Trypanosomiasis

Sleeping Sickness

American trypanosomiasis, also known as Chagas disease, affects millions of people throughout the Americas.

Carlos Chagas first described this disease in 1911 when he discovered the parasite in the blood of a Brazilian child with fever, lymphadenopathy, and anemia.

Trypanosoma cruzi, a protozoan hemoflagellate, is the parasite that causes this disease.

When humans are infected, the parasite can cause acute illness; however, the infection is generally asymptomatic. In some cases, usually many years after initial infection, the affected individual can have clinical signs and symptoms from damage to the heart or GI tract.

The disease is the leading cause of non-ischemic congestive heart failure worldwide and notably in Latin America where it is endemic.

Human African trypanosomiasis, or sleeping sickness, is caused by infection with parasites of the genus Trypanosoma, transmitted by the tsetse fly.

tsetse fly

The tsetse fly bite erupts into a red chancre sore and within a few weeks, the person can experience fever, enlarged lymph nodes, hematuria, aching muscles and joints, headaches and irritability. In the first phase, the patient has only intermittent bouts of fever with lymphadenopathy together with other non-specific signs and symptoms. The second stage of the disease is marked by the involvement of the central nervous system with extensive neurological effects like changes in personality, alteration of the biological clock (the circadian rhythm), confusion, slurred speech, seizures and difficulty in walking and talking. These problems can develop over many years and if not treated, the person dies. It is common to the African continent.

tsetse fly bite-chancre

The disease has two forms, Trypanosoma brucie (T b) rhodesiense and T b gambiense; and is almost always fatal if untreated.

Despite a recent reduction in the number of reported cases, patients with African trypanosomiasis continue to present major challenges to clinicians. Because treatment for CNS-stage disease can be very toxic, diagnostic staging to distinguish early-stage from late-stage disease when the CNS invaded is crucial but remains problematic.

Melarsoprol is the only available treatment for late-stage T b rhodesiense infection, but can be lethal to 5% of patients owing to post-treatment reactive encephalopathy. Eflornithine combined with nifurtimox is the first-line treatment for late-stage T b gambiense.

New drugs are in the pipeline for treatment of CNS human African trypanosomiasis, giving rise to cautious optimism.

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