Sleeping Beauty Syndrome

Trypanosoma brucei are parasitic protests which are responsible for African sleeping sickness in 36 countries of sub-Saharan Africa. It is comprised of three sub-species Trypanosoma brucei brucei, Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense. Of these three subspecies, only the last two are infectious in humans. Sleeping sickness can be very devastating to humans and there are over .5 million cases of sleeping sickness and 70,000 deaths caused by it each year. In addition, the diseases is always fatal if it is left untreated. In the past thirty years, failures in control measures and treatments have caused the fatality rate of this parasite to increase so much that it is now the biggest killer in parts of Africa such as in areas in Angola, Congo and Southern Sudan.

Tsetse Fly [2]

Trypanosoma brucei is transmitted between mammals by its intermediate host the tsetse fly which acquires the parasite by biting mammals and feeding on their blood. In mammals the parasite lives freely in the blood stream which is why it can be easily acquired by tsetse flies through biting mammals. Once in the tsetse fly the parasite establishes itself in the midgut of the fly but then migrates to the salivary glands in order to be transmitted to another mammal.

Trypanosoma brucei life cycle [3]

In a more detailed look at the life cycle of Trypanosoma brucei, the parasite divides rapidly in the blood stream of its mammal host as morphologically slender forms. Then following this proliferation, the parasite expresses the bloodstream-stage-specific VSG coat to evade the mammalian immune response. The mitochondrial genome of the parasite is located in the posterior end of the parasite and during this phase the mitochondrial activity is relatively repressed. As the number of parasites increases in the bloodstream, the parasite undergoes a change in morphology from their slender form to a stumpy form. The stumpy phase is a division-arrested form which is adapted for transmission to the tsetse fly. Following the transfer to the tsetse fly the parasite undergoes another morphological change into its procyclic form and resides in the flies midgut. The procyclic form looses the VSG from the parasite form and replaces it with a coat composed of and GPEET procyclins. After establishment in the fly midgut, the parasite stop division and then migrate to the tsetse salivary gland, where they attach as epimastigote forms. These divide rapidly and multiple and are attached through elaboration of their flagellum. Eventually they generate metacyclic forms, which have re-acquired a VSG coat in preparation for transmission to a new mammalian host. Then when the tsetse fly next bites a mammal the parasites are transferred to a new host where the cycle starts over again.

[1] Matthews, K,R. 2005 The developmental cell biology of Trypanosoma brucei. Journal of Cell Science 118, 283-290.

[2] http://media-1.web.britannica.com/eb-media/99/24099-004-EB15ADB7.jpg

[3]http://www.dpd.cdc.gov/dpdx/images/ParasiteImages/S-Z/TrypanosomiasisAfrican/AfrTryp_LifeCycle.gif