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Streptococcus anginosus has long been recognized to cause invasive pyogenic infections. This holds true for thoracic infections where S. anginosus has a propensity for abscess and empyema formation. Early diagnosis is important given the significant morbidity and mortality associated with thoracic S. anginosus infections. Yet, distinguishing thoracic S. anginosus clinically is difficult. We present three cases of thoracic S. anginosus that demonstrated radiographic extension across tissue planes, including the interlobar fissure, diaphragm, and chest wall. Few infectious etiologies are known to cross tissue planes. Accordingly, we propose S. anginosus be considered among the differential diagnosis of potential infectious etiologies causing radiographic extension across tissue planes.

Multiple causes for tree-in-bud (TIB) opacities have been reported. However, to our knowledge the relative frequencies of the causes have not been evaluated. The purpose of this study was to determine the relative frequency of causes of TIB opacities and identify patterns of disease associated with TIB opacities.Cases with TIB opacities in the radiology report in 2010 were identified by searching the Radiology Information System. Medical records and CT scan examinations were reviewed for the causes of TIB opacities. Patterns of disease associated with TIB opacities were evaluated.Causes for TIB opacities were established in 166 of 406 (40.9%) cases. Respiratory infections (119 of 166, 72%) with mycobacteria (65 of 166, 39%), bacteria (44 of 166, 27%), viruses (four of 166, 3%), or multiple organisms (six of 166, 4%) were most common. Aspiration was the cause in 42 of 166 (25%). Alternating areas of normal lung with regions of small airways disease (TIB opacities, bronchiectasis) (random small airways pattern) was specific (0.92) for Mycobacterium avium complex infection. Nearly uniform distribution of bronchiectasis (widespread bronchiectasis pattern) was specific for "diseases predisposing to airway infection" (specificity 0.92), such as cystic fibrosis, primary ciliary dyskinesia, allergic bronchopulmonary aspergillosis, and immunodeficiency states. Consolidation and TIB opacities (bronchopneumonia pattern) were usually due to bacterial infection or aspiration. Dependent distribution (specificity 0.79) and esophageal abnormality (specificity 0.86) with TIB opacities were associated with aspiration. Chronicity of findings was associated with mycobacterial infection (Plt; .0001, sensitivity 0.96). Acuteness of findings was associated with bacterial infection (Plt; .001, specificity 0.87).TIB opacities are most often a manifestation of infections or aspiration. Patterns of disease can provide clues to the most likely diagnosis.

Background CT scan measures of emphysema and airway disease have been correlated with lung function in cohorts of subjects with a range of COPD severity. The contribution of CT scan-assessed airway disease to objective measures of lung function and respiratory symptoms such as dyspnea in severe emphysema is less clear. Methods Using data from 338 subjects in the National Emphysema Treatment Trial (NETT) Genetics Ancillary Study, densitometric measures of emphysema using a threshold of −950 Hounsfield units (%LAA-950) and airway wall phenotypes of the wall thickness (WT) and the square root of wall area (SRWA) of a 10-mm luminal perimeter airway were calculated for each subject. Linear regression analysis was performed for outcome variables FEV 1 and percent predicted value of FEV 1 with CT scan measures of emphysema and airway disease. Results In univariate analysis, there were significant negative correlations between %LAA-950 and both the WT ( r = −0.28, p = 0.0001) and SRWA ( r = −0.19, p = 0.0008). Airway wall thickness was weakly but significantly correlated with postbronchodilator FEV 1 % predicted (R = −0.12, p = 0.02). Multivariate analysis showed significant associations between either WT or SRWA (β = −5.2, p = 0.009; β = −2.6, p = 0.008, respectively) and %LAA-950 (β = −10.6, p = 0.03) with the postbronchodilator FEV 1 % predicted. Male subjects exhibited significantly thicker airway wall phenotypes (p = 0.007 for WT and p = 0.0006 for SRWA). Conclusions Airway disease and emphysema detected by CT scanning are inversely related in patients with severe COPD. Airway wall phenotypes were influenced by gender and associated with lung function in subjects with severe emphysema.

Streptococcus anginosus has long been recognized to cause invasive pyogenic infections. This holds true for thoracic infections where S. anginosus has a propensity for abscess and empyema formation. Early diagnosis is important given the significant morbidity and mortality associated with thoracic S. anginosus infections. Yet, distinguishing thoracic S. anginosus clinically is difficult. We present three cases of thoracic S. anginosus that demonstrated radiographic extension across tissue planes, including the interlobar fissure, diaphragm, and chest wall. Few infectious etiologies are known to cross tissue planes. Accordingly, we propose S. anginosus be considered among the differential diagnosis of potential infectious etiologies causing radiographic extension across tissue planes.

Background Pulmonary infection and tumor in the AIDS population has a variable clinical and radiographic presentation. The association between the radiographic presentation of pulmonary tuberculosis and CD4 T lymphocyte count in the HIV-infected patient is investigated in order to provide an empirical approach for early diagnosis, treatment, and isolation of infected subjects. Methods: A retrospective analysis of chest radiographs, CD4 T lymphocyte counts, and clinical history of 35 subjects from 3 urban hospitals was performed. All subjects were HIV-seropositive and had culture-proven pulmonary tuberculosis. Radiographs were evaluated for the presence of either a pattern characteristic of post-primary tuberculosis (typical pattern) or a pattern uncharacteristic of post-primary infection (atypical pattern). Results: Twenty-one of 26 subjects with a CD4 T lymphocyte count less than 0.20×10 9 cells/L, whereas only 1 of 9 subjects with a CD4 T lymphocyte count of 0.20×10 9 cells/L or more presented with an atypical pattern of pulmonary tuberculosis (p with atypical versus typical radiographic pattern of post-primary pulmonary tuberculosis were 0.069 × 10 9 cells/L (n=22) and 0.323×10 9 cells/L (n=13), respectively (p 9 cells/L). Atypical radiographic pattern included diffuse and lower lobar opacities, pleural effusion, mediastinal adenopathy, interstitial nodules, and a normal chest radiograph. Conclusion: AIDS patients presenting with CD4 count less than 0.20×10 9 cells/L and an atypical radiographic pattern for pulmonary tuberculosis are at risk for tuberculous infection requiring appropriate treatment and isolation until the diagnosis of pulmonary tuberculosis has been excluded.

Objective To evaluate the clinical and radiographic features of pulmonary aspergillosis as they present in AIDS patients; in particular, to determine similarities and differences between Aspergillus infection in patients with AIDS vs those without AIDS. Subjects and Methods Six new cases of confirmed or probable pulmonary aspergillosis were discovered during a search of hospital records. These are reviewed with 30 previously reported cases with special attention to radiographic appearance of disease and how radiographic appearance influences clinical outcome. Results Symptoms of pulmonary aspergillosis in AIDS were nonspecific, most often including fever, cough, and dyspnea, and less commonly, chest pain or hemoptysis. Major risk factors for the development of pulmonary aspergillosis in patients with AIDS were steroid administration and neutropenia. Neutropenia was often a complication of therapies for AIDS, in particular, ganciclovir and zidovudine. Radiographic appearance of disease could be divided into three general categories. One third of the patients (13/36) presented with cavitary upper lobe disease resembling noninvasive or chronic necrotizing aspergillosis. Fatal hemoptysis occurred in 42 percent of patients with this form of disease. Twenty-two percent (8/36) of the cases presented as a nondescript focal alveolar opacity similar to invasive aspergillosis. In several patients, the focal infiltrate remained stable for several months, a feature that is unusual for aspergillosis in non-AIDS patients. The air crescent sign was present in none of the 36 reported cases. Patients with only focal disease had the best prognosis of patients with pulmonary aspergillosis. Bilateral alveolar or interstitial disease similar to invasive aspergillosis was present in 23 percent (9/36) of the patients. Bilateral disease appears to be a marker for disseminated infection and was associated with a high mortality due to aspergillosis. Two new forms of bronchial aspergillosis (5/36 cases) have been described previously. These patients presented with either obstructing fungal casts or bronchial pseudomembranes demonstrated bronchoscopically. In some patients with the bronchial forms of aspergillosis, transient alveolar opacities were seen on chest radiographs. These opacities may represent regions of atelectasis due to airway obstruction. One patient who had bilateral pneumothoraces without parenchymal opacities did not correspond to any of the three previously mentioned categories. Mortality due to aspergillosis was greater than 50 percent among AIDS patients. Death was subsequent to fatal hemoptysis or widespread pulmonary or systemic infection. Conclusion Unlike other risk groups that tend to contract only one form of pulmonary aspergillosis, AIDS patients can develop the whole spectrum of aspergillosis-related pulmonary disorders, including chronic cavitary, invasive, and bronchial forms of aspergillosis. Clinical symptoms are nonspecific and major risk factors include neutropenia, which is often a side effect of various therapies for AIDS, and steroid administration. Patients with the chronic cavitary form of disease have an unusually high mortality due to fatal hemoptysis. Patients with bilateral pulmonary infiltrates and aspergillosis have a high mortality due to disseminated infection.

Background Neurofibromatosis type 1 (NF1) is a common disorder of dysregulated tissue growth secondary to mutations in the tumor suppressor gene NF1. Pulmonary arterial hypertension (PAH) in patients with NF1 is hypothesized to be secondary to an underlying vasculopathy. Methods We describe the entity we term NF1-associated PAH (NF1-PAH) in four new patients and update the data on four previously published reports of patients with PAH and NF1. We performed genetic testing of the bone morphogenic protein receptor 2 (BMPR2) gene, which is mutated in 70% of patients with familial PAH and approximately 25% of patients with idiopathic PAH. We report, for the first time, pathologic findings in the autopsy-obtained lung of one patient with NF1-PAH. Results Patients with NF1-PAH have a generally poor long-term prognosis. In four patients, we observed the mosaic pattern of lung attenuation on a CT scan of the chest, a radiographic finding that can be consistent with an underlying vasculopathy. No mutations or rearrangements in the BMPR2 gene were found. We observed complex plexiform lesions in the one available autopsy specimen. Similar lesions are a hallmark of plexogenic pulmonary arteriopathy and are associated with several severe types of PAH. (Plexiform lesions should not be confused with plexiform neurofibromas, which are distinctive tumors seen in NF1.) Conclusions Our findings suggest that NF1 should be considered as being "associated with PAH" as outlined in the Revised Clinical Classification of Pulmonary Hypertension. Understanding the mechanism of PAH in NF1 may inform the pathogenesis of PAH, NF1-PAH itself, and other NF1-associated vasculopathies. The pulmonary vasculature should now be included among the arterial beds affected by NF1 vasculopathy.

While a number of recent reports have documented the changing clinical and radiographic spectrum of parenchymal tuberculosis, relatively little attention has been paid to changes in the patterns of pleural tuberculosis. We therefore reviewed the clinical, laboratory, and radiographic characteristics of 26 adult patients with tuberculous pleural effusions. We found that pleural tuberculosis has become a disease of older adults (median age, 56 years) and that 19 percent (5/26) of the cases were due to postprimary (reactivation) disease. This shift in age led to problems in diagnosis, since many of these older patients had underlying or coexisting disease that could have caused a pleural effusion. Both specimens of pleural fluid and pleural biopsy were useful in establishing the diagnosis. Examination of sputum was less helpful. All patients who were not anergic had positive cutaneous reactions to first-strength purified protein derivative of tuberculin. Lymphocytosis of the pleural fluid was not a uniform finding; only 62 percent of our patients had greater than 50 percent lymphocytes on their initial examinations of pleural fluid, and four patients had greater than 90 percent polymorphonuclear cells. All of the effusions were exudates, and four had glucose levels in the pleural fluid that were less than 30 mg/dl. Pleural tuberculosis is an important diagnostic consideration in adult or elderly patients with exudative pleural effusions.