Synonym: African trypanosomiasisGerman: (Afrikanische) Schlafkrankheit, Afrikanische Trypanosomiasis </br> German':Schlafkrankheit
Sleeping sickness is a tropical disease elicited by Trypanosoma brucei.
The reservoir of trypanosomes are humans, cattle and antelopes. Carriers of the sleeping sickness are diurnal biting houseflies (tsetse fly). They are endemic to tropical Africa, predominantly in wetlands (rivers, swamps), but also in dry savannahs (e.g. Kalahari). Its sting is very painful and can occur even through fabric. The protozoa enter the bite lesion with the flyâ€™s saliva. The saliva primarily inhibits the coagulation processes. One bite can transmit several thousand protozoa. Theoretically, one single trypansome is enough to trigger the disease.
Not all tsetse flies are trypanosome vectors, so not every bite inevitably leads to an infection. The rate of endemic infection varies widely regionally and is given as 1:100 to 1:1000. The risk thereby increases proportionally to the number of bites. The infection predominantly affects the indigenous population. Tourists are mainly at risk, if they stay for a longer period in the endemic area.
The incidence pattern of the sleeping sickness is difficult to ascertain regionally; the disease occurs in Africaâ€™s entire tropical region. According to WHO estimates, more than 500,000 humans are affected by trypanosomiasis. Due to the volatile political situation in many regions (refugees), the rate of the disease has increased in recent years.
The course of the disease depends on the triggering protist. In an infection with trypanosomea brucei gambiense, the course of the disease is slower, and in an infection with trypanosomea brucei rhodesiense, it is as a rule faster and more pronounced.
The trypanosomes are surrounded by glycoproteins, the so-called "variable surface glycoproteins" (VSGs). The VSGs are regularly varied by the protozoa during reproduction to escape the immune response of the host (antigenic variation). In the trypanosome genome, more than 1000 different VSG genes are coded, which are alternatively expressed. Even though the human immune system can produce antibodies against the prevalent antigenes, it can only eliminate part of the protist, since new variants already circulate in the blood.
In stage I, the protozoa can be detected microscopically in the blood ("thick drop") or by biopsy of the lymphatic nodes. If the pathology corresponds to stage II, the cerebrospinal fluid is additionally examined. Immunodiagnostic procedures include ELISA, IFT and PHA.
At present (2004), there exists no medicinal prophylaxis for sleeping sickness. The only option is the avoidance of bites. Tourists should protect themselves with repellents, mosquito nets and long-sleeved clothes. However, these measures are successful only to a limited extent, since tsetse flies are very aggressive, and there are always unprotected areas on the body.
Due to the toxicity of available medicines, sleeping sickness is treated in most cases in the hospital. In stage II, arsenic compounds are given that trigger pronounced side effects. Lethality may be up to 5%.
[http://www.who.int/mediacentre/factsheets/fs259/en/index.html WHO-Factsheet sleeping sickness]
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