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Starting in 541–542 AD, the Plague of Justinian and a series of subsequent outbreaks killed between 13-26% of the world's population. The plagues were caused by Yersinia pestis, the same microorganism that would cause the Black Death in the 14th century. However, each subsequent outbreak during this period was less deadly than the previous; likely due to the propensity of pathogenic organisms to adapt in such a way that they actually don't kill their host!

My question is this: What mechanisms exist that might have made a subsequent outbreak of Yersinia pestis more virulent and more deadly that those that preceded it?

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    $\begingroup$ Killing off the last hope of survival for the classical civilization is not enough for you? When Justinian's plague struck, the (Eastern) Roman Empire had reconquered Italy, northern Africa and a fair chunk of Iberia, and had re-established its control over the Mediterranean. Then the plague struck, the economic base collapsed, and the descent into the Middle Ages became unavoidable. $\endgroup$ – AlexP Oct 28 '18 at 21:57
  • $\begingroup$ Are we talking natural mechanisms, or deliberate engineering or use as a weapon? $\endgroup$ – Cadence Oct 28 '18 at 21:58
  • $\begingroup$ @Cadence Natural mechanisms, yes. $\endgroup$ – Arkenstein XII Oct 28 '18 at 22:00
  • $\begingroup$ @AlexP Yeah, I'm looking for a historical divergence through which Europe fails entirely. $\endgroup$ – Arkenstein XII Oct 28 '18 at 22:02
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    $\begingroup$ "Europe fails entirely": but it did fail entirely, didn't it? In the 6th century the economic base of the Roman Empire was in Syria and Egypt, and to lesser extent in Asia Minor. Europe remained an utterly unimportant place until the 13th century, and then it took it four more centuries to build an economic base (and military power) comparable with the Ottoman, or Persian, or Chinese empires. We study the history of Europe not because it was important at that time, but because the European civilization eventually won; but that was a thousand years later. $\endgroup$ – AlexP Oct 28 '18 at 22:18
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Make the incubation period longer.

Traveling in Ancient/Medieval times was slow. A person infected with bubonic plague only had an incubation period of 2-5 days (1-3 if the plague was pulmonary). After that, the disease killed its host in less than 72 hours. There wasn't much time to infect other people and that is why quarantine more or less worked and the cities (specially the ones with good naval communications) were more affected.

By making bubonic plague less "effective", you increase the possibilities of contagion. Mountainous remote populations (like the Pyrenees) aren't safe anymore.

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    $\begingroup$ +1, Basically what I would have answered. Incubation periods can be months long, and people can be infectious during that time. In the time period described, people likely would not even realize what was happening, not mentally linking a touch, cough, or other minor incident a few months ago with their disease and demise now. This was a time in Europe before sanitation, when people still accepted having fleas, before they believed in anything even a proxy for germ theory. Infected people would run when the plague hit their town, thinking they escaped to safety, and spreading the plague fast. $\endgroup$ – Amadeus Oct 29 '18 at 10:40
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I'm not convinced that your assumption that the plagues were less virulent over time because of pathogenic evolution; I think it's more to do with the evolution of the host. This is the same problem we currently have with anti-biotics and pesticides; the organisms that are not killed by them have a form of natural resistance, which (because of the mass extinctions of those organisms without that resistance) gets propagated through the rest of the species pretty quickly.

Ultimately, the humans that survived the plagues in the days of Justinian, and the Black Death of the 14th century were more likely to be resistant to the pathogen, which means subsequent outbreaks are going to be less effective.

THAT SAID;

One way to do it is to have 2x pathogens, each of which exploit an aspect of humans that serves as the resistance to the alternate pathogen. Let's call one the black plague and the other the white plague, for simplicity.

So; you start with the black plague in Justinian's time. That wipes out most of the population with the lowest resistance to it. The survivors breed through several subsequent generations, and then in about 2 centuries, the white plague hits. It specifically targets that part of the genome (or a biological consequence of it) that serves to give resistance to the black plague, so it's very effective. BUT, many out there still have a resistance to the white plague (which means a weakness for the black plague) and then survive, interbreed for a couple of centuries before the black plague hits again.

The white plague has effectively selected weakness to the black plague, meaning this time it'll be more devastating. The advantage (if you want to call it that) to this situation is that you can use a leapfrogging of the pathogens so that each sets up the human race to be hit even harder by the alternate plague.

Eventually (and hopefully), you'll find some human mutation of the human genome that makes a human resistant to both, but in the first instance, this type of leapfrogging pathogen is what would make each turn of the plague more devastating, at least for a millenia or two.

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First lets fix this:

likely due to the propensity of pathogenic organisms to adapt in such a way that they actually don't kill their host!

This is unlikely and flat wrong with respect to the black plague. Microbes generally don't evolve to be less lethal. The microbial world is fairly simply, they do whatever works to reproduce more effectively. Caring about where their nutrition comes from is about the furthest consideration conceived by their short existences.

Immune systems in a similar respect are equally simple, they kill whatever tries to grow where it shouldn't. In many illnesses it is not actually the pathogen itself that kills the host but the immune systems amplified response to the foreign intrusion that ultimately kills the host. Fevers aren't caused by a bacteria they are an immune response in an effort to kill the bacteria.

This brings us to why subsequent outbreaks of a pathogen are less devastating in ancient populations. Previous outbreaks killed off the immunologically weak members of the populace while surviving members passed on both resistant genes and antibodies to the next generation. So in subsequent outbreaks the pathogen is now dealing with immune systems that are more versed in how to deal with the pathogen. This results in both less fatalities as well as less dramatic manifestations of trademark symptoms.

Now for your actual question:

What mechanisms exist that might have made a subsequent outbreak of Yersinia pestis more virulent and more deadly that those that preceded it?

Virulency: Pathogens can evolve certain changes in their structure that make it more difficult for white blood cells to identify them. This can increase the time between which a pathogen reaches a criticality needed to infect other members of a species and the time at which symptoms present themselves. Similarly, the pathogen can also evolve structures that make it more transmittable like being able to survive in an exposed environment or sticking to surfaces.

Lethality: As stated before, simply existing can cause the immune system to kill itself. By being identifiable to the immune system but unkillable the immune system can amplify and amplify till it kills itself. Though that isn't the only means, like any good domineering organism, generalization is key. Being able to spread, adapt to different conditions, and exploit new resources is the key to success. For pathogens this means being able to conquer different tissues/organelles. Encephalitis is condition caused when an infection has compromised the brain. This is one of many means where an infection can directly kill the host as it eats away at brain cells eventually terminating the very controls that keep the body moving.

The challenge To be worse all Yersinia pestis, or any pathogen really, has to do is evolve traits that enable some of the above outcomes. This is generally hard to achieve when the host population is concurrently adapting to its changes. This brings us back to the first point and highlights this cyclical process of adaptation and why the first epidemic is worse than subsequent outbreaks, because the first one is new and unchallenged. I do now want to point out that just because the pathogen appears less deadly does not mean it is.

Did It Become Cuddlier?

HECK NO! If you understand the fact that the bubonic plague still exists today and actually look at plague maps of Europe and Asia over time you might notice What is reported as 3 different plagues isn't necessarily 3 different plagues but really the same plague just evolved each time. See if you pine over maps of Europe, Asia, and Africa the black plague (or some variant of) is always present after the first epidemic. What happens is the local population becomes immune to it preventing it from spreading. Similarly while it is suppressed by that immunity it is learning how to counter it, until finally it does in which case the new and improved form spreads again.

To be even more clear, it never became weaker. From what I've seen the mortality ratings of the Asian, African, and European variants never seem to cull more than 25% of the population. That is until the Spanish Conquests of the New World. The native Americans had never once before been exposed to the disease so it's no wonder that it and other experienced diseases managed to rack up death tolls estimated as high as 90% of the indigenous. Now to be fair it is not definitive whether it was bubonic plague, and or smallpox and or some other pathogen that led to such a number or what the exact number really was. Do bare in mind that an entire empires (that spanned many modern day countries) fall coincides with the Spanish Conquests with Spanish suffering nowhere near the same percent in casualties.

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