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

Comments

  1. #1 Left_Wing_Fox
    January 16, 2008

    Neat stuff! I’m looking forward to reading more. :D

  2. #2 J-Dog
    January 16, 2008

    Tara – You tease! Well, it worked – I’ll be back tomorrow.

    Thanks for the research and the post!

  3. #3 chezjake
    January 16, 2008

    Thanks, Tara. This is the best summation of the evidence against Yersinia that I’ve seen so far. I’ll be interested to read your follow-up tomorrow.

  4. #4 e okul
    January 16, 2008

    thanks tara well it worked.I’ll be interested to read your follow-up tomorrow.

  5. #5 Algerine
    January 16, 2008

    I don’t get how anthrax would be considered as a viable suspect. Sure the symptoms are similar, but person-to-person transmission of anthrax is pretty rare. Has that been explained, or is that a big sticking point for the hypothesis?

  6. #6 Tara C. Smith
    January 16, 2008

    When anthrax is brought up, it’s usually as a second pathogen that may confuse the issue of Y. pestis causation–a second outbreak rather than a sole cause of Black Death, or a localized outbreak in one village that may have a common source. Indeed, it’s not really a viable alternative for Black Death as a whole.

  7. #7 jen_m
    January 16, 2008

    Algerine – just a guess, but maybe in 14th century England, where there was a lot of casual daily contact between livestock and humans even in the cities, it might be pretty hard to distinguish between person-to-person transmission and livestock-to-person transmission.

  8. #8 DouglasG
    January 16, 2008

    One of the flaws that I see in this report is the No Rats means no fleas argument. Fleas can reside on any fur baring animal. Cats, dogs, deer, bear, etc. Thus, an absence of rats would not necessitate the absence of fleas. A few rats coming over on boats into Iceland could spread their fleas onto any animal that preyed upon the rats. I don’t know much about the fauna of Iceland, but I am sure there were plenty of fur bearing (and fur wearing) animals around.

    Secondly, haven’t there been a few outbreaks of Bubonic plague recently? We certainly know plenty about these recent outbreaks. Are they claiming that the recent outbreaks are different than the Middle ages?

    It sounds sketchy to me, and I anxiously await tomorrow’s report!

  9. #9 jspreen
    January 16, 2008

    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.

    What? They dare disagree with the consensus? Heretics! Dissidents! Denialists!

    Stop it, Tara, now. You give ‘em denialists importance they do not merit. I think you should “treat them with the utter contempt that they deserve and expose them for the charlatans that they are”.

  10. #10 Algerine
    January 16, 2008

    jen_m — I did some investigating on my own and discovered one of the sources of the anthrax hypothesis was historian Norman Cantor. His argument was not that anthrax was the true cause but that perhaps some of the deaths attributed to the plague were actually due to other causes. That I can buy.

  11. #11 jen_m
    January 16, 2008

    Algerine, that seems plausible to me, as well.

    DouglasG – yeah, although Y. pestis is transmitted via bites from Xenopsylla cheopsis, the oriental rat flea, many other fleas, including the human flea Pulex irritans can transmit the bacteria. Black-tailed prairie dogs, which are an important species in domestic plague cases in the US, are associated with five different species of flea, all of which have been documented with plague (Cully et al., 2006, Mammalogy 82(4):894.) Domestic cats can transmit pneumonic plague by droplet transmission, for that matter, so once a human epidemic is in the pneumonic stage, or if a rodent epidemic happens to coincide with a vulnerable domestic cat population, you really don’t need human-rat contact for the disease to spread to humans.

  12. #12 Chris Noble
    January 17, 2008

    Fred Hoyle solved all of the inconsistencies in the Yersinia pestis/Black death theory by invoking panspermia.

    It wasn’t being transmitted by fleas or rats. It was coming from outer space.

  13. #13 Jim
    January 17, 2008

    Recently they were able to exhume victims of the 1918 flu epidemic in Alaska and recreate the virus that killed them by isolating lung tissue. Could a similar process recover enough genetic material for analysis from victims in Iceland and put the issue to rest?

  14. #14 Tara C. Smith
    January 17, 2008

    Jim,

    That’ll be the topic of Friday’s post.

  15. #15 Jag
    January 17, 2008

    I find this highly suspect:
    “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?”

    For the main bulk of Europe (France, England, Germany, ect), fleas and lice WERE present and a ever present problem. It can be documented: You can see it in the folk remdies, fleas are mentioned by some writers, ect.

    Even outside of the highly favorable areas, human tructures could have provided a favorable micro-climate and overwintering spot untill the summer brought enough warmth to get a few flea generations in.

    Fleas can have a wide host range. Infested humans, livestock, pets and unwanted pests would provide a means to spread.
    So spreading at human walk rate (and not rat rate) still does NOT rule out fleas. Nothing would prevent the flea from hitchhiking in human clothing, or luggage/trade goods.

    In most of Europe, temperature and humidity requirements of the flea are met, and allow the flea to complete its lifecycle (see below for temp info), the cat flea can complete its lifecycle in 21-28 days (so a few generations in the summer) and overwintering is definately possible inside (adults can live long without feeding), and quite probably outside during a mild winter or in a favorable micro climate as well (for example, on a host – seeing that even today, every hedgehog found outside seems to be crawling with fleas)

    The living conditions at the time were quite favorable for human and flea contact. Human houses and structures such as barns were probably prime habitat for fleas, and a perfect overwintering site.

    Further, I wonder if the authors take into account how different the living conditions, sanitation wise, were.

    Floors of dirt (for the lower classes) or stone and wood, covered in rushes (straw, herbs). Swept out and replaced maybe once a month, maybe less. (perfect flea larvae habitat, and nice overwintering site)

    No vaccum cleaner that removes adults, eggs and larvae from the floor, just a broom.

    No modern pesticides.

    People had fewer clothes (particularly the lower classes), changed the clothes (also linens, straw matress) less often. May have washed less.

    People (particularly the pesant or surf classes) lived in close quarters with animals. REAL CLOSE – same room, same small building close, and not just with dogs, cats and rodents.
    Livestock also served as a heat source. Even as late as the 16th century you see farm houses in some areas, where the first floor is all the livestock area, and the living area is the floor right above.

    Consider, for example, the temperature and humidity requirements for flea growth
    (From http://www.wvu.edu/~agexten/ipm/insects/hpm4001.pdf )
    ” Adult fleas thrive at temperatures between 66
    degrees and 84 degrees F and at relative humidities
    between 70 and 90 percent. Flea eggs don’t hatch if
    the temperature is below 40 degrees F. A temperature
    below 46 degrees F for 10 days or 37 degrees F
    for five days will kill flea eggs. A relative humidity
    of less than 50 percent will reduce egg hatch by 20
    to 60 percent.
    Flea larvae are the stage that is most sensitive
    to extremes in temperature and humidity. They are
    especially prone to drying out and will die at humidities
    below 45 percent. Larvae will not grow or
    mature at temperatures below 55 degrees F or above
    95 degrees F.”

    A nice link on cat fleas:
    http://www.entm.purdue.edu/publichealth/insects/flea.html

    Cool and rainy Europe would meet those conditions outside for a chunk of the year, and inside even longer.

    Fleas would overwinter quite well in a mideval house, castle or barn.

    - Jag

  16. #16 Sock Puppet of the Great Satan
    January 18, 2008

    “I did some investigating on my own and discovered one of the sources of the anthrax hypothesis was historian Norman Cantor.”

    Naw, Cantor was citing Duncan and Scott’s work. I thought Cantor’s book on the plague was very disappointing, BTW. It was obvious he didn’t have a clue about epidemiology.

  17. #17 Sock Puppet of the Great Satan
    January 18, 2008

    “I did some investigating on my own and discovered one of the sources of the anthrax hypothesis was historian Norman Cantor.”

    Naw, Cantor was citing Duncan and Scott’s work. I thought Cantor’s book on the plague was very disappointing, BTW. It was obvious he didn’t have a clue about epidemiology.