Demographic and environmental risk factors for infection by Theileria equi in 590 horses in Israel.

The prevalence of Theileria equi infection as well as the environmental and demographic risk factors for infection was studied in 590 healthy horses from 46 farms in Israel. The prevalence of T. equi DNA was assessed using a polymerase chain reaction for a segment of the Theileria 18S rRNA gene. The overall prevalence was 26.4% (156/590). There was a significant geographical variation in the prevalence of T. equi infection, ranging from 9.3% (25/270) in the central lowlands to 81.7% (49/60) in the Golan Heights. The prevalence of T. equi infection was found to be significantly associated with management types with more horses with access to pasture being positive. Breed was identified as a risk factor for T. equi infection in a univariate analysis with relatively high infection rates in the Quarter horse and local breeds (41.1% and 36.3% respectively), while ponies and Arabian horses had a relatively low prevalence (10% and 9.1%, respectively). However, since a correlation between geographic location and breed was found, it is difficult to draw definite conclusions regarding this risk factor. Age and gender were not found as risk factors for T. equi infection in this study. The environmental variables that were significantly associated with positivity were relative humidity and minimum land surface temperature at day which both showed negative correlation with T. equi prevalence. In conclusion, Israel was found to be enzootic for T. equi infection, as indicated by the high sub-clinical infection rate, which differed between geographical areas.

Neurotropism of herpes simplex virus type 1 in brain organ cultures.

The mechanism of herpes simplex virus type 1 (HSV-1) penetration into the brain and its predilection to infect certain neuronal regions is unknown. In order to study HSV-1 neurotropism, an ex vivo system of mice organotypic brain slices was established and the tissue was infected with HSV-1 vectors. Neonate tissues showed restricted infection confined to leptomeningeal, periventricular and cortical brain regions. The hippocampus was the primary parenchymatous structure that was also infected. Infection was localized to early progenitor and ependymal cells. Increasing viral inoculum increased the intensity and enlarged the infected territory, but the distinctive pattern of infection was maintained and differed from that observed with adenovirus and Vaccinia virus. Neonate brain tissues were much more permissive for HSV-1 infection than adult mouse brain tissues. Taken together, these results indicate a complex interaction of HSV-1 with different brain-cell types and provide a useful vehicle to elucidate the mechanisms of viral neurotropism.