Human African trypanosomiasis (HAT, or sleeping sickness) is a protozoan parasitic infection caused by Trypanosoma brucei rhodesiense or Trypanosoma brucei gambiense. These are neglected tropical diseases, and T.b. rhodesiense HAT is a zoonosis. We review current knowledge on the burden of HAT in sub-Saharan Africa, with an emphasis on the disability-adjusted life year (DALY), data sources, and methodological issues relating to the use of this metric for assessing the burden of this disease. We highlight areas where data are lacking to properly quantify the impact of these diseases, mainly relating to quantifying under-reporting and disability associated with infection, and challenge the HAT research community to tackle the neglect in data gathering to enable better evidence-based assessments of burden using DALYs or other appropriate measures.

/pdf/the-burden-of-human-african-trypanosomiasis-3bwyagdchl.pdf

The Burden of Human African Trypanosomiasis

High systemic drug toxicity and increasing prevalence of drug resistance hampers efficient treatment of human African trypanosomiasis (HAT). Hence, development of new highly specific trypanocidal drugs is necessary. Normal human serum (NHS) contains apolipoprotein L-I (apoL-I), which lyses African trypanosomes except resistant forms such as Trypanosoma brucei rhodesiense. T. b. rhodesiense expresses the apoL-I-neutralizing serum resistance-associated (SRA) protein, endowing this parasite with the ability to infect humans and cause HAT. A truncated apoL-I (Tr-apoL-I) has been engineered by deleting its SRA-interacting domain, which makes it lytic for T. b. rhodesiense. Here, we conjugated Tr-apoL-I with a single-domain antibody (nanobody) that efficiently targets conserved cryptic epitopes of the variant surface glycoprotein (VSG) of trypanosomes to generate a new manmade type of immunotoxin with potential for trypanosomiasis therapy. Treatment with this engineered conjugate resulted in clear curative and alleviating effects on acute and chronic infections of mice with both NHS-resistant and NHS-sensitive trypanosomes.

Experimental therapy of African trypanosomiasis with a nanobody-conjugated human trypanolytic factor.

Salivarian trypanosomes are single cell extracellular parasites that cause infections in a wide range of hosts. Most pathogenic infections worldwide are caused by one of four major species of trypanosomes including (i) Trypanosoma brucei and the human infective subspecies T. b. gambiense and T. b. rhodesiense, (ii) Trypanosoma evansi and T. equiperdum, (iii) Trypanosoma congolense and (iv) Trypanosoma vivax. Infections with these parasites are marked by excessive immune dysfunction and immunopathology, both related to prolonged inflammatory host immune responses. Here we review the classification and global distribution of these parasites, highlight the adaptation of human infective trypanosomes that allow them to survive innate defense molecules unique to man, gorilla, and baboon serum and refer to the discovery of sexual reproduction of trypanosomes in the tsetse vector. With respect to the immunology of mammalian host-parasite interactions, the review highlights recent findings with respect to the B cell destruction capacity of trypanosomes and the role of T cells in the governance of infection control. Understanding infection-associated dysfunction and regulation of both these immune compartments is crucial to explain the continued failures of anti-trypanosome vaccine developments as well as the lack of any field-applicable vaccine based anti-trypanosomosis intervention strategy. Finally, the link between infection-associated inflammation and trypanosomosis induced anemia is covered in the context of both livestock and human infections.

https://biblio.ugent.be/publication/8614888/file/8614889.pdf

Salivarian Trypanosomosis: A Review of Parasites Involved, Their Global Distribution and Their Interaction With the Innate and Adaptive Mammalian Host Immune System.

Trypanosome lytic factor (TLF) is a high-density lipoprotein (HDL) subclass providing innate protection to humans against infection by the protozoan parasite Trypanosoma brucei brucei. Two primate-specific plasma proteins, haptoglobin-related protein (Hpr) and apolipoprotein L-1 (ApoL-1), have been proposed to kill T. b. brucei both singularly or when co-assembled into the same HDL. To better understand the mechanism of T. b. brucei killing by TLF, the protein composition of TLF was investigated using a gentle immunoaffinity purification technique that avoids the loss of weakly associated proteins. HDL particles recovered by immunoaffinity absorption, with either anti-Hpr or anti-ApoL-1, were identical in protein composition and specific activity for T. b. brucei killing. Here, we show that TLF-bound Hpr strongly binds Hb and that addition of Hb stimulates TLF killing of T. b. brucei by increasing the affinity of TLF for its receptor, and by inducing Fenton chemistry within the trypanosome lysosome. These findings suggest that TLF in uninfected humans may be inactive against T. b. brucei prior to initiation of infection. We propose that infection of humans by T. b. brucei causes hemolysis that triggers the activation of TLF by the formation of Hpr–Hb complexes, leading to enhanced binding, trypanolytic activity, and clearance of parasites.

/pdf/hemoglobin-is-a-co-factor-of-human-trypanosome-lytic-factor-1nm72jk4e3.pdf

Hemoglobin Is a Co-Factor of Human Trypanosome Lytic Factor

Leprosy and women

Objective: To find out if indeed anaemia is a major sign in human trypanosomiasis caused by Trypanosoma brucei rhodensiense . 
Design: A one year cross-sectional study of all admitted and surveyed Trypanosoma brucei rhodensiense infected patients (June 2001-June 2002) 
Setting: Nkhotakota District Hospital-Central Region of Malawi. 
Results: After survey and investigations, 28 patients (16 males and 12 females) were admitted to Nkhotakota District Hospital with a parasite positive Trypanosoma brucei rhodensiense infection. Twenty four (85.7%) of them were anaemic. Their mean haemoglobin was 8.96 ± 3.07 g/dl compared to controls that had a mean haemoglobin concentration of 12.17 ± 1.35 g/dl (p 
Conclusion: Though basic, this study has shown that anaemia is indeed a complication of human Africa trypanosomiasis caused by Trypanosoma brucei rhodensiense . There is need for further investigation to investigate the type of anaemia that is caused by this disease. East African Medical Journal Vol.81(10) 2004: 505-508

/pdf/anaemia-in-human-african-trypanosomiasis-caused-by-1gk8bwukfn.pdf

Anaemia in human African trypanosomiasis caused by Trypanosoma brucei rhodesiense.

Objective: To study the profile of leprosy cases at Nkhotakota District Hospital in Central 
Region of Malawi. 
Design: Retrospective cross-sectional study of all registered cases of leprosy from records over a nine year period (January 1992 to April 2001) 
Setting: Nkhotakota District Hospital-Central Region of Malawi. 
Results: In total 526 cases of leprosy were identified from the records. The prevalence rates gradually increased from 0.998 per 10,000 cases in 1992 to 3.39 cases per 10,000 in 1995. There was however a gradual decline of prevalence rates from 1997/1998 that had 3.17 cases per 10,000 to 1.3 cases per 10,000 in 2001. 1996 registered 2.34 cases per 10,000. Fifty seven cases (10.8%) were found with children of the age of 14 or below and 469 (89.2%) cases were of adults. Paucibacillary leprosy presented with more cases than multibacillary leprosy (p East African Medical Journal Vol.80(12) 2003: 635-639

/pdf/leprosy-in-nkhotakota-district-hospital-opwi8xnitp.pdf

Leprosy in Nkhotakota District Hospital.

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Anaemia in human African trypanosomiasis caused by Trypanosoma brucei rhodesiense.

Leprosy in Nkhotakota District Hospital.