Sorry, server stalled and… well you know the story.
It would be possible to release Y. pestis in rat fleas, but not very practical.
Naturally occurring Y. pestis infection is relatively easily treated with antibiotics, and the bacteria generally does not carry antibiotic resistance (although there is one strain recently isolated in Madagascar that was multiply resistant).
Another problem with the rat infection:
Even if rats were infected there isn’t any evidence that people would be infected at a significant rate. Generally natural outbreaks occur when the rats are disturbed, and when people and rats are forced to live closely together. The last big outbreak in the US was after the 1906 San Francisco earthquake. The last big outbreak in the world was in Sarat, India, also after an earthquake. So unless you could somehow get New Yorkers to live with the rats happily you probably couldn’t get too many of them infected.
However, there is evidenice that Y. pestis has been weaponized. According to the Johns Hopkins Center for Civilian Biodefense Strategies "In the 1950s and 1960s, the U.S. and Soviet biological weapons programs developed techniques to directly aerosolize plague particles, a technique that leads to pneumonic plague, an otherwise uncommon, highly lethal and potentially contagious form of plague. A modern attack would most probably occur via aerosol dissemination of Y pestis, and the ensuing outbreak would be almost entirely pneumonic plague.
More than 10 institutes and thousands of scientists were reported to have worked with plague in the former Soviet Union"
Sparc My understanding is that the number of Black Rat subspecies is legion ( no cite handy, sorry ). I think the “three subspecies” thing is from oft reported number of subspecies in the U.S. ( no longer considered all that valid any more around here because they’ve all interbred ). And I’ve seen names other than the five you’ve listed. There is also a constantly shifting dispute over which is a distinct species - For example one reference considers your R. rattus diardii to be a distinct species, R. diardii.
At any rate Twigg suggests that Rattus rattus is a problematic host for plague in northern Europe, due to temperture constraints. Today it is not found outside of seaports and canal-attached towns in England and this does not seem to be purely a situation of compeitition by the more recently introduced Norway Rat as was once thought. Fossil data backs this up as well ( in fact there is some uncertainty as to if the black Rat was even established in England at all in the 14th century ). The colder it gets, the less successful Rattus rattus is. There are no Black Rats in Greenland for example and the historical record indicates that Greenland was hit even harder by the Black Death than England was. Further tempertures were even colder then and populations much less dense ( which would affect the carrying capacity of the human-tied Black Rats ). All in all there is good evidence, that at least in northern Europe, that Black Rats were not a good candidate for an explosive epizootic in 14th century northern Europe.
- Tamerlane
Thanks, Tamerlane.
I had a vague feeling that the answer would be something in that direction. It obviously still leaves open the question as to what actually caused the plague (if it was the plague) to spread, but I guess this is neither the forum nor the time to start such an exploration.
I’ll go take my tinfoil hat off now.
Sparc
Evidence has come to light in the last few years that Y. pestis really was the 14th-century plague bug. Scientists have extracted Y. pestis DNA from the remains of victims. Here are a couple of cites:
Excellent Bob Scene :)!
Of course if this result has held up it still raises question as to what the vector biology was and why the modern disease doesn’t seem to correlate with the extreme virulence we see in the middle ages. I’d like to see these techniques applied in Britain and on a wider scale to test the hypotheses of a “complex of diseases” in the 14th century epidemic. There is also the question of whether this was a different, more virulent strain of plague or if we just have seen a worldwide increase in resistance ( and what about Justinisn’s “plague”? ).
Always more questions with every answer :).
- Tamerlane
Did enough people die to cause a true genetic drift? (Those who survived had children who would not contract or at least die from the disease?)
Do we really recognize how the huge advances in simple hygiene might effect the spread of the disease? Not just not living with rats and fleas, but washing one’s hand before eating?
Has the bacillus or the flea mutate in any small but significant way?
Tamerlane, thanks for your posts.
A quick question regarding “definitions” if I may. I often hear the terms “vector management” and “reservoir” being used when discussing viral and bacterial outbreaks. What do these terms mean?
Also, Tamerlane, you were kind enough earlier to explain that naturally ocurring outbreaks of “Y Pestis” is found in certain squirrel populations in Nevada (as an example). I’m just a bit confused on something… does “Y Pestis” pretty well kill ‘everything’ it comes into contact with? Or are there some certain animals who naturally carry the bacteria without ever contracting symptoms themselves? And in doing so, are free to pass it on to other organisms without tha natural defence mechanisms?
Oh, I’m sorry - one very last question. The human immune system uses white blood cells to fight off viruses doesn’t it? Hoever, bacterial infections are different beasts I’m told. If it’s not too much of an imposistion, how does the body fight a bacterial infection versus a viral infection?
Thanks guys for the great responses.
A vector is an organism that harbors a disease-causing pathogen and acts as a source of infection for other animals ( including humans ). So vector management refers to controlling the animal vectors that transmit the disease to humans. In this case there is a proximate vector, the infected flea, and a remote vector, the infected rodent. So in this case vector control might consist of culling populations of rodents near habitations and dusting their bodies and burrows for fleas.
A reservoir in this case refers to a species or population of animal that provides a semi-stable residence for some pathogen that can infect humans. In other words they are sort of “maintanence infections” that allow the parasite to hum along. This may consist of animals which are immune or at least highly resistant to a disease ( like native big game is highly resistant to nagana, or “animal sleeping sickness” in Africa that will kill horses dead ). Or it may consist of populations that are strongly affected but the rate of transmission is low enough that it never completely overwhelms the population ( forest monkeys and Yellow Fever ). A pathogen of man that is maintained by another host species is often referred to as a zoonosis ( plural=zoonoses ).
I was referring to a large mountain range called the ‘Sierra Nevada’ in California actually, but it is found in the state of Nevada as well :).
Plague is essentially a disease of rodents and only secondarily man. I think at last count it has been recorded in well over 200 species of rodent. The level of resistance among those species apparently varies a fair bit and there may even be differential resistance at the population level. So, no, it doesn’t always kill. But it often ( usually ) does. In resistant populations what you may have is animals that linger, sick, for quite awhile before finally dieing, while others may shake it off temporarily. For example one species of marmot native to Siberia and Manchuria apparently has such low body tempertures that it retards the infection and allows the animals to survive from one season to the next with the infection. But in the case of Plague I don’t think it is ever completely asymptomatic. This seems to be born out by many rodent species appearing to have regular cycles of epizootics ( just means an epidemic in a non-human animal ) where the populations will crash as infection levels reach periodic highs.
Large topic :). But briefly the term “white blood cell” encompasses something like 15 ( that might be a little off ) different basic varieties of cells from macrophages to eosinophils to killer T-cells. Different varieties separately and in concert serve to deal with both bacteria and viruses ( and other “stuff” ).
I’ll let someone else try summarizing the different responses of the immune systems to viruses vs. bacteria.
- Tamerlane
Oh and I should add that resistant populations of animals may be resistant in the sense that it requires a relatively large quantity of the pathogen in their bodies before they start showing an effect. So it could become infected, but if not constantly reinoculated it will fight it off OR it might become infected and only manifest symptoms days, weeks, or months down the road as the pathogen multiplies to a certain level in their system. So it might appear asymptomatic for awhile before the disease really kicks in.
I’ll also note just for fun that dogs seem more resistant to plague than cats - There have been recorded cases of feline plague.
- Tamerlane
Tamerlane there really isn’t any evidence that the 1400 strain was indeed any more virulent than the current strain.
What most like occurred was; first folks got the bubonic form of the disease, which has about a 50-60% fatality rate when left untreated. Undoubtedly this would have moved to the pneumonic form. Due to overpopulation and unsanitary conditions, the pneumatic form would have quickly spread (bypassing the rat/flea cycle), and killed nearly 100% of the people who caught it. Thus the high death rates.
The Justinian epidemic was also most likely Y. pestis. The symptoms certainly matched; as recorded by Procopius.
Boo Boo Foo any parasite that kills it’s host is an unsuccessful parasite. Ideally (for the bacteria) an infection will be comensial like the bacteria in your gut. That way the little guys get everything they need for their entire lifespan. What this means is that the Y. pestis found in the fleas of rats shouldn’t kill the rats or the fleas, or it becomes unsuccessful and will cause it’s own extinction. The human infection is a side effect (if you will) of a successful parasitic infection of the flea/rat.
Except some population densities weren’t all that great. An analysis of English populations in 1377 showed that 90% of the population lived in small villages of 50-200 which were generally reasonably well spaced out. Northern Europe in general was much less densely crowded ( even if above overall environmental carrying capacity ) than southern Europe where you had ( particularly in the Italian cities ) more of the phenomena of small buildings crowded with many people ( for example the populations of Genoa had perhaps 545 people/hectare vs. Brussels at 56/hectare ). Further to ramp up pneumonic plague you first have to have established bubonic plague and analyses of the Indian epidemic have indicated that small communities ( such as predominated in England ) may not be capable of establishing an active bubonic phase ( to be fair there may be other factors confoundin that comparison ).
Further further ( 
) later outbreaks do not appear to follow that explosive death toll model. The 1665 London outbreak appears to have killed 68,596 out of perhaps 350,000-450,000, a death rate 0f 15-20%. This compared to 30-50% for England as a whole ( far less crowded overall than London ) during the Black Death. In India between 1897 and 1907 the death toll very slowly ratcheted up from 20/100,000 to a peak of 410/100,000 in 1907 ( then declining somewhat quickly. 6,000,000 people died in extremely crowded India ( without widespread availability of antibiotics ) during those eleven years out of a population of 329 million ( estimates of 70-80 million deaths a al Shrewsbury appear to be errors, at least according to Twigg ).
And blah, blah, blah - I could go on ;). I’m not really disagreeing with you per se, as you may well be right :). Just saying that there have been conflicting arguments on this issue.
Certainly appears that way, I agree. But some authors have argued that it wasn’t purely plague, but rather a melange of different epidemics including smallpox.
Not necessarily - If it can successfully reproduce and transfer to a new host AND the rate of transmission or course of the infection is not enough to permantly deabilitate the host species population, ultimate individual host survival is irrelevant.
Yes, but it does kill them in this case. Or at least a very significant proportion of the infected hosts anyway, depending on species of rodent or flea. It may be that all roads lead towards commensalism ( though I doubt that, personally ), but Y. pestis obviously isn’t there yet. We can see all sorts of progressions like this. Plasmodium vivax and P. falciparum both appear to be human-adapted species of malaria with no stable zoonoses, yet one is considerably more malign than the other. On the other hand the relatively rare P. ovale causes a relatively mild infection, definitely milder than P. falciparum, yet it IS a zoonosis, in this case probably being synonomous with the non-human primate malaria P. schwetzi.
On that, I agree :).
- Tamerlane
Tamerlane I concede to your obviously superior knowledge on this subject. I don’t know nothin’ 'bout no population densities in the Middle ages!
As an undergrad I did my research on Y. pseudotuberculosis. It’s a useful organism to study because it’s about 95% similar to *Y. pestis[/y] and has multiple plasmids which are fun to play with. So if there are any question about Yops. I’m your girl!
You guys! Thank you ever so much for your wonderful input.
“Bio Brat”? May I ask you a question regarding tuberculosis then? I watched (yet another) documentary in the last 6 months on tuberculosis in the Russian city of Tomsk. If memory serves me correctly, I understand that the prison system in Tomsk has turned out to be (unknowingly) the world’s perfect incubator for a totally antibiotic resistant strain of tuberculosis due it’s dark, cramped, damp conditions. The prison’s doctors pumped generic forms of antibiotics into their prisoners for 50 years and in doing so, created a ‘super TB microbe’ I’m told.
How much chance is there of that super-strain of TB getting out into the wider population? And that’s what ‘consumption’ was, wasn’t it?
Am I correct in understanding that TB is a pneumonic airosol microbe which prefers dark damp environments and that we’d be pretty safe here in Australia?
This is such an old argument, you know.
On one side are people who:
- Want to cause harm.
- Want to be able to say whatever they want, whenever they want.
- Understand there’s risk, but in their worldly wisdom have considered all possible outcomes, and have decided, unilaterally, that if the chance is only X%, then it’s ok by them!
- Don’t understand what the risk is, and have no way to evaluate it, so imagine there isn’t any.
On the other are:
- People who know what they are talking about, and are worried about the risk.
- People who don’t know about the risk, but aren’t willing to accept much…especially when in the hands of types 1, 2, 3, 4 above who are obviously capable of causing a great deal of harm without caring much about their responsibility.
I suggested this thread’s information could be misused, and your answer was: “But I want to talk about it.”
P.S. And if I want to contradict your statement that the discussion’s impractical… wouldn’t that support exactly the kind of discussion we’d all like to avoid?
The discussion’s impractical, until we discover it isn’t, then we take it all back in a hurry?
Boo Boo Foo First I should preface this by saying that Y.
pseudoturbroculosis is not Mycobacterium tuberculosis which is
the causative agent in TB (aka Consumption aka white death). However, I think
I can still give you a pretty good answer.
Mycobacterium spp. has some advantages when it comes to causing disease in modern humans. First off, it’s highly mutatable. It is naturally resistant to a wide variety of antibiotics. Also it’s a very slow grower. It lurks around forever before actually forming a colony. This makes it much harder to detect in a sample unless you’re looking for it. It’s easily out-competed by other, faster growing bacteria. But when grown in the presence of multiple antibiotics, it’s usually the only guy to show up.
This mutatability makes it difficult to control, and in fact, TB is usually treated with an antibiotic cocktail, so that all of the bacteria are killed off, and no resistant strains are created. It is very important when treating a TB infection to test for resistance in the lab, so that the proper treatment can be given. This is why your prison was such a good incubator. Apparently the prison docs were just throwing antibiotics at the sick, thus allowing the development of multiply resistant strains. Prisons, are ideal breeding grounds for M. tuberculosis, since TB is spread by aerosol. TB is also easily spread in hospitals and schools, if they aren’t fanatical about cleanliness (with alcohol, or bleach- not those antibiotic soaps and lotions). Much like Y. pestis, M. tuberculosis thrives where there is overpopulation and unsanitary conditions.
However, the dampness and the darkness would only be side issues. They would allow environmental bacteria to hang around a bit linger, but since TB is a direct airborne transmission it probably didn’t effect it too much. Bacteria in general like damp, dark places. This is why they love your kitchen sponges and your bath towel. It’s also why they like your nose, gut and lungs. So really, the fact that you’re an Aussie doesn’t effect a bacteria’s love of your mouth. However, Australia’s TB rates have varied little in the past decade, ranging from 3.7 to 4.1 cases per 100,000 population. (Just as a side note: Australia is the only continent other than Antarctica that has never had an incidence of Y. pestis infection).
bio-brat, as your name suggests, shall we just mark you down for one of those who doesn’t care about the consequences of their statements and won’t accept reponsibility for them?
This is how “irresponsibility” is defined. Your statements are irresponsible.
Unless, of course, you’re prepared to pay for damages. Can we see evidence that you’ve got enough money put aside to pay restitution to the survivors of an outbreak in your town?
Um, partly_warmer, why did you not respond to Point 3? To my mind, that’s the kicker.
The information in this thread already exists and is available to the public.
your point appears to be
Well, it’s already been done. Not only by the CDC. Hell, I’ve read a fictional novel about the bubonic plague hitting NYC - through the rats.
If you are Joe Terrorist, where are you going to look for ideas about bioterrorism? The JAMA, CDC publications, epidemiology and infectious disease textbooks - or the GQ forum of the SDMB?
Sua