This analysis of the Black Death in the Middle East and Central Asia consists of two sections:
SECTION ONE sums up results found via (1) Table of mortality of the Black Death in the Middle East and (2) Transmission Timeline East (a) and West (b) for the Black Death in the Middle East and Central Asia.
SECTION TWO is an introduction, a review of the literature on the subject and a discussion of quantitative methods that were used to determine plague mortality.
(1) TABLE OF BLACK DEATH MORTALITY
(2) TRANSMISSION TIMELINE
Black Death Timeline-Transmission (a) East
Black Death Timeline-Transmission (b) West
INTRODUCTION – SURVEY OF THE LITERATURE
The Black Death (1347 – 1351 CE) was the first and greatest of the many plague outbreaks of the second plague pandemic in the Middle East (1347 CE to 1877 CE).[2] While the Black Death’s mortality and impact in Europe has received a great deal of attention, the same cannot be said for the case of the Black Death in the Middle East. This study will present newly discovered evidence and a fresh analysis of quantification as part of our ongoing efforts to examine and interpret the mortality of the Black Death in the Middle East.[3] We will use data and information compiled from medieval Arabic texts and thus expand upon our recent analyses that have dealt with this subject. In particular we examine in this study new data for the Black Death’s mortality in Samarqand, Khurasan, Iraq, Andalusia, and North Africa – in addition to our review and reexamination of the data for Egypt and Syria.
As our analysis in this study will show, the Black Death in the Middle East had an approximate mortality of 42% (in the areas for which we were able to gather sufficient data to make estimates). It stands without question that an event with such a high mortality would have had a serious and profound impact on all regions of the Middle East, and this proposes that more studies consider the historical importance and long-term impact of the Black Death. In this context, it’s also worth emphasizing that the Black Death was only the first in a series: there were over 150 plague outbreaks in the Middle East’s second plague pandemic and it was a pandemic far longer in duration than that of Europe. Furthermore, it is clear that severe plague outbreaks with large-scale mortality occurred over this long interval at a rate of roughly ten per century. A great deal of work remains to be done in terms of our understanding of how such serious and repeated demographic blows affected the Middle East socially, economically, and otherwise.
Of the formal studies that have analyzed the Black Death in the Middle East, Michael Dols’ seminal work, The Black Death in the Middle East, included a lengthy analysis of the demography of this initial plague outbreak as well as its social and economic impact. His work remains the standard source of reference for the Black Death in the Middle East. His well-informed conclusion was that between one-third and one-half of the inhabitants of Egypt were carried off by this outbreak. In his subsequent work, Dols developed a series of detailed estimates of the Black Death’s mortality in Cairo, expanding on the work he had done in his monograph. At the same time, the economic historian Boaz Shoshan furnished us with a comprehensive list of the timings of every single outbreak that followed the Black Death for the duration of the Mamlūk Dynasty in the Middle East (12150 -1517 CE).[4] Shoshan’s meticulous work at documenting the timing of outbreaks is more comprehensive and accurate than the tables provided by Dols, though scholarship has generally overlooked this study. Shoshan’s tables, should, we argue, be the standard for any scholar working on the plague in the Middle East. Shoshan’s detailed tabulations allow us to estimate how frequently plague struck this core area of the Middle East; there was approximately one outbreak every two years for Egypt (73 over 169 years, i.e., one per 2.31 years) and roughly one outbreak every four years for Syria (exactly 41 in 169 years, i.e., one per 4.12 years).
As other scholars have pointed out, plague outbreaks continued to have a serious demographic impact through the course of the Ottoman era. The contributions of André Raymond, Daniel Panzac, Alan Mikhail and Nukhet Varlik should be consulted here.[5] The severity of plague was sustained in Egypt and in Syria over the course of the Ottoman era and in fact continued with even greater frequency severity. Panzac has shown that Ottoman-era plague outbreaks occurred with a frequency of approximately one every 2.5 years – with 59 plague outbreaks occurring between 1700 CE and 1844 CE.[6]
METHODOLOGY: PLAGUE AND QUANTITATIVE MODELS
Plague is a disease caused by the rod-shaped gram-negative bacterium Yersinia pestis. Yersinia pestis evolved from the closely related environmental progenitor Yersinia pseudotuberculosis, a mild pathogen that was spread by oral-fecal transmission. This event happened quite recently – some 4,000 years ago during the Bronze Age.[7] As it diverged from Yersinia pseudotuberculosis, it acquired the ability to be transmitted by insect vector (primarily the rat-flea Xenopsylla cheopis). It also developed its high pathogenicity; this was required for the successful infection of its host (primarily the rodent species, Rattus rattus) in its new mode of transmission. In this way, Yersinia pestis developed the ability to spread between rodents via fleas since fleas – in the process of feeding on infected rats – ingest plague bacilli.
In this mode of transmission, Yersinia pestis bacilli ingested during the flea’s blood meal build up as a biofilm in the flea’s proventriculus (a reuptake valve located between the flea’s esophagus and its mid-gut).[8] The block formed by this bacterial biofilm shuts off the passageway to the flea’s mid-gut and thereby renders the flea incapable of ingesting its food and drink (rat-blood). The flea then begins to starve and dehydrate and – as it becomes desperately hungry and thirsty – it engages in continuous efforts at feeding, biting the rat-host with steadily increasing frequency and in growing agitation as it attempts to relieve the obstruction in its proventriculus. Subsequently, each time the infectious flea attempts to feed, it regurgitates accumulated rat-blood into its rat-host and thereby delivers to the rat’s bloodstream a mass of Yersinia pestis bacilli from its biofilm. The rat becomes sick with plague and as it weakens and dies, the flea moves on to another rat, infecting it in turn.
A zoonosis of rats thus develops and the rats die in increasing numbers. As the rat population dwindles, fleas leave their rat hosts and become “free” fleas – i.e. fleas without a rat host (see the model below). These free fleas begin a desperate search for a new source of food and drink – and this is when they make the transition to any humans that are in proximity to the dying rat colony. The transition to humans is not a normal one for the rat-flea, as it typically disdains a human blood-meal. Yet in their desperate and steadily increasing state of hunger and thirst, the fleas migrate to humans in rapidly growing numbers. In this fashion, the human plague outbreak begins as these rat fleas continue their attempts to relieve their state of dehydration and starvation by feeding on humans. Thus the human outbreak begins only after most of the rat colony has perished. In this sense the human epidemic is a sort of footnote to the rat zoonosis.
The process of plague zoonosis has been successfully modeled by Matthew Keeling and Christopher Gilligan who developed a quantitative system that simulates the zoonosis via nine differential equations. These equations reproduce – in quantitative fashion – each step of the rat zoonosis: achieving Keeling and Gilligan’s primary goal. However, these same equations can also be employed to represent the human epidemic as well. In the image below, the dynamic stages of rat zoonosis and human epidemic are depicted via a graph in which time in days is plotted on the x-axis.
Application of the Keeling and Gilligan Plague Model
On the y-axis there are three curved lines: one (on the left, dotted-black) for the number of rats (which can be seen to dwindle as the rat zoonosis depletes the rat colony’s numbers), a second (in the middle, dashed-blue) for the “free” infectious flea population that spikes upward as the number of fleas without rat hosts grows exponentially toward the tail-end of the rat zoonosis. These are the fleas that cause the human plague outbreak and the outbreak itself is represented in the third line (at center-right, solid-red) which represents the number of human deaths that occurs as free fleas without rat hosts make the transition to the human population.
Three of the differential equations of the Keeling and Gilligan model are shown below. The quantification of plague outbreak is represented primarily in the rate of change in the number of fleas without a rat host as this is the motor that drives the human epidemic. The parameters and variables composed in this equation follow beneath.
What we have done in our efforts to simulate past plague outbreaks is to apply our data from medieval Arabic texts to the Keeling and Gilligan plague model. What we do is to take the fatality data from our texts and adjust the parameters of the nine-differential equations so that they yield – within the fixed parameters boundaries of the model as a whole – a regression line that can fit our data in least-squares fashion and provide an r-squared that is acceptable (r^2 > .9). Our goal has been to use this model in such a way that we can quantify the human outbreak and its fatalities with as much realism as possible.
From this perspective, one of our primary objectives has been to quantify the trajectory of a human plague epidemic for those cases in which our medieval source data is limited, i.e., for those cases in which the fatality data for the outbreak is very sparse. By using the Keeling and Gilligan model, we can provide for such limited data a solution for cumulative fatalities that has a solid quantitative underpinning. We also note that in the process of working with these differential equations we also developed our own equations that simulate episodes of pneumonic plague that often accompany the primary bubonic plague outbreak. Our pneumonic plague model was useful for simulating cases where there were twin peaks in the number of plague fatalities. We had speculated that bimodal peaks seen in other plague outbreaks: Sydney (1903), Freiberg (1613–14), Bombay (1905–6), and Coventry (1348) might well be the result of episodes of pneumonic plague – as suggested by descriptions found in our medieval Arabic texts. Such twin crests in daily plague fatalities were highlighted by Monecke and Monecke in their application of the Keeling and Gilligan model to the Freiburg outbreak of 1613-14 CE.[9]
As a final note regarding the transmission and quantitative modeling of plague outbreaks, we should mention that alternative approaches have recently been proposed. A new study has demonstrated the viability of modeling European plague outbreaks of the second plague pandemic not as the product of a rat zoonosis spread by rat-fleas but rather as the product of a disease spread directly from human to human. This alternative approach – which is based upon new interpretations of the historical evidence from European plague outbreaks of the Black Death takes the major step of restructuring our working framework for plague transmission as it argues that human-to-human transmission of Yersinia pestis occurred by means of the ectoparasites, human flea (Pulex irritans) and human louse (Pediculus humanus humanus), rather than the rat-flea (Xenopsylla cheopis). This study based its statistical conclusions upon the method of Bayesian inference – and produced results that suggested that more accurate regressions of historical plague fatality data could be obtained by using this human-human transmission model.[10] In light of these results, it may well be that future studies will take advantage of this alternate approach when it comes to quantifying the mortality of the Black Death – and the mortality of the second plague pandemic as a whole.
Notes:
[1] I would like to thank Tarek Sabraa (Independent Researcher, Bonn, Germany) and Arthur Andreev (Independent Researcher, U.S.) for research assistance.
[2] Beginning with the Black Death in Alexandria (November 1347 CE, see Barker, 2021) with the last documented plague of the second plague pandemic occurring in Iran in 1877.
[3] See our previous work on the particular subject of the Black Death in Stuart Borsch and Tarek Sabraa, “Refugees of the Black Death: Quantifying rural migration for plague and other environmental disasters,” Annales de démographie historique 134, no. 2 (2017): 63-93, as part of a special edition introduced and edited by Isabelle Séguy and Guido Alfani. We will also discuss here our analyses from 2016 and 2014, where we derived methods that are discussed below: Stuart Borsch and Tarek Sabraa, “Plague mortality in late medieval Cairo: Quantifying the plague outbreaks of 833/1430 and 864/1460,” Mamlūk Studies Review 19 (2016): 115; Stuart Borsch, “Plague depopulation and irrigation decay in Medieval Egypt,” The Medieval Globe 1, no. 1 (2014): 125.
[4] Boaz Shoshan, “Notes sur les épidémies de peste en Egypte,” Annales de démographie historique (1981) : 387.
[5] Nükhet Varlık, Plague and Empire in the Early Modern Mediterranean World: The Ottoman Experience, 1347–1600 (Cambridge: Cambridge University Press, 2015); Alan Mikhail, “The Nature of Plague in Late Eighteenth-Century Egypt,” Bulletin of the History of Medicine 82, no. 2 (2008): 249; Daniel Panzac, La Peste dans L’Empire Ottoman, 1700–1850 (Leuven: Éditions Peeters, 1985); André Raymond, “Les Grandes Epidemies de Peste au Caire aux XVIIe et XVIIIe Siecles,” Bulletin d’études orientales 25 (1973): 203-210.
[6] Daniel Panzac, La Peste dans L’Empire Ottoman, 1700–1850.
[7] Y. pestis evolved from Y. pseudotuberculosis so recently that it still retains much of the former species’ genetic structure. The primary characteristics that distinguish it from Y. pseudotuberculosis developed as a consequence of chromosomal gene loss on the one hand and the acquisition of two key plasmids (DNA fragments) on the other. The plasmids (pMT1 and pPCP1) were responsible for enabling Yersinia pestis’ high level of pathogenicity as distinct from Y. pseudotuberculosis as well as its ability to transmit infection via arthropod (the flea).
[8] The proventriculus also serves as a pre-digestive system, by which the spines of the proventriculus break up the incoming food before it reaches the flea’s midgut. The blocking of the flea’s digestive system caused by the proliferation of masses of plague bacilli in the flea’s proventriculus was first discovered and documented by Ada White Bacot and C. J. Martin, “LXVII. Observations on the mechanism of the transmission of plague by fleas,” The Journal of Hygiene 13 Suppl. (1914): 431–37.
[9] Stefan Monecke, Hannelore Monecke, and Jochen Monecke, “Modelling the Black Death: A Historical Case Study and Implications for the Epidemiology of Bubonic Plague,” International Journal of Medical Microbiology 299, no. 8 (2009): 588.
[10] Bayesian inference is a mode of statistical inference which tests hypothesis’ probability.