Cerebral trypanosomiasis in native cattle

Tuntasuvan, Darunee; Sarataphan, Nopporn; Nishikawa, Hiroaki

doi:10.1016/s0304-4017(97)00128-3

Cited by 45 publications

(35 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…8,11,16,41 Natural infection by T. evansi is rarely considered a cause of encephalitis in horses. 40 Neurologic signs have been reported in cattle 47 and hog deer 46 naturally infected by T. evansi; however, the histopathologic changes in the brain of these species were either not described 47 or just briefly described. 45,46 On the other hand, mild lymphoplasmacytic meningoencephalitis was reported in horses, 21 donkeys, 3 dogs, 2 goats, 6 coatis (N. nasua), 15 and buffaloes 5 experimentally infected by T. evansi.…”

Section: Discussionmentioning

confidence: 99%

“…Neurologic signs have been described occasionally in the terminal phase of natural infection by T. evansi in horses, 40 cattle, deer, 46,47 and buffaloes, 45 but have not been well documented in horses. In Brazil, T. evansi is enzootic in horses from the midwestern part of the country, specifically the Pantanal region, 7,8,10,15,[41][42][43] where the disease has great economic importance because of the large equine population.…”

Section: 22mentioning

confidence: 99%

See 1 more Smart Citation

Neuropathology of Naturally Occurring Trypanosoma evansi Infection of Horses

Rodrigues

Fighera

Souza

et al. 2009

Veterinary Pathology

View full text Add to dashboard Cite

Abstract. The clinical signs and pathology of the central nervous system in 9 horses with naturally occurring neurologic disease due to Trypanosoma evansi are described. The clinical course was 2 to 20 days; clinical signs included marked ataxia, blindness, head tilt and circling, hyperexcitability, obtundity, proprioceptive deficits, head pressing, and paddling movements. Grossly, asymmetric leukoencephalomalacia with yellowish discoloration of white matter and flattening of the gyri were observed in the brain of 7 of 9 horses. Histologically, all 9 horses had necrotizing encephalitis that was most severe in the white matter, with edema, demyelination, and lymphoplasmacytic perivascular cuffs. Mild to moderate meningitis or meningomyelitis was observed in the spinal cord of 5 of 7 horses. T. evansi was detected immunohistochemically in the perivascular spaces and neuropil of formalin-fixed, paraffin-embedded brain tissue in 8 of 9 horses.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: 22mentioning

confidence: 99%

Neuropathology of Naturally Occurring Trypanosoma evansi Infection of Horses

Rodrigues

Fighera

Souza

et al. 2009

Veterinary Pathology

View full text Add to dashboard Cite

show abstract

“…No entanto, jumentos infectados experimentalmente com T. evansi (Cadioli 2001) apresentaram sinais clínicos de distúrbios encefálicos, caracterizados por torcicolo, dismetria e andar em círculos, e lesões encefálicas semelhantes às descritas em nossos eqüinos. Bovinos (Tuntasuvan et al 1997, Tuntasuvan & Luckins 1998 e veados (Tuntasuvan et al 2003) naturalmente infectados desenvolveram um quadro clínico e lesões semelhantes.…”

Section: Discussão Discussão Discussão Discussão Discussãounclassified

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

et al. 2005

View full text Add to dashboard Cite

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 "dogseating 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 streptavidinbiotin 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.

show abstract

“…Animals recovering from the disease can become reservoirs, with low or even undetectable blood levels of the parasite (Plata 1931b). In the aparasitemic phases, trypanosomes can be found extravascularly, in lymph nodes (Hoare 1972), eyes (in the choroid plexus and aqueous humor) (Whitelaw et al 1988), and cerebrospinal fluid (Tuntasuvan et al 1997). Occult infections can be reactivated by stress.…”

Section: Pathogenesis and Symptomsmentioning

confidence: 99%