Trypanosomiasis African

African trypanosomiasis (sleeping sickness) and American trypanosomiasis (Chagas disease) are caused by Trypanosoma brucei and Trypanosoma cruzi, respectively. Sleeping sickness results from being bitten by the insect vector, the tsetse fly. At first there is only local lymphadenitis but about a month later generalized malaise, fever, and systemic disease involving skeletal muscle is seen. 

Indeed, a bDNA assay for diagnosis of African trypanosomiasis was developed and compared with buffy coat microscopy for detection of T brucei in human blood samples (Harris etal., 1996). Two repetitive DNA sequences found only in the T. brucei complex, a 177-bp satellite repeat and the ribosomal mobile element, were selected as targets in the bDNA assay. The assay used the standard bDNA components capture probes, target probes, amplifier molecules, and alkaline phosphatase-labeled probes. Various blood fractions and sample preparation methods were examined. Ultimately, buffy coat samples resulted in the highest sensitivity. Although typanosomes do not infect leukocytes, they cosediment with them. 

African Regional Industrial Property Organization (ARIPO), 78 198 African trypanosomiasis... 

The second parasitic disease we want to consider is sleeping sickness, or African trypanosomiasis, as it is also known. Sleeping sickness results from an infection by protozoa called trypanosomes that are closely related to Leishmania, and, like leishmaniasis, sleeping sickness is spread by flies. On a more general level, however, the two diseases seem quite distinct. Leishmaniasis takes several forms, only one of which is fatal, but untreated sleeping sickness invariably leads to death. Leishmaniasis is a menace in much of the... 

Flies and mosquitoes are vectors for a number of other diseases that constitute significant menaces to public health, but we do not yet know what role chemical signals play in all of them. Where natural chemicals are important, much additional research will be essential to establish whether they offer realistic approaches to managing these afflictions. The results with leishmaniasis and African trypanosomiasis indicate that such research can both increase our understanding of how fly vectors live and also lead to practical measures for fighting the diseases they carry. 

Pepin, J., and F. Milford. "The Treatment of Human African Trypanosomiasis." Advances in Parasitology 33 (1994) 2-47. 

Belete, H., Tikubet, G., Petros, B., Oyibu, W. A., and Otigbuo, I. N. (2004). Control of human African trypanosomiasis trap and odour preference of tsetse flies (Glossina morsitans submorsitans) in the upper Didessa River Valley of Ethiopia. Tropical Medicine and International Health 9,710-714. 

Conclusion. In African trypanosomiasis there is a very marked increase of the serum IgM—about 10-20 times the normal level. Estimation of the serum IgM can be regarded as a very useful test in the diagnosis of African sleeping sickness. The concentration of serum IgG is slightly raised and serum IgA is normal. In the tropics, trypanosomiasis may be regarded as one of the chief factors which contribute to secondary macroglobulinaemia. 

Chagas disease, the South American variety of trypanosomiasis, is caused by Trypanosoma cruzi. It is quite different from African trypanosomiasis in its clinical and pathological presentation and in its failure to respond to many agents effective in that disease. It has both an acute and chronic phase. The latter frequently results in gastrointestinal and myocardial disease that ends in death. 

Suramin is used primarily to treat African trypanosomiasis, for which it is the drug of choice. It is effective in treating disease caused by Trypanosoma gam-biense and T. rhodesiense but not T. cruzi (Chagas ... 

For obvious reasons of structural analogy to heparinoids the focus of this review is on sulfated carbohydrate derivatives. While it is not in all cases clear that these compounds really mimic the physiological activity of heparinoids, it is even less so for non-carbohydrate sulfates or sulfonates. Examples of the latter class include suramin and the simple 1,3-propanediol disulfate. Suramin is a sulfonat-ed bis-naphthalene derivative used as a drug to treat African trypanosomiasis and onchocerciasis (a filarial infection) it was also tested in a number of other indications including adrenocortical carcinomas and AIDS. A wider use is, however, restricted by various toxic effects [66]. 1,3-Propanediol disulfate reduced inflammation-associated amyloid progression in vivo after oral administration which may be relevant to the treatment of Alzheimer s disease [67]. 

Unlabeled Uses Treatment of African trypanosomiasis, cutaneous or visceral leishma-... 

It is used in the treatment of pneumocystosis (pulmonary and extrapulmonary disease caused by P. carinii), African trypanosomiasis (disease caused by Trypanosoma brucei) and leishmaniasis. Systemic pentamidine is highly toxic and can lead to severe hypotension, tachycardia, dyspnea, dizziness, hypoglycemia. Other adverse effects are skin rash, metallic taste, gastrointestinal symptoms, thrombocytopenia and cardiac arrhythmias. 

It is a sulfated napthylamine and used as first line therapy for early hemolymphatic African trypanosomiasis (caused by T. brucei gambiense). It has very tight protein binding and having short initial half life but terminal half life is about 50 days and is excreted by kidney. It is also used for chemoprophylaxis against African trypanosomiasis. 

Chemically it is trivalent arsenical used for advanced CNS African trypanosomiasis. It is administered IV in propylene glycol and after administration it is rapidly excreted. It is highly toxic and used only in advanced trypanosomiasis when no alternative is there. 

It is an inhibitor of ornithine decarboxylase and is used as second line therapy for advanced CNS African trypanosomiasis. After oral or IV administration, peak plasma level is reached rapidly and elimination half life is approximately three hours. 

The primary drugs used to treat African trypanosomiasis are set forth in Table 52-6, and those for other protozoal infections are listed in Table 52-7. Important drugs that are not covered elsewhere in this or other chapters are discussed below. 

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