Trypanosoma Evansi

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Bruno Goddeeris - One of the best experts on this subject based on the ideXlab platform.

  • Genome-Wide SNP Analysis Reveals Distinct Origins of Trypanosoma Evansi and Trypanosoma equiperdum.
    2017
    Co-Authors: Bart Cuypers, Nick Van Reet, Julien Cauchard, Filip Claes, Bruno Goddeeris, Frederik Van Den Broeck, Conor J. Meehan, Jonathan M. Wilkes, Hadush Birhanu, Jean-claude Dujardin
    Abstract:

    Trypanosomes cause a variety of diseases in man and domestic animals in Africa, Latin America, and Asia. In the Trypanozoon subgenus, Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense cause human African trypanosomiasis, whereas Trypanosoma brucei brucei, Trypanosoma Evansi, and Trypanosoma equiperdum are responsible for nagana, surra, and dourine in domestic animals, respectively. The genetic relationships between T. Evansi and T. equiperdum and other Trypanozoon species remain unclear because the majority of phylogenetic analyses has been based on only a few genes. In this study, we have conducted a phylogenetic analysis based on genome-wide SNP analysis comprising 56 genomes from the Trypanozoon subgenus. Our data reveal that T. equiperdum has emerged at least once in Eastern Africa and T. Evansi at two independent occasions in Western Africa. The genomes within the T. equiperdum and T. Evansi monophyletic clusters show extremely little variation, probably due to the clonal spread linked to the independence from tsetse flies for their transmission.

  • variable surface glycoprotein rotat 1 2 pcr as a specific diagnostic tool for the detection of Trypanosoma Evansi infections
    2004
    Co-Authors: Filip Claes, Bruno Goddeeris, Magdalena Radwanska, Toyo Urakawa, Phelix Ao Majiwa, Philip Büscher
    Abstract:

    Background Based on the recently sequenced gene coding for the Trypanosoma Evansi (T. Evansi) RoTat 1.2 Variable Surface Glycoprotein (VSG), a primer pair was designed targeting the DNA region lacking homology to other known VSG genes. A total of 39 different trypanosome stocks were tested using the RoTat 1.2 based Polymerase Chain Reaction (PCR).

  • the effect of Trypanosoma Evansi infection on pig performance and vaccination against classical swine fever
    2003
    Co-Authors: Wicher Holland, Bruno Goddeeris, Nt Huong, Nt Dung, Ng Thanh, Jozef Vercruysse
    Abstract:

    Although Trypanosoma Evansi is not considered as an important pathogen in pigs, it may interfere with other pathogens or vaccinations by its immunosuppressive nature. In order to determine whether T. Evansi alters pig performance and induces immunosuppression in pigs, induction of immune responses by vaccination against classical swine fever (CSF) and by immunization with a control antigen, human serum albumin (HSA), was assessed in T. Evansi-infected and non-infected animals. Although T. Evansi infection did not have a significant influence on growth performance, feed conversion or PCV, antibody responses against both the test antigen HSA and the CSF vaccine were significantly reduced in T. Evansi-infected animals as compared to uninfected animals. Moreover, the reduced response against the CSF vaccine appears to be accompanied by a less well-developed protection against CSF with higher fever responses and leukopenia. This immunosuppression might explain the accounts of poor protection of CSF-vaccinated pigs reported in T. Evansi-endemic areas of Vietnam, and suggests that prior treatments with trypanocidal drugs to improve the efficacy of CSF vaccination, may be justified.

Heitor Miraglia Herrera - One of the best experts on this subject based on the ideXlab platform.

  • modulating variables of Trypanosoma cruzi and Trypanosoma Evansi transmission in free ranging coati nasua nasua from the brazilian pantanal region
    2011
    Co-Authors: Fernanda Moreira Alves, Paulo Marcelo Tenório Cotias, Natalie Olifiers, Matthew Edzart Gompper, Guilherme Mourão, Heitor Miraglia Herrera, Rita De Cassia Bianchi, Ana Claudia Machado Duarte, Paulo Sergio Dandrea, Ana Maria Jansen
    Abstract:

    Abstract This is a long-term follow-up of infection by Trypanosoma cruzi (TC) and Trypanosoma Evansi (TE) in the free-ranging coatis (Procyonidae: Nasua nasua) from Pantanal region (Mato Grosso do ...

  • enzootiology of Trypanosoma Evansi in pantanal brazil
    2004
    Co-Authors: Heitor Miraglia Herrera, Paulo Sergio Dandrea, Alberto M R Davila, A Norek, Urbano Gomes Pinto De Abreu, S S Souza, Ana Maria Jansen
    Abstract:

    In order to better understand the enzootiology of trypanosomiasis caused by Trypanosoma Evansi in the Brazilian Pantanal we examined domestic and wild mammals by microhematocrit centrifuge technique (MHCT), immunofluorescence antibody test (IFAT) and polymerase chain reaction (PCR). T. Evansi infection was detected in all species sampled with exception of the sheep and the feral pig. High parasitemias were observed in capybaras (5/24), coatis (18/115), horses (31/321) and dogs (3/112). Among these species, only the capybaras did not develop anemia. Low parasitemias, only detected by PCR, were found in buffaloes (18/43), bovines (29/331), marsupials (1/4), small rodents (14/67), bats (7/18), and one armadillo (1/8). The highest prevalence of T. Evansi infection was recorded in horses (73%), although no neurological signs in infected horses were observed. Diagnosis through standard parasitological tests and IFAT should be used with caution since they may overlook comprovedly infected horses. The relationship between ranch management and T. Evansi infection in horse was investigated. The importance of other transmission mechanisms apart from the tabanids and reservoir hosts are discussed.

  • Experimental Trypanosoma Evansi infection in South American coati (Nasua nasua): hematological, biochemical and histopathological changes.
    2002
    Co-Authors: Heitor Miraglia Herrera, Antonio Carlos Alessi, Luiz Carlos Marques, A.e Santana, L.p.c.t Aquino, R.f Menezes, M.a.v Moraes, R. Z. Machado
    Abstract:

    The course of an experimental Trypanosoma Evansi infection in coatis (Nasua nasua, carnivora, Procyonidae) was followed for 262 days. Hematological analysis of the infected coatis revealed a marked decline in hemoglobin, packed-cell volume, and total erythrocyte count. An intense anemia followed the first wave of parasitemia and persisted until the end of the experimental period. Biochemical analysis showed increased serum levels of alanine aminotransferase and aspartate aminotransferase and decreased albumin. The main histopathological features consisted of myocarditis with the presence of degenerate cardiac fibers and meningoencephalitis. This study has shown that coatis infected with T. Evansi develop a chronic disease.

  • Trypanosoma Evansi experimental infection in the South American coati (Nasua nasua): clinical, parasitological and humoral immune response.
    2001
    Co-Authors: Heitor Miraglia Herrera, Luiz Carlos Marques, R.f Menezes, M.a.v Moraes, Lucia Padilha Cury Thomaz De Aquino, Karin Werther, Rosangela Zacarias Machado
    Abstract:

    The course of Trypanosoma Evansi infection in coatis (Carnivora, Procionidae) was followed for 262 days. Parasites were detected in all infected animals from day 2 post infection until the end of the study. No correlation between temperature and parasitemia was observed. Animals of the infected group demonstrated depression, weakness, lethargy and pale mucous membranes. Indirect fluorescent antibody tests detected anti-T. Evansi antibodies within 7 to 14 days post infection and showed high levels until the end of the experimental period. The persistent parasitemia in coati and their relative tolerance to clinical signs suggested that this species develops a chronic disease and plays an important role in the epidemiology of trypanosomosis due to T. Evansi in enzootic regions.

Diana Bahia - One of the best experts on this subject based on the ideXlab platform.

  • molecular characterization of Trypanosoma Evansi mevalonate kinase temvk
    2018
    Co-Authors: Daniel Pereira Duarte, Eden Ramalho Ferreira, Fabio Mitsuo Lima, Franciane Batista, Michel De Groote, E Horjales, Luiz Claudio Miletti, Diana Bahia
    Abstract:

    The mevalonate pathway, present in eukaryotes, archaea, and some bacteria, is an essential part of isoprenoid biosynthesis leading to production of isoprenoids, a diverse class of >30,000 biomolecules including cholesterol, heme, and all steroid hormones. Isoprenoid biosynthesis involves one of the most highly regulated enzymes in nature, 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), which catalyzes conversion of HMG-CoA to mevalonic acid. The enzyme mevalonate kinase (MVK) subsequently converts mevalonic acid to 5-phosphomevalonic acid. Trypanosoma Evansi is a flagellate protozoan parasite that causes the disease “Surra” in domesticated large mammals, with great economic impact. T. Evansi has only a trypomastigote bloodstream form, and requires constant modification of the VSG (variant surface glycoprotein) coat for protection against the host immune system. We characterized the MVK of T. Evansi (termed TeMVK) at molecular, biochemical, and cellular levels. TeMVK from parasite extract had molecular weight ~36 KDa, was colocalized with aldolase (a glycosomal marker enzyme) in glycosomes, and was structurally similar to Leishmania major MVK. Interestingly, the active form of TeMVK was the tetrameric oligomer form, in contrast to other MVKs in which the dimeric form is active. TeMVK was detected in parasites isolated directly from mice and was colocalized with aldolase in glycosomes. Despite lacking organized mitochondria, T. Evansi synthesizes both HMGCR transcripts and protein. The mevalonate pathway also generates dolichols, which play an essential role in construction of glycosylphosphatidylinositol (GPI) anchors, and VSGs are attached to the plasma membrane via GPI anchors. MVK and HMGCR in T. Evansi are therefore potentially useful targets for therapeutic drug design.

  • Molecular Characterization of Trypanosoma Evansi Mevalonate Kinase (TeMVK)
    2018
    Co-Authors: Daniel Pereira Duarte, Eden Ramalho Ferreira, Fabio Mitsuo Lima, Franciane Batista, Michel De Groote, E Horjales, Luiz Claudio Miletti, Diana Bahia
    Abstract:

    The mevalonate pathway is an essential part of isoprenoid biosynthesis leading to production of a diverse class of >30,000 biomolecules including cholesterol, heme, and all steroid hormones. In Trypanosomatids, the mevalonate pathway also generates dolichols, which play an essential role in construction of glycosylphosphatidylinositol (GPI) molecules that anchor variable surface proteins (VSGs) to the plasma membrane. Isoprenoid biosynthesis involves one of the most highly regulated enzymes in nature, 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), which catalyzes the conversion of HMG-CoA to mevalonic acid. The enzyme mevalonate kinase (MVK) subsequently converts mevalonic acid to 5-phosphomevalonic acid. Trypanosoma Evansi is a flagellate protozoan parasite that causes the disease “Surra” in domesticated large mammals, with great economic impact. T. Evansi has only a trypomastigote bloodstream form and requires constant modification of the variant surface glycoprotein (VSG) coat for protection against the host immune system. We identified MVK of T. Evansi (termed TeMVK) and performed a preliminary characterization at molecular, biochemical, and cellular levels. TeMVK from parasite extract displayed molecular weight ~36 kDa, colocalized with aldolase (a glycosomal marker enzyme) in glycosomes, and is structurally similar to Leishmania major MVK. Interestingly, the active form of TeMVK is the tetrameric oligomer form, in contrast to other MVKs in which the dimeric form is active. Despite lacking organized mitochondria, T. Evansi synthesizes both HMGCR transcripts and protein. Both MVK and HMGCR are expressed in T. Evansi during the course of infection in animals, and therefore are potential targets for therapeutic drug design

  • Image_1_Molecular Characterization of Trypanosoma Evansi Mevalonate Kinase (TeMVK).TIF
    2018
    Co-Authors: Daniel Pereira Duarte, Eden Ramalho Ferreira, Fabio Mitsuo Lima, Franciane Batista, Michel De Groote, E Horjales, Luiz Claudio Miletti, Diana Bahia
    Abstract:

    The mevalonate pathway is an essential part of isoprenoid biosynthesis leading to production of a diverse class of >30,000 biomolecules including cholesterol, heme, and all steroid hormones. In Trypanosomatids, the mevalonate pathway also generates dolichols, which play an essential role in construction of glycosylphosphatidylinositol (GPI) molecules that anchor variable surface proteins (VSGs) to the plasma membrane. Isoprenoid biosynthesis involves one of the most highly regulated enzymes in nature, 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), which catalyzes the conversion of HMG-CoA to mevalonic acid. The enzyme mevalonate kinase (MVK) subsequently converts mevalonic acid to 5-phosphomevalonic acid. Trypanosoma Evansi is a flagellate protozoan parasite that causes the disease “Surra” in domesticated large mammals, with great economic impact. T. Evansi has only a trypomastigote bloodstream form and requires constant modification of the variant surface glycoprotein (VSG) coat for protection against the host immune system. We identified MVK of T. Evansi (termed TeMVK) and performed a preliminary characterization at molecular, biochemical, and cellular levels. TeMVK from parasite extract displayed molecular weight ~36 kDa, colocalized with aldolase (a glycosomal marker enzyme) in glycosomes, and is structurally similar to Leishmania major MVK. Interestingly, the active form of TeMVK is the tetrameric oligomer form, in contrast to other MVKs in which the dimeric form is active. Despite lacking organized mitochondria, T. Evansi synthesizes both HMGCR transcripts and protein. Both MVK and HMGCR are expressed in T. Evansi during the course of infection in animals, and therefore are potential targets for therapeutic drug design.

Reto Brun - One of the best experts on this subject based on the ideXlab platform.

  • in vitro activity and preliminary toxicity of various diamidine compounds against Trypanosoma Evansi
    2010
    Co-Authors: Kirsten Gillingwater, Arvind Kumar, David W Boykin, Richard R Tidwell, Mohamed A Ismail, Reem K Arafa, Chad E Stephens, Reto Brun
    Abstract:

    Trypanosoma Evansi is an animal pathogenic protozoan, causing a wasting disease called Surra, which is broadly distributed in a wide range of mammalian hosts. Chemotherapy is the most efficient control method, which depends on four drugs. Unfortunately, with the appearance of resistance to these drugs, their effective use is threatened, emphasising a need to find new drugs. Diamidines bind to the minor groove of DNA at AT-rich sites and exert their anti-Trypanosomal activity by inhibiting one or more DNA dependent enzymes or by directly impeding the transcription process. In total, 67 novel diamidine compounds were tested in vitro to determine activity against an animal pathogenic Chinese kinetoplastic T. Evansi strain. In comparison, a human pathogenic Trypanosoma brucei rhodesiense strain and a P2 transporter knock out of a Trypanosoma brucei brucei strain were also tested. All diamidine compounds tested in this study against T. Evansi produced inhibitory concentration (IC(50)) values below 50 nM. The results demonstrate that these compounds are highly active against T. Evansi in vitro. In addition, preliminary in vivo toxicity tests were performed on all 67 diamidines with 69% of the compounds showing no acute toxicity at an intra-peritoneal dose of 100mg/kg.

  • in vivo investigations of selected diamidine compounds against Trypanosoma Evansi using a mouse model
    2009
    Co-Authors: Kirsten Gillingwater, Arvind Kumar, Mariappan Anbazhagan, David W Boykin, Richard R Tidwell, Reto Brun
    Abstract:

    Surra is an animal pathogenic protozoan infection, caused by Trypanosoma Evansi, that develops into a fatal wasting disease. Control measures rely on diagnosis and treatment. However, with the continuous emergence of drug resistance, this tactic is failing, and the pressing need for new chemotherapeutic agents is becoming critical. With the introduction of novel aromatic diamidines, a new category of antiTrypanosomal drugs was discovered. Nevertheless, their efficacy within a T. Evansi-infected mouse model was not known. In total, 30 compounds previously selected based on their in vitro activity were tested in a T. Evansi mouse model of infection. Six of the compounds were capable of curing T. Evansi-infected mice at drug doses as low as 0.5 and 0.25 mg/kg of body weight administered for 4 consecutive days, and they were more effective than the standard drugs suramin, diminazene, and quinapyramine. After all selection criteria were applied, three diamidine compounds (DB 75, DB 867, and DB 1192) qualified as lead compounds and were considered to have the potential to act as preclinical candidates against T. Evansi infection.

  • Trypanosoma Evansi and t equiperdum distribution biology treatment and phylogenetic relationship a review
    1998
    Co-Authors: Reto Brun, Hermann Hecker, Zhao-rong Lun
    Abstract:

    Trypanosoma Evansi and T. equiperdum were compared regarding their ultrastructure, their mammalian hosts, way of transmission, pathogenicity, diagnosis and treatment, and biochemical and molecular characteristics. Electron microscopic investigation revealed no ultrastructural differences between the two species except that there were more coated vesicles in the flagellar pocket of T. equiperdum. Biological, biochemical and molecular studies were reviewed and exhibited many similarities between T. Evansi and T. equiperdum. The most prominent differences between the two species are the presence of maxicircles in T. equiperdum, which are missing in T. Evansi, and the route of transmission. While T. Evansi is transmitted by biting flies, T. equiperdum is transmitted from one equine host to another during copulation when mucous membranes come into contact. Otherwise the two species are remarkably similar. The phylogenetic relationship between the two species and T. b. brucei is being discussed, and the hypothesis is proposed that T. Evansi arose from a clone of T. equiperdum which lost its maxicircles.

  • Drug sensitivity of Chinese Trypanosoma Evansi and Trypanosoma equiperdum isolates.
    1994
    Co-Authors: Reto Brun, Z.-r. Lun
    Abstract:

    Abstract The drug sensitivities of eleven Trypanosoma Evansi isolates from China were examined using two different in vitro assays, a 3 H-hypoxanthine incorporation assay and a long incubation low inoculation test (LILIT). Better discrimination of the drug susceptibility of the strains was observed with the LILIT. The drug responses of all the isolates to the arsenical melarsoprol were very similar. In contrast, for suramin, minimal inhibitory concentrations (MIC) varied within a 27-fold range and for diminazene within a 55-fold range. Comparison of MIC values with expected drug levels in the host as well as in vivo experiments with selected isolates and drugs indicated that all the isolates examined would be sensitive to melarsoprol, diminazene and suramin under in vivo conditions. for isometamidium, the difference in MIC values between the most and the least sensitive isolate was 724-fold. Neither of two isolates tested in mice—the most resistant and the second most sensitive—was cured with the highest acceptable dose of 10 mg kg −1 isometamidium chloride. Comparison of our results with blood levels of drug to be expected in cattle support the assumption that the Chinese T. Evansi isolates have more or less innate resistance to isometamidium under in vivo conditions. One Trypanosoma equiperdum isolate was tested in the 3 H-hypoxanthine incorporation assay. The results indicated that this isolate was highly sensitive to melarsoprol, isometamidium and suramin; with regard to diminazene, T. equiperdum was not as sensitive as the most sensitive T. Evansi strains.

  • Kinetoplast DNA and molecular karyotypes of Trypanosoma Evansi and Trypanosoma equiperdum from China.
    1992
    Co-Authors: Zhao-rong Lun, Reto Brun, Wendy Gibson
    Abstract:

    We compared 12 stocks of Trypanosoma Evansi and 1 recently isolated stock of Trypanosoma equiperdum from different regions of China by analysis of kinetoplast DNA (kDNA), nuclear DNA and molecular karyotypes. The T. equiperdum stock was remarkably similar to the T. Evansi stocks, except for the possession of kDNA maxi-circles, suggesting a very close evolutionary relationship between T. Evansi and T. equiperdum. The maxi-circles of the Chinese T. equiperdum stock were approximately 14.3 kb in size, i.e., about half the size of those of Trypanosoma brucei. This stock is thus similar to an old laboratory stock of T. equiperdum, which also has maxi-circles with a sizeable deletion. Both T. equiperdum and T. Evansi kDNA mini-circles hybridised with a T. Evansi-specific mini-circle fragment isolated from a Kenyan T. Evansi stock. Our results extend the generality that T. Evansi and T. equiperdum mini-circles are microheterogeneous rather than homogeneous. Molecular karyotypes obtained by pulsed field gradient gel electrophoresis provided a more sensitive way of distinguishing the T. Evansi stocks than isoenzymes or restriction fragment length polymorphisms in kDNA mini-circles, genes for ribosomal RNAs and variant surface glycoproteins. Our results fit the general idea that T. Evansi stocks worldwide have a single origin.

Livia Perles - One of the best experts on this subject based on the ideXlab platform.