ing P. malariae and P. vivax. While these are not to be unleashed the malarial potential of the landscape. The underestimated, they caused a milder, feverish disease Romans felled forests in great swaths, accelerating run- with lower rates of mortality than the great killer, P. fal- off and making it easier for mosquitos to breed. They ciparum. As Newfield shows in his wide analysis of the drained and built roads through pestilential source material, P. malariae and P. vivax were dangers landscapes, and their civil engineering brought water even in more northern parts of Europe in Late Antiquity into close proximity to human habitations everywhere. and the , while P. falciparum seems Wherever it takes hold, malaria is not just one disease only to have been endemic in southern Europe.30 Both among others; it is a burdensome presence, exacer- the protozoa and the mosquito vectors are ecologically bating malnutrition and weakening immunity against sensitive, and, in Newfield’s words, “the less severe the other pathogens. It seemed to hasten the corruption of malaria the more tolerant its parasite and its vectors are all life: “Why do men grow old slowly in places with fresh of cold weather”. and pure air, while those in hollow and marshy places Plasmodium diseases are old. They originated in the grow old rapidly?”34 African tropics; but now, genomic evidence is sharpen- If human transformations of the landscape shaped ing the picture. The deadliest branch of Plasmodium, the , so too did natural climate change. P. falciparum, is an evolutionary novelty. It is a descen- The breeding habits of the Anopheles mosquito are sen- dant of a pathogen, and may be less than 10,000 sitive to climate parameters, on multiple time-scales. In years old.31 It moved into the Mediterranean in the mil- the long term, the climatic conditions of the early impe- lennia before the Romans built their empire, but a vari- rial period may have been propitious for the mosquitos. ety of factors aligned in the Roman period to make it an The Roman Climate Optimum (RCO) (ca. 200 BC–AD 150) especially formidable nemesis. was a phase of Late Holocene history when the circum- Roman medical authors, including the 2nd c. AD phy- Mediterranean was not only consistently warm but also sician , reveal an intimate familiarity with malaria, anomalously wet.35 A range of climate proxies suggest which they knew, in its most virulent form, as semi- that the conditions of the RCO mirrored the millennia of tertian fever. They associated it closely with life in the the Mid Holocene, which were much warmer and wetter itself: in the regions controlled by the Roman empire. It is alto- gether likely that these climate parameters exacerbated We no longer need the word of Hippocrates or the impact of malaria in core regions of the empire. anyone else as witness that there is such a [semi- On shorter timescales, inter-annual variability in tertian] fever, since it is right in our sight every day, the climate drove wild oscillations in the incidence of and especially in Rome. Just as other diseases are malaria. Much of the Roman empire sat along the bor- der between the temperate mid-latitudes and the sub- tropics, and the prevalence of malaria here could be

32 Gal., De morborum temporibus 7.435K. 28 See e.g. Prowse et al. (2008) for important bioarchaeological 33 Marciniak (2016). evidence. 34 Pseudo-, Problemata 14.7.909 (transl. in Sallares 29 Sallares (2002). (2002) 2820). 30 Newfield (2017); Newfield, in this volume. 35 Harper (2017) chapter 1; Hin (2013); Manning (2013); 31 Loy et al. (2017). McCormick et al. (2012).

Kyle Harper - 9789004392083 Downloaded from Brill.com10/01/2021 05:10:18AM via free access 304 Harper exquisitely sensitive to the fluctuation of the climate, is such an important factor in determining mortality, which might send the disease escalating toward epidemic the arrival of new pathogens has continually reshaped heights. Galen reported the conventional wisdom, while the demographic regime and, in some cases, intervened remaining unaware of the actual mechanisms: “… when forcefully in the course of events at the highest level. the entire year becomes wet or hot, there necessarily One notable instance in which the Roman disease occurs a very great plague.”36 In early modern Italy, epi- pool witnessed change was the diffusion of tuberculo- demic outbreaks of malaria erupted on average every sis in the centuries of Roman rule.40 TB is, still today, a five-eight years.37 The ancients, lacking germ theory, did devastating respiratory illness caused by the bacterium not imagine, much less specify, the pathogenic agents Mycobacterium tuberculosis. The bacterium causes a of epidemic events; their terminology for ‘plagues’ or chronic , grinding down its victims over the ‘pestilences’ was stubbornly generic (lues, loimoi). It is course of weeks or often years with coughing and con- evident that short-term climate anomalies (hot or wet sumption. In the past, it was a lethal presence, rather years) were the proximate cause of most disease out- like malaria, casting a spell over entire societies where breaks recorded in the sources. It is also likely, but not it took hold. The history of TB has been rewritten in the provable, that malaria was a principal cause of many of last few years, thanks to genomic evidence. Here is a par- these ‘plagues’. adigmatic case where the classic model of disease his- The incidence of epidemic events, malarial or other- tory has been overturned: while it was long believed that wise, points toward one of the most important features humans contracted TB from cattle, in fact human TB is of the demographic regime in Late Antiquity: its insta- ancestral to bovine TB:41 we made the cows sick, not vice bility. The endemic disease pool is the ‘background’ set versa. TB is a relatively young disease, maybe only 5,000 of diseases present in a population. Epidemic disease re- years old, but even within its short time as a species, fers to the sudden upsurge in death due to one or more Mycobacterium tuberculosis has experienced an event- pathogens, and just as the cycle of the year was marked ful history, with evolutionary developments that have by strong variations in the timing of mortality, so there altered its virulence. Genomic analysis has revealed that was enormous volatility between years. Death came in a major evolutionary event occurred between 1800 and waves, not as a steady drip. The causes of an epidemic 3400 years ago, leading to the most virulent modern lin- can be extraordinarily complex. Climate variability can eage. Future work will narrow this event window, but affect the behaviour of pathogen, vector, or host; food sometime in the centuries of classical antiquity, TB took shortage may lower the nutritional status, and there- a turn towards a deadlier career. fore the immune resistance, of a population. External The example of TB is interesting for another reason, factors, like siege warfare or army movements, can stir too. Whereas most infectious diseases do not leave char- ; and other more purely biological factors, acteristic marks on skeletons, the pathology of TB leaves like changes in the balance of people with acquired im- visible traces of its presence in bones. Thus, bioarchae- munity in a population, or changes in the virulence of a ologists can follow its diffusion in the skeletal record. TB pathogen, can also trigger disease outbreaks.38 is hard to find in pre-Roman skeletons in Europe, but it In the deep background of changes to the disease en- becomes far more common in the period of the Roman vironment lies the constant evolution of the microscopic empire. These centuries have been called “… a water- organisms themselves, as the interplay of mutation and shed moment for the spread of tuberculosis in Europe”.42 natural selection creates novel forms of old pathogens The empire created the ecology where TB could thrive; and also new species. It should also be acknowledged the interconnectedness of the empire, and its dense that horizontal gene transfer—in which genes are trans- urban habitats, were conducive to the spread of a truly mitted between organisms, instead of vertically from devastating killer. The genomic and skeletal evidence parent to offspring—has been important in the evolu- alike are pointing to the Roman empire as an important tion of microbial organisms. In a sense, pathogens can part of the story of TB. bypass some of the ‘trial and error’ of random mutation Tuberculosis was a chronic disease. It moved slowly, by absorbing already functional genetic tools from other claiming its victims in an unhurried way and diffused bacteria.39 Because the particularity of individual germs across the Roman empire at a snail’s pace. In this, it was

36 Gal., De Temperamentis 1.4.531 (transl. Singer (1997) 212). 40 Overviews of TB: Roberts (2015); Müller et al. (2014); Roberts 37 Sallares (2002) 229. and Buikstra (2003). 38 Landers (1993). 41 TB genome: Achtman (2016); Bos et al. (2014); Comas et al. 39 See McNally et al. (2016), for the role of horizontal gene trans- (2013); Stone et al. (2009). fer in the specific case of Yersinia. 42 Eddy (2015).

Kyle Harper - 9789004392083 Downloaded from Brill.com10/01/2021 05:10:18AM via free access Invisible Environmental History: Infectious Disease in Late Antiquity 305 limited by its own mechanisms of dispersal. We should In AD 165, a pestilence arrived in the Roman empire,43 pause to appreciate how historically contingent the and contemporary observers were shocked by its scale Roman disease pool was; it was shaped by the biology and its toll. The was associated in an- of the pathogens that existed in this time and place. The cient sources with the invasion of Parthia under Marcus movement of these pathogens was constrained by their Aurelius and Lucius Verus, and specifically the sack of mechanisms of transmission. Parasites that depend on Seleucia on the . It was said that a Roman soldier mosquito vectors or the faecal-oral route can only spread opened a chest in a temple of the “unshorn Apollo” and so far, so fast. The spread of slow-moving, chronic infec- released a miasma that spread over the whole world. tions like tuberculosis highlights the potential inherent While it is plausible that one spur of the pandemic in Roman systems of communication, but, in the early ran through Parthia, and was accelerated by the return empire, acute infectious diseases seem strongly limited of Roman legions to the empire, we should not be too by their inherent constraints. On close inspection, there credulous. The disease was inside the empire at least a were no large-scale, inter-regional epidemics over a long year before the return of the troops, and it is probable span of time between the late republic and early em- that evidence for a devastating pestilence in Arabia re- pire. Disease outbreaks were local or regional in scale, corded in the AD 150s—noted, somewhat unusually, in spatially limited by the agents of diseases like malaria or both Roman sources and Arabian inscriptions—reflects paratyphoid fever. The arrival of highly communicable the march of the same disease towards Roman borders.44 acute infectious diseases in the auspicious conditions of There had simply never been anything like this dis- the Roman empire would prove to be explosive. ease event before; within a few years, it was taking vic- In Late Antiquity, the Roman empire intersected with tims from one end of the empire to the other. It has left the evolutionary history of some of the worst pathogens a large amount of evidence, of various kinds. The pan- humanity has ever encountered. The entire period be- demic motivated a sudden outburst of religious activity tween the 2nd and 7th c. might be considered an age aimed at the god Apollo, the debris from which are re- of . By giving attention to the spatial and markably preserved in inscriptions across the empire.45 temporal dynamics of disease events, we can put into The written sources testify to a disease event that un- how exceptional in scope and magnitude a series settled contemporaries, laid waste whole regions, and of outbreaks in Late Antiquity truly were. Whereas pre- decimated the army. By sheer luck, the Antonine Plague vious epidemics were regionally confined, starting with overlapped the career of the most prolific ancient medi- the pestilence in the reign of Marcus Aurelius (known cal writer, Galen, whose observations of the “greatest as the Antonine Plague), new germs—what we would plague” are vitally important for understanding the dis- today call ‘emerging infectious diseases’—began to ar- ease. He describes a disease that caused oesophageal rive to rattle the foundations of Roman civilisation. For lesions, bloody diarrhoea, a black extrusive rash cover- the first time, there were disease events truly deserving ing the whole body, with scabbing and scarring in the the label of pandemic, an excess mortality event on an aftermath, and a crisis around days nine-twelve.46 His inter-regional or continental scale. descriptions of the pathology have led modern histori- The reasons for the advent of pandemic mortality ans to identify the agent of the Antonine Plague as the events are ecological, environmental, and evolutionary. smallpox virus. Retrospective diagnosis is full of uncer- The Roman empire fostered an ecology that was con- tainty, and it should be pointed out that Galen’s descrip- ducive to the transmission of acute infections: its thick tion does not unequivocally point to the differentiating web of connections and dense were advantageous symptoms of smallpox. The consensus that has formed for microbes. At the same time, repeatedly, sharp envi- among modern historians needs to remain a hypothe- ronmental changes seem to lie in the background of the sis, until there is positive paleomolecular identification major pandemic events. Given the nature of the ancient from an archaeological victim. But smallpox remains evidence, the causal links between climate change and pandemic events remain obscure, tantalizingly out of reach. But in each case, we can note the circumstan- tial evidence and consider reasonable hypotheses. The 43 A select bibliography would include Elliott (2016); Lo Cascio coincidence between global-scale climate change and (2012); Bruun (2012), (2007) and (2003); Jones (2006) and the eruption of Roman pandemics is not disputable; the (2005); Gourevitch (2005); Zelener (2003); Marcone (2002); Duncan-Jones (1996); Littman and Littman (1973). The over- causal links are necessarily speculative. Along with this, view presented in brief here is covered more extensively in finally, there is evolution. The picture that is coming to- Harper (2017). gether, from a combination of molecular and historical 44 SHA, Ant. Pius 9.4. sources: Robin (1992). evidence, points to the role of evolutionary novelties in 45 Collected in Harper (2017). causing pandemic events. 46 Gourevitch (2005); Littman and Littman (1973).

Kyle Harper - 9789004392083 Downloaded from Brill.com10/01/2021 05:10:18AM via free access 306 Harper the best candidate, and it is likely that genomic evidence Mortality estimates for the Antonine Plague have var- will eventually confirm the hypothesis. ied from as little as 2% of the population to as much as Certainly, the genomic evidence is already starting 25–30%, although I have argued for something in the to fill in the broader . Two recent realm of 10% of the empire’s population as a whole. studies are of particular relevance for understanding That would represent an astonishing 7–8 million vic- the history of the virus. One reconstructs the phyloge- tims, probably the largest single mortality event in abso- netic tree of the orthopoxviruses, which include Variola lute terms up to that point. Nonetheless, the pestilence major, the smallpox virus.47 It shows that the closest did not topple the empire; even if staggered, the empire relatives of smallpox are camelpox virus and Taterapox proved resilient and enjoyed a period of renewed demo- virus. The latter infects only the naked sole gerbil, a graphic and economic expansion under the Severan dy- small rodent that inhabits the dry forests of . All nasty. The next pandemic event, however, proved more three diverged from an ancestral rodent poxvirus, only fundamentally disruptive. 2,000–4,000 years ago, somewhere in Africa. A 2016 In recent work, I have tried to call attention to the study reconstructed the genome of Variola from a 17th importance of the episode known (somewhat mis- c. mummy from Lithuania; the startling discovery was leadingly) as the ‘’.52 This pestilence that this virus sat on a lineage ancestral to all known struck the empire in the obscure and tumultuous years 20th c. smallpox specimens. What this implies is an ex- ca. AD 249–62. Despite the relative paucity of source ma- tremely volatile and extremely recent evolutionary his- terial for this period, the attestation of a massive disease tory, closely connected with modern globalisation.48 So, event is abundant. Some 24 testimonies, including seven at present, the early history of smallpox is a story full of independent eyewitness sources, describe a disease that gaps, to be filled in with more molecular evidence. struck, again within the space of a couple of years, from The case of the Antonine Plague is important, since it one end of the empire to the other. Contemporaries is conceivably the historical debut of the smallpox virus were horrified by the grisly course of the disease and its in Eurasia. It could have evolved in Africa, very shortly huge death tolls. Although this event has been neglect- before the Roman pestilence, and travelled along the ed in recent , it in fact belongs among the trading networks that the empire had intensified along few pandemic events of the ancient world. the and Indian Ocean. The middle of the 2nd c. Once again, we sense the role of global climate events was also a period of climate reorganisation on a global in the background of the pestilence. The empire was scale; it marked the end of the Roman Climate Optimum afflicted by an epochal inter-regional drought from and the beginning of a period of much sharper climate ca. 244. It included Egypt, which points to the role of variability.49 The global nature of this change is reflected global-scale climate perturbations. The drought is at- in the fact that even the Nile flood, dependent on the tested by contemporaries, one of whom claimed that the monsoons, suddenly becomes more erratic. Perhaps bed of the Nile River was dry.53 It is also evident in the these vibrations in the climate system helped to stir papyri, which reflect what has been called the worst food viral evolution, or somehow encouraged the spill-over shortage in Egypt throughout the entire span of Roman events that allowed the smallpox race onto the conveyor history.54 Yet, as with the case of the Antonine Plague, belt of global trade; but these are speculative hypoth- we cannot offer firm hypotheses about the mechanisms eses. However, it does not seem to be the case that the of the relationship between climate turbulence and the Antonine Plague was brought on by the greater vulner- disease event. In this case, it is more likely that the wide- ability of the population due to Malthusian pressures; spread food crisis rendered the population susceptible real wages were rising right down to the advent of the to infectious disease, but this does not exclude other pandemic.50 The background of the pandemic is to be possibilities. We do not know the causative agent of the found in the ecology of the empire, global climate tur- Plague of Cyprian, although I have outlined the hypo- bulence, and the evolutionary history of the smallpox thetical case for a viral haemorrhagic fever.55 It was an virus.51

India—demonstrate familiarity with an endemic form of 47 Babkin and Babkina (2015). smallpox. So, what can be said securely, is that going forward, 48 Duggan et al. (2016). the combination of traditional and novel forms of evidence 49 Harper (2017); Elliott (2016). will be necessary to fill out the history of smallpox, a virus 50 Harper (2016a). whose evolutionary history is recent and eventful. 51 The pestilence in Edessa is also of particular importance 52 Harper (2017); (2016b); (2015b). potentially, since it provides strong observational evi- 53 Euseb., Hist. eccl. 7.21. dence for epidemic smallpox in the 5th c. Medical sources 54 Rathbone and von Reden (2015) 184. from the 7th to 9th c.—from to Iraq, Persia and 55 Harper (2017) chapter 3.

Kyle Harper - 9789004392083 Downloaded from Brill.com10/01/2021 05:10:18AM via free access Invisible Environmental History: Infectious Disease in Late Antiquity 307 exotic pathogen of exceptional virulence, and this time ‘year without a summer’,59 but for various reasons, in- the empire was not able to endure the environmental cluding a lack of calibration in the proxy records, the and demographic shocks. The empire experienced a precise sequence of natural events remained uncertain. multi-faceted social, economic, political, and military Recently, however, a satisfying alignment in the physical crisis, of which environmental factors were a major proxy record—especially ice cores and tree rings—has cause. Whereas the empire emerged on the other side been achieved, as Newfield describes in this volume.60 of the Antonine Plague in relatively unchanged form, In early 536, there was a huge volcanic eruption in the the Plague of Cyprian helped to precipitate more radical northern hemisphere; megatons of sulphate aerosols transformations in the basic structures of empire. This were ejected into the stratosphere, reflecting solar radia- crisis cut deep, although the new empire that took shape tion back into space. Then, in 539 or 540, a second and would endure for centuries. even more powerful tropical explosion occurred. These After the dual blow of these two pandemics, there was events are registered in proxy records around the world, nothing on a similar scale for a long time. The disease and they constitute one of the strongest climate anoma- environment of the later empire remained unfavourable lies in the last several millennia. The decade 536–45 was and volatile, but disease outbreaks were regionally con- the coldest decade in the last 2000 years.61 tained. This lull would end, however, in dramatic fash- The effects of climate turbulence were felt principal- ion, when the single most violent sequence of climate ly in the long run.62 The Roman empire seemed able to change and biological catastrophe in all of antiquity un- withstand a year of poor harvests, but the instantaneous ravelled in the 530s and 540s. cooling was not transient. Independently, the levels of solar energy emitted by the sun declined in the 6th and 7th c., and the entire period has started to be charac- The Great Event: The terised as the ‘Late Antique ’. Yet, the most consequential effect of this raucous climate instability From his accession as sole ruler in AD 527 down until was registered in changes within the biological environ- 541, the career of Justinian was a resounding success. He ment. Right in the aftermath of the spasm of volcanic had made peace with Persia, reconquered Africa, and activity came the worst mortality event of the ancient subdued most of Italy. He survived a coup, reformed the world: the Plague of Justinian. imperial administration and codified all of Roman law. We cannot say with certainty how the climate catas- He went on a building binge as expansive as any emper- trophe sparked the disease outbreak, but we must be- or in Roman history, crowned by the construction of the lieve that the two were causally linked. To understand in . Behind two centuries why, we must appreciate that an epidemic of bubonic of demographic and economic growth in the eastern plague, caused by the bacterium Yersinia pestis, requires provinces, the eastern Roman empire was resurgent. an exquisitely complex ecological platform. Yersinia Then the environment intervened to turn the course of pestis has been the agent of three historical pandemics.63 events. The reversals of the age shocked contemporaries: The first of these erupted under Justinian,64 the sec- “I cannot understand why it should be the will of God to ond was the medieval pandemic that started with the exalt the fortunes of a man or place, and then to cast in 1346. A third erupted in 1894 in Yunnan them down and destroy them for no cause that is ap- Province, China and diffused globally. The first two pan- parent to us.”56 In contrast to the famous achievements demics were probably the most devastating mortality in the earlier part of Justinian’s rule, Mischa Meier has events, in proportionate terms, in all of human history. evocatively called the rest of the emperor’s reign “the other age of Justinian”.57 The environmental crisis in the age of Justinian was marked by changes in the physical as well as the bio- 59 Arjava (2005) on the written evidence. logical climate.58 In both cases, natural archives play 60 Sigl et al. (2015). a crucial role in complementing the written evidence. 61 Toohey et al. (2016); Kostick and Ludlow (2015); Buntgen et al. Historians have long known that the year 536 was a (2016). 62 Harper (2017) chapter 6. 63 Slack (2012). 64 The essays in Little (2007) represent the state of the field. Major treatments include Meier (2016); Mitchell (2015) 409–13, 56 Procop., Pers. 2.10.4 (transl. Kaldellis (2014) 93). 479–91; Horden (2005); Meier (2003); Stathakopoulos (2004); 57 Meier (2003). Sarris (2002); Stathakopoulos (2000); Conrad (1981); Durliat 58 All of what follows is treated more extensively in Harper (1989); Allen (1979); Biraben (1975) 22–48; Biraben and Le Goff (2017) chapters 5 and 6. (1969).

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Humans, though, have been merely incidental vic- up to the Plague of Justinian.71 These genetic adapta- tims in what is really an animal disease; Y. pestis is a tions allowed Y. pestis to become the deadly germ be- bacterium of rodents spread principally by flea bite, and hind the pandemic event. colonies of burrowing rodents are its natural reservoir.65 The abrupt climatic changes preceding the outbreak The bacterium probably evolved in central Asia, whose triggered the spill-over event, even if the mechanisms highlands are home to great colonies of marmots and remain uncertain. Still today, climate perturbations reg- gerbils. Most of the time, the plague remains enzootic, ulate the incidence of plague. In China, El Niño years are quietly lurking in its maintenance hosts.66 Under the correlated with plague outbreaks, and there is a strong right conditions, plague will become epizootic, spilling relationship between volcanism and El Niño, so the vol- beyond its host species into other animals, including canic eruptions of 536 and 539/40 could have sparked rodents like the black rat, Rattus rattus. In recent years, the sequence of events leading to the pandemic.72 In the versatility of Y. pestis has become more broadly truth, though, the climate could have acted on any appreciated; it is capable of infecting a wide range of of the five organisms involved in a plague event. Rain species.67 But, its most notorious historical spill-over might have fostered vegetation growth, that instigated events seem closely connected to Rattus rattus, a com- runaway population explosions among the burrowing mensal rodent that lives in close quarters with humans.68 rodents. Indeed, in a recent book, I argue that both long- A human epidemic is actually the collateral damage of term and short-term climate mechanisms played a role, an underlying epizootic event. Thus, there are at least with several decades of heavier precipitation in central five species involved in a plague outbreak: the bacteri- Asia leading up to the plague probably resulting in rapid um, the maintenance host, the commensal rodent, the growth in rodent populations. Sudden cooling may have flea vector, and humans. The sheer complexity of this ar- helped the temperature-sensitive rat flea to continue to rangement, and the intricate dependence on the black reproduce in the sweltering Indian Ocean, and survive rat epizootic, long engendered doubt that Y. pestis could the southern passage into the Roman empire. Grain have been the agent of the historical pandemics. But in shortages could have stirred human movements, or ren- recent years, genomic confirmation has laid to rest any dered hungry bodies vulnerable to infection, though I doubts that Y. pestis was the guilty party, in what were in am in agreement with Newfield’s arguments, in this vol- fact disease events of stunning contingency.69 ume, that famine is so far a weak candidate for a trigger The plague came to the Roman empire from beyond. of the plague. In all likelihood, several of these climate Genomic evidence indicates that the lineage of Y. pestis mechanisms were at play simultaneously. that caused the Plague of Justinian is most closely relat- Perhaps the most intricate requirements for the ed to specimens in present-day grey marmots and long- plague pandemic, though, were ecological. If the hand tailed ground squirrels in the Xinjiang region of western of nature was at work in genetic evolution and the cli- China. In the words of Monica Green, “All narratives matic background, the human role was supreme in of plague’s history must be connected to that place of constructing the ecological platform for the plague. In origin.”70 The arrival in 541 of Y. pestis at , on at least two senses, human civilisation was responsible the southern shore of the Mediterranean, was a con- for establishing the conditions under which the plague spiracy of evolutionary, environmental and ecological pandemic could occur. The first was the web of connec- circumstances. In evolutionary terms, we are learning tions binding east and west.73 A robust trade network that Y. pestis is not an ancient pathogen that has existed across the Red Sea and Indian Ocean carried silk, spices, unchanged, since time immemorial. It has been found slaves, ivory, aromatics, and other commodities: as well in a range of Bronze Age burials from Eurasia, and these as germs. Tellingly, the Plague of Justinian first appeared archaeological samples of the bacterium have revealed at Pelusium, right at the hinge of the Mediterranean and important genetic changes in the millennium leading the Indian Ocean worlds. The second human factor was the diffusion of the black rat. Native to south-east Asia, Rattus rattus is an invasive species, and McCormick has

65 Cui et al. (2013). 71 Specifically, the late development of the ability to make Ymt, 66 Eisen and Gage (2009); Gage and Kosoy (2005). a protein that lets the bacterium survive in the mid-gut of the 67 Of both mammals and fleas. See Campbell (2016) esp. 232–33 flea, as well as an amino acid substitution in the pla protein for the medieval Black Death. that heightens the virulence of the pathogen. 68 McCormick (2003). 72 Plague and climate generally: Ari et al. (2011); Kausrud et al. 69 Feldman et al. (2016); Wagner et al. (2014); Harbeck et al. (2010); Gage et al. (2008). El Niño: Zhang et al. (2007). Xu et al. (2013); Wiechmann and Grupe (2005). (2015) and (2014); Enscore et al. (2002). 70 Green (2014) 37. 73 A point I emphasise in Harper (2017) chapter 5.

Kyle Harper - 9789004392083 Downloaded from Brill.com10/01/2021 05:10:18AM via free access Invisible Environmental History: Infectious Disease in Late Antiquity 309 shown that its colonisation of the West was part and At first only a few people died above the usual parcel of Romanisation.74 The storage and transport of death rate but then the mortality rose higher until grain was conducive to the expansion of rat colonies all the toll in deaths reached five thousand a day, and over the empire. The massive rat colonies of the Roman after that it reached ten thousand, and then even world were the fuel to the fire of the pandemic. In 541, more.79 Y. pestis met the rats of the Roman empire, and the con- sequences were explosive. According to John, the dead were counted until the The transmission of the disease by flea bite is the key number reached 230,000, but after that the authorities to its insidious power.75 In the most common course lost count. Both authors claim that basic order broke of infection, the dermis is inoculated with Y. pestis, down, in the food supply, retail commerce, and munici- and the lymphatic system drains the bacterium to the pal governance. At first the dead were buried, but when nearest lymph node. There Y. pestis replicates, causing room ran out, piles of corpses were ferried across the the visible swelling of the lymph node, called a bubo in inlet to Sykai, where the dead were thrown en masse Greek. , chills, headache, malaise, and delirium into giant military towers. The events at Constantinople move quickly, and the lymph node grows like a tumid are described in the greatest detail, but the disease orange or grapefruit.76 The victim succumbs to sep- reached the , Italy, , , Spain, sis, with case fatality rates around 80%. Less often, the and the British Isles. According to , half the bacterium can enter directly into the bloodstream and population was lost. cause sepsis with exceptional speed, a course of infec- Historians of Late Antiquity have struggled to know tion called primary septicaemic plague. The bacterium what to make of the Plague of Justinian; was it a truly can also spread from the lymphatic system into the destructive event?80 The preponderance of the evidence lungs, causing secondary pneumonic plague. This form has always leaned towards the conclusion that it was an of the disease was uniformly fatal. All of these courses episode on a par with the medieval Black Death. The derive from the flea bite. It seems increasingly likely that literary sources insist on the plague’s massive toll, and plague could travel not only by the rat flea but via other these accounts deserve more sympathetic reading than ectoparasites, including human fleas. Furthermore, the they have sometimes been given. They are independent, plague could also spread directly between humans via vivid, and credible. Attestations of pandemic events in aerosol droplet expelled by coughing. When plague was the ancient record are truly limited, and deserve cau- inhaled into the lungs and induced respiratory infec- tious consideration, not brash dismissal. Moreover, the tion, it caused primary pneumonic plague. But the sig- continued accumulation of evidence underscores the nificance of primary pneumonic plague was probably credibility of the literary texts. McCormick has just pub- limited in the pandemic, and fleas remained integral to lished a database of mass graves from Late Antiquity the dynamics of the outbreak. and found a major rise in the 6th and 7th c.; he cautious- We have two star witnesses, as well as a number ly and plausibly associates this phenomenon with the of minor ones, to the first outbreak of the Plague of arrival of pandemic plague.81 Justinian.77 The eastern churchman John of , The maximalist case for the plague’s impact, though, and the classicising Procopius, each provided has received stunning confirmation in the last few vivid testimonies to the plague’s destruction. Despite years. Two cemeteries, from Aschheim and Altenerding their radically different cultural outlooks, their accounts outside Munich, have yielded ancient DNA evidence are remarkably consistent, and allow us to reconstruct for Yersinia pestis from the 6th c.82 The significance of in outline the course of the event. It erupted in Egypt these discoveries could not be greater. First, the positive in 541 and diffused over land and sea across the eastern Mediterranean. By 542 it was in Constantinople, and the next year in the West.78 Its destruction was vast in town McCormick (1998) more convincing, and think it is far prefer- and country, and in the capital it was horrific: able to follow Procopius. 79 Procop., Pers. 2.23.2 (transl. Kaldellis (2014) 123). 80 For expressions of minimalist views, see Wickham (2016) 43–44 and (2005), building on Durliat (1989), which is still the 74 McCormick (2003). most important version of the sceptical case, although I think 75 Harper (2017). See Campbell (2016) and Benedictow (2004) for it is deeply flawed. For a recent presentation of the maximalist the Black Death. case, Meier (2016) is convincing. 76 Benedictow (2004) is clear, reliable, and helpful. 81 McCormick (2016) and (2015). 77 Harper (2017) for a fuller account. 82 Aschheim: Wagner et al. (2014); Harbeck et al. (2013); 78 Meier (2003) 92–93 offers a slightly different dating, with Wiechmann and Grupe (2005). Altenerding: Feldman et al. the outbreak arriving in the capital by AD 541, but I find (2016).

Kyle Harper - 9789004392083 Downloaded from Brill.com10/01/2021 05:10:18AM via free access 310 Harper identification of Y. pestis vindicates the description of onwards, the importance of Constantinople declined, the disease in the written accounts. Second, the bacteri- while the focus of the disease in and Iraq remained al genomes recovered show that the agent of the plague intense.85 Then, in the middle of the 8th c., the disease was a form of Y. pestis similar to the lineage that caused disappeared as mysteriously as it had arrived. The DNA the medieval pandemic. Third, the place of the discov- evidence shows that the Justinianic Plague was caused ery matters: the bacterium was found in some rather by an extinct branch of Y. pestis. The bacterium retreat- modest multiple burials in tiny villages in the German ed to its haunts in central Asia, and the Black Death was countryside. By far the most uncertain hypothesis in the a new introduction event. The role of climate change in maximalist case for the Plague of Justinian was that the the end of the First Pandemic deserves more attention, disease spread far and wide, including into rural settle- and a comparative analysis with the medieval pandemic, ments. In short, the discovery of the bubonic plague at too. Certainly, public health responses centred on ‘quar- Aschheim and Altenerding confirms the worst: if the antine’ played no role in the end of the First Pandemic, monster was here, it was everywhere. so answers must be sought in some combination of the What made the plague so devastating was its mode physical climate, rodent ecology, and epidemiology. of transmission, which relied on the underlying rat epi- zootic. It was thus able to penetrate more easily into the rural sphere, where most of the population lived. Conclusion The medieval Black Death carried off 50–60% of the European population. Our 6th c. evidence does not The impact of the Plague of Justinian was registered in allow for the same analysis or confidence that supports the long term, in two centuries of demographic history such conclusions, but we can say that everything we burdened by the presence of this single, devastating know is consistent with a death toll in the same range germ. Moreover, the longer term effects of a cooler, less for the first episode in 541–43.83 And even with this vio- hospitable climate acted in synergy with biological ca- lence, the pandemic was not finished. After the initial tastrophe. The ultimate result, I argue in a recent book, outbreak, the bubonic plague recurred for over two cen- was a prolonged sequence of stagnation and state fail- turies in the circum-Mediterranean and . Every ure, stretching from the 540s to the 630s. The particular 10–20 years, the disease erupted again, and was able to history experienced by each of the societies under the do so for two reasons. First, the immunity conferred on umbrella of Roman rule was determined by a range of survivors of infection by Y. pestis is weak and transient. local factors, and some regions suffered worse than oth- Second, and more importantly, I argue in a recent book ers. But the general fact of demographic volatility and that the bacterium became established in host rodent decline, and the fiscal disequilibria of the central state, populations in the West.84 We should imagine the re- proved insuperable. lapse events not as reintroductions from without, but We should not discount the resilience of these ancient as amplifications from interior plague reservoirs. Hence, societies, nor the circumstantial and human element in the metaphor of epidemic ‘waves’ is misleading. The the final events of the later Roman period. But it would recurrent plague events were explosions from within, be distorting not to attribute strong agency to nature as spatially complex events shaped by physical and human well. We have learned, thanks to new physical evidence, geography. As Newfield observes in this volume, the ‘Late that the worst biological enemy in the history of human- Antique Little Ice Age’ is the backdrop for the broader ity arrived on Roman shores at this time, and that the First Pandemic, and recurring climate anomalies could most pronounced episode of climate change in the Late have played a role in each of the amplification events. Holocene struck almost simultaneously. The history of We do not know where, exactly, the plague reser- Late Antiquity needs to be written, in the provocative voir was, and there could have been more than one. words of a recent book on modern environmental his- From the first outbreak down to around 620, it is clear tory, “as if nature existed.”86 Late Antiquity witnessed that Constantinople was a major node in amplification violent turbulence in the physical and biological en- events. Probably, the disease found its way to the capital vironment. We do justice to the men and women who of the empire, which then acted as a nexus of metastatic worked to make their world out of such conditions by dispersal. Even the western amplifications depended on acknowledging the powerful role of nature in their story. an integration with eastern networks. Then, from 620

83 See Harper (2017). 85 See Conrad (1981). 84 Harper (2017). 86 McNeill, Pádua, and Rangarajan (2015).

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