Why trypanosomes cause sleeping sickness.

@article{Lundkvist2004WhyTC,
  title={Why trypanosomes cause sleeping sickness.},
  author={Gabriella B. S. Lundkvist and Krister Kristensson and Marina Bentivoglio},
  journal={Physiology},
  year={2004},
  volume={19},
  pages={
          198-206
        }
}
African trypanosomiasis or sleeping sickness is hallmarked by sleep and wakefulness disturbances. In contrast to other infections, there is no hypersomnia, but the sleep pattern is fragmented. This overview discusses that the causative agents, the parasites Trypanosoma brucei, target circumventricular organs in the brain, causing inflammatory responses in hypothalamic structures that may lead to dysfunctions in the circadian-timing and sleep-regulatory systems. 
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Research on sleeping sickness parasite biology and the impact it has on host health is summarized and the possible evolutionary advantages of sleep and circadian deregulation for the parasite are considered.
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It is shown that the robust circadian rhythms of mice become phase advanced upon infection, with abnormal activity occurring during the rest phase, and proposed that T. brucei causes an advanced circadian rhythm disorder, previously associated only with mutations in clock genes, which leads to changes in the timing of sleep.
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The sleep architecture of male mice infected with T. brucei was assessed and it was found that infected mice had drastically altered sleep patterns, suggesting that signaling of adenosine, a neuromodulator involved in mediating homeostatic sleep drive, may be reduced in infected mice.
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Although a great deal of progress has been made in recent years, the advent and application of sophisticated analysis techniques, to decipher the complexities of HAT pathogenesis, herald an exciting and rewarding period for advances in trypanosome research.
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Experimental results that support crossing of the blood–brain barrier and of theBlood–CSF barrier are listed and the implications that either pathway would have on infection progress and on the survival strategy of the parasite are discussed.
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The symptomatology of travellers is markedly different from the usual textbook descriptions of African HAT patients and a promising new drug combination is currently evaluated in a phase 3 b study and further new drugs are under evaluation.
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