Previous studies suggested that the persistence in eukaryotic cells of a Bordetella bronchiseptica mutant carrying an insertion in the locus encoding the response regulator RisAS is impaired. This suggested that ris-dependent products are required for the intracellular survival of bacteria. In this study we demonstrate that ris-regulated products play a role in B. bronchiseptica resistance against both phagosomal acidification and reactive oxygen intermediates.

Background Amyloidosis is an uncommon condition, which results from accumulation of misfolded extracellular insoluble protein in tissues and organs of the body, causing its damage and dysfunction. Histologically, after staining with Congo red, the amyloid deposits show an apple-green birefringence under polarized light microscope. Amyloidosis can affect all organ systems and is classified into hereditary or acquired, localized or systemic. Respiratory involvement occurs in 50% of the patients with amyloidosis and it may take tracheobronchial, nodular parenchymal, diffuse alveolar septal and lymphatic forms. Methods We report four cases of pulmonary amyloidosis. A female patient with localized form of tracheobronchial and nodular parenchymal pulmonary amyloidosis, which was initially misdiagnosed as sarcoidosis. A male patient who was referred to our department for further evaluation of multiple tumors in lungs accompanied by mediastinal lymphadenopathy, liver and peritoneal tumors. A male patient with suspect of lung malignancy. A male patient with diagnosed idiopathic pulmonary fibrosis and the possibility of malignancy. Results All the diagnoses were established by demonstration of amyloid protein in tissue specimens obtained in transbronchial or open lung biopsies. Conclusions Due to its nonspecific clinical and radiological findings, amyloidosis can often mimic other diseases and should be considered as one of the differential diagnoses. In order to confirm the diagnosis, proving the presence of amyloid deposition with positive Congo red staining in respiratory specimen is mandatory.

Background Idiopathic pulmonary fibrosis (IPF) and chronic hypersensitivity pneumonitis share commonalities in pathogenesis shifting haemostasis balance towards the procoagulant and antifibrinolytic activity. Several studies have suggested an increased risk of venous thromboembolism in IPF. The association between venous thromboembolism and chronic hypersensitivity pneumonitis has not been studied yet. Methods A retrospective cohort study of IPF and chronic hypersensitivity pneumonitis patients diagnosed in single tertiary referral center between 2005 and 2018 was conducted. The incidence of symptomatic venous thromboembolism was evaluated. Risk factors for venous thromboembolism and survival among those with and without venous thromboembolism were assessed. Results A total of 411 (259 IPF and 152 chronic hypersensitivity) patients were included (mean age 66.7 ± 8.4 vs 51.0 ± 13.3 years, respectively). There were 12 (4.6%) incident cases of venous thromboembolism in IPF and 5 (3.3%) in chronic hypersensitivity pneumonitis cohort. The relative risk (RR) of venous thromboembolism in chronic hypersensitivity pneumonitis was not significantly different to that found in patients with IPF (7.1 vs 11.8/1000 person-years, RR 1.661 95% CI 0.545–6.019, respectively). The treatment with systemic steroids (OR 5.38; 95% CI 1.65–18.8, p = 0.006) and GAP stage 3 (OR 7.85; 95% CI 1.49–34.9; p = 0.037) were significant risk factors for venous thromboembolism in IPF. Arterial hypertension and pulmonary hypertension significantly increased risk of venous thromboembolism in chronic hypersensitivity pneumonitis. There were no significant differences in survival between patients with and without venous thromboembolism. Conclusions The patients with chronic hypersensitivity pneumonitis have a marked increase in the risk of venous thromboembolism, similar to the patients with IPF. Venous thromboembolism does not affect the survival of patients with IPF and chronic hypersensitivity pneumonitis.

Lipoid pneumonia is a rare pulmonary disease, classified in terms of the source of lipid exposure into two variants: exogenous and endogenous. We present a patient with exogenous lipoid pneumonia, acquired after chronic exposure to paraffin oil-containing nasal drops. The diagnosis was established by demonstration of lipid-laden macrophages in bronchoalveolar lavage, chest computed tomography results and a history of lipid exposure.

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