Neuropathology of Naturally Occurring Trypanosoma evansi Infection of Horses

Department of Veterinary Pathobiology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, 4467 TAMU, College Station, TX 77843-4467, USA.
Veterinary Pathology (Impact Factor: 1.87). 04/2009; 46(2):251-8. DOI: 10.1354/vp.46-2-251
Source: PubMed


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.

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    • "Neurological signs have occasionally been reported in the terminal phase of natural infection in horses (Seiler et al. 1981). Neurological signs appear to be variable and include generalized weakness, progressive hind limb paralysis, restlessness , circling, incoordination, gait instability (wobbling) involving the pelvic limb, atrophy of the heavy muscles of the hind quarters, and difficulty in rising (Furr 2008; Rodrigues et al. 2009). The CNS form of trypanosomiasis can occur during the early stages of infection, during which time the T. "
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    ABSTRACT: Trypanosoma evansi infection typically produces wasting disease, but it can also develop into a neurological or meningoencephalitis form in equids. Trypanosomiasis in horses was treated with quinapyramine sulfate, and all the 14 infected animals were recovered clinically. After clinical recovery, four animals developed a neurological form of the disease at various intervals. Two of these animals treated with diminazene aceturate recovered temporarily. Repeated attempts failed to find the parasite in the blood or the cerebrospinal fluid (CSF), but all of the animals were positive in enzyme-linked immunosorbent assay. The calculation of the antibody index (AI) in the serum and the CSF and polymerase chain reaction (PCR) analysis of the CSF and brain tissue were carried out to confirm the neuro-infection. We found PCR and AI analyses of the CSF to be useful tools in the diagnosis of the neurological form of trypanosomiasis when the organism cannot be found in the blood or CSF. The increased albumin quotient is indicative of barrier leakage due to neuroinflammation. The biochemical changes in the CSF due to nervous system trypanosomiasis include increases in the albumin quotient, total protein, and urea nitrogen. It seems to be the first report on relapse of the nervous form of trypanosomiasis in equids even after quinapyramine treatment in endemic areas.
    Tropical Animal Health and Production 11/2013; 46(2). DOI:10.1007/s11250-013-0498-9 · 0.82 Impact Factor
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    • "Regardless of these findings, the involvement of the CNS in infection is widely discussed, because brain lesions are occasionally observed. Some authors have reported the appearance of lesions in the brain and presence of the parasite (Berlin et al. 2009; Rodrigues et al. 2009). Data based from animal Fig. 5. Evaluation of Na + , K + -ATPase activity in cortex, striatum and hippocampus of rats infected by Trypanosoma evansi at 5 (T5) and 30 (T30) dpi. "
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    ABSTRACT: The aim of this study was to investigate neurochemical and enzymatic changes in rats infected with Trypanosoma evansi, and their interference in the cognitive parameters. Behavioural assessment (assessment of cognitive performance), evaluation of cerebral L-[3H]glutamate uptake, acetylcholinesterase (AChE) activity and Ca+2 and Na+, K+-ATPase activity were evaluated at 5 and 30 days post infection (dpi). This study demonstrates a cognitive impairment in rats infected with T. evansi. At 5 dpi memory deficit was demonstrated by an inhibitory avoidance test. With the chronicity of the disease (30 dpi) animals showed anxiety symptoms. It is possible the inhibition of cerebral Na+, K+-ATPase activity, AChE and synaptosomal glutamate uptake are involved in cognitive impairment in infected rats by T. evansi. The understanding of cerebral host–parasite relationship may shed some light on the cryptic symptoms of animals and possibly human infection where patients often present with other central nervous system (CNS) disorders.
    Parasitology 09/2013; 140(11):1432-41. DOI:10.1017/S003118201300108X · 2.56 Impact Factor
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    • "After treatment the detection methods were repeated after every two weeks, clinical symptoms disappeared during the course of medication, while microscopic examination remained positive after six weeks however PCR results took 2 months to give negative results. DISCUSSION Trypanosomes have wide range of hosts, and are responsible for variety of diseases in mammals, reptiles, rodents as well as in amphibians (Muhammad et al., 2007; Ravindran et al., 2008; Da Silva et al., 2009, 2011a, 2011b; Fernández et al., 2009; Rodrigues et al., 2009; Umezawa et al., 2009; Tamarit et al., 2010). The Fig. 2: 1.5% Agarose gel of PCR product of TR3/TR4 primer pair stained with ethidium bromide. "
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    ABSTRACT: Clinical signs, viz lethargy, increased heart rate and reduced appetite, making trypanosomiasis a possible differential diagnosis, were found in five out of twenty semi-captive Asiatic black bears (Ursus thibetanus) in a sanctuary, located in Kund, District Sawabi, KPK, Pakistan. Microscopic examination of blood samples of bears expressing clinical signs and symptoms revealed the presence of haemoflagellates, which was found to be trypanosomes. Subsequently, the PCR technique was exploited to screen for the presence of trypanosomal species in all bears’ blood samples. Blood samples from 20 individual bears were screened using three sets of primers specific to Trypanosoma evansi species. Three primer pairs used are equally effective in successful detection of the parasite. Two out of five, diseased bears died prior to any trypanosoma specific medication while the rest were given an administered dose of Melarsomine (Immiticide). The treated bears survived and were assured to be aparasitemic on post-treatment examination after six weeks.
    Pakistan Veterinary Journal 04/2013; 33(4):442-445. · 1.39 Impact Factor
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