We prospectively compared healthcare worker-collected nasopharyngeal swabs (NPS) to self-collected anterior nasal swabs (ANS) and straight saliva for the diagnosis of COVID-19 in 354 patients. The positive percent agreement between NPS and ANS or saliva was 86.3% (95% CI: 76.7-92.9) and 93.8% (95% CI: 86.0-97.9), respectively. Negative percent agreement was 99.6% (95% CI: 98-100) for NPS vs. ANS and 97.8% (95% CI: 95.3 – 99.2) for NPS vs. saliva. NPS (n=80) and saliva (n=81) detected more cases than ANS (n=70), but no single specimen type detected all SARS-CoV-2 infections.

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Vascular dysfunction has been reported in human cases of anthrax, in mammalian models of Bacillus anthracis, and in animals injected with anthrax toxin proteins. To examine anthrax lethal toxin effects on intact blood vessels, we developed a zebrafish model that permits in vivo imaging and evaluation of vasculature and cardiovascular function. Vascular defects monitored in hundreds of embryos enabled us to define four stages of phenotypic progression leading to circulatory dysfunction. We demonstrated increased endothelial permeability as an early consequence of toxin action by tracking the extravasation of fluorescent microspheres in toxin-injected embryos. Lethal toxin did not induce a significant amount of cell death in embryonic tissues or blood vessels, as shown by staining with acridine orange, and endothelial cells in lethal toxin-injected embryos continued to divide at the normal rate. Vascular permeability is strongly affected by the VEGF/ vascular permeability factor (VPF) signaling pathway, and we were able to attenuate anthrax lethal toxin effects with chemical inhibitors of VEGFR function. Our study demonstrates the importance of vascular permeability in anthrax lethal toxin action and the need for further investigation of the cardiovascular component of human anthrax disease.endothelial ͉ vascular permeability ͉ VEGF

SummaryPseudomonas aeruginosa and other bacterial pathogens express one or more homologous extracellular phospholipases C (PLC) that are secreted through the inner membrane via the twin arginine translocase (TAT) pathway. Analysis of TAT mutants of P. aeruginosa uncovered a previously unidentified extracellular PLC that is secreted via the Sec pathway (PlcB). Whereas all presently known PLCs of P. aeruginosa (PlcH, PlcN and PlcB) hydrolyse phosphatidylcholine (PC), only PlcB is active on phosphatidylethanolamine (PE). plcB candidates were identified based on deductions made from bioinformatics data and extant DNA microarray data. Among these candidates, a gene (PA0026) required for the expression of an extracellular PE-PLC was identified. The protein encoded by PA0026 has limited, but significant similarity, over a short region ( ~ 60aa of 328), to a class of zinc-dependent prokaryotic PLCs. A conserved His residue of PlcB (His216) that is required for coordinate binding of zinc in this class of PLCs was mutated. Analysis of this mutant established that the protein encoded by PA0026 is PlcB. Three independent recently published reports indicate that homoserine lactone-mediated quorum sensing regulates the expression of PA0026 (i.e. plcB ). PlcB, but not PlcH or PlcN, is required for directed twitching motility up a gradient of certain kinds of phospholipids. This response shows specificity for the fatty acid moiety of the phospholipid.