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Could trypanosomes evolve to attack their invertebrate hosts?


Zirojtan

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Hey guys, my name's Nate (Zirojtan), and this is my first post on these forums.

 

 

I'm writing an alternate history timeline that concerns a point of departure around 176,000 years ago, and recently I've been looking into the possible extinction of the tsetse as one of the butterflies of the timeline.

 

 

I don't really know if this is any of your thing our not, so I won't go into a lot of detail about the timeline itself, and just skip ahead to the question I had: is it biologically feasible for a species of trypanosome, specifically one that effects antelope/equids, to evolve to attack the tsetse itself? If so, how would you explain such a mutation and the advantages posed by it, if any?

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I only know of trypanosomes that are harmful, such as the one that causes sleeping sickness. So having a species within within that phyla become harmful to another species isn't unbelievable.

No, but the new strain would have a difficult time spreading if it's killing off its primary transmission vector.

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No, but the new strain would have a difficult time spreading if it's killing off its primary transmission vector.

I agree, but if it doesn't attack the other reservoir species and uses a different transmission vector it's plausible. Not to say it wouldn't take a suspension of disbelief, but any sort alternate history book like this would have some difficulty being perfectly accurate.

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My friend and I were discussing it a little more and I've decided that it's not entirely plausible, at least the way I had originally thought it out. The trypanosomes associated with sleeping sickness, specifically those in the species Trypanosoma brucei spend their larval stage inside the tsetse, and mature into their adult form inside their human/cattle/equine/camelid/antelopine host. Unfortunately, the trypanosomes once in their vertebrate hosts are able to adapt too quickly for the immune system to handle, so the idea that my friend had was that the trypanosomes would adapt to live out their entire life cycle within the flies instead of requiring the transfer between species. This way, the trypanosomes could possibly remain inside the former vector, the fly, and nature might select for those that can mature inside the vector instead over those that need another host to complete their life cycle. At that point, the trypanosomes may not attack the flies until they're in their adult stage, killing only mature adults. It may shorten the lives of the flies by a day or two, but it won't drive them into extinction. Instead, it would mean that the trypanosomes that cause sleeping sickness would become specifically adapted to fly hosts, and not infect humans/other mammals.

 

 

Although, there is the obvious problem that "sleeping sickness" is actually caused by a few different species of trypanosomes that occur in a number of different varieties of tsetse. So, if I applied this to one species of trypanosome in one variety of fly (specifically the morsitans variety, as they are the most widespread), I can see it creating an advantage for Africans in some areas of Africa, allowing for an increased human population and possibly the domestication of some native fauna (the common eland, specifically), but I think that by and large, sleeping sickness would still exist, and there's still malaria to worry about when it comes to empire-building in Africa as well...

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