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Journal articles on the topic 'Nagana'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Yalew, Shimels Ayele. "Historical analysis of animal diseases: Nagana in Southwestern Ethiopia, Gambella." Ethiopian Veterinary Journal 27, no. 1 (2023): 55–71. http://dx.doi.org/10.4314/evj.v27i1.3.

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Animals and humans have been intimate companions since antiquity. The history of animals discloses diverse episodes in human history. However, the history of animal disease via humans has been the least researched theme. Therefore, this study aimed to explore animal disease history with a special focus on Nagana in Gambella, Ethiopia. The study utilized content analysis of travelers’ accounts, archival documents, reports, and secondary sources. It revealed that nagana was endemic in the region due to the presence of dense forests, abundant game resources, and climatic factors. Nagana had direc

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2

Martini, Oberstabsarzt. "Aus der Epidemiologie der Schlafkrankheit und Nagana." Zeitschrift für Angewandte Entomologie 28, no. 2-3 (2009): 488–500. http://dx.doi.org/10.1111/j.1439-0418.1941.tb01037.x.

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Minnaar, A. de V. "Nagana, big-game drives and the Zululand game reserves (1890s-1950s)." New Contree 25 (June 28, 2024): 10. http://dx.doi.org/10.4102/nc.v25i0.684.

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Zululand's world-renowned Hluhluwe and Umfolozi game reserves are today two of the most popular of their kind. But in the effort to establish and keep them, the cattle disease nagana and the accompanying use of big-game drives as a preventative measure to combat the tsetse fly proved to be a serious problem. The game reserves were blamed for harbouring game which carried the nagana parasite, and were therefore regarded as a food source and infection pool for the tsetsefly. Conservationists therefore had to struggle continually to protect the existence of Zululand's game reserves in the face of

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Boulanger, Nathalie, Rebecca J. L. Munks, Joanne V. Hamilton, et al. "Epithelial Innate Immunity." Journal of Biological Chemistry 277, no. 51 (2002): 49921–26. http://dx.doi.org/10.1074/jbc.m206296200.

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The gut epithelium is an essential interface in insects that transmit parasites. We investigated the role that local innate immunity might have on vector competence, takingStomoxys calcitransas a model.S. calcitransis sympatric with tsetse flies, feeds on many of the same vertebrate hosts, and is thus regularly exposed to the trypanosomes that cause African sleeping sickness and nagana. Despite this,S. calcitransis not a cyclical vector of these trypanosomes. Trypanosomes develop exclusively in the lumen of digestive organs, and so epithelial immune mechanisms, and in particular antimicrobial

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Authié, Édith, Frédéric Bringaud, Norbert Bakalara, Emmanuel Tetaud, and Théo Baltz. "Trypanosomoses humaines et animales: maladie du sommeil et Nagana." Annales de l'Institut Pasteur / Actualités 10, no. 1 (1999): 27–50. http://dx.doi.org/10.1016/s0924-4204(99)80021-3.

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6

Alexeyenkova, S. V. "The current diagnostic challenges of equid trypanosomoses: nagana, surra and dourine." "Veterinary Medicine" Journal 24, no. 12 (2021): 35–39. http://dx.doi.org/10.30896/0042-4846.2021.24.12.35-39.

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Cauchard, S., N. Van Reet, P. Büscher, et al. "Killing of Trypanozoon Parasites by the Equine Cathelicidin eCATH1." Antimicrobial Agents and Chemotherapy 60, no. 5 (2016): 2610–19. http://dx.doi.org/10.1128/aac.01127-15.

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ABSTRACTTrypanozoonparasites infect both humans, causing sleeping sickness, and animals, causing nagana, surra, and dourine. Control of nagana and surra depends to a great extent on chemotherapy. However, drug resistance to several of the front-line drugs is rising. Furthermore, there is no official treatment for dourine. Therefore, there is an urgent need to develop antiparasitic agents with novel modes of action. Host defense peptides have recently gained attention as promising candidates. We have previously reported that one such peptide, the equine antimicrobial peptide eCATH1, is highly a

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Słomka vel Słomiński, Krystian. "Przekłady i parafrazy „Vitae Regum Polonorum” Klemensa Janicjusza od XVI do XVIII wieku – sposoby kreowania wizerunku doskonałego władcy." "Res Rhetorica" 8, no. 3 (2021): 4–19. http://dx.doi.org/10.29107/rr2021.3.1.

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W artykule analizowane są podobieństwa i różnice w sposobie kreowania wizerunków doskonałego władcy, które występują w zbiorze epigramatów Janicjusza oraz w tekstach inspirowanych jego dziełem, napisanych przez S. F. Klonowica, J. A. Kmitę, J. Głuchowskiego, M. Paszkowskiego i J. Bielskiego. Fakt, iż teksty te w różnym stopniu nawiązują do pierwowzoru, a ponadto powstawały na przestrzeni 200 lat, sprawia, że w kolejnych zbiorach zmienia się wymowa poszczególnych epigramów (ocena czynów władcy ulega złagodzeniu lub wyostrza się nagana); ponadto modyfikacji poddany jest zespół cech monarchów. Sł

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Płońska, Anna. "Problematyka racjonalizacji kar za wykroczenia." Przegląd Prawa i Administracji 124 (November 18, 2021): 203–17. http://dx.doi.org/10.19195/0137-1134.124.15.

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Przedmiotem niniejszego opracowania jest zagadnienie racjonalizacji kar orzekanych na gruncie prawa wykroczeń. Autorka zwięźle przedstawia dyrektywy i zasady wymiaru poszczególnych kar za wykroczenia oraz wskazuje na potrzebę wprowadzenia zmian w tym zakresie. Przedstawione rozważania zasadniczo prowadzą do konstatacji, iż w obliczu nieuchronnej gruntownej nowelizacji unormowań kodeksu wykroczeń korzystne z punktu widzenia usprawnienia systemu kar za wykroczenia wydaje się nie tylko podnoszone przez doktrynę wyeliminowanie kary aresztu i pozostawienie do dyspozycji sędziego jedynie zastępczej

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D'Amico, F., J. M. Poussinga, C. Le Masson, Alain Le Masson, and Dominique Cuisance. "Pratiques pastorales Mbororo et trypanosomoses bovines dans une zone de savanes humides de Centrafrique." Revue d’élevage et de médecine vétérinaire des pays tropicaux 48, no. 2 (1995): 203–12. http://dx.doi.org/10.19182/remvt.9473.

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L'étude a porté sur l'agencement de l'espace pastoral chez les éleveurs Mbororo de Centrafrique et les mouvements de leurs zébus à robe acajou. Outre le campement des éleveurs, cet espace est divisé en trois compartiments principaux : l'aire de repos, l'abreuvoir et le Pâturage sillonné de sentiers. Son utilisation repose sur une ségrégation spatiale et temporelle des déplacements des animaux. Dans le contexte particulier des savanes humides du centre de la République centrafricaine, où l'espèce riveraine Glossina fuscipes fuscipes Newst. 1910 est le vecteur principal des trypanosomoses bovine

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Haynes, Carole L. F., Paul Ameloot, Han Remaut, Nico Callewaert, Yann G. J. Sterckx, and Stefan Magez. "Production, purification and crystallization of atrans-sialidase fromTrypanosoma vivax." Acta Crystallographica Section F Structural Biology Communications 71, no. 5 (2015): 577–85. http://dx.doi.org/10.1107/s2053230x15002496.

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Sialidases andtrans-sialidases play important roles in the life cycles of various microorganisms. These enzymes can serve nutritional purposes, act as virulence factors or mediate cellular interactions (cell evasion and invasion). In the case of the protozoan parasiteTrypanosoma vivax,trans-sialidase activity has been suggested to be involved in infection-associated anaemia, which is the major pathology in the disease nagana. The physiological role of trypanosomaltrans-sialidases in host–parasite interaction as well as their structures remain obscure. Here, the production, purification and cry

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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 (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 simil

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13

Cook, G. C. "Sir David Bruce's elucidation of the aetiology of nagana—exactly one hundred years ago." Transactions of the Royal Society of Tropical Medicine and Hygiene 88, no. 3 (1994): 257–58. http://dx.doi.org/10.1016/0035-9203(94)90068-x.

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14

Nagamune, Kisaburo, Alvaro Acosta-Serrano, Haruki Uemura, et al. "Surface Sialic Acids Taken from the Host Allow Trypanosome Survival in Tsetse Fly Vectors." Journal of Experimental Medicine 199, no. 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 abunda

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15

Lorger, Mihaela, Markus Engstler, Matthias Homann, and H. Ulrich Göringer. "Targeting the Variable Surface of African Trypanosomes with Variant Surface Glycoprotein-Specific, Serum-Stable RNA Aptamers." Eukaryotic Cell 2, no. 1 (2003): 84–94. http://dx.doi.org/10.1128/ec.2.1.84-94.2003.

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ABSTRACT African trypanosomes cause sleeping sickness in humans and Nagana in cattle. The parasites multiply in the blood and escape the immune response of the infected host by antigenic variation. Antigenic variation is characterized by a periodic change of the parasite protein surface, which consists of a variant glycoprotein known as variant surface glycoprotein (VSG). Using a SELEX (systematic evolution of ligands by exponential enrichment) approach, we report the selection of small, serum-stable RNAs, so-called aptamers, that bind to VSGs with subnanomolar affinity. The RNAs are able to r

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16

Gumbo, Maureen, Richard Beteck, Tawanda Mandizvo, et al. "Cinnamoyl-Oxaborole Amides: Synthesis and Their in Vitro Biological Activity." Molecules 23, no. 8 (2018): 2038. http://dx.doi.org/10.3390/molecules23082038.

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Due to the increased interest in their application in the treatment of infectious diseases, boron-containing compounds have received a significant coverage in the literature. Herein, a small set of novel cinnamoly-oxaborole amides were synthesized and screened against nagana Trypanosoma brucei brucei for antitrypanosomal activity. Compound 5g emerged as a new hit with an in vitro IC50 value of 0.086 μM against T. b. brucei without obvious inhibitory activity against HeLa cell lines. The same series was also screened against other human pathogens, including Mycobacterium tuberculosis, the causa

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Fuchs, Alicia G., María C. Soraires Santacruz, Octavio A. Fusco, et al. "Trypanocidal effect of Diminazene aceturate by intranasal administration. Comparison among formulations." Interamerican Journal of Health Sciences, no. 1 (December 3, 2021): 33. http://dx.doi.org/10.59471/ijhsc202133.

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Background: The standard treatment for nagana and surra, vector–born parasite diseases, is a single intramuscular (i.m.) dose of diminazene aceturate (Berenil), an aromatic diamidine. Due to discontinuation of public provision of veterinary services or to lack of access to remote areas, low income farmers inject livestock and other domestic animals by themselves. We tested a not explored administration route for drugs against parasitological infections: the intranasal one. Berenil alone dissolved in water did not reach an effective drug concentration. Methods: Mice were infected with Try

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Blom-Potar, Marie Christine, Nathalie Chamond, Alain Cosson, et al. "Trypanosoma vivax Infections: Pushing Ahead with Mouse Models for the Study of Nagana. II. Immunobiological Dysfunctions." PLoS Neglected Tropical Diseases 4, no. 8 (2010): e793. http://dx.doi.org/10.1371/journal.pntd.0000793.

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Magri, Alice, Roberta Galuppi, and Marialetizia Fioravanti. "Autochthonous Trypanosoma spp. in European Mammals: A Brief Journey amongst the Neglected Trypanosomes." Pathogens 10, no. 3 (2021): 334. http://dx.doi.org/10.3390/pathogens10030334.

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The genus Trypanosoma includes flagellated protozoa belonging to the family Trypanosomatidae (Euglenozoa, Kinetoplastida) that can infect humans and several animal species. The most studied species are those causing severe human pathology, such as Chagas disease in South and Central America, and the human African trypanosomiasis (HAT), or infections highly affecting animal health, such as nagana in Africa and surra with a wider geographical distribution. The presence of these Trypanosoma species in Europe has been thus far linked only to travel/immigration history of the human patients or intr

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Vidilaseris, Keni, Nicolas Landrein, Yulia Pivovarova, et al. "Crystal structure of the N-terminal domain of the trypanosome flagellar protein BILBO1 reveals a ubiquitin fold with a long structured loop for protein binding." Journal of Biological Chemistry 295, no. 6 (2019): 1489–99. http://dx.doi.org/10.1074/jbc.ra119.010768.

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Trypanosoma brucei is a protist parasite causing sleeping sickness and nagana in sub-Saharan Africa. T. brucei has a single flagellum whose base contains a bulblike invagination of the plasma membrane called the flagellar pocket (FP). Around the neck of the FP on its cytoplasmic face is a structure called the flagellar pocket collar (FPC), which is essential for FP biogenesis. BILBO1 was the first characterized component of the FPC in trypanosomes. BILBO1's N-terminal domain (NTD) plays an essential role in T. brucei FPC biogenesis and is thus vital for the parasite's survival. Here, we report

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Panethymitaki, Chrysoula, Paul W. Bowyer, Helen P. Price, Robin J. Leatherbarrow, Katherine A. Brown, and Deborah F. Smith. "Characterization and selective inhibition of myristoyl-CoA:protein N-myristoyltransferase from Trypanosoma brucei and Leishmania major." Biochemical Journal 396, no. 2 (2006): 277–85. http://dx.doi.org/10.1042/bj20051886.

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The eukaryotic enzyme NMT (myristoyl-CoA:protein N-myristoyltransferase) has been characterized in a range of species from Saccharomyces cerevisiae to Homo sapiens. NMT is essential for viability in a number of human pathogens, including the fungi Candida albicans and Cryptococcus neoformans, and the parasitic protozoa Leishmania major and Trypanosoma brucei. We have purified the Leishmania and T. brucei NMTs as active recombinant proteins and carried out kinetic analyses with their essential fatty acid donor, myristoyl-CoA and specific peptide substrates. A number of inhibitory compounds that

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Matovu, Enock, Thomas Seebeck, John C. K. Enyaru, and Ronald Kaminsky. "Drug resistance in Trypanosoma brucei spp., the causative agents of sleeping sickness in man and nagana in cattle." Microbes and Infection 3, no. 9 (2001): 763–70. http://dx.doi.org/10.1016/s1286-4579(01)01432-0.

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Lillico, Simon, Mark C. Field, Pat Blundell, Graham H. Coombs, and Jeremy C. Mottram. "Essential Roles for GPI-anchored Proteins in African Trypanosomes Revealed Using Mutants Deficient in GPI8." Molecular Biology of the Cell 14, no. 3 (2003): 1182–94. http://dx.doi.org/10.1091/mbc.e02-03-0167.

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The survival of Trypanosoma brucei, the causative agent of Sleeping Sickness and Nagana, is facilitated by the expression of a dense surface coat of glycosylphosphatidylinositol (GPI)-anchored proteins in both its mammalian and tsetse fly hosts. We have characterized T. brucei GPI8, the gene encoding the catalytic subunit of the GPI:protein transamidase complex that adds preformed GPI anchors onto nascent polypeptides. Deletion ofGPI8 (to give Δgpi8) resulted in the absence of GPI-anchored proteins from the cell surface of procyclic form trypanosomes and accumulation of a pool of non–protein-l

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Awuoche, E., and No author No author. "Tsetse fly saliva: Could it be useful in fly infection when feeding in chronically aparasitemic mammalian hosts." Open Veterinary Journal 5, no. 2 (2012): 95. http://dx.doi.org/10.5455/ovj.2012.v2.i0.p95.

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Sleeping sickness and nagana are two important diseases cuased by African trypanosomes in humans and animals respectively, in tropical african countries. A number of trypanosome species are implicated in these diseases, but it is the Trypanosoma brucei group that is responsible for the chronic form of sleeping sickness. During the course of this chronic infection the parasite shows a clear tropism for organs and tissues and only sporadically appears in the blood stream. Notwithstanding this feature, tsetse flies normally get infected from chronically infected apparasitemic hosts. For some path

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Iribarren, Paula Ana, Lucía Ayelén Di Marzio, María Agustina Berazategui, et al. "Depolymerization of SUMO chains induces slender to stumpy differentiation in T. brucei bloodstream parasites." PLOS Pathogens 20, no. 4 (2024): e1012166. http://dx.doi.org/10.1371/journal.ppat.1012166.

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Trypanosoma brucei are protozoan parasites that cause sleeping sickness in humans and nagana in cattle. Inside the mammalian host, a quorum sensing-like mechanism coordinates its differentiation from a slender replicative form into a quiescent stumpy form, limiting growth and activating metabolic pathways that are beneficial to the parasite in the insect host. The post-translational modification of proteins with the Small Ubiquitin-like MOdifier (SUMO) enables dynamic regulation of cellular metabolism. SUMO can be conjugated to its targets as a monomer but can also form oligomeric chains. Here

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Chamond, Nathalie, Alain Cosson, Marie Christine Blom-Potar, et al. "Trypanosoma vivax Infections: Pushing Ahead with Mouse Models for the Study of Nagana. I. Parasitological, Hematological and Pathological Parameters." PLoS Neglected Tropical Diseases 4, no. 8 (2010): e792. http://dx.doi.org/10.1371/journal.pntd.0000792.

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Echodu, Richard, Mark Sistrom, Rosemary Bateta, et al. "Genetic Diversity and Population Structure of Trypanosoma brucei in Uganda: Implications for the Epidemiology of Sleeping Sickness and Nagana." PLOS Neglected Tropical Diseases 9, no. 2 (2015): e0003353. http://dx.doi.org/10.1371/journal.pntd.0003353.

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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 (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 try

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Ebhodaghe, Faith I., Michael N. Okal, Shewit Kalayou, Armanda D. S. Bastos, and Daniel K. Masiga. "Tsetse Bloodmeal Analyses Incriminate the Common Warthog Phacochoerus africanus as an Important Cryptic Host of Animal Trypanosomes in Smallholder Cattle Farming Communities in Shimba Hills, Kenya." Pathogens 10, no. 11 (2021): 1501. http://dx.doi.org/10.3390/pathogens10111501.

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Trypanosomes are endemic and retard cattle health in Shimba Hills, Kenya. Wildlife in the area act as reservoirs of the parasites. However, wild animal species that harbor and expose cattle to tsetse-borne trypanosomes are not well known in Shimba Hills. Using xeno-monitoring surveillance to investigate wild animal reservoirs and sources of trypanosomes in Shimba Hills, we screened 696 trypanosome-infected and uninfected tsetse flies for vertebrate DNA using multiple-gene PCR-High Resolution Melting analysis and amplicon sequencing. Results revealed that tsetse flies fed on 13 mammalian specie

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van Hellemond, J. J., F. R. Opperdoes, and A. G. M. Tielens. "The extraordinary mitochondrion and unusual citric acid cycle in Trypanosoma brucei." Biochemical Society Transactions 33, no. 5 (2005): 967–71. http://dx.doi.org/10.1042/bst0330967.

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African trypanosomes are parasitic protozoa that cause sleeping sickness and nagana. Trypanosomes are not only of scientific interest because of their clinical importance, but also because these protozoa contain several very unusual biological features, such as their specially adapted mitochondrion and the compartmentalization of glycolytic enzymes in glycosomes. The energy metabolism of Trypanosoma brucei differs significantly from that of their hosts and changes drastically during the life cycle. Despite the presence of all citric acid cycle enzymes in procyclic insect-stage T. brucei, citri

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Namangala, Boniface, Chihiro Sugimoto та Noboru Inoue. "Effects of Exogenous Transforming Growth Factor β on Trypanosoma congolense Infection in Mice". Infection and Immunity 75, № 4 (2007): 1878–85. http://dx.doi.org/10.1128/iai.01452-06.

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ABSTRACT The socioeconomic implications of trypanosomosis in sub-Saharan Africa and the limitations of its current control regimes have stimulated research into alternative control methods. Considering the pro- and anti-inflammatory properties of transforming growth factor β1 (TGF-β1) and its potential to enhance immunity against protozoan parasites, we examined the effects of intraperitoneally delivered TGF-β1 in C57BL/6 mice infected with Trypanosoma congolense, the hemoprotozoan parasite causing nagana in cattle. A triple dose of 10 ng TGF-β1 significantly reduced the first parasitemic peak

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Pereira, Samille Henriques, Felipe Paladino Alves, and Santuza Maria Ribeiro Teixeira. "Animal Trypanosomiasis: Challenges and Prospects for New Vaccination Strategies." Microorganisms 12, no. 12 (2024): 2575. https://doi.org/10.3390/microorganisms12122575.

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Animal trypanosomiasis, such as nagana, surra, and dourine, represent a significant challenge to animal health and economic development, especially in tropical and subtropical regions where livestock production is an essential component of a country’s economy. Despite advances in the control of human trypanosomiasis, animal diseases caused by several species of trypanosomes remain neglected. The lack of funding for the development of new treatments and vaccines contributes to sustaining the severe economic impacts these diseases have on the farming industry, especially in low-income rural area

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Giordani, Federica, Daniel Paape, Isabel M. Vincent, et al. "Veterinary trypanocidal benzoxaboroles are peptidase-activated prodrugs." PLOS Pathogens 16, no. 11 (2020): e1008932. http://dx.doi.org/10.1371/journal.ppat.1008932.

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Livestock diseases caused by Trypanosoma congolense, T. vivax and T. brucei, collectively known as nagana, are responsible for billions of dollars in lost food production annually. There is an urgent need for novel therapeutics. Encouragingly, promising antitrypanosomal benzoxaboroles are under veterinary development. Here, we show that the most efficacious subclass of these compounds are prodrugs activated by trypanosome serine carboxypeptidases (CBPs). Drug-resistance to a development candidate, AN11736, emerged readily in T. brucei, due to partial deletion within the locus containing three

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CLAES, F., E. C. AGBO, M. RADWANSKA, et al. "How does Trypanosoma equiperdum fit into the Trypanozoon group? A cluster analysis by RAPD and Multiplex-endonuclease genotyping approach." Parasitology 126, no. 5 (2003): 425–31. http://dx.doi.org/10.1017/s0031182003002968.

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The pathogenic trypanosomes Trypanosoma equiperdum, T. evansi as well as T. brucei are morphologically identical. In horses, these parasites are considered to cause respectively dourine, surra and nagana. Previous molecular attempts to differentiate these species were not successful for T. evansi and T. equiperdum; only T. b. brucei could be differentiated to a certain extent. In this study we analysed 10 T. equiperdum, 8 T. evansi and 4 T. b. brucei using Random Amplified Polymorphic DNA (RAPD) and multiplex-endonuclease fingerprinting, a modified AFLP technique. The results obtained confirm

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CAPEWELL, PAUL, ANNELI COOPER, CAROLINE CLUCAS, WILLIAM WEIR, and ANNETTE MACLEOD. "A co-evolutionary arms race: trypanosomes shaping the human genome, humans shaping the trypanosome genome." Parasitology 142, S1 (2014): S108—S119. http://dx.doi.org/10.1017/s0031182014000602.

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SUMMARYTrypanosoma brucei is the causative agent of African sleeping sickness in humans and one of several pathogens that cause the related veterinary disease Nagana. A complex co-evolution has occurred between these parasites and primates that led to the emergence of trypanosome-specific defences and counter-measures. The first line of defence in humans and several other catarrhine primates is the trypanolytic protein apolipoprotein-L1 (APOL1) found within two serum protein complexes, trypanosome lytic factor 1 and 2 (TLF-1 and TLF-2). Two sub-species of T. brucei have evolved specific mechan

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McGettrick, Anne F., Sarah E. Corcoran, Paul J. G. Barry та ін. "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, № 48 (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

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Dera, Kiswend-Sida M., Mouhamadou M. Dieng, Percy Moyaba, et al. "Prevalence of Spiroplasma and interaction with wild Glossina tachinoides microbiota." Parasite 30 (2023): 62. http://dx.doi.org/10.1051/parasite/2023064.

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Tsetse flies (Diptera: Glossinidae) are vectors of the tropical neglected diseases sleeping sickness in humans and nagana in animals. The elimination of these diseases is linked to control of the vector. The sterile insect technique (SIT) is an environment-friendly method that has been shown to be effective when applied in an area-wide integrated pest management approach. However, as irradiated males conserve their vectorial competence, there is the potential risk of trypanosome transmission with their release in the field. Analyzing the interaction between the tsetse fly and its microbiota, a

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Hoppenheit, Antje, Stephan Steuber, Burkhard Bauer, et al. "Host preference of tsetse: an important tool to appraise the Nagana risk of cattle in the cotton zone of Mali." Wiener klinische Wochenschrift 122, S3 (2010): 81–86. http://dx.doi.org/10.1007/s00508-010-1443-9.

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Brown, K. "From Ubombo to Mkhuzi: Disease, Colonial Science, and the Control of Nagana (Livestock Trypanosomosis) in Zululand, South Africa, c. 1894-1953." Journal of the History of Medicine and Allied Sciences 63, no. 3 (2008): 285–322. http://dx.doi.org/10.1093/jhmas/jrn003.

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Alam, Uzma, Chaz Hyseni, Rebecca E. Symula, et al. "Implications of Microfauna-Host Interactions for Trypanosome Transmission Dynamics in Glossina fuscipes fuscipes in Uganda." Applied and Environmental Microbiology 78, no. 13 (2012): 4627–37. http://dx.doi.org/10.1128/aem.00806-12.

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ABSTRACTTsetse flies (Diptera: Glossinidae) are vectors for African trypanosomes (Euglenozoa: kinetoplastida), protozoan parasites that cause African trypanosomiasis in humans (HAT) and nagana in livestock. In addition to trypanosomes, two symbiotic bacteria (Wigglesworthia glossinidiaandSodalis glossinidius) and two parasitic microbes,Wolbachiaand a salivary gland hypertrophy virus (SGHV), have been described in tsetse. Here we determined the prevalence of and coinfection dynamics betweenWolbachia, trypanosomes, and SGHV inGlossina fuscipes fuscipesin Uganda over a large geographical scale sp

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Mosimann, Marc, Shinobu Goshima, Tanja Wenzler, Alexandra Lüscher, Nobuyuki Uozumi, and Pascal Mäser. "A Trk/HKT-Type K+ Transporter from Trypanosoma brucei." Eukaryotic Cell 9, no. 4 (2010): 539–46. http://dx.doi.org/10.1128/ec.00314-09.

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ABSTRACT The molecular mechanisms of K+ homeostasis are only poorly understood for protozoan parasites. Trypanosoma brucei subsp. parasites, the causative agents of human sleeping sickness and nagana, are strictly extracellular and need to actively concentrate K+ from their hosts’ body fluids. The T. brucei genome contains two putative K+ channel genes, yet the trypanosomes are insensitive to K+ antagonists and K+ channel-blocking agents, and they do not spontaneously depolarize in response to high extracellular K+ concentrations. However, the trypanosomes are extremely sensitive to K+ ionopho

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Favaro, Annagiulia, Giovanni Bolcato, Marcelo A. Comini, Stefano Moro, Massimo Bellanda, and Mattia Sturlese. "Drugging the Undruggable Trypanosoma brucei Monothiol Glutaredoxin 1." Molecules 28, no. 3 (2023): 1276. http://dx.doi.org/10.3390/molecules28031276.

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Trypanosoma brucei is a species of kinetoplastid causing sleeping sickness in humans and nagana in cows and horses. One of the peculiarities of this species of parasites is represented by their redox metabolism. One of the proteins involved in this redox machinery is the monothiol glutaredoxin 1 (1CGrx1) which is characterized by a unique disordered N-terminal extension exclusively conserved in trypanosomatids and other organisms. This region modulates the binding profile of the glutathione/trypanothione binding site, one of the functional regions of 1CGrx1. No endogenous ligands are known to

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Possart, Katharina, Fabian C. Herrmann, Joachim Jose, and Thomas J. Schmidt. "In Silico and In Vitro Search for Dual Inhibitors of the Trypanosoma brucei and Leishmania major Pteridine Reductase 1 and Dihydrofolate Reductase." Molecules 28, no. 22 (2023): 7526. http://dx.doi.org/10.3390/molecules28227526.

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The parasites Trypanosoma brucei (Tb) and Leishmania major (Lm) cause the tropical diseases sleeping sickness, nagana, and cutaneous leishmaniasis. Every year, millions of humans, as well as animals, living in tropical to subtropical climates fall victim to these illnesses’ health threats. The parasites’ frequent drug resistance and widely spread natural reservoirs heavily impede disease prevention and treatment. Due to pteridine auxotrophy, trypanosomatid parasites have developed a peculiar enzyme system consisting of dihydrofolate reductase-thymidylate synthase (DHFR-TS) and pteridine reduct

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Krstin, Sonja, Herbenya Silva Peixoto, and Michael Wink. "Combinations of Alkaloids Affecting Different Molecular Targets with the Saponin Digitonin Can Synergistically Enhance Trypanocidal Activity against Trypanosoma brucei brucei." Antimicrobial Agents and Chemotherapy 59, no. 11 (2015): 7011–17. http://dx.doi.org/10.1128/aac.01315-15.

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ABSTRACTThe flagellateTrypanosoma bruceicauses sleeping sickness in humans and nagana in animals. Only a few drugs are registered to treat trypanosomiasis, but those drugs show severe side effects. Also, because some pathogen strains have become resistant, new strategies are urgently needed to combat this parasitic disease. An underexplored possibility is the application of combinations of several trypanocidal agents, which may potentiate their trypanocidal activity in a synergistic fashion. In this study, the potential synergism of mutual combinations of bioactive alkaloids and alkaloids with

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Oli, Monika W., Laura F. Cotlin, April M. Shiflett, and Stephen L. Hajduk. "Serum Resistance-Associated Protein Blocks Lysosomal Targeting of Trypanosome Lytic Factor in Trypanosoma brucei." Eukaryotic Cell 5, no. 1 (2006): 132–39. http://dx.doi.org/10.1128/ec.5.1.132-139.2006.

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ABSTRACT Trypanosoma brucei brucei is the causative agent of nagana in cattle and can infect a wide range of mammals but is unable to infect humans because it is susceptible to the innate cytotoxic activity of normal human serum. A minor subfraction of human high-density lipoprotein (HDL) containing apolipoprotein A-I (apoA-I), apolipoprotein L-I (apoL-I), and haptoglobin-related protein (Hpr) provides this innate protection against T. b. brucei infection. This HDL subfraction, called trypanosome lytic factor (TLF), kills T. b. brucei following receptor binding, endocytosis, and lysosomal loca

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Possart, Katharina, Fabian C. Herrmann, Joachim Jose, Maria P. Costi, and Thomas J. Schmidt. "Sesquiterpene Lactones with Dual Inhibitory Activity against the Trypanosoma brucei Pteridine Reductase 1 and Dihydrofolate Reductase." Molecules 27, no. 1 (2021): 149. http://dx.doi.org/10.3390/molecules27010149.

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The parasite Trypanosoma brucei (T. brucei) is responsible for human African trypanosomiasis (HAT) and the cattle disease “Nagana” which to this day cause severe medical and socio-economic issues for the affected areas in Africa. So far, most of the available treatment options are accompanied by harmful side effects and are constantly challenged by newly emerging drug resistances. Since trypanosomatids are auxotrophic for folate, their pteridine metabolism provides a promising target for an innovative chemotherapeutic treatment. They are equipped with a unique corresponding enzyme system consi

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Anghel, Nicoleta, Joachim Müller, Mauro Serricchio, et al. "Cellular and Molecular Targets of Nucleotide-Tagged Trithiolato-Bridged Arene Ruthenium Complexes in the Protozoan Parasites Toxoplasma gondii and Trypanosoma brucei." International Journal of Molecular Sciences 22, no. 19 (2021): 10787. http://dx.doi.org/10.3390/ijms221910787.

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Toxoplasma gondii is an apicomplexan parasite that infects and proliferates within many different types of host cells and infects virtually all warm-blooded animals and humans. Trypanosoma brucei is an extracellular kinetoplastid that causes human African trypanosomiasis and Nagana disease in cattle, primarily in rural sub-Saharan Africa. Current treatments against both parasites have limitations, e.g., suboptimal efficacy and adverse side effects. Here, we investigate the potential cellular and molecular targets of a trithiolato-bridged arene ruthenium complex conjugated to 9-(2-hydroxyethyl)

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Wall, Richard J., Eva Rico, Iva Lukac, et al. "Clinical and veterinary trypanocidal benzoxaboroles target CPSF3." Proceedings of the National Academy of Sciences 115, no. 38 (2018): 9616–21. http://dx.doi.org/10.1073/pnas.1807915115.

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African trypanosomes cause lethal and neglected tropical diseases, known as sleeping sickness in humans and nagana in animals. Current therapies are limited, but fortunately, promising therapies are in advanced clinical and veterinary development, including acoziborole (AN5568 or SCYX-7158) and AN11736, respectively. These benzoxaboroles will likely be key to the World Health Organization’s target of disease control by 2030. Their mode of action was previously unknown. We have developed a high-coverage overexpression library and use it here to explore drug mode of action in Trypanosoma brucei.

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Chang, Tunhan, Kenneth G. Milne, Maria Lucia Sampaio Güther, Terry K. Smith, and Michael A. J. Ferguson. "Cloning ofTrypanosoma bruceiandLeishmania majorGenes Encoding the GlcNAc-Phosphatidylinositol De-N-acetylase of Glycosylphosphatidylinositol Biosynthesis That Is Essential to the African Sleeping Sickness Parasite." Journal of Biological Chemistry 277, no. 51 (2002): 50176–82. http://dx.doi.org/10.1074/jbc.m208374200.

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The second step of glycosylphosphatidylinositol anchor biosynthesis in all eukaryotes is the conversion of D-GlcNAcα1–6-d-myo-inositol-1-HPO4-sn-1,2-diacylglycerol (GlcNAc-PI) tod-GlcNα1–6-d-myo-inositol-1-HPO4-sn-1,2-diacylglycerol by GlcNAc-PI de-N-acetylase. The genes encoding this activity arePIG-LandGPI12in mammals and yeast, respectively. Fragments of putative GlcNAc-PI de-N-acetylase genes fromTrypanosoma bruceiandLeishmania majorwere identified in the respective genome project data bases. The full-length genesTbGPI12andLmGPI12were subsequently cloned, sequenced, and shown to complement

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Yang, Xiao, Xuelei Wu, Jiahai Zhang, et al. "Recognition of hyperacetylated N-terminus of H2AZ by TbBDF2 from Trypanosoma brucei." Biochemical Journal 474, no. 22 (2017): 3817–30. http://dx.doi.org/10.1042/bcj20170619.

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Histone modification plays an important role in various biological processes, including gene expression regulation. Bromodomain, as one of histone readers, recognizes specifically the ε-N-lysine acetylation (KAc) of histone. Although the bromodomains and histone acetylation sites of Trypanosoma brucei (T. brucei), a lethal parasite responsible for sleeping sickness in human and nagana in cattle, have been identified, how acetylated histones are recognized by bromodomains is still unknown. Here, the bromodomain factor 2 (TbBDF2) from T. brucei was identified to be located in the nucleolus and b

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