African Trypanosomiasis (Sleeping Sickness)

Essentials of Diagnosis

Inconspicuous local inflammatory reaction (trypanosomal chancre).

Irregular fever, tachycardia, lymphadenitis, splenomegaly, transient rashes.

Prolonged course (Gambian trypanosomia-sis): Personality changes, headache. apathy. somnolence, tremors, speech and gait distur-bances, anorexia, malnutrition. coma.

Rapid course (Rhodesian trypanosomiasis): Findings as above, but lymph nodes less often enlarged.

Death may occur before signs of CNS involvement appear.

Trypanosomes in thick blood films or lymph node aspirates (early stages); CSF with trypanosomes, increased cells and protein (late stages).

General Considerations

Rhodesian and Gambian trypanosomiasis are caused by 2 morphologically similar protozoan parasites, Trypanosorna rhodesiense and T gambiense, found only as the mature trypanosome form in the blood stream, lymph nodes, myocardium, CSF, and brain. The disease occurs focally throughout tropical Africa. Both trypanosomes are transmitted by the bites of tsetse flies (Glossina sp).

Clinical Findings

A. Symptoms and Signs: The trypanosomal chancre, a local inflammatory reaction which appears about 48 hours after the tsetse fly bite, is the first sign of infection. Many patients give no history of such a reaction; in others the lesions are painful or pruritic and persist up to 3 weeks. The second stage, invasion of the blood stream and reticuloendothelial system, usually begins several weeks later. Symptoms may appear at once, particularly in rhodesiense infections, or after several years. An irregular fever pattern with persistent tachycardia is characteristic. Transient rashes, often circinate. and scattered areas of firm edema may appear. There may be delayed sensation to pain with deep hyperesthesia. The spleen is usually enlarged. Enlarged, rubbery, and painless lymph nodes, particularly those of the posterior cervical group (Winterbottom's sign) are commonly found in gam-biense infection; lymph nodes are not often enlarged in rhodesiense infection. Signs of myocardial involvement appear early in Rhodesian trypanosomiasis. The patient may succumb to myocarditis before signs of CNS invasion appear. Manifestations of the final CNS stage appear within a few weeks or months of onset in rhodesiense infection. Gambian sleeping sickness dif-fers from the acute and virulent Rhodesian form in that it develops more insidiously. starting 6 months to several years from onset. Personality changes, apathy, and headaches are among the early Iindings. Tremors, disturbances of speech and gait, mania, aomnolence, and anorexia appear late. The patient becomes severely emaciated, and finally comatose. Death often results from secondary infection.

B. Laboratory Findings: Lymph node puncture and examination of fresh and stained aspirates is the method of choice for finding T gambiense prior to invasion of the CNS. In early rhodesiense infections blood films will usually reveal a few trypanosomes. In advanced cases lumbar puncture is necessary for diagnosis. the CSF, which is clear, colorless, and under normal pressure, shows increased cells (lymphocytes) and elevated protein. Trypanosomes may be demonstrated in the centrifuged CSF specimen. Serologic tests are of little value in diagnosis.

Other laboratory findings include microcytic anemia, increased sedimentation rate, increased serum globulin, and reduced total serum protein.

Differential Diagnosis

Trypanosomiasis may be mistaken for a variety of other diseases, including malaria, kala-azar, cerebral tumors, encephalitis, and cerebral syphilis. Serologic tests for syphilis may be falsely positive in trypanosomiasis. Malaria, suggested by fever and splenomegaly, may be ruled out by blood examinations; kala-azar, considered because of irregular fever, anemia, splenomegaly, and lymphadenitis, can usually be ruled out clinically without resorting to spleen or marrow puncture. Other CNS conditions are differentiated by neurologic examination and lumbar puncture findings.


Excretion of pentamidine isethionate and suramin sodium (see below) from the body is slow. Either drug will prevent infection for a considerable time after injection. A single injection of 0.3-0.7 gm of suramin (IM or IV) will give protection for 6-12 weeks. One IM injection of pentamidine (3 mg/kg) will protect against rhodesiense infection for 2 months and against gambiense infection for 3-6 months.


A. Specific Measures:

1. Suramin sodium (Naphuride®, Antrypol®) is the drug of choice in the early stages of trypanosomiasis before the CNS is invaded. This organic urea compound is administered intravenously in freshly prepared 10 per cent solution in distilled water. Start treatment with a test dose of 100 mg. For adults, continue with 1 gm doses at 5-7 day intervals to a total of 10 gm. Because of occasional renal toxicity, frequent urinalyses are essential during therapy. Dermatitis and gastrointestinal disturbances are also reported. The drug is contraindicated in renal disease.

2. Pentamidine isethionate (Lomidine®)is somewhat less effective alternative to suramin in treating early trypanosomiasis. It is administered as a 2 per cent solution intramuscularly. The drug may induce a sudden fall in blood pressure or hypoglycemia if given intravenously. It is contraindicated in renal disease. Administer in doses of 4 mg/kg daily or every other day for 10-15 injections.

3. Tryparsamide, a pentavalent arsenical, has long been used in the treatment of gambiense infections of the CNS. It is much less effective against rhodesiense meningoencephalitis. The drug may cause dermatitis or optic atrophy. Discontinue treatment if eye pain, excessive lacrimation, or photophobia develops.

Administer intravenously in a 20 per cent solution in water. The dosage is 20-40 mg/kg, given at weekly intervals to a total course of 10-12 injections. The usual initial dose for adults is 1-1.5 gm; subsequent doses, 2-3 gm. Repeat the course if necessary after a rest period of at least 1 month. A course of suramin or pentamidine should be given simultaneously to remove any parasites remaining in the blood or lymph nodes.

4. Melarsoprol (Mel B®; melarsen oxide/BAL) is effective for the treatment of gambiense and rhodesiense infections of the CNS, but undesirable drug effects are not uncommon. A second course may be given for a relapse, but resistance develops rapidly. Melarsoprol must be given intravenously in 5 per cent solution in propylene glycol.

A recently introduced derivative, Mel W®, is water-soluble and may be given intramuscularly or subcutaneously. It is necessary to use either suramin sodium or pentamidine isethionate in conjunction with melarsoprol to remove trypanosomes from the blood and lymph nodes. A recommended schedule is 3.6 mg/kg daily for 4 consecutive days, a rest of 7 days, and then a second series of 4 daily doses.

B. General Measures:

Good nursing care, treatment of anemia and concurrent infections, and correction of malnutrition are essentials in the management of patients with advanced African trypanosomiasis.


Without treatment, 25-50 per cent of gambiense infec-tions and over 50 per cent of rhodesiense infections are fatal. With treatment, 5-15 per cent of gambiense infections and up to 50 per cent of rhodesiense infections are fatal. Prognosis is considerably more favorable if treatment is started before invasion of the CNS occurs.

The author is practicing medicine.

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