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51 pages 1 hour read

Ole Jørgen Benedictow

The Black Death 1346-1353: The Complete History

Nonfiction | Book | Adult | Published in 2004

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Part 3Chapter Summaries & Analyses

Part 3: “Patterns and Dynamics of the Black Death”

Part 3, Chapter 25: “Patterns of Conquest, Dynamics of Spread”

Port cities acted as epicenters for the Black Death’s transmission in medieval Europe. These epicenters were infected through shipping connections with Eurasia as Italian merchants fled Kaffa. Although the plague also traveled over land, ships were the primary vehicles of transport, allowing the Black Death to make numerous metastatic leaps, as it did when it entered Weymouth in England by ship from France and then jumped to Norway through the grain trade that departed Weymouth. These leaps “greatly hastened the Black Death’s conquest of Europe, and, arguably, made the almost total success of the European campaign possible” (231). The average rate of transport by ship was 40 kilometers per day, while overland plague traveled roughly two kilometers per day. Thus, the plague had the ability to travel more swiftly by sea. Furthermore, the slow pace at which the plague spread by land, according to the epidemiological evidence outlined above, confirms that the Black Death was bubonic, not pneumonic, plague because the latter would have spread more swiftly.

Pace of spread and population density also interacted to affect the dynamics of plague’s spread. As the author notes, “high population density […] increased the pace of spread along communication lines,” but it also “slowed down the pace of conquest” (231) due to the time required for the illness to reach epidemic levels in a larger population. For example, the plague arrived in Norway in the late autumn of 1349 and attacked on two fronts, with the first epicenter at Oslo. From Oslo, plague began its spread the following April. The country was fully contaminated within the year. Conversely, the plague’s spread in Denmark was much slower due to its greater population density. A similar pattern occurred in densely populated Italy and France. The plague arrived in Italy as early as 1347 but did not fully consume the region until 1350.

The plague’s seasonality also provides information on how it propagated and suggests that the Black Death was dominated by the bubonic variety of plague. Patterns of spread in Europe show that the Black Death slowed—or even vanished—in the winter, and its spread slowed in cooler, mountainous areas. For example, in northeastern France, the plague’s spread over land between the towns of Besançon and Chalon was approximately 1.1 km per day but in the winter slowed to 0.4 km between Besançon and Montbéliard. Likewise, although the Black Death appeared in Austria by 1348, it was unable to cross the mountains into Bavaria until the spring of 1349. Pneumonic plague is transmitted from one person to another by respiratory droplets in the air, so that it is not driven by temperature.

Although it was not impossible for cases of plague to appear in winter, it was less common for them to do so. The plague’s winter crawl, therefore, suggests that the bubonic version dominated the pandemic of the mid-1300s. Bubonic plague, spread by fleas, “requires a climate with moderately warm temperatures that promote the procreation of fleas and the reproduction of the flea population” (235). Although primary source descriptions of the Black Death suggest that it may have been both bubonic and pneumonic plague, these descriptions make clear, based on the symptoms, that these victims suffered from secondary—not primary—pneumonic plague, which follows the bubonic infection. Indeed, “secondary pneumonic plague is a normal feature of bubonic plague epidemics, comprising 10-25 per cent of all cases” (238).

Part 3 Analysis

In the third section of The Black Death, Benedictow builds on evidence outlined in Part 2 to make a pointed case for bubonic plague as the disease that characterized the Black Death. Here, he addresses a series of problems that the Black Death’s historiography—the scholarship of history—has raised over the years, many of which appeared in earlier chapters. This section of the book mostly serves to synthesize, summarize, and streamline his earlier arguments. Again, the Black Death was bubonic, depended on seasonality and population density, traveled frequently by metastatic leaps, and was spread by black rats.

First, metastatic leaps by ship were the major way plague spread, as when the plague left Kaffa and entered the Byzantine city of Constantinople with Italian merchant vessels. This method of spread turned port cities into plague epicenters that further infected the European continent and the British Isles. Such leaps, however, could also happen overland, as occurred when the plague leapt from Pisa to other Italian cities including Modena, Bologna, Perugua, and Orvieto or when the plague leapt from the French city of Arles to other urban centers along a major road that linked Arles and Carcassonne. Benedictow asserts that these kinds of leaps “greatly hastened the Black Death’s conquest of Europe” (229).

Second, Benedictow argues for a pace of spread of 40 km by day by ship and varying daily averages over land, all of which are under two km by day. Because the pace of spread slowed, according to the epidemiological data, as the Black Death moved into northern Europe, Benedictow confirms this as evidence that the Black Death’s movement was inhibited by cold weather and, therefore, was bubonic plague.

Demographic data related to population density also support this assertion. Although high population density allowed the plague to swiftly move along major routes of trade and communication, high density also meant that the plague spread more slowly through these areas due to the time required for a larger number of people to become infected and the factors mentioned in Part 1, such as the decreased likelihood of one rat colony’s co-residence with a single household in an urban area. While plague eventually became spread throughout densely populated regions, that process required more time than in the countryside. Benedictow asserts that these facts further confirm his thesis that the Black Death was bubonic plague due to the form of its spread, such as its seasonality. For example, airborne exposure via respiratory droplets is characteristic of pneumonic plague, so that its transmission would be expected to increase during the winter months, but bubonic plague cases decreased during cold weather. Bubonic plague correlates with the warmer months, when the flea population thrives. As a result, historian Emmanuel Le Roy Ladurie’s argument that the Black Death was both bubonic and pneumonic is not supported by the evidence. Rather, Benedictow suggests that human behavior, especially bodily contact with the sick—not weather—explains pneumonic plague’s spread.

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