Raoultella ornithinolytica is an encapsulated Gram-negative, oxidase-negative, catalase-positive, aerobic, non-motile rod that belongs to the Enterobacteriaceae family. This bacterium was initially classified in the genus Klebsiella as Klebsiella ornithinolytica, until the creation of the genus Raoultella in 2001. R. ornithinolytica is usually found in water environments and soil, and due to its ability to convert histidine to histamine, it has been associated with histamine poisoning in humans. R. ornithinolytica is an emerging entity in human infections, with several reports of virulent infections in comorbid at-risk patients. Increasing reports are potentially due to better and more precise identification tools. The objective of this article is to provide a comprehensive review of reported cases of R. ornithinolytica infections, the emergent virulence of described multiresistant strains, and an overview of currently used identification methods.

Background Nonmyeloablative (NMA) stem cell transplant (HSCT) regimens have expanded in the past decade, but little data exists to support antiviral prophylaxis to prevent zoster in recipients seropositive for varicella-zoster virus in this population. The objectives of this study were to describe the clinical features, incidence and risk factors for herpes zoster (HZ) in a homogeneous cohort of NMA allogeneic HSCT recipients. Methods Retrospective cohort study assessing all patients undergoing sibling NMA HSCT at Hôpital Maisonneuve-Rosemont (Montréal, Canada) between 7/2000-12/2008. All patients transplanted received the same conditioning regimen, immunoprophylaxis and graft-versus-host therapy. Herpes zoster diagnosis was defined clinically. Factors associated with HZ occurrence were identified using a Cox proportional hazards model. Results A total of 179 patients were followed for 33 months (median, IQR: 21-59). Zoster developed in 66 patients (37%) at a median of 8.3 months post-HSCT; the incidence rate was 175 cases/1,000 person-years. Estimated cumulative HZ incidence was 27, 36, and 44% at 1, 2, and 3 years respectively. Thoracic dermatomes were most frequently involved (30%); dissemination occurred in 5 patients. No death resulted from HZ, but 23% developed post-herpetic neuralgia. In multivariate analysis, CMV and HSV reactivations were associated with a reduced likelihood of HZ (hazard ratios=0.54 and 0.33, respectively). Conclusion The incidence of HZ in our cohort of NMA allogeneic transplant recipients is similar to the incidence reported following myeloablative regimens. Antiviral prophylaxis or treatment for CMV and HSV reactivations were protective against HZ. Given the observed high risk, we conclude that recommendations for antiviral prophylaxis should also apply, at least for the first year, to the NMA HSCT population.

We aimed to develop a risk model, based on single-nucleotide polymorphism (SNP) markers associated with an increased risk of organ-specific GVHD in 394 transplant pairs. A total of 259 SNPs were genotyped in 53 genes and evaluated for their associated risk of organ-specific GVHD. Risk models were generated using both clinical factors and genetic SNP markers. Patients were stratified by quartiles according to their risk scores and then categorized into three groups (low, intermediate and high risk) according to this model. We compared the risk of overall and organ-specific GVHD amongst these groups. Several SNP markers in the cytokine-, apoptosis-, TGF-b-and PDGF-mediated pathways were identified as correlative markers of acute and chronic GVHD. Each organspecific GVHD shared some common biologic pathway such as cytokine, TGF-b-or PDGF-mediated pathways. However, we also identified different SNP markers that correlated with increased risk of organ-specific GVHD (for example, FCGR2A SNP for oral GVHD, and FAS and TGFB1 SNP for lung GVHD). The incorporation of genetic risk factors into the clinical factors risk model improved stratification power for organ-specific GVHD. The SNP-based approach was suggested to improve risk stratification of organ-specific GVHD.

Raoultella ornithinolytica and Raoultella planticola are histamine-producing bacteria that are usually found in fish and water. They are associated with scombroid syndrome that presents with vomiting and flushing. A wide range of infections with these germs is reported, but mainly in fragile hospitalized patients with multiple comorbidities. We report the case of a 54-year-old healthy patient who presented with 24-hours abdominal pain, vomiting, flushing and shock. The abdominal examination showed guarding in the right lower quadrant (RLQ), and the abdominal CT scan images showed a thickened terminal ileum and a distended appendix. The patient underwent a surgical exploration revealing a normal terminal ileum but an inflamed appendicular base. Raoultella ornithinolytica was found in blood cultures and in the liquid retrieved from the RLQ. To the best of our knowledge, this is the first report of a severe life-threatening intra-abdominal presentation due to a community-acquired R. ornithinolytica infection.

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To determine the profile for risk of disease relapse following definitive radiation therapy/chemotherapy (RT/CRT) in human papillomavirus-unrelated (HPV[-]) oropharyngeal cancer (OPC) patients (pts). Materials/Methods: All newly diagnosed p16-confirmed HPV(-) OPC pts treated with RT/CRT from 2000 to 2012 were included. Overall survival (OS), relapse-free survival (RFS), locoregional control (LRC), distant control (DC), and grade 3e4 late toxicity (LT) were estimated using Kaplan-Meier or competing risk method. Multivariable analysis (MVA) identified predictors for RFS. Recursive partitioning analysis (RPA) derived low and high RFS risk groups. Results: A total of 314 HPV(e) (stage I, II, III, and IV: 13, 39, 51, and 211) pts were identified, including 231 (74%) males with median age of 65 years (range, 33e89 years). Primary tumors originated from tonsil or tongue base in 230 (73%) cases. Two hundred and ten (67%) cases were treated with RT alone, 87 (28%) with concurrent cisplatin (100 mg/m 2 x 3 on days 1, 22, and 43), and 17 (5%) with cetuximab. Median follow-up was 3.9 years. Relapse occurred in 112 cases (57 locoregional only, 33 distant only, 22 locoregional-distant). At 5 years, OS, RFS, LRC, DC, and LT were 45%, 64%, 74%, 83%, and 25%, respectively. MVA identified the N2be3 category as a predictor for disease relapse (hazard ratio [HR] 2.6 95% CI: 1.7e4.1, P < .01); age (HR Z 1.03, P Z .06), T3e4 (HR Z 1.4, P Z .09), and RT alone (HR Z 1.4, P Z .13) were marginally predictive; smoking pack-years was nonpredictive (P Z .94). RPA stratified the entire cohort into low (T1e2N0e2a, n Z 77) and high (T3e4 or N2be3, n Z 237) relapse risk groups with 5-year RFS of 86% and 56%, respectively. In the low-risk group, 74 of 77 (96%) pts received RT alone, and their 5-year RFS was 86% (95% CI: 74e92). For the highrisk group, the RT alone (n Z 136) subgroup had a lower RFS compared to the CRT (n Z 84) or RT + cetuximab (n Z 17) subgroups (51% vs 63%, P Z .03). Conclusion: Locoregional failure is the main form of treatment failure for the HPV(e) OPC population. A low-relapse-risk subgroup, defined as T1eT2N0eN2a, may be appropriately treated with RT alone. Highrelapse-risk HPV(-) OPC pts have a poor prognosis, and while intensified treatment schedules (e.g., high dose cisplatin) appear to suggest benefit in this subgroup, further research on novel treatment strategies is warranted.