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Relevant bibliographies by topics / Trypanosoma. Trypanosomiasis

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Academic literature on the topic 'Trypanosoma. Trypanosomiasis'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

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Journal articles on the topic "Trypanosoma. Trypanosomiasis"

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Morais, Mayara Castro de, Jucieudo Virgulino de Souza, Carlos da Silva Maia Bezerra Filho, Silvio Santana Dolabella, and Damião Pergentino de Sousa. "Trypanocidal Essential Oils: A Review." Molecules 25, no. 19 (October 6, 2020): 4568. http://dx.doi.org/10.3390/molecules25194568.

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Trypanosomiases are diseases caused by parasitic protozoan trypanosomes of the genus Trypanosoma. In humans, this includes Chagas disease and African trypanosomiasis. There are few therapeutic options, and there is low efficacy to clinical treatment. Therefore, the search for new drugs for the trypanosomiasis is urgent. This review describes studies of the trypanocidal properties of essential oils, an important group of natural products widely found in several tropical countries. Seventy-seven plants were selected from literature for the trypanocidal activity of their essential oils. The main chemical constituents and mechanisms of action are also discussed. In vitro and in vivo experimental data show the therapeutic potential of these natural products for the treatment of infections caused by species of Trypanosoma.

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Katabazi, Aziz, Adamu Almustapha Aliero, Sarah Gift Witto, Martin Odoki, and Simon Peter Musinguzi. "Prevalence of Trypanosoma congolense and Trypanosoma vivax in Lira District, Uganda." BioMed Research International 2021 (June 14, 2021): 1–7. http://dx.doi.org/10.1155/2021/7284042.

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Trypanosomes are the causative agents of animal African trypanosomiasis (AAT) and human African trypanosomiasis (HAT), the former affecting domestic animals prevalent in Sub-Saharan Africa. The main species causing AAT in cattle are T. congolense, T. vivax, and T. b. brucei. Northern Uganda has been politically unstable with no form of vector control in place. The return of displaced inhabitants led to the restocking of cattle from AAT endemic areas. It was thus important to estimate the burden of trypanosomiasis in the region. This study was designed to compare the prevalence of animal African trypanosomes in cattle in Lira District using microscopy and polymerase chain reaction amplification (PCR) methods. In this cross-sectional study, a total of 254 cattle from the three villages of Acanakwo A, Barropok, and Acungkena in Lira District, Uganda, were selected by simple random sampling technique and screened for trypanosomiasis using microscopy and PCR methods. The prevalence of trypanosomiasis according to microscopic results was 5/254 (2.0%) as compared to 11/254 (4.3%) trypanosomiasis prevalence according to PCR analysis. The prevalence of trypanosomiasis infection in the animal studied is 11/254 (4.3%). Trypanosoma congolense was the most dominant trypanosome species with a proportion of 9/11 (81.8%), followed by T. vivax 1/11 (9.1%) and mixed infection of T. congolense/T. vivax1/11 (9.1%). Barropok village had the highest prevalence of trypanosomiasis with 6/11 (54.5%). There is a statistically significant relationship ( OR = 6.041 ; 95% CI: 1.634-22.331; p < 0.05 ) between abnormal PCV and trypanosome infection. Polymerase reaction amplification was the most reliable diagnostic method due to its high sensitivity and specificity as compared to the conventional microscopic method. Polymerase reaction amplification appears to have adequate accuracy to substitute the use of a microscope where facilities allow. This study, therefore, underscores the urgent need for local surveillance schemes more especially at the grassroots in Uganda to provide data for reference guideline development needed for the control of trypanosomiasis in Uganda.

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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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ALSFORD, SAM, JOHN M. KELLY, NICOLA BAKER, and DAVID HORN. "Genetic dissection of drug resistance in trypanosomes." Parasitology 140, no. 12 (April 3, 2013): 1478–91. http://dx.doi.org/10.1017/s003118201300022x.

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SUMMARYThe trypanosomes cause two neglected tropical diseases, Chagas disease in the Americas and African trypanosomiasis in sub-Saharan Africa. Over recent years a raft of molecular tools have been developed enabling the genetic dissection of many aspects of trypanosome biology, including the mechanisms underlying resistance to some of the current clinical and veterinary drugs. This has led to the identification and characterization of key resistance determinants, including transporters for the anti-Trypanosoma bruceidrugs, melarsoprol, pentamidine and eflornithine, and the activator of nifurtimox-benznidazole, the anti-Trypanosoma cruzidrugs. More recently, advances in sequencing technology, combined with the development of RNA interference libraries in the clinically relevant bloodstream form ofT. bruceihave led to an exponential increase in the number of proteins known to interact either directly or indirectly with the anti-trypanosomal drugs. In this review, we discuss these findings and the technological developments that are set to further revolutionise our understanding of drug-trypanosome interactions. The new knowledge gained should inform the development of novel interventions against the devastating diseases caused by these parasites.

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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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Makhulu, Edward Edmond, Jandouwe Villinger, Vincent Owino Adunga, Maamun M. Jeneby, Edwin Murungi Kimathi, Enock Mararo, Joseph Wang’ang’a Oundo, Ali Abdulahi Musa, and Lillian Wambua. "Tsetse blood-meal sources, endosymbionts and trypanosome-associations in the Maasai Mara National Reserve, a wildlife-human-livestock interface." PLOS Neglected Tropical Diseases 15, no. 1 (January 6, 2021): e0008267. http://dx.doi.org/10.1371/journal.pntd.0008267.

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African trypanosomiasis (AT) is a neglected disease of both humans and animals caused by Trypanosoma parasites, which are transmitted by obligate hematophagous tsetse flies (Glossina spp.). Knowledge on tsetse fly vertebrate hosts and the influence of tsetse endosymbionts on trypanosome presence, especially in wildlife-human-livestock interfaces, is limited. We identified tsetse species, their blood-meal sources, and correlations between endosymbionts and trypanosome presence in tsetse flies from the trypanosome-endemic Maasai Mara National Reserve (MMNR) in Kenya. Among 1167 tsetse flies (1136 Glossina pallidipes, 31 Glossina swynnertoni) collected from 10 sampling sites, 28 (2.4%) were positive by PCR for trypanosome DNA, most (17/28) being of Trypanosoma vivax species. Blood-meal analyses based on high-resolution melting analysis of vertebrate cytochrome c oxidase 1 and cytochrome b gene PCR products (n = 354) identified humans as the most common vertebrate host (37%), followed by hippopotamus (29.1%), African buffalo (26.3%), elephant (3.39%), and giraffe (0.84%). Flies positive for trypanosome DNA had fed on hippopotamus and buffalo. Tsetse flies were more likely to be positive for trypanosomes if they had the Sodalis glossinidius endosymbiont (P = 0.0002). These findings point to complex interactions of tsetse flies with trypanosomes, endosymbionts, and diverse vertebrate hosts in wildlife ecosystems such as in the MMNR, which should be considered in control programs. These interactions may contribute to the maintenance of tsetse populations and/or persistent circulation of African trypanosomes. Although the African buffalo is a key reservoir of AT, the higher proportion of hippopotamus blood-meals in flies with trypanosome DNA indicates that other wildlife species may be important in AT transmission. No trypanosomes associated with human disease were identified, but the high proportion of human blood-meals identified are indicative of human African trypanosomiasis risk. Our results add to existing data suggesting that Sodalis endosymbionts are associated with increased trypanosome presence in tsetse flies.

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Kubata, Bruno Kilunga, Michael Duszenko, Zakayi Kabututu, Marc Rawer, Alexander Szallies, Ko Fujimori, Takashi Inui, et al. "Identification of a Novel Prostaglandin F2α Synthase in Trypanosoma brucei." Journal of Experimental Medicine 192, no. 9 (November 6, 2000): 1327–38. http://dx.doi.org/10.1084/jem.192.9.1327.

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Members of the genus Trypanosoma cause African trypanosomiasis in humans and animals in Africa. Infection of mammals by African trypanosomes is characterized by an upregulation of prostaglandin (PG) production in the plasma and cerebrospinal fluid. These metabolites of arachidonic acid (AA) may, in part, be responsible for symptoms such as fever, headache, immunosuppression, deep muscle hyperaesthesia, miscarriage, ovarian dysfunction, sleepiness, and other symptoms observed in patients with chronic African trypanosomiasis. Here, we show that the protozoan parasite T. brucei is involved in PG production and that it produces PGs enzymatically from AA and its metabolite, PGH2. Among all PGs synthesized, PGF2α was the major prostanoid produced by trypanosome lysates. We have purified a novel T. brucei PGF2α synthase (TbPGFS) and cloned its cDNA. Phylogenetic analysis and molecular properties revealed that TbPGFS is completely distinct from mammalian PGF synthases. We also found that TbPGFS mRNA expression and TbPGFS activity were high in the early logarithmic growth phase and low during the stationary phase. The characterization of TbPGFS and its gene in T. brucei provides a basis for the molecular analysis of the role of parasite-derived PGF2α in the physiology of the parasite and the pathogenesis of African trypanosomiasis.

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Sarataphan, Nachai, Montakan Vongpakorn, Bandit Nuansrichay, Nonglux Autarkool, Tiemjan Keowkarnkah, Pranee Rodtian, Roger W. Stich, and Sathaporn Jittapalapong. "Diagnosis of a Trypanosoma lewisi-like (Herpetosoma) infection in a sick infant from Thailand." Journal of Medical Microbiology 56, no. 8 (August 1, 2007): 1118–21. http://dx.doi.org/10.1099/jmm.0.47222-0.

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Trypanosomes were observed in a peripheral blood smear from a 45-day-old Thai infant displaying fever, anaemia, cough and anorexia. Human trypanosomiasis is not endemic to Thailand, so parasite identification was undertaken to determine likely sources of the infection. Several morphological parameters of the trypanosomes were similar to those of Trypanosoma evansi and statistically different from those of Trypanosoma lewisi-like parasites from a naturally infected indigenous rat. However, duplicate PCR assays with primers flanking trypanosome rRNA internal transcribed spacer 1 (ITS1) resulted in amplicons of ~623 bp that corresponded to the expected size for T. lewisi-like parasites. The ITS1 sequence from the infant's blood was 98 and 49 % identical to T. lewisi and T. evansi sequences, respectively. Based on molecular results, it was concluded that the infant was infected with a T. lewisi-like (Herpetosoma) species.

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Pereira, Glaécia AN, Lucianna H. Santos, Steven C. Wang, Luan C. Martins, Filipe S. Villela, Weiting Liao, Marco A. Dessoy, et al. "Benzimidazole inhibitors of the major cysteine protease of Trypanosoma brucei." Future Medicinal Chemistry 11, no. 13 (July 2019): 1537–51. http://dx.doi.org/10.4155/fmc-2018-0523.

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Aim: Limitations in available therapies for trypanosomiases indicate the need for improved medicines. Cysteine proteases cruzain and rhodesain are validated targets for treatment of Chagas disease and human African trypanosomiasis. Previous studies reported a benzimidazole series as potent cruzain inhibitors. Results & methodology: Considering the high similarity between these proteases, we evaluated 40 benzimidazoles against rhodesain. We describe their structure-activity relationships (SAR), revealing trends similar to those observed for cruzain and features that lead to enzyme selectivity. This series comprises noncovalent competitive inhibitors (best Ki = 0.21 μM against rhodesain) and micromolar activity against Trypanosoma brucei brucei. A cheminformatics analysis confirms scaffold novelty, and the inhibitors described have favorable predicted physicochemical properties. Conclusion: Our results support this series as a starting point for new human African trypanosomiasis medicines.

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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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Dissertations / Theses on the topic "Trypanosoma. Trypanosomiasis"

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Tchamo, Cesaltina da Conceicao Lopes Menete. "Evaluation of the pathogenicity in goats of Trypanosoma congolense from Matutuine, Mozambique." Pretoria : [s.n.], 2007. http://upetd.up.ac.za/thesis/available/etd-04212008-143822/.

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Aboubaker, Eltayb Abdelwahab Mohamed. "Trypanosomiasis : molecular diagnosis of Trypanosoma evansi infection and endotoxaemia during Trypanosoma brucei rhodesiense infection." Thesis, University of Aberdeen, 2017. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=231772.

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Two aspects of trypanosomiasis have been investigated in this study. First, molecular methods were applied to the diagnosis of T.evansi in camels in South Libya. The aim of the study was to determine if FTA card blood sampling and PCR amplification could detect parasites and this be used as tool for diagnosis and epidemiology. Targeted samples of 70 camels were identified on the basis of symptoms of infection and blood was collected on FTA cards. PCR primers and conditions for the amplification of T.evansi DNA were developed on the basis of the literature and a positive control clone grown in the laboratory. The assay found 84.3% of camel samples positive using TBR primers (177bp amplicon) and ITS nested primers (611-1513bp amplicons). This result demonstrated that Surra is endemic in this area, and that T.evansi was the species that was involved. The ITS and TBR loci in the parasites identified in Libya were almost identical to those previously reported in the genbank database, though with some polymorphisms. Dullness and emaciation were the clinical signs of camels infected by trypanosomes, and these two symptoms were significantly related to the 1200bp ITS nested PCR amplicon. These two symptoms can be thus used as a sign an initial diagnosis of T.evansi infection in camels. The second aspect of trypanosomiasis studied was the occurrence of endotoxaemia in infection. The first part of this research investigated endotoxin levels in clinical human African trypasnosomiasis using the Limulus Amoebocyte lysate assay. Endotoxin levels were significantly increased over control individuals in the plasma of T.b.rhodesiense patients. This endotoxaemia was unrelated to infection duration, parasitaemia or clinical stage but resolved after clearance of parasites by drug treatment. In the cerebrospinal fluid there was no significant difference in endotoxin level between early and late stage cases and no relationship to parasite loads. It is argued on the basis of the data that endotoxaemia in trypanosomiasis most likely results from increases in permeability of the gut to endotoxins from gram negative enter bacteria. This conclusion was further supported from a study using cell culture adapted T.brucei and secreted products which gave no evidence of any endotoxin activity. Also samples of an acute experimental mouse infection with T.brucei gave no endotoxin activity, suggesting that this phenomenon requires a more chronic infection in mice. No relationships were found between plasma or CSF endotoxin levels to neurological signs of infection. However the presence of a gross inflammatory clinical symptom, splenomegaly, was associated with endotoxaemia and the concentrations of 3 plasma cytokines associated with the immune response in trypanosome infection were associated with correlated to plasma endotoxin levels. In order to determine the nature of the endotoxin activity, a biosensor cell assay for LPS was used, based on human embryonic kidney cells transfected with TLR4/MD3 and a NF-κB induced alkaline phosphatase reporter gene. This assay revealed low or undetectable levels of LPS in clinical samples from T.b.rhodesiense patients, in mouse samples from T.b.brucei infections and in vitro cultured trypanosomes. This suggests that either the endotoxin activity detected using the LAL assay is an unconventional endotoxin signalling via a TLR4 independent pathway or that the human plasma was in some way toxic to the reporter cell and this requires further investigation. In conclusion, this study has provided the first clear evidence of an association of endotoxaemia and inflammatory responses in clinical African trypansomiasis and helps resolve the question of whether endotoxaemia is a parasite or host-microbiota related phenomenon.

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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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Mhlanga, Jama Donewell Mayixeke. "Antigenic variation in Trypanosoma brucei, a relationship with poly ADP-ribose polymerase." Thesis, University of Sussex, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240553.

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Hickey, Meghan C. "Exploring an unusual beta-hydroxybutyrate dehydrogenase from Trypanosoma brucei." Click here for download, 2010. http://proquest.umi.com.ps2.villanova.edu/pqdweb?did=2011158651&sid=1&Fmt=7&clientId=3260&RQT=309&VName=PQD.

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Guegan, Fabien. "Caractérisation des sialidases chez le parasite Trypanosoma vivax : rôle dans l’anémie." Thesis, Bordeaux 2, 2010. http://www.theses.fr/2010BOR21775/document.

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La trypanosomiase animale africaine (TAA) est une pathologie qui sévit en Afrique sub-saharienne et qui représente un obstacle majeur à l’élevage du bétail et à la production agricole. Cette pathologie est causée principalement par les parasites T. congolense et T. vivax. Elle affecte le bétail, les animaux domestiques et sauvages, sur un territoire de 10 millions de km2 où ces animaux cohabitent avec l’insecte vecteur, la mouche Tsé-Tsé. L’infection du bétail par ces parasites provoque une anémie sévère pouvant entraîner la mort de l’animal. Dans ce contexte, nous nous sommes intéressés à l’étude des mécanismes impliqués dans le développement de l’anémie lors de l’infection de l’animal par T. vivax. Pour cela, nous avons développé un modèle murin d’infection par T. vivax. Nous avons démontré que l’infection à T. vivax induit d’importantes modifications des acides sialiques présents à la surface des érythrocytes. De plus, nous avons établi un système expérimental « ex-vivo » qui nous a permis de montrer que l’anémie observée au cours de l’infection était dépendante du mécanisme d’érythrophagocytose. Les modifications en acides sialiques des érythrocytes constitueraient un signal de reconnaissance des érythrocytes par les cellules phagocytaires de l’hôte. Par ailleurs, nous avons mis au point des conditions de culture in vitro pour tous les stades parasitaires de T. vivax et T. congolense afin de développer des outils de génomique fonctionnelle. Ces avancées nous ont notamment permis d’identifier des enzymes de type sialidase et trans-sialidase et de détecter les activités enzymatiques correspondantes dans les formes infectieuses de ces parasites. Nous avons exprimé des trans-sialidases recombinantes et démontré qu’elles étaient capables de reproduire in vitro certaines des caractéristiques pathologiques définies in vivo : modifications en acides sialiques des érythrocytes et augmentation de l’érythrophagocytose. Par conséquent, ces travaux ont permis pour la première fois de mettre en évidence un lien entre l’expression des sialidases et trans-sialidases chez le parasite T. vivax et le développement de l’anémie au cours de la TAA
African animal trypanosomiasis (AAT) is a parasitic disease occurring in sub-Saharan Africa. It impairs livestock development and agricultural production. This disease is mainly caused by T. congolense and T. vivax parasites and is present in livestock, domestic and wild animals, covering an area of over a 10 millions km2, that is known as the Tsé-Tsé fly belt. These infections cause severe anaemia leading to animal death in most cases. In this context, we were interested in unravelling the mechanisms responsible for anaemia caused by T. vivax infection. We developed a murine model for T. vivax infection and our data pointed out important sialic acid modifications of the mouse erythrocyte surface during infection. Additionally, an ex-vivo experimental model was established which proved that anaemia associated with infection depends on erythrophagocytosis. Consequently, we propose that sialic acid modifications associated with infection are involved in the erythrophagocytosis mechanism. Furthermore, in order to develop genetic tools we established in vitro culture conditions for all parasite forms of T. vivax and T. congolense. Parasite cultivation allowed the detection of sialidase and trans-sialidase activity and identifies the presence and function of these proteins in the mammalian form of the parasite. Moreover, trans-sialidase recombinant proteins reproduced some of the T. vivax infection characteristics such as sialic acid modification and increased erythrophagocytosis. Consequently, this work provides the first evidence that links the expression of sialidases and trans-sialidases in T. vivax with the development of anemia during AAT

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Mabbott, Neil A. "Nitric oxide : host-protective or host-destructive during African trypanosomiasis." Thesis, University of Aberdeen, 1995. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU543723.

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The aims of the research presented in this thesis were concerned with investigating the effect of inducible nitric oxide (NO) synthase expression during Trypanosoma brucei infections on both host and parasite. NO was shown to exhibit a potent cytostatic effect on parasite proliferation. Oxyhaemoglobin is a potent scavenger of NO. The cytostatic effects of NO on the trypanosomes were completely prevented through the addition of erythrocytes to the cultures. This implies that in the host blood-stream, NO is unlikely to be involved in the eradication of the parasites. Through the adoptive transfer of suppressor macrophages from T.brucei-infected donor mice to naive recipients, it was demonstrated that NO mediates a suppressive effect on host lymphocyte responses in vivo. Furthermore, suppressor macrophages were shown to have a finite life-span and undergo NO-mediated apoptosis. Evidence also suggested that elevated NO production in the bone marrow of T.brucei -infected mice is likely to play a significant role in the anaemia resulting from T.brucei infection. Experiments demonstrated that a soluble lysate prepared from freeze-thawed blood-stream form T.brucei, activated interferon (IFN)-gamma primed macrophages to express high levels of NO synthase. Experiments also demonstrated that viable blood-stream forms, but not procyclic form trypanosomes, released a soluble factor which in combination with IFN-gamma induced NO synthase. The absolute requirement of IFN-gamma priming for NO synthase activation by T.brucei was studied using macrophages from mutant mice lacking functional IFN-gamma receptors (IFN-gamma R -/- mutant mice). In comparison to macrophages from wild-type mice, cells from IFN-gamma-R-/- mutant mice were unable to produce NO following stimulation in vitro or infection in vivo. Finally, utilising mice with specific immunodeficiencies it was demonstrated that natural killer cells and a/b T-lymphocytes were important sources of IFN-gamma during murine T.brucei infections.

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Giles, Natalie Lydia. "Exploitation of the protein tubulin for controlling African trypanosomiasis /." Access via Murdoch University Digital Theses Project, 2005. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20060315.191003.

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Ndoutamia, Guelmabye. "Derivation and characterisation of a quinapyramine-resistant clone of Trypanosoma congolense." Thesis, Brunel University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286698.

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Jaye, Assan. "Characterisation of Trypanosoma (Nannomonas) congolense-specific antigen : identification as a thiol protease precursor." Thesis, Brunel University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296197.

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Books on the topic "Trypanosoma. Trypanosomiasis"

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Magez, Stefan, and Magdalena Radwanska, eds. Trypanosomes and Trypanosomiasis. Vienna: Springer Vienna, 2014. http://dx.doi.org/10.1007/978-3-7091-1556-5.

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2

Budd, Leonard T. DFID-funded tsetse and trypanosome research and development since 1980. London: DFID, 1999.

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Onah, Denchris Nnabuike. The elegance and success of trypanosomes as parasites: Immunological perspective : an inaugural lecture of the University of Nigeria, delivered on June 4, 2009. Nsukka: University of Nigeria, Senate Ceremonials Committee, 2009.

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Magez, Stefan, and Magdalena Radwanska. Trypanosomes and Trypanosomiasis. Springer, 2013.

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Leslie, Hudson, ed. The Biology of trypanosomes. Berlin: Springer-Verlag, 1985.

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Hudson, Leslie, and Rudolf Jaenisch. The Biology of Trypanosomes. Brand: Springer, 2011.

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Altcheh, Jaime, Guillermo Moscatelli, and Facundo Garcia Bournissen. Chagas Disease (Trypanosoma cruzi). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190604813.003.0016.

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Chagas disease (CD), or American trypanosomiasis, is caused by the hemoflagellate parasite Trypanosoma cruzi and has evolved from a regional, Latin American disease to one that is becoming widespread in other parts of the world. Mother-to-child transmission (MTCT) of Chagas disease has become the primary means of transmission of T. cruzi worldwide. Congenital Chagas disease can be prevented by treating women of reproductive age. It is important to develop strategies for the systematic screening of pregnant women for CD, as well as all children born to infected mothers, and also to treat every infected child as early as possible.

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G, Hide, ed. Trypanosomiasis and leishmaniasis: Biology and control. Wallingofrd, Oxon, UK: CAB International, 1997.

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(Editor), Kevin M. Tyler, and Michael A. Miles (Editor), eds. American Trypanosomiasis (World Class Parasites). Springer, 2002.

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Mwamachi, Derrick Mwanyalo. Immune colostrum induces trypanotolerance in goat kids challenged with Trypanosoma congolense. 1987.

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Book chapters on the topic "Trypanosoma. Trypanosomiasis"

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Gonzatti, Mary Isabel, Bernardo González-Baradat, Pedro M. Aso, and Armando Reyna-Bello. "Trypanosoma (Duttonella) vivax and Typanosomosis in Latin America: Secadera/Huequera/Cacho Hueco." In Trypanosomes and Trypanosomiasis, 261–85. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1556-5_11.

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Leung, Ka Fai, Paul T. Manna, Cordula Boehm, Luke Maishman, and Mark C. Field. "Cell Biology for Immune Evasion: Organizing Antigenic Variation, Surfaces, Trafficking, and Cellular Structures in Trypanosoma brucei." In Trypanosomes and Trypanosomiasis, 1–39. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1556-5_1.

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Gries, Oliver, and Thomas Ly. "Trypanosoma brucei: Afrikanische Trypanosomiasis, „Schlafkrankheit”." In Infektologie - Kompendium humanpathogener Infektionskrankheiten und Erreger, 433–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-58219-0_63.

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Bello, Zoraida Díaz, and Belkisyolé Alarcón de Noya. "Biological Aspects of American Trypanosomiasis." In Trypanosoma cruzi as a Foodborne Pathogen, 7–19. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-23410-6_2.

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Leppla, Norman C., Bastiaan M. Drees, Allan T. Showler, John L. Capinera, Jorge E. Peña, Catharine M. Mannion, F. William Howard, et al. "Rodent Trypanosomiasis: A Comparison Between Trypanosoma lewisi and Trypanosoma musculi." In Encyclopedia of Entomology, 3208–10. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_3429.

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Black, Samuel J. "Control of pathogenesis in African animal trypanosomiasis: a search for answers at ILRAD, ILCA and ILRI, 1975-2018." In The impact of the International Livestock Research Institute, 103–47. Wallingford: CABI, 2020. http://dx.doi.org/10.1079/9781789241853.0103.

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Abstract This book chapter describes the management of animal trypanosomiasis: (i) vector control/eradication; (ii) use of trypanocides; and (iii) use of trypanotolerant breeds of cattle. Vector control includes reducing the tsetse fly population with traps and insecticides, and in areas with a high population of trypanosome infected tsetse, animals are prophylactically administered antiparasitic drugs. To date, there is no AAT vaccine available, as discussed below. While disappointing with respect to AAT control, studies of AAT pathogenesis at ILRAD/ILRI did identify the definitive question for immunological research on AAT, namely, how do trypanosomes eliminate TD antibody responses in trypanosomiasis-susceptible mammals? In addition, the work at ILRI on the genetic basis of trypanotolerance contributed a high-density singlenucleotide polymorphism (SNP) map of the bovine genome that has intrinsic value for analysis of QTLs that control other traits, including susceptibility to other diseases.

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Namangala, Boniface, and Steven Odongo. "Animal African Trypanosomosis in Sub-Saharan Africa and Beyond African Borders." In Trypanosomes and Trypanosomiasis, 239–60. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1556-5_10.

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Caljon, Guy, Linda De Vooght, and Jan Van Den Abbeele. "The Biology of Tsetse–Trypanosome Interactions." In Trypanosomes and Trypanosomiasis, 41–59. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1556-5_2.

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Hall, James Peter John, and Lindsey Plenderleith. "Withstanding the Challenges of Host Immunity: Antigenic Variation and the Trypanosome Surface Coat." In Trypanosomes and Trypanosomiasis, 61–87. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1556-5_3.

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Mansfield, John M., Donna M. Paulnock, and Gina M. Hedberg. "Bridging Innate and Adaptive Immunity in African Trypanosomiasis." In Trypanosomes and Trypanosomiasis, 89–114. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1556-5_4.

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Conference papers on the topic "Trypanosoma. Trypanosomiasis"

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Marcelino Pacheco Neto, Joao, and Otavio Noura Teixeira. "Reconhecimento de Padrões em Imagens de Triatomíneos Usando Redes Neurais Artificiais com Algoritmo Backpropagation." In Computer on the Beach. Itajaí: Universidade do Vale do Itajaí, 2020. http://dx.doi.org/10.14210/cotb.v11n1.p455-460.

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Chagas disease, also known as American trypanosomiasis isone of the consequences of the human infection caused by theflagellate protozoan called Trypanosoma cruzi transmittedby the barbeiro of the subfamily Triatominae known as triatomines.In the Lower Tocantins region of the state of Para,three genera of barbers transmitting the disease are found.Searching for a way to automate the manual recognition process,this work aimed to implement a Model of Recognitionand Classification of Images of barbers found in the LowerTocantins region in order to recognize the genus of the insectthrough the use of Artificial Neural Networks PerceptronMulti-layered and performing training with Backpropagationalgorithm, helping to identify the transmitters. In themiddle of this recognition, the Digital Image Processing isperformed to extract important characteristics relevant to theclassification. This entire process is performed in MATLABsoftware through scripts and the creation of the ArtificialNeural Network in the toolbox called Pattern RecognitionApp.

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Dardonville, Christophe, Francisco José Fueyo González, Carolina Izquierdo García, Teresa Díaz Ayuga, Godwin Ebiloma, Emmanuel Balogun, Kiyoshi Kita, and Harry de Koning. "Targeting the Trypanosome Alternative Oxidase (TAO) as Promising Chemotherapeutic Approach for African Trypanosomiasis." In 3rd International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2017. http://dx.doi.org/10.3390/ecmc-3-04641.

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