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In the third season (2002) of the West Nile virus epidemic in the United States, two canids (wolf and dog) were diagnosed with West Nile virus encephalitis and myocarditis with [...]

Research has been conducted on Escherichia coli filamentous prophage. Results demonstrate that this prophage can be integrated into the chromosomal homologue of Escherichia coli O18:K1:H7 high-virulence clone.

Evidence supports a pathogenic role of arachidonic acid - derived inflammatory mediators within the gastrointestinal tract of patients with inflammatory bowel disease. The purpose of this study was to assess the effects of an ulcerative colitis nutritional formula (UCNF) containing oligosaccharides, fish oil, gum arabic and antioxidants on plasma and colonic phospholipid fatty acid and prostaglandin profiles in pigs. Twenty-four growing barrows in two replications were equally randomized among four killing times (d 0, 7, 14 and 21), and one of two diets, a control and the UCNF. Diets contained comparable levels of protein, fat, and nonstructural carbohydrate and met 100% of the energy requirements of the pig. Intake and body weight were recorded daily while blood, urine and tissue samples were collected at time of kill. Within 1 wk of ingestion of the UCNF, the composition of plasma phospholipid fatty acids showed an increase in 20:5(n-3) and 22:6(n-3) (P < 0.0001) and a decrease in 20:4(n-6) and 18:2(n-6) (P < 0.0001). Similar effects were observed for the phospholipids in the colonic and cecal mucosa. Plasma prostaglandin E was unaffected by treatment, whereas thromboxane [B.sub.2] and 6-ketoprostaglandin [F.sub.1[Alpha]] levels were significantly decreased after 7 d of UCNF ingestion. Ingestion of the UCNF resulted in a suppression in the synthesis of proinflammatory prostaglandins by cecal and colonic mucosal cells. Levels of colonic and cecal prostaglandin E, 6-ketoprostaglandin [F.sub.1[Alpha]] and thromboxane [B.sub.2] were significantly decreased after 7 d of UCNF ingestion. These changes may have been mediated by rapid increases of (n-3) fatty acids into cellular phospholipids. Dietary supplementation with the UCNF may prove beneficial for patients with ulcerative colitis by modulating colonic prostaglandin synthesis. J. Nutr. 127: 137-145, 1997. KEY WORDS: fish oil oligosaccharides pigs inflammatory bowel disease ulcerative colitis

Most microorganisms do not produce sialic acid (sialate), andthose that do appear to use a biosynthetic mechanism distinct frommammals. Genetic hybrids of nonpathogenic, sialate-negative laboratory Escherichia coli K-12 strains designed for the de novo synthesis of the polysialic acid capsulefrom E. coli K1 proved useful in elucidating the geneticsand biochemistry of capsule biosynthesis. In this article we proposea dynamic model of sialometabolism to investigate the effects ofbiosynthetic neu (N-acetylneuraminicacid) and catabolic nan (N-acylneuraminate) mutationson the flux of intermediates through the sialate synthetic pathway.Intracellular sialate concentrations were determined by high pHanion exchange chromatography with pulsed amperometric detection.The results indicated that a strain carrying a null defect in thegene encoding polysialyltransferase (neuS) accumulated > 50times more CMP–sialic acid than the wild type when strainswere grown in a minimal medium supplemented with glucose and casaminoacids. Metabolic accumulation of CMP–sialic acid dependedon a functional sialic acid synthase (neuB), as shownby the inability of a strain lacking this enzyme to accumulate adetectable endogenous sialate pool. The neuB mutantconcentrated trace sialate from the medium, indicating its potentialvalue for quantitative analysis of free sialic acids in complexbiological samples. The function of the sialate aldolase (encodedby nanA) in limiting intermediate flux throughthe synthetic pathway was determined by analyzing free sialate accumulationin neuA (CMP–sialic acid synthetase) nanA double mutants. The combined results demonstratehow E. coli avoids a futile cycle in which biosyntheticsialate induces the system for its own degradation and indicatethe feasibility of generating sialooligosaccharide precursors throughtargeted manipulation of sialate metabolism. [ABSTRACT FROM PUBLISHER]

The article focuses on the case of pharyngeal-laryngeal blastomycosis in a 6-year-old, male black Labrador retriever dog. Based on history, signalment and clinical presentation, a tentative diagnosis of laryngeal paralysis was made. In order to relieve the upper airway obstruction, a permanent tracheostomy was performed. The drug prescribed following the operation was itraconazole.