Journal articles: 'Trypanosomiasis; Sleeping sickness'

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Kennedy, Peter G. E. "Sleeping sickness - human African trypanosomiasis." Practical Neurology 5, no. 5 (October 2005): 260–67. http://dx.doi.org/10.1111/j.1474-7766.2005.00324.x.

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Burri, Christian. "Sleeping Sickness at the Crossroads." Tropical Medicine and Infectious Disease 5, no. 2 (April 8, 2020): 57. http://dx.doi.org/10.3390/tropicalmed5020057.

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Gibson, Wendy. "Report on African Trypanosomiasis (Sleeping Sickness)." Transactions of the Royal Society of Tropical Medicine and Hygiene 98, no. 6 (June 2004): 392. http://dx.doi.org/10.1016/j.trstmh.2004.02.001.

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Cox, Francis E. G. "History of sleeping sickness (African trypanosomiasis)." Infectious Disease Clinics of North America 18, no. 2 (June 2004): 231–45. http://dx.doi.org/10.1016/j.idc.2004.01.004.

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Kirchhoff, Louis V. "American trypanosomiasis (Chagasʼ disease) and African trypanosomiasis (sleeping sickness)." Current Opinion in Infectious Diseases 7, no. 5 (October 1994): 542–46. http://dx.doi.org/10.1097/00001432-199410000-00004.

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Lundkvist, Gabriella B., Krister Kristensson, and Marina Bentivoglio. "Why Trypanosomes Cause Sleeping Sickness." Physiology 19, no. 4 (August 2004): 198–206. http://dx.doi.org/10.1152/physiol.00006.2004.

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African trypanosomiasis or sleeping sickness is hallmarked by sleep and wakefulness disturbances. In contrast to other infections, there is no hypersomnia, but the sleep pattern is fragmented. This overview discusses that the causative agents, the parasites Trypanosoma brucei, target circumventricular organs in the brain, causing inflammatory responses in hypothalamic structures that may lead to dysfunctions in the circadian-timing and sleep-regulatory systems.

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Baker, John. "Progress in human African Trypanosomiasis, sleeping sickness." Transactions of the Royal Society of Tropical Medicine and Hygiene 94, no. 1 (January 2000): 82. http://dx.doi.org/10.1016/s0035-9203(00)90449-8.

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Kennedy, Peter G. E. "Update on human African trypanosomiasis (sleeping sickness)." Journal of Neurology 266, no. 9 (June 17, 2019): 2334–37. http://dx.doi.org/10.1007/s00415-019-09425-7.

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Kennedy, Peter G. E. "The continuing problem of human African trypanosomiasis (sleeping sickness)." Annals of Neurology 64, no. 2 (August 2008): 116–26. http://dx.doi.org/10.1002/ana.21429.

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P. De Koning, Harry. "The Drugs of Sleeping Sickness: Their Mechanisms of Action and Resistance, and a Brief History." Tropical Medicine and Infectious Disease 5, no. 1 (January 19, 2020): 14. http://dx.doi.org/10.3390/tropicalmed5010014.

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With the incidence of sleeping sickness in decline and genuine progress being made towards the WHO goal of eliminating sleeping sickness as a major public health concern, this is a good moment to evaluate the drugs that ‘got the job done’: their development, their limitations and the resistance that the parasites developed against them. This retrospective looks back on the remarkable story of chemotherapy against trypanosomiasis, a story that goes back to the very origins and conception of chemotherapy in the first years of the 20 century and is still not finished today.

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Rogers, D. J., and B. G. Williams. "Monitoring trypanosomiasis in space and time." Parasitology 106, S1 (January 1993): S77—S92. http://dx.doi.org/10.1017/s0031182000086133.

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SUMMARYThe paper examines the possible contributions to be made by Geographic Information Systems (GIS) to studies on human and animal trypanosomiasis in Africa. The epidemiological characteristics of trypanosomiasis are reviewed in the light of the formula for the basic reproductive rate or number of vector-borne diseases. The paper then describes how important biological characteristics of the vectors of trypanosomiasis in West Africa may be monitored using data from the NOAA series of meteorological satellites. This will lead to an understanding of the spatial distribution of both vectors and disease. An alternative, statistical approach to understanding the spatial distribution of tsetse, based on linear discriminant analysis, is illustrated with the example of Glossina morsitans in Zimbabwe, Kenya and Tanzania. In the case of Zimbabwe, a single climatic variable, the maximum of the mean monthly temperature, correctly predicts the pre-rinderpest distribution of tsetse over 82% of the country; additional climatic and vegetation variables do not improve considerably on this figure. In the cases of Kenya and Tanzania, however, another variable, the maximum of the mean monthly Normalized Difference Vegetation Index, is the single most important variable, giving correct predictions over 69 % of the area; the other climatic and vegetation variables improve this to 82 % overall. Such statistical analyses can guide field work towards the correct biological interpretation of the distributional limits of vectors and may also be used to make predictions about the impact of global change on vector ranges. Examples are given of the areas of Zimbabwe which would become climatically suitable for tsetse given mean temperature increases of 1, 2 and 3 °Centigrade. Five possible causes for sleeping sickness outbreaks are given, illustrated by the analysis of field data or from the output of mathematical models. One cause is abiotic (variation in rainfall), three are biotic (variation in vectorial potential, host immunity, or parasite virulence) and one is historical (the impact of explorers, colonizers and dictators). The implications for disease monitoring, in order to anticipate sleeping sickness outbreaks, are briefly discussed. It is concluded that present data are inadequate to distinguish between these hypotheses. The idea that sleeping sickness outbreaks are periodic (i.e. cyclical) is only barely supported by hard data. Hence it is even difficult to conclude whether the major cause of sleeping sickness outbreaks is biotic (which, in model situations, tends to produce cyclical epidemics) or abiotic. The conclusions emphasize that until we understand more about the variation in space and time of tsetse and trypanosomiasis distribution and abundance we shall not be in a position to benefit from the advances made by GIS. The potential is there, however, to re-introduce the spatial and temporal elements into epidemiological studies that are currently often neglected.

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Blum, Johannes A., Christian Burri, Christoph Hatz, Leon Kazumba, Patrick Mangoni, and Michael J. Zellweger. "Sleeping hearts: the role of the heart in sleeping sickness (human African trypanosomiasis)." Tropical Medicine & International Health 12, no. 12 (December 7, 2007): 1422–32. http://dx.doi.org/10.1111/j.1365-3156.2007.01948.x.

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HIDE, G., and A. TAIT. "Molecular epidemiology of African sleeping sickness." Parasitology 136, no. 12 (June 26, 2009): 1491–500. http://dx.doi.org/10.1017/s0031182009990333.

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SUMMARYHuman sleeping sickness in Africa, caused by Trypanosoma brucei spp. raises a number of questions. Despite the widespread distribution of the tsetse vectors and animal trypanosomiasis, human disease is only found in discrete foci which periodically give rise to epidemics followed by periods of endemicity A key to unravelling this puzzle is a detailed knowledge of the aetiological agents responsible for different patterns of disease – knowledge that is difficult to achieve using traditional microscopy. The science of molecular epidemiology has developed a range of tools which have enabled us to accurately identify taxonomic groups at all levels (species, subspecies, populations, strains and isolates). Using these tools, we can now investigate the genetic interactions within and between populations of Trypanosoma brucei and gain an understanding of the distinction between human- and nonhuman-infective subspecies. In this review, we discuss the development of these tools, their advantages and disadvantages and describe how they have been used to understand parasite genetic diversity, the origin of epidemics, the role of reservoir hosts and the population structure. Using the specific case of T.b. rhodesiense in Uganda, we illustrate how molecular epidemiology has enabled us to construct a more detailed understanding of the origins, generation and dynamics of sleeping sickness epidemics.

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Kennedy, Peter GE. "Clinical features, diagnosis, and treatment of human African trypanosomiasis (sleeping sickness)." Lancet Neurology 12, no. 2 (February 2013): 186–94. http://dx.doi.org/10.1016/s1474-4422(12)70296-x.

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Cook, G. C. "Patrick Manson (1844–1922) FRS:Filaria (Mansonella) perstansand sleeping sickness (African trypanosomiasis)." Journal of Medical Biography 20, no. 2 (May 2012): 69. http://dx.doi.org/10.1258/jmb.2010.010051.

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Blum, Johannes A., Caecilia Schmid, Christoph Hatz, Leon Kazumba, Patrick Mangoni, Jonas Rutishauser, Anna la Torre, and Christian Burri. "Sleeping glands?—The role of endocrine disorders in sleeping sickness (T.b. gambiense Human African Trypanosomiasis)." Acta Tropica 104, no. 1 (October 2007): 16–24. http://dx.doi.org/10.1016/j.actatropica.2007.07.004.

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Xiao, Zhengguang, Aisheng Dong, and Yang Wang. "FDG PET/CT in a Case of Human African Trypanosomiasis (Sleeping Sickness)." Clinical Nuclear Medicine 43, no. 8 (August 2018): 619–22. http://dx.doi.org/10.1097/rlu.0000000000002149.

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Wéry, M. "Drug used in the treatment of sleeping sickness (human African trypanosomiasis: HAT)." International Journal of Antimicrobial Agents 4, no. 3 (August 1994): 227–38. http://dx.doi.org/10.1016/0924-8579(94)90012-4.

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Carvalho, Luis, Marta Martínez-García, Ignacio Pérez-Victoria, José Ignacio Manzano, Vanessa Yardley, Francisco Gamarro, and José M. Pérez-Victoria. "The Oral Antimalarial Drug Tafenoquine Shows Activity against Trypanosoma brucei." Antimicrobial Agents and Chemotherapy 59, no. 10 (July 20, 2015): 6151–60. http://dx.doi.org/10.1128/aac.00879-15.

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ABSTRACTThe protozoan parasiteTrypanosoma bruceicauses human African trypanosomiasis, or sleeping sickness, a neglected tropical disease that requires new, safer, and more effective treatments. Repurposing oral drugs could reduce both the time and cost involved in sleeping sickness drug discovery. Tafenoquine (TFQ) is an oral antimalarial drug belonging to the 8-aminoquinoline family which is currently in clinical phase III. We show here that TFQ efficiently kills differentT. bruceispp. in the submicromolar concentration range. Our results suggest that TFQ accumulates into acidic compartments and induces a necrotic process involving cell membrane disintegration and loss of cytoplasmic content, leading to parasite death. Cell lysis is preceded by a wide and multitarget drug action, affecting the lysosome, mitochondria, and acidocalcisomes and inducing a depolarization of the mitochondrial membrane potential, elevation of intracellular Ca2+, and production of reactive oxygen species. This is the first report of an 8-aminoquinoline demonstrating significantin vitroactivity againstT. brucei.

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Mulenga, Gloria M., Lars Henning, Kalinga Chilongo, Chrisborn Mubamba, Boniface Namangala, and Bruce Gummow. "Insights into the Control and Management of Human and Bovine African Trypanosomiasis in Zambia between 2009 and 2019—A Review." Tropical Medicine and Infectious Disease 5, no. 3 (July 11, 2020): 115. http://dx.doi.org/10.3390/tropicalmed5030115.

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Tsetse transmitted trypanosomiasis is a fatal disease commonly known as Nagana in cattle and sleeping sickness in humans. The disease threatens food security and has severe economic impact in Africa including most parts of Zambia. The level of effectiveness of commonly used African trypanosomiasis control methods has been reported in several studies. However, there have been no review studies on African trypanosomiasis control and management conducted in the context of One Health. This paper therefore seeks to fill this knowledge gap. A review of studies that have been conducted on African trypanosomiasis in Zambia between 2009 and 2019, with a focus on the control and management of trypanosomiasis was conducted. A total of 2238 articles were screened, with application of the search engines PubMed, PubMed Central and One Search. Out of these articles, 18 matched the required criteria and constituted the basis for the paper. An in-depth analysis of the 18 articles was conducted to identify knowledge gaps and evidence for best practices. Findings from this review provide stakeholders and health workers with a basis for prioritisation of African trypanosomiasis as an important neglected disease in Zambia and for formulation of One Health strategies for better control and/or management of the disease.

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Castaño, M. Soledad, Maryam Aliee, Erick Mwamba Miaka, Matt J. Keeling, Nakul Chitnis, and Kat S. Rock. "Screening Strategies for a Sustainable Endpoint for Gambiense Sleeping Sickness." Journal of Infectious Diseases 221, Supplement_5 (December 26, 2019): S539—S545. http://dx.doi.org/10.1093/infdis/jiz588.

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Abstract Background Gambiense human African trypanosomiasis ([gHAT] sleeping sickness) is a vector-borne disease that is typically fatal without treatment. Intensified, mainly medical-based, interventions in endemic areas have reduced the occurrence of gHAT to historically low levels. However, persistent regions, primarily in the Democratic Republic of Congo (DRC), remain a challenge to achieving the World Health Organization’s goal of global elimination of transmission (EOT). Methods We used stochastic models of gHAT transmission fitted to DRC case data and explored patterns of regional reporting and extinction. The time to EOT at a health zone scale (~100 000 people) and how an absence of reported cases informs about EOT was quantified. Results Regional epidemiology and level of active screening (AS) both influenced the predicted time to EOT. Different AS cessation criteria had similar expected infection dynamics, and recrudescence of infection was unlikely. However, whether EOT has been achieved when AS ends is critically dependent on the stopping criteria. Two or three consecutive years of no detected cases provided greater confidence of EOT compared with a single year (~66%–75% and ~82%–84% probability of EOT, respectively, compared with 31%–51%). Conclusions Multiple years of AS without case detections is a valuable measure to assess the likelihood that the EOT target has been met locally.

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Bakshi, Rahul P., Dongpei Sang, Andrew Morrell, Mark Cushman, and Theresa A. Shapiro. "Activity of Indenoisoquinolines against African Trypanosomes." Antimicrobial Agents and Chemotherapy 53, no. 1 (September 29, 2008): 123–28. http://dx.doi.org/10.1128/aac.00650-07.

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ABSTRACT African trypanosomiasis (sleeping sickness), caused by protozoan Trypanosoma brucei species, is a debilitating disease that is lethal if untreated. Available drugs are antiquated, toxic, and compromised by emerging resistance. The indenoisoquinolines are a class of noncamptothecin topoisomerase IB poisons that are under development as anticancer agents. We tested a variety of indenoisoquinolines for their ability to kill T. brucei. Indenoisoquinolines proved trypanocidal at submicromolar concentrations in vitro. Structure-activity analysis yielded motifs that enhanced potency, including alkylamino substitutions on N-6, methoxy groups on C-2 and C-3, and a methylenedioxy bridge between C-8 and C-9. Detailed analysis of eight water-soluble indenoisoquinolines demonstrated that in trypanosomes the compounds inhibited DNA synthesis and acted as topoisomerase poisons. Testing these compounds on L1210 mouse leukemia cells revealed that all eight were more effective against trypanosomes than against mammalian cells. In preliminary in vivo experiments one compound delayed parasitemia and extended survival in mice subjected to a lethal trypanosome challenge. The indenoisoquinolines provide a promising lead for the development of drugs against sleeping sickness.

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Wendel, S. "Transfusion-transmitted American and African trypanosomiasis (Chagas disease and sleeping sickness): neglected or reality?" ISBT Science Series 1, no. 1 (September 2006): 140–51. http://dx.doi.org/10.1111/j.1751-2824.2006.00023.x.

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Akazue, Pearl Ihuoma, Godwin U. Ebiloma, Olumide Ajibola, Clement Isaac, Kenechukwu Onyekwelu, Charles O. Ezeh, and Anthonius Anayochukwu Eze. "Sustainable Elimination (Zero Cases) of Sleeping Sickness: How Far Are We from Achieving This Goal?" Pathogens 8, no. 3 (August 29, 2019): 135. http://dx.doi.org/10.3390/pathogens8030135.

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The recent massive reduction in the numbers of fresh Human African Trypanosomiasis (HAT) infection has presented an opportunity for the global elimination of this disease. To prevent a possible resurgence, as was the case after the reduced transmission of the 1960s, surveillance needs to be sustained and the necessary tools for detection and treatment of cases need to be made available at the points of care. In this review, we examine the available resources and make recommendations for improvement to ensure the sustenance of the already achieved gains to keep the trend moving towards elimination.

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Kagira, J. M., N. Maina, J. Njenga, S. M. Karanja, S. M. Karori, and J. M. Ngotho. "Prevalence and Types of Coinfections in Sleeping Sickness Patients in Kenya (2000/2009)." Journal of Tropical Medicine 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/248914.

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The occurrence of coinfections in human African trypanosomiasis (HAT) patients was investigated using a retrospective data of hospital records at the National Sleeping Sickness Referral Hospital in Alupe, Kenya. A total of 31 patients, 19 males and 12 females, were diagnosed with HAT between the years 2000 and 2009. The observed co-infections included malaria (100%), helminthosis (64.5%), typhoid (22.5%), urinary tract infections (16.1%), HIV (12.9%), and tuberculosis (3.2%). The species of helminthes observed includedAncylostoma duodenale(38.7%),Ascaris lumbricoides(45.7%),Strongyloides stercoralis(9.7%), andTaeniaspp. (3.2%). The patients were also infected withEntamoebaspp. (32.3%) andTrichomonas hominis(22.6%) protozoan parasites. The main clinical signs observed at the point of admission included headache (74.2%), fever (48.4%), sleep disorders (45.2%), and general body pain (41.9%). The HAT patients were treated with suramin (early stage, 9/31) and melarsoprol (late stage, 22/31). In conclusion, the study has shown that HAT patients have multiple co-infections which may influence the disease pathogenesis and complicate management of HAT.

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Parwan, Deepika, Ranjan Kumar, and Sumit Aggrawal. "African Trypanosomiasis in Young Female in North India - A Rare Case Report." Annals of Pathology and Laboratory Medicine 8, no. 4 (May 10, 2021): C71–73. http://dx.doi.org/10.21276/apalm.2997.

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Human African trypanosomiasis, also known as sleeping sickness, is a vector-borne parasitic disease. It is caused by infection with protozoan parasites belonging to the genus Trypanosoma. They are transmitted to humans by tsetse fly (Glossina genus) bites which have acquired their infection from human beings or from animals harboring human pathogenic parasites. Tsetse flies are found just in sub-Saharan Africa though only certain species transmit the disease. We report a case of human African trypanosomiasis in a 28-year-old Indian female who had a travel history to sub–Saharan Africa, Uganda and she presented with a history of fever, body ache, headache, decreased oral intake, pain lower abdomen, swelling and discharge from forearm chancre since last 4-5 days. Peripheral smear showed heavy parasitemia by flagellated forms of Trypanosoma and the diagnosis of Trypanosoma brucei was given on Peripheral smear report. Serological testing was also done and a diagnosis of West-African trypanosomiasis was confirmed. The patient was successfully treated and made a good recovery. So West-African trypanosomiasis should be considered in the differential diagnosis with presentation of fever with chancre in every person with recent history of travel to African countries as it is universally fatal without treatment.

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Havik, Philip Jan. "Public health and tropical modernity: the combat against sleeping sickness in Portuguese Guinea, 1945-1974." História, Ciências, Saúde-Manguinhos 21, no. 2 (May 20, 2014): 641–66. http://dx.doi.org/10.1590/s0104-59702014005000013.

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Until the establishment of the “Commission for the study of and combat against sleeping sickness” (Missão de estudo e combate à doença do sono) in 1945, underfunded and understaffed health services had not been a priority for the colonial administration in Portuguese Guinea. The Commission not only implemented endemic disease control in the territory under the auspices of metropolitan institutions, but also provided preventive public healthcare to the local population. Its relative success in reducing the negative impact of Human African Trypanosomiasis turned the colony into an apparent model of tropical modernity. In the process, the local evolution of the disease was marginalized, despite the tacit but contested recognition by some health professionals of the role of popular healthcare.

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Olet, Pamela, and Joseph Othieno. "How to do mass media publicity for a neglected disease. Lessons from Tsetse and Trypanosomiasis in Kenya." Journal of Science Communication 14, no. 03 (August 19, 2015): Y03. http://dx.doi.org/10.22323/2.14030403.

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The prioritization of neglected diseases in the policy making framework requires heightened advocacy [WHO, 2006]. Mass media positive publicity is among approaches that can be used to achieve this. This paper discusses practical use of mass media to do publicity and advocacy for a neglected disease and its vector. It uniquely presents online links to the analyzed newspaper and television news and opinion articles on tsetse and Trypanosomiasis. The paper shares entry points into mass media advocacy from a lessons learned perspective and notes the importance of understanding how the mass media works in order to achieve advocacy of neglected diseases using sleeping sickness as a case study.

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Njiru, Zablon K., Cecilia K. Mbae, and Gitonga N. Mburugu. "Loop-Mediated Isothermal Amplification Test forTrypanosoma gambienseGroup 1 with Stem Primers: A Molecular Xenomonitoring Test for Sleeping Sickness." Journal of Tropical Medicine 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/8630708.

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The World Health Organization has targeted Human African Trypanosomiasis (HAT) for elimination by 2020 with zero incidence by 2030. To achieve and sustain this goal, accurate and easy-to-deploy diagnostic tests for Gambian trypanosomiasis which accounts for over 98% of reported cases will play a crucial role. Most needed will be tools for surveillance of pathogen in vectors (xenomonitoring) since population screening tests are readily available. The development of new tests is expensive and takes a long time while incremental improvement of existing technologies that have potential for xenomonitoring may offer a shorter pathway to tools for HAT surveillance. We have investigated the effect of including a second set of reaction accelerating primers (stem primers) to the standardT. brucei gambienseLAMP test format. The new test format was analyzed with and without outer primers. Amplification was carried out using Rotorgene 6000 and the portable ESE Quant amplification unit capable of real-time data output. The stem LAMP formats indicated shorter time to results (~8 min), were 10–100-fold more sensitive, and indicated higher diagnostic sensitivity and accuracy compared to the standard LAMP test. It was possible to confirm the predicted product using ESE melt curves demonstrating the potential of combining LAMP and real-time technologies as possible tool for HAT molecular xenomonitoring.

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RADWANSKA, MAGDALENA. "Emerging trends in the diagnosis of Human African Trypanosomiasis." Parasitology 137, no. 14 (April 12, 2010): 1977–86. http://dx.doi.org/10.1017/s0031182010000211.

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SUMMARYHuman African trypanosomiasis (HAT) or sleeping sickness is caused by protozoan parasitesTrypanosoma brucei gambienseandT. b. rhodesiense. Despite the enormous technological progress in molecular parasitology in recent years, the diagnosis of HAT is still problematic due to the lack of specific tools. To date, there are two realities when it comes to HAT; the first one being the world of modern experimental laboratories, equipped with the latest state-of-the-art technology, and the second being the world of HAT diagnosis, where the latest semi-commercial test was introduced 30 years ago (Magnuset al.1978). Hence, it appears that the lack of progress in HAT diagnosis is not primarily due to a lack of scientific interest or a lack of research funds, but mainly results from the many obstacles encountered in the translation of basic research into field-applicable diagnostics. This review will provide an overview of current diagnostic methods and highlight specific difficulties in solving the shortcomings of these methods. Future perspectives for accurate, robust, affordable diagnostics will be discussed as well.

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Gervas, Hamenyimana Emanuel, Nicholas Kwasi-Do Ohene Opoku, and Shamsuddeen Ibrahim. "Mathematical Modelling of Human African Trypanosomiasis Using Control Measures." Computational and Mathematical Methods in Medicine 2018 (November 22, 2018): 1–13. http://dx.doi.org/10.1155/2018/5293568.

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Human African trypanosomiasis (HAT), commonly known as sleeping sickness, is a neglected tropical vector-borne disease caused by trypanosome protozoa. It is transmitted by bites of infected tsetse fly. In this paper, we first present the vector-host model which describes the general transmission dynamics of HAT. In the tsetse fly population, the HAT is modelled by three compartments, while in the human population, the HAT is modelled by four compartments. The next-generation matrix approach is used to derive the basic reproduction number, R0, and it is also proved that if R0≤1, the disease-free equilibrium is globally asymptotically stable, which means the disease dies out. The disease persists in the population if the value of R0>1. Furthermore, the optimal control model is determined by using the Pontryagin’s maximum principle, with control measures such as education, treatment, and insecticides used to optimize the objective function. The model simulations confirm that the use of the three control measures is very efficient and effective to eliminate HAT in Africa.

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Keck, Devin, Callie Stuart, Josie Duncan, Emily Gullette, and Rodrigo Martinez-Duarte. "Highly Localized Enrichment of Trypanosoma brucei Parasites Using Dielectrophoresis." Micromachines 11, no. 6 (June 26, 2020): 625. http://dx.doi.org/10.3390/mi11060625.

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Human African trypanosomiasis (HAT), also known as sleeping sickness, is a vector-borne neglected tropical disease endemic to rural sub-Saharan Africa. Current methods of early detection in the affected rural communities generally begin with general screening using the card agglutination test for trypanosomiasis (CATT), a serological test. However, the gold standard for confirmation of trypanosomiasis remains the direct observation of the causative parasite, Trypanosoma brucei. Here, we present the use of dielectrophoresis (DEP) to enrich T. brucei parasites in specific locations to facilitate their identification in a future diagnostic assay. DEP refers to physical movement that can be selectively induced on the parasites when exposing them to electric field gradients of specific magnitude, phase and frequency. The long-term goal of our work is to use DEP to selectively trap and enrich T. brucei in specific locations while eluting all other cells in a sample. This would allow for a diagnostic test that enables the user to characterize the presence of parasites in specific locations determined a priori instead of relying on scanning a sample. In the work presented here, we report the characterization of the conditions that lead to high enrichment, 780% in 50 s, of the parasite in specific locations using an array of titanium microelectrodes.

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Magez, Stefan, Joar Esteban Pinto Torres, Seoyeon Oh, and Magdalena Radwanska. "Salivarian Trypanosomes Have Adopted Intricate Host-Pathogen Interaction Mechanisms That Ensure Survival in Plain Sight of the Adaptive Immune System." Pathogens 10, no. 6 (May 31, 2021): 679. http://dx.doi.org/10.3390/pathogens10060679.

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Salivarian trypanosomes are extracellular parasites affecting humans, livestock and game animals. Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense are human infective sub-species of T. brucei causing human African trypanosomiasis (HAT—sleeping sickness). The related T. b. brucei parasite lacks the resistance to survive in human serum, and only inflicts animal infections. Animal trypanosomiasis (AT) is not restricted to Africa, but is present on all continents. T. congolense and T. vivax are the most widespread pathogenic trypanosomes in sub-Saharan Africa. Through mechanical transmission, T. vivax has also been introduced into South America. T. evansi is a unique animal trypanosome that is found in vast territories around the world and can cause atypical human trypanosomiasis (aHT). All salivarian trypanosomes are well adapted to survival inside the host’s immune system. This is not a hostile environment for these parasites, but the place where they thrive. Here we provide an overview of the latest insights into the host-parasite interaction and the unique survival strategies that allow trypanosomes to outsmart the immune system. In addition, we review new developments in treatment and diagnosis as well as the issues that have hampered the development of field-applicable anti-trypanosome vaccines for the implementation of sustainable disease control.

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Madeja, Ulrich-Dietmar, and Ulrike Schroeder. "From Colonial Research Spirit to Global Commitment: Bayer and African Sleeping Sickness in the Mirror of History." Tropical Medicine and Infectious Disease 5, no. 1 (March 10, 2020): 42. http://dx.doi.org/10.3390/tropicalmed5010042.

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In the early 20th century, a series of epidemics across equatorial Africa brought African sleeping sickness (human African trypanosomiasis, HAT) to the attention of the European colonial administrations. This disease presented an exciting challenge for microbiologists across Europe to study the disease, discover the pathogen and search for an effective treatment. In 1923, the first “remedy for tropical diseases”—Suramin—manufactured by Bayer AG came onto the market under the brand name “Germanin.” The development and life cycle of this product—which today is still the medicine of choice for Trypanosoma brucei (T.b), hodesiense infections—reflect medical progress as well as the successes and failures in fighting the disease in the context of historic political changes over the last 100 years.

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von Wissmann, Beatrix, Jenna Fyfe, Kim Picozzi, Louise Hamill, Charles Waiswa, and Susan C. Welburn. "Quantifying the Association between Bovine and Human Trypanosomiasis in Newly Affected Sleeping Sickness Areas of Uganda." PLoS Neglected Tropical Diseases 8, no. 6 (June 5, 2014): e2931. http://dx.doi.org/10.1371/journal.pntd.0002931.

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Sutherland, C. Simone, Joshua Yukich, Ron Goeree, and Fabrizio Tediosi. "A Literature Review of Economic Evaluations for a Neglected Tropical Disease: Human African Trypanosomiasis (“Sleeping Sickness”)." PLOS Neglected Tropical Diseases 9, no. 2 (February 5, 2015): e0003397. http://dx.doi.org/10.1371/journal.pntd.0003397.

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Kaboré, Jacques, Hamidou Ilboudo, Charlie FA Compaoré, Oumou Camara, Mohamed Bamba, Hassane Sakandé, Mamadou Camara, et al. "PO 8441 EXPERIMENTAL COMPARISON OF SENSITIVITY OF LAMP AND REAL-TIME PCR." BMJ Global Health 4, Suppl 3 (April 2019): A37.3—A38. http://dx.doi.org/10.1136/bmjgh-2019-edc.98.

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BackgroundHuman African trypanosomiasis, or sleeping sickness, remains a serious problem in tropical Africa. Timely diagnosis of this disease requires systematic population screening, particularly for Trypanosoma brucei gambiense, which has a long asymptomatic period.The lack of sensitivity and specificity of conventional diagnostic tests has led in recent years to the use of molecular tools. Amplification of parasite-specific DNA sequences significantly improved diagnosis of infection. However, these molecular tools still have some limitations especially in the case of low parasitaemia. Furthermore, research is still needed to make molecular detection a real control tool for the fight against sleeping sickness. The purpose of this study is to determine the threshold of sensitivity of real-time PCR using the 18S and TgsGp primers and of the LAMP technique, applied in the DiTECT-HAT project as molecular reference tests.MethodsWe used serial dilutions containing 0, 1, 10, 100, 103, 104, 105, 106 parasites per ml of blood. Samples were extracted, and DNA was amplified.ResultsThe analytical sensitivity of the 18S real-time PCR with the Taqman probe of the filter paper samples is 100 parasites/ml and that of the TgsGp real-time PCR with the Taqman probe of filter paper samples is 104 parasites/ml. For Lamp technique, the analytical sensitivity is 103 parasites/ml.ConclusionThis study shows that a ‘negative PCR’ would not mean ‘no parasite’. It suggests that DNA detection techniques should still be improved.

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Szabó, Lara U., Marcel Kaiser, Pascal Mäser, and Thomas J. Schmidt. "Antiprotozoal Nor-Triterpene Alkaloids from Buxus sempervirens L." Antibiotics 10, no. 6 (June 10, 2021): 696. http://dx.doi.org/10.3390/antibiotics10060696.

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Malaria and human African trypanosomiasis (HAT; sleeping sickness) are life-threatening tropical diseases caused by protozoan parasites. Due to limited therapeutic options, there is a compelling need for new antiprotozoal agents. In a previous study, O-tigloylcyclovirobuxeine-B was recovered from a B. sempervirens L. (common box; Buxaceae) leaf extract by bioactivity-guided isolation. This nor-cycloartane alkaloid was identified as possessing strong and selective in vitro activity against the causative agent of malaria tropica, Plasmodium falciparum (Pf). The purpose of this study is the isolation of additional alkaloids from B. sempervirens L. to search for further related compounds with strong antiprotozoal activity. In conclusion, 25 alkaloids were obtained from B. sempervirens L., including eight new natural products and one compound first described for this plant. The structure elucidation was accomplished by UHPLC/+ESI-QqTOF-MS/MS and NMR spectroscopy. The isolated alkaloids were tested against Pf and Trypanosoma brucei rhodesiense (Tbr), the causative agent of East African sleeping sickness. To assess their selectivity, cytotoxicity against mammalian cells (L6 cell line) was tested as well. Several of the compounds displayed promising in vitro activity against the pathogens in a sub-micromolar range with concurrent high selectivity indices (SI). Consequently, various alkaloids from B. sempervirens L. have the potential to serve as a novel antiprotozoal lead structure.

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Varanda, Jorge, and Josenando Théophile. "Putting Anthropology into Global Health." Anthropology in Action 26, no. 1 (March 1, 2019): 31–41. http://dx.doi.org/10.3167/aia.2019.260104.

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This analysis of over a century of public health campaigns against human African trypanosomiasis (sleeping sickness) in Angola aims to unravel the role of (utopian) dreams in global health. Attention to the emergence and use of concepts such as neglected tropical diseases (NTDs) and ideas about elimination or eradication highlights how these concepts and utopian dreams are instrumental for the advancement of particular agendas in an ever-shifting field of global health. The article shows how specific representations of the elimination and eradication of diseases, framed over a century ago, continue to push Western views and politics of care onto others. This analysis generates insight into how global health and its politics of power functioned in Angola during colonialism and post-independence.

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Carrington, Mark. "Slippery customers: How African trypanosomes evade mammalian defences." Biochemist 31, no. 4 (August 1, 2009): 8–11. http://dx.doi.org/10.1042/bio03104008.

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African trypanosomes are excellent parasites and can maintain an infection of a large mammalian host for months or years. In endemic areas, Human African Trypanosomiasis, also called sleeping sickness, has been largely unaffected by the advent of modern medicine, and trypanosomiasis of domestic livestock is a major restraint on productivity in endemic areas and is arguably the major contributor to the institutionalized poverty in much of rural sub-Saharan Africa1,2. A simple way of visualizing the effect of the livestock disease is to compare maps showing the distribution of livestock (www.ilri.org/InfoServ/Webpub/Fulldocs/Mappoverty/index.htm) and tsetse flies, the insect vector (www.fao.org/ag/AGAinfo/programmes/en/paat/maps.html): the lack of overlap is remarkable. Tsetse flies are only present in sub-Saharan Africa, and this probably restricted the spread of African trypanosomiasis until historical times. Livestock infections are now present in much of South Asia and South America, a product of long distance trade and adaptation of the trypanosomes to mechanical transmission3. The majority of research is on Trypanosoma brucei as this includes the human infective subspecies. This article provides a description of progress in the understanding the molecular details of how the trypanosome interacts with the mammalian immune system and how these studies have extended beyond this to fundamental aspects of eukaryotic cell biology.

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Cestari, Igor, and Kenneth Stuart. "Inhibition of Isoleucyl-tRNA Synthetase as a Potential Treatment for Human African Trypanosomiasis." Journal of Biological Chemistry 288, no. 20 (April 2, 2013): 14256–63. http://dx.doi.org/10.1074/jbc.m112.447441.

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Trypanosoma brucei sp. causes human African trypanosomiasis (HAT; African sleeping sickness). The parasites initially proliferate in the hemolymphatic system and then invade the central nervous system, which is lethal if not treated. New drugs are needed for HAT because the approved drugs are few, toxic, and difficult to administer, and drug resistance is spreading. We showed by RNAi knockdown that T. brucei isoleucyl-tRNA synthetase is essential for the parasites in vitro and in vivo in a mouse model of infection. By structure prediction and experimental analysis, we also identified small molecules that inhibit recombinant isoleucyl-tRNA synthetase and that are lethal to the parasites in vitro and highly selective compared with mammalian cells. One of these molecules acts as a competitive inhibitor of the enzyme and cures mice of the infection. Because members of this class of molecules are known to cross the blood-brain barrier in humans and to be tolerated, they may be attractive as leading candidates for drug development for HAT.

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Kaiser, Marcel, Michael A. Bray, Monica Cal, Bernadette Bourdin Trunz, Els Torreele, and Reto Brun. "Antitrypanosomal Activity of Fexinidazole, a New Oral Nitroimidazole Drug Candidate for Treatment of Sleeping Sickness." Antimicrobial Agents and Chemotherapy 55, no. 12 (September 12, 2011): 5602–8. http://dx.doi.org/10.1128/aac.00246-11.

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ABSTRACTFexinidazole is a 5-nitroimidazole drug currently in clinical development for the treatment of human sleeping sickness (human African trypanosomiasis [HAT]), caused by infection with species of the protozoan parasiteTrypanosoma brucei. The compound and its two principal metabolites, sulfoxide and sulfone, have been assessed for their ability to kill a range ofT. bruceiparasite strainsin vitroand to cure both acute and chronic HAT disease models in the mouse. The parent molecule and both metabolites have shown trypanocidal activityin vitroin the 0.7-to-3.3 μM (0.2-to-0.9 μg/ml) range against all parasite strains tested.In vivo, fexinidazole is orally effective in curing both acute and chronic diseases in the mouse at doses of 100 mg/kg of body weight/day for 4 days and 200 mg/kg/day for 5 days, respectively. Pharmacokinetic data indicate that it is likely that the sulfoxide and sulfone metabolites provide most, if not all, of thein vivokilling activity. Fexinidazole and its metabolites require up to 48 h exposure in order to induce maximal trypanocidal efficacyin vitro. The parent drug and its metabolites show noin vitrocross-reactivity in terms of trypanocidal activity with either themselves or other known trypanocidal drugs in use in humans. Thein vitroandin vivoantitrypanosomal activities of fexinidazole and its two principal metabolites provide evidence that the compound has the potential to be an effective oral treatment for both theT. b. gambienseandT. b. rhodesienseforms of human sleeping sickness and both stages of the disease.

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Mamani-Matsuda, Maria, Jérôme Rambert, Denis Malvy, Hélène Lejoly-Boisseau, Sylvie Daulouède, Denis Thiolat, Sara Coves, Pierrette Courtois, Philippe Vincendeau, and M. Djavad Mossalayi. "Quercetin Induces Apoptosis of Trypanosoma brucei gambiense and Decreases the Proinflammatory Response of Human Macrophages." Antimicrobial Agents and Chemotherapy 48, no. 3 (March 2004): 924–29. http://dx.doi.org/10.1128/aac.48.3.924-929.2004.

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ABSTRACT In addition to parasite spread, the severity of disease observed in cases of human African trypanosomiasis (HAT), or sleeping sickness, is associated with increased levels of inflammatory mediators, including tumor necrosis factor (TNF)-α and nitric oxide derivatives. In the present study, quercetin (3,3′,4′,5,7-pentahydroxyflavone), a potent immunomodulating flavonoid, was shown to directly induce the death of Trypanosoma brucei gambiense, the causative agent of HAT, without affecting normal human cell viability. Quercetin directly promoted T. b. gambiense death by apoptosis as shown by Annexin V binding. In addition to microbicidal activity, quercetin induced dose-dependent decreases in the levels of TNF-α and nitric oxide produced by activated human macrophages. These results highlight the potential use of quercetin as an antimicrobial and anti-inflammatory agent for the treatment of African trypanomiasis.

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Pereira, Claudio A., León A. Bouvier, María de los Milagros Cámara, and Mariana R. Miranda. "Singular Features of Trypanosomatids' Phosphotransferases Involved in Cell Energy Management." Enzyme Research 2011 (April 4, 2011): 1–12. http://dx.doi.org/10.4061/2011/576483.

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Trypanosomatids are responsible for economically important veterinary affections and severe human diseases. In Africa, Trypanosoma brucei causes sleeping sickness or African trypanosomiasis, while in America, Trypanosoma cruzi is the etiological agent of Chagas disease. These parasites have complex life cycles which involve a wide variety of environments with very different compositions, physicochemical properties, and availability of metabolites. As the environment changes there is a need to maintain the nucleoside homeostasis, requiring a quick and regulated response. Most of the enzymes required for energy management are phosphotransferases. These enzymes present a nitrogenous group or a phosphate as acceptors, and the most clear examples are arginine kinase, nucleoside diphosphate kinase, and adenylate kinase. Trypanosoma and Leishmania have the largest number of phosphotransferase isoforms ever found in a single cell; some of them are absent in mammals, suggesting that these enzymes are required in many cellular compartments associated to different biological processes. The presence of such number of phosphotransferases support the hypothesis of the existence of an intracellular enzymatic phosphotransfer network that communicates the spatially separated intracellular ATP consumption and production processes. All these unique features make phosphotransferases a promising start point for rational drug design for the treatment of human trypanosomiasis.

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Sanderson, Lisa, Adil Khan, and Sarah Thomas. "Distribution of Suramin, an Antitrypanosomal Drug, across the Blood-Brain and Blood-Cerebrospinal Fluid Interfaces in Wild-Type and P-Glycoprotein Transporter-Deficient Mice." Antimicrobial Agents and Chemotherapy 51, no. 9 (June 18, 2007): 3136–46. http://dx.doi.org/10.1128/aac.00372-07.

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ABSTRACT Although 60 million people are exposed to human African trypanosomiasis, drug companies have not been interested in developing new drugs due to the lack of financial reward. No new drugs will be available for several years. A clearer understanding of the distribution of existing drugs into the brains of sleeping sickness patients is needed if we are to use the treatments that are available more safely and effectively. This proposal addresses this issue by using established animal models. Using in situ brain perfusion and isolated incubated choroid plexus techniques, we investigated the distribution of [3H]suramin into the central nervous systems (CNSs) of male BALB/c, FVB (wild-type), and P-glycoprotein-deficient (Mdr1a/Mdr1b-targeted mutation) mice. There was no difference in the [3H]suramin distributions between the three strains of mice. [3H]suramin had a distribution similar to that of the vascular marker, [14C]sucrose, into the regions of the brain parenchyma that have a blood-brain barrier. However, the association of [3H]suramin with the circumventricular organ samples, including the choroid plexus, was higher than that of [14C]sucrose. The association of [3H]suramin with the choroid plexus was also sensitive to phenylarsine oxide, an inhibitor of endocytosis. The distribution of [3H]suramin to the brain was not affected by the presence of other antitrypanosomal drugs or the P-glycoprotein efflux transporter. Overall, the results confirm that [3H]suramin would be unlikely to treat the second or CNS stage of sleeping sickness.

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Camara, Oumou, Sylvain Biéler, Bruno Bucheton, Moïse Kagbadouno, Joseph Mathu Ndung’u, Philippe Solano, and Mamadou Camara. "Accelerating elimination of sleeping sickness from the Guinean littoral through enhanced screening in the post-Ebola context: A retrospective analysis." PLOS Neglected Tropical Diseases 15, no. 2 (February 16, 2021): e0009163. http://dx.doi.org/10.1371/journal.pntd.0009163.

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Background Activities to control human African trypanosomiasis (HAT) in Guinea were severely hampered by the Ebola epidemic that hit this country between 2014 and 2016. Active screening was completely interrupted and passive screening could only be maintained in a few health facilities. At the end of the epidemic, medical interventions were progressively intensified to mitigate the risk of HAT resurgence and progress towards disease elimination. Methodology/Principal findings A retrospective analysis was performed to evaluate the medical activities that were implemented in the three most endemic prefectures of Guinea (Boffa, Dubreka and Forecariah) between January 2016 and December 2018. Passive screening using rapid diagnostic tests (RDTs) was progressively resumed in one hundred and one health facilities, and active screening was intensified by visiting individual households and performing RDTs, and by conducting mass screening in villages by mobile teams using the Card Agglutination Test for Trypanosomiasis. A total of 1885, 4897 and 8023 clinical suspects were tested in passive, while 5743, 14442 and 21093 people were actively screened in 2016, 2017 and 2018, respectively. The number of HAT cases that were diagnosed first went up from 107 in 2016 to 140 in 2017, then subsequently decreased to only 73 in 2018. A progressive decrease in disease prevalence was observed in the populations that were tested in active and in passive between 2016 and 2018. Conclusions/Significance Intensified medical interventions in the post-Ebola context first resulted in an increase in the number of HAT cases, confirming the fear that the disease could resurge as a result of impaired control activities during the Ebola epidemic. On the other hand, the decrease in disease prevalence that was observed between 2016 and 2018 is encouraging, as it suggests that the current strategy combining enhanced diagnosis, treatment and vector control is appropriate to progress towards elimination of HAT in Guinea.

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Simo, Gustave, Jean Mbida, Vincent Eyenga, Tazoacha Asonganyi, Flobert Njiokou, and Pascal Grébaut. "Challenges towards the elimination of Human African Trypanosomiasis in the sleeping sickness focus of Campo in southern Cameroon." Parasites & Vectors 7, no. 1 (2014): 374. http://dx.doi.org/10.1186/1756-3305-7-374.

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Ofon, Elvis, Harry Noyes, Vincent Ebo’o Eyanga, Flobert Njiokou, Mathurin Koffi, Pythagore Fogue, Christiane Hertz-Fowler, Annette MacLeod, Enock Matovu, and Gustave Simo. "Association between IL1 gene polymorphism and human African trypanosomiasis in populations of sleeping sickness foci of southern Cameroon." PLOS Neglected Tropical Diseases 13, no. 3 (March 25, 2019): e0007283. http://dx.doi.org/10.1371/journal.pntd.0007283.

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Soudan, Benoit, Daniel Tetaert, André Racadot, Pierre Degand, and Arnold Boersma. "Decrease of testosterone level during an experimental African trypanosomiasis: involvement of a testicular LH receptor desensitization." Acta Endocrinologica 127, no. 1 (July 1992): 86–92. http://dx.doi.org/10.1530/acta.0.1270086.

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To investigate gonadal disorders and changes of the testicular receptors occurring during the sleeping sickness disease (African trypanosomiasis), an experimental model was developed with 10-month-old rats infested by bloodstream forms of two variants of Trypanosoma brucei brucei (AnTat 1.1 A and AnTat 1.8). At the acute phase, three days after inoculation, the animals were sacrificed for estimating the serum levels of LH and testosterone and the number of testicular LH receptors. Considering a possible intervention of the stress during the infestation and to improve our investigations on gonadal imbalance related to trypanosomasis, levels of additional parameters [corticosterone, glucose and transaminases (glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase)] were determined. Stimulation testing with hCG was likewise assessed in infested rats to analyse the testicular testosterone response to gonadotropin. A significant decrease was demonstrated for serum LH and testosterone levels in the infested rats, as well as the loss of: (i) the testicular responsiveness to exogenous gonadotropin; (ii) the number of testicular LH receptors. Moreover, the remaining testicular receptors of infested rats showed an increase in their equilibrium association constant (Ka). Our study suggests that dysfunction of Leydig cells occurring during African trypanosomiasis is in part related to stress induced by the presence of the parasites.

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McGettrick, Anne F., Sarah E. Corcoran, Paul J. G. Barry, Jennifer McFarland, Cécile Crès, Anne M. Curtis, Edward Franklin, et al. "Trypanosoma bruceimetabolite indolepyruvate decreases HIF-1α and glycolysis in macrophages as a mechanism of innate immune evasion." Proceedings of the National Academy of Sciences 113, no. 48 (November 15, 2016): E7778—E7787. http://dx.doi.org/10.1073/pnas.1608221113.

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The parasiteTrypanasoma bruceicauses African trypanosomiasis, known as sleeping sickness in humans and nagana in domestic animals. These diseases are a major burden in the 36 sub-Saharan African countries where the tsetse fly vector is endemic. Untreated trypanosomiasis is fatal and the current treatments are stage-dependent and can be problematic during the meningoencephalitic stage, where no new therapies have been developed in recent years and the current drugs have a low therapeutic index. There is a need for more effective treatments and a better understanding of how these parasites evade the host immune response will help in this regard. The bloodstream form ofT. bruceiexcretes significant amounts of aromatic ketoacids, including indolepyruvate, a transamination product of tryptophan. This study demonstrates that this process is essential in bloodstream forms, is mediated by a specialized isoform of cytoplasmic aminotransferase and, importantly, reveals an immunomodulatory role for indolepyruvate. Indolepyruvate prevents the LPS-induced glycolytic shift in macrophages. This effect is the result of an increase in the hydroxylation and degradation of the transcription factor hypoxia-inducible factor-1α (HIF-1α). The reduction in HIF-1α levels by indolepyruvate, following LPS or trypanosome activation, results in a decrease in production of the proinflammatory cytokine IL-1β. These data demonstrate an important role for indolepyruvate in immune evasion byT. brucei.

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Journal articles on the topic 'Trypanosomiasis; Sleeping sickness'

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