2.1Athens: an account, a tooth and a reply
The dispute over Athens has three positions, and they are not symmetrical. Morens and Littman treat the text as the evidence. Their reading takes Thucydides's account apart into the features an epidemiologist would ask about: when the disease began, how it spread, who caught it, what it did to the body, and whether those who survived were protected. With those features in hand they weigh the diseases that had been proposed and find that the account does not allow a firm identification (Morens and Littman 1992).
Papagrigorakis and colleagues turn to the dead. Their material is dental pulp from people buried in a mass grave in the Kerameikos, dated to the time of the plague. From it they report DNA sequences resembling those of the typhoid organism, and on that basis they propose typhoid fever as a probable cause of the plague that Thucydides described (Papagrigorakis et al. 2006). What ties their material to the plague Thucydides described, as the reading note gives it, is the grave's dating to the time of the plague.
Shapiro, Rambaut and Gilbert reply on the material's own terms: they argue that the sequences do not place the organism as Typhi with confidence, that the methods used do not exclude contamination, and that the identification of the plague's cause therefore remains unproven (Shapiro, Rambaut and Gilbert 2006).
Laid side by side, the three positions have a shape. Morens and Littman end where the text ends. Papagrigorakis and colleagues try to go beyond the text with other evidence. Shapiro and colleagues return the question to unproven, for reasons about the material. The text's limits are the floor under the whole dispute, which turns on whether material evidence can lift the question off that floor.
2.2Florence and the Black Death: description against genome
The dispute over the Black Death has two positions, and here the material evidence came second. Cohn's argument rests on contemporary records. The medieval disease's patterns of spread, seasonality and symptoms, as contemporaries recorded them, differ from those of the bubonic plague observed from the 1890s, and he questioned whether the two were the same disease. He also argued that culture changed as later waves struck, with physicians and communities growing more confident (Cohn 2002). Bos and colleagues then reconstructed a draft genome of Yersinia pestis from the teeth of people buried in a London cemetery used for the dead of 1348 to 1350, and in doing so established that the Black Death was caused by that organism (Bos et al. 2011).
Set beside the Athenian dispute, this one runs in the opposite direction. At Athens, a textual reading that declined to identify was followed by a material claim that was contested. For the Black Death, a textual reading that questioned an identification was followed by material evidence that settled it. The two disputes therefore offer a modest contrast: in one the material evidence has not, on the reading notes, closed the question; in the other it has.
What the genome settles, and what it leaves, is the point where this article enters. The genome settles the organism. Cohn's argument was about what contemporaries recorded: patterns of spread, season and symptoms. A genome from teeth does not change what a contemporary wrote. It changes what a reader can infer from the gap between the writing and the modern disease. If the organism is settled, then any difference between a contemporary description and the modern clinical picture becomes a fact about the description, or about the disease's behaviour in its setting, rather than evidence of a different disease. That is this article's reading of how the two positions now stand to each other; neither work's note puts it that way. It makes the contemporary descriptions more interesting, not less, because they become evidence about what people in 1348 noticed and how they put it into words.
There is a second limit in the material. The East Smithfield dead were buried in London. Boccaccio described Florence. The reading note for Bos and colleagues states the finding for the Black Death as a whole, and this article does not go beyond that note; but it is worth saying plainly that nothing in Boccaccio's text or in Skeptron's record of Florence was tested by the London genome. The identification of what killed Florentines in 1348 rests, in this article's evidence, on the general finding.
2.3How an epidemic comes to be known
The disputes ask what the disease was. A prior question is how an epidemic comes to be known at all, and three works in the study's list help with it.
Charles Rosenberg describes an epidemic as having a dramaturgic form, unfolding as if in acts: a slow and often reluctant recognition, which he calls progressive revelation; the framing of an explanation that manages randomness; the negotiation of a collective public response, often with a ritual side; and a subsidence followed by retrospection. He also distinguishes explanatory styles in which disease is read as configuration, an imbalance of the whole person and environment, or as contamination, a specific agent passing between people (Rosenberg 1992). Both Thucydides and Boccaccio write in Rosenberg's last act, looking back, and their texts contain the earlier acts as remembered. Both of Rosenberg's styles appear in Boccaccio's text within a few paragraphs.
Richard Neustadt and Ernest May propose that decision makers separate what is known, what is unclear and what is presumed about a situation, ask what the story of an issue is and when it began, and test analogies by listing likenesses and differences (Neustadt and May 1986). Their subject is decision makers, not ancient historians, but the three-way separation suits two authors who mark the difference between what they saw, what was said and what was believed.
Reinhart Koselleck describes historical time as shaped by the relation between the space of experience, the past present in memory, and the horizon of expectation, the future anticipated now (Koselleck 1985). Thucydides's stated purpose joins the two directly: an experience written down for an expected recurrence. Boccaccio's purpose looks only backward. That difference is the hinge of this article's comparison.
2.4What a pair of cases can carry
Two texts cannot settle what two diseases were, and this article does not try. Alexander George and Andrew Bennett describe heuristic case studies, which use cases to find new variables, paths and questions, and the method of structured, focused comparison, which asks the same questions of each case (George and Bennett 2005). The reading below is heuristic in that sense: it asks the same questions of both texts to find which features of a description bear on a later identification.
One more work bears on the counting. Marc Lipsitch and colleagues set out why estimates of the share of cases who die, made during an outbreak, are biased: deaths lag behind cases, so early ratios understate; mild cases are missed, so ratios overstate; and case definitions, testing and reporting differ between places and over time (Lipsitch et al. 2015). Their subject is modern outbreak statistics, and neither text gives a ratio; but both make statements about who died and who recovered, and Boccaccio's depends on how a case was recognised.