Tsetse flies and Trypanosomes?

Reply Sun 4 Aug, 2013 01:59 pm
Alright, so my name's Nathan, and I'm currently working on an alternate history timeline with a point of departure 176,000 years ago. I'm about 105,000 years or so into the timeline during the Weichselian Glacial Period, and I've been looking for ways to make the tsetse go extinct without some sort of mass extinction of other African fauna.I had initially sought out a way for the trypanosomes to mutate to attack the flies, but since they've evolved over millions of years together with one another, establishing a relationship in which the fly serves as a vector in a very important part of the trypanosome life cycle, that's probably unlikely. So another idea would be a possible evolutionary jump in trypanosomes that would affect tsetse flies and how the parasites are spread.

An idea that a friend of mine (who unfortunately doesn't know much more about the subject) had was to have the parasites evolve instead to live out their entire life cycles within the flies themselves, instead of requiring a vertebrate host for the second part. This would happen specifically in the species Trypanosoma brucei and its susbepcies and initially affect the morsitans variety of tsetse, which are primarily found in savannas in East and Central Africa.

There are a few problems with this however...

As insects have open circulatory systems, it would be very easy for the parasite to transfer into different organ systems if it were to live in the blood, thus making them more easily sexually transmissible. There are two clear problems with that though: A) the trypanosomes live out the initial stage of their lives within the digestive system of the fly as they are picked up in their blood meals, so getting them outside into the circulatory system is... hard to explain, and then B ) insect blood, more properly termed hemolymph, has a different composure than vertebrate blood, so how would it adapt to survive?

After these two problems, I can think of at least two others off the top of my head, such as how to prevent the trypanosomes from attacking infected young before they reach maturity, and how to ensure that the trypanosomes, while infecting the fly, allow the fly to at least reproduce so that it is not so detrimental to the livelihood of the fly so as to be selected against.

Any pointers? Because this has been stumping me for weeks...
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Reply Sun 4 Aug, 2013 02:50 pm
Let me sleep on that a bit.
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Reply Sun 4 Aug, 2013 07:34 pm
Perhaps human could develop their own parasite, residing most of the time in our blood supply, and for the most part relatively harmless to us, its primary hosts. This new parasite could infect and kill any tsetse fly that fed on us. Before long tsetse flies would evolve to feed on other animals besides humans. Their species might or might not go extinct, but what matters is they would cease to trouble us.
Reply Mon 5 Aug, 2013 03:48 am
Heres a summary of the co-evolution of the tse tse and its role as a vector of Trypanosomes. Seems that much isn't really known, so perhaps you oughta consider doing a proposal to NIH or CDC

The epidemiological significance of tsetse fly population structures vis a vis population structures of trypanosomes is virtually unknown and requires both laboratory and field research. These endeavours will not be easy, however.

Clearly, demes in two (of nine) Palpalis group taxa, like those in the Morsitans group, are localized, with little detectable gene flow among demes. The extent of genetic sampling in Palpalis group species, however, is limited taxonomically and geographically. Clearly, gene flow in G. p. gambiensis should be investigated further by using markers that afford higher resolution than our use of SSCPs. A number of G. palpalis and G. fusca subspecies, G. tachinoides and G. pallicera s.l., remain to be studied. Our knowledge of Fusca group genetics is virtually nil.

Sampling of Morsitans group flies, while genetically and geographically much greater than Palpalis and Fusca taxa, has many deficiencies. In particular, G. longipalpis and G. austeni require investigation. For Morsitans group taxa, cytogenetical work at a population level should prove highly interesting given the polymorphisms already detected in G. morsitans s.l. and G. pallidipes.

In terms of population biology, G. pallidipes is probably the most thoroughly investigated tsetse fly. The most recent distribution map of G. pallidipes shows highly fragmented populations (Rogers and Robinson, 2004) and compelling genetic evidence indicates little gene flow among them. Yet gene flow among G. pallidipes demes within environmentally suitable patches also seems restricted, as genetic sampling in Ethiopia, Zambia, Tanzania, and Zimbabwe has shown. Distribution maps of the other genetically sampled morsitans group and palpalis group show much less fragmentation than that for G. pallidipes. Indeed, G. morsitans s.l., G. palpalis s.l. and G. fuscipes s.l. distributions are more or less continuous throughout their ranges (Rogers and Robinson, 2004) yet the patterns of genetic differentiation in these taxa do not seem greatly different than G. pallidipes. Tsetse fly demes seem structured much like island populations. To be sure, there must be gene flow, at least historically, but its magnitude seems small. Even populations of species that recovered from earlier, severe bottlenecks are highly structured – for example, G. morsitans s.l. and G. pallidipes in southern Africa.

What may account for this structure? And how well does the hypothesis of little gene flow agree with ecological knowledge of this important group of vector insects? As we have seen earlier in this essay, tsetse dispersal has been measured and thoroughly analyzed (e.g., Rogers, 1977; Williams et al., 1992; Hargrove, 1981, 2000). Based on earlier direct estimates of movement, tsetse dispersal has been simulated (Hargrove, 2000; Vale and Torr, 2004). All the foregoing evidence strongly suggests there should be abundant gene flow among tsetse demes. Are conclusions drawn from the ecological research false? Or do the simplifying assumptions of population genetic theory render false conclusions when applied to tsetse populations?

Of course not. Ecologists and geneticists have measured different things at different scales (Krafsur, 2002b). Ecological estimates are based on scales of one to tens of kilometers measured over short time intervals. The genetic scales are tens to thousands of kilometers and represent demographic phenomena integrated over intervals of many thousands of generations. Let’s go back to the underlying model against which geneticists test hypotheses about gene flow. The model is an ideal population established by Hardy-Weinberg assumptions, viz., populations of infinite size, discrete generations, of randomly mating individuals, and uninfluenced by natural selection. Few taxa, if any, conform to such a model. Genetic inferences about tsetse population structure include small effective population sizes (Ne) of continuously overlapping generations and geographically fragmented populations. Genetic drift is inversely proportional to Ne so is an especially potent force in tsetse population structure, accounting for most, if not all, of the measured differentiation. Also contributing to the genetic differentiation must be numerous and widespread inhospitable patches, in which the precise biotic and abiotic criteria vary greatly (review in Rogers and Randolph, 1985). There is a strong historical component to the picture, that of the rinderpest epizootic beginning in 1887 that killed out 90% of more of the mammalian fauna upon which tsetse feed. Although the epizootic occurred throughout much of sub-Saharan Africa, its effects on tsetse flies seemed to have been particularly severe in southern Africa, as documented by stockmen, entomologists, and veterinarians during the colonial era (Buxton, 1955; Ford, 1971; Jordan, 1986). Morsitans group flies were diminished to only a few, relict refugia. It is important to note that resurgence of G. morsitans s.l. and G. pallidipes there required many years to return to economically significant levels. A more recent example is afforded by results of the Okavango project in which G. m. centralis has failed to reappear after the six years since control operations ceased. Their slow recovery should be an important consideration in examining cost-benefit analysis of thorough, area-wide tsetse control schemes. As pointed out by Rogers and Randolph (2002), tsetse populations are extremely resilient. Adult female average daily survival probabilities are of the order of 98% or more. The half-life of an adult female cohort born simultaneously on day zero is approximately 35 days. Tsetse populations are able to recover from as few as 16 inseminated females, according to Hargrove’s (2005) estimates. Whether that is actually 10 or 100 inseminated females is moot because such small tsetse populations are not likely to be detected even with intensive sampling. Genetic studies support the existence of highly resilient G. pallidipes populations in two ecologically well-studied sites, Lambwe and Nguruman in Kenya. It was shown that populations there shared little genetic variation with the populations nearby. Hypotheses of massive immigration following control measures or seasonal declines were invoked to explain the reappearance of G. pallidipes in Lambwe and Nguruman (Turner and Brightwell, 1986; Williams et al., 1992). Based on genetic evidence, however, it seems those hypotheses are likely to be false.

Genetic models of population structure are gross oversimplifications of natural demographic phenomena, for example, FST and Ne (Whitlock and McCauley, 1999). Simulation modeling has shown that large variances in deme size, caused by environmental or temporal heterogeneity, can produce high values of FST even when dispersion rates are large (Wegmann et al., 2006). It is clear that estimates of Nem are no substitute for estimates based on mark, release, and recapture trials. Based on the oversimplified genetic models, all we can really say about tsetse dispersion is that the subpopulations sampled contain numerically very few individuals that originated in other subpopulations and genetic drift is the dominant force in population structure. A scenario of massive exchange of individuals among any of the populations sampled to date, however, seems to be untenable when based on the genetic evidence
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