Thromboxane B2 in dogs with babesiosis

Babesiosis can cause severe tissue hypoxia with consequent widespread tissue damage and probable release of inflammatory mediators (Lobetti, 1998). The major mediators are cytokines, nitric oxide, free oxygen radicals, eicosanoids, and platelet-activating factor (Purvis et al., 1994). Eicosanoids are a family of lipid mediators regulating numerous physiological processes (Hwang, 1989). There is clear evidence that the eicosaniod pathway is involved in many metabolic diseases of animals and humans (Cook, 2002). Thromboxanes (TX) are part of a family of biologically active lipids derived from eicosanoids. They are the major arachidonic acid metabolite produced by platelet (via COX-1). The platelet accounts for about 95% of the TX detectable in serum with neutrophils being another source (Higgs et al., 1985). Thromboxane is a very potent vasoconstrictor and agonist for platelet aggregation. We investigated the serum levels of the thromboxanes B2 (TXB2) in Babesia canis patients. Twentysix dogs presented at the Veterinary Hospital with clinical signs of acute babesiosis were prospectively studied. In all cases Babesia canis infection was confirmed by detection of the parasite using Romanowsky- stained thin blood smears. The control group consisted of 17 healthy dogs, clinically normal and aparasitemic. Blood was collected before treatment with imidocarb dipropionat (Imizol, Schering Plough) and on the 1st, and 2nd day after treatment. The thromboxane serum concentration was measured using a competitive enzyme immunoassay test kit (Thromboxane B2 EIA Kit, Catalog No.519031, Cayman Chemical Company). Statistical analysis of the data were carried out by the Mann-Whitney U test at p