Non Tuberculous Cutaneous Mycobacteriosis in a primary school in Rome: epidemiological and microbiological investigation.

During the school years 2009-2010 and 2010-2011 a total of 25 cases of Non Tuberculous Cutaneous Mycobacteriosis (NTCM) were notified in children attending the same school with a swimming pool in Rome. Environmental microbiological and epidemiological investigations (only for suspected outbreaks in 2009-2010) were conducted. We screened students with skin lesions, and environmental samples were collected from the school area and the swimming pool. During the school year 2009-10 18 cases were clinically identified among 514 primary school children (3.50%) and all cases attended the swimming pool. Only 2 out of 18 cultures were positive for Mycobacterium chelonae complex (Group III, M. abscessus). Attack Rate for swimming pool use was 13,10% (17/130), with a Relative Risk 54,70 (95% CI: 9,4 - ∞). In February 2011 additional 7 cases of cutaneous NTM among children - who attended the same primary school and swimming pool were notified to the local public health authority followed by environmental microbiological investigation. Environmental samples were positive for NTM but not for M. abscessus. Mycobacteria are not included in water-quality criteria in Italy for this reason it is important to collect evidences of NTM cases caused by these infrequent pathogens, to be able to perform rapid risk assessment and to identify the best practices in prevention and management of such a risk.

All-cause mortality in hospitalized patients with infectious diarrhea: Clostridium difficile versus other enteric pathogens in Austria from 2008 to 2010.

BACKGROUND: Clostridium difficile infection is the leading cause of gastroenteritis-associated deaths in the industrialized world, followed by infection with norovirus. METHODS: Using a cohort study design, we compared 90 inpatients with diarrhea due to C. difficile infection (CDI) with 180 inpatients with diarrhea due to other infectious agents (including 55% with norovirus infection) with respect to complications and all-cause mortality. The effects of age, severity of underlying diseases and additional infections were assessed by stratified analyses. RESULTS: Diarrhea recurrence occurred 8.9 (95%CI: 2.9-27.3) times more often in CDI independent of age and severity of comorbidities. The all-cause mortality in CDI patients pre-discharge and at 30 and 180 days, respectively, was 20.0%, 17.0% and 42.3% versus 7.2%, 6.7% and 22.5% in non-CDI diarrhea patients. Among those patients with low comorbidities, who were younger than 65 years and without additional infections, the all-cause pre-discharge, 30-day and 180-day mortality risks were significantly higher for the CDI diarrhea patients than the non-CDI diarrhea patients. This association was not observed among patients with an older age, more severe comorbidities or additional infections. CONCLUSION: CDI results in higher all-cause mortality than diarrhea due to other infectious agents in younger patients with low comorbidities.

The molecular archaeology of a mitochondrial death effector: AIF in Drosophila.

Apoptosis-inducing factor (AIF) is a phylogenetically conserved redox-active flavoprotein that contributes to cell death and oxidative phosphorylation in Saccharomyces cerevisiae, Caenorhabditis elegans, mouse and humans. AIF has been characterized as a caspase-independent death effector that is activated by its translocation from mitochondria to the cytosol and nucleus. Here, we report the molecular characterization of AIF in Drosophila melanogaster, a species in which most cell deaths occur in a caspase-dependent manner. Interestingly, knockout of zygotic D. melanogaster AIF (DmAIF) expression using gene targeting resulted in decreased embryonic cell death and the persistence of differentiated neuronal cells at late embryonic stages. Although knockout embryos hatch, they undergo growth arrest at early larval stages, accompanied by mitochondrial respiratory dysfunction. Transgenic expression of DmAIF misdirected to the extramitochondrial compartment (DeltaN-DmAIF), but not wild-type DmAIF, triggered ectopic caspase activation and cell death. DeltaN-DmAIF-induced death was not blocked by removal of caspase activator Dark or transgenic expression of baculoviral caspase inhibitor p35, but was partially inhibited by Diap1 overexpression. Knockdown studies revealed that DeltaN-DmAIF interacts genetically with the redox protein thioredoxin-2. In conclusion, we show that Drosophila AIF is a mitochondrial effector of cell death that plays roles in developmentally regulated cell death and normal mitochondrial function.