Trypanosoma (Duttonella) vivax and Typanosomosis in Latin America: Secadera/Huequera/Cacho Hueco

Gonzatti, Mary Isabel; González-Baradat, B.; Aso, Pedro María; Reyna-Bello, Armando

doi:10.1007/978-3-7091-1556-5_11

Cited by 26 publications

(30 citation statements)

References 102 publications

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“…T. vivax can also be transmitted mechanically by bloodsucking insects, and such transmission has been found in Central and South America (Gonzatti et al, 2014), and in non-tsetse infested regions of Ethiopia (Cherenet et al, 2006; Fikru et al, 2012). The disease Surra, a similar wasting disease to nagana, is caused by T. evansi , which has lost its maxicircle kinetoplast DNA and thus the procyclic stage of its lifecycle, and as such does pass through an insect vector, instead being mechanically transmitted between hosts by blood-feeding insects (Lun et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Transport proteins determine drug sensitivity and resistance in a protozoan parasite, Trypanosoma brucei

2015

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Drug resistance in pathogenic protozoa is very often caused by changes to the ‘transportome’ of the parasites. In Trypanosoma brucei, several transporters have been implicated in uptake of the main classes of drugs, diamidines and melaminophenyl arsenicals. The resistance mechanism had been thought to be due to loss of a transporter known to carry both types of agents: the aminopurine transporter P2, encoded by the gene TbAT1. However, although loss of P2 activity is well-documented as the cause of resistance to the veterinary diamidine diminazene aceturate (DA; Berenil®), cross-resistance between the human-use arsenical melarsoprol and the diamidine pentamidine (melarsoprol/pentamidine cross resistance, MPXR) is the result of loss of a separate high affinity pentamidine transporter (HAPT1). A genome-wide RNAi library screen for resistance to pentamidine, published in 2012, gave the key to the genetic identity of HAPT1 by linking the phenomenon to a locus that contains the closely related T. brucei aquaglyceroporin genes TbAQP2 and TbAQP3. Further analysis determined that knockdown of only one pore, TbAQP2, produced the MPXR phenotype. TbAQP2 is an unconventional aquaglyceroporin with unique residues in the “selectivity region” of the pore, and it was found that in several MPXR lab strains the WT gene was either absent or replaced by a chimeric protein, recombined with parts of TbAQP3. Importantly, wild-type AQP2 was also absent in field isolates of T. b. gambiense, correlating with the outcome of melarsoprol treatment. Expression of a wild-type copy of TbAQP2 in even the most resistant strain completely reversed MPXR and re-introduced HAPT1 function and transport kinetics. Expression of TbAQP2 in Leishmania mexicana introduced a pentamidine transport activity indistinguishable from HAPT1. Although TbAQP2 has been shown to function as a classical aquaglyceroporin it is now clear that it is also a high affinity drug transporter, HAPT1. We discuss here a possible structural rationale for this remarkable ability.

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Section: Introductionmentioning

confidence: 99%

Transport proteins determine drug sensitivity and resistance in a protozoan parasite, Trypanosoma brucei

2015

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“…Desquesnes (2004) estimated that an outbreak of trypanosomosis in beef cattle cost the equivalent of 3.3 % live weight per animal; which can be split into 30€ of weight loss and 3€ of treatment per head. These haemoparasites cause reproductive disorders such as infertility and abortions, as well as growth delay, weight loss and diminished physical condition that can lead to animal death (Desquesnes 2004;Gonzatti et al 2014). In horses, T. evansi produces central nervous system disorders and muscle atrophy in the limbs which causes animal prostration (Desquesnes et al 2013a) and death.…”

Section: Introductionmentioning

confidence: 99%

Molecular diagnosis of cattle trypanosomes in Venezuela: evidences of Trypanosoma evansi and Trypanosoma vivax infections

et al. 2016

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In South America has been determined by molecular methods in cattle from Bolivia, Brazil, Colombia and Peru, reason for which the presence of this parasite is not excluded in Venezuelan livestock. Therefore, the aim of this study was to perform parasitological and molecular diagnosis of cattle trypanosomosis in small livestock units from two regions in this country. The parasitological diagnosis was carried out by MHCT and the molecular by PCR using genus-specific ITS1 primers that differentiate and infections. 47 cattle were evaluated in the "Laguneta de la Montaña" sector, Miranda State, where 3 animals were diagnosed as positive (6.4 %) by MHCT and 14 (30 %) by PCR as spp., out of which 9 animals resulted positive for , 3 for and 2 with double infections. Whilst in the "San Casimiro" sector, State of Aragua, out of the 38 cattle evaluated 7 animals were diagnosed as positive (18.4 %) by MHCT and 19 (50 %) by PCR, determining only the presence of in this locality. The molecular diagnosis by PCR using ITS1 primers allowed detection in cattle field populations, which suggests the possible role of these animals as reservoirs in the epidemiology of the disease caused by in Venezuela.

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“…Trypanosomosis is responsible for tangible economic losses due to impaired livestock production. The detrimental effects produced by T. vivax in livestock include growth retardation, loss of body weight, low production of animal proteins (meat and milk) [1, 2], and diminished fertility [3]. These effects are responsible for increasing production costs through an increased need for treatment and veterinary care [4–6].…”

Section: Introductionmentioning

confidence: 99%

“…The pathogenesis, characterized by anemia and fever, seriously compromises the animal's health [1, 6, 18]. The aim of this study was to examine, with a scanning electron microscope (SEM), the cellular interactions and alterations in ovine RBCs experimentally infected with a Venezuelan T. vivax isolate.…”

Section: Introductionmentioning

confidence: 99%

Trypanosoma vivax Adhesion to Red Blood Cells in Experimentally Infected Sheep

Boada-Sucre

Spadafora

Tavares-Marques

et al. 2016

Pathology Research International

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Trypanosomosis, a globally occurring parasitic disease, poses as a major obstacle to livestock production in tropical and subtropical regions resulting in tangible economic losses. In Latin America including Venezuela, trypanosomosis of ruminants is mainly caused by Trypanosoma vivax. Biologically active substances produced from trypanosomes, as well as host-trypanosome cellular interactions, contribute to the pathogenesis of anemia in an infection. The aim of this study was to examine with a scanning electron microscope the cellular interactions and alterations in ovine red blood cells (RBC) experimentally infected with T. vivax. Ovine infection resulted in changes of RBC shape as well as the formation of surface holes or vesicles. A frequent observation was the adhesion to the ovine RBC by the trypanosome's free flagellum, cell body, or attached flagellum in a process mediated by the filopodia emission from the trypanosome surface. The observed RBC alterations are caused by mechanical and biochemical damage from host-parasite interactions occurring in the bloodstream. The altered erythrocytes are prone to mononuclear phagocytic removal contributing to the hematocrit decrease during infection.

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Trypanosoma (Duttonella) vivax and Typanosomosis in Latin America: Secadera/Huequera/Cacho Hueco

Cited by 26 publications

References 102 publications

Transport proteins determine drug sensitivity and resistance in a protozoan parasite, Trypanosoma brucei

Transport proteins determine drug sensitivity and resistance in a protozoan parasite, Trypanosoma brucei

Molecular diagnosis of cattle trypanosomes in Venezuela: evidences of Trypanosoma evansi and Trypanosoma vivax infections

Trypanosoma vivax Adhesion to Red Blood Cells in Experimentally Infected Sheep

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