Pathogenic animal trypanosomes affecting livestock have represented a major constraint to agricultural development in Africa for centuries, and their negative economic impact is increasing in South America and Asia. Chemotherapy and chemoprophylaxis represent the main means of control. However, research into new trypanocides has remained inadequate for decades, leading to a situation where the few compounds available are losing efficacy due to the emergence of drug-resistant parasites. In this review, we provide a comprehensive overview of the current options available for the treatment and prophylaxis of the animal trypanosomiases, with a special focus on the problem of resistance. The key issues surrounding the main economically important animal trypanosome species and the diseases they cause are also presented. As new investment becomes available to develop improved tools to control the animal trypanosomiases, we stress that efforts should be directed towards a better understanding of the biology of the relevant parasite species and strains, to identify new drug targets and interrogate resistance mechanisms.

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The animal trypanosomiases and their chemotherapy: a review.

This paper reviews the transmission modes of Trypanosoma evansi. Its worldwide distribution is attributed to mechanical transmission. While the role of tabanids is clear, we raise questions on the relative role of Haematobia sp. and the possible role of Stomoxys sp. in delayed transmission. A review of the available trypanocidal drugs and their efficacy in various host species is useful for understanding how they interact in disease epidemiology, which is complex. Although there are similarities with other mechanically transmitted trypanosomes, T. evansi has a more complex epidemiology due to the diversity of its hosts and vectors. The impact of clinical and subclinical disease is difficult to establish. A model was developed for buffaloes in the Philippines, which could be transferred to other places and livestock systems. Since Trypanosoma evansi was reported in humans, further research is required to investigate its zoonotic potential. Surra remains a potentially emerging disease that is a threat to Australia, Spain, and France. A number of questions about the disease have yet to be resolved. This brief review of the basic knowledge of T. evansi suggests that there is renewed interest in the parasite, which is spreading and has a major economic impact.

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Trypanosoma evansi and Surra: A Review and Perspectives on Transmission, Epidemiology and Control, Impact, and Zoonotic Aspects

Surra is an animal trypanosomosis, caused by infection with Trypanosoma evansi and leading to severe economic loss due to mortality and morbidity. Compared to tsetse-transmitted animal trypanosomoses, little attention is given to the epidemiology and control of surra. Understanding its epidemiology is a first step in local and global efforts to control the disease. We conducted a systematic review and meta-analysis of published studies on distribution, host ranges and prevalence of T. evansi infection. Four electronic databases were searched for publications on T. evansi that met our inclusion criteria for the systematic review. Subsets of publications were subjected to meta-analysis for the pooled prevalence of T. evansi in various hosts as determined by multiple detection methods. A total of 272 references published between 1906–2017 were included. Trypanosoma evansi was reported from 48 countries; largely confined to Africa and Asia with publications on natural T. evansi infections from 77% (n = 48) of countries, contrasting with seven countries in South America, and four in Europe where T. evansi is not endemic but was imported with infected animals. Although surra is a notifiable disease, many countries do not report surra cases to OIE. Trypanosoma evansi was mainly reported from dromedary camels in Africa and the Middle East, water buffaloes, cattle, dogs and horses in East and Southeast Asia. In South America, the acute form of the disease was reported in horses and dogs. Surra was also reported in a wide range of wild animals. Some rare human cases occurred in India and Vietnam. Meta-analysis on a subset of 165 publications indicated pooled prevalence of T. evansi in domestic animals ranging from 14–31%, 6–28% and 2–9% using respectively antibody detection, molecular and parasitological tests, with camels as the most affected, followed by buffalo and cattle. This study illustrates that T. evansi affects a wide range of domestic and wild animals in Africa, Asia and South America with highest prevalence observed in dromedary camels. For successful control of T. evansi, both locally and globally, the role of wild animals in the epidemiology of surra needs further investigation.

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Systematic Review and Meta-Analysis on the Global Distribution, Host Range, and Prevalence of Trypanosoma Evansi

Cases of trypanosomiasis by Trypanosoma evansi were diagnosed in horses in the state of Rio Grande do Sul, Brazil, between 2003 and 2004. In one stud farm (Farm A) with 125 horses, 52 died. Additionally, around 80 mares were sent to Farm A to be bred. Of those, 66 became ill and 56 died after being returned to their farms of origin. Twenty one horses clinically affected by the disease were observed. Clinical signs included loss of weight (despite voracious appetite), lethargy, incoordination and instability of hindlimbs, atrophy of the large muscles of the hindlimbs, muscle weakness and paleness of mucosae. Specimens of T. evansi were detected in the blood drawn from four affected horses. Normocytic normochromic anemia with PCVs ranging from 15 to 31%, leucocytosis due to lymphocytosis associated to large atypical lymphocytes was observed in several affected horses. High levels of antibodies against T. evansi were detected in the serum of six horses from Farm A. Eight horses presented encephalic neurological signs such as circling, ataxia, blindness, excitation, falls, listlessness, proprioception deficits and head tilt. One horse assumed a "dog-seating position". Necropsy findings included muscle atrophy, enlargement and lymphoid hyperplasia of the spleen and lymphnodes, edema and softening of the white and grey matter of the brain. Histologically, an overwhelming necrotizing panencephalitis was observed in the seven horses with encephalic signs. This panencephalitis was characterized by marked edema, demyelination and necrosis and perivascular infiltrates of 6-10 layers of lymphocytes and plasm cells affecting both the white and gray matter. Several plasm cells in the inflammatory infiltrate contained numerous eosinophilic globules in their cytoplasm (Mott cells). Similar histological lesions were observed in the spinal cord of the horse with the "dog-seating position". The brains of five horses with the encephalic signs were submitted to immunohistochemistry stain by the streptavidin-biotin technique. In all of those five brains moderate to abundant specimens of T. evansi in the perivascular spaces and neuropile were marked by the specific antibody. Epidemiological, clinical, hematological, and pathological aspects of equine trypanosomiasis caused by T. evansi are discussed.

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Surtos de tripanossomíase por Trypanosoma evansi em eqüinos no Rio Grande do Sul: aspectos epidemiológicos, clínicos, hematológicos e patológicos

Humans have three functioning genes that encode copper-containing amine oxidases. The product of the AOC1 gene is a so-called diamine oxidase (hDAO), named for its substrate preference for diamines, particularly histamine. hDAO has been cloned and expressed in insect cells and the structure of the native enzyme determined by X-ray crystallography to a resolution of 1.8 A. The homodimeric structure has the archetypal amine oxidase fold. Two active sites, one in each subunit, are characterized by the presence of a copper ion and a topaquinone residue formed by the post-translational modification of a tyrosine. Although hDAO shares 37.9% sequence identity with another human copper amine oxidase, semicarbazide sensitive amine oxidase or vascular adhesion protein-1, its substrate binding pocket and entry channel are distinctly different in accord with the different substrate specificities. The structures of two inhibitor complexes of hDAO, berenil and pentamidine, have been refined to resolutions of 2.1 and 2.2 A, respectively. They bind noncovalently in the active-site channel. The inhibitor binding suggests that an aspartic acid residue, conserved in all diamine oxidases but absent from other amine oxidases, is responsible for the diamine specificity by interacting with the second amino group of preferred diamine substrates.

A Theeraphan

Papers

Chemotherapy of surra in horses and mules with diminazene aceturate