Human African Trypanosomiasis:
A Critical Review
Human African Trypanosomiasis (HAT) or more commonly known as African sleeping sickness is an endemic that is responsible for posing a risk to 60 million people in 36 countries in sub-Saharan Africa( Fig 1) (Brun et al 2009). It is a vector- borne disease which is transmitted by the bite of Tsetse flies of the Glossina genus which injects the protozoan parasite of the genus trypanasoma to humans (Rodgers 2009).
The disease appears to occur in two forms which depend on the subspecies of the parasite involved which include Trypanosoma brucie (T.b) gambiense and Trypanosoma brucie (T.b) rhodesiense. The former is the more common, accounting to be the cause of more than 90% of reported cases and is seen in the Western and Central Africa. The latter causes less than 10% of the disease and prevails in the East and South Africa (Cattand et al 2001, WHO 2006).
Fig 1: Showing distribution of HAT in Sub- Saharan Africa (Brun et al 2009)
After the trypanosomes are injected into the host, the disease is said to be in the first (hemo- lymphatic) stage and as the disease spreads attacking the CNS, it is said to be in the second or meningo- encephalitic stage. T.b gambiense causes a chronic infection with the slow invasion of the CNS which lasts for several years without any major clinical signs and symptoms and T.b rhodesiense leads to an acute infection with the fast invasion of the CNS and clinical presentations are observed from a few weeks or months. Both forms are lethal without any treatment (Cattand et al 2001, Lejon et al 2005, WHO 2006).
In terms of the clinical presentations both forms of Trypanosomiasis vary considerably and many symptoms are non- specific, variable and inconstant. With chronic T.b. gambiense the most prominent symptom is gland enlargement mainly in the neck. Other symptoms in the first stage include general malaise, headache, fever, pruritus, oedema, splenomegaly, hepatomegaly and weight loss. With the invasion of the CNS and the onset of the second stage; the symptoms seen are more of a neural nature and include sleeping disorders, sensory disturbances, endocrine dysfunction, tone & mobility disorders, abnormal movements and mental changes. Eventually the patient stops eating, goes into a deep coma and gradually dies. In T.b. rhodesiense, cardiac failure is the most cardinal symptom and eventual cause is death. Some other symptoms that have been noticed are anaemia, thrombocytopenia and abnormal liver function (Louis et al 2001).
Diagnosis and treatment
Diagnosis is crucial in the treatment of the disease as without it a patient would merely die. It is also very important as without diagnosis, it’s not just the patient that is affected but other people in the population as the patient acts as a reservoir for the disease. On this basis, this essay will aim to critically review some of the methods used for the diagnosis for the T.b. gambiense disease as it is the most prevalent cause of death (fig 2). But the diagnosis is often very difficult as the symptoms are often variable and for this reason prove to be unreliable. As Bouteille et al (2003) and WHO (2006) suggests, the best strategy for treatment is early diagnosis but they say this is not always possible due to the absence of clinical presentations in the hemo-lymphatic stage and also to the fact that parasitological methods available are not sensitive to diagnose the condition at an early stage. The detection of parasitemia is achieved by techniques like lymph node puncture, blood film test and other tests which can detect the trypanosomes in blood. This according to Stich et al (2002) is not reliable as the concentration of the parasites in the blood undulates making them hard to detect especially in the chronic Trypanosomiasis disease.
Fig 2: Showing the steps in diagnosis and treatment stage of HAT (Lejon et al 2005)...
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