Malevolent Designer News - Sleeping Sickness

The parasite that causes African sleeping sickness can cause death in humans if not treated.

Credit: College of Science

Researchers reveal secrets of parasite that causes African sleeping sickness

The intelligent designer hates Africans. This is obvious from the way it has designed a nasty little parasite and a clever delivery system, that is designed not only to make Africans sick and die but also prevents them using the same domestic animals that allowed Eurasians to develop agriculture. The nasty little parasite is a trypanosome that causes sleeping sickness.

This parasitic trypanosome and its tsetse fly vector have huge economic importance to Africa because while the African native megafauna are all unsuitable for domestication, the Eurasian animals that were used as transport and to pull ploughs in agricultural cultures are all susceptible to it and so agriculture could never spread south of the Sahara to any significant extent, nor could food sources such as sheep and pigs, save in the highlands of Ethiopia, where the tsetse fly is absent.

This means that subsistence agriculture in Africa could never progress much beyond what manpower alone could produce. There appears to be no other purpose for either the trypanosome or the tsetse fly apart from making copies of themselves.

Now a group of researchers has gone some way to discovering just how ingenious this malevolent designer needed to be to make it's hateful plan work.

Abstract
The African trypanosome has evolved mechanisms to adapt to changes in nutrient availability that occur during its life cycle. During transition from mammalian blood to insect vector gut, parasites experience a rapid reduction in environmental glucose. Here we describe how pleomorphic parasites respond to glucose depletion with a focus on parasite changes in energy metabolism and growth. Long slender bloodstream form parasites were rapidly killed as glucose concentrations fell, while short stumpy bloodstream form parasites persisted to differentiate into the insect-stage procyclic form parasite. The rate of differentiation was lower than that triggered by other cues but reached physiological rates when combined with cold shock. Both differentiation and growth of resulting procyclic form parasites were inhibited by glucose and nonmetabolizable glucose analogs, and these parasites were found to have upregulated amino acid metabolic pathway component gene expression. In summary, glucose transitions from the primary metabolite of the blood-stage infection to a negative regulator of cell development and growth in the insect vector, suggesting that the hexose is not only a key metabolic agent but also an important signaling molecule.

IMPORTANCE As the African trypanosome Trypanosoma brucei completes its life cycle, it encounters many different environments. Adaptation to these environments includes modulation of metabolic pathways to parallel the availability of nutrients. Here, we describe how the blood-dwelling life cycle stages of the African trypanosome, which consume glucose to meet their nutritional needs, respond differently to culture in the near absence of glucose. The proliferative long slender parasites rapidly die, while the nondividing short stumpy parasite remains viable and undergoes differentiation to the next life cycle stage, the procyclic form parasite. Interestingly, a sugar analog that cannot be used as an energy source inhibited the process. Furthermore, the growth of procyclic form parasite that resulted from the event was inhibited by glucose, a behavior that is similar to that of parasites isolated from tsetse flies. Our findings suggest that glucose sensing serves as an important modulator of nutrient adaptation in the parasite.

Qiu, Y., Milanes, J. E., Jones, J. A., Noorai, R. E., Shankar, V., & Morris, C. (2018).
Glucose Signaling Is Important for Nutrient Adaptation during Differentiation of Pleomorphic African Trypanosomes,
mSphere 3(5), 1–18. DOI: 10.1128/mSphere.00366-18

Copyright: © 2018 Qiu et al.
Open Access
Reprinted under a Creative Commons Attribution 4.0 International license (CC-BY 4.0)

One of the key things that happens is that, as the parasite is floating around in (mammalian) blood, it perceives its neighbors and says ‘oh, there are a lot of us,’ and becomes a different form that is ready to go into a fly, if the fly were to happen to bite that person. That form that’s ready for life in the fly doesn’t grow – it’s not a growing form – it’s really sitting there, waiting to be taken up by a fly. Once it passes into the fly, though, it begins to grow again. It becomes a form that can live in the fly, and that’s the insect-stage form, or procyclic form.

What has been a mystery, and still is a mystery, is how the parasite really knows where it is. It turns out that if you take the form that lives in the fly and inject it into a mammal, it is killed instantly by the mammal’s immune system. So, the parasite really has to do an excellent job of recognizing its environment.

We’ve always suspected the sugar was the cause, but it’s been hard to prove... We felt, wouldn’t it be interesting if the parasite is monitoring that sugar to know when it has moved into a fly, because when there’s lots of sugar, the parasite thinks ‘I’m in a mammal,’ and when there’s no sugar, the parasite thinks ‘oh, I’m in a fly’. We found that if you take the parasites and remove glucose nearly completely, they’re still alive, which was: A, very surprising because they’re so reliant on the sugar; but B, they also then quickly changed into the form that can live in the fly...

That’s the first step in understanding that pathway and trying to confuse the parasite with drugs later, so that when they’re in your blood, perhaps you could give them a drug and make them think ‘oh, there’s no glucose around, I should become the insect stage,’ and they would be killed.

James C Morris, Co-author
Department of Genetics and Biochemistry,
Eukaryotic Pathogens Innovation Center,
Clemson University, Clemson, South Carolina, USA

The problem the malevolent designer had to overcome was a problem of its own making due to a lack of foresight, as with so many of its malevolent designs. Although it had designed a whole range of other parasites, like bacteria and viruses to make humans (and other animals) sick, it had also, in what was probably a moment of amnesia, forgetting why it had designed things to cause sickness in the first place, had designed a whole complex immune system so animals could defend themselves against the parasites it had designed.

So, having realised its silly mistake in making an immune system, it has had to redesign the parasites so they could overcome it.

The team at the Department of Genetics and Biochemistry, Eukaryotic Pathogens Innovation Center, Clemson University, Clemson, South Carolina, USA, has explained is what triggers the trypanosomes that cause sleeping sickness to change form so it can move from the delivery system - the tsetse fly - to the human and animal host and make them sick.

What they were trying to explain is why, if you take the trypanosomes from a tsetse fly and inject them into a human, the human immune system recognises them immediately as foreign and kills them, yet when they are injected by the tsetse fly, the human immune system doesn't notice them.

Obviously there is something different about the tsetse fly-injected trypanosomes that protects them from a human immune response. Exactly what this is has yet to be explained but what triggers it has now been shown to be the presence of glucose.

So here we have as clear an example as you could wish for of the malevolent intent of any intelligent designer such as creationists insist is managing the design of organisms. This intelligent designer, if it were intelligent and a designer would have a clear purpose for its designs and its designs would do exactly what they are designed to do; nothing more and nothing less.

So, if you subscribe to the claim of intelligent design behind all living things it is impossible not to conclude that this putative designer firstly gave humans and other animals an immune system specifically to protect them against the parasites it designed to attack them. Then, it designed the parasites like this trypanosome to get round the defences it had designed.


And, it is also impossible not to conclude, if you subscribe to the intelligent design idea, because that was the effect of it, that this putative designer intended to have a devastating economic impact on human development in African and designed both the trypanosome that causes sleeping sickness and the tsetse fly to deliver it specifically and deliberately to do it.

Perhaps an ID advocate would explain to people who think making people sick and keeping them in poverty is an evil thing to do, why they are so keen to persuade others to worship this malevolent thing.

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