Ruairidh Macleod
If you mention the plague, most people think of the classic features of the Black Death: bubonic plague, spread by flea bites from infected rats, causing painful swellings ('buboes') that turn black and necrotic, giving the disease it's nickname. But this is actually only just one way that the plague bacteria can infect humans. As septicaemic plague, the bacteria enters the bloodstream directly, through injuries breaking the skin, and causes a severe multi-organ infection that quickly results in death if untreated. As pneumonic plague, bacteria are spread through the air by coughing, and aggressively infect the lungs of victims breathing them in, also leading rapidly to death.
Pneumonic plague presents the greatest public health threat: it is the only form known to spread rapidly between humans directly, and in 1910-1911 an outbreak killed around 60,000 people in China. Better contained outbreaks in the past decade have still killed dozens of people. Septicaemic plague and pneumonic plague both have a higher fatality rate (up to 100%) than bubonic plague (30-60%). While the Black Death is widely viewed as bubonic plague, some historians and scientists have recently argued that other forms of plague infection (pneumonic plague in particular) could have contributed to the very high historical death toll of the disease.
Historical disease outbreaks can give us vital insights into the transmission dynamics and pathogenicity of infectious diseases, revealing how these can evolve and change across much longer time scales than we can get from modern records. Unfortunately, we have extremely limited records for plague cases across the second pandemic, when the disease was endemic in Eurasia betwen the 14th and the 19th Centuries.
A new discovery and analysis of an extraordinarily detailed record of cases during the 1820 plague outbreak in Mallorca shows that this outbreak doesnt match what we would expect for rat-borne bubonic plague. Using rigourous methods from modern-day disease outbreak modelling, the authors find that instead, the high fatality rate (78%) and short infectious time among victims implies that pneumonic or septicaemic plague were responsible. Once the first cases arrived from infected sailors, the disease seems to have spread either by coughing (pneumonic plague) or as septicaemic plague spread by bites from human parasites like body lice (instead of the rodent flea bites which cause bubonic plague). This presents a significant challenge to the assumption that epidemics at this time were driven and maintained by continuous infections from rodents as bubonic plague.
These findings are also exciting given the level of statistical modelling that can be applied with this data, showing how this epidemic was shaped by how humans responded to the disease, and that socioeconomic status was likely a major factor in getting infected (accounting, for example, for why so many excess children also died).