SEASONALITY of BUBONIC PLAGUE Introduction

CHAPTER ELEVEN

DEFINING FEATURE 5: SEASONALITY OF BUBONIC PLAGUE

Introduction: Bubonic Plague’s Association with Moderately Warm Temperatures and Seasons

Bubonic plague has a distinctive seasonal pattern. According to observations and studies performed in India and other developing countries with a more or less tropical climate, when humidity is reasonably favourable, favourable temperatures for plague epidemics are generally around 20 °C, while temperatures much above or below this range, generally above about 30 °C and below 10 °C, will weaken or suppress them. I have pointed out above that it is a fallacy of methodology to assume that these precise climatic limits apply in more northerly countries with the implication that bubonic plague is not possible in the north, since one must take into account the ability of rats and fl eas to evolutionarily adapt to various climates and ecological niches.1 In the words of G. Lamb, Senior Member of the IPRC: “While plague can exist and spread under a great range of climatic conditions, it exhibits a marked seasonal prevalence, which is the most striking feature of the epidemiology of the disease.”2 Lamb considers the seasonality of bubonic plague in terms approaching the concept of defi ning feature; he also emphasizes that it can spread effi ciently under “a great range of climatic variation.” Th is defi ning feature is mainly due to two central structural aspects of the epidemiology of bubonic plague springing from its basis in (black) rats and their fl eas: (1) Th e natural mortality rate of fl eas is high. Levels of temperature and humidity aff ect the reproduction of fl eas, the rates of egg-laying and development of fertilized eggs, and the rates of survival and development of larvae and cocoons on the ground. Th is means that in adverse temperatures and conditions of humidity, the population of

1 See above: 116–22. 2 Lamb 1908: 1, 85.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access seasonality of bubonic plague 397 fl eas will not be replenished by reproductive processes and their number will fall. Th is will aff ect the intensity with which a rat-fl ea population can transmit and disseminate plague and therefore the dynam- ics of the epidemic process. (2) Plague septicaemia in rats falls strongly at temperatures below 10 °C. Consequently, in chilly and cold circumstances rat fl eas which draw blood from plague-diseased rats will become much less infected and will, therefore, develop blockage far more slowly and at much lower rates. Protraction of this process also implies higher death rates of fl eas from other causes which will contribute to a corresponding reduction of infected fl eas and the further weakening of the disseminative powers of the fl ea population.3 Th is means that the plague season will vary with temperature and humidity in various countries or within the same country if it covers two or more climate zones.4 In India and other countries with very warm summers bubonic plague epidemics will subside and disappear with the advent of the warm season. In India, for instance, epidemics normally attain their maximum severity in Bombay in October; in the Central Provinces in February; in the United Provinces and Bihar in March; and in the Punjab in April. In the remaining provinces, taken together, March is the month of maximum mortality.5 In Egypt, the plague seasons were March to May in Upper Egypt, April to June in Middle Egypt, April to July in the Nile Delta and Suez, and May to October in Mediterranean ports. In Peru, “as elsewhere the plague seasons fell into an earlier period in areas where the winter months were warm than in localities with a colder climate.”6 Th e same two basic factors also explain why historical plague epidemics in Europe are strongly associated with the warmer seasons and falter, subside or disappear with the advent of chilly autumn weather and cold winter weather. Th e use of words like “falter” and “subside” is not fortuitous. One should note that rat fl eas are typical fur fl eas (and not nest fl eas),7 which means that they spend much of their adult lives

3 IPRC 1908c: 285–8; Lamb 1908: 88–90; Hirst 1953: 270–82, 340–5; Seal 1969: 288–9; Benedictow 1993/1996: 156–70, 227–64. 4 See, for instance, Pollitzer 1954: 20, 22, 24–5, 28, 33, 37, 43, 46, 48–50, 58, 60, 63, 65, 487–90. 5 Pollitzer 1954: 28, 487–90. 6 Pollitzer 1954: 33, 63. 7 IPRC 1908b: 245–6, 258; Liston 1924: 997; Pollitzer 1953: 321; Pollitzer and Meyer 1961: 461; Busvine 1976: 37.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access 398 chapter eleven in the fur of their hosts, enjoying there a relatively warm microclimate even in chilly or cold weather and ample feeding opportunities. Th is explains why plague epidemics can produce cases in chilly or cold autumnal weather, although at a rapidly diminishing rate. Th e notion that plague epidemics stop abruptly with the advent of chilly or cold weather is erroneous. Th e notion of Shrewsbury (and some other scholars who have apparently picked up this notion from his monograph) that the usual fl ea of the black rat, Xenopsylla cheopis, hibernates in the winter is a misunderstanding. It is also a misunderstanding that it is a typical nest fl ea, although this is the case for most species of fl eas.8 Consequently it is a double misunderstanding that this fl ea normally hibernates in the host’s nest.9 Th e same two basic factors explain also why historical plague epidemics tended to start earlier and to last longer in Southern Europe than in Northern Europe.

Seasonality of Historical Bubonic-Plague Epidemics with Emphasis on the Transseasonal Form

For the same basic two reasons, epidemics in the northerly parts of Europe will oft en not have taken their full course through the rat colonies when they are suppressed by cold weather. In many cases, plague contagion transported by rat fl eas or (less oft en) by infected rats will arrive late in the plague season, oft en on merchant ships returning from abroad at the end of the sailing season, which will have the same eff ect. At the end of the plague season, there will therefore quite oft en remain a murine epidemic potential that can permit the epidemic to recrudesce with the advent of warmer spring weather (see below). As shown in my monograph on the Black Death, this pattern is very evi- dent in the Black Death in central and northerly parts of Europe (see below).10 Th is alternative transseasonal pattern of bubonic plague associated with late arrival in the plague season, withdrawal with cold weather and recrudescence with warmer spring weather was also

8 Shrewsbury 1971: 3, 21, 62, 117; Scott and Duncan 2001: 26. 9 It is another matter that when extra-mural rat colonies die out from plague, fl eas from rats dying in the nest will be forced to stay in the nest, dependent on re-occupation by new rats for their survival. 10 See Benedictow 2004: 233–5, which contains a summary of these data and the page references in the index under “seasonality” (418).

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studied in India at the beginning of the twentieth century, especially in the Punjab where this pattern was quite frequent: Th is recrudescence was not due to importation but apparently to an epizootic continuing below ground, progressing slowly during the off - season on account of a scarcity of fl eas, or at least highly infective fl eas, but quickening up with a return of conditions suitable for fl ea transmission. Th e study of seventeen villages in the Pune (Poona) region roughly 100 km south-east of Mumbai revealed the following pattern: If infection of a village occurred early in the plague season the epidemic died out before the arrival of the off -season, but when a village was infected late in the season the disease was apt to linger through the off - season and to reappear the next season […] the important fact was established that all the 17 villages had been infected late in the preceding plague season. On this background, a practical scheme was developed for “predicting the carrying over of epidemics, based upon (1) the size of the community and (2) the month in which it was primarily infected.”11 It is correct that bubonic plague in full epidemic form (in contrast to the endemic or sporadic occurrence) requires a certain minimum level of temperature in Europe and is dependent on the temperatures of the warmer seasons. But it is erroneous or fallacious, as has been empha- sized several times, to assume that this level was exactly the same in Europe (and across Europe) as in India and to deny or ignore the possibility of evolutionary adaptation by natural selection of rats and fl eas to various European biotopes or climatic zones. Also in the winter, the temperatures would in many areas in the southerly parts of Europe quite oft en allow a certain low-scale, lingering epidemic or endemic activity at least temporally, and this could also have overarching seasonal eff ects. One should also take into account the eff ects of ocean- regulated and Gulf-Stream-aff ected coastal climates in western and north-western Europe that tend to produce relatively mild winters, which would no doubt dampen or restrain epidemic activities but not necessarily suppress them into an enzootic existence among rats or complete extinction. Th is is the case even along the coasts of Norway since the Gulf Stream raises average temperatures by 10 °C.12

11 Wu Lien-Teh 1936c: 397–9. 12 See above: 139.

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With this background we may consider H. Dubois’s summary of the seasonal pattern of the Black Death in France: “Almost everywhere in France, the plague has taken on the bubonic form with secondary manifestations, and most oft en it has been inhibited or slowed down by the winter, staying away to re-emerge in the spring.”13 In Rheims, for instance, the Black Death arrived in the autumn of 1348, too late to develop an epidemic form, but aft er the disease had smouldered in the rat colonies during the winter the outbreak started in April at the latest, was raging in the summer and reached its “paroxysm” in August.14 Biraben generalizes this information from a historical perspective, pointing out that the epidemics of bubonic plague which dominate the scene in France “are arrested or diminished by the cold season.”15 Carmichael states: “Also characteristic was the season of the plague: throughout the fourteenth century, chroniclers reported a faithful May-to-September course of plague in each city epidemic.”16 In Northern Europe the plague took on a somewhat diff erent but predictable version of this pattern. In my doctoral thesis I found no instance of a winter epidemic in late medieval Norway, and aft er having fi nished my history of Norwegian plague epidemics in 2002, ten years later, I could conclude that in the 300 years of Norwegian plague history, from the Black Death to the last epidemics in 1654, i.e., in the course of more than 30 (waves of) epidemics, there never was a case of a winter epidemic of plague.17 In his 2008 paper, Cohn maintains, nonetheless, that “the seasonality of the late medieval plagues does not resemble that of modern plague […] could occur at any time of year, including January in places as inhospitable to the subtropical rat fl ea […] as Norway.” He refers for support to my doctoral thesis and to Walløe 1982, the English translation of “199518 pp. 25 passim” maintaining that For the Black Death in Bergen, Norway, in January, see Ole Jørgen Benedictow, Plague in the Late Medieval Nordic Countries: Epidemiological Studies, Oslo, Middelalderforlaget, 1992, p. 44. For plague in Trondheim,

13 Dubois 1988: 316. My translation from French. 14 Desportes 1977–2: 795–6. 15 Biraben 1975–1: 86. My translation from French. 16 Carmichael 1983: 514. 17 Benedictow 2002: 320. 18 Walløe mentions in the preface that it was mostly fi nished by 1977, Walløe 1995: 4.

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Norway, that peaked in February 1566 and many other examples of winter outbreaks in Scandinavia, see Lars Walløe, Plague and Population: Norway 1350–750.19 Neither on page 44 in my doctoral thesis nor elsewhere in it, is it stated that the Black Death raged in Bergen in January 1350 simply because there is no evidential basis for it. Th e few dated or datable sources relat- ing to the Black Death in Bergen are from September 1349, the earliest from briefl y aft er 8 September and the last from 26 September. On page 44, the account in the Icelandic Lawman’s Annal is cited on the circumstances leading to the contamination of Bergen by a ship from England. In my Norwegian plague history, I have quite likely identifi ed this ship together with the merchants from King’s Lynn who in early May, while the Black Death raged in the areas on the Wash, received royal permis- sion to sail to Norway with 1000 quarters of grain,20 the most dangerous of all goods with respect to metastatic spread of rat-fl ea-borne plague. Th e time perspective fi ts nicely to a scenario where a ship sailing from King’s Lynn in the early summer of 1349 and putting into the harbour of Bergen in the fi rst half of July with a cargo of grain infested with infective rat fl eas which fi rst unleashed a rat-epizootic. According to the usual development pattern of rat-fl ea-borne plague, it would produce an early epidemic phase among the human population about six weeks later and develop into a full-blown epidemic in September, when it would start to take its toll among the upper classes and scare them into making their wills. According to the mortality pattern of Table 7 showing the development of mortality in the plague epidemic in Bergen 1565–6, the Black Death would be expected to begin to diminish abruptly in November or perhaps in late October since it apparently arrived earlier in the season than the 1565–6 epidemic, and it would disappear around the turn of the year. Cohn refers also to Walløe 1995: 25 passim for support of the assertion that a plague epidemic peaked in Trondheim in February 1566. Th is assertion is also without basis in the text referred to. Th e historical source on plague in Trondheim on this occasion is a notice in the Diary of Absalon Pederssøn (Beyer),21 the highly regarded Norwegian humanist and ecclesiastic in Bergen, where it is stated in his entry for February 1566 that he had

19 Cohn 2008: 78 and 92, fn. 38. 20 Benedictow 2004: 137–40, 149, 154–6. 21 Absalon Pederssøn 1963. My translation of the title into English.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access 402 chapter eleven received a letter from a priest in Trondheim informing him that “600 persons had died from plague in this town.” Walløe cites the source correctly, and there is no way it can be understood to the eff ect that the epidemic peaked in Trondheim in February or that it took the form of a winter epidemic.22 On the contrary, it is implied by the use of the past tense and by the rough estimate of the number of victims that the epidemic had been over in this small town for some unspecifi ed time. Clearly, this indicates the normal seasonal pattern, the epidemic having broken in the early autumn, quite likely aft er importation from Bergen, and declined and disappeared with the arrival of cold weather. Moreover, during the plague epidemic in Bergen 1565–6, Absalon Pederssøn indicates in his diary the number of dead persons brought each day to the Cathedral in Bergen for burial in its function as a parish church. Th is information provides the opportunity to follow closely the development of the plague epidemic in detail, particularly as he specifi es the few cases which were not caused by plague and because he provides increasing information on the number of plague victims being brought to the other three parish churches in the city. Th is information is summarized in Table 7 and Figure 2 below, which shows that the epidemic broke out in early September 1565, peaked predictably in November and then was rapidly diminishing until it disappeared, a pattern that was repeated the next autumn. Th e number of victims in February 1566 was only a small fraction of the number of victims in November. Th is seasonal pattern is, of course, inexplicable with respect to diseases spread by cross-infection and must almost inevitably refl ect a disease transmitted and disseminated by insects on which chilly and cold weather have strong deleterious eff ects (above). Cohn’s further reference to “many other examples of winter outbreaks in Scandinavia” according to Walløe’s account is also not correct. Since Walløe mentions only Norwegian epidemics, this can be confi rmed in my history of Norwegian plague where all epidemics are identifi ed and all sources are presented and discussed extensively. In his Diary, Absalon Pederssøn provides information on the introduction of the contagion and the fi rst cases which lends itself to epidemiological analysis and makes it possible to identify a period of latency which is a defi ning feature of rat- fl ea-borne plague (see above).23

22 Benedictow 2002: 211–2. 23 Benedictow 2002: 190–4. Above, Chapter 7.

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In the period 1348–1599 plague was mainly imported into Norway from England, occasionally also from the Netherlands, probably from England:24 the microbiological basis would have to be the same. In Norway, the Black Death evidently arrived in Oslo in the autumn of 1348 with ship(s) returning from south-eastern England, was suppressed by cold weather, and broke out again in April, as it seems; a new introduction of plague from England took place in Bergen in the summer of 1349. From these two bridgeheads or epicentres the epidemic spread across Norway in 1349 and petered out and became extinguished at the end of the year with the advent of winter weather; there is no evidence of epidemic activity in the winter of 1350. Only one person is known to have died from the Black Death in Norway in 1350, namely the bishop of Stavanger who died 7 January, which confi rms the seasonal pattern and the Black Death’s rapid disappearance with cold winter weather.25 In Sweden the Black Death was introduced into a few localities across the border in late 1349, from Halland (Denmark) whence the Black Death had presumably come by ship from Oslo to Halmstad, into Småland, from south-eastern Norway into Västergötland, and to Visby in Gotland Island in the Baltic Sea late in 1349 by a Hanseatic ship. In all three cases, the epidemic was suppressed by cold weather and broke out again in the spring to spread all over the country in 1350 from the bridgeheads in the west and disappeared at the end of that year. In Denmark, the Black Death was introduced in Halland in the summer whence it spread southwards along the coast to the cathedral city of Lund which it reached at the end of 1349, and was also introduced in the town of Ribe in the south-western corner of the country (Jutland) at the end of 1349. Also in these cases, the epidemic developments were arrested by cold winter weather and recrudesced with warmer spring weather, and from these bridgeheads spread all over Denmark in 1350, again to disappear with cold weather at the end of the year.26 Th is means that in the case of Oslo in Norway, and the points of introduction in Sweden and Denmark, the Black Death developed according to the transseasonal model or pattern. Probably in all these cases plague was introduced in Sweden and Denmark from Norway

24 Benedictow 2002: 103–8, 131, 139–43. 25 Benedictow 2002: 47–82; Benedictow 2004: 149–58; Benedictow 2006: 86–123, 128–31. 26 Benedictow 2004: 159–78.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access 404 chapter eleven which had received the contagion from England, and one should therefore expect that the disease was the same with the same basic epidemiological properties and that the seasonal pattern should be broadly similar when it is taken into account that England is situated south of Scandinavia and enjoys a milder Atlantic climate and the eff ects of the Gulf Stream. Predictably some subsequent plague epidemics took on this transseasonal form, being suppressed by chilly and cold weather but breaking out again in the spring, producing a bimodal curve of mortality showing two peaks. Some examples may be useful. At the end of August 1547 plague broke out in Oslo; around 20 September the epidemic had developed such a severe form that the commander of Akershus Castle in Oslo left the castle for his manor in a nearby island where he could isolate himself and his family. With the advent of cold(er) weather the plague declined and disappeared. However, 24 April the commander wrote to the Chancellor of the Realm Eske Bille that “the plague had broken out again and raged severely.”27 Importantly, this pattern does not manifest itself only in Northern Europe but also in the Alpine areas much further to the south where it is high altitude that makes for cold winter climate. Spreading northwards from its original epicentre in Venice, the Black Death crossed the Tyrolese Alps at the Brenner Pass in July 1348, reaching deep into Austria in some areas in the autumn of 1348, ravaging the inner mountain areas of the province of the Tyrol in September, and breaking out in areas west of Innsbruck, among other places. Th e distance from Innsbruck to the present-day German border is roughly twenty-fi ve km which distance the disease should have been able to cover in (less than) a month. However, the Black Death did not advance further into the Alpine areas and did not break out in southern Germany until the following (late) spring. At lower altitudes the epidemic could continue its spread, although at a moderate pace: spreading westwards the Black Death reached Pfäfers about 200 km from the Brenner Pass in eastern present-day Switzerland in May 1349. Presumably the onset of cold winter weather is the reason that the Black Death did not proceed directly from its outbreak in November in Constance on the central Swiss-German border into Germany’s south-western province of Baden-Würtemberg. Th e Black Death was forced to postpone its

27 Benedictow 2002: 163–4.

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invasion of south-western Germany from this advanced position until the arrival of spring brought warmer weather. Much the same appears to have happened with the Black Death’s spread out of the Swiss city of Basle on southern Germany’s south-western corner in the spring. Many German Hanseatic cities on the North Sea and the Baltic Sea were infected in the late autumn of 1349 with the return of the ships. However, except for a few recognized outbreaks that soon were suppressed by the advent of cold winter weather, it was not until the following spring that the Black Death broke out in force and formed a northern plague front spreading southwards which met the southern plague front which was moving northwards somewhere in central Germany.28 Th us, clearly the transseasonal pattern was an important feature of the Black Death in Austria, Switzerland and Germany. Since the plague contagion of the Black Death was introduced into England from France where, as underlined by Dubois and Biraben, the transseasonal form of the epidemic was usual, it is diffi cult to imagine why the Black Death should not tend to take on the same pattern in England when diff erences in climate are taken into account. Twigg takes another view: “high mortality in late spring and early summer would not be typical of bubonic plague and illustrates the point that the disease produced heavy loss of life when it fi rst made contact in a new area, no matter what time of year that was.”29 Th is means that he has overlooked or ignored the transseasonal form of plague. Twigg uses as evidential support the sequence of plague events at the manor of Fing rith in south-western Essex where the outbreak manifested itself in an abrupt increase in the registered deaths among the tenants at the court of 23 March and raged during the following months.30 Interpretation of the events at this manor requires a much broader perspective. Th e Black Death broke out in London at the end of September and had by the end of 1348 broken out in various localities along the south-eastern coast up to the R. Stour, the border river between Essex and Suff olk/ East Anglia. Since Fingrith is situated only about twenty-fi ve km from London, it appears quite likely that the manor was infected from London some time in the late autumn of 1348, and that the epidemic processes had been suppressed by cold weather but re-emerged with the advent of mild spring weather, according to a usual pattern of bubonic plague.

28 Benedictow 2004: 120, 181–2, 186–7, 194–201. 29 Twigg 1984: 69. 30 Fisher 1943: 13–4, 19–20.

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Table 7. Plague in Bergen 1565–6. Mortality in the Cathedral’s parish Year Month Deaths 1565 September 33 October 66 November 113 December 66 1566 January 27 February 14 March 7 April 0 May 1 June 2 July 0 August 70 September 229 October 133 November 35 December 4 1567 January 0

Schofi eld comments sensibly on such matters in his study of plague in Colyton in 1645–6 where plague fi rst struck in the autumn but was soon wholly or mainly suppressed by cold autumn and winter weather, so that the level of mortality was quite modest until late spring or the early summer, when the plague epidemic took on a dramatic character. Schofi eld points out that there are “few examples of plague persisting as a human epidemic through the inhospitable north European winter months.” Th e ability of plague to carry episodically on through adverse climatic circumstances refl ects that “the micro-climates of rodents’ habitats continue to provide favourable conditions regardless of seasonal changes outside,” which was, as shown above, also true for black rats in the Nordic countries. One should in this context keep in mind that the black rat’s fl eas are fur fl eas riding in the fur of their hosts, there enjoying a relatively warm micro-climate even in cold weather and easy access to nutriment, and that the black rat with its fondness for human habitats, including the housing of domestic farm animals

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(where maids or farm-hands oft en slept), would tend to live in considerably higher temperatures than prevailed outside during Nordic winters. It is the reproduction of fl eas that is seriously aff ected by chilly or cold weather and, thus, the size of the fl ea population and its collective vector capacity and also the level of septicaemia in rats (see above). Another point is that “if the winter were warm and wet, the persistence of plague through an English winter must be entertained as a serious possibility.”31 Th us, the view that Twigg and Scott and Duncan present as an absolute truth, that plague epidemics could never take place in the winters in England, is not warranted, and does not constitute proof that these epidemics could not have been bubonic plague. Episodically, higher temperatures and other circumstances could allow plague epidemics to continue through the mild English winter months, albeit at a relatively low level of intensity. Schofi eld emphasizes that the transseasonal pattern (without using the term) with bimodal mortality curve is typical of plague, referring to a number of later outbreaks of bubonic plague epidemics in England and Sweden as evidence.32 A beautiful instance of an epidemic with this transseasonal form is provided by Shrewsbury, namely the epidemic at Colchester 1665–6.33 Th is pattern is, of course, inexplicable for diseases spread by cross-infection, but easily explicable for rat-fl ea- based epidemics of bubonic plague. Other aspects of the seasonality of the Black Death in England will be discussed at quite some length below. Th e information Absalon Pederssøn gives on a daily basis in his diary on the number of dead persons brought to the Cathedral in the plague epidemic 1565–6 indicates an interesting alternative, the two- seasonal plague epidemic. In Table 7 and Figure 2 the development of mortality in the Cathedral’s parish is organized according to month and shows a very distinctive seasonal pattern. Th e surge in mortality was clearly checked by chilly autumn weather followed by moderately wintry weather typical of this south-western coastal town on the North Sea, which fi rst produced a rapid fall which developed into a slower fi nal phase of decline ending in no plague cases in April and insignifi - cant or no plague mortality the following months. However, the plague

31 Schofi eld 1977: 101 and footnotes 33–4. 32 Schofi eld 1977: 101. 33 Shrewsbury 1971: 499–501.

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250

200 1565 1566 1567

150

100

April May June July March January August January October February October September NovemberDecember September NovemberDecember Figure 2. Plague in Bergen 1565–6. Mortality in the cathedral’s parish. broke dramatically out again in August and developed explosively until chilly autumn weather and increasingly wintry weather again caused a rapid decline; in December only four cases of plague mortality were registered, in January there was no case and the epidemic was fi nally over. Late autumn and wintry temperatures hit at the heart of the epidemic’s dynamic powers and set it on a more or less rapidly declining course that refl ected the degree of chilliness or coldness of prevailing temperatures, in both cases ending with the complete disappearance of plague cases. Th e long interval of four months (April to July) with no cases or with one or two cases respectively, and no case in July at the height of warm summer temperatures, is conspicuous and indicates that the epidemic was extinguished by the winter weather of 1566 without having exhausted the murine epidemic potential and that the outbreak in August 1566 was due to re-importation. Th e epidemic clearly took up its course where it had ended and died out in the same order as it had broken out in the parishes. Th e two-seasonal pattern based on re-introduction draws support from the fact that there was one plague death in August and one in October 1567, eight to nine months aft er the last plague death in December 1566. Th ese cases must also refl ect independent re-introduction, however, at a time when the murine basis was exhausted in a city of 5000–6000 inhabitants,34 but suggest that in big urban centres a multi-seasonal pattern could occur.

34 Benedictow 2002: 197.

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Th ese epidemic case histories illustrate the deleterious eff ects of chilly and cold weather on plague epidemics: cold weather could either lead to the extinction of the epidemic or diminish it to the point that it would go underground and disappear from the human scene, smoul- dering in the rat colonies in a process that could be revealed by the occasional case. In order to understand the developments more fully, one should take into account the fact that there would be a delay of a couple of weeks from when chilly weather sets in and when the negative eff ects on the reproduction of fl eas and the reduction in the levels of septicaemia in rats would start to aff ect the development of the epidemic, since the number of heavily infected and infective fl eas will not fall instantaneously but in a gradual process. Th is characteristic temperature-dependent feature of plague epidemics was recognized by contemporaries. In November 1545, the Danish Chancellor of the Exchequer Joakim Beck wrote from Roskilde, Zealand Island’s cathedral city situated about thirty km north of Copenhagen, to the soon-to-be Chancellor of the Realm Eske Bille: “I will not advise you to go to Copenhagen before it begins to freeze and the plague stops to reign there in the city. I intend to pass the waiting time here in Roskilde.”35 In 1641, a Londoner claimed that a proposed day for religious humiliation to ward off plague was unneces- sary, because “winter was coming on, and then the plague would be s t ay e d .” 36 Th e peculiar pattern of seasonality in historical plague epidemics can, as shown above, be explained by the properties of rats and rat fl eas and their roles or functions when contaminated by plague contagion. All alternative theories of the microbiological nature of historical plague epidemics which cannot on empirical grounds explain why the mechanisms of transmission and dissemination would produce such a seasonal pattern and be compatible with this feature are ipso facto falsi- fi ed. Th e central argument of this chapter has three main parts: (1) this seasonal pattern can only be explained by the epidemiological properties of rat-fl ea-borne bubonic plague; (2) this seasonal pattern is incompatible with diseases spread by cross- infection; and (3) none of the alternative theories can explain this pattern.

35 Benedictow 2002: 40. My translation from the source into English. 36 Slack 1985: 239.

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Th e plague epidemics at Penrith in 1597–8 and Eyam in 1665–6, which both display a transseasonal pattern, are incompatible with any viral theory based on interhuman transmission, but are easily compatible with bubonic plague. Scott and Duncan’s discussion of these epidemics is peculiarly strained and untenable.37 Eyam has been studied by L. Bradley and M.P. Coleman on the basis of demographic parish reconstitution techniques and the disease has been shown by both scholars to be compatible with bubonic plague, including with respect to the seasonal pattern,38 a fact which is conspicuously diffi cult to dis- cern in Scott and Duncan’s discussion of it. Th is seasonal pattern is incompatible with all epidemic diseases spreading by cross-infection because it does not comply with the central principle of epidemiology which is formulated so well by Burnet (and White)39: “no matter by what method a parasite passes from host to host, an increased density of the susceptible population will facilitate its spread from infected to uninfected individuals.” All infectious diseases spread by cross-infection fl ourish in chilly and cold weather: they gain strength from people’s intuitive and practical reactions which are to stay or huddle closer together, remain indoors more and restrict living space for better and more effi cient heating. Th e net ect eff is to bring people closer together, in other words to increase population density at the micro-level of human behaviour, which means that all interperson- ally communicable diseases will gain increasing powers of spread. By implication, all alternative theories based on assumptions that historical plague was spread by cross-infection must be untenable, namely the theories of Morris and Karlsson, Scott and Duncan and Cohn. Th is seasonal pattern is a defi ning feature of bubonic plague. How do the advocates of alternative theories address the compelling evidence on plague seasonality and defend their theories against its potentially devastating eff ects? Th ey employ three strategies: (1) they attempt to reject the evidence of seasonality; (2) they argue that seasonality did not apply to their alternative infection for some special reason; (3) they argue that the Black Death did not exhibit seasonality, though subsequent plague epidemics did, but that the Black Death and

37 Scott and Duncan 2001: 114–48 (Penrith), 261–83 (Eyam); Scott and Duncan 2004: 5–8, 153–62 (Penrith), 191–206, 212–3 (Eyam). 38 Bradley 1977a; Coleman 1986. 39 Revised edn. of 1972.

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subsequent epidemics were, nonetheless, the same disease, and that the pattern of the Black Death proves that historical plague epidemics were not bubonic plague. Although anthrax is not generally, or is only sporadically, transmitted by cross-infection between human beings, Twigg realizes the inherent danger to his theory posed by the question of compatibility with plague seasonality and presents some peculiar arguments which later are picked up by Scott and Duncan, while Cohn relies mainly on his own line of arguments and again more or less confi nes his attention to northern Italy and Italian chroniclers. Twigg’s fi rst climatic argument against the possibility that the Black Death was bubonic plague is that the epidemic, he asserts, moved (freely) across the Alps into southern Germany in the winter of 1348–9, and Davis and Scott and Duncan pick up the argument in closely related wordings.40 As shown above, this is wrong. Twigg also launched the argument that the Black Death ravaged Greenland, which would, of course, have been a good argument if it were not fi ctitious.41 Since Greenland is not mentioned in Twigg’s index, the whole monograph must be read carefully in order to discover the argument and reveal its true character. Cohn starts his discussion of the seasonality of plague by citing Burnet’s prestigious monograph Natural History of Infectious Disease (3rd. ed.) to the eff ect that diseases of the past must be studied not only according to clinical indications but also according to their epidemiology. Of course, the seasonality of epidemic diseases is part of their epidemiology. However, Cohn passes again in silence by Burnet’s presentation of the central principle of epidemiology, the link between increasing density of (susceptible) population and the powers of spread of infectious diseases disseminated by cross-infection, whatever the means or mechanisms of transmission. Th e reason for Cohn’s neglect of this principle seems obvious: it would immediately reveal the unten- ability of his alternative theory based on a viral disease spread by cross- infection which would inevitably present itself as a disease thriving in cold weather when people stay closer together and the density of people is higher. All alternative theories on the microbiological and epidemiological nature of historical plague must satisfy the criterion of a

40 Twigg 1984: 57; Davis 1986: 460; Scott and Duncan 2001: 87. 41 Above: 98–9.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access 412 chapter eleven disease strongly associated with the warmer seasons and exhibit weak properties for spreading in chilly and cold weather. Cohn’s approach also to this matter of seasonality is characterized by his neglect of the work of historical demographers with their demand for quantifi able source material in order to secure a high level of empirical tenability. Instead, Cohn considers that the sources suited for the study of the seasonality of historical plague are chronicles, which however are characterized by their inaccuracy and subjectivity, especially in the relatively narrow perspective of Italian chronicles. However, plague’s typical association with the warmer seasons is a very conspicuous feature even of Cohn’s material and cannot simply be explained away: a summary of his citations of various chroniclers will show a very heavy preponderance of references to the warmer seasons.42 It is not correct that “a reading of the chronicles might suggest that the medieval bubonic plague had no season and could strike at any time.”43 Th e distribution of seasonal identifi cations of plague epidemics by chroniclers relates overwhelmingly to the warmer seasons. As underlined above, in Southern Europe weather conditions may occasionally allow plague in epidemic form in the winter, albeit at quite a low level of intensity. Sporadic outbreaks in chilly weather or winter months, which can refl ect mild weather for the season, cannot override the fact that in the overwhelming number of cases historical plague epidemics are associated with the warmer seasons. It is erroneous not to take into account the fact that bubonic plague can arrive in the late autumn or winter with contaminated goods or luggage, progress slowly among the rats and produce sporadic human cases for some time, and with the advent of warmer spring temperatures develop into a serious epidemic form that would impress chroniclers. Also in the case of Italy, the results of studies on the seasonality of plague by historical demographers are very clear, but since Cohn has succeeded in avoiding all of them, some central fi ndings shall be presented here. Herlihy and Klapisch-Zuber provide very strong material on the seasonality of plague in Tuscany. For the period 1251–1500 they succeeded in individualizing according to month the deaths of 939 persons who died in plague years and 1614 persons who died in plague- free years. Th ey found that 85.6 per cent of all deaths in plague years

42 Cohn 2002: 140–87, 209–10. 43 Cohn 2002: 140.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access seasonality of bubonic plague 413 occurred in the six months April to September, whilst 54 per cent of all deaths took place in these six months in plague-free years, near the normal distribution. Th ey were also able to distinguish the cause of death for 4711 persons in the period 1424–30. Among these 4711 persons 3296 or 70 per cent died from plague, and among those who died from plague 3091 or 93.8 per cent died in the six months May to October.44 Th is reveals that 5.85 per cent of plague mortality in this southern European city occurred in the months January to March and almost the same percentage in the months November and December. In Southern Europe, plague cases can occur in any month, but the overwhelming majority take place in the warmer months or seasons. In fact, with the arrival of the Black Death and subsequent plague epidemics in the period 1348–75 nearly a quarter of all Florentine deaths took place in July, which contrasts sharply with the preceding period 1276–1347 when 9.4 per cent of all deaths took place in this month.45 Herlihy and Klapisch-Zuber conclude: “Th e concentration of the deaths in the summer months corresponds well to the description which contemporaries make on the great plague epidemics,” and go on to cite Giovanni Morelli, the chronicler, who writes that plague “begins to make itself felt in February and goes on to grow until it peaks in July […].”46 Th is seasonal pattern corresponds quite closely to that of the Black Death in Tuscany where the outbreaks were noted in Pisa in January, in Lucca in February, and in March in Florence where according to Matteo Villani the disease developed rapidly from April reaching its peak in the summer and lasting until the end of September.47 Th is pattern is strongly refl ected in the dates at which many wills were written, if we take into account the usual delay between the outbreak and the time the will-producing social classes feel threatened.48 Del Panta provides other instances of transseasonal plague epidemics in Italy, in Mantua 1575–6, in many localities in Tuscany 1630–1, and in Genoa 1656–7. In all three cases, the original outbreaks were quite late in the autumn, in October, and seemingly disappeared with the arrival of winter weather, but recrudesced in the spring.49 In Rome,

44 Herlihy and Klapisch-Zuber 1978: 192, 465. 45 Herlihy and Klapich-Zuber 1978: 193–4. 46 Herlihy and Klpaisch-Zuber 1978: 192. My translation from French. 47 Matteo Villani Cronica 1995–1: 13; Falsini 1972: 432–3; Benedictow 2004: 93–5. 48 See Cohn 2002: 158. Cf. 150–71, 178–84. See above: 401; below: 431. 49 Del Panta 1980: 50–1, 53–4.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access 414 chapter eleven where the epidemic of 1656–7 broke out in July, the epidemic completed its course in the plague season, albeit with the peak skewed towards the autumn months, indicating that if the contamination of the city and the subsequent outbreak had been a little later, the epidemic process would not have been completed in the warmer seasons and could have taken on the transseasonal form. Del Panta also points out the association of bubonic plague with warmer seasons and underlines its connection with the role of rat fl eas,50 the only viable explanation. Th is helps to explain why Cohn, who relies so heavily on Italian material, especially chroniclers and wills, passes in silence by this standard work by a leading Italian historical demographer. Whatever chroniclers wrote, the hard demographic statistical data speak loudly to the eff ect that a new disease had arrived in Italy that dramatically changed the usual seasonal pattern of mortality and produced a heavy preponderance of mortality in the summer months and adjacent relatively warm spring and autumn months. Only bubonic plague is characterized by this seasonal pattern of mortality and only in the case of bubonic plague can this pattern be epidemiologically explained. Importantly, Herlihy and Klapisch-Zuber and Del Panta have made both their data and their conclusions testable by other scholars. Italian chroniclers can be shown to provide valuable information on the matter: they overwhelmingly relate plague epidemics to the warm(er) seasons. Cohn’s citations of various types of statistics regarding wills and mortality in the form of fi gures associated with various hospitals and a couple of burial grounds of ecclesiastical institutions in the period 1348–1400, mostly in Italy but also in other regions, overwhelmingly show plague’s association with warm(er) months and seasons.51 Much of Cohn’s presentation of this material deserves serious criticism, but since he cannot get away from the pivotal point, historical plague epidemics’ close association with the warmer seasons or months, this can be dispensed with. Th ere is much more severe criticism to come. However, seasonality is a material feature of epidemiology. Cohn starts his chapter on seasonality by citing Burnet to the eff ect that historical epidemic diseases must be studied according to their epidemiology, but in the presentation and discussion of his material he ignores this

50 Del Panta 1980: 48–9. 51 Cohn 2002: 156–9, 161–73, 181–5.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access seasonality of bubonic plague 415 crucial point. Instead, he attempts to explain away the strong seasonality of plague epidemics with some rather peculiar arguments on fl eas and climate that he maintains prove that this seasonality, nonetheless, was not an epidemiological refl ection of the central role of rats and their fl eas.52 Cohn makes extraordinary comments on some of the developments of plague seasonality in England, and claims that there should be peaks in the late autumn and criticizes Slack and Schofi eld for maintaining the established view of plague seasonality.53 As underlined repeatedly above, the peaks of plague epidemics are aff ected by the time of arrival in the plague season, and especially under favourable climatic circumstances late arrivals would make for late peaks. A couple of late autumnal peaks in Bristol in the sixteenth century do not constitute a change of pattern, and Slack and Schofi eld, who know that plague epidemics in England continued to be overwhelmingly associated with the warmer seasons according to a long established systematic pattern, have no reason to change their views on the matter. Th ere will be occasion to present much of this material below. Cohn tries to undermine the rat-fl ea theory when he asserts in the concluding pages of his monograph that plague epidemics in the Mediterranean regions strike con- sistently “during the hottest and driest months of the year” but “north of the Alps” broke out “in the cooler and wetter autumn.”54 Th is is not correct: all over Europe plague epidemics were associated with the warmer months or seasons. Th e point is simply that since warmer weather develops later north of the Alps, plague epidemics there will tend to rise later and not complete their spread in the rat colonies before later in the autumn, a pattern that is, of course, easily explicable on the basis of the rat-fl ea theory of plague. Cohn naturally does not make the point that this epidemiological pattern of seasonality which is so easily compatible with the rat-fl ea theory of bubonic plague is incompatible with his theory of a viral disease spread by interhuman cross-infection. Scott and Duncan enlarge on Twigg’s false arguments that the Black Death crossed the Alps into Southern Germany in the winter of 1348–9 and his statements about plague in Greenland. Th ey assert that this “pandemic [the Black Death: my insertion] even reached the polar

52 Cohn 2002: 175–8. 53 Cohn 2002: 185. 54 Cohn 2002: 251.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access 416 chapter eleven regions,” reiterating six times that also Greenland and Iceland were invaded by the Black Death and claim that this constitutes proof that the epidemic could not have been bubonic plague: “It is inconceivable that bubonic plague could have spread rapidly in winter, over alpine passes and through sub-Arctic regions including Iceland, Norway and Greenland.”55 Th e fact that I have written a monograph on plague in the Nordic countries in the Late Middle Ages is ignored. Th e juxtaposition and implied identity of the concepts “polar regions” and “sub-Arctic regions” are quite extraordinary: according to dictionaries the term polar means “of or near the North or South Pole,” hence “the polar regions.”56 No scholars other than Scott and Duncan have asserted that there ever was a bubonic plague epidemic on or near any of the poles, for obvious demographic reasons. As shown above, the Black Death never came to Greenland or Iceland, there is no factual basis for this assertion, it has been taken out of thin air. And as shown below, the two purported plague epidemics in Iceland in the fi ft eenth century cannot for several independent suffi cient reasons have been plague. In short there never was an epidemic of plague in Iceland, neither bubonic plague nor primary pneumonic plague. Scott and Duncan also accept uncritically Twigg’s assertion that the climate in Northern Europe was too cold to allow fl eas to breed and that for this reason there could not have been plague epidemics in England, Scotland or Norway. Th is contrasts sharply with the brief opening statement of the IPRC in a chapter on the “Distribution of Fleas, Geographically and on Animals”: “Fleas are found in all climates from the arctic regions to the tropical zones.”57 Scott and Duncan also add unreservedly as an objective fact: “It is important to remember that during the Little Ice Age, when the plague was rampaging most fi ercely, the conditions would have ensured that fl ea breeding was absolutely impossible.”58 Obviously if fl ea-breeding was impossible in Northern Europe there could not have been any fl eas there or bubonic plague. One may wonder how it could be that medieval and early modern Scandinavians, obviously inhabitants of Northern Europe were plagued by fl eas in the period covered by the misnomer “the Little Ice Age” (see below). Colloquially, with an element of black humour, old-time

55 Scott and Duncan 2001: 57, 81, 98, 108, 109, 357, 376. 56 Oxford Advanced Learners Dictionary 1990: 957. 57 IPRC 1908b: 245. 58 Scott and Duncan 2004: 178–9.

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Norwegians called their beds “fl eaboxes,” so as the English “hit the hay,” old-time Norwegians hit the “fl eabox.” And how can it be that in the Nordic countries many types of wild animals and birds are plagued by fl eas, although they do not live indoors in heated rooms but have to endure the cold winter climate in nests and lairs in the “woods so wild”? A shown above, this was also the case with rats, and the black rat was the only rat in the Nordic countries in the Middle Ages. Th e modern grey or brown rat, which was fi rst described in the Nordic countries in Norway around 1750 (which is the reason it is called Rattus norvegi- cus), have substantial numbers of fl eas in their nests in the Nordic countries. Scott and Duncan’s concept of the Little Ice Age is an exaggerated version of a misnomer. In the period ca. 1540–1830, there was indeed a slight fall in average temperatures in Europe, however, the tiny signifi cance of this development is demonstrated by the fact that the fi rst hundred years of this period saw the taking up of all lands all over Europe that had become deserted in the late medieval period and the recuperation of European populations aft er the precipitous decline of that period.59 In the period c. 1520–1666, the number of agricultural holdings in operation in such a northerly country as Norway increased from c. 23,500 to 58,000; in addition many thousands of new undersettlers/ sub-tenancies were established within their territories, and the number of both holdings and undersettlers continued to expand all through the so-called Little Ice Age: even the deserted mountain settle- ments were resettled and expanded. And this development took place even in northern Norway. In a broader European perspective, this subject should certainly be discussed in relation to E. Le Roy Ladurie’s sober works on the interaction of historical climate and historical change with emphasis on the period in question.60 Th e implication that Norway is situated in the “polar regions,” whatever the meaning of this term, even in the implied highly unconven- tional meaning of sub-Arctic, must be taken as an expression of great geographical and conceptual confusion. Norway is not situated in a sub-Arctic region, this is only the case for the northernmost parts of Norway containing only a tiny part of the Norwegian population; in

59 Th e exception is England, but this was not due to climate but to profound demographic changes. Hatcher 2003. 60 Le Roy Ladurie 1965: 899–922; Le Roy Ladurie 1967. Le Roy Ladurie 1974: 3–30.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access 418 chapter eleven the Middle Ages this proportion was even smaller than it is today. It is an expression of great geographical and conceptual confusion also because the term is climatically and biologically determined and not mechanically associated with latitude.61 One should note that the Gulf Stream produces a climate in Norway with average temperatures about 10 °C. higher than would otherwise be the case.62 Central Norway (Trøndelag), situated roughly at latitudes 63–65°, corresponding to the southern half of Iceland and the region around Godthåb about 500 km north of the southern tip of Greenland, is a rich agricultural area producing, among other things, large amounts of Norway’s grain, vegeta- bles and strawberries. In the Middle Ages Norway was generally self-suffi cient in grain, and the central region of Trøndelag produced a surplus which was sold in the adjacent eastern county of Jemtland, in the western coastal areas of Namdalen and Fosen, and to some extent in southern parts of northern Norway.63 Th e situation was entirely diff erent in Greenland or Iceland, in fact, early attempts at growing grain in those regions were rapidly given up. Only the tiny fi shing population in villages along the coasts of northern Norway was largely dependent on importation of grain from abroad, exchanging stockfi sh for grain with Hanseatic merchants in Bergen. Th ese fi shing villages were mainly established on this economic basis, and at the time of the Black Death this development was in an early phase. Unfortunately, the fi shers and fi sher-peasants

61 It is also highly surprising that Norway should be thought to be part of sub-Arctic regions in the ordinary scholarly meaning of a border zone between the Arctic regions and the temperate climatic regions. Assuming that the point relates to the part of Norway situated north of the Arctic Circle and the population living there at the time of the Black Death, the following remarks will be relevant: this population consisted mainly of an ethnic Norwegian population living up to or quite near to the border of the most northerly county of Finnmark, on about 2400 individual agricultural settle- ments (subsisting mainly on a combination of animal husbandry and fi shing) comprising a population of about 11,000 persons, and in addition those living in the few fi shing villages in operation at the time. At the time, Finnmark was mainly inhabited by Saami people, nomadic hunter-gatherers numbering perhaps a couple of thousand persons (at the most). In all, the part of Norway situated north of the Arctic Circle contained some 14,000–16,000 persons or about 4–4.5 per cent of the national population. Th us this line of argument is untenable. See Sandnes, 1968: 289; Benedictow 1996b: 179–81; Benedictow 1996c: 155–6, 179–81; Benedictow 2003: 245, 248–9; Benedictow 2004: 147–8, fns. 5–6; Benedictow 2006: 125–7, 131–57, contains a new thorough discussion of the size and composition of the Norwegian population at the time of the Black Death, confi rming, supporting and supplementing previous conclusions. 62 Eldevik 2006: 48. 63 Sandnes 1971: 69–70; Benedictow 2002: 161.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access seasonality of bubonic plague 419 who sailed to Bergen in the spring with their stockfi sh returned with grain that could be contaminated with dangerous rat fl eas, or Norwegian traders could bring contaminated Norwegian grain with them from Bergen or Trondheim. A few later outbreaks of plague in northern Norway are mentioned in the sources. Th e parson in Rødøy, a parish situated just north of the Arctic Circle, provides in his chronicle-like notes information on outbreaks of plague in Bergen and the devastating spread to Trondheim and northern Norway in 1599–1600 and 1618. In 1618, he specifi ed the areas ravaged by plague in northern Norway as the contemporary baili- wicks of “Helgeland, Salten, Lofoten, etc.,” comprising most of the present-day county of Nordland; only the northernmost bailiwick of Andenes is not mentioned.64 Th e northern part of the bailiwick of Helgeland, where the parson’s parish of Rødøy is situated, and also Salten and Lofoten are situated north of the Arctic Circle. Since skeletal remains of black rats have been found in Trondheim (see above), and the climate in the inland city of Trondheim is considerably colder in the late autumn, winter and early spring than the coastal areas around the Arctic circle, there is no reason why the black rat should not have spread much earlier in sacks or barrels of grain or fl our to northern Norway in fi shing boats or in ships belonging to Norwegian traders from Bergen and Trondheim, and why black rats should not have thrived there and provided a basis for epidemics of bubonic plague. Some of the observations of the IPRC may here be usefully recalled: We would, however, like to draw attention to the ease with which rats with their fl eas can be transported in certain kinds of merchandise. We have seen rats dive, as it were, into bags containing bran and disappear, so that the bags could be moved without any evidence of the presence of the rats within. M. rattus [= Rattus rattus, the black rat] from its habits is particularly liable to be transported in this way […]. From what has been said above it will be apparent that merchandise and grain, which have been visited by rats, may have fl eas deposited on them and these fl eas may be transferred with these articles to distant places.65 Th ese are important points that should be kept in mind. Twigg’s and Scott and Duncan’s assertions on climate are arguably not the result of serious scholarly work.

64 Benedictow 2002: 234, 240–3, 258–60. 65 IPRC 1908b: 254–5. Above: 105, 160.

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Th e Seasonality of Plague and Mortality in England 1340–1666

Both Twigg and Scott and Duncan maintain that the Black Death spread in the south-western counties or dioceses of England in the winter months and that this constitutes proof that the Black Death could not have been bubonic plague. Th e Black Death was introduced into Norway from England and to the other Scandinavian countries probably mostly from Norway. It has been shown that the Black Death in these countries was temperature dependent, spreading only in warmer seasons and disappearing with cold winter weather. In Norway, it has been shown that there was never a winter epidemic of plague in the country’s whole plague history of over 300 years. It has been shown above that this was also the case with the Black Death all over Europe.66 In view of these facts, one should expect that the Black Death’s seasonal pattern in England was similar. Since Shrewsbury and especially Twigg and Scott and Duncan play such a central part in this discussion, English evidence tends to play a central and even disproportionate role. However, in defence of their theories Twigg and Scott and Duncan focus only on small and selected parts of the seasonal history of the Black Death’s spread in England and base their arguments on sources which are highly problematic for inference to the reality of these matters, as will be seen below. It is therefore important to construct a rather complete overview of the sta- tus of English research on the seasonal pattern of historical plague epidemics in England throughout the whole plague period of over 300 years and apply source-criticism in quantum satis (suffi cient quantity). An overview which is complete for all practical purposes will provide the strongest possible basis for identifi cation of the seasonal pattern of plague and for inference to the causal nexus underlying the particular form of correlation of plague epidemics and climate, i.e. their seasonality. Only a qualitatively secured and, for all practical purposes, complete overview can provide a holistic perspective and framework within which their arguments can be satisfactorily considered. A methodological and source-critical point that may appear self- evidently true must be stated for reasons that soon will be clear: only empirical evidence consisting of generally accurate identifi cations of

66 Th ere may have been a case of a mixed epidemic of bubonic and primary pneumonic plague which spread also in the winter in the pneumonic mode, or just possible two cases. Benedictow 2004: 236–41.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access seasonality of bubonic plague 421 day of death or burial of a suffi ciently large sample of persons dead from plague can provide reliable information on the seasonality of plague, providing that the registration is seasonally independent. Th e reliability of information will decrease (1) with increasing temporal distance or uncertainty as to the time of death of plague victims and the registration of their demise, it will also decrease (2) as the number of persons included in the sample diminishes, and it will (3) lose its evidential power if the number falls under a critical minimum level. Th e arrival of the Black Death and subsequent plague epidemics caused a dramatic transformation of the seasonal distribution of mortality in England throughout the Late Middle Ages and well into the Early Modern Period, that is, for the duration of the plague period. Russell produced data on the seasonality of the time of death of tenants-in-chief, the noble class that held feudal land directly from the king, in the period 1340–1450 and 1476–1500.67 Th e high social class of the subject of Russell’s work will exclude direct infl uence from hun- ger, malnutrition or undernutrition associated with bad harvests which among the poorer classes would tend to cause increased mortality in the summer and early autumn of the following year as reserves of foodstuff s were being depleted and unavailable at aff ordable prices in the market. Since tenants-in-chief had large households and an active social pattern of behaviour, they would tend to be exposed to conta- gious diseases as much as or perhaps more than the average population without having normal consumption patterns of foodstuff s that would signifi cantly increase resistance to disease. Th is material will therefore refl ect more clearly the seasonal distribution of mortality caused by epidemic disease and be reasonably representative in this respect also for the general population. Tenants-in-chief lived at their manors or estates around the country, and thus the material is probably geographically well distributed. Assuming that historical plague was bubonic plague, this representativeness is negatively aff ected by the fact that tenants-in-chief tended to live in stone buildings which were less ame- nable to rats than ordinary housing at the time, and this fact would presumably tend to reduce this disease’s impact on this social class relative to peasants and burghers who lived in far more unfavourable dwellings in this respect. In principle, the representativeness would tend to deteriorate to the extent that the incidence and demographic

67 Russell 1948: 195–9.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access 422 chapter eleven impact of plague epidemics became relatively more urban, a development that did not, however, become pronounced until about the mid- 1550s, and therefore does not aff ect Russell’s data here. As can be seen from Table 8, the temporal coverage is suffi ciently large to provide good data.68 It should be noted that as outstanding medieval demographer as Hatcher, who oft en is very critical of Russell’s material and his handling of it, and rightly and fairly so, has no diffi culty in accepting the useful- ness of Russell’s data and the validity of the inferences drawn from it on this point of the seasonality of mortality.69 Russell found that before the Black Death, in the eight pre-plague years 1340–7, the “heaviest mortality was in the late autumn and winter months, in January and February, in October and November,” and he adds correctly: “Th e heavy mortality of the winter months requires no other explanation than winter severity.” Traditionally, the months of November and December were regarded as the fi rst winter months, the “forewinter.” With the advent of the Black Death, the seasonal distribution of mortality changed dramatically. In the period 1348–1375 cover- ing the Black Death and the subsequent three plague epidemics (1360–1, 1369, 1374), Russell’s data show an abrupt surge of mortality in July, the heaviest impact on mortality in September or more broadly the months August to October, with an abrupt tendency of decline starting in October. Conspicuously, the seven years of plague in this period accounted for twenty per cent more deaths than the remaining twenty- one non-plague years taken together.70 Twigg’s eff orts to render these fi ndings harmless to his theory are curious: he divides his discussion of seasonality and Russell’s fi ndings into two parts more than hundred pages apart, which means that important argumentative connections are severed, the critical reader is put at a disadvantage, and the problematic character and lack of real signifi cance of his discussion in the second part tends to be veiled.71 Curious also is Twigg’s dismissal of Russell’s fi ndings on the grounds that in the fi rst plague period 1348–75, “the death rate is only four in

68 One should note that even in countries the size of the U.K. or U.S.A. national political Gallup polls are oft en based on a sample of about a thousand persons, which provide national polls with an uncertainty margin of about 3 per cent. It is all a question of reasonable or adequate representativeness. 69 Hatcher 1977/1987: 25–6. 70 Russell 1948: 195–8. 71 Twigg 1984: 59–69, 175–85.

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January,”72 which refl ects his usual carelessness: in fact it is the number of deaths that is four. If this fi gure is taken at face value, the death rate as proportion of deaths in this month in the period is 0.9.73 Some sort of numerical error is involved, since among the remaining seventy-one mortality datapoints distributed according to month and temporal subdivisions in the period February 1348 to December 1500 on which the data presented in Table 7 are based, the lowest fi gure is 18. However, on statistical grounds one should take heart from the fact that material for correction is available: for the other months of January in the respec- tive subperiods the fi gures are 42, 47, 56, and 53. Th e fact that these numbers are quite closely bunched inspires confi dence. Th e average is 49.5 deaths, and since there is a noticeable tendency of increase throughout the period as a whole from 42 to the mid-fi ft ies, it appears reasonable, in our attempt to fi nd the true fi gure for January in the fi rst plague period of 1348–75, to weight this average in the direction of forty. Th us, it seems that the fi gure four is a slip of the pen for forty, a zero has slipped away, and forty can readily be substituted for four in the tables. Th is means that 52 per cent of total yearly mortality in the period 1348–75 was distributed on the four months July–October. Th is confi rms that Hatcher’s use of Russell’s seasonality data is justifi ed. One could also remark that it does not seem that anomalous fi gures concern Twigg much when they seemingly strengthen his case. Since he must try to reduce mortality in the Black Death as much as he can,

Table 8. Percentage of mortality July–October 1340–1500 among English tenants-in-chiefs Period Nos. % 1340–7 159 33 1348–75 426/466 56/52 1376–1400 632 43 1401–25 759 42 1426–50 640 35 1476–1500 791 40

1348–1500 3248 43

72 Twigg 1984: 181. 73 Russell 1948: 197.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access 424 chapter eleven far more than anyone else has found possible, in order to make the facts fi t his alternative anthrax theory,74 he accepts without objections Russell’s crude mortality data on the Black Death based on inquisi- tions post mortem as a realistic factual basis, and not only for mortality among the tenants-in-chief but also for the general population. In the age group 0–1, this material contains no infants, implying, consequently, a mortality rate of zero for this age, or alternatively, that there were no infants, neither of which is a realistic possibility. In ages 1–5, Russell’s material includes three young children, of whom one died. Th us, in ages 0–5, Russell’s total child population consists of three persons of whom one died, which he assumes permits the conclusion that the mortality rate in ages 0–5 was a ludicrous 33 per cent.75 Th e result is a very low mortality rate among the population of tenants-in-chief in the Black Death as a whole that suits his case, especially when Russell considers the mortality rate among tenants-in-chief representative for the general population. However, Life Tables Model West for populations with life expectancy at birth of twenty-fi ve years show a normal infant mortality of 30.5 per cent for female infants and of 35 per cent for male infants, and of 21 per cent for young children of ages 1–4.76 It should have been impossible not to note that the mortality rates according to age imply that adult cohorts in this material were very much larger than child cohorts since far more adults die according to age cohorts in this social class than is warranted by the implied birth rates. Th is should make it clear that Russell’s data are out of touch with reality and do not allow any sort of statistical use but probably refl ect interesting aspects of culture and mentality. Th ere can only be one explanation for Russell’s registrations of children of these ages, namely that the mortality rates of infants and young children were so high that their deaths were taken for granted and parents quite generally did not bother to register the deaths of their youngest children, only of their somewhat older children who had greatly improved survival rates and were of greater interest for questions of inheritance and line- age. Th us, these data do not refl ect realities of mortality in these age cohorts but cultural and practical attitudes of parents. Th e use of statistics and demographic sociology apart, Russell’s estimate of mortality among infants and young children is at gross variance with medieval

74 Below: 595–608. 75 Russell 1948: 216. 76 Coale and Demeny 1983: 43.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access seasonality of bubonic plague 425 demography on these ages.77 Th is explains why Russell’s estimate of mortality in the Black Death has been generally rejected.78 Twigg’s peculiar eff orts to reduce Russell’s mortality fi gure to c. 16.5 per cent for tenants-in-chief in the Black Death and to argue that they are representative for the general population will be commented on below. Russell made the same type of estimate of the seasonality of mortality for the subsequent subperiods 1375–1400, 1401–25, 1426–50, and 1476–1500. Th e central data are presented in a highly concentrated form in Table 8 which is so constructed that average mortality for a four-month period is, other things being equal, 33 per cent; higher percentages must refl ect higher than average mortality, and vice versa. Th e average of 33 per cent was the case in the months July–October of the eight pre-plague years, importantly, in these years almost 45 per cent of all mortality occurred in the four months January–February plus October–November. Th is underlines the great change in seasonal mortality heralded by the advent of the Black Death better than the bare numbers in Table 8. In the period 1348–1450 and 1476–1500 as a whole and in all its constituent subperiods there was a consistent supermortality in the four-month period July–October. A reservation is called for in the penultimate subperiod 1426–50 as there was hardly a statistically signifi cant supermortality in these months. Th e main reason is that a smaller or secondary peak had emerged in the months April–May which drained off some of the relative distribution of mortality.79 However, it is diffi cult to explain this as a real or factual change, because in the next subperiod for which Russell provides data, namely the last of 1476–1500, the seasonal pattern reverts by and large to the previous level of supermortality in these months. It is therefore more likely that there is some fl aw in Russell’s material for 1426–50, which also saw some very serious plague epidemics (see below). Th is may also serve to explain the gap in the series caused by Russell’s inability to present data for the implied following sub-period 1451–1475: there seem to be serious problems associated with this specifi c material for the decades around 1450, at least as collected by Russell. Th e data may not be erroneous or skewed, but need further study, perhaps a heavier input of source-criticism, and increased substantiation. Only Russell’s data for the period 1340–1426 can be considered reliable and usable

77 Benedictow 2004: 246–56. 78 See for instance Titow 1969: 68; Razi 1980: 100; Hatcher 1977/1987: 13. See also below: 596–602, 605–07. 79 Ibid.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access 426 chapter eleven here. Fortunately, there are alternative sources of information on the distribution of mortality according to season for the fi ft eenth century which allow the development of an overview of the seasonality of mortality in this period on independent material, and also correction or adjustment of Russell’s data for the periods aft er 1426 (see below). Th e seasonal pattern of mortality uncovered by Russell does not mean that the incidence of mortality in the late autumn/early winter months and central winter months had decreased signifi cantly, although, of course, persons with poor health now died from plague who would otherwise have died in the subsequent winter months. Mainly, it means that winter mortality now was overshadowed by new forces of death with their greatest impact in the late summer and early autumn as would be the case with bubonic-plague epidemics. Th e sudden transformation of the seasonal distribution of mortality from the pre-plague to the plague-era uncovered by Russell is a very important fi nding. Certainly, it is entirely compatible with bubonic plague with its basis in rats and fl eas which would develop its highest epidemic intensity in the months of (late) summer and early autumn and subside and (almost) disappear with the advent of chilly and cold weather in the late autumn and winter, as has also been pointed out by several prominent historians.80 Th e easy explanation of this transformation of the seasonal distribution of mortality on the basis of central aspects of bubonic-plague epidemiology strengthens the positive assessment of Russell’s material and the good level of tenability of observations inferred from it. Its incompatibility with diseases spread by cross-infection should be clear: they would tend to increase winter mortality.

Th e attainment of reliable general knowledge of the seasonality of plague in the fi ft eenth century requires that information be collected from several studies and pieced together. Hatcher has, as mentioned, published an important study of the mortality among the monks of Christ Church Priory, Canterbury. Obituary lists and other evidence permit a complete registration of the day of death of the great majority of monks who died there in the period 1395–1507, and to make good assumptions as to the time of death for the remainder.81 In this period,

80 Hatcher 1977/1987: 25–6; Slack 1979: 43. 81 Hatcher 1986: 23–5; Hatcher 1977/1987: 17–8.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access seasonality of bubonic plague 427 plague visited the priory in 1413, 1419–20, 1431, 1447, 1457, 1465, 1467, 1470–1, 1487, 1501, 1504, 1507.82 Th ere were also a couple of epidemics there in the preceding eighteen years that could quite likely have been plague as indicated by high mortality at the very end of the fourteenth century and c. 1407, years corresponding to known or pre- sumed national plague epidemics in the years 1400 and 1405–7.83 Since monks are a special social category and live in quite a diff erent way from the various segments of the ordinary population, the representativeness and, thus, the usability of this material for the question must be clarifi ed and corroborated before inference to society at large can be made. Th e monks were “exceedingly well fed, clothed and sheltered,” and “they benefi ted from levels of sanitation, hygiene and medical care which were wholly exceptional for the times.” On the other hand, the monks did not live reclusive or isolated lives. Th ere were twice as many servants as monks, the priory housed an “unquan- tifi able” number of permanent and temporary lay residents and corrodians.84 Th ere was also a “constant stream of visitors,” so monks made “frequent contact with the wider world,” and it was centrally located in a bustling market town containing a population of about 4,000–5,000 persons with which there was lively social exchange, townspeople visiting the monastery, and monks frequenting the town. In market towns there was a strong confl uence of people and with them of various epidemic diseases which caused high urban mortality rates. Also Canterbury’s population was declining throughout the fi ft eenth century. Clearly, the monks were exposed to diseases transmitted by cross-infection both by visitors who would quite likely suff er from an unrepresentative incidence and array of diseases and by their own vis- its in the town. Th e problem of cross-infectious diseases must have been exacerbated by their communal living: the rank and fi le monks, the younger monks or ordinary cloister-monks, “invariably slept in common dormitories and ate the common meals,”85 which must have “further facilitated the transmission of a range of diseases.”86

82 Hatcher 1977/87: 17. 83 Hatcher 1986: 26; Hatcher 1977/1987: 57; Shrewsbury 1971: 138, 141–3. Cf. Harvey 1993: 125. 84 See for instance Harvey 1993: 179–209. “A corrody was a special form of pension or annuity. Some corrodians enjoyed their privileges as a gift from the monks, but many, as will appear, paid for them.” 85 Hatcher, Piper and Stone 2006: 682; Harvey 1993: 77. 86 Hatcher 1986: 34–6; Bailey 1996: 2; Hatcher 2003: 97.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access 428 chapter eleven

Th e great similarity of the highly negative developments of life expectancy of monks and their risk of disease in such distant localities as Canterbury, Westminster and Durham (see below) to more general demographic developments in English society at the time are striking. Hatcher uses the terms “symmetry” and “synchronized” about this concurrence of similar demographic patterns of people and monks in the fi ft eenth century.87 Considering this concomitant demographic evidence Hatcher fi rst concluded that the monks’ health was “likely to have been driven in major part by the same forces which were deter- mining the health of the population at large.”88 In his latest paper, he argues that there may have been a certain supermortality associated with monastic life in the past, a view which tends to underline the importance of infectious diseases spread by cross-infection in this specifi c environment.89 Th is may have been the case, but Hatcher also argues convincingly that the size of the general population was falling in the fi ft eenth century, markedly aft er 1450 until some time in the early sixteenth century.90 It is therefore not clear that the possible diff erence between the levels of mortality of people and monks was pronounced, although the mortality profi les may quite likely have diverged. One point of importance could be that the monks lived in buildings of stone or bricks that would, presumably, be an environment less ame- nable to rats than ordinary housing at the time. Th is suggests that monastic buildings would tend to reduce the numerical incidence of rats and rat fl eas in relation to monastic men compared to the situation in environments of the general population in town and country. Th e general analysis would therefore tend to suggest that these monastic communities may have been relatively more at risk of contracting infectious diseases spread by cross-infection and less at risk of contracting bubonic plague than the general population. And this seems to have indeed been the case. Th ere is a clear increase of mortality in the winter months among the monks. However, in general terms the

87 Hatcher 2003: 97; Hatcher, Piper and Stone 2006: 667: “[…] no doubt, the symmetry that has been established between mortality in three monasteries located in dif- ferent parts of the country has important implications for our understanding of the demographic history of late medieval England.” 88 Hatcher 2003: 97–8. 89 Hatcher, Piper and Stone 2006: 682–3. 90 Hatcher 1977/87: 43–57, 64–5; Hatcher and Bailey 2001: 31; Hatcher 2003: 95–9; Hatcher, Piper and Stone 2006: 683–5.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access seasonality of bubonic plague 429 seasonal pattern of mortality among the monks at Christ Church Priory in the period 1395–1504 still shows heaviest mortality in the months July–October, a mortality profi le that is clear all through the period, but markedly stronger aft er 1450 than in the preceding period,91 which may have been the case also for the “population at large” for the same (main) causal reason, namely an increased incidence of bubonic plague epidemics. Arguably, the supermortality among the monks in the months July–October as a refl ection of bubonic plague would tend to understate the impact of bubonic plague on the ordinary population in the same months and as such the importance of bubonic plague as a demographic factor in the lives of the English population in the period. In a fi ne monograph, B. Harvey has studied the lives of monks at Westminster Abbey, London, in about the same period. Unfortunately, the material at her disposal for the demographic study of mortality is considerably weaker, because, among other things, the obituaries are lost, so that the day of death of the monks cannot be identifi ed with the same accuracy as in the case of Christ Church Priory in Canterbury. However, other sources make it possible to address usefully the question of the seasonal pattern of mortality in the period 1390–515. It hap- pens that 28 per cent of deaths occurred in winter or early spring, 69 percent in the late spring, summer, and autumn, and 3 per cent of deaths cannot be temporally accounted for. Furthermore, mortality in the warmer seasons “claimed more victims in the crisis years” than in years of “high mortality of the second order.” Importantly, in some of the crisis years the summer and autumn were actually the “dangerous seasons—and dangerous by any standards.”92 In a less specifi c and compelling way, this material shows much the same pattern as was identifi ed in the case of Christ Church Priory, that the mortality among the community of monks, despite the particularly high level of expo- sure to cross-infection, was much the highest in the warmer seasons, especially in the summer and the autumn, and that this pattern is closely associated with known plague epidemics in this period, namely those in 1400, 1420, 1434, 1458, 1464, 1471, 1479, 1491, and 1500. Evidently these studies of monastic mortality accord completely with Russell’s fi ndings, link up to his data around 1400, overlap his data

91 Hatcher 1986: 26. 92 Harvey 1993: 135–8.

O. Benedictow - 9789004193918 Downloaded from Brill.com09/24/2021 11:29:50AM via free access 430 chapter eleven for the periods 1401–26, and extend the seasonal overview up to about 1500, and as such also overlap and confi rm the value of his data for the period 1476–1500. Th e similarity of these fi ndings based on unrelated source materials is strongly corrobatory. Th ey also strengthen the prob- ability that Russell’s dat