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  • br Acknowledgements We thank A Devia


    Acknowledgements We thank A. Devia-Barros and S.A. Barrios Latorre for invaluable technical support during the collection, maintenance and exposure of oysters. We are, furthermore, grateful to the municipal marina of Santa Marta for authorizing access to their facilities and to A. Franco for facilitating use of the laboratory of the Jorge Tadeo Lozano University campus in Santa Marta. We are also indebted to H. Thomas-Guyon and colleagues of the LIENS laboratory (Littoral Environnement et Sociétés), University of La Rochelle (France) for metal analyses of oyster tissues. Two anonymous reviewers provided helpful comments to improve the manuscript. This study was carried out in accordance with decree 1376–2013 of the Pentamidine dihydrochloride clinical Colombian Ministry for the Environment and Sustainable Development (MADS) under general collection permit issued to Jorge Tadeo Lozano University by the Colombian National Authority for Environmental Licenses (ANLA, Res.1271-2014). Financial resources for this study were kindly provided by research Grant 560-10-13 from Jorge Tadeo Lozano University (project MOSAICO-II) and a scholarship to A.M. from Colciencias (Convocatoria No. 528).
    Introduction Trypanosoma evansi (T. evansi), belongs to the subgenus Trypanozoon, a group of Trypanosomes has a large Pentamidine dihydrochloride clinical of mammalian hosts (Da Silva et al., 2010) and can affect both humans and animals (Desquesnes et al., 2013). Its infection is mainly disseminated by Tabanid species (Tabanus sp., Chrysops sp. and Hematopota sp.) (Otto et al., 2010). T. evansi is considered as both a blood and tissue parasite owing to its ability to invade the nervous system not only in horses and dogs but also in cattle, buffaloes, deer and pigs (Rodrigues et al., 2009). Although trypanosomosis has long been recognized as an important disease in tropical and subtropical countries (Herrera et al., 2004, Da Silva et al., 2010), but the situation in India is quite different as pathogenic effects of trypanosomosis had been recorded long back in 1891 with very high mortality (>90%) as documented by Gill (1977) from different parts of India. T. evansi infection results in anemia, reproductive disorders, loss in body weight, milk and meat production and loss in draught power, and most often during chronic evolution, it leads to totally wasted animals (Desquesnes et al., 2013). Clinical signs of neurological disorders are reported in horses, camels, buffaloes, cattle, deer and cats infected by T. evansi (Desquesnes et al., 2013). In spite of enormous advancements in diagnosis, understanding of pathogenesis of experimental T. evansi infection and therapeutic approaches, mechanism of T. evansi-induced neurological disorders in buffaloes are yet to be unraveled especially in view of the fact that trypanosomes evade the immune defense mechanism of host, and thus it has become one of the major and puzzling issues in host-parasite interaction studies (Zambrano-Villa et al., 2002). Existence of cholinergic anti-inflammatory pathway is well documented (Pavlov and Tracey, 2006) and acetylcholine (ACh) plays an important role in attenuating the release of pro-inflammatory cytokines such as tumour necrosis factor (TNF), interleukin-1 (IL-1), interleukin-6 (IL-6) and interleukin-18 (IL-18), without affecting the production of interleukin-10 (IL-10), an anti-inflammatory cytokine (Pavlov and Tracey, 2004). Concentration of ACh is regulated by cholinesterases e.g. acetylcholinesterase (AchE), which is expressed in nerve cells and erythrocytes, and butyrylcholinesterase (BuChE), which is found in plasma. Therefore, cholinesterase activity is considered as an indirect indicator of ACh levels. Alterations in acetyltransferase and acetylcholinesterase (AChE) activities (Brennessel et al., 1985) and increased dopamine and norepinephrine levels (Amole et al., 1989) have been associated with trypanosomosis in mice due to T. cruzi and T. brucei infections. Therefore, determination of cholinesterase activity in clinical cases of trypanosomosis will be of significance in further understanding the pathogenesis and host immune evasion mechanisms. Reduction in cholinesterase activity might be a possible cause of neurological disorders in trypanosomosis since this enzyme is essential in nerve impulse transmission during nerve signal relay (Bartels et al., 2000).