African Trypanosomiasis Treatment in India

African trypanosomiasis is a protozoan infection of the species Trypanosoma brucei, transmitted by the bite of a tsetse fly. Symptoms include characteristic skin lesions, intermittent fever, headache, and stiffness, transient enema, generalized. Diagnosis involves the identification of the organism in the blood, lymph node suction, or cerebrospinal fluid, or sometimes serum tests. Treatment is performed with suramine, pentamidine, melarsoprol, or eflornithine, depending on the infective subspecies, clinical stage, and availability of drugs.

African trypanosomiasis is caused by Trypanosoma brucei gambiense in West and Central Africa and East Africa, both of which are endemic in Uganda. African trypanosomiasis has been targeted for eradication by the World Health Organization and as a result of control efforts; there has been a dramatic decrease in the number of reported cases worldwide over the last 20 years.

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African trypanosomiasis has 3 stages:

•         Cutaneous
•         Hemolymphatic
•      Central nervous system

Cutaneous

A papule may develop at the site of a tsetse fly bite within a few days to two weeks. It develops into a dusty red, painful, indurated nodule that can ulcerate (tripanosomal chancre). The chancre is present in about half of Caucasians with rhodesiens, but it is less common in Africans with Rhodesiense and this is rarely the case.

Hemolymphatics

Rhodesiensis, intermittent fever, headaches, rigors, muscle, and joint pain, and transient facial swelling develop. An evanescent, circumcised erythematous rash may develop. It is most easily seen in light-skinned patients.

The central nervous system (CNS)

In the Gambia, CNS involvement occurs months to several years after the onset of acute illness. In the Rhodesian form, the disease is more fulminant, and the invasion of the CNS often occurs within a few weeks. SNC involvement causes a persistent headache, inability to concentrate, personality changes, daytime somnolence, tremor, ataxia, and terminal coma.

Diagnosis

Light microscopy of blood (thin or thick) or other fluid samples. Antibody detection tests are not very useful clinically, as seroconversion occurs after symptoms begin. However, the T-card agglutination test. b. Gambiense is useful in mass screening programs to identify candidates for microscopic examinations. Other non-specific laboratory findings include anemia, monocytosis, and significantly elevated polyclonal serum levels.

Treatment:

WHO recommends eflornithine in combination with nifurtimox 5 mg/kg 3 times daily for ten days. Adverse effects of eflornithine include gastrointestinal symptoms, suppression of bone marrow, and seizures. Common side effects of nifurtimox include anorexia, nausea, vomiting, weight loss, polyneuropathy, headache, dizziness, and dizziness.

Alternative regimens have been proposed for weakened patients with severe CNS involvement. Serial follow-up tests, including a cerebrospinal fluid analysis, are recommended every 6 months (sooner if symptoms return) for 2 years.

Serious side effects of melarsoprol include encephalopathy reactions, exfoliative dermatitis, cardiovascular toxicity (hypertension, arrhythmia, heart problems), and arsenic gastrointestinal and renal damage.

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