Feline Emphysematous Gastritis in a Cat with Pancreatitis and Secondary Hepatic Lipidosis.

A 7 yr old female neutered domestic shorthair was presented with a 2 mo history of lethargy and hyporexia progressing to anorexia. Initial diagnostics indicated pancreatitis with secondary hepatic lipidosis. Supportive care, including the placement of an esophageal feeding tube, was initiated. The feeding tube was removed traumatically by the cat and thus replaced. The cat acutely deteriorated while hospitalized, developing marked hypersalivation and an obtunded mentation. Radiographs were taken to confirm placement of the feeding tube in case tube dislodgement was contributing to the hypersalivation; results confirmed appropriate positioning and gastric pneumatosis. Despite intensified medical management, the patient suffered cardiopulmonary arrest 7 days after hospital admission. Post-mortem examination confirmed necrotizing gastritis with emphysema alongside segmental mucosal necrosis in the jejunum, focal pancreatic necrosis, and diffuse hepatic lipidosis. Gas in the gastric wall is a rare finding in veterinary medicine and can arise due to gastric pneumatosis or emphysematous gastritis; there are scant reports of either in feline medicine. This report documents a case of emphysematous gastritis in a cat with concurrent pancreatitis and hepatic lipidosis. The cat developed emphysematous gastritis without undergoing gastrointestinal surgery which is currently the only reported feline predis-posing factor for development.

Long-range dispersal moved Francisella tularensis into Western Europe from the East.

For many infections transmitting to humans from reservoirs in nature, disease dispersal patterns over space and time are largely unknown. Here, a reversed genomics approach helped us understand disease dispersal and yielded insight into evolution and biological properties of Francisella tularensis, the bacterium causing tularemia. We whole-genome sequenced 67 strains and characterized by single-nucleotide polymorphism assays 138 strains, collected from individuals infected 1947-2012 across Western Europe. We used the data for phylogenetic, population genetic and geographical network analyses. All strains (n=205) belonged to a monophyletic population of recent ancestry not found outside Western Europe. Most strains (n=195) throughout the study area were assigned to a star-like phylogenetic pattern indicating that colonization of Western Europe occurred via clonal expansion. In the East of the study area, strains were more diverse, consistent with a founder population spreading from east to west. The relationship of genetic and geographic distance within the F. tularensis population was complex and indicated multiple long-distance dispersal events. Mutation rate estimates based on year of isolation indicated null rates; in outbreak hotspots only, there was a rate of 0.4 mutations/genome/year. Patterns of nucleotide substitution showed marked AT mutational bias suggestive of genetic drift. These results demonstrate that tularemia has moved from east to west in Europe and that F. tularensis has a biology characterized by long-range geographical dispersal events and mostly slow, but variable, replication rates. The results indicate that mutation-driven evolution, a resting survival phase, genetic drift and long-distance geographical dispersal events have interacted to generate genetic diversity within this species.