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Climate, pathogens and mammals: England in the age of emerging diseases, c. 1275–1362

Philip Slavin

Between 1275 and 1348 (i.e., within the space of some seventy years) no less than three major outbreaks on a pandemic/panzootic scale occurred in England: sheep epizootic of 1275–80 (with its recurrent waves into at least 1320) caused by scab; the Great Bovine Pestilence of 1319–20 (with two minor outbreaks in 1324–27 and 1333–34); and the bubonic plague of 1348–50, aka the Black Death, with recurrent waves into the seventeenth century, the deadliest of which was the ‘second pestilence’ (pestis secunda) of 1361–62. In all three cases, these were new emerging diseases, with no previous exposure of local mammal populations. The sudden appearance of these infectious epidemics is puzzling to historians and is only most recently, through the appreciation of their wider climatic, ecobiological and genetic contexts and the complex interaction between them that historians and palaeoscientists have begun to acquire some initial understanding about these sudden outbreaks, the Black Death in particular. Indeed, as some recent studies have established, both short-term weather shocks and long-term climatic shifts had a decisive impact on the health of humans and other mammals.¹ Short-term weather vagaries dictated the annual levels of food and fodder availability and supply and, thus, the well-being of humans and animals. A short-term episode of exposure to a harvest-failure and malnourishment could compromise the immune system of starving humans and animals and make them prone to various pathogens and diseases.² Likewise, long-term and large-scale climatic shifts, such as prolonged periods of cooling and warming, increasing incidence in storminess or periods of climatic instability, may drastically alter wider bioecological contexts, by creating peculiar conditions in air, water or soil that would encourage the activity and migration of new or dormant pathogens.³

Setting the stage for disease: climate change

To appreciate this complex interaction between climate, environment and pathogens, it is necessary to establish a wider climatic context of late-medieval England and elsewhere in the North Atlantic region. The three emerging diseases are to be seen in a much wider context of profound climatic changes occurring from c. 1250/70 onward. Although the exact chronology of these shifts is being debated, it is now generally accepted that by the second half of the thirteenth century (ca. 1250/70), the North Atlantic climate entered a new transitional phase, leading from the so-called Medieval Climate Anomaly (MCA) (c. 1050/70–c. 1250/70) to the Little Ice Age (LIA) (c. 1420–c. 1850). The MCA was dominated by a strongly positive North Atlantic Oscillation (NAO), when strong winter Westerlies brought mildly wet and relatively warm weather to north-western Europe and arid conditions to the Mediterranean and North Africa, with average annual temperatures in Europe approaching those of ca. 2000 CE. During the transitional phase from the MCA to the LIA (c. 1250/70–1420), one witnesses a general weakening of the NAO, especially since the 1320s, to the point that by the 1430s it became firmly negative. The gradual NAO weakening during the transitional period caused a highly unstable climatic regime, characterised by high variability of year-to-year sea-surface and air temperatures, as well as year-to-year precipitation levels. The weak winter Westerlies brought increasingly stormy conditions and cold spells into much of Europe, and these conditions were dominant during most of the LIA.⁴

The shift from the positive to the negative NAO was not the only fact that caused the increased climatic instability and the piecemeal cooling. In addition, we have to account for a gradual reduction in solar irradiance, partially caused by the ongoing volcanic activity. In 1257, there was a mega-eruption in Samalas (Indonesia), the single largest volcanic eruption in the last 7,000 years, which released between 300 and 600 megatons of sulfuric acid. The Samalas eruption was followed by five major volcanic eruptions in 1268/69, 1275/76, 1285/86 (most likely, the VEI-6 eruption Quilotoa in Ecuador), 1328/29 and 1342/43.⁵ In particular, solar irradiance was depressed between c. 1280 and c. 1340, a period known as the ‘Wolf Minimum’. During this period, levels of solar irradiance were significantly lower than average for the period 1000–1500.⁶

Piecemeal weakening of the NAO on the one hand and reduced levels of sunshine on the other meant gradual cooling. Indeed, Greenland witnessed a period of severe cold spells, peaking in 1303, 1320 and 1353, while Iceland saw sea-ice formation along its northern coast in the 1310s and 1330s.⁷ The period 1315–18, overlapping with the Great Famine of 1315–17, coincided with unusually warm North Atlantic sea-surface temperatures, which created atmospheric conditions encouraging unusually wet, cold and stormy weather all over northern Europe.⁸ The excessive storminess caused several major sand-blowing and dune deflation events across coastal areas all over Britain in the fourteenth and the fifteenth centuries.⁹ Although solar levels began picking up in the 1340s, the period of c. 1341–53 was marked by exceptionally cold summer temperatures, with 1348–53 standing out as the coldest years during the transitional period. Likewise, the period of c. 1357–62 was exceedingly damp and cold. From the early 1360s, temperatures started catching up with the increased levels of solar irradiance, and for some thirty five or so years (c. 1360–95), Englishmen and other Europeans enjoyed what has recently been coined as ‘Chaucerian maximum’. This warm and sunny period was, however, short-lived. From the early fifteenth century onward, we enter a new phase of cooling, the so-called ‘Spörer Minimum’ (c. 1416–1534), which reached its peak between c. 1437 and 1460, when the levels of solar irradiances and air temperatures plunged to the lowest level in the previous 1,500 years.¹⁰

These climatic changes had some far-reaching implications on the bioecological environment and consequently, the health of its inhabitants. Within the arable sector, dominating most England, south and south-east Scotland, south and east Wales and east Ireland, weather anomalies caused a series of bad harvests, the worst of which were the two three-back-to-back harvest failures of 1315–17 and 1349–51. Additional bad harvests in the period of 1270 and 1450, with composite net crop yields standing at 20% or higher below average, are reported in 1270, 1283, 1293, 1304, 1321, 1328, 1346, 1362–63, 1367, 1369, 1374–75, 1390, 1401, 1406, 1408–09, 1413, 1416, 1418, 1420, 1422, 1424, 1428–29, 1435–38, 1442, 1445 and 1450.¹¹ Within the pastoral sector, the climatic deterioration reduced the grazing season by approximately one month, with early May and late September being effectively eliminated.¹² This meant that the annual biomass for grazing animals was now reduced by some 10%–15%. This made the situation especially grave in upland and highland areas of the British Isles, where cattle and sheep farming were the single most predominant type of local economies.

These climatic changes and environmental crises had a profound impact on health of humans and other mammals – first and foremost, domesticated livestock. For instance, torrential rain can ruin not only grain for humans, but also fodder for animals. Even though excessive rain creates an abundance of grass, damp conditions can make hay-making very challenging. This was indeed the case during the excessively pluvial 1314–16.¹³ The fact that bad harvests can happen once every decade implies that worse-off individuals and their stocks would experience events of shortage and malnourishment and in some extreme cases – hunger. To make things even worse, poor housing conditions meant that starving humans and their domesticates had to waste more energy to maintain body heat. These factors would undoubtedly compromise the immune system of humans and animals and render them susceptible to various pathogens and diseases. It is equally essential to appreciate that the same climatic conditions can create the optimal environmental context for new diseases to emerge and spread. As we shall see in the following discussion, all three biological shocks – sheep scab, cattle pestilence and human plague –originated in the context of particular weather anomalies, which encouraged active and aggressive behaviour of both pathogens and vectors. If weather anomalies were bad for humans and their livestock, they were good for pathogens.

The scab panzootics of 1275–80 and its recurrent outbreaks

The first biological shock on a national level was the emergence of scab panzootics in sheep flocks, commencing in Northern England in 1275–6 and spreading southwards between 1276 and 1280 (with the 1279–80 outbreak being a particularly pervasive and devastating one), and carrying on in several recurrent waves for several decades. Scab is a highly acute and transmissive form of dermatitis, caused by faeces and bites of nonburrowing sheep mites (Psoroptes ovis). The two-week lifecycle evolves from the egg, through hexapod larvae, octopod protonymphs and tritonymphs into adult mites. After mating and fertilising, female mites will live for some forty days, laying one or two eggs a day and never mating again.¹⁴ In appropriately cold temperatures (~10 C), the mites can be viable off the host for seventeen days (in wool sacks, woollen clothes, barns and soil), during which period eggs can hatch. The off-host longevity is shorter in warmer Wallingford.¹⁵ It is unclear if the 1275–80 outbreak was the first historical incidence of scab murrain in England, on the national level: the incidence of sheep panzootics were uncommon before the thirteenth century, especially when compared to the incidence of human and cattle diseases.¹⁶ Several English chronicles mention the outbreaks of sheep murrain, whose character is unknown, in 1201, 1225 and 1258, but those seem to be regional, rather than national murrains in character. A reference to a possibly localised outbreak of scab in 1231–32 is found in a manorial account from the manor of East Meon (Hampshire), where thirty two ewes (out of 1,075) were described as ‘scabious’.¹⁷ It is possible that scab was present for some time in various loci in England in an endemic form, without turning into a major national epizootic. What is clear, however, is that scab murrain of 1275–80 was a disaster of alarming proportions. Within the space of some eighteen months, England lost around half of its sheep flocks (Table 10.1). The outbreak is also reported in east Wales and east Ireland in 1280–81, and it is unclear if the disaster prevailed in Gaelic-speaking parts of the British Isles. In relative terms, the mortality discriminated between different sex- and age-groups. Male animals were hit worse than their female counterparts. Among male animals, wethers (castrated rams) were faring worse than sexually active rams. This is largely because they grew longer and heavier fleeces than sexually active sheep, which facilitated the dissemination of scab, either through direct contact with live mites, or through shearing combs and cutters. But it was lambs that suffered the highest mortality rates. Scab tends to be particularly devastating in lambs born to ewes with scab during pregnancy. Mortality rates varied from place to place and, as I have shown elsewhere, these differences in figures cannot be explained by a single variable. Rather, it was a complex combination of various factors, varying from place to place, that determined different rates of morbidity and mortality.¹⁸

Although the first major wave of scab was over by 1281, recurrent, more minor outbreaks of scab continued well into the 1320s (in particular, in 1283–4, 1293–4, 1313–4).

Table 10.1 Mortality rates of sheep flocks on English demesnes, by sex and age group, 1275–80
	Total sheep sampled	Deaths through murrain		Total losses (through murrain + butchery + ‘panic sales’)
	Heads	Heads	As (%)	Heads	As (%)
All animals	47,655	16,805	35.3	26,559	55.7
Female animals (excluding lambs)	18,265	5,329	29.2	9,450	51.7
Male animals (excluding lambs)	18,896	7,124	37.7	10,609	56.1
Mature, sexually active animals (ewes and rams)	16,135	4,836	30.0	8,850	54.8
Immature animals (hoggets and gimmers)	8,038	3,249	40.4	3,618	45.0
Lambs	10,495	4,353	41.5	6,500	61.9
Neutered animals (wethers)	12,988	4,367	33.6	7,591	58.4

Source: Derive from Slavin, 2020, p. 890

How do we explain the sudden outbreak of scab in 1275–80? Or, if our hypothesis regarding the tacit existence of scab in an endemic form is correct, how do we explain its advance from an enzootic to an epizootic stage sometime in the late 1270s? Again, it is necessary to establish the particular climatic context of the 1270s, and see how those specific conditions may have affected the activity of scab mites (Psoroptes ovis). Scab mites favour cold and wet conditions, with winter being the period of aggressive mating and egg-laying. Chronicles report the years of 1273, 1275, 1278 and 1280 as being wet and cold.¹⁹ Likewise, dendrochronological record from East Anglia and western counties reveals excessively high levels of March-to-July precipitation in 1271, 1273, 1274, 1278 and 1280–81.²⁰ These would have been the ideal conditions to encourage the growth of Psoroptes ovis population, to the point that by the late 1270stheir population was large and dense enough to drift the scab cycle from an enzootic to epizootic stage.²¹

While natural forces may have played a detrimental role in initiating the scab outbreak, they seem to have had only a limited impact on its spread across the British Isles. True, some exogenous factors, including local microclimates, vegetation types of landscapes, population densities and demographic composition of flocks, as well as wool-types may have had partial impact on variations in mortality rates, they do not explain the dissemination of the disease. It was anthropogenic factors that accounted for that. In order to spread any vector-host based disease, a metastatic movement of both vectors and hosts is required. Sheep are domesticated animals, whose movements were restricted and conditioned by managerial decisions, preferences and arrangements of their human owners. Thus, sheep could be moved between manors, when local managers decided to replenish depleted flocks, hit by scab, with healthy animals from elsewhere. Likewise, some manors housing large flocks tended to herd their sheep cooperatively, and this fact implied a back-and-forth movement of animals. Furthermore, sheep could be moved from the countryside to towns, to be sold and butchered there for consumption. Finally, scab mites could potentially be transported to towns in wool sacks. After all, by c. 1280, the textile industry was still largely an urban phenomenon, regulated by local guilds.²² The spread of scab was also conditioned by the ability of local demesne managers, shepherds and tenants to contain the disease on a local level. As some accounts from the Chalkland region of Hampshire-Wiltshire indicate, there were serious efforts to stop the spread of the disease, by applying various types of biological and chemical medicaments, most efficient of which was tar, usually mixed with oil or fat.²³

The Great Cattle Pestilence of 1319–20

Likewise, the Great Cattle Pestilence of 1319–20 was a disaster in its own league. Most likely, it was caused by Rinderpest, a highly communicable viral disease, caused by the Rinderpest Virus (RPV), which killed no less than about 63% of English bovine stocks between April 1319 and Summer 1320.²⁴ The pathogen incubates from three to nine days and gets transmitted mostly through respiratory means (through aerosol secretions and droplets) and sexual contacts, as well as by drinking contaminated water. The speed of its dissemination was remarkably fast: between early April and early September 1319, it travelled all the way from the Essex coast to Berwick-upon-Tweed, making the total route of about 370 miles (595 kilometres) at the approximate speed of 2.43 miles (=3.91 kilometres) a day.²⁵ This could be possible only metastatically via constant movement of infected cattle, through sales, intermanorial transfers and army provisioning, in the context of the ongoing Anglo-Scottish conflict. Rinderpest is characterised by haemorrhaging, fever, erosion of lower intestine, debilitating diarrhoea and nasal and ocular discharge. Animals succumb between six and twelve days; during the pandemic and postmortem, succumbed animals contaminate fodder, pasture and sources of water.²⁶

Just as scab, Rinderpest mortality rates varied across different sex- and age-groups (Table 10.2). Mature female animals were hit the worst, with about 75% of cows and heifers perishing, while mortality rates of cows alone standing at the overwhelming 80%. By comparison, average mortality rates of male animals stood at 57%, with the lowest figures reported in oxen (54%). This is hardly surprising given that cows and older heifers spent much of their time in pregnancy and lactation, which may have weakened their immune system. Oxen, on the other hand, were draught animals, with a strong muscular system and enjoying a better fodder intake than nonworking cattle.²⁷ Intriguingly, there seems to be a gap in reported mortality figures between calves (53%) and yearlings (74%).

Table 10.2 Mortality rates of bovine stocks on English demesnes, by sex and age group, 1319–20
	Total cattle sampled	Deaths through murrain		Total losses (through murrain + butchery + ‘panic sales’)
	Heads	Heads	As (%)	Heads	As (%)
Oxen	3,095	1,537	49.7	1,674	54.1
Bulls	257	139	54.1	171	66.3
Cows	1,809	1,247	68.9	1,447	80.0
Young cattle	1,001	548	54.7	597	59.7
Yearlings	576	429	74.4	429	74.4
Calves	865	410	47.4	454	52.5
All animals	7,605	4,310	56.7	4,773	62.8

Source: Recalculated from Slavin (2015).

Although both scab and Rinderpest outbreaks were both devastating in their scale and impact, the main difference was that the former seems to have been an epizootic confined endemically to the British Isles, while the latter was clearly a panzootic spreading on a quasi-global scale. Although it is impossible to establish, at this point, the exact geography of its dissemination, cattle mortality outbreaks have been reported in Outer Mongolia in the 1280s, from where it may have spread, the Ilkhanate (in the 1290s), the territories of the Golden Horde (in the 1290s or the 1300s), and in Russian principalities (c. 1298–309), eastern and central Europe (c. 1314–16), northern France (1317/8), the Low Countries (1318) and Denmark (1318). Whether East and West Eurasian cattle plague outbreaks were caused by the same disease or not remains to be thoroughly investigated. It was from the Low Countries that the pestilence arrived in Essex in Easter 1319. In the British Isles, the disease spread all over England (1319–20), arriving at the Scottish borderlands in early September 1319, reaching Wales in the Summer of 1320 and finally making it to Ireland in 1321.²⁸

Given the possible Asian origins and the quasiglobal proportions of the Rinderpest outbreak, it is necessary to set it into an appropriately broad ecobiological and climatic context. The shift from the MCA to the transitional phase leading to the onset of the LIA was a global phenomenon, whose effects were equally pronounced around the Pacific Rim. The MCA in the Pacific was characterised by the dominance of La Niña, causing low precipitation levels along the west coast of the Americas and south-Asian monsoons. During the last two decades of the thirteenth century, the monsoon levels declined considerably, giving way to unprecedentedly dry and cold weather in the Pacific and Central Asia, as is evidenced in local dendrochronological record in Siberia, Mongolia, India and Vietnam.²⁹ According to Bruce Campbell, these new climate conditions were ideal for the emergence and spread of the RPV across Eurasia.³⁰ While Rinderpest indeed favours cold conditions and tends to be most virulent in winter, it also likes damp, rather than dry weather, which reduces its activity.³¹ Therefore, whether the ensuing climatic changes had a pronounced impact on the emergence and spread of the virus remains an open question, subject to further investigation.

It is equally important to appreciate the impact of climate on the availability of fodder resources and, consequently, the health of bovids. The abnormal weather conditions that prevailed from Summer 1314 until Summer 1316, and characterised by a virtually incessant torrential rain and cold temperatures, depressed hay produce a great deal. Firstly, it made mowing extremely difficult, costly and long. Secondly, in many instances, grass remained unmown, destined to be consumed by water and rot. The consumption of rotten straw and hay can pose a dangerous threat to the health of domesticated animals. Putrefied herbage can easily encourage the activity of parasitic fungi, bacteria, worms and gastropods, which, if ingested, can compromise the health of animals easily. Thirdly, in those instances, when some meadow was mown, it could not be dried easily and converted into hay. To make things worse, however, cattle and other domestic animals also suffered from wet weather and cold temperature. Exposed to colder temperatures and deprived of their fodder resources, they had to waste more energy to maintain body heat. This, in turn, would have lowered their resistance to pathogens and diseases within a short period of time.³² The cold weather and malnourishment, especially in young cattle, would imply harsh, long-term implications for their health and physical growth, chiefly the development of muscles in subadult animals. The period of growth in cattle is significantly shorter than in humans: normally, it takes about eighteen months for calves to develop into physically and sexually mature animals. Therefore, a six-month deprivation and malnutrition in a calf, bullock or a heifer, caused by the cold weather and unavailability of good-quality fodder, is undoubtedly much worse than a year-long deprivation in a subadult human. Thus, young bullocks were more likely to have grown into sterile bulls and weak oxen, while heifers were destined to develop into infertile and aborting cows.

When Rinderpest arrived in Essex in early April 1319, a large proportion of Britain’s cattle were, in fact, the survivors of the 1314–16 crisis. Approximately 87% of local bovine stocks consisted of animals born before the fodder crisis ended in Summer/early Autumn 1316, and about 39% of animals were either born or maturing into their second year of age during the episode of the weather anomaly, between Autumn 1314 and Summer/Early Autumn 1316. The latter figure is inflated to 47% if we add those animals that were in utero between Autumn 1315 and Summer/Early Autumn 1316.

What is important to appreciate is that while the climatic conditions might well have influenced the emergence and the initial activity of the RPV, they cannot, alone, explain its spread. Just as with scab, its dissemination was largely determined by purely anthropogenic factors. As far as the English experience goes, we can identify at least three channels of the pathogen spread. Firstly, we have to account for trade in cattle, which could be conducted on either a local level, with animals being marketed between manorial manager and local tenants, or on a regional level, when one manor could supply another manor, or when live animals were driven to local towns for slaughter and consumption. Secondly, there were intermanorial transfers of cattle, with stock shuffling being a commonplace practice in the late-medieval period. In particular, bulls had to be either castrated or transferred elsewhere after two years of sexually active life to prevent inbreeding. Finally, the ongoing warfare with Scotland was another mode of dissemination. In Summer 1319, Edward II mustered a 10,000-strong army, recruited from different parts of the country, marching to the north.³³ Food provisioning logistics were essential to the viability of the army and large amounts of grain, ale, fish, meat and wine were duly supplied by local sheriffs. In particular, beef played an important role in an English soldier’s diet during the Scottish campaign and live cattle were driven to the Siege of Berwick.³⁴ According to one chronicle, nearly all oxen driven to the Siege of Berwick (8–12 September 1319) suddenly died.³⁵ To make things even worse, Scottish marauders carried large-scale cattle raids in northern England around the same time, driving locally plundered bovids into Scotland. It should be borne in mind that animal husbandry played a crucial role in Scotland’s economy, and cattle rearing was of a particular importance to the well-being of local communities. Furthermore, in the undermonetised economy of Scotland, cattle were regarded not only as a measure of one’s wealth, power and prestige, but also as a universal currency.³⁶

Linked to that, one may add yet another mode of dissemination: summer transhumance, which was an important herding practice in Cymric and Gaelic parts of the British Isles, but also in upland parts of England, and in particularly in the north. The most omnipresent system was shieling, whereby herders would move their livestock from their valley farms into more mountainous areas for grazing for the summer, while spending that season in temporary huts or cottages.³⁷ In theory, the seasonal transhumance would have facilitated physical contacts between cattle and, thus, expose them to the disease. This is especially true given the communal nature of shieling pastoralism. Unfortunately, the impact of the shieling system on the spread of the cattle pestilence is not documented in any surviving source, and should, therefore, remain as a mere hypothesis.

Postfamine health crisis

The torrential rain of 1314–16 initiated what may be regarded the single worst subsistence crisis in European history in the last two millennia: the Great European Famine of 1315–17. The abnormally wet and cold weather ruined three back-to-back harvests of 1315, 1316 and 1317, with composite net crop yields standing at about thirty eight, fifty and twenty six below average. This created an omnipresent shortage of food into famine, and it was not before too long that the shortage was transformed into an acute famine, through a number of anthropogenic and institutional factors, including managerial decisions, failed market performance, grain hoarding, rising transportation costs, deficient storage facilities and ongoing military conflict in Wales and Scotland – to name but a few. Although any attempts to estimate the fall in population are far from being secure, all available evidence hints that England may have lost at least 15% of her population (and most likely in the area of 15%–20%).³⁸

As palaeopathological evidence from the Black Death burials at East Smithfield (London), Hereford Cathedral and recently excavated Chaterhouse (London) demonstrates, it appears that the famine mortality was selective, targeting frailer individuals who were more prone to diseases than their healthier peers. This can be gathered from the fact that the prefamine cohorts tend to exhibit less pathological signs and higher stature than those born after 1317. In other words, the Great Famine weeded out weaker and frailer individuals, while the famine survivors may have been healthier than both famine victims and the postfamine cohort.³⁹ Conversely, the postfamine cohorts (and in particular those born shortly after the famine) exhibit various pathological signs, including shorter stature; enamel hypoplasia (horizontal lines on the enamel of an affected tooth); cribra orbitalia (lesions on orbital roofs); and porotic hyperostosis (lesions on cranial vault bones). As Sharon DeWitte and I have argued elsewhere, these pathologies may have been caused by the chronic shortage of dairy products in the 1320s, in conjunction with the impact of the Great Bovine Pestilence (1319–20), which, as we have seen, killed about 63% of English and Welsh cattle, with mortality rates of cows standing at the overwhelming 80%.⁴⁰

Despite the relatively commercialised nature of the English economy c. 1300, and particularly of its arable sector, livestock markets were comparatively underdeveloped. Cattle trade was confined primarily to a local or regional level, while long-distance trade in livestock was extremely rare. This fact meant that securing large numbers of healthy animals from panzootic-free regions was, more or less, an impossible task and the most obvious strategy to replenish the depleted bovine cohorts was to rely on the biological cycle of reproduction. It was a long and painful process. Oxen were the most important draught animal in the British Isles, and to avoid potential grain scarcity, they had to be replenished first, at the expense of dairy cattle. It was not until the late 1320s that dairy cattle started catching up. All in all, the dairy industries were depressed for at least fifteen years, which had some harsh consequences for human diet and health. In late-medieval England, dairy products constituted the single most important source of protein, calcium and vitamin B12. A long-term deprivation of these nutrients can be devastative for human health. Thus, chronic deficiency of calcium-based products may be reflected in the fact that a larger proportion of individuals born after the famine tended to develop enamel hypoplasia and be of a shorter height. A long-term deprivation of vitamin B12 could have been one of the factors causing higher frequencies of cribra orbitalia and porotic hyperostosis within the same postfamine cohort.

The dairy crisis, however, could be just one contributing factor to the deteriorated health of the postfamine cohort. We also have to bear in mind the possible epigenetic alterations within young famine survivors and their progenies. As some work on later historical famines have shown, prolonged malnourishment (and other extreme environmental shocks) can have some far-reaching epigenetic consequences for those being in utero (especially the first two trimesters), born or growing up into the famine (especially during the so-called ‘Slow Growth Period’ (SGP), between the ages of 8 and 12).⁴¹ Thus, it has been found that malnourishment in those individuals can produce a trigger causing schizophrenic, depression-related and other mental alterations within the epigenome. It has also been established that the same epigenetic alterations compromise the immune system in foetuses and children and make them weaker and more prone to various pathogens and diseases.⁴² To make things even worse, however, famines do not only affect starving populations, but also have transgenerational effects, whereby the same changes in genomic expression continue to be shared by progenies of starving individuals for up to two subsequent generations.⁴³ If the same reasoning can be applied to the Great Famine and its aftermath, then the crisis may indeed have had a long-lasting impact on health of pre-Black Death population, by causing some epigenetic alterations in the generation of ‘famine children’ and potentially their offspring, and making them prone to mental disorders and physical debilitation. This is in addition to the harsh implications of the chronic deficiency of dairy products on the health of the same generation, at least half of which succumbed to the first wave of bubonic plague. Is it coincidental that the Black Death, or at least its first outbreak in the British Isles (1348–50), was so devastating not only because of its biological force, but also because of the biological weakness of its human victims?

Plague of 1348–50 and its recurrent outbreaks

Just like the scab and Rinderpest, plague, too, was an emerging disease. Its first late-medieval outbreak, known as the Black Death, which ravaged Europe between 1347 and 1353, has been a subject of centuries-long scholarly debates and controversies – in particular, in reference to its nature and origins. In 2011, an interdisciplinary team of palaeogeneticists managed to detect, isolate and sequence a complete pathogen genome from dental pulp of skeletons from the East Smithfield Black Death burial in London. The results yielded that the mortality was caused by a strain of Yersinia pestis coccobacillus, the same pathogen responsible for the Third Human Pandemic of the late nineteenth century (and, indeed, for the First Human Pandemic of 541–750).⁴⁴ As of 2021, palaeogenetic analysis of ten fully sequenced from eight Black Death burials (Laishevo (Tatarstan), Saint-Laurent-de-la-Cabrerisse, Toulouse, Barcelona, Sienna, London East Smithfield, Oslo and Nabburg (Bavaria) ) has confirmed the presence of Yersinia pestis, beyond any doubt, putting an end to decades-long scholarly controversies about the nature of the Black Death.⁴⁵

The geographic origins of the Black Death have been another subject of scholarly and scientific controversies, with historians and plague ecologists suggesting China, Central Asia, the Caspian region, the Pontic Steppe and Western Siberia as the original homes of the catastrophe.⁴⁶ Likewise, the timing of the beginning of the Black Death has been, too, debated. In 2013, a team of geneticists managed to reconstruct the phylogenetic tree of Yersinia pestis and identify a major polytomy (aka, the ‘Big Bang’) preceding the Black Death. The authors dated the event to 1142–1339, with the median date of c.1268.⁴⁷ This led some historians to suggest that the late-medieval plague may have commenced in Central Asia in the early thirteenth century, some hundred years before the Black Death.⁴⁸ The ongoing palaeogenetic work, however, will sooner or later answer the question of the spatio-temporal origins of the Black Death in particular and the polytomy in general, and settle these debates.

Although the Black Death is associated, in a popular imagination, with human mortality, its bacterial agent, Yersinia pestis, attacks primarily rodents, rather than humans. Plague outbreaks originate in sylvatic rodent reservoirs, in which bacteria are capable of being present for centuries, if not thousand years. Plague is a complex disease, involving bacteria, vectors and hosts. There are three possible vectors: fleas, ticks and lice. Of these, the most common ones are Oriental rat flea (Xenopsylla cheopis); Human flea (Pulex irritans) feeding on both humans and a variety of mammals; and Human lice (Pediculus humanus capitis), feeding exclusively on humans.⁴⁹ The notion that fleas can transmit the disease only in a blocked state (after sufficient ingestion of the bacillus) has now been dismissed.⁵⁰ Identifying hosts presents an even greater challenge. Although rats have been, for a long time, considered to be the initial host of the disease, recent research has shown that sylvatic ground-burrowing rodents, including native Central Asian marmots, gerbils, and susliks and indigenous European common voles, play a paramount role as initial plague carriers, before the disease crosses over to either commensal rodents (primarily, rats) or directly humans.⁵¹ The time-lag between rodent panzootic and human pandemic is about 19–27 days.⁵²

In theory, Yersinia pestis-caused plague can manifest itself in three forms: bubonic, pneumonic and septicemic. By far, bubonic is the most common type of plague, whose symptoms include painful and swelled lymph nodes (primarily in groin, armpits, upper femoral and neck), chills, headache, fever and weakness. On average, it takes the bacillus 3–5 days to incubate and then one to three days for humans to die.⁵³ Pneumonic plague, infecting the lungs, is a rarer, but deadlier type, with the incubation period of just one to three days. Finally, septicemic plague is the deadliest type, which infects the blood and has a similar incubation length to pneumonic plague. Although it is possible that all three types of plague coexisted during the Black Death outbreak, it should be borne in mind that both pneumonic and septisemic are ‘supplementary’ plagues, and cannot exist independently without the initial presence of bubonic plague. Therefore, it is probable that bubonic plague accounted for at least the majority of deaths during the first outbreak.

Just like Rinderpest, the dissemination path of the plague is incredibly perplexing and still badly understood. It is complicated by the fact that it passed through a number of climatic and bioecological zones, each dictating a different pace and mode of dissemination. Between its outbreaks in Tian-Shan in the later 1330s and its eventual appearance in the Pontic-Caspian region in 1345–6, the plague presumably travelled some 3,000 km along trans-Asian inland trade routes (often referred to as the ‘Silk Roads’). It is equally important to consider the wider bioecological and climatic context to appreciate the timing of the pathogen. As several recent studies have shown, emerging diseases and their recurrent waves tend to break out in very specific environmental contexts.⁵⁴ As dendrochronological record from the Tian-Shan region reveals, the period of c.1325–50 was characterised by a high amplitude of year-to-year summer temperatures. The summers of 1326–8 were both cold and damp weather, with rainfall levels standing at 30% above average in 1327; the precipitation levels were again about the average in 1329–31. These conditions may have created abundant grassland on lowland pastures, encouraging population growth in both vectors (ectoparasites) and hosts (marmots), and facilitating plague activity in existing reservoirs. This phase was followed by a dry and cold event of 1332–4, with 1334 being the second driest year in the fourteenth century, with rainfall levels standing at 34% below average. After a short-lived episode of average rainfall in 1335, there was another damp year (1336), followed by a fall in precipitation in 1337 and an episode of extreme drought, with 1339 being the single driest year of the fourteenth century.⁵⁵ The reversal of climatic conditions towards dry and hot summers in 1337–9 meant decreased availability of biomass for marmots who were now forced to move around seeking fodder, intermingling (and conflicting) with other marmot colonies, thus facilitating the spread of plague. Once plague in marmots reached an epizootic proportions, the plague (and ectoparasites) would cross over to humans.

Once active among humans, the speed of plague dissemination became much faster, certainly with the help of maritime and transportation means. Having traversed some 3,000 km from Tian-Shan to the Black Sea shores, it carried on to Constantinople (May 1347), before arriving in Sicily in the autumn. It entered England, through the port of Melcombe Regis in Dorset in late June 1348, via the sea, from English-controlled Gascony. Later in the summer, the plague was introduced into the ports of Bristol and Southampton. It ravaged southern England in 1348, before spreading to the rest of England and Wales in 1349. In Ireland, the plague is attested along the east coast already in late 1348, where it came from Bristol, before spreading to other parts of the island in 1349. It came to Scotland in late 1349, and ravaged the already frail kingdom, devastated by years of war with England, in 1350.⁵⁶ On average, the pathogen travelled with the speed of about 0.62 miles (=1 kilometres) a day.⁵⁷ As far as England goes, the seasonality of plague mortality was altogether different from that in ‘normal years’. As expected, mortality peaked between June and September, with August deaths accounting for approximately 20% of all annual deaths in 1349.⁵⁸ Yersinia pestis and its vectors are particularly active in warm and especially humid weather. This is in contrast with nonplague years, when mortality peaks occurred in the cold and damp period between December and March.⁵⁹

Just as in the context of its putative Central Asian origins, the plague disseminated in England in the context of a short-term climatic anomaly. As we have seen, the period of c. 1341–54 was marked by exceptionally cold summer weather, with 1348–53 standing out in particular. To make things even worse, the years 1348–51 were also excessively damp.⁶⁰ As English manorial accounts indicate, there was a second incidence of three back-to-back harvest failures, with composite crop yields standing at, approximately, 51%, 60% and 42% below average in 1349, 1350 and 1351, respectively.⁶¹ Although there is no doubt that those abysmally low figures may be partially caused by the widespread harvest labour deficiency, on the account of human mortality, the ability of abnormally bad weather to ruin harvests is a truism that cannot be dismissed. Thanks to excessive deaths, relieving food crisis, England (and indeed other parts of Europe) may have been spared of another ‘Great Famine’.

It would not be an overstatement that the Black Death was the single deadliest pandemic in documented human history, in terms of its absolute morbidity and mortality rates. Current estimates vary, but scholars agree that at least 40%–50% of European population perished in the first outbreak of the plague. The figures obviously varied from place to place. In England proper, estimates vary, depending on interpretations of the total population size on the eve of the plague outbreak. According to one recent estimate, England’s population declined from 4.8 to 2.6 million people between 1348 and 1351, namely by some 46%.⁶² This, however, seems to have been an under-estimate. For instance, tenant mortality on the estates of Winchester Bishopric in south England amounted to well over 70%.⁶³ Similarly high losses are reported on the estates of Glastonbury Abbey and Titchfield Abbey in south England.⁶⁴ On the estates of Durham Cathedral Priory, the corresponding figure is about 48%.⁶⁵ The total sample of eighty-six manors yields the cumulative mortality rates of about 62.7%, deriving from the deaths of 3,434 out of the total 5,476 male tenants, between c. 1348 and 1350.⁶⁶ Although these statistics do not account for female tenants and children, and they cover only a very small fraction of the English population, they still indicate that England seems to have lost well over half of its population: possibly in the area of 60%. After all, rural inhabitants accounted for about 85% of the total population and, consequently, they bore the heaviest share within the total population loss. If this interpretation is correct, then it corroborates with higher estimates of preplague population, proposed by some scholars to have been somewhere between five and six million people.⁶⁷

Urban settlements are said to suffer heavy losses, too. In London, home to some 60,000–70,000 people, the plague ravaged for fifteen months, between November 1348 and February 1350, killing at least half of its population, of which about 14,000 people are said to have died between early February and mid-April 1349 alone.⁶⁸ Other towns, including Norwich, Great Yarmouth, Canterbury, Leicester, Lincoln and Colchester, too, lost over half of their preplague population.⁶⁹ Mortality rates were almost as high among parish priests (45%) and monastic communities (43%).⁷⁰ The former worked among lay people, including plague-infected individuals, while the latter resided in cloistered communities. In either scenario, a close contact with potentially infected people would facilitate an easy pathogen transmission and, thus, high mortality rates. Higher social echelons were faring better, on the account of their ability to segregate themselves from the wider world. Thus, the respective mortality rates among bishops and royal tenants-in-chief amounted to 18% and 27%.⁷¹

Did the Black Death kill indiscriminately across genders and age groups? In nonepidemic years, testosterone reduces the resistance to pathogens, while oestrogen, by contrary, increases it, which explains why men are normally frailer than women. But this rule may or may not have worked in the context of the plague and the available evidence is incredibly contradictory. To begin with, sex ratios from different skeletal assemblages vary from place to place. Thus, at East Smithfield, adult female skeletons accounted for 40% of the total assemblage of sexed adult skeletons, while at Hereford Cathedral and Dreux (north-western France), the respective figures stood at 56% and 58%, respectively.⁷² The preponderance of one sex does not, however, mean that the same sex was at a higher risk of mortality than the other. As Sharon DeWitte has established, applying the biostatistical Gompertz Model of mortality, there is no evidence that the Black Death was sex-selective.⁷³ Likewise, Castex and Kacki concluded that the sheer number of sexed skeletons at both Hereford and Dreux was too small to be reflective of the Black Death sex-selectivity.⁷⁴ Conversely, Daniel Curtis and Joris Roosen’s work on plague mortality in Hainault (Belgium), based on the analysis of death duties (‘mortmains’), found that the Black Death and the recurrent outbreaks tended to kill higher proportions of women than in noncrisis years. Here, the sex ratio in mortality stood at 0.89:1.00 during the 1349–50 outbreak and 0.94:1.00 during recurrent plague waves – in contrast with 1.07:1.00 for nonplague years.⁷⁵ Similarly, the sex-ratio analysis of thirteenth- and fourteenth-century East Syriac (Nestorian) burials in Kara-Djigach (the Tian-Shan region in North Kyrgyzstan) has established that women were far more susceptible during the 1338–9 plague outbreak than men.⁷⁶ Although it is possible that the contradiction between these sets of data may have something to do with regional differences, much new work, based on fresh archival and skeletal data alike, needs to be done, to solve this conundrum.

Likewise, DeWitte and her colleagues have established that the plague targeted frailer individuals of all age groups.⁷⁷ This is hardly surprising, given the prolonged food and health crisis in England, stretching far beyond the famine years of 1315–17. As we have seen, the famine- and postfamine cohorts, growing up during the famine or dairy deficiency crisis of the 1320s, tended to exhibit more pathological signs than the prefamine cohort and, as such, were more likely to be killed by the plague.⁷⁸ Likewise, mortality risk rose with age, with older individuals being at an elevated risk of mortality than their younger counterparts.⁷⁹ In other words, those individuals born in the 1290s who survived the Great Famine were more likely to die than individuals born in the 1330s after the end of dairy deficiency crisis. At the same time, however, those born or growing between c. 1315 and 1330, who suffered episodes of malnourishment and exhibiting various pathological signs (including cribra orbitalia and porotic hyperostosis), were similarly more likely to die than those born after c. 1330.

The pestis secunda of 1361–62

Despite the remarkable and transdisciplinary progress in the study of the Black Death, the second outbreak of the plague pandemic (1361–62) remains badly understudied, notwithstanding its harsh implications. This is largely due to the fact that historians and scientists alike tend to devote disproportionate attention to initial outbreaks of emerging diseases, often ignoring their recurrent waves. Indeed, the phenomenon of the disease recurrence is still largely under-appreciated in both historical and scientific literature.

The geography of the origins and spread of the pestis secunda differed considerably from that of the previous wave, namely the Black Death. As a recent study has shown, it originated in a woodland reservoir in South-Central Germany (possibly in the Dreieich forest around Frankfurt-am-Main), which seemed to have been seeded there during the Black Death outbreak in summer 1349. As all the available evidence points out, the pestis secunda broke out in late summer 1356 in southern Hesse. It is unclear what rodents were its initial carriers, before it crossed over to humans, although the common vole seems to have been the most likely candidate, given its proliferation in that region.⁸⁰ From Hesse, the plague spread all over the German Empire in 1357–8, before spreading in all four directions between 1358 and 1366. It arrived in London, the first place to be infected in England, in March 1361, seemingly from English-controlled Gascony (just as the Black Death thirteen years earlier). This was undoubtedly facilitated by Anglo-French trade and the presence of English garrisons and administration in Gascony. The plague ravaged the city until at least August, concurrently penetrating into the metropolitan hinterland. The plague is attested in the East Midlands and East Anglia in late summer; by October it reached as far as eastern Wales, via the West Country and the West Midlands, and around the same time, it crossed the Humber in the north. By early 1362, it arrived in the Anglo-Scottish borders (Cumberland in the west and Northumberland in the east), before carrying on to lowland Scotland.⁸¹

Just as the Black Death, the pestis secunda seems to have originated in very particular climatic circumstances. According to dendrochronological evidence from Central Germany, it appears that the 1356 outbreak was preceded by hot and dry summers of 1353 and 1354, which could be potentially beneficial for good masting, and excessively wet summers of 1355 and 1356, potentially favourable for grass abundance. There were also three back-to-back cold and snowy winters of 1353/4, 1354/5 and 1355/6, which may have been good for burrow insulation and consequently, winter survival of sylvatic rodents, such as voles.⁸² Taking together, the availability of both tree mast and grass biomass, as well as burrow insulation, may have encouraged the vole population growth (and eventual outbreak) in Hessian woodland, on the eve of the pestis secunda outbreak. The multitude of rodents (eventually succumbing and dying en mass) has often been seen as an omen of plague outbreak in humans by nomadic communities in Central Asia, as data from early Soviet Kazakhstan and Kyrgyzstan suggests.⁸³ Moreover, the wet summers of 1355 and 1356 could also present optimal conditions for the hatching and survival of flea larvae, which is equally crucial to the outbreak and spread of plague, first in rodents and later in humans.⁸⁴

Recent palaeogenetic work has advanced our knowledge regarding the genetic peculiarities of the pestis secunda. So far, four genomes from three pestis secunda burials (St Mary Graces, London; Bergen-op-Zoom, Netherlands; and Bolghar City, Tatarstan) have been sequenced. As the palaeogenomic sequencing indicates, although the pestis secunda genomes are related to the Black Death ones (and the subsequent Second Plague Pandemic ones), they also differed in their genetic signature. In fact, they were the product of the post-Black Death split of Branch 1 into two sub-lineages: Branch 1A and Branch 1B.⁸⁵ All the sequenced pestis secunda genomes belong to Branch 1B, which has been attested, so far, only in the pestis secunda genomes (with all the subsequent Second Plague Pandemic genomes belonging to Branch 1A). It is possible that Branch 1B radiated out of or entirely left its Central German reservoir (and indeed the continent) shortly after the pestis secunda and migrated eastwards, to break out again, at a much later stage, during the Third Human Pandemic, which commenced in the Yunnan province of China in 1855.⁸⁶ The almost concurrent processes of the establishment of the Central German reservoir and the split within Branch 1 are separate (and highly complicated) topics, which cannot be dealt with in the present study.

The estimates of demographic losses are currently few, but all the available research indicates that the second plague outbreak killed about 10%–20% of England’s population, making it the second deadliest mortality crisis of the last millennium. According to some written narratives, the pestis secunda outbreak was more discriminative than the previous one: several chroniclers describe it as ‘the plague of children, men and nobles’.⁸⁷ Indeed, it killed almost one-fourth of the English nobility.⁸⁸ The mortality of parish clergy varied from parish to parish, varying between the average of 30% in Winchester Diocese and 14% in York Diocese.⁸⁹ Likewise, demographic losses among manorial tenants varied from place to place. Thus, in Bishop’s Waltham (Hampshire) and Halesowen (on the Shropshire-Worcestershire border), the population of male tenants declined by just under 15%.⁹⁰ The communities of Great Waltham and High Easter (both in Essex) seem to have gotten away with lighter losses, standing at below 10%.⁹¹ On the other hand, several Hampshire and Wiltshire manors of Winchester Bishopric appear to have been hit as severely as during the first outbreak.⁹² A preliminary survey of the surviving manorial court rolls from over 70 English manors, recording heriot payments (entry fines paid by unfree tenants, usually upon the death of deceased relatives), indicates that the excess mortality ratio between the pestis secunda and the non-plague years during the 1355–65 period was about 8:1.⁹³ If we were to take 3% as ‘normal’ annual mortality rates, then the mortality rates of unfree tenants may have stood around 20%–25%.⁹⁴ Similarly, in London, mortality rates seem to have stood at about 20%.⁹⁵

Was the pestis secunda sex-selective, killing more men than women, as some chroniclers suggest? At this stage, the available evidence is ambiguous. On the one hand, the sudden surge of land inheritance applications by female tenants after the deaths of their male relatives may indeed indicate that. As Mullan’s study of the situation on Winchester Bishopric manors reveals, in 1361–2, female inheritance accounted for as much as 61% of the total inheritance, in contrast with 37% during the first outbreak and 40% in 1351–60.⁹⁶ This is partially corroborated by the skeletal evidence from St Mary Graces, where adult male skeletons accounted for 53% of the total sexed adult sample (110 in total).⁹⁷ On the other hand, just as with the first outbreak, this does not mean that men were more susceptible than women. As DeWitte has shown, using the Gompertz model of mortality, there was no significant difference in risk of mortality between men and women during the 1361–2 outbreak at St Mary Graces.⁹⁸

Skeletal evidence from the 1361–2 outbreak may partially support the chroniclers’ statement that it was ‘the plague of the children’. At St Mary Graces, the combined proportion of infants and child aged 10 and less accounted for about 23%, which was indeed higher than 17% at the 1349–50 burial at East Smithfield and 13% in fifteenth-century non-plague burials at St Mary Graces.⁹⁹ The proportion of children could, in theory, be even higher, given that child skeletons are more fragile and, thus, more prone to destruction than the adult ones. The skeletal data, when conjoined with chronicle evidence, reflects the fact that children, born in the ‘inter-plague’ decade of the 1350s, constituted a substantial proportion within the total population and, thus, among the plague victims: certainly higher than during the first outbreak. But just as with the first outbreak, the risk of death increased with adult age: that is, older adults were more likely to die than the younger ones.¹⁰⁰ And similarly to the 1348–50 wave, frailer adults were more prone to mortality than the healthier ones.¹⁰¹

Even though the pestis secunda was, in demographic terms, less destructive than the first outbreak, its consequences were by far more enduring. It was this outbreak that made a huge demographic difference, by wiping out the temporary surge in fertility of the inter-plague decade of the 1350s, and setting the stage for a new demographic regime, marked by low fertility and high mortality. With the massive deaths of young and immunologically ‘naïve’ population, born after the first outbreak and thus lacking any immunity to plague, the reproductive ability of England (and indeed other parts of Eurasia and Africa) was depressed for many decades to come. All at sudden, England shifted from ‘bottom-heavy’ to ‘top-heavy’ demographic regime, characterised by a relatively large proportion of older people and low fertility. Without a sufficient share of young people, England was doomed for a long-term demographic stagnation and decline, going on for about a hundred years. According to one recent estimate, the population of England declined from about 2.5 million in 1377 to about 2 million in 1400, remaining more or less stagnant until the late fifteenth century.¹⁰² This gloomy demographic behaviour was determined not only by low fertility, but also by high mortality. After three additional ‘national’ outbreaks of 1368–70, 1373–7, 1382–3, 1389–91, 1398–1400 and 1403–7, England was visited by a series of more localised waves in the course of the fifteenth century. As of now, no systematic research has been undertaken to study the scale and impact of these outbreaks, which would be instrumental in improving our current knowledge about the changing demographic, economic and social landscape in late-medieval England and elsewhere. After all, the decline and demise of centuries-old systems of feudalism, manorialism and serfdom, the rise in real wages and living standards of commoners and the appearance of a more consumerist culture cannot be understood, unless studied against the context and impact of the ongoing disease. It was the 1361–2 outbreak, rather than the 1348–50 one that set the stage for all these profound changes.

Conclusions

The period of c. 1275–348 was truly unique in the sense that it witnessed the emergence of no less than three emerging diseases on a panzootic/pandemic scale. These emerging diseases, with their recurrent outbreaks, claimed millions of human and animal lives in England (and indeed elsewhere) and were one of the triggers of what Bruce Campbell has aptly called ‘the Great Transition’ of the late medieval world. The outbreaks have profoundly altered the complex interactions between climatic, ecobiological and genetic contexts, which, in turn, changed the existing demographic and socioeconomic order for good.

Emerging diseases is one of the most complex and pressing topics that not only historians and medicine and health but also scientists and policy makers are struggling with. While some diseases have disappeared, others such as Swine influenza (2009) and Ebola (2014–16) have recently emerged, claiming approximately 284,500 and 11,310 human lives so far, respectively.¹⁰³ Both disease, however, pale in comparison to recently emerging COVID-19. As of August 2021, it killed 4.2 million people and infected almost 200 million people worldwide, since its beginning in late 2019.¹⁰⁴ Many of the characteristics of emerging diseases remain poorly understood. Even worse understood is the phenomenon of their recurrence. To be able to respond to or even prevent future emerging diseases and their recurrent outbreaks, we need a better understanding of their determinants and dynamics in a long-run historical context. The late-medieval period represents an ideal ‘lab’, which allows us to study the same determinants and dynamics, thanks to the remarkable abundance of source material, both written and palaeoscientific.

Pathogens do not appear out of nowhere. As we have seen, England, and indeed the rest of Europe and beyond, entered the ‘age of pathogens’, marked by the appearance of emergent diseases, their recurrent outbreaks and high mortality regime, in a very turbulent bioecological and climatic context. The transitional period from the Medieval Climate Anomaly to the Little Ice Age was characterised by a high degree of instability and piecemeal deterioration, causing climatic and biological shocks. These conditions would be highly unfavourable for human and animal health, yet highly favourable for pathogen activity. The frail health preconditions in hosts and aggressive behaviour of pathogens and vectors was that killer combination that set the stage for the emergence and recurrence of new diseases. Although local climatic conditions are vitally important, they did not exist in isolation: rather, they formed a part of a much wider and complex global climatic regime. In the case of Rinderpest and plague, these were global diseases, originating in Central Eurasia, in specific bioclimatic contexts. We cannot understand how these diseases ended up in Western Europe, unless we consider their initial outbreak in the context of climatic and ecological shifts in their original loci. As Monica Green has stated, it is time now to treat the Black Death as a global disease in a global context.¹⁰⁵ Much the same can be said of other pandemics and panzootics.

Although various exogenous factors played an enormous role in initiating the emergence of new pandemics and panzootics and their recurrent waves, they cannot account for their dissemination, while blaming everything on nature means to fall into the trap of environmentalist reductionism and determinism. It is essential to analyse various anthropogenic and institutional aspects that were instrumental in spreading pathogens. Thus, trade, which implied the movement of people, animals and goods, played an enormous role in spreading all three diseases under study. In the case of scab and Rinderpest, livestock management was another factor encouraging the spread of the panzootics. Ongoing military conflicts, too, should be taken into account. When Edward II’s army was marching northward to the Siege of Berwick (August-September 1319), it was carrying not only soldiers and arms, but also infected cattle. Just as with famines and other disasters, diseases, too, cannot be understood through a singular prism of either nature or anthropogenics. Only when both exogenous and endogenous factors are considered together can we understand the incredible complexity of the origins, spread and impact of emerging diseases.

Notes

1. See, for instance, Tamara Ben Ari, Simon Neerinckx, Kenneth L. Gage, Katharina Kreppel, Anne Laudisoit, Herwig Leirs, and Nils Chr. Stenseth, ‘Plague and Climate: Scales Matter,’ PLOS Pathogens, 8 (2012), http://doi.org/10.1371/journal.ppat.1002160; Boris Schmid, Ulf Büntgen, W. Ryan Easterday, Christian Ginzler, Lars Walløe, Barbara Bramanti, and Nils Chr. Stenseth, ‘Climate-Driven Boris Introduction of the Black Death and Successive Plague Reintroductions into Europe,’ PNAS, 12 (2015), pp. 3020–5; Bruce M.S. Campbell, The Great Transition: Climate, Disease and Society in the Late Medieval World (Cambridge: Cambridge University Press, 2016), pp. 209–331, Kathleen Pribyl, Farming, Famine and Plague. The Impact of Climate in Late Medieval England (Berlin: Springer, 2017), and most recently Philip Slavin, ‘Out of the West: Formation of a Permanent Plague Reservoir in South-Central Germany (1349-1356) and Its Implications’, Past & Present 252 (August 2021), pp. 3–51.

2. Timothy Newfield, ‘A Cattle Panzootic in Early Fourteenth-Century Europe,’ Agricultural History Review, 57 (2009), pp. 176–7; Philip Slavin, ‘The Great Bovine Pestilence and Its Economic and Environmental Consequences in England and Wales, 1318–50,’ Economic History Review, 65 (2012), p. 1246; Philip Slavin, Experiencing Famine in Fourteenth-Century Britain (Turnhout: Brepols, 2019), pp. 357-63.

3. Philip Slavin, ‘Death by the Lake: Mortality Crisis in Early Fourteenth-Century Central Asia’, Journal of Interdisciplinary History 50 (2019), pp. 70-5; Slavin, ‘Out of the West

4. A.G. Dawson, K. Hickey, P.A. Mayewski, and A. Nesje, ‘Greenland (GISP2) Ice Core and Historical Indicators of Complex North Atlantic Climate Changes during the Fourteenth Century,’ Holocene, 17 (2007), pp. 427–34; Philip Slavin, ‘The 1310s Event’, in Palgrave Handbook of Climate History, eds. Christian Pfister, Franz Mauelshagen and Sam White (London: Palgrave Macmillan, 2018), pp. 95-7; Slavin, Experiencing Famine, pp. 13-4

5. Clive Oppenheimer, Eruptions that Shook the World (Cambridge: Cambridge University Press, 2011), pp. 263–7.

6. Raimund Muscheler, Fortunat Joos, Jürg Beer, Simon A. Müller, Maura Vonmoos, and Ian Snowball, ‘Solar Activity during the Last 1000 yr Inferred from Radionuclide Record,’ Quaternary Science Reviews, 26 (2007), p. 82–97.

7. Bruce M.S. Campbell, ‘Panzootics, Pandemics and Climatic Anomalies in the Fourteenth Century,’ in Berndt Herrmann (ed.), Beiträge zum Göttinger Umwelthistorischen Kolloquium 2010 – 2011 (Göttingen: Universitätsverlag Göttingen, 2011), p. 186.

8. Dawson et al., ‘Greenland (GISP2) Ice,’ p. 431.

9. David Griffiths, ‘Medieval Coastal Sand Inundation in Britain and Ireland,’ Medieval Archaeology, 59 (2015), pp. 103–21.

10. Campbell, Great Transition, pp. 337–9.

11. Calculated from Campbell, Bruce M.S. Campbell, Three Centuries of English Crops Yields, 1211-1491 (http://www.cropyields.ac.uk) (accessed July 2017).

12. Richard Oram and W. Paul Adderley, ‘Lordship and Environmental Change in Central Highland Scotland c. 1300–c. 1400,’ Journal of the North Atlantic, 1 (2008), p. 79.

13. Philip Slavin, ‘Experiencing Famine in Fourteenth-Century Britain’ (Turnhout: Brepols, 2019), pp. 59–67.

14. P. Bates, ‘Sheep Scab (Psoroptes ovis),’ in I.D. Aitken (ed.), Diseases of Sheep (Fourth Edition) (Oxford: Oxford University Press, 2007), pp. 321–5.

15. R.L. Coop, I. Barger, and F. Jackson, ‘The Use of Macrocyclic Lactones to Control Parasites of Sheep and Goats,’ in J. Vercruysse, and R.S. Rew (eds.), Macrocyclic Lactones in Antiparasitic Therapy (Wallingford: Cab International, 2002), pp. 303–21.

16. Timothy P. Newfield, ‘Early Medieval Epizootics and Landscapes of Disease: The Origins and Triggers of European Livestock Pestilences, 400-1000 CE’, in Sunhild Kleingärtner, Timothy P. Newfield, Sebastien Rossignol, and Donat Wehner (eds.), Landscapes and Societies in Medieval Europe East of the Elbe: Interactions between Environmental Settings and Cultural Transformations (Toronto: Pontifical Institute of Medieval Studies, 2013), pp. 79–84.

17. Philip Slavin, ‘Flogging a Dead Cow: Coping with Animal Panzootics on the Eve of the Black Death,’ in Alex Brown, Andy Burn and Rob Doherty (eds.), Crises in Economic and Social History: A Comparative Perspective (Woodbridge: Boydell and Brewer, 2015), p. 115.

18. Philip Slavin, ‘Landscapes of Panzootics: Sheep Scab and Rural Environment in England in 1279-1280,’ Landscapes, 17 (2016), pp. 156–70; Philip Slavin, ‘‘Mites and Merchants: The Crisis of English Wool and Textile Trade Revisited, c.1275-1330,’ Economic History Review 73 (2020), 885-913

19. Charles E. Britton, A Meteorological Chronology to AD 1450 (London: Meteorological Office, 1937), pp. 115–9.

20. R.J. Cooper, et al. 2012, East Anglia 1,100 Year Spring-Summer Precipitation Reconstruction, IGBP PAGES/World Data Center for Paleoclimatology Data Contribution Series # 2012-043. NOAA/NCDC Paleoclimatology Program, Boulder CO, USA (https://www.ncdc.noaa.gov/paleo/study/12896) (accessed July 2017); R. Wilson, et al., Southern-Central England 1000 Year March-July Precipitation Reconstruction, IGBP PAGES/World Data Center for Paleoclimatology Data Contribution Series # 2012-054. NOAA/NCDC Paleoclimatology Program, Boulder CO, USA (https://www.ncdc.noaa.gov/paleo/study/12907) (accessed July 2017).

21. Slavin, ‘Landscapes of Panzootics,’ p. 159.

22. John H. Munro, ‘The Symbiosis of Towns and Textiles: Urban Institutions and the Changing Fortunes of Cloth Manufacturing in the Low Countries and England, 1270-1570,’ The Journal of Early Modern History: Contacts, Comparisons, Contrasts, 3 (1999), pp. 1–74.

23. Slavin, ‘Flogging a Dead Cow,’ pp. 123–5.

24. Newfield, ‘Cattle Panzootic,’ pp. 155–90; Slavin, ‘Great Bovine Pestilence,’ pp. 1239–66.

25. Wendy R. Childs (ed. and trsl.), Vita Edwardi Secundi (Oxford: Oxford University Press, 2005), pp. 162–7.

26. T.U. Obi, P.L. Roeder, and W.A. Geering, Manual on the Preparation of Rinderpest Contingency Plans (Rome: Food and Agriculture Organization of the United Nations, 1999), p. 6; J. Anderson and Gordon Scott, Manual on the Diagnosis of Rinderpest (Rome: Food and Agriculture Organization of the United Nations, 1996), p. 7.

27. Slavin, ‘Great Bovine Pestilence,’ pp. 1247–8.

28. Newfield, ‘Cattle Panzootic,’ pp. 159–63.

29. Campbell, ‘Panzootics, Pandemics,’ pp. 186–9, 192, 196, 199; R. D’Arrigo, G. Jacoby, D. Frank, N. Pederson, E. Cook, B. Buckley, B. Nachin, R. Mijiddorj, and Ch. Dugarjav., ‘1738 Years of Mongolian Temperature Variability Inferred from a Tree-Ring Width Chronology of Siberian Pine,’ Geophysical Research Letters, 28 (2001), pp. 543–6; Max Berkelhammer, Ashish Sinha, Manfred Mudelsee, Hai Cheng, Lawrence Edwards, and Kevin Cannariato, ‘Persistent Multidecadal Power of the Indian Summer Monsoon,’ Earth and Planetary Science Letters, 290 (2010), 166–172; Ashish Sinha, Lowell Stott, Max Berkelhammer, Hai Cheng, R. Lawrence Edwards, Brendan Buckley, Mark Aldenderfer, and Manfred Mudelsee, ‘A Global Context for Megadroughts in Monsoon Asia during the Past Millennium,’ Quaternary Science Reviews, 30 (2011), pp. 47–62.

30. Campbell, Great Transition, pp. 215–20.

31. Clive Spinage, Cattle Plague: A History (New York: Kluwer Academic, 2003), p. 19.

32. Timothy Newfield, A Great Destruction of Cattle: The Impact and Extent of Epizootic Disease in Early Fourteenth-Century Northwestern Europe (unpublished MA thesis, University of Toronto, 2005), p. 64.

33. Seymour Phillips, Edward II (New Haven, CT: Yale University Press, 2010, pp. 342–5.

34. Michael Prestwich, ‘Victualling Estimates for English Garrisons in Scotland during the Early Fourteenth Century,’ English Historical Review, 82:324 (1967), pp. 536–43.

35. Vivian H. Galbraith, ‘Extracts from the Historia Aurea and a French ‘Brut’ (1317-47),’ English Historical Review, 43 (1928), p. 210.

36. Philip Slavin, ‘Warfare and Ecological Destruction in Early Fourteenth-Century British Isles,’ Environmental History, 19 (2014), p. 536.

37. Richard C. Hoffmann, An Environmental History of Medieval Europe (Cambridge: Cambridge University Press, 2014), p. 175.

38. Slavin, Experiencing Famine, Chapter 7.

39. Philip Slavin and Sharon DeWitte, ‘Between Famine and Death. Physiological Stress and Dairy Deficiency in England on the Eve of the Black Death (1315–50): New Evidence from Paleoepidemiology and Manorial Accounts,’ Journal of Interdisciplinary History, 44 (2013), pp. 37–60; Sacha Kacki, Influence de l’état sanitaire des populations anciennes sur la mortalité en temps de peste. Contribution à la paléoépidémiologie (unpublished doctoral thesis, University of Bordeuax, 2016), pp. 286–7; Sam Pfizenmaier (ed.), Charterhouse Square: Black Death Cemetery and Carthusian Monastery, Meat Market and Suburb (London: Museum of London Archaeology, 2016), pp. 132–3.

40. Slavin and DeWitte, ‘Between Famine and Death’.

41. Gunnar Kaati, Lars Olov Bygren, Marcus Pembrey, and Michael Sjöström, ‘Transgenerational Response to Nutrition, Early Life Circumstances and Longevity,’ European Journal of Human Genetics, 15 (2007), pp. 784–90.

42. Mervyn Susser and Zena Stein, ‘Timing in Prenatal Nutrition: A Reprise of the Dutch Famine Study,’ Nutrition Reviews, 52 (1994), pp. 84–94; Ezra Susser, Richard Neugebauer, Hans W. Hoek, Alan S. Brown, Shang Lin, Daniel Labovitz, and Jack M. Gorman, ‘Schizophrenia after Prenatal Famine,’ Archives of General Psychiatry, 53 (1996), 25–31; Bastiaan T. Heijmans, Elmar W. Tobi, Aryeh D. Stein, Hein Putter, Gerard J. Blauw, Ezra S. Susser, e P. Eline Slagboom, and L. H. Lumey ‘Persistent Epigenetic Differences Associated with Prenatal Exposure to Famine,’ PNAS, 105 (2008), pp. 17046–9; Oonagh Walsh, Insanity, Power and Politics in Nineteenth-Century Ireland: The Connaught District Lunatic Asylum (Manchester: Manchester University Press, 2013).

43. Marjolein V.E. Veenendaal, Rebecca C. Painter, Susanne R. de Rooij, Patrick M.M. Bossuyt, Joris A.M. van der Post, Peter D. Gluckman, Mark A. Hanson, and Tessa J. Roseboom, ‘Transgenerational Effects of Prenatal Exposure to the 1944-45 Dutch Famine,’ in Marjolein Veenendaal (ed.), The Fetal Origins of Adult Disease, the Evidence and Mechanisms (Rotterdam: Legatron Electronic Publishing, 2012), pp. 96–104.

44. Kirsten I. Bos, Verena J. Schuenemann, G. Brian Golding, Hernán A. Burbano, Nicholas Waglechner, Brian K. Coombes, Joseph B. McPhee, Sharon N. DeWitte, Matthias Meyer, Sarah Schmedes, James Wood, David J.D. Earn, D. Ann Herring, Peter Bauer, Hendrik N. Poinar, and Johannes Krause, ‘A Draft Genome of Yersinia pestis from Victims of the Black Death,’ Nature, 478:7370 (2011), pp. 506–10; Marcel Keller, Maria A. Spyrou, Christiana L. Scheib, Gunnar U. Neumann, Andreas Kröpelin, Brigitte Haas-Gebhard, Bernd Päffgen, Jochen Haberstroh, Albert Ribera i Lacomba, Claude Raynaud, Craig Cessford, Raphaël Durand, Peter Stadler, Kathrin Nägele, Jessica S. Bates, Bernd Trautmann, Sarah A. Inskip, Joris Peters, John E. Robb, Toomas Kivisild, Dominique Castex, Michael McCormick, Kirsten I. Bos, Michaela Harbeck, Alexander Herbig, and Johannes Krause, ‘Ancient Yersinia Pestis Genomes from across Western Europe Reveal Early Diversification during the First Pandemic (541–750),’ Proceedings of the National Academy of Sciences 116, no. 25 (June 4, 2019): 12363–72. doi:10.1073/pnas.1820447116.

45. Bos et al., ‘Draft Genome’; Maria A. Spyrou, Rezeda I. Tukhbatova, Michal Feldman, Joanna Drath, Sacha Kacki, Julia Beltrán de Heredia, Susanne Arnold, Airat G. Sitdikov, Dominique Castex, Joachim Wahl, Ilgizar R. Gazimzyanov, Danis K. Nurgaliev, Alexander Herbig, Kirsten I. Bos, and Johannes Krause, ‘Historical Y. pestis Genomes Reveal the European Black Death as the Source of Ancient and Modern Plague Pandemics,’ Cell Host and Microbe, 19 (2016), pp. 874–81; Amine Namouchi, Meriam Guellil, Oliver Kersten, Stephanie Hänsch, Claudio Ottoni, Boris V. Schmid, Elsa Pacciani, et al. “Integrative Approach Using Yersinia Pestis Genomes to Revisit the Historical Landscape of Plague during the Medieval Period.” Proceedings of the National Academy of Sciences 115, no. 50 (November 26, 2018): E11790–97. doi:10.1073/pnas.1812865115.Maria A. Spyrou, Marcel Keller, Rezeda I. Tukhbatova, Christiana L. Scheib, Elizabeth A. Nelson, Aida Andrades Valtueña, Gunnar U. Neumann, et al. “Phylogeography of the Second Plague Pandemic Revealed through Analysis of Historical Yersinia pestis Genomes.” Nature Communications 10, no. 1 (October 2, 2019). doi:10.1038/s41467-019-12154-0.

46. For the Chinese origin hypothesis, see: Justus Friedrich Carl Hecker, Der schwarze Tod im vierzehnten Jahrhundert: Nach den Quellen für Ärzte und gebildete Nichtärzte bearbeitet (Berlin: Herbig, 1832): pp. 15, 26; Francis Aidan Gasquet, The Great Pestilence (A.D. 1348-9), Now Commonly Known as the Black Death (London: Simpkin Marshall, 1893), p. 4; William McNeill, Plagues and Peoples (New York: Anchor Books, 1976), p. 43; M.l.W. Dols, The Black Death in the Middle East (Princeton, 1977), pp. 35-8; U. Schamiloglu, “The End of Volga Bulgarian,” Varia Eurasiatica. Festschrift für Professor András Róna Tas. (Szeged, 1991), pp. 159-62; U. Schamiloglu, "Preliminary remarks on the Role of Disease in the History of the Golden Horde," Central Asian Survey 12 (1993), p. 448; R. Hymes, ‘A Hypothesis on the East Asian beginnings of the Yersinia pestis polytomy’, The Medieval Globe 1 (2014), pp. 285-308; Campbell, Great Transition, pp. 246–247. The Central Asian theory has been advanced by D. Chwolson, "Syrisch-Nestorianische Grabinschriften aus Semirjetschie," Memoires de l’Académie Impériale des Sciences de St. Petersbourg 37 (1890), p. 33; Wu Lien-teh, ‘The Original Home of Plague,’ in A. L. Hoops and J. W. Scharff, eds., Far Eastern Association of Tropical Medicine, Transactions of the Fifth Biennial Congress Held at Singapore, 1923 (London, 1924), p. 301; John Stewart, Nestorian Missionary Enterprise: The Story of a Church on Fire (Edinburgh, 1928), p. 209; G.P. Kalina, Chuma v Sredney Azii (Arkhangelsk, 1936), pp. 9-10; R. Pollitzer, Plague (Geneva, 1954), p. 14; Dols, Black Death, pp. 35-8 (as another possibility in addition to the ‘Chinese origin’ theory); Philip Slavin, ‘Death by the Lake: Mortality Crisis in Early Fourteenth-Century Central Asia’, Journal of Interdisciplinary History 50 (2019), pp. 82-7; M. H. Green, ‘Four Black Deaths’, American Historical Review 125 (2020), pp. 1601-31; Nahyan Fancy and Monica H. Green, 'Plague and the Fall of Baghdad (1258),' Medical History 65 (2021), 157-177. The Caspian hypothesis has been in J. Norris, ‘East or West? The Geographic Origin of the Black Death’, Bulletin of the History of Medicine 51 (1977), pp. 10-11. The Pontic origin theory has been advanced by Ole J. Benedictow, The Complete History of the Black Death (Woodbridge: The Boydell Press, 2021), pp. 137-44. The Western Siberian hypothesis has been proposed (together with the Central Asian one) in Slavin, ‘Death by the Lake,’ pp. 86-7.

47. Y. Cui, C. Yu, Y. Yan, D. Li, Y. Li, T. Jombart, L.A. Weinert, Z. Wang, Z. Guo, L. Xu, Y. Zhang, H. Zheng, N. Qin, X. Xiao, M. Wu, X. Wang, D. Zhou, Z. Qi, Z. Du, H. Wu, X. Yang, H. Cao, H. Wang, J. Wang, S. Yao, A. Rakin, Y. Li, D. Falush, F. Balloux, M. Achtman, Y. Song, J. Wang, and R. Yang, ‘Historical Variations in Mutation Rate in an Epidemic Pathogen, Yersinia pestis,’ PNAS, 110:2 (2013), pp. 577–82.

48. Hymes, ‘Hypothesis,’ pp. 285-308; Green, ‘Four Black Deaths,’ pp. 1615-6 and 1620; Fancy and Green, 'Plague and the Fall of Baghdad

49. M. Drancourt and D. Raoult, ‘Molecular History of Plague,’ Clinical Microbiology and Infection, 22 (2016), pp. 911–5.

50. R.J. Eisen, D.T. Dennis, and K.L Gage, ‘The Role of Early-Phase Transmission in the Spread of Yersinia pestis,’ Journal of Medical Entomology, 52 (2015), pp. 1183–92.

51. K.L. Gage and M.Y. Kosoy, ‘Natural History of Plague: Perspectives from More Than a Century of Research,’ Annual Review of Entomology, 50 (2005), pp. 505–28; Pribyl, Farming, Famine and Plague.

52. Ole J. Benedictow, What Disease was Plague? On the Controversy over the Microbiological Identity of Plague Epidemics of the Past (Leiden: Brill, 2010), p. 6.

53. Campbell, Great Transition, p. 296.

54. Ari et al., ‘Plague and Climate’; Kyrre Linné Kausrud, Mike Begon, Tamara Ben Ari, Hildegunn Viljugrein, Jan Esper, Ulf Büntgen, Herwig Leirs, Claudia Junge, Bao Yang, Meixue Yang, Lei Xu, and Nils Chr Stenseth, ‘Modeling the Epidemiological History of Plague in Central Asia: Palaeoclimatic Forcing on a Disease System over the Past Millennium,’ BMC Biology, 8:112 (2010), http://doi.org/10.1186/1741-7007-8-112.

55. Derives from: J. Esper, Shiyatov, S.G., Mazepa, V.S., Wilson, R.J.S., Graybill, D.A., and Funkhouser, G., "Temperature-Sensitive Tian Shan Tree Ring Chronologies Show Multicentennial Growth Trends," Climate Dynamics 21 (2003), 699-706 (I am grateful for Prof. Esper for being kind and supplying me with the annual data in conjunction with this study); Olga Solomina, Olga Maximova and Edward Cook, "Picea Schrenkiana Ring Width and Density at the Upper and Lower Tree Limits in the Tien Shan Mts, Kyrgyz Republic as a Source of Paleoclimatic Information," Geography, Environment, Sustainability 1 (2014), 66-79 (annual data available at https://www.ncdc.noaa.gov/paleo-search/study/15248); Jens Fohlmeister, Birgit Plessen, Alexey Sergeevich Dudashvili, Rik Tjallingii, Christian Wolff, Abror Gafurov and Hai Cheng, "Winter Precipitation Changes during the Medieval Climate Anomaly and the Little Ice Age in Arid Central Asia," Quaternary Science Reviews 178 (2017), 24-36; Hui-Qin Wang, Fenga Chen, Bakytbek Ermenbaev and Rysbek Satylkanov, ‘Comparison of Drought-Sensitive Tree-Ring Records from the Tien Shan of Kyrgyzstan and Xinjiang (China) during the Last Six Centuries,’ Advances in Climate Change Research, 8, 2017, 21-2

56. The geography of the spread of the Black Death is meticulously surveyed in Ole J. Benedictow, The Black Death, 1346-1353. The Complete History (Woodbridge: Boydell and Brewer, 2004), pp. 55–215, also Map 1.

57. G. Christakos, R.A. Olea, and H.L. Yu, ‘Recent Results on the Spatiotemporal Modelling and Comparative Analysis of Black Death and Bubonic Plague Epidemics,’ Public Health, 121 (2007), p. 715.

58. Campbell, Great Transition, p. 295.

59. E.A. Wrigley and R.S. Schofield, The Population History of England 1541—1871: A Reconstruction (Cambridge, MA: Harvard University Press, 1981), pp. 288–9.

60. Jan Z. Titow, ‘Evidence of Weather in the Account Rolls of the Bishopric of Winchester 1209-1350,’ Economic History Review, 12 (1960), pp. 401–2; idem, ‘Le climat à travers les rôles de comptabilité de l'évêché de Winchester (1350-1450),’ Annales. Économies, Sociétés, Civilisations, 25 (1970), pp. 314–5.

61. Calculated from Campbell, Bruce M.S. Campbell, Three Centuries of English Crops Yields, 1211-1491 (http://www.cropyields.ac.uk) (accessed July 2017).

62. Stephen Broadberry, Bruce M.S. Campbell, Alexander Klein, Mark Overton, and Bas van Leeuwen, British Economic Growth, 1270-1870 (Cambridge: Cambridge University Press, 2015), p. 20.

63. Paula Arthur, ‘The Black Death and Mortality: A Reassessment,’ in Chris Given-Wilson (ed.), Fourteenth Century England VI (Woodbridge: Boydell and Brewer, 2010), pp. 49–72.

64. Martin Ecclestone, ‘Mortality of Rural Landless Men before the Black Death: The Glastonbury Head-Tax Lists,’ Local Population Studies, 63 (1999), pp. 25–6; D.G. Watts, ‘The Black Death in Dorset and Hampshire,’ in T.B. James (ed.), The Black Death in Wessex; (Southampton: The Hatcher Review Trust, 1999), p. 27.

65. Richard A. Lomas, Durham Cathedral Priory as a Landowner and a Landlord, 1290 - 1540 (unpublished doctoral thesis, Durham University, 1973), pp. 298–313.

66. The references to the published figures are given in Benedictow, Black Death, pp. 360–76 (esp. 364–5).

67. Richard Smith, ‘Plagues and People: The Long Demographic Cycle, 1250 - 1670,’ in Paul Slack and Ryk Ward (eds.), The Peopling of Britain: The Shaping of a Human Landscape (Oxford: Oxford University Press, 2002), pp. 177–209; David J. Stone, ‘Consumption of Field-Crops in Late-Medieval England,’ in C.M. Woolgar, D. Serjeantson, and T. Waldron (eds.), Food in Medieval England: Diet and Nutrition (Oxford: Oxford University Press, 2006), pp. 19–25. Likewise, in my Experience Famine, I suggest a somewhat more conservative figure of (Experiencing Famine, pp. 18–9).

68. Rosemary Horrox (ed. and trans.), The Black Death (Manchester: Manchester University Press, 1994), pp. 64–5.

69. Richard Britnell, ‘The Black Death in English Towns,’ Urban History, 21 (1994), pp. 198–205.

70. Josiah Cox Russell, British Medieval Population (Albuquerque: University of New Mexico Press, 1948), pp. 221–5.

71. Russell, British Medieval Population, p. 216; John Hatcher, Plague, Population and the English Economy 1348–1530 (London: Macmillan), p. 22.

72. Sharon DeWitte, ‘The Effect of Sex on Risk of Mortality during the Black Death in London, A.D. 1349-1350,’ American Journal of Physical Anthropology, 139 (2009), p. 228; D. Castex and S. Kacki, ‘Demographic Patterns Distinctive of Epidemic Cemeteries in Archaeological Samples,’ Microbiology Spectrum, 4 (2016), pp. 7–8.

73. DeWitte, ‘The Effect of Sex,’ pp. 230–1.

74. Castex and Kacki, ‘Demographic Patterns,’ p. 8.

75. Daniel Curtis and Joris Roosen, ‘The Sex-Selective Impact of the Black Death and Recurring Plagues in the Southern Netherlands, 1349-1450,’ American Journal of Physical Anthropology 164 (2017), pp. 246–59.

76. Philip Slavin, ‘A Rise and Fall of a Chaghadaid Community: Demographic Growth and Crisis in ‘Late-Medieval’ Semirech’ye (Zhetysu), c.1248-1345’ Journal of the Royal Asiatic Society (forthcoming in 2022).

77. Sharon N. DeWitte and James W. Wood, ‘Selectivity of Black Death Mortality with Respect to Preexisting Health,’ Proceedings of the National Academy of Sciences of the United States of America, 105 (2008), pp. 1436–41.

78. Slavin and DeWitte, ‘Between Famine and Death’.

79. Sharon N. DeWitte, ‘Age Patterns of Mortality During the Black Death in London, A.D. 1349-1350,’ Journal of Archaeological Science, 37 (2010), pp. 3394–400.

80. The candidacy of the common vole as a likely carrier of plague in late-medieval England has been suggested by Pribyl, in her Farming, Famine and Plague, 213-23.

81. Slavin, ‘Out of the West,’

82. The Central German weather information derives from Rüdiger Glaser, Klimageschichte Mitteleuropas. 1000 Jahre Wetter, Klima, Katastrophen (Darmstadt: Wissenschaftliche Buchgesselschaft, 2001), 67-89; On the impact of weather on beech masting and vole population dynamics, see J.D. Matthews, “The Influence of Weather on the Frequency of Beech Mast Years in England,” Forestry: An International Journal of Forest Research 28 (1955), 107–116 and C. Imholt et al., “Identification of Weather Parameters Related to Regional Population Outbreak Risk of Common Voles (Microtus arvalis) in Eastern Germany,” Wildlife Research 38 (2011), 551–559

83. Pr. Nikanoroff, “Rapport URSS,” in Les faunes régionales des rongeurs et des puces dans leurs rapports avec la peste. Résultats de l'enquête du Comité permanent de l'Office International d'Hygiène publique, ed. : R. Jorge (Paris: Masson et Cie, 1928), 126-7

84. Rebecca J. Eisen and Kenneth L. Gage, “Transmission of Flea-Borne Zoonotic Agents,” Annual Revue of Entomology 57 (2012), 69

85. That Branch 1 split into Branch 1A and 1B was discovered by Monica Green, who detected that one skeletal sample from the Museum of London (Sample 6330), originally thought to be from the East Smithfield burial of 1349, comes, in fact, from St Mary Graces burial of 1361. This finding was subsequently announced in “Plague Dialogues: Monica Green and Boris Schmid on Plague Phylogeny” (https://contagions.wordpress.com/2016/06/29/plague-dialogues-monica-green-and-boris-schmid-on-plague-phylogeny-ii/). The genetic and environmental context of the split is discussed, in a detailed manner, in Slavin, ‘Out of the West’.

86. For the spinoff of 1.ORI and its dating from the main Branch 1B tree nodes, see Cui et al., “Historical Variations”

87. Horrox, Black Death, p. 85

88. Russell, British Medieval Population, pp. 217 and 224

89. Russell, British Medieval Population, p. 222; John Mullan, ‘Mortality, Gender and the Plague of 1361-2 on the Estate of the Bishop of Winchester,’ Cardiff Historical Papers (Cardiff: Cardiff University Press, 2007-8), pp. 14-6

90. Jan Z. Titow, English Rural Society, 1200-1350 (London: Allen and Unwin, 1969), p. 70; Zvi Razi, Life, Marriage and Death in a Medieval Parish (Cambridge: Cambridge University Press, 1980), pp. 126-7; Watts, ‘Black Death in Dorset,’ pp. 23-25

91. Lawrence Poos, A Rural Society after the Black Death: Essex, 1350–1525 (Cambridge: Cambridge University Press, 1991), p. 96

92. Mullan, ‘Mortality, Gender and Plague,’ pp. 21-2

93. The mortality rates and demographic impact of the pestis secunda in England will be discussed in a greater length in my separate study of the subject, currently in progress

94. For the 3 per cent as an average year figure, see Jens Röhrkasten, ‘Trends of Mortality in Late Medieval London, 1348-1400,’ Nottingham Medieval Studies, 45 (2001), p. 182

95. Röhrkasten, ‘Trends of mortality,’ 192

96. Mullan, ‘Mortality, Gender and Plague,’ 23

97. Sharon N. DeWitte and Maryanne Kowaleski, ‘Black Death Bodies,’ Fragments 6 (2017), 14

98. DeWitte, ‘The Effect of Sex’; DeWitte and Kowaleski, ‘Black Death Bodies,’ 13-4

99. DeWitte and Kowaleski, ‘Black Death Bodies,’ 14

100. DeWitte, ‘Effect of Sex’

101. DeWitte and Wood, ‘Selectivity of Black Death’

102. Broadberry et al, British Economic Growth, p. 21

103. F.S. Dawood, A Danielle Iuliano, Carrie Reed, Martin I Meltzer, David K Shay, Po-Yung Cheng, Don Bandaranayake, Robert F Breiman, W Abdullah Brooks, Philippe Buchy, Daniel R Feikin, Karen B Fowler, Aubree Gordon, Nguyen Tran Hien, Peter Horby, Q Sue Huang, Mark A Katz, Anand Krishnan, Renu Lal, Joel M Montgomery, Kåre Mølbak, Richard Pebody, Anne M Presanis, Hugo Razuri, Anneke Steens, Yeny O Tinoco, Jacco Wallinga, Hongjie Yu, Sirenda Vong, Joseph Bresee, Marc-Alain Widdowson., ‘Estimated Global Mortality Associated with the First 12 Months of 2009 Pandemic Influenza A H1N1 Virus Circulation: A Modelling Study,’ Lancet Infectious Diseases, 12 (2012), pp. 687–95; WHO (World Health Organization), Ebola data and statistics (http://apps.who.int/gho/data/view.ebola-sitrep.ebola-summary-latest?lang=en) (accessed July 2017).

104. https://www.worldometers.info/coronavirus/?utm_campaign=homeAdvegas1?

105. Monica H. Green, ‘Taking ‘Pandemic’ Seriously: Making the Black Death Global,’ The Medieval Globe, 1 (2014), pp. 27–61.