Fatal outbreaks in dogs associated with pantropic canine coronavirus in France and Belgium

Infection with pantropic canine coronavirus was detected during outbreaks in France and Belgium. This was concurrent in most cases with canine parvovirus 2c. One outbreak was a deadly acute systemic disease with a single pantropic canine coronavirus infection. This is the first report of a fatality associated with pantropic canine coronavirus alone outside Italy

Ticagrelor Conditioning Effects Are Not Additive to Cardioprotection Induced by Direct NLRP3 Inflammasome Inhibition: Role of RISK, NLRP3, and Redox Cascades

Inhibition of either P2Y12 receptor or the nucleotide-binding oligomerization domain- (NOD-) like receptor pyrin domain containing 3 (NLRP3) inflammasome provides cardioprotective effects. Here, we investigate whether direct NLRP3 inflammasome inhibition exerts additive effects on myocardial protection induced by the P2Y12 receptor antagonist Ticagrelor. Ticagrelor (150 mg/kg) was orally administered to rats for three consecutive days. Then, isolated hearts underwent an ischemia/reperfusion (30 min ischemia/60 min reperfusion; IR) protocol. The selective NLRP3 inflammasome inhibitor INF (50 μM) was infused before the IR protocol to the hearts from untreated animals or pretreated with Ticagrelor. In parallel experiments, the hearts isolated from untreated animals were perfused with Ticagrelor (3.70 μM) before ischemia and subjected to IR. The hearts of animals pretreated with Ticagrelor showed a significantly reduced infarct size (IS, 49±3% of area at risk, AAR) when compared to control IR group (69±2% of AAR). Similarly, ex vivo administration of INF before the IR injury resulted in significant IS reduction (38±3% of AAR). Myocardial IR induced the NLRP3 inflammasome complex formation, which was attenuated by either INF pretreatment ex vivo, or by repeated oral treatment with Ticagrelor. The beneficial effects induced by either treatment were associated with the protective Reperfusion Injury Salvage Kinase (RISK) pathway activation and redox defence upregulation. In contrast, no protective effects nor NLRP3/RISK modulation were recorded when Ticagrelor was administered before ischemia in isolated heart, indicating that Ticagrelor direct target is not in the myocardium. Our results confirm that Ticagrelor conditioning effects are likely mediated through platelets, but are not additives to the ones achieved by directly inhibiting NLRP3

Histologic and Molecular Correlation in Shelter Cats with Acute Upper Respiratory Infection ▿

This is a descriptive study designed to correlate diagnostic real-time PCR results with histopathologic lesions in cats with clinical signs of upper respiratory infection (URI). The study occurred over a 9-month period in a single open-intake animal shelter. Cats that were selected for euthanasia by the shelter staff and additionally had URI were included in the study, for a total of 22 study cats. Combined conjunctival and oropharyngeal swab specimens were tested by quantitative real-time PCR (qPCR) for feline herpesvirus type 1 (FHV-1), feline calicivirus (FCV), Mycoplasma felis, Chlamydophila felis, and Bordetella bronchiseptica. Necropsy was performed on all cats, and a complete set of respiratory tract tissues was examined by histopathology. Among 22 cats, 20 were qPCR positive for FHV-1, 7 for M. felis, 5 for FCV, 1 for C. felis, and 0 for B. bronchiseptica. Nine cats were positive for two or more pathogens. Histopathologic lesions were present in all cats, with consistent lesions in the nasal cavity, including acute necroulcerative rhinitis in 16 cats. Histologic or antigenic detection of FHV-1 was seen in 18 of 20 cats positive for FHV-1 by qPCR. No lesions that could be specifically attributed to FCV, M. felis, or C. felis were seen, although interpretation in this cohort could be confounded by coinfection with FHV-1. A significant agreement was found between the amount of FHV-1 DNA determined by qPCR and the presence of specific histopathologic lesions for FHV-1 but not for the other respiratory pathogens