Detection of Coxiella burnetii antibodies in sheep and cattle on a veterinary campus in St. Kitts: Implications for one health in the Caribbean region.

Coxiella burnetii is a ubiquitous zoonotic bacterium reported worldwide that causes Q-fever. Infections result in profound economic losses to livestock producers by causing abortions and low birth weights. Current information about the disease in the Caribbean region is scarce. With multiple small islands and territories, it is often considered that the bacterium is absent or circulates at a low prevalence. Our study aimed to determine whether sheep and cattle housed at a veterinary campus in St Kitts had previous exposure to C. burnetii. Blood samples were taken from cattle (n = 63; 72% of the herd) and sheep (n = 133; 71% of the flock). Antibodies to C. burnetii were detected by a commercial indirect enzyme-linked immunosorbent assay (IDvet® ELISA) test. The seroprevalence was estimated at 26.3% (95% CI: 19.1-34.7%) in sheep and 0% (95% CI: 0-5.7%) in cattle. Sheep importation to St. Kitts is very rare, thus, these results suggest that C. burnetii is present on the island. The seronegativity of all the cattle highlights the absence of the bacterium on the veterinary campus. The high seroprevalence in sheep, however, has potentially important implications for animal health and public health as well as for wildlife conservation. Further investigation about animal seroprevalence and human exposure are warranted in St. Kitts and in the Caribbean region.

Constitutive expression of c-FLIP in Hodgkin and Reed-Sternberg cells.

Crosslinking of the transmembrane receptor CD95/Fas leads to activation of a signaling cascade resulting in apoptosis. c-FLIP is a recently described protein that potently inhibits Fas-mediated apoptosis and has been shown to be a key factor in germinal center B cell survival. Because Hodgkin and Reed-Sternberg cells in classical Hodgkin's disease (cHD) are also resistant to Fas-mediated apoptosis we studied the role of c-FLIP in classical HD. High levels of c-FLIP protein were identified in two Fas-resistant Hodgkin-derived cell lines. In contrast to other tumor cells, inhibition of protein synthesis by cycloheximide did not lead to down-regulation of c-FLIP protein in these HD cell lines. Furthermore, Fas-mediated apoptosis was only partially restored suggesting that normal regulation of c-FLIP was disrupted. The in vivo relevance of these findings was supported by demonstration of significant c-FLIP expression by immunohistochemistry in 18 of 19 evaluable cases of primary HD. Taken together, c-FLIP is constitutively expressed in HD and may therefore be a major mechanism responsible for Fas-resistance in HD.