|Apr29-12, 11:39 AM||#1|
Some Questions On the Bubonic Plague
Why did these plagues come in waves (Justinian Plague, Black Death of 1347, etc.)? I mean, even when the Silk Road is restricted, the contact and trade never stopped. Rats will always get to be transferred from one end of Eurasia to the other.
Also, I have heard that all of the main Bubonic plagues began in Yunnan, China.
Do you guys know of any very credible books that deal with the origin and "Birthday" of the Bubonic plagues?
|Aug8-12, 02:27 PM||#2|
Hypothesize that there is a species of pathogen with many varieties. It attacks a species of host which itself has many individuals. Each variety can overcome a certain type of antibody or defense of the host. Hosts have a wide variety of antibodies and other defenses, some of which are hereditary and some are developed by the individual in response to sickness. For example, every host of vertebrate can have a histoimmune profile consisting of the specific antibodies it makes to resist pathogens.
The general pathogen infects some hosts all the time. For long periods of time, the pathogen is in equilibrium with the host. The pathogen isn't spreading, infects only a fraction of the host, and causes very few symptoms. However, there is a finite rate at which mutants and other inherited variations occur in the pathogen. Most mutations end up killing the pathogen that has it. For instance, the pathogen could become more sensitive to the antibodies in most hosts. However, a few mutations improve the ability of the pathogen to reproduce and survive. A few mutations will be immune to the antibodies or host.
A new variety of pathogen, that can overcome all the available antibodies in the host, can develop in a single mutation or in a series of mutations. The series of mutations are especially likely if there are small isolated communities inside the larger population of hosts. I won't go into into the second possibility, but it has been studied a great deal in both epidemiology and paleontology. The new variety in the isolated community inevitably gets out to infect the larger host population. Either way, the general host population meets a new variety of pathogen that can overcome the defenses left from the last outbreak.
The pathogen is no longer at equilibrium with the host. The new variety of pathogen spreads rapidly. The pathogen spreads until it has either killed all the individuals that don't resist it or when the majority of individuals have developed antibodies to resist the pathogen. Then, this variety of the pathogen either goes extinct.
Once the new variety of pathogen becomes extinct, the extant varieties of pathogen are in equilibrium with the host. As many hosts catch the disease as become immune to it every day. Because there are so few each day who catch the disease associated with the pathogen, the pandemic becomes unnoticed. The cycle can start over.
New variety develops by one or a few sequential mutations. Overwhelms most of the host. Maybe it kills or immunizes the sensitive host. It leaves a few hardy individuals immune to the new variety. Host population goes into equilibrium with the large population of hosts.
At some point, there will be a mutation or other variation that overcomes the defenses of the remaining host. The newest variety is different from the previous variety in that it can overcome the antibodies of the hosts that are left. Then a new epidemic breaks out.
Basically, it is the same reason that new species of organisms suddenly appear in the fossil record even though evolution is slow. After a mass extinction, there are isolated communities of the organisms. Mutations have less competition than before. New species develop rapidly, taking over host environments. However, eventually the system goes back to equilibrium until the next mass extinction.
This seems antiintuitive to some people. Here is how I think of it.
The development of new varieties is slow, just as Darwin described. However, Darwin was wrong about one thing. The extinction of a species can be very fast. Therefore, the time that a species exists at equilibrium can be very large. Sudden changes of any type can make a new variety that spreads like a wildfire. Like a wildfire, it burns itself out. It immunizes the host, or it kills all susceptible hosts. When a rabid variety goes extinct, there is an illusion that every last member of the species has disappeared. This is wrong. A new variety of that species can reappear at any time. However,
Lets us consider bubonic plague, which is caused by the Yersinai pestis bacterium. Even though it is considered one species, the individual bacterium varies quite a lot. Different individual bacterium have differing ability to infect people with different antibodies. Like all gram-negative bacteria, it conjugates. It exchanges genetic material with others of its kind. It reproduces by splitting, but it also can trade genetic material with others. So there are communities of Yersina pestis bacteria that are similar genetically, but vary a bit from other communities. Occasionally, a Y. pestis bacterium mutates. Most mutations die quickly.
Yersinia is never wiped out. Not only are there many communities in human hosts, but there are many communities in rodent hosts. Every species of rodent has some Yersina, and there are small populations of humans that have it. Most varieties of Yersinia are hardly noticed unless they can overcome the majority of antibodies.
Occasionally, a new variety develops which can overcome all the antibodies among the hosts. It spreads like wild fire. Eventually, people recognize it. They quarantine the victims. They give specific antibiotics to cure the victims. The new variety goes extinct or evolves into a less active bacteria.
A mutation occurs that is immune to common antibodies and to the antibiotics. It spreads. It makes people sick. The cycle occurs again.
Note that today, scientists can identify the new strains. They know these germs are constantly changing. One can never catch the same cold twice. This is why many health organizations try to stop the new varieties soon after they develop.
When I was younger, I read "The Coming Plague" by Laurie Garrett. Some of this information is outdated now. She takes an alarmist stance which in my opinion is slightly exaggerated. However, it describes some of the details very well.
I also recommend: "The Evolution Explosion" by Stephen R. Palumbi. It describes the situation with some pathogens, but not in detail. He is not as alarmist as Palumbi, so maybe you will find what he says less questionable. He makes a strong connection between Darwin's theory of evolution and the spread of disease. I think he is a clearer writer than Garrett, but you can decide. Palumbi focuses on the general theory, and doesn't go into the very fine details.
There are a bunch of more recent books that describe the situation better. I have been out of the loop for some time.
My own opinion is that what we see today is a sort of break. The cycle of disease has been going on for millions of years. Things aren't going to Hell. Things are going back to normal.
|Aug8-12, 03:14 PM||#3|
Paul Ewald. See:
This deals with several different diseases, and the evolution of virulence and why virulence can "go away". Which is what you are asking.
And I disagree with Darwin123. We have recently exploited "holes" in the biochemistry of pathogens. They are evolving in response, so we see antibiotic resistance, for example. We are by no means currently in a lull. And holding pathogens at bay is more a function of socio-economic resources.
An example, phrased another way: who can afford to pay for the newest antibiotic, and who can fund research into more new antibiotics, a third world country or a country like Germany?
For history of disease and human impact:
Hans Zinnser 'Rats, Lice, and History'
Jared Diamond 'Guns, Germs, and Steel'
|Aug8-12, 04:54 PM||#4|
Some Questions On the Bubonic Plague
What I meant was that this wasn't the first time in history that new varieties of diseases are evolving and spreading. The OP asked about the bubonic plague. Clearly, the era of the bubonic plague was a time of rapidly evolving disease. Any time there is a change in environment, one has new diseases. Any time populations are taken out of isolation, one has an explosion of new diseases.
I believe that there are threats of new pandemics. In the long run, we may be faced with a cocktail of infectious diseases. Yet, I doubt that any one of these diseases will by itself match the per capita infectious lethality that was caused by Yersinia pestis during the Black Plague part of its history. Or of small pox and measles after the Europeans started to invade the Americas.
Evolving disease aren't the "end of the world". However, they are not at a lull.
Also note that the two references that I gave are not directly about Yersinia pestis. They are about some of these modern varieties of disease. There was no theory of evolution in medieval times. The Black Plague occurred before humans knew any biochemistry, or even about germs. However, the spread of HIV and other "modern" pandemics has been studied with modern science and technology. Therefore, to catch up on modern understanding of disease one should read up about HIV and other "modern" diseases. Once the basics are understood, he can understand conjectures about bubonic plague.
The OP asked for references specifically about bubonic plague. However, not everything is known about the spread of bubonic plague in medieval times. Research is still being done. However, we should understand modern biology and modern medicine before we discuss historic outbreaks of bubonic plague.
|Aug8-12, 09:54 PM||#5|
|Aug10-12, 01:46 PM||#6|
1) C.Darwin, "Origin of the Species"
2) S. R. Palumbi, "The Evolution Explosion"
3) L. Garret, "The Coming Plague".
These were books readily available in my personal library. They didn't come with links. However, I think they are reputable sources.
I have a large library in my study filled with paper (!) books. I have a cabinet with drawers full of paper (!) articles that I clipped out of journals and magazines. I don't keep an organized list of computer links. Maybe I better start. However, I am a a paper junky.
I read a lot of books on the subject, many of which I had to buy. Some books have been taken from libraries. I also have read a lot of articles on the subject. Many of the articles that I read are from peer-reviewed refereed journals. I thought that peer reviewed publications were considered the most reliable sources for information. Books present knowledge in an organized fashion. The index of a book provides a chain of reference.
Not all good references come with a link. Not all links are reliable sources of information.
I started studying science way before Google existed. Not everything has been placed on a blog.
Next time that I use a reference without a link, I will quote a paragraph from the reference. I will try to look up links that quote that paragraph. However, I don't think it is fair to restrict my citations to references with computer links.
|Aug10-12, 03:54 PM||#7|
I believe a reasonable argument can be made that climate change facilitated the spread of bubonic plague. Here's one link:
|Aug10-12, 03:55 PM||#8|
|Aug10-12, 05:31 PM||#9|
I am answering your question regarding the general pattern of epidemics, rather than focusing on bubonic plague itself. Because bubonic plagues happened mostly in the past, there will always be controversy on the precise way it originated. However, once it originated it kept on appearing and disappearing just as you described. Therefore, you asked a general question as to why epidemics often follow that same pattern.
Please note that the "punctuated equilibrium" theory of disease is not mutually exclusive of other explanations. The mechanism described by "punctuated equilibrium" is very general. The theory does not specify what type of mutations take place, the sudden environmental changes that break the equilibrium, or other specific conditions. The punctuated equilibrium model shows why the pattern of short outbreaks followed by long periods of stasis is common to many pathogens.
Here are some links with corresponding quotes that show the connection between epidemics and punctuated equilibrium. The first link addresses the general connection between sporadic outbreaks of disease and bacterial evolution. The second one concentrates on the influenza virus. The third one on “Sudden Oak Death”. The fourth on vesicular stomatitis virus. The fifth is influenza again.
Genes 2011, 2, 804-828; doi:10.3390/genes2040804
Ecological and Temporal Constraints in the Evolution of Bacterial Genomes
by Luis Boto 1,* and Jose Luis Martínez
Bacterial experimental evolution studies as those performed by the groups of Lenski [2-7],
Rainey [8-13], Levin [14,15] or Kolter [16-19] among several others, have served to experimentally test several general evolutionary processes, which would not be easily tested using multicellular organisms as models. These processes include sympatric diversification, punctuated evolution, kin selection, prey-predator interactions, bet-hedging or the effect of cheating on group selection among others…
One important issue to be mentioned here is the fact that, in addition to the universal principle of evolution based in the selection of gradual modified descendants (mutants) claimed by Darwin  and the proponents of the Modern Synthesis  , HGT, which allows fast, stepwise adaptation by quantum leaps , is a major evolutionary force in bacteria , and an example of punctuated evolution …
Temporal Constraints in the Evolution of Bacterial Genomes: Punctuated Equilibrium and Short-Sighted Evolution…
However, despite this fast adaptation, bacterial core genomes are
rather stable (see above), and it can be stated that the evolution of bacterial genome is an example of punctuated evolution in which periods of fast evolution are followed by stasis...
The relative importance of these mechanisms for bacterial evolution is determined by the ecological scenarios in which bacteria live and follows specific temporal patterns such as those driven by punctuated equilibrium and short-sighted evolution…
“Short-term Evolution In the short-term evolution of influenza A virus, a 2006 study found that stochastic, or random, processes are key factors. Influenza A virus HA antigenic evolution appears to be characterized more by punctuated, sporadic jumps as opposed to a constant rate of antigenic change.
Phenotypic Diversification Is Associated with Host-Induced Transposon Derepression in the Sudden Oak Death Pathogen Phytophthora ramorum
“The emergence of such lineages could be considered examples of “punctuated equilibrium” where evolution proceeds through bursts of rapid morphological change and speciation followed by long term stasis . Zeh and coworkers  have proposed the “epi-transposon hypothesis” in which TEs play a major role in punctuated equilibria.”
“Punctuated equilibrium and positive Darwinian evolution in vesicular stomatitis virus
This is also a demonstration of punctuated equilibrium at the molecular level…
Indeed, the branch length discontinuities are suggestive of punctuated equilibrium. In addition, despite the extensive overall genetic diversity, several specific examples of genetic stasis can be seen…
The punctuated character can not be explained by any heterogeneity of geographic sampling because the geographical breaks in the sampling do not correspond to the long lineages of the phylogeny…”
“A major challenge is the prediction of patterns of evolution and emergence of disease agents. The antigenic evolution of influenza virus is known to follow a punctuated equilibrium model in which periods of relative virus stability around the globe are followed by periods of rapid change, requiring modification of the influenza vaccine.”
|Aug10-12, 05:54 PM||#10|
Although punctuated equilibria likely play a role in the outbreaks of some diseases (like pandemic influenza), in the case of the plague (infection by Yersinia pestis), recent studies suggest that the bacterium that caused the black death did not harbor any mutations that increased its pathogenicity relative to modern, seemingly less deadly strains of the bacterium. From the abstract of the study, which appeared last year in the journal Nature:
For a non-technical summary of the Nature paper, see the link presented by jackmell or the following NY Times writeup:
|Aug10-12, 06:50 PM||#11|
The last great outbreak of bubonic plague in Europe was the Great Plague. This is the plague that drove Isaac Newton into the countryside. The Great Plague "only" killed ten percent of England in a decade. Explain how bubonic plague hid between the Black Plague, later outbreaks, and the Great Plague.
There are two questions asked by the OP. First, how did bubonic plague originate in Europe. Second, how did it come and go for centuries>
I am not addressing the question of origin. I am addressing the issue of why it is sporadic. I agree that the great lethality of the Black Death was not by itself caused by genetic change. Yersinia pestis hasn't changed very much genetically since the Black Death. Therefore, the decrease in over all lethality is mostly due to changes in hygiene, architexture, climate and other environmental factors.
However, how come Yersinia pestis became so sporadic after it was first introduced? I suspect that the epidemiology of later outbreaks wasn't much different from the epidemiology of influenza. You can't blame all these separate outbreaks on one factor alone.
|Aug10-12, 07:20 PM||#12|
One thing to keep in mind is that flea-bitten rats don't have to be transported all across Eurasia to cause outbreaks of plague. Rats breed prolifically and they walk and swim quite well. They can easily repopulate areas in which they have died off.
Rat-infestations on cargo ships, etc, can be documented (you can Wiki for examples), but we can't discount the fact that rats are prolific breeders and can spread into areas where their numbers have diminished for one reason or another.
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