ABSTRACT
We describe cases of donor-derived transmission of Cryptococcus deuterogattii in 2 kidney transplant recipients in Brazil and published information on other cases. Prompt reduction of immunosuppression and initiation of antifungal therapy was required to successfully control the fungal infections and preserve engraftment.
Subject(s)
Cryptococcosis , Cryptococcus gattii , Cryptococcus neoformans , Kidney Transplantation , Antifungal Agents/therapeutic use , Brazil , Cryptococcosis/diagnosis , Cryptococcosis/drug therapy , Cryptococcus gattii/genetics , Humans , Kidney Transplantation/adverse effects , Transplant RecipientsSubject(s)
Bronchiolitis Obliterans/diagnostic imaging , Cysts/diagnostic imaging , Biopsy , Bronchiolitis Obliterans/pathology , Cysts/pathology , Diagnosis, Differential , Female , Humans , Lung/diagnostic imaging , Lung/pathology , Middle Aged , Respiratory Function Tests/methods , Tomography, X-Ray Computed/methodsABSTRACT
CONTEXT: Prolonged exposure to ambient particles is associated with premature mortality due to cardio-respiratory diseases and lung cancer. The size and composition of these particles determine their toxicity, which is aggravated by their long-term retention in the lungs. OBJECTIVE: To compare the elemental profile of particles retained along the bronchial tree and lymph nodes by combining laser capture microdissection (LCM) and elemental composition analysis through energy dispersive x-ray (EDX) and scanning electron microscopy (SEM). MATERIAL AND METHODS: Twenty-four right lung middle lobes from autopsied cases were obtained from two cities with different pollution backgrounds. Lung samples were collected from three distinct sites within the lung at the time of autopsy: peribronchial tissue, peripheral parenchyma and hilar lymph nodes. Areas of potentially increased particle deposition were microdissected using LCM and analyzed for elemental composition through EDX "allied" with SEM. RESULTS: Elemental analyses of the particles retained along the bronchial tree showed two groups of distribution: peribronchiolar or lymph node deposition. The elemental profile of peribronchial areas were significantly different between the two cities and were better discriminators of past air pollution exposure. CONCLUSION: Our data suggest that particle uptake varies along the bronchial tree and human lung tissue retains particles indicative of regional air pollution background.
Subject(s)
Air Pollutants/toxicity , Bronchi/drug effects , Inhalation Exposure/adverse effects , Lymph Nodes/drug effects , Metals/analysis , Particulate Matter/toxicity , Adult , Aged , Aged, 80 and over , Air Pollutants/analysis , Brazil , Bronchi/chemistry , Bronchi/ultrastructure , Environmental Monitoring , Female , Humans , Lasers , Lymph Nodes/chemistry , Lymph Nodes/ultrastructure , Male , Microdissection , Microscopy, Electron, Scanning , Middle Aged , Particulate Matter/analysis , Spectrometry, X-Ray Emission , Urban HealthABSTRACT
Small airway disease is thought to contribute significantly to functional impairment caused by asthma. Functional evidence of airway-parenchyma uncoupling in asthma, such as loss of deep breath bronchodilator effect in bronchoconstrictive episodes and enhanced airway closure, has been previously demonstrated. Elastic fibers are essential to maintain adequate elastic recoil of the lungs. In this study, we hypothesized that alveolar attachments could be abnormal and that elastic fibers could be damaged in the distal lungs of patients with fatal asthma. For this purpose, we measured the number of abnormal alveolar attachments and quantified the content of elastic fibers in the adventitial layer of small airways and in the peribronchial and distal alveolar septa of 15 patients who died of asthma (FA) and 9 control subjects (CTRL). Our data (geometric mean [range]) showed an increased proportion of abnormal alveolar attachments per centimeter of basement membrane perimeter in fatal asthma (FA, 0.18 [0.03-4.00]; CTRL, 0.00 [0.00-0.12]; p < 0.001) and decreased elastic fiber content in the small airway adventitial layer (FA, 4.08 [2.22-11.46] microm; CTRL, 6.79 [5.62-10.0] microm; p = 0.01) and in the peribronchial alveoli (FA, 1.08 [0.46-1.91] microm; CTRL, 1.81 [1.22-1.74] microm; p = 0.003), but not in the distal alveoli. We propose that structural alterations at the peribronchiolar level might contribute to the pathogenesis of some functional abnormalities observed in patients with severe asthma.