Medical management of esophageal food impaction refractory to endoscopic interventions.

Most esophageal food impactions either pass spontaneously or are treated endoscopically. Severe food impactions can require extensive endoscopic therapy that potentially could lead to procedure-related complications. There are few alternate therapies available when endoscopy fails. Traditionally, pharmacologic therapy with glucagon has been performed with varying success. This case report and discussion will outline the management of a complete food impaction and medical therapies available when first-line endoscopic treatment fails. We present a case in which the endoscopic intervention for esophageal food bolus impaction was unsuccessful.

A Rare Report of Infectious Emphysematous Aortitis Secondary to Clostridium septicum without Prior Vascular Intervention.

The term "mycotic aneurysm" was first used by Osler in 1882 to describe a mushroom-shaped aneurysm in subacute bacterial endocarditis. Mycotic aneurysms account for only 2.6% of all aneurysms of the aorta. Rarer still are anaerobic infections secondary to organisms such as Clostridium septicum, which results in emphysematous aortitis. The vast majority of emphysematous aortic infections occur as a result of instrumentation; however, in this case we present an infection de novo. A 75-year-old male presented with a 2-week history of progressive fatigue and chest pain that then developed into constitutional symptoms. Chest radiograph demonstrated an obvious widened mediastinum. CT angiogram of his chest then confirmed this finding as well as significant periaortic gas and focal outpouching. Numerous diverticuli with inflammatory changes consistent with diverticulitis was observed on CT abdomen. Blood cultures returned positive for Clostridium septicum. Definitive treatment was discussed including debridement and graft insertion; however, patient decided on conservative management and was discharged on intravenous antibiotics. Unfortunately, as in most cases of emphysematous aortitis that do not undergo surgical management, the patient succumbed to his illness. The lesson provided will be the epidemiology of emphysematous aortitis, presentation, diagnosis, management, and prognosis through a case report.

The bacterial virulence factor NleA inhibits cellular protein secretion by disrupting mammalian COPII function.

Enterohemorrhagic and enteropathogenic Escherichia coli (EHEC and EPEC) maintain an extracellular lifestyle and use a type III secretion system to translocate effector proteins into the host cytosol. These effectors manipulate host pathways to favor bacterial replication and survival. NleA is an EHEC/EPEC- and related species-specific translocated effector protein that is essential for bacterial virulence. However, the mechanism by which NleA impacts virulence remains undetermined. Here we demonstrate that NleA compromises the Sec23/24 complex, a component of the mammalian COPII protein coat that shapes intracellular protein transport vesicles, by directly binding Sec24. Expression of an NleA-GFP fusion protein reduces the efficiency of cellular secretion by 50%, and secretion is inhibited in EPEC-infected cells. Direct biochemical experiments show that NleA inhibits COPII-dependent protein export from the endoplasmic reticulum. Collectively, these findings indicate that disruption of COPII function in host cells contributes to the virulence of EPEC and EHEC.