As I noted last week, Shelley mentioned a topic that’s been brought up here a few times in the comments section: alternative theories for causes of the Black Plague (the devastating plague that ravaged Europe beginning in ~1347 and eventually killed more than a third of the population). Though the bacterium Yersinia pestis is almost universally accepted as the causative organism, like many areas of science, there are a few individuals who disagree with the consensus. To this end, several alternative etiologies for Black Plague have been put forth, and shortcomings with the mainstream Y. pestis causation assumption have been suggested. More on that after the jump…
Today, I’ll discuss the alleged shortcomings with Y. pestis causation, which is really what has driven exploration of the “alternative” hypotheses. Though several scientists throughout the years have suggested that perhaps Black Plague wasn’t caused by Y. pestis, the current champions of this line of thought are Susan Scott and Christopher Duncan, who have co-authored several papers and books either addressing or focusing on this topic. Indeed, Duncan has definitively stated:
“Historians jumped on the bubonic plague idea in the early 20th-century when the disease was first described in India but … it was certainly not the causative agent in the Black Death or in any other of the outbreaks in England.”
Scott and Duncan argue that several points don’t jibe when it comes to Y. pestis and Black Death. They’ve investigated historical records in a number of areas and concluded that many different lines of evidence converge and suggest that the Black Death couldn’t have been caused by Y. pestis.
First, they suggest that these records show that the organism that caused the Black Death was directly transmitted, rather than having a vector intermediate (such as the flea). They claim this for several reasons. They claim that their perusal of historical records in several towns suggest that the writers (and townspeople) “knew” that the infection was directly transmitted person-to-person. They also argue that the speed with which the infection spread far exceeded that which rats could travel, but it was right on target with the pace of human walking. Therefore, they suggest that humans spread the infection directly while moving from village to village (either trying to escape plague-ridden towns, or wandering travelers or merchants who may have been infected but didn’t yet realize it).
Second, they argue that the incubation period for the disease was 32 days, much longer than Y. pestis’ incubation period of ~1-6 days. They came to this conclusion also based on analysis of historical records, under the assumption that in the records they examined, contacts and deaths were carefully documented.
Third, Scott and Duncan report that Black Plague occurred in areas where black rats (the primary urban source of infected fleas) weren’t supposed to be present, such as Iceland and rural England. Iceland was certainly hard-hit by plague, resulting in death of half to two-thirds of the population, so how could that happen without the presence of rats? Additionally, they claim that fleas couldn’t even replicate in the colder parts of Europe; therefore, how could they be expected to transmit bubonic plague?
It is also argued by Scott and Duncan that a quarantine period of 40 days was “completely successful” in stopping the spread of Black Death. This wouldn’t be expected if Black Death was a vector-borne disease carried by rats, which wouldn’t be stopped by quarantine. Indeed, Scott and Duncan point out an outbreak of “genuine” bubonic plague in Marseille, France, in 1720. Quarantine was instituted, but ineffective (as expected).
Finally, Scott and Duncan argue that a pandemic of Y. pestis wouldn’t explain the frequency of the CCR5Δ32 allele we see today. This is a gene that encodes a chemokine receptor: molecules on the surface of cells that bind chemokines, which are signals produced by the immune system. This particular allele has a mutation: a deletion of 32 nucleotides which renders the receptor non-functional. It also happens to be most common in individuals of European descent, and early studies on the allele suggested that it had increased in frequency in the population around the time of the Black Death. Therefore, Scott and Duncan suggest that those who carried the CCR5Δ32 allele (and especially those who were homozygous) were more resistant to whatever organism caused this pandemic, similar to what we see with HIV–and that these resistant individuals survived the Black Death at higher rates than their countrymen who didn’t carry the mutation, thus driving up the frequency of the CCR5Δ32 allele in the population. But was it Y. pestis that caused this? Scott and Duncan, obviously, argue no. At least one study showed that CCR5Δ32 didn’t provide protection against Y. pestis infection in mice–so it’s unlikely that Y. pestis was the cause of this purported increase in CCR5Δ32 in the medieval European population.
For mainly these reasons, Scott and Duncan (and a few other historians and scientists) have argued that something else besides Y. pestis must have caused the Black Death. Though a number of other pathogens have been suggested, two have received much of the recent focus: anthrax, or a currently-unknown type of hemorrhagic fever virus, akin to Ebola or Marburg.
Why these pathogens? Anthrax, like bubonic plague, can cause blackening of the skin, and certainly was an organism that would have been present in 14th century Europe. A hemorrhagic fever virus is hypothesized by Scott and Duncan based on the presence of what were called “God’s tokens,” a bruising or hemorrhage beneath the skin. Additionally, they suggest that a virus would be more likely than a bacterium to use CCR5 as a receptor for entry into cells (as HIV does), so they claim that this has greater biological plausibility and is a better fit to the data than anthrax or Y. pestis.
So, are these objections valid? I’ll examine the evidence tomorrow in part 2.
For further reading
Scott and Duncan. 2004. Return of the Black Death. Wiley and Sons.
Scott and Duncan. 2001. Biology of Plagues. Cambridge University Press.
Duncan and Scott. 2005. What caused the Black Death? Postgrad. Med. J. 81:315-320.
Duncan et al. 2005. Reappraisal of the historical selective pressures for the CCR5-Δ32 mutation. J Med Genet. 42:205-208.
Mescas et al. 2004. Evolutionary genetics: CCR5 mutation and plague protection. Nature. 427:606.
Karlsson G. 1996. Plague without rats: the case of fifteenth-century Iceland. Journal of Medieval History. 22:263-284.
Image from http://sphtc.org/timeline/plague.jpg