AFRICAN TRYPANOSOMIASIS ( SLEEPING SICKNESS ) : CLINICALASPECTS
The trypanosomal chancre appears 2 to 3 days after the bite of the tsetse fly as a raised, reddened nodule on one of the exposed surfaces of the body. With the onset of para-sitemia 2 to 3 weeks later, the patient develops recurrent bouts of fever, tender lym-phadenopathy, skin rash, headache, and impaired mentation. In the Rhodesian form of disease, myocarditis and CNS involvement begin within 3 to 6 weeks. Heart failure, con-vulsions, coma, and death follow in 6 to 9 months. Gambian sleeping sickness pro-gresses more slowly. Bouts of fever often persist for years before CNS manifestations gradually appear. Spontaneous activity progressively diminishes, attention wavers, and the patient must be prodded to eat or talk. Speech grows indistinct, tremors develop, sphincter control is lost, and seizures with transient bouts of paralysis occur. In the terminal stage, the patient develops a lethal intercurrent infection or lapses into a final coma.
A definitive diagnosis is made by microscopically examining lymph node aspirates, blood, or cerebrospinal fluid for the presence of trypomastigotes. Early in the disease, ac-tively motile organisms can often be seen in a simple wet mount preparation coat smear; identification requires examination of an appropriately stained smear. If these tests prove negative, the blood can be centrifuged and the stained buffy coat examined. Inoculation of rats or mice can also prove helpful in diagnosing the Rhodesian disease. The patient may also be screened for elevated levels of IgM in the blood and spinal fluid or specific trypanosomal antibodies by a variety of techniques. A simple card agglutination test, which can be performed on finger-stick blood, can provide serologic confirmation within minutes. Subspecies-specific DNA probes may eventually prove useful for the identifica-tion of organisms in clinical specimens.
Lumbar puncture must always be performed before initiation of therapy. If the specimen reveals evidence of CNS involvement, agents that penetrate the blood – brain barrier must be included. Unfortunately, the most effective agent of this type is a highly toxic arseni-cal, melarsoprol (Mel B). Although this agent occasionally produces a lethal hemorrhagic encephalopathy, the invariably fatal outcome of untreated CNS disease warrants its use. The ornithine decarboxylase inhibitor, eflornithine appears capable, when used alone, or together with suramin, of curing CNS disease caused by T. brucei gambiense without the serious side effects associated with melarsoprol. Unfortunately, it is very expensive and is only variably effective in T. brucei rhodesiense infections. If the CNS is not yet involved, less toxic agents, such as suramin, pentamidine, or eflornithine, can be used. In such cases, the cure rate is high and recovery complete.
Although a variety of tsetse fly control measures, including the use of insecticides, defor-estation, and the introduction of sterile males into the fly population, have been at-tempted, none has proved totally practicable. Similarly, eradication of disease reservoirs by the early detection and treatment of human cases and the destruction of wild game has had limited success. Attempts to develop effective vaccines are currently under way but are complicated by the antigenic variability of most trypomastigotes. A degree of per-sonal protection can be achieved with insect repellents and protective clothing. Although prophylactic use of pentamidine was once advocated, enthusiasm for this treatment has waned.
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