Gemella morbillorum as the Culprit Organism of Post-Colonoscopy Necrotizing Perineal Soft Tissue Infection in a Diabetic Patient With Crohn's Disease.

Gemellsa morbillorum (G. morbillorum) is a Gram-positive facultative anaerobe and a known commensal organism of the oropharyngeal and gastrointestinal tracts. It is considered a rare cause of infections in humans. Most of the documented infections, whereas G. morbillorum has been implicated as a causative pathogen, were infective endocarditis and deep visceral abscesses. However, there are only a handful of cases in the current literature that have reported G. morbillorum as the primary organism causing necrotizing soft tissue infections. The authors presented a rare case of post-colonoscopy necrotizing perineal soft tissue infections in an elderly patient with poorly controlled diabetes mellitus and Crohn's disease with G. morbillorum being the culprit pathogen of this necrotizing infection. The reported case raises concerns for this commensal organism as an emerging virulent pathogen in certain high-risk patients. The authors proposed that a combination of the long-standing Crohn's disease and the recent colonoscopy with rectal polypectomy has predisposed the patient to G. morbillorum bacteremia with perineal sepsis in the setting of diabetic immunosuppression. Further studies are warranted to ascertain whether G. morbillorum is acquiring increased virulence that would have enabled this organism to cause novel soft tissue infections.

Tissue-dependent effects of cis-9,trans-11- and trans-10,cis-12-CLA isomers on glucose and lipid metabolism in adult male mice.

Mixtures of the two major conjugated linoleic acid (CLA) isomers trans-10,cis-12-CLA and cis-9,trans-11-CLA are used as over the counter supplements for weight loss. Because of the reported adverse effects of CLA on insulin sensitivity in some mouse studies, we sought to compare the impact of dietary t10c12-CLA and c9t11-CLA on liver, adipose tissue, and systemic metabolism of adult lean mice. We fed 8 week-old C57Bl/6J male mice with low fat diets (10.5% Kcal from fat) containing 0.8% t10c12-CLA or c9t11-CLA for 9 or 38 days. Diets containing c9t11-CLA had minimal impact on the endpoints studied. However, 7 days after starting the t10c12-CLA diet, we observed a dramatic reduction in fat mass measured by NMR spectroscopy, which interestingly rebounded by 38 days. This rebound was apparently due to a massive accumulation of lipids in the liver, because adipose tissue depots were visually undetectable. Hepatic steatosis and the disappearance of adipose tissue after t10c12-CLA feeding was associated with elevated plasma insulin levels and insulin resistance, compared to mice fed a control diet or c9t11-CLA diet. Unexpectedly, despite being insulin resistant, mice fed t10c12-CLA had normal levels of blood glucose, without signs of impaired glucose clearance. Hepatic gene expression and fatty acid composition suggested enhanced hepatic de novo lipogenesis without an increase in expression of gluconeogenic genes. These data indicate that dietary t10c12-CLA may alter hepatic glucose and lipid metabolism indirectly, in response to the loss of adipose tissue in mice fed a low fat diet.