We report the primary sequence analyses of two loci, hel and ccl, whose gene products are required specifically for the biogenesis of c-type cytochromes in the Gram-negative photosynthetic bacterium Rhodobacter capsulatus. Genetic and molecular analyses show that the hel locus contains at least four genes, helA, helB, helC, and orf52, and the ccl locus contains two genes, cell and ccl2, that are essential for cytochromes c biogenesis. HelA is homologous to a class of proteins called ABC transporters and helA, belB, and helC are proposed to encode an export complex. Cytochrome C2-alkaline phosphatase gene fusions were used to show that apocytochrome C2 synthesis and secretion are not affected by the hel and ccl defects. Cell and Ccl2 possess typical signal sequences to direct them to the periplasm. The periplasmic orientation of Cell was confirmed using a CcU-alkaline phosphatase gene fusion. The CcU-alkaline phosphatase gene fusion analysis also demonstrated that Cell does not require hel genes for its synthesis and secretion. Cell is homologous to proteins encoded by chloroplast and mitochondrial genes, suggesting analogous functions in these organelles. Taken together, these results support the hypothesis that the hel-encoded proteins are required for the export of heme to the periplasm where it is subsequently ligated to the c-type apocytochromes.

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Introduction: Several risk stratification tools are available to predict short-term mortality in patients with acute pulmonary embolism (PE). The presence of ventricular (RV) dysfunction is an independent predictor of mortality and may be a more efficient way to stratify risk for patients assessed by a Pulmonary Embolism Response Team (PERT). Methods:We evaluated 571 patients presenting with acute PE, then stratified them by the Pulmonary Embolism Severity Index (PESI), by the BOVA score, or categorically as low risk (no RV dysfunction by imaging), intermediate risk (RV dysfunction by imaging), or high risk PE (RV dysfunction with sustained hypotension). Using imaging data to firstly define the presence of RV strain, and plasma cardiac biomarkers as additional evidence for myocardial dysfunction, we evaluated whether PESI, BOVA, or RV strain were more appropriate for determining patient risk by a PERT where rapid decision making is important.Results: Cardiac biomarkers poorly distinguished between PESI classes and BOVA stages in patients with acute PE. Cardiac TnT and NT-proBNP easily distinguished low risk from submassive PE with an area under the curve (AUC) of 0.84 (95% C.I. 0.73 -0.95, p< 0.0001), and 0.88 (95% C.I. 0.79-0.97, p< 0.0001), respectively. Cardiac TnT and NT-proBNP easily distinguished low risk from massive PE with an area under the curve (AUC) of 0.89 (95% C.I. 0.78 -1.00, p< 0.0001), and 0.89 (95% C.I. 0.82-0.95, p< 0.0001), respectively. In patients with RV dysfunction, the predicted short-term mortality by PESI score or BOVA stage was lower than the observed mortality by a two-fold order of magnitude.

Legionella pneumophila is an important cause of community-acquired and nosocomial pneumonia. We describe an immunocompromised patient with severe pneumonia from whom Legionella species were isolated from sputum samples by culture for 30 days, despite administration of treatment with appropriate antimicrobial agents. However, clear improvement in the patient's respiratory condition was evident, and he subsequently recovered completely.

Respiratory involvement is a frequent complication of Stevens-Johnson syndrome (SJS). However, there are very few convincing reports of persistent pulmonary sequelae, as demonstrated by spirometry, radiology and pathology.The current study presents a case of a 13-yr-old female with T-cell acute lymphocytic leukaemia who developed persistent, severe, obstructive lung disease following an episode of SJS.A lung biopsy demonstrated bronchiolar submucosal fibrosis consistent with constrictive bronchiolitis, as well as eosinophilic micro-abscesses, which, to the current authors' knowledge, has not been previously described.The present study illustrates specific histopathological features that highlight a possible association between Stevens-Johnson syndrome, constrictive bronchiolitis and eosinophilic micro-abscesses. The eosinophils may be associated with permanent mucosal damage, as seen in the present case, by releasing mediators that have a pro-fibrogenetic role. However, further investigation is warranted.

We present a case of invasive pulmonary aspergillosis (IPA) in a previously healthy young woman who presented with what initially appeared to be an acute eosinophilic pneumonia. A second lung biopsy taken after treatment with steroids showed invasive Aspergillus with associated necrotizing granulomas, a pattern commonly found in chronic granulomatous disease (CGD). Both siblings, and by extrapolation, the patient, were actually found to have CGD. A review of the literature revealed other cases of presumed immunocompetent patients with IPA with presentations and lung histopathology similar to that of our patient.We conclude that chronic granulomatous disease presenting in the adult may be more common than previously assumed, and that patients previously presumed immunocompetent, but with granulomatous invasive pulmonary aspergillosis, may have chronic granulomatous disease. Furthermore, and most devastatingly in this case, the presentation may simulate a recently described steroid responsive acute lung disease, acute eosinophilic pneumonia.