Epidemiologic Findings and Management Response During a Bighorn Sheep Die-Off in the Elkhorn Mountains of West-Central Montana

Bighorn sheep (Ovis canadensis) were introduced into the Elkhorn Mountains of west-central Montana in the mid 1990s. The population increased in number to approximately 250 animals until the winter of 2007-2008 when about 84 percent of the population died from a pneumonia related epizootic. Management actions during the die-off were geared toward removing as many sick animals as possible in efforts to reduce overall mortality. Due to the stage of the epizootic removal of sick sheep was not effective in interrupting the die-off. Samples were collected from bighorn sheep, domestic sheep, mule deer (Odocoileus hemionus), elk (Cervus elaphus) and domestic goats utilizing the same winter range. Pasteurella spp, Moraxella ovis and Mycoplasma ovipneumonia were isolated from lung tissue of dead bighorns and pharyngeal swabs collected from domestic sheep occupying similar range during the epizootic. Both the bighorn sheep and domestic sheep also shared similar gastro-intestinal parasites including Nematodirus spp and Eimeria spp. Testing tissues and fecal samples from sympatric mule deer suggested no shared bacterial pathogens and limited shared gastrointestinal parasites. Evaluation of fecal samples from domestic goats and elk also occupying bighorn sheep range identified few shared parasites that may have contributed to the epizootic

Transferring from clopidogrel loading dose to prasugrel loading dose in acute coronary syndrome patients High on-treatment platelet reactivity analysis of the TRIPLET trial

High on-treatment platelet reactivity (HPR) has been identified as an independent risk factor for ischaemic events. The randomised, double-blind, TRIPLET trial included a pre-defined comparison of H PR in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI) following a placebo/600-mg clopidogrel loading dose (LD) immediately before a subsequent prasugrel 60-mg or 30-mg LD. Platelet reactivity was assessed using the VerifyNow (R) P2Y12 assay (P2Y12 Reaction Units, PRU) within 24 hours (h) following the placebo/clopidogrel LD (immediately prior to prasugrel LD), and at 2, 6, 24, 72 h following prasugrel LDs. The impact of CYP2C19 predicted metaboliser phenotype (extensive metabolisers [EM] and reduced metabolisers [RM])) on HPR status was also assessed. HPR (PRU >= 240) following the clopidogrel LD (prior to the prasugrel LD) was 58.5% in the combined clopidogrel LD groups. No significant difference was noted when stratified by time between the clopidogrel and prasugrel LDs (56 hs vs >6 h). At 6 h following the 2nd loading dose in the combined prasugrel LD groups, HPR was 7.1%, with 0% HPR by 72 h. There was no significant effect of CYP2C19 genotype on pharmacodynamic (PD) response following either prasugrel LD treatments at any time point, regardless of whether it was preceded by a clopidogrel 600-mg LD. In conclusion, in this study, patients with ACS intended for PCI showed a high prevalence of HPR after clopidogrel 600-mg LD regardless of metaboliser status. When prasugrel LD was added, HPR decreased substantially by 6 h, and was not seen by 72 h