Relevant bibliographies by topics / Sleeping sickness ; Trypanosomes

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Academic literature on the topic 'Sleeping sickness ; Trypanosomes'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "Sleeping sickness ; Trypanosomes"

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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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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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HUTCHINSON, RACHEL, and JAMIE R. STEVENS. "Barcoding in trypanosomes." Parasitology 145, no. 5 (November 23, 2017): 563–73. http://dx.doi.org/10.1017/s0031182017002049.

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SUMMARYTrypanosomes (genus Trypanosoma) are parasites of humans, and wild and domestic mammals, in which they cause several economically and socially important diseases, including sleeping sickness in Africa and Chagas disease in the Americas. Despite the development of numerous molecular diagnostics and increasing awareness of the importance of these neglected parasites, there is currently no universal genetic barcoding marker available for trypanosomes. In this review we provide an overview of the methods used for trypanosome detection and identification, discuss the potential application of different barcoding techniques and examine the requirements of the ‘ideal’ trypanosome genetic barcode. In addition, we explore potential alternative genetic markers for barcoding Trypanosoma species, including an analysis of phylogenetically informative nucleotide changes along the length of the 18S rRNA gene.
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Matovu, Enock, Claire Mack Mugasa, Peter Waiswa, Annah Kitibwa, Alex Boobo, and Joseph Mathu Ndung’u. "Haemoparasitic Infections in Cattle from a Trypanosoma brucei Rhodesiense Sleeping Sickness Endemic District of Eastern Uganda." Tropical Medicine and Infectious Disease 5, no. 1 (February 7, 2020): 24. http://dx.doi.org/10.3390/tropicalmed5010024.

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We carried out a baseline survey of cattle in Kaberamaido district, in the context of controlling the domestic animal reservoir of Trypanosoma brucei rhodesiense human African trypanosomiasis (rHAT) towards elimination. Cattle blood was subjected to capillary tube centrifugation followed by measurement of the packed cell volume (PCV) and examination of the buffy coat area for motile trypanosomes. Trypanosomes were detected in 561 (21.4%) out of 2621 cattle screened by microscopy. These 561 in addition to 724 apparently trypanosome negative samples with low PCVs (≤25%) were transported to the laboratory and tested by PCR targeting the trypanosomal Internal Transcribed Spacer (ITS-1) as well as suspect Tick-Borne Diseases (TBDs) including Anaplasmamosis, Babesiosis, and Theileriosis. PCR for Anaplasma sp yielded the highest number of positive animals (45.2%), followed by Trypanosoma sp (44%), Theileria sp (42.4%) and Babesia (26.3%); multiple infections were a common occurrence. Interestingly, 373 (29%) of these cattle with low PCVs were negative by PCR, pointing to other possible causes of aneamia, such as helminthiasis. Among the trypanosome infections classified as T. brucei by ITS-PCR, 5.5% were positive by SRA PCR, and were, therefore, confirmed as T. b. rhodesiense. Efforts against HAT should therefore consider packages that address a range of conditions. This may enhance acceptability and participation of livestock keepers in programs to eliminate this important but neglected tropical disease. In addition, we demonstrated that cattle remain an eminent reservoir for T. b. rhodesiense in eastern Uganda, which must be addressed to sustain HAT elimination.
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Griffin, Gabriel K. "Trypping up antigenic variation in sleeping sickness." Science Immunology 3, no. 29 (November 2, 2018): eaav7758. http://dx.doi.org/10.1126/sciimmunol.aav7758.

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Kanté Tagueu, Sartrien, Oumarou Farikou, Flobert Njiokou, and Gustave Simo. "Prevalence of Sodalis glossinidius and different trypanosome species in Glossina palpalis palpalis caught in the Fontem sleeping sickness focus of the southern Cameroon." Parasite 25 (2018): 44. http://dx.doi.org/10.1051/parasite/2018044.

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Tsetse flies are the cyclical vector of human and animal African trypanosomiasis. To improve vector control in order to achieve the elimination of human African trypanosomiasis (HAT) and boost the control of animal diseases, investigations have been undertaken on the tripartite association between tsetse, trypanosome, and symbionts. It is in this light that Sodalis glossinidius and different trypanosomes were identified in Glossina palpalis palpalis caught in Fontem in southern Cameroon. For this study, DNA was extracted from whole flies, and S. glossinidius and different trypanosome species were identified by polymerase chain reaction (PCR). Statistical analyses were performed to compare the trypanosome and S. glossinidius infection rates and to look for an association between these microorganisms. Of the 274 G. p. palpalis caught, 3.3% (9/274) were teneral. About 35% (96/274) of these flies harbored S. glossinidius. Of the 265 non-teneral flies, 37.7% were infected by trypanosomes. The infection rates of Trypanosoma congolense “forest type” and Trypanosoma vivax were 26.04% and 18.11%, respectively. About 6.41% of tsetse harbored mixed infections of T. congolense and T. vivax. Of the 69 tsetse with T. congolense infections, 33.33% (23/69) harbored S. glossinidius while 71.86% (69/96) of flies harboring S. glossinidius were not infected by trypanosomes. No association was observed between S. glossinidius and trypanosome infections. Some wild tsetse harbor S. glossinidius and trypanosomes, while others have no infection or are infected by only one of these microorganisms. We conclude that the presence of S. glossinidius does not favor trypanosome infections in G. p. palpalis of the Fontem focus.
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Nagamune, Kisaburo, Alvaro Acosta-Serrano, Haruki Uemura, Reto Brun, Christina Kunz-Renggli, Yusuke Maeda, Michael A. J. Ferguson, and Taroh Kinoshita. "Surface Sialic Acids Taken from the Host Allow Trypanosome Survival in Tsetse Fly Vectors." Journal of Experimental Medicine 199, no. 10 (May 10, 2004): 1445–50. http://dx.doi.org/10.1084/jem.20030635.

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The African trypanosome Trypanosoma brucei, which causes sleeping sickness in humans and Nagana disease in livestock, is spread via blood-sucking Tsetse flies. In the fly's intestine, the trypanosomes survive digestive and trypanocidal environments, proliferate, and translocate into the salivary gland, where they become infectious to the next mammalian host. Here, we show that for successful survival in Tsetse flies, the trypanosomes use trans-sialidase to transfer sialic acids that they cannot synthesize from host's glycoconjugates to the glycosylphosphatidylinositols (GPIs), which are abundantly expressed on their surface. Trypanosomes lacking sialic acids due to a defective generation of GPI-anchored trans-sialidase could not survive in the intestine, but regained the ability to survive when sialylated by means of soluble trans-sialidase. Thus, surface sialic acids appear to protect the parasites from the digestive and trypanocidal environments in the midgut of Tsetse flies.
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MacLEOD, E. T., I. MAUDLIN, A. C. DARBY, and S. C. WELBURN. "Antioxidants promote establishment of trypanosome infections in tsetse." Parasitology 134, no. 6 (February 19, 2007): 827–31. http://dx.doi.org/10.1017/s0031182007002247.

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SUMMARYEfficient, cyclical transmission of trypanosomes through tsetse flies is central to maintenance of human sleeping sickness and nagana across sub-Saharan Africa. Infection rates in tsetse are normally very low as most parasites ingested with the fly bloodmeal die in the fly gut, displaying the characteristics of apoptotic cells. Here we show that a range of antioxidants (glutathione, cysteine, N-acetyl-cysteine, ascorbic acid and uric acid), when added to the insect bloodmeal, can dramatically inhibit cell death of Trypanosoma brucei brucei in tsetse. Both L- and D-cysteine invoked similar effects suggesting that inhibition of trypanosome death is not dependent on protein synthesis. The present work suggests that antioxidants reduce the midgut environment protecting trypanosomes from cell death induced by reactive oxygen species.
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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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Mogk, Stefan, Hartwig Wolburg, Claudia Frey, Bruno Kubata, and Michael Duszenko. "Brain infection by African trypanosomes during sleeping sickness." Neurology, Psychiatry and Brain Research 18, no. 2 (March 2012): 49–51. http://dx.doi.org/10.1016/j.npbr.2012.02.012.

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Dissertations / Theses on the topic "Sleeping sickness ; Trypanosomes"

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Toleman, Mark Alexander. "Cloning, sequencing and sequence analysis of a chitinase gene from secondary endosymbiont of Glossina morsitans morsitans : a step towards pseudo-transgenic tsetse." Thesis, University of Bristol, 1998. http://hdl.handle.net/1983/0c82830d-945e-443b-b2e7-8f4d1a1b239a.

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Lane-Serff, Harriet. "Structural insights into innate immunity against African trypanosomes." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:3a1415e6-3df4-42dd-827b-d05edb2137be.

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The haptoglobin-haemoglobin receptor (HpHbR) is expressed by the African try- panosome, T. brucei, whilst in the bloodstream of the mammalian host. This allows ac- quisition of haem, but also results in uptake of trypanolytic factor 1, a mediator of in- nate immunity against non-human African trypanosomes. Here, the structure of HpHbR in complex with its ligand, haptoglobin-haemoglobin (HpHb), is presented, revealing an elongated binding site along the membrane-distal half of the receptor. A ~50° kink allows the simultaneous binding of two receptors to one dimeric HpHb, increasing the efficiency of ligand uptake whilst also increasing binding site exposure within the densely packed cell surface. The possibility of targeting this receptor with antibody-drug conjugates is ex- plored. The characterisation of the unexpected interaction between T. congolense HpHbR and its previously unknown ligand, haemoglobin, is also presented. This receptor is iden- tified as an epimastigote-specific protein expressed whilst the trypanosome occupies the mouthparts of the tsetse fly vector. An evolutionary pathway of the receptor is proposed, describing how the receptor has changed to adapt to a role as a bloodstream form-specific protein in T. brucei. Apolipoprotein L1 (ApoL1) is the pore-forming component of the trypanolytic factors. An expression and purification protocol for ApoL1 is presented here, and the functionality of the protein established. Initial attempts to characterise the pores and structure of ApoL1 are described.
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Masiga, Daniel Kanani. "The development and application of a polymerase chain reaction methodology for the identification of African trypanosomes." Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386509.

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Poole, Lindsey. "The role of intraflagellar transport in signaling in the African trypanosome Trypanosoma brucei /." Connect to online version, 2008. http://ada.mtholyoke.edu/setr/websrc/pdfs/www/2008/282.pdf.

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Kanmogne, Georgette Djuidje. "Genetic characterization of Trypanosoma brucei gambiense isolates from Cameroon." Thesis, University of Bristol, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319021.

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Millar, Amanda E. "T-cell responses during Trypanosoma brucei infections." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363151.

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Ford, Jack Ragnar. "Cyclin dependent kinases and cell cycle control in Trypanosoma brucei." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312512.

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Hare, Julie D. "Mutational analysis of T. brucei components of motile flagella (TbCMF) genes in the African trypanosome /." Connect to online version, 2007. http://ada.mtholyoke.edu/setr/websrc/pdfs/www/2007/218.pdf.

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Dantas, Sonia N. "Mutational analysis of a gene required for flagellar motility in the African sleeping sickness parasite /." Connect to online version, 2008. http://ada.mtholyoke.edu/setr/websrc/pdfs/www/2008/260.pdf.

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Bernstein, Bradley E. "Crystallographic investigations of phosphoglycerate kinase from the causative agent of sleeping sickness /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/9232.

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Books on the topic "Sleeping sickness ; Trypanosomes"

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Gibson, W. African trypanosomosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0049.

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The African trypanosomoses are diseases of both man and his livestock. There are two forms of human trypanosomosis or sleeping sickness: Gambian or Rhodesian sleeping sickness, roughly corresponding to a West, Central or East African distribution respectively. Gambian sleeping sickness runs a more protracted and chronic course than the Rhodesian form; nevertheless, human trypanosomosis is invariably fatal if not treated. Animal reservoir hosts, both wild and domestic, assume greater importance for Rhodesian sleeping sickness than Gambian sleeping sickness, and the former is often an occupational hazard of those visiting or working in wildlife areas, e.g. tourists, hunters. Animal trypanosomosis transmitted by tsetse is generally referred to as Nagana, while the disease transmitted by other bloodsucking flies outside the African tsetse belt is known chiefly as Surra, but also by a variety of local names.Sleeping sickness control measures are aimed either at the trypanosome or the fly. Human cases are detected by active or passive surveillance and cured by treatment with trypanocidal drugs.Control of the tsetse vector is by application of residual insecticides or bush clearing and, more recently, by traps or insecticide-impregnated targets, or by wholesale release of sterile males. Tsetse control is more widely employed for the control of animal trypanosomosis than sleeping sickness.
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Mott, Frederick Walker. Histological Observations on Sleeping Sickness and Other Trypanosome Infections. Adamant Media Corporation, 2004.

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1934-, Dumas Michel, Bouteille Bernard 1952-, and Buguet Alain, eds. Progress in human African trypanosomiasis, sleeping sickness. Paris: Springer, 1999.

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Book chapters on the topic "Sleeping sickness ; Trypanosomes"

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Pays, E. "Antigenic variation in African trypanosomes." In Progress in Human African Trypanosomiasis, Sleeping Sickness, 31–52. Paris: Springer Paris, 1999. http://dx.doi.org/10.1007/978-2-8178-0857-4_3.

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Gibson, W., J. Stevens, and P. Truc. "Identification of trypanosomes: from morphology to molecular biology." In Progress in Human African Trypanosomiasis, Sleeping Sickness, 7–29. Paris: Springer Paris, 1999. http://dx.doi.org/10.1007/978-2-8178-0857-4_2.

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Steverding, Dietmar. "Sleeping Sickness and Nagana Disease Caused by Trypanosoma brucei." In Arthropod Borne Diseases, 277–97. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-13884-8_18.

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Brun, Reto, and Johannes Blum. "Human African trypanosomiasis." In Oxford Textbook of Medicine, edited by Christopher P. Conlon, 1451–59. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0169.

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Human African trypanosomiasis (sleeping sickness) is caused by subspecies of the protozoan parasite Trypanosoma brucei. The disease is restricted to tropical Africa where it is transmitted by the bite of infected tsetse flies (Glossina spp.). Control programmes in the 1960s were very effective, but subsequent relaxation of control measures led to recurrence of epidemic proportions in the 1980s and 1990s. Control is now being regained. Untreated human African trypanosomiasis is almost invariably fatal. Specific treatment depends on the trypanosome subspecies and the stage of the disease. Drugs used for stage 1 include pentamidine and suramin, and for stage 2 include melarsoprol, eflornithine, and nifurtimox, but regimens are not standardized, and treatment is difficult and dangerous; all of the drugs used have many side effects, some potentially lethal.
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Stich, August. "Human African trypanosomiasis." In Oxford Textbook of Medicine, 1119–27. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.070810_update_001.

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Human African trypanosomiasis (HAT, sleeping sickness) is caused by two subspecies of the protozoan parasite Trypanosoma brucei: T. b. rhodesiense is prevalent in East Africa among many wild and domestic mammals; T. b. gambiense causes an anthroponosis in Central and West Africa. The disease is restricted to tropical Africa where it is transmitted by the bite of infected tsetse flies (...
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Salvana, Edsel Maurice T., and Robert A. Salata. "African Trypanosomiasis (Sleeping Sickness; Trypanosoma brucei Complex)." In Nelson Textbook of Pediatrics, 1190–93. Elsevier, 2011. http://dx.doi.org/10.1016/b978-1-4377-0755-7.00278-5.

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