PESQUISA VETERINÁRIA BRASILEIRA

Abstract in English:

Trypanosoma evansi can affect a broad range of domestic and wild animals, such as feral pigs, horses, cattle, goats, dogs, and other carnivores. The growth in wild boar (Sus scrofa) populations is considered a significant risk factor, given their status as known reservoirs. This article reviews the epidemiological, clinicopathological, and molecular dimensions, including the identification and genetic characterization, of a T. evansi outbreak in dogs. Thirty-four dogs, utilized for wild boar management, underwent physical examinations, complete blood counts, hemoparasite detection via direct microscopic examination of blood smears, DNA detection using polymerase chain reaction, and serological testing for antibodies against Trypanosoma spp., alongside post mortem analyses of two deceased animals. Clinical signs observed included changes in the color of ocular, oral, and genital mucous membranes, lymphadenomegaly, subcutaneous edema, and anemia. Trypanosoma spp. DNA was detected in blood and tissue samples, while blood smears (8/34) revealed the presence of organisms morphologically consistent with the trypomastigote forms of Trypanosoma spp. Serological testing failed to detect antibodies. Our results suggest that the dogs were likely infected with T. evansi through contact with the blood and/or tissues of infected wild boars. Given the spread of wild boars and their role as reservoirs of T. evansi, we emphasize the need to incorporate this protozoan species into routine diagnostic procedures for dogs and the urgency of preventive measures to reduce contact between dogs and wildlife, along with wild boar control initiatives.

• Oral transmission dogs Trypanosoma evansi PCR anatomopathological findings Sus scrofa

Abstract in Portuguese:

Trypanosoma evansi pode afetar uma ampla variedade de animais domésticos e selvagens, como javalis, cavalos, bovinos, caprinos, cães e outros carnívoros. O crescimento das populações de javalis (Sus scrofa) é considerado um fator de risco significativo, visto que são conhecidos como reservatórios. Este artigo revisa as dimensões epidemiológicas, clinicopatológicas e moleculares, incluindo a identificação e caracterização genética, de um surto de T. evansi em cães. Trinta e quatro cães, utilizados no manejo de javalis, foram submetidos a exames físicos, hemogramas completos, detecção de hemoparasitas por exame microscópico direto de esfregaços sanguíneos, detecção de DNA utilizando a reação em cadeia da polimerase (PCR) e testes sorológicos para anticorpos contra Trypanosoma spp., além de análises post mortem de dois animais que vieram a óbito. Nossos resultados sugerem que a infecção dos cães por T. evansi provavelmente ocorreu devido ao contato com sangue e/ou tecidos de javalis infectados. Considerando a disseminação dos javalis e sua importância como reservatórios de T. evansi, ressaltamos a necessidade de incorporar essa espécie do protozoário na rotina diagnóstica de cães e a urgência de medidas preventivas para reduzir o contato entre cães e animais selvagens, junto com iniciativas de controle dos javalis.

• Transmissão oral caninos cães Trypanosoma evansi PCR achados anatomopatológicos Sus scrofa

Abstract in English:

Rodrigues A., Fighera R.A., Souza T.M., Schild A.L., Soares M.P., Milano J. & Barros C.S.L. 2005. [Outbreaks of trypanosomiasis in horses by Trypanosoma evansi in the state of Rio Grande do Sul, Brazil: epidemiological, clinical, hematological, and pathological aspects.] Surtos de tripanossomíase por Trypanosoma evansi em eqüinos no Rio Grande do Sul: aspectos epidemiológicos, clínicos, hematológicos e patológicos. Pesquisa Veterinária Brasileira 25(4):239-249. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br 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.

• Trypanosomiasis Trypanosoma evansi infectious diseases encephalitis hematology pathology diseases of horses.

Abstract in Portuguese:

Rodrigues A., Fighera R.A., Souza T.M., Schild A.L., Soares M.P., Milano J. & Barros C.S.L. 2005. [Outbreaks of trypanosomiasis in horses by Trypanosoma evansi in the state of Rio Grande do Sul, Brazil: epidemiological, clinical, hematological, and pathological aspects.] Surtos de tripanossomíase por Trypanosoma evansi em eqüinos no Rio Grande do Sul: aspectos epidemiológicos, clínicos, hematológicos e patológicos. Pesquisa Veterinária Brasileira 25(4):239-249. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br 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.