California woman has plague

I thought one only still found bubonic plague in India. I find it kind of alarming that it's found in North America.

I'm actually collaborating with a post-doc on plague: he's in Colorado at the moment (he thinks that plague is just moss on speed). They have it in prairie dogs, and there seem to be quite a few poeple working on it.

Bob

Interesting, but I think those cute little ferrets are at greater risk.

For those interested, Igor Domaradsky's "Biowarrior" is an interesting autobiography of a scientist who went from plague prevention to working on the Soviet Union's infamous Biopreparat BW program.

On Tuesday nite HOUSE had a woamn with the plague. Wednesday I awoke to here this- is life imitating art again?

What is the evidence that the Black Death was bubonic plague? I've never managed to find out. A few years ago I read Biology of Plagues by Scott and Duncan. (See also http://jmg.bmjjournals.com/cgi/reprint/42/3/205). They believe it was a haemorrhagic virus with an unusually long (~32 days) infectious latent period.

I found it quite persuasive, but am no epidemiologist.

s.

You're really asking 2 questions there: 1) re: Black death/bubonic plague, and 2) regarding whether a mutation in CCR5 spread due to black plague. For 1, there are a number of lines of evidence, but it's largely the symptomology. The "buboes" caused by Yersinia pestis are fairly diagnostic, and they were frequently reported in contemporary descriptions of Black Plague victims. Timing was another line of evidence--the plague dissipated in the colder months, as the fleas that carried it died off. More recently, Yersinia pestis DNA has been found in the teeth of some plague victims, pretty much sealing the deal. It's still possible that a hemorrhagic fever virus was circulating at the same time, or perhaps causing co-infections, but there's not a lot of good evidence to support that.

Regarding #2, that one is less clear. It's fairly well-established that the CCR5 mutation spread through the European population at some point in the last 1000-ish years, but the timing varies a bit depending on the assumptions and models, so it's not really known whether smallpox, or Y. pestis, or some other agent played a role in the increase in prevalence of that mutation.

Yes, I know it's really two questions. Biology of Plagues was a book, but really like an immensely long paper, where Duncan and Scott used good records of the progression of the plague through various towns and cities to argue that the symptoms and mechanism of spread were not consistent with Y. pestis. For example, they claim that the plague moved faster and over bigger distances between settlements than it would have done if it was transported by rats, and that even in the mediaeval period people knew about quarantine, which would not have worked if the rats were carrying the pathogen rather than humans.

At the end, they talk a wee bit about CCR5d32. I think that there is at least one paper out there that says this mutation is irrelevant to Y. pestis infection. It makes more intuitive sense that a virus (whether smallpox, a haemorrhagic plague or whatever) was the selective agent than a bacterium.

s.

Right. I'm familiar with the book (though I've not yet read it because of the expense; I see now they've released a paperback for $60), but I was referring to the paper you linked. Apologies for the confusion.

One problem (that I don't know if they address) is that we don't know the extent of bubonic vs. pneumonic plague during the Black Death. From reading other work by Duncan and Scott, it just seems that they put too much on what "couldn't have" happened. I think this is a bad premise in biology, where even the highly unlikely sometimes happens. Add to that the uncertainty of talking about what "couldn't have" been 700 years ago, and I just think it makes it all the more speculative, and they tend to pass over inconsistencies in their own ideas that other biologists find unlikely (such as a 32-day incubation period for a viral hemorrhagic fever, which is pretty long compared to most of those we know today). I think their ideas are intriguing, but still really without much evidence to support them.

It makes more intuitive sense that a virus (whether smallpox, a haemorrhagic plague or whatever) was the selective agent than a bacterium.

How so? I'd agree if it was an extracellular bacterium, but Y. pestis lives intracellularly, so it makes more sense. And indeed, there are a number of papers that go back and forth about whether Y. pestis played a role in selection for the mutation, or if there even was positive selection for it at all. It's definitely a hot area of research, and one where each new paper seems to bring up more questions than answers.

"a 32-day incubation period for a viral hemorrhagic fever is pretty long compared to most of those we know today"
Yes. And a good thing too, if they are right! I agree with you that they are certainly opinionated, and obviously lack convincing evidence of their hypothesis. Digging up a suitable virus from plague graves would be good. But if the Black Death was bubonic plague, one would surely have expected epidemics subsequent to the most recent recorded ones? This is why I set some store by what they suggest: The last plague in Britain was 1665. (In Scandinavia, possibly 1700s). Antibiotics only appeared in the mid-twentieth century. There are still rats in our cities.
There are plenty of accounts of people dying within 24 hours of presenting during the plagues. This seems too fast for bubonic plage even in an untreated patient. So perhaps you are right, and pneumonic plague was more significant. Alternatively, the Black Death might have been a Y. pestis variant which is, thankfully, no longer extant. It's an interesting idea though.
"Y. pestis lives intracellularly..."
Doh! Good point, forgot that...
s.

Digging up a suitable virus from plague graves would be good.

Indeed--but 1) viruses are less protected than bacteria, and may not be preserved; and 2) what one to look for? Ones we know of, such as Ebola or its relatives? Something totally novel? It's something that's really difficult to test, because negative data doesn't really tell you much.

But if the Black Death was bubonic plague, one would surely have expected epidemics subsequent to the most recent recorded ones? This is why I set some store by what they suggest: The last plague in Britain was 1665. (In Scandinavia, possibly 1700s). Antibiotics only appeared in the mid-twentieth century. There are still rats in our cities.

Actually, there's no reason to expect outbreaks to keep re-occurring like that, even if the rats and fleas remain. There's no reason to assume that the same proprtion of rats, for example, were infected with Y. pestis from one year (or one decade, or one score etc.) to another, and even small variations in the percentage of infected animals may have had a large effect. Or as you mention, perhaps there were some changes in the bacterium, where even something minor could cause it to be less deadly (and therefore, less likely to cause severe outbreaks, and more intermittent cases wouldn't be newsworthy enough to deserve comment). There's just a lot of gaps in our knowledge. I don't think any, or even all of them together, are enough to overturn the Y. pestis-->Black Plague idea, though.

There are plenty of accounts of people dying within 24 hours of presenting during the plagues. This seems too fast for bubonic plage even in an untreated patient. So perhaps you are right, and pneumonic plague was more significant. Alternatively, the Black Death might have been a Y. pestis variant which is, thankfully, no longer extant. It's an interesting idea though.

Or they could be exaggerations. During the Spanish flu, there are similar reports of people dying quickly--in some cases, boarding a bus as a well person and dying in their seat a half-hour later. Sure, it's possible for death to be quick, but it's likely (IMO) that some stories are embellished as well, and again, looking back that far in history, it's tough to say what's accurate and what's fictionalized.

Searching around Amazon, I found that Duncan and Scott have a more recent (and significantly cheaper!) book, so I ordered that and I'll write something on the whole black death/Y. pestis/hemorrhagic fever virus/CCR5 topic in the future. I think it's a very interesting topic and appreciate your questions.

" I'll write something on the whole black death/Y. pestis/hemorrhagic fever virus/CCR5 topic in the future."

Kewl. I'll wear my "Celebrating 650 years of Bubonic Plague" T-shirt that my brother-in-law gave me.

"I'll write something on the whole black death/Y. pestis/hemorrhagic fever virus/CCR5 topic in the future"

I look forward to it! It's several years since I read Biology of Plagues. Maybe I'll have a look at their more recent effort as well. With respect to "what virus do you look for?": Ah, there's the rub. If it's real it's clearly not a modern haemorrhagic virus. Even if one could come up with some reasonable primers, it mightn't even be a DNA virus. I wonder if there are any plague graves in the Arctic permafrost?

s.

You can't be 31407 serious?!?

The Great Fire of London 1666 has been mentioned as a possible reason that Plague did not recur. It burned the homes of 70,000 people. Most of the people got out but the rats and fleas might not have.