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Back To Vidyya Trypanosoma Brucei Gambiense - African Trypanosomiasis (Sleeping Sickness)

Causal Agents:
Protozoan hemoflagellates belonging to the complex Trypanosoma brucei. Two subspecies that are morphologically undistinguishable cause distinct disease patterns in humans: T. b. gambiense causes West African sleeping sickness and T. b. rhodesiense causes East African sleeping sickness. (A third member of the complex, T. b. brucei, under normal conditions does not infect humans.)

Life Cycle:
T. brucei is transmitted by tsetse flies of the genus Glossina. Parasites are ingested by the fly when it takes a blood meal on an infected mammal. The parasites multiply in the fly, going through several developmental stages in the insect gut and salivary glands (procyclic trypanosomes, epimastigotes, metacyclic trypanosomes). The cycle in the fly takes approximately 3 weeks. When the fly bites another mammal, metacyclic trypanosomes are inoculated, and multiply in the host's blood and extracellular fluids such as spinal fluid. Humans are the main reservoir for T. b. gambiense, but this species can also be found in animals. Wild game animals are the main reservoir of T. b. rhodesiense.

Geographic Distribution:
T. b. gambiense is found in foci in large areas of West and Central Africa. The distribution of T. b. rhodesiense is much more limited, with the species found in East and Southeast Africa.

Clinical Features:
Infection occurs in 3 stages. A trypanosomal chancre can develop on the site of inoculation. This is followed by a hemolymphatic stage with symptoms that include fever, lymphadenopathy, and pruritus. In the meningoencephalitic stage, invasion of the central nervous system can cause headaches, somnolence, abnormal behavior, and lead to loss of consciousness and coma. The course of infection is much more acute with T. b. rhodesiense than T. b. gambiense.

Laboratory Diagnosis:
The diagnosis rests upon demonstrating trypanosomes by microscopic examination of chancre fluid, lymph node aspirates, blood, bone marrow, or, in the late stages of infection, cerebrospinal fluid. A wet preparation should be examined for the motile trypanosomes, and in addition a smear should be fixed, stained with Giemsa (or Field), and examined. Concentration techniques can be used prior to microscopic examination. For blood samples, these include centrifugation followed by examination of the buffy coat; mini anion-exchange/centrifugation; and the Quantitative Buffy Coat (QBC) technique. For other samples such as spinal fluid, concentration techniques include centrifugation followed by examination of the sediment. Isolation of the parasite by inoculation of rats or mice is a sensitive method, but its use is limited to T. b. rhodesiense. Antigen detection assays, in a test format suitable for field use, are being developed and evaluated. Antibody detection has sensitivity and specificity that are too variable for clinical decisions. In addition, in infections with T. b. rhodesiense, seroconversion occurs after the onset of clinical symptoms and thus is of limited use. However, the Card Agglutination Trypanosomiasis Test (CATT) test is of value for epidemiologic surveys or screening of T. b. gambiense.

The drug regimen depends on the infecting species and the stage of infection. For the hemolymphatic stage, the Medical Letter recommends suramin or eflornithine, with pentamidine isethionate as an alternative. The drugs of choice recommended for late disease with central nervous system involvement are melarsoprol or eflornithine, with tryparsamide plus suramin as an alternative regimen (for T. b. gambiense only). (Notes: a) the remaining worldwide supply of eflornithine is very limited, and it is advisable to reserve this drug for the treatment of late stage T. b. gambiense; b) in the hemolymphatic stage, suramin is the drug of choice for T. b. rhodesiense and pentamidine is the drug of choice for T. b. gambiense.)

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Editor: Susan K. Boyer, RN
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