Background: Sleeping sickness (human African trypanosomiasis) is a parasitic infection transmitted by day-biting tsetse flies. The diagnostic standard is microscopy of blood, lymph node aspirates, or cerebrospinal fluid. The disease is invariably fatal if not treated. There are >300,000 new cases of sleeping sickness each year and ~100,000 deaths. Case Presentation: We describe a British soldier who acquired sleeping sickness in Malawi. He gave no history of a painful insect bite but presented with classic early signs of sleeping sickness (a primary chancre, regional lymphadenopathy, circinate erythema, and a cyclical fever pattern). His condition worsened in the next week, and trypanosomes were observed in a blood sample. The patient was aeromedically evacuated to Johannesburg, where stage 1 Trypanosoma brucei rhodesiense infection was confirmed; he also had renal and liver failure, pancytopenia, and heart block. He was treated with intravenously administered suramin, and he recovered fully over the next 5 months. Recommendations: Medical officers deploying to eastern and southeastern Africa must be familiar with the common presenting signs and symptoms of T. b. rhodesiense sleeping sickness and should have 24-hour access to a reliable, local, clinical microscopy service. Confirmed sleeping sickness requires immediate transfer to a tertiary diagnostic and treatment center, where suramin (for T. b. rhodesiense infection), pentamidine (for Trypanosoma brucei gambiense infection), and melarsoprol (for stage 2 disease) must be immediately available.

Human African trypanosomiasis, or sleeping sickness, affects one-half of Africa’s continental land mass. The disease is considered to have had a greater negative  impact on the economic development of central Africa than any other.1 There are >300,000 new cases of sleeping sickness each year and -100,000 deaths.2·3 Since 1990, the rate of infection has risen tenfold.4

Sleeping sickness is confined to the equatorial region and occurs in a patchy distribution throughout central and southeastern Africa, including Malawi.5 During a 3-year period of national surveillance (November 1986 to September 1989), 33 cases of sleeping sickness were recorded from the Kasungu National Park.6 The greatest risk of acquiring sleeping sickness in Malawi is during the dry season, which in most years runs from May to October.5

Sleeping sickness is transmitted by tsetse flies of the genus Glossma and is caused by two different parasite subspecies, that is, Trypanosoma brucei rhodesiense, which causes acute sleeping sickness, and Trypanosoma brucei gambiense, which causes a more-chronic disease presentation.7 Key differences between the two forms of the disease are summarized in Table I. Game animals and cattle are the natural reservoirs of T. b. rhodesiense, and humans, domestic pigs, and some wild mammals are the natural reservoirs of T. b. gambiense.8

The survival of Trypanosoma brucei in mammalian hosts derives from its ability to very readily alter its antigenic profile.9 The bloodstream forms of T. brucei are covered with a dense coat of highly immunogenic glycoproteins, which stimulate the production of specific antibodies, mainly of the IgM subclass.10 Approximately 2% of each new T. brucei generation expresses a different surface glycoprotein, thus stimulating the production of a new IgM population; this process enables the parasite to elude the host immune response. ‘ ‘ Over time, trypanosomes are able to penetrate the central nervous system (CNS), probably through damage to and breakdown of the choroid plexus.” Death is most commonly attributable to neurological involvement, leading to neglect, malnutrition, infection, and eventual coma.7·11

Clinical Presentation

The early symptoms of sleeping sickness can be nonspecific, and it is essential for medical officers in disease-endemic areas to consider trypanosomiasis in the differential diagnosis of any patient with a febrile illness.12 Tsetse bites can be quite painful, and they often leave a small, self-healing mark.13 Wien trypanosomal infection follows a tsetse bite, a more-pronounced, longerlasting, local reaction occurs, with injected trypanosomes multiplying at the bite site.

A small red papule develops after ~5 days, expanding over the next 7 to 10 days to a hard, painful, round, pruritic nodule, the “erythematous pseudo-furuncle” (up to 3 cm in diameter).13 At this stage, the lesion usually is warm, painful, and somewhat tender (although it is painless in some cases) and typically is surrounded by an intense erythematous tissue reaction, with local edema; the whole complex is called a primary chancre, or trypanosomal chancre.2 The chancre usually persists for ~3 weeks and then subsides spontaneously, to be replaced by a hyperpigmented, painless, nontender eschar (Fig. I).7 During this time, lymph nodes in the region of the bite may become enlarged as drainage from the bite site occurs.