Outbreak of bacterial endocarditis associated with an oral surgery practice: New Jersey public health surveillance, 2013 to 2014.

BACKGROUND: In October and November 2014, the New Jersey Department of Health received reports of 3 patients who developed Enterococcus faecalis endocarditis after undergoing surgical procedures at the same oral surgery practice in New Jersey. Bacterial endocarditis is an uncommon but life-threatening condition; 3 patients with enterococcal endocarditis associated with a single oral surgery practice is unusual. An investigation was initiated because of the potential ongoing public health risk. METHODS: Public health officials conducted retrospective surveillance to identify additional patients with endocarditis associated with the practice. They interviewed patients using a standardized questionnaire. An investigative public health team inspected the office environment, interviewed staff, and reviewed medical records. RESULTS: Public health officials identified 15 confirmed patients with enterococcal endocarditis of those patients who underwent procedures from December 2012 through August 2014. Among these patients, 12 (80%) underwent cardiac surgery. One (7%) patient died from complications of endocarditis and subsequent cardiac surgery. Breaches of recommended infection prevention practices were identified that might have resulted in transmission of enterococci during the administration of intravenous sedation, including failure to perform hand hygiene and failure to maintain aseptic technique when performing procedures and handling medications. CONCLUSIONS: This investigation highlights the importance of adhering to infection prevention recommendations in dental care settings. No additional patients with endocarditis were identified after infection prevention and control recommendations were implemented. PRACTICAL IMPLICATIONS: Infection prevention training should be emphasized at all levels of professional dental training. All dental health care personnel establishing intravenous treatment and administering intravenous medications should be trained in safe injection practices.

PPARdelta modulates lipopolysaccharide-induced TNFalpha inflammation signaling in cultured cardiomyocytes.

Peroxisome proliferator activated receptors (PPARs: PPARalpha, gamma and delta) regulate fatty acid metabolism, glucose homeostasis, cell proliferation, differentiation and inflammation. Tumor necrosis factor alpha (TNFalpha) is one of the important pathological factors in inflammatory responses during the pathological progression of myocardial ischemic/reperfusion and hypertrophy. Accumulating evidence shows that synthetic ligands of PPARalpha and PPARgamma suppress myocardial inflammatory responses, such as the production of TNFalpha, thus exerting beneficial effects in animals who had undergone ischemia/reperfusion injury or cardiac hypertrophy. However, it remains obscured if PPARdelta and its ligands exert any effect on the production of TNFalpha, thus influencing cardiac inflammatory responses. In this study, we investigated the effects of PPARdelta and its synthetic ligand GW0742 on TNFalpha production in cultured cardiomyocytes. Our studies indicate that a PPARdelta-selective ligand inhibited lipopolysaccharide (LPS)-induced TNFalpha production from cardiomyocytes. Adenoviral-mediated overexpression of PPARdelta substantially inhibited TNFalpha expression in cultured cardiomyocytes compared to controls, whereas overexpression of a PPARdelta mutant with ablated ligand binding domain did not show similar effect. Conversely, absence of PPARdelta in cardiomyocytes further exaggerated LPS-induced TNFalpha production. Moreover, activation of PPARdelta abrogated LPS-induced degradation of IkappaBs, thus suppressing LPS-induced nuclear factor kappaB (NF-kappaB) activities. Therefore, PPARdelta is an important determinant of TNFalpha expression via the NF-kappaB signaling pathway, thus serving as therapeutic targets to attenuate inflammation that are involved in cardiac pathological progression.