I’ve been reading Robert Sallares book chapter “Ecology, Evolution, and Epidemiology of Plague” this weekend. Its a fascinating read. Epidemiology of the plague brings up all kinds of factors of medieval culture that are largely invisible by other means.
In his contribution to the same book, Michael McCormick wrote that “it is just imaginable that the broad routes and patterns of long-distance transmission of the plague pathogen, we might be able to discern the changing constellations of long-distance ship movements in the late Roman and early Islamic empires with a precision and detail that would render obsolete my own recent efforts to do so from the written and archaeological sources”. His own recent efforts are found in the highly acclaimed book Origins of the European Economy.
Sallares hypothesizes that it was a cold snap in 540-541 that initially pushed the plague from highly local epidemics in Egypt and Syria to a pandemic largely because pnuemonic plague spreads better in cooler temperatures. This brings to mind one of the largely overlooked consequences of global warming today. We have already seen one pathogen, cholera (Vibrio cholerae), make an evolutionary leap to adapt to new climate patterns and this accounts for our inability to get the current Asian epidemic under control. Epidemics and pandemics occur when the right series of events fall into place. For the Justinian plague, it was the coincidence of the plague bacterium (Yersinia pestis), black rats, rat fleas, and humans to start the first epidemics and perhaps, if Sallares is correct, a cool enough time period in the Middle East to promote the beginning of a pneumonic plague. Once the plague becomes pneumonic, then it only needs a constant supply of vulnerable hosts and the right temperature and humidity to promote respiratory spread. At the beginning of the Justianian plague, these conditions only improved the further north the plague moved. As far north as Ireland, it was recorded as an unusually cool and wet year. Rats and their fleas still play a vital role primarily at maintaining the pandemic. Respiratory spread may have given it the explosive start necessary to move it from a local epidemic to a pandemic. The plague seems to have been incubating in local epidemics in normally hot and dry Egypt and nearby areas, possibly waiting for the write climate conditions to go pneumonic.
Sallares (p. 240) made the important connection between neck bubos and pneumonic plague. Plague can spread by respiratory droplets. Small droplets are inhaled directly into the alveoli of the lungs staring the rapid pneumonic plague pattern. This form of plague kills its host rapidly and usually without the development of the characteristic bubo. However, plague spread by large respiratory droplets does not reach the alveoi directly and settles on the tonsils. Tonsillar plague forms neck bubos and follows the bubonic plague timescale. Sallares notes that neck bubos are described frequently in both the Justianian plague and the Black Death of the 14th century but were very rare in the third pandemic of the 1890s and in modern cases. Neck bubos are not a sign of fleas biting the head but of pneumonic transmission. Of course, this calls to mind for me that Æthelthryth of Ely died of a neck swelling in an epidemic that killed many others at Ely in 679.
Lester Little, ed. (2007) Plague and the End of Antiquity: The Pandemic of 541-750. Cambridge UP.