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28 5 Hemoflagellates
vector from human to human. Its morphology, habitat and life cycle are similar to
that of T. brucei gambiense.
Pathogenesis and Clinical Features
Trypanosoma brucei rhodesiense causes East African sleeping sickness. It is more
acute than the Gambian form and appears after an incubation period of 4 weeks. It
may end fatally within a year of onset, before the CNS symptoms develop.
Pathological features are similar in both diseases with some variations. Lymphadenitis
is less prominent and typical sleeping sickness picture is seldom seen in East African
trypanosomiasis.
Diagnosis
The diagnosis of both types of human African trypanosomiasis (HAT) is similar.
1. Microscopic examination
Wet mount preparation of lymph node aspirates, CSF, and chancre fluid are
used for demonstration of trypomastigotes. These specimens can be fixed and
stained with Giemsa.
2. Culture
Culture is not routinely used.
3. Animal inoculation
Inoculation of specimens from suspected cases to rats/mice is a highly sensi-
tive procedure.
4. Serodiagnosis
Specific antibodies or antigens can be detected in serum and CSF.
5. Molecular diagnosis
PCR on clinical specimens.
Treatment
Before CNS involvement, pentamidine (i.m. 4 mg/kg daily for 10 days) is the drug
of choice for gambiense human African trypanosomiasis (HAT). This drug does
not cross the blood–brain barrier and hence is ineffective during the CNS stage of
the disease. Suramin (1 g i.v. on days 1, 3, 5, 14 and 21) is the drug of choice for
rhodesiense HAT. In patients with CNS involvement, melarsoprol (2–3.6 mg/kg/
day i.v. for 3 days, a week later, 3.6 mg/kg/day for 3 days followed by a third
series of 3.6 mg/kg/day after a week) is the drug of choice, as it can cross the
blood–brain barrier.