Article

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: 2.04). 04/2009; 46(2):251-8. DOI: 10.1354/vp.46-2-251
Source: PubMed

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.

0 Followers
 · 
192 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: The aim of this study was to investigate the behavioral assessment and activities of important enzymes involved in the phosphoryl transfer network in rat brains that were experimentally infected with Trypanosoma evansi. Behavioral assessment (cognitive performance), pro-inflammatory cytokines in serum and activities of adenylate kinase (AK), pyruvate kinase (PK), and creatine kinase (CK) in brain were evaluated at 5 and 15 days post-infection (PI). Here we demonstrate a cognitive impairment in the rats infected with T. evansi. At 5 and 15 days PI, a memory deficit and a depressant activity were demonstrated by an inhibition avoidance test and increase in the immobility time in a tail suspension test, respectively. On day 5 PI, a decrease in the CK activity and an increase in the AK activity were observed. On day 15 PI, an increase in the CK activity and a decrease in the AK activity were observed. Considering the importance of energy metabolism for brain functioning, it is possible that the changes in the activity of enzymes involved in the cerebral phosphotransfer network and an increase in the proinflammatory cytokines (TNF and IFN) may be involved at least in part in the cognitive impairment in infected rats with T. evansi.
    Experimental Parasitology 02/2015; 151-152. DOI:10.1016/j.exppara.2015.01.015 · 1.86 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The present study is an observation of transplacental transmission of T. evansi in a donkey neonatal foal. One experimentally infected pregnant donkey mare gave a normal birth to a foal after three months of experimental infection. No trypanosome was seen in wet blood film on microscopic examination in the experimentally infected donkey mare at time of birth of foal, however in serum a significant level of antitrypanosmal IgG antibodies in ELISA and many immunodominant polypeptide bands on immunoblotting were observed. In neonatal foal, live moving trypanosomes were observed in wet blood film just after birth before colostrum feeding. The foal serum sample (collected before colostrum feeding) was found negative in ELISA and immunoblotting indicating that IgG antibodies have not crossed placental barrier in mother donkey mare. After 24 h of birth, the clinical symptoms appeared in foal showing recumbancy, unable to stand and suckle, and poor reflexes. The foal was administered fluid therapy, but could survive only up to 36 h after birth. The study indicated transplacental transmission of T. evansi in donkey but the mechanism responsible for crossing the placental barrier need to be further elucidated.
    Journal of Equine Veterinary Science 02/2015; DOI:10.1016/j.jevs.2015.02.004 · 0.89 Impact Factor
  • Journal of parasitic diseases 01/2015; DOI:10.1007/s12639-014-0633-1