Pyoderma Gangrenosum after Fat Grafting in Alloplastic Breast Reconstruction: An Unusual Outcome.

Pyoderma gangrenosum (PG) is a rare and painful inflammatory skin disorder that has been recently associated with breast surgery. It is commonly mistaken for postoperative ischemia or wound infection and does not show response to antibiotics or debridement. We describe the first case of post-surgical PG (PSPG) after alloplastic breast reconstruction involving fat grafting. A 47-year-old woman underwent bilateral mastectomy and 2-stage alloplastic breast reconstruction, with fat grafting from the abdomen. Two days post-surgery, she developed bilateral erythema with tender grouped pustules that progressed rapidly into necrotic ulcerations. She did not respond to antibiotics and serial debridement. Subsequent biopsy confirmed a diagnosis of PG. She was started on steroid therapy and responded well. She was discharged on a steroid regimen, local wound care, and eventually a T-cell inhibitor. Over the next 12 months, her wounds healed without surgical intervention. PSPG has been observed in a variety of reconstructive breast surgeries, but never reported in the setting of fat grafting. As PG involves subcutaneous fat, fat grafting may accelerate and exacerbate the course of disease. Treatment for PSPG includes systemic steroid therapy or other immunomodulatory agents (or both). Surgical management remains controversial, as serial debridement and reconstruction have shown to exacerbate and stimulate disease progression. A long-term follow-up is recommended to monitor for wound healing. Delayed diagnosis of PG in breast reconstruction patients can lead to severe morbidity and disfigurement. This is first case of PSPG following fat grafting in the literature

The Teaching Leader Series: Interprofessional Faculty Development Update

Seminar (24 PowerPoint slides) Purpose: The mission of the Teaching Leader Series is to strengthen teaching, learning and assessment skills by providing opportunities and support for faculty to achieve educational excellence, promote interdisciplinary collaboration and encourage instructional innovation. Background: The Series is based on the assumption that an inclusive strategy would help ensure sustainability and that unique learning experiences occur when two or more professions together learned with, from, and about each other’s teaching practice. Since the Series began in 2008 over 20 different topics have been presented including Adult Learning, Curriculum Development, Narrative Medicine, and Teaching with Simulation and Standardized Patients. Description of Intervention or Program: We recognize individuals who have made the Series a part of their educational process and their development as teaching leaders with a pin. In order to receive a pin, participants must attend at least 6 workshops, prepare a report describing how they have applied information from the workshop and must agree to participate in a best practice focus group. Our goal is to have these individuals team teach a workshop with a current presenter who serves as their mentor. Results: The Series demographics are 50% nurses, 25% physicians, and 25% other educators. At the conclusion of each workshop, participants are asked to complete a self-retrospective evaluation. During AY 2011 92% of participants agreed that they would be able to apply what they learned to their job. Pin recipients (physician, pharmacists, nurse) have presented Teaching at the Bedside and Small Group Teaching with a PhD medical educator mentor. Relevance to interprofessional education or practice: Healthcare is practiced in teams and the Series models the importance and effectiveness of interprofessional learning and teaching. Not only are the participants from different disciplines, we also pair presenters from different disciplines. Learning Objectives: Upon completion of this session the participants will be able to Identify the effectiveness of providing interprofessional faculty development. Identify how interprofessional faculty development facilitates collaboration of clinical educators across traditional boundaries. Identify strategies used to integrate interprofessional education into faculty development

Crystal Structures of Cif from Bacterial Pathogens Photorhabdus luminescens and Burkholderia pseudomallei

A pre-requisite for bacterial pathogenesis is the successful interaction of a pathogen with a host. One mechanism used by a broad range of Gram negative bacterial pathogens is to deliver effector proteins directly into host cells through a dedicated type III secretion system where they modulate host cell function. The cycle inhibiting factor (Cif) family of effector proteins, identified in a growing number of pathogens that harbour functional type III secretion systems and have a wide host range, arrest the eukaryotic cell cycle. Here, the crystal structures of Cifs from the insect pathogen/nematode symbiont Photorhabdus luminescens (a γ-proteobacterium) and human pathogen Burkholderia pseudomallei (a β-proteobacterium) are presented. Both of these proteins adopt an overall fold similar to the papain sub-family of cysteine proteases, as originally identified in the structure of a truncated form of Cif from Enteropathogenic E. coli (EPEC), despite sharing only limited sequence identity. The structure of an N-terminal region, referred to here as the ‘tail-domain’ (absent in the EPEC Cif structure), suggests a surface likely to be involved in host-cell substrate recognition. The conformation of the Cys-His-Gln catalytic triad is retained, and the essential cysteine is exposed to solvent and addressable by small molecule reagents. These structures and biochemical work contribute to the rapidly expanding literature on Cifs, and direct further studies to better understand the molecular details of the activity of these proteins

Lumbar vertebral osteomyelitis with mycotic abdominal aortic aneurysm caused by highly penicillin-resistant Streptococcus pneumoniae.

We present a case of vertebral osteomyelitis with an adjacent abdominal aortic mycotic aneurysm caused by a highly penicillin-resistant Streptococcus pneumoniae strain. The occurrence of all three phenomena in a single patient has not been previously described. This presentation offers the opportunity to reflect on the increasing incidence of S. pneumoniae as a resistant pathogen, the treatment of highly penicillin-resistant S. pneumoniae, and the etiologic agents of both vertebral osteomyelitis and mycotic aneurysm

The RovA regulons of Yersinia enterocolitica and Yersinia pestis are distinct: evidence that many RovA-regulated genes were acquired more recently than the core genome.

RovA is a transcriptional activator of Yersinia invasin, an outer membrane protein involved in bacterial attachment and invasion across the intestinal epithelium. In Y. enterocolitica, a rovA mutant is attenuated for virulence compared with either wild-type or inv mutant strains, indicating that RovA may regulate additional virulence factors. Here, we used microarray analysis to define the RovA regulon. Curiously, there was little overlap between the RovA regulons of Y. enterocolitica and Y. pestis despite the fact that RovA itself is highly conserved between the two species. Some of these differences are explained by the observation that a number of RovA-regulated loci in Y. enterocolitica do not have orthologues in Y. pestis and vice versa, suggesting that RovA established regulatory control over genetic material acquired after the divergence of the species. Electromobility shift assays demonstrated that 15 of these RovA-regulated loci directly interact with RovA, and 11 of these promoters had similar affinity as observed for the inv promoter. H-NS and YmoA are believed to form a transcriptional repression complex on the inv promoter, and several studies indicate that RovA and H-NS have overlapping DNA binding sites. H-NS and YmoA regulated a subset of the RovA-regulated loci. Furthermore, H-NS directly bound to 14 of the 15 promoters bound by RovA. From these data, we hypothesize that RovA generally behaves as an anti-H-NS factor to alleviate transcriptional repression in Y. enterocolitica. A number of recent studies have presented data and a model suggesting that H-NS functions as a transcriptional silencer of horizontally acquired genes. This repression can be selectively relieved by regulators such as RovA, and the observation that nearly all RovA-activated genes are repressed by H-NS is consistent with this model