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For genetically monomorphic bacteria, current typing methods often prove inadequate for outbreak detection, trace back, and identification of transmission routes. Some of these bacteria, such as Salmonella enterica serovar Enteritidis, [...]

In a series of 116 Salmonella enterica Newport isolates that included 64 multidrug-resistant (MDR) isolates, automated ribotyping and pulsed-field gel electrophoresis (PFGE) discriminated MDR S. Newport with a sensitivity of [...]

The Oregon Health Authority routinely investigates clusters of reportable enteric diseases identified by whole-genome sequencing. While investigating 2 cases of Escherichia coli O157:H7 in 2019, in which both patients were exposed to the same home-processed "jerky" and clinical isolates matched within 2 single nucleotide polymorphisms (SNPs), we discovered, by searching the National Library of Medicine's National Center for Biotechnology Information website, 3 other cases of E coli O157:H7 from 3 Oregon counties—Tillamook, Umatilla, and Douglas—whose clinical isolates were within 9 SNPs of the 2 initial matched cases. We analyzed interview data for 3 case patients and followed up with additional hypothesis-generating questions. Onset of illness for the Tillamook, Umatilla, and Douglas county cases were October 7, 2017, October 27, 2017, and April 30, 2018, respectively. The median age of the 5 case patients was 16 years. Parents of 2 of the 5 case patients, each from a different county, had harvested deer approximately 20 miles from each other in the same Douglas County wildlife hunting unit in late September 2017. The case from Umatilla County was lost to follow-up. Although it is well documented that deer are a viable and substantial reservoir of E coli O157:H7, to our knowledge, this is the first time that venison from a common wildlife hunting unit was found to be associated with a cluster of illnesses. This finding suggests a geographic nidus for E coli O157:H7. We recommend routinely asking about wildlife hunting units when developing exposure hypotheses involving potential venison-associated clusters. [ABSTRACT FROM AUTHOR]

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Pyruvate (PYR) improves cellular and organ function hypoxia and ischemia by stabilizing the reduced nicotinamide adenine dinucleotide redox state and cytosolic ATP phosphorylation potential. In this in vivo study, we evaluated the effects of intravenous pyruvate on neocortical function, indexes of the cytosolic redox state, cellular energy state, and ischemia during a prolonged (4 h) controlled arterial hemorrhage (40 mmHg) in swine. Thirty minutes after the onset of hemorrhagic shock, sodium PYR (n = 8) was infused (0.5 g [multiplied by] [kg.sup.-1] [multiplied by] [h.sup.-1)] to attain arterial levels of 5 mM. The volume and osmotic effects were matched with 10% NaCl [hypertonic saline (HTS)] (n = 8) or 0.9% NaCl [normal saline (NS)] (n = 8). During the hemorrhage protocol, the time to peak hemorrhage volume was significantly delayed in the PYR group compared with the HTS and NS groups (94 [+ or -] 5 vs. 73 [+ or -] 6 and 72 [+ or -] 4 min, P [is less than] 0.05). In addition to the early onset of the decompensatory phase of hemorrhagic shock, the complete return of the hemorrhage volume during decompensatory shock resulted in the death of five and four animals, respectively, in the HTS and NS groups. In contrast, in the PYR group, reinfusion of the hemorrhage volume was slower and all animals survived the 4-h hemorrhage protocol. During hemorrhage, the PYR group also exhibited improved cerebral cortical metabolic and function status. PYR slowed and reduced the rise in neo-cortical microdialysis levels of adenosine, inosine, and hypoxanthine and delayed the loss of cerebral cortical biopsy ATP and phosphocreatine content. This improvement in energetic status was evident in the improved preservation of the electrocorticogram in the PYR group. PYR also prevented the eightfold increase in the excitotoxic amino acid glutamate observed in the HTS group. The findings show that PYR administered after the onset of hemorrhagic shock markedly improves cerebral metabolic and functional status for at least 4 h. microdialysis; glutamate; pyruvic acid

Mongan, Paul D., John L. Fontana, Rouyan Chen, and Rolf Bringer. Intravenous pyruvate prolongs survival during hemorrhagic shock in swine. Am. J. Physiol. 277 (Heart Circ. Physiol. 46): H2253-H2263, 1999.--Pyruvate improves cellular and organ function during hypoxia and ischemia and stabilizes the NADH redox state and cytosolic ATP phosphorylation potential. In this in vivo study, we evaluated the effects of intravenous pyruvate on cardiovascular and neocortical function, indexes of the cytosolic redox state (lactate/pyruvate ratio, LfP) and cellular energy state (adenosine and degradative products hypoxanthine and inosine, ADO + HX + Ino) during controlled arterial hemorrhage (40 mmHg) in sedated swine (45 kg). [Na.sup.+] pyruvate was infused i h before (1 g [multiplied by] [kg.sup.-1] [multiplied by] [h.sup.-1]) and 2 h during (0.5 g [multiplied by] [kg.sup.-1] [multiplied by] [h.sup.-1]) hemorrhage to attain arterial pyruvate levels of 6 mM. Volume (0.9% NaCl) and osmotic (10% NaCl) effects were matched in controls. Time to peak hemorrhage (57 min) and peak hemorrhage volume (43 ml/kg) were similar in all groups. The volume and osmotic groups experienced spontaneous cardiovascular decompensation between 60 and 90 min, with an average time until death of 82.7 [+ or -] 5.5 and 74.8 [+ or -] 8.2 min. In contrast, survival in the pyruvate group was 151.2 [+ or -] 10.0 min (P [is less than] 0.001). During hemorrhage, the pyruvate group had better cardiovascular and cerebrovascular function with significantly higher systemic and cerebral oxygen consumption and less attenuation of the amplitude and frequency of the electrocorticogram. In addition, pyruvate prevented metabolic acidosis and stabilized the L/P. Pyruvate slowed the rise in neocortical microdialysis levels of ADO + HX + Ino, and prevented the net efflux of ADO + HX + Ino into the sagittal sinus. The findings reveal considerable metabolic and functional enhancement by pyruvate during severe hemorrhagic shock with a 75-min delay in spontaneous cardiovascular decompensation and death. ischemia tolerance; microdialysis; cerebral blood flow; cardiovascular decompensation