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Relevant bibliographies by topics / Trypanosomiasis; Sleeping sickness

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Academic literature on the topic 'Trypanosomiasis; Sleeping sickness'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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Journal articles on the topic "Trypanosomiasis; Sleeping sickness"

1

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

1

Bailey, Wendi. "The diagnosis of human African trypanosomiasis." Thesis, University of Liverpool, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260319.

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Nyasulu, Yohane. "The study of human trypanosomiasis in Malawi." Thesis, University of Salford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304724.

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Gichuki, Charity Wangui. "The role of astrocytes in the neuropathogenesis of African trypanosomiasis." Thesis, University of Glasgow, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294595.

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Mungongo, Singfrid Gasper. "The design, synthesis and biological evaluation of novel antitrypanosomal drugs." Thesis, University of Sunderland, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284073.

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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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Acup, Christine Amongi. "Epidemiology and control of human African trypanosomiasis in Uganda." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/16246.

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Poverty and disease are bound together in rural communities of sub-Saharan Africa (SSA) exacerbated by weak social services and conflict. The infectious disease burden in SSA combines the neglected tropical diseases (NTDs) and the 'big three' (malaria, HIV/AIDS and tuberculosis), so-called because they attract more global attention and hence funding. NTDs include human African trypanosomiasis (HAT or sleeping sickness), first noticed by the outside world during the slave trade era and later in the 2-th century by widespread epidemics of disease across the tsetse fly belt. HAT describes two diseases: i) Gambian HAT caused by Trypanosoma brucei gambiense is characteristically chronic with an infectious period lasting up to three years and ii) Rhodesian HAT caused by T.b. rhodesiense is an acute disease, killing its victim within weeks of infection. The two diseases are frequently considered together as both are transmitted by tsetse flies, the parasites are morphologically indistinguishable and the associated diseases are both fatal if left untreated. However, the two diseases are clinical, epidemiologically and geographical distinct, each requiring different control strategies. Under field conditions, where microscopy is the basic diagnostic tool, differentiation is simply by geographical location of the patient; the Great Rift Valley separates the Gambian disease present in West and Central Africa, from East and southern Africa's Rhodesian disease. Control strategies are also distinct; while the Belgian and French colonial strategies to control the disease were patient-centred, the British colonial powers in East Africa were motivated by the effect of tsetse borne diseases on animal health. Towards the end of the colonial ear, both types of disease were heading for elimination but during the immediate post-colonial era in the 1960s, political instability compromised the rigid HAT control programs that had been put in place. For zoonotic Rhodesian sleeping sickness, complex tsetse control programmes proved difficult to maintain and to justify economically; for Gambian sleeping sickness the generalised breakdown of medical services allowed the disease to return, sometimes to devastating levels. The millennium development goals (MDGs) set out in 2000, highlighted specific challenges and opportunities for national and global development. HAT impacts national health goals of national development plans and MDGs and impedes rural development of SSA. NTDs were not addressed directly by MDGs but the World Health Organization (WHO) has reaffirmed its commitment not only to control of HAT but also to eliminate it as a public health problem by 2020. Currently there are 25 countries reporting HAT to WHO, and while the overall prevalence of HAT across Africa continues to fall, epidemics have been recorded, particularly from central Africa, South Sudan and Uganda. Uganda is uniquely, the only country affected by both T.b. gambiense and T.b. rhodesiense and until the present study, there was no evidence to suggest that the two parasite species co-existed in Uganda. The development of a new control paradigm for T.b. rhodesiese in South East Uganda has lowered the incidence of human infections and, more importantly, halted the northerly spread of this parasite. However, recurring epidemics in several established and new disease foci in central Uganda highlight the difficulties involved in eliminating this disease. The present study assesses past and present HAT control strategies centred on Dokolo, Kaberamaido and Soroti Districts located at the centre of Uganda. These districts are highly endemic for T.b. rodesiense, they represent the region of concern for overlap with T.b. gambiense foci in central Uganda, and are the current focus of the Stamp out Sleeping sickness control initiative. The point prevalence of T. brucei s.1 in cattle reservoir from villages with (out) reported human disease located at specific distances to Otuboi, Chagwere and Ochero cattle markets, was evaluated before and six months after trypanocidal treatment, to assess the transferrable impact of zoonotic T.b. rhodesiense to the human population. Overall, the proportion of T. brucei s.1 in cattle dropped significantly from 22% at baseline to 9% six months after trypanocide treatment (P < 0.05, Chi-square + 17.92, 95% C.I. + 1.71 to 4.49). All villages located in sub-counties that received at least 80% treatment coverage had a drop in T. brucei s.1 prevalence from 30.4% (95%, C.I + 22.8 to 38.0) before treatment was done, to 12.9% (95%, C.I. + 7.4 to 18.4) six months after treatment. More specifically, impact on human infective T.b. rhodesiense was also halved. In fact only three cattle were detected with the parasite six months after treatment compared with six from those sampled as baseline. This study also utilises documented cases between 2009 and 2012 to assess the current HAT reporting system for monitoring and evaluating transmission dynamics of the disease. Using a questionnaire, capacity and preparedness of healthcare professionals to respond to disease epidemics was assessed. The point prevalence of sleeping sickness in the three districts in 2009 was determined by screening volunteers. Microscopic examinations detected trypanosomes in four volunteers (4/5311 or 0.075 %) while PCR detected significantly more infections (24, p < 0.001). Multiplex PCR showed that ten of the Trypanozoon infections were T.b. rhodesiense while nested PCR identified four infections as T.b. gamiense, indicating that the distribution of the two forms of sleeping sickness overlaps in Uganda. Second phase investigations followed up the PCR positive cases; these people were screened again, together with members of their homestead and the inhabitants of three neighbouring homes. Besides microscopy and PCR, study subjects were examined clinically for sleeping sickness and completed a questionnaire to assess community recognition of the disease. This extended screen revealed no new cases underlining the importance of stringent early screening that PCR techniques can provide. At local healthcare centres, 54% of reported sleeping sickness cases were diagnosed only at the late stage, indicating a weakness in early diagnosis and hence early reporting. Interviews with local health workers also revealed weaknesses in recognition of clinical signs and a gap in diagnostic capacity. While records at treating hospitals remain a useful indicator for targeting active foci of infection, improvement in capacity to diagnose HAT at an early stage should contribute both to rural health and disease control strategies and also towards WHO's 2020 target of elimination of HAT.

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7

Batchelor, Nicola Ann. "Spatial epidemiology of Rhodesian sleeping sickness in recently affected areas of central and eastern Uganda." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4432.

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The tsetse transmitted fatal disease of humans, sleeping sickness, is caused by two morphologically identical subspecies of the parasite T. brucei; T. b. rhodesiense and T. b. gambiense. Current distributions of the two forms of disease are not known to overlap in any area, and Uganda is the only country with transmission of both. The distribution of Rhodesian sleeping sickness in Uganda has expanded in recent years, with five districts newly affected since 1998. This movement has narrowed the gap between Rhodesian and Gambian sleeping sickness endemic areas, heightening concerns over a potential future overlap which would greatly complicate the diagnosis and treatment of the two diseases. An improved understanding of the social, environmental and climatic determinants of the distribution of Rhodesian sleeping sickness is required to allow more effective targeting of control measures and to prevent further spread and possible concurrence with Gambian sleeping sickness. The work presented in this thesis investigates the drivers of the distribution and spread of Rhodesian sleeping sickness in districts of central and eastern Uganda which form part of the recent disease focus extension. The spatial distribution of Rhodesian sleeping sickness was examined in Kaberamaido and Dokolo districts where the disease was first reported in 2004, using three different methodologies. A traditional one-step logistic regression analysis of disease prevalence was compared with a two-step hierarchical logistic regression analysis. The two-step method included the analysis of disease occurrence followed by the analysis of disease prevalence in areas with a high predicted probability of occurrence. These two methods were compared in terms of their predictive accuracy. The incorporation of a stochastic spatial effect to model the residual spatial autocorrelation was carried out using a Bayesian geostatistical approach. The geostatistical analysis was compared with the non-spatial models to assess the importance of spatial autocorrelation, to establish which method had the highest predictive accuracy and to establish which factors were the most significant in terms of the disease’s distribution. Links between Rhodesian sleeping sickness and landcover in Soroti district were also assessed using a matched case-control study design. Temporal trends in these relationships were observed using an annually stratified analysis to allow an exploration of the disease’s dispersion following its introduction to a previously unaffected area. This work expands on previous research that demonstrated the source of infection in this area to be the movement of untreated livestock from endemic areas through a local livestock market. With regards to the comparison of regression frameworks, the two-step regression compared favourably with the traditional one-step regression, but the Bayesian geostatistical analysis outperformed both in terms of predictive accuracy. Each of these regression methods highlighted the importance of distance to the closest livestock market on the distribution of Rhodesian sleeping sickness, indicating that the disease may have been introduced to this area via the movement of untreated cattle from endemic areas, despite the introduction of regulations requiring the treatment of livestock prior to sale. In addition, several other environmental and climatic variables were significantly associated with sleeping sickness occurrence and prevalence within the study area. The temporal stratification of the matched case-control analysis highlights the dispersion of sleeping sickness away from the point of introduction (livestock market) into more suitable areas; areas with higher proportions of seasonally flooding grassland, lower proportions of woodland and dense savannah and lower elevations. These findings relate to the habitat preferences of the predominant vector species in the study area; Glossina fuscipes fuscipes, which prefers riverine vegetation. The findings presented highlight the importance of the livestock reservoir as well as the climatic and environmental preferences of the tsetse fly vector for the introduction of Rhodesian sleeping sickness into previously unaffected areas, the subsequent spread of infection following an introduction and the equilibrium spatial distribution of the disease. By enhancing the knowledge base regarding the spatial determinants of the distribution of Rhodesian sleeping sickness within newly affected areas, future control efforts within Uganda may be better targeted to decrease prevalence and to prevent further spread of the disease.

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8

Makumi, Joseph Njuguna. "The behaviour and role of Glossina longipennis as a vector of trypanosomiasis in cattle at Galana Ranch, south-eastern Kenya." Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385471.

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9

West, Ryan. "The design and synthesis of drug-like trypanosome alternative oxidase inhibitors for the treatment of African trypanosomiasis." Thesis, University of Sussex, 2019. http://sro.sussex.ac.uk/id/eprint/81228/.

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Trypanosome alternative oxidase (TAO) is the sole terminal oxidase responsible for the aerobic respiration of the parasite T. b. brucei. Specific strains of this parasite cause the neglected tropical disease Human African trypanosomiasis (HAT), and thus TAO is an interesting target for the potential treatment of this disease. Inhibition of TAO with the natural product inhibitors colletochlorin B or ascofuranone has been shown to clear infections of T. b. brucei in mice at high concentrations. However, these natural product inhibitors contain undesirable chemical functionality and have poor physicochemical properties, preventing adequate drug exposure to effectively treat HAT. Robust protocols for the expression and purification of recombinant TAO were developed, which enabled the development of biochemical assays to identify inhibitors of TAO function. Single point inhibition screening of the Medicines Malaria Venture 'kinetoplastid collection' of 400 compounds identified a range of micro-molar inhibitors of TAO. A program of chemical optimisation was carried out around the natural product inhibitor colletochlorin B, with the aim to improve the physicochemical properties and retain inhibitory potency against TAO. The structure activity relationships generated over the course of this exploration identified a dependency on high lipophilicity to retain potent TAO inhibition. The TAO inhibitors synthesised were also assessed for parasite growth inhibition and mammalian cell cytotoxicity to correlate inhibition data with cellular efficacy, in collaboration with Novartis. The physicochemical properties of these novel compounds showed improvement over the natural product colletochlorin B and prompted further assessment of leading compounds in advanced parasite kill kinetic and parasite clearance assays at Novartis. The data generated in these assays for compounds synthesised in this thesis determined that TAO inhibition results in a trypanostatic response, and not a preferred trypanocidal response in T. b. brucei.

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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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Books on the topic "Trypanosomiasis; Sleeping sickness"

1

James, Grant. Sleeping sickness. Ottawa: J. Hope & Sons, 1996.

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2

Dumas, Michel, Bernard Bouteille, and Alain Buguet, eds. Progress in Human African Trypanosomiasis, Sleeping Sickness. Paris: Springer Paris, 1999. http://dx.doi.org/10.1007/978-2-8178-0857-4.

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Ramen, Fred. Sleeping sickness and other parasitic tropical diseases. New York: Rosen, 2002.

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Musere, Jonathan. African sleeping sickness: Political ecology, colonialism, and control in Uganda. Lewiston, N.Y., USA: E. Mellen Press, 1990.

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The colonial disease: A social history of sleeping sickness in northern Zaire, 1900-1940. Cambridge: Cambridge University Press, 1992.

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Cattand, Pierre D. Human African trypanosomiasis: Assessment of serological methods in T.B. Gambiense sleeping sickness. Salford: University of Salford, 1987.

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Lords of the fly: Sleeping sickness control in British East Africa, 1900-1960. Westport, Conn: Praeger, 2003.

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Hoppe, Kirk Arden. Lords of the fly: Sleeping sickness control in British East Africa, 1900-1960. Westport, CT: Praeger, 2004.

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Hoppe, Kirk Arden. Lords of the flies: British sleeping sickness policies as environmental engineering in the Lake Victoria region, 1900-1950. Boston, Mass: African Studies Center, Boston University, 1995.

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Freiburghaus, Franziska. African medicinal plants used in the treatment of sleeping sickness: An evaluation. Bern: Wittwer Service AG, 1996.

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Book chapters on the topic "Trypanosomiasis; Sleeping sickness"

1

Domachowske, Joseph, and Manika Suryadevara. "African Sleeping Sickness: African Trypanosomiasis." In Clinical Infectious Diseases Study Guide, 307–11. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-50873-9_50.

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Heppner, John B., David B. Richman, Steven E. Naranjo, Dale Habeck, Christopher Asaro, Jean-Luc Boevé, Johann Baumgärtner, et al. "Sleeping Sickness or African Trypanosomiasis." In Encyclopedia of Entomology, 3387–90. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_4225.

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Vincendeau, P., M. O. Jauberteau-Marchan, S. Daulouède, and Z. Ayed. "Immunology of African trypanosomiasis." In Progress in Human African Trypanosomiasis, Sleeping Sickness, 137–56. Paris: Springer Paris, 1999. http://dx.doi.org/10.1007/978-2-8178-0857-4_8.

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Kristensson, K., and M. Bentivoglio. "Pathology of African trypanosomiasis." In Progress in Human African Trypanosomiasis, Sleeping Sickness, 157–81. Paris: Springer Paris, 1999. http://dx.doi.org/10.1007/978-2-8178-0857-4_9.

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Radomski, M. W., and G. Brandenberger. "Hormones in human African trypanosomiasis." In Progress in Human African Trypanosomiasis, Sleeping Sickness, 183–90. Paris: Springer Paris, 1999. http://dx.doi.org/10.1007/978-2-8178-0857-4_10.

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Dumas, M., and S. Bisser. "Clinical aspects of human African trypanosomiasis." In Progress in Human African Trypanosomiasis, Sleeping Sickness, 215–33. Paris: Springer Paris, 1999. http://dx.doi.org/10.1007/978-2-8178-0857-4_13.

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Van Meirvenne, N. "Biological diagnosis of human African trypanosomiasis." In Progress in Human African Trypanosomiasis, Sleeping Sickness, 235–52. Paris: Springer Paris, 1999. http://dx.doi.org/10.1007/978-2-8178-0857-4_14.

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Chauvière, G., and J. Périé. "The nitroimidazoles and human African trypanosomiasis." In Progress in Human African Trypanosomiasis, Sleeping Sickness, 281–87. Paris: Springer Paris, 1999. http://dx.doi.org/10.1007/978-2-8178-0857-4_16.

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Stanghellini, A. "Prophylactic strategies in human African trypanosomiasis." In Progress in Human African Trypanosomiasis, Sleeping Sickness, 301–13. Paris: Springer Paris, 1999. http://dx.doi.org/10.1007/978-2-8178-0857-4_18.

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Frézil, J. L. "‘Trypanosomiasis exists when it is searched for…’." In Progress in Human African Trypanosomiasis, Sleeping Sickness, 1–5. Paris: Springer Paris, 1999. http://dx.doi.org/10.1007/978-2-8178-0857-4_1.

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