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Casos de tripanossomíase por Trypanosoma evansi foram diagnosticados em eqüinos no Rio Grande do Sul entre 2003 e 2004. Em uma propriedade (Propriedade A) com 125 eqüinos, 52 morreram. A Propriedade A recebeu ao redor de 80 éguas de outras propriedades para cobertura. Dessas, 66 adoeceram e 56 morreram após voltarem para suas propriedades de origem. A doença clínica observada em 21 eqüinos caracterizava-se por emagrecimento (apesar de apetite voraz), letargia, incoordenação e instabilidade dos membros pélvicos, atrofia das grandes massas musculares dos membros pélvicos, fraqueza muscular e palidez das mucosas. Exemplares de T. evansi foram observados na corrente sangüínea de 4 eqüinos. Anemia normocítica normo-crômica, com hematócritos que variavam de 15-31%, e leuco-citose por linfocitose associada à presença de linfócitos atípicos foram observadas em vários eqüinos. Altos níveis de anticorpos contra T. evansi foram detectados em 6 eqüinos da Propriedade A. Oito eqüinos desenvolveram um quadro neurológico encefálico caracterizado por andar em círculos, ataxia, cegueira, hiperexcitabilidade, quedas, embotamento, déficits proprioceptivos e desvio da cabeça. Um eqüino desenvolveu "posição de cão sentado". Nas 13 necropsias, havia espleno-megalia, linfadenomegalia, hiperplasia linfóide no baço e linfo-nodo, atrofia das grandes massas musculares dos membros pélvicos, edema e malacia na substância branca e cinzenta do encéfalo. Histologicamente, uma panencefalite devastadora foi observada nos 7 casos e caracterizada por marcado edema, desmielinização, necrose e infiltrado perivascular de 6-10 camadas de células linfoplasmocitárias afetando tanto a substância branca quanto a cinzenta. Muitos plasmócitos do infiltrado inflamatório continham numerosos grânulos eosinofílicos no citoplasma (células de Mott). Lesões semelhantes foram observadas na medula espinhal do eqüino que desenvolveu "posição de cão sentado". Os encéfalos de 5 eqüinos com quadro encefálico foram submetidos à técnica de imunoistoquímica estrepto-avidina-biotina; em todos eles observou-se a marcação de números moderados ou elevados de espécimes de T. evansi pelo anticorpo específico nos espaços intravasculares e na neurópila. Os aspectos epidemiológicos, clínicos, hematológicos e patológicos da tripanossomíase por T. evansi em eqüinos são discutidos. 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

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