Sometimes, I love being wrong


It seems I may have spoken too soon. Quoting myself:

One historical event that has been the subject of much speculation over the decades has been the Plague of Athens, a mysterious outbreak that is thought to have changed the direction of the Peloponnesian War, and for which the cause still remains uncertain.

This plague has been attributed to bubonic plague, toxic shock syndrome and/or necrotizing fasciitis due to Streptococcus pyogenes or Staphylococcus aureus, Salmonella, yellow fever, malaria, Ebola, influenza, and smallpox, to name just a few. Typhus seems to fit the description best, but it’s likely that a cause will never be known with certainty.

Little did I know when I posted that on my old blog (just last month!) that a study had already been accepted to the International Journal of Infectious Diseases suggesting that it’s not typhus (caused by Rickettsia prowazekii), but typhoid fever (Salmonella enterica serovar Typhi) that appears to be the cause of the plague.

(Find out how over at Aetiology)


As an undergrad I attended the national conference for Eta Sigma Phi. One of the students there discussed the possible causes of the Plague of Athens. However, I forget what his conclusion was.

Heh. For those without access to the paper, the entire list of hypothesized causes that have previously been proposed are:

Alimentary toxic aleukia anthrax bubonic plague cholera dengue Ebola/marburg ergotism erysipelas glanders influenza influenza complicated by Guillian Barre syndrome or toxic shock syndrome Lassa fever malaria measles meningitis rift valley fever scarlatina maligna scarlet fever scurvy smallpox sweating sickness toxic shock syndrome tularemia typhoid fever typhus typhus complicated by bubonic plague/dysentery/yellow fever yellow fever complicated by scurvy

It’s been so tought to diagnose because the symptoms described (which can be found here) don’t fit neatly with any contemporary disease. Hence the “X complicated by Y” suggestions.

Intriguing stuff! Thanks, Tara.

And note how a real scientist reacts when new evidence comes along that changes her former “best” understanding of how things work in the real world: she doesn’t whine, cry, or pout.

No way! She loves it! It makes her day! It makes her brain cells itch! It gets her charged up! It may improve our ability to help people avoid plagues like this! This is why she does what she does for a living! It’s fun, it’s cool, it’s neat, it’s just wicked awesome!

Of course, to do this stuff, you also have to be curious, well-educated, mentally flexible, indefatigable, smart as heck, and darn hard-working. Which leaves most of the IDists of the world out of the running right at the start.

And, in saying that “most” of the IDists are left out of the running, I may well have spoken too soon.

And been overly-generous to the IDists.

Extremely interesting.

We should bear in mind that bacteria can be opportunistic super-infectors, though. Haemophilus influenza is so named because it killed many (viral) influenza victims in 1918. However, it was the influenza virus that weakened the victims and set them up for the bacterial infection. H. influenza is a persistent cause of pediatric and opportunistic illnesses (actually, now there’s a vaccine against it). But it wasn’t the cause of the 1918 epidemic. The authors allude to the possibility that other agents may have been involved.

Typhoid fever is still common. It’s a food and water-borne. Sadly, it’s not uncommon when homeless or otherwise desperate people eat from garbage cans. But I’ve never heard of it causing mortality like the level one presumes was associated with the Athenian plague. Even in the pre-antibiotic era, people often survived it. But of course, that’s the recent past. A particularly virulent strain could have been present in Athens at the time of the epidemic.

And of course, one final non-mutually exclusive possibility is that people in Athens had been weakened by malnutrition or some other environmental stressor.

All of these ideas are touched on in the paper.

Since this is PT, I would like to point out the the theory of evolution is extraordinarily good at explaining pathogens.

Oops, I should clarify…I just realized that the confusing nomenclature may be, well, confusing…

Haemophilus influenza is a bacterial species. It owes its confusing name to the fact that it was the final insult for many 1918 victims, and was officially described around that time. However, it does NOT cause influenza. It can cause bacterial meningitis, pneumonia, ear infections, and other things, but not influenza. Influenze predisposed people to an infection with it, and it was named as a result of its association with influenza. (Actually, there was a time when many wrongly believed it to be the cause of influenza. But only briefly.)

The influenza viruses, the true causers of influenza, are, of course, viruses. Not bacteria.


Absolutely. The possibility that these bacteria might just be colonizers and not the primary cause exists. Examining more teeth would help clear this up. Even in 1918, they knew they weren’t seeing H. flu in *all* the cases, so it would help to know if this is present in *all* the individuals in this mass grave? some of them? Is it present in conjunction with other pathogens? etc. The findings so far are intriguing, but still speculative.

Tara – wow, what a great detective story (and obviously one that’s far from being a closed case)! Is it common for human pathogens to be found in dental pulp, even if that’s not the tissue that they normally attack? Do they get released into distant tissues via the circulatory system after the death of the host terminates all immune defenses?

Now that’s a good question, Julie.


The dental pulp is vascularized, so anything that travels via the bloodstream will pass through there. The organisms will be cleared out eventually by the immune system, so using the dental pulp provides a “snapshot” of what was infecting the person at the time of death. As far as release of organisms after death, that’s a good question. Obviously some organisms bloom for awhile after the host dies (leading to its decomposition), but without the heart to pump them through the veins, I don’t think many (any?) would get to the dental pulp. Indeed, that’s one reason it’s used: because it’s largely resistant to bacterial invaders after death.

Julie and Tara -

I’m going to have to do a little reading on dental pulp.

Drancourt et al seem to be the originators of the technique (the link should open a page with six references, including the one discussed above).[…]mp;DB=pubmed

They claim to have sequenced Y. pestis from mediaeval plague victims.

The work is not entirely free of controversy (as you can see from the link above). The “Black Death” is a heated subject for some, and certainly seemed to behave differently from the flea-bite carried bubonic plague of today. Others have claimed not to replicate the Y. pestis result. Pcre is always to be viewed with some caution. On one hand, PCR from tiny amounts of material has proven itself many times, on the other, an element of “art” is often needed.

It is said to be sterile in non-bacteremic people (ie normal people - the blood shouldn’t have any significant number of ciculating bacteria, to put it mildly). Note some immediate limitations. Many people are very sick without having bacteremia.

The problem of post-mortem diagnosis of infectious disease is an important one. As Tara mentioned, post-mortem cultures for bacteria and fungi are potentially contaminated by decomposers who were absent or harmless in life.

If recent autopsy tissue is cultured, you can believe the results if it’s an organism that’s virtually certain to be a pathogen and fits the clinical picture - N. meningitides (which does, however, harmlessly colonize many people in low numbers, but is virtually certain to be a pathogen in the right context), Y. pestis, or something like that. You can disregard results if they don’t make sense and involve a well-known commensal/decomposer type. But there are a lot of organisms, like E. coli and Enterococcus species, to throw out a couple of examples, which can play either role. I have personally experienced situations where this distinction could not be made with certainty.

If dental pulp and PCR continue to show interesting results, it could become a very valuable combination.

Crap, the link doesn’t work. You can go to (not the real url but it works) and seach for “y. pestis dental pulp”.

Also, the “it” in “It is said to be sterile…” above is dental pulp, of course.


There’s some discussion of PCR and their methods over on Aetiology as well that you might be interested in. As you mention, the work Drancourt and others have done has been controversial and is not universally accepted–which is one of the reasons for so much concern about contamination and controls. It’s definitely still a young field and one in which all the kinks haven’t quite been worked out yet, but certainly one to watch.

Weird, that stripped my link. Anyhoo, it’s in the main post.

Here is a new take on the “Black Death” was it a virus ?[…]/blackdeath/

A few clips…

Christopher Duncan and Susan Scott from the University of Liverpool, who in 2001 published a book called Biology of Plagues: Evidence from Historical Populations.…

…They say that during the period of the Great Pestilence there were probably two separate plagues - a viral haemorrhagic fever in Europe, the Black Death; and a bubonic plague in Asia and parts of the Mediterranean coast caused by Yersinia.…

.….Both epidemics are examples of an evolutionary struggle that has gone on for millions of years between disease causing micro-organisms and hosts. If a micro-organism mutates into a form that makes transmission easier - to a new host for example - then it has the advantage. If the host in turn develops a mutation that protects it from the micro-organism, or develops immunity to it, then it has an advantage over that micro-organism.

Man, am I glad my ancestors had a mutated white blood cell gene ;>

Yeah, a problem with that is that (to my knowledge) they’ve only published their ideas in that book, not in the scientific literature. And, the book costs ~$130. [ETA: ah, I see it’s now out in paperback for a mere $60…] It’s an interesting idea (and IIRC, I think part of it deals with the presence of black rats), but it’s a shame they published it there instead of where more scientists could comment on and critique it.

Are you certain this confirmation of the actual cause is new? I thought I read the same conclusion in Italian scientific papers in 1999.

Do you have a reference?

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This page contains a single entry by Tara Smith published on January 24, 2006 12:32 PM.

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