Fatal Theileria orientalis N2 genotype infection among Asian water buffaloes (Bubalus bubalis) in a commercial dairy farm in Kerala, India.

Fifteen dairy buffaloes of a farm in the state of Kerala, India developed fatal oriental theileriosis within 2 months of their procurement. Typical piroplasms of Theileria orientalis were observed in the erythrocytes of all affected animals by Giemsa-Leishman staining of blood smears. Case fatality rate was 87·5% (seven out of eight) in the clinically progressed cases. Therapeutic management with anti-theilerial drugs buparvaquone and oxytetracycline led to recovery of seven other animals in less advanced stages of the disease. The aim of this study was to determine the reasons for increased virulence of this pathogen, hitherto considered to be benign. Acute haemolytic anaemia was the predominant haematological finding in the affected animals. Lymphocytic infiltration and degeneration of vital organs leading to functional derangement was the cause of the high mortality. Identification of T. orientalis was confirmed by polymerase chain reaction (PCR). DNA sequencing of the PCR products revealed close identity with already reported sequences of T. orientalis/buffeli N2 genotype. The sequences were deposited in GenBank with accession number KM609973 and KM043772. Rhipicephalus ticks, previously not reported as vectors for oriental theileriosis, were identified as the potential vectors. This is the first report of fatal oriental theileriosis in Asian water buffaloes.

Enhanced NMDAR1, NMDA2B and mGlu5 receptors gene expression in the cerebellum of insulin induced hypoglycaemic and streptozotocin induced diabetic rats.

Glucose homeostasis in humans is an important factor for the functioning of the nervous system. A decrease in glucose content below a minimal level or hypoglycemia is dangerous for cells of the central and peripheral nerve system. In the present study we showed the effects of insulin induced hypoglycaemia and streptozotocin induced diabetes on the cerebellar glutamate receptor subunits and glutamate transporter. Cerebellar dysfunction is associated with seizure generation, motor deficits and memory impairment. We found an up regulation in NMDA receptor number and gene expression of N-methyl-d-aspartic acid (NMDA(R1)), NMDA(2B), metabotrophic glutamate 5 (mGlu(5)) glutamate receptor subunits in experimental rats. The glutamate content was shown to be increased with decreased glutamate aspartate transporter (GLAST) gene expressions indicating lower reuptake of glutamate. The enhanced gene expression of NMDA(R1), NMDA(2B), mGlu(5) glutamate receptors were confirmed by immunohistochemistry studies. At the second messenger level, the IP3 content and IP3 receptors were enhanced in the cerebellum of both hypoglycaemic and diabetic rats increased. The present study showed that the enhanced glutamate content activates NMDA receptors, increasing the inositol triphosphate (IP3) content which mediates Ca(2+) overload in cells causing cell damage and neurodegeneration. Our results also showed that the enhanced glutamate receptor activity were more prominent in hypoglycaemic group compared to diabetic group. Further the neurodegeneration by the up regulation of glutamate receptor activity causing motor dysfunction was demonstrated by the Rotarod test. Thus our results suggest that enhanced NMDA receptor mediated neurodegeneration affect the motor learning and memory ability of an individual.