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COVID-19 has quickly reached pandemic levels since it was first reported in December 2019. The virus responsible for the disease, named SARS-CoV-2, is enveloped positive-stranded RNA viruses. During its replication in the cytoplasm of host cells, the viral genome is transcribed into proteins, such as the structural protein spike domain S1, which is responsible for binding to the cell receptor of the host cells. Infected patients have initially flu-like symptoms, rapidly evolving to severe acute lung injury, known as acute respiratory distress syndrome (ARDS). ARDS is characterized by an acute and diffuse inflammatory damage into the alveolar-capillary barrier associated with a vascular permeability increase and reduced compliance, compromising gas exchange and causing hypoxemia. Histopathologically, this condition is known as diffuse alveolar damage which consists of permanent damage to the alveoli epithelial cells and capillary endothelial cells, with consequent hyaline membrane formation and eventually intracapillary thrombosis. All of these mechanisms associated with COVID-19 involve the phenotypic expression from different proteins transcription modulated by viral infection in specific pulmonary microenvironments. Therefore, this knowledge is fundamentally important for a better pathophysiological understanding and identification of the main molecular pathways associated with the disease evolution. Evidently, clinical findings, signs and symptoms of a patient are the phenotypic expression of these pathophysiological and molecular mechanisms of SARS-CoV-2 infection. Therefore, no findings alone, whether molecular, clinical, radiological or pathological axis are sufficient for an accurate diagnosis. However, their intersection and/or correlation are extremely critical for clinicians establish the diagnosis and new treatment perspectives., Highlights • The RNA virus SARS-COv-2 is responsible for COVID-19. • Some COVID-19 patients rapidly evolve to acute respiratory distress syndrome (ARDS). • COVID-19 can cause diffuse alveolar damage (DAD) and thrombotic events. • Temporal heterogeneity of lung damage is caused by SARS-CoV-2. • Clinical-radio-pathologic correlation is critical for an accurate diagnosis.

Summary Introduction In our institution, patients with suspected pulmonary TB undergo multiple induced-sputum sampling for microscopy, culture and nucleic acid amplification (NAA) with the MTD ® Gen-probe assay. Those with negative induced-sputum results still suspected with TB are then referred for bronchoscopy. We sought to determine the diagnostic yield of bronchoscopy in these patients with negative initial induced-sputum results both via smear and NAA testing. Methods We identified 30 consecutive cases of suspected pulmonary TB between 2001 and 2007, who had undergone a diagnostic bronchoscopy after negative results on induced-sputum smears and the MTD ® Gen-probe on at least 2 samples. Results The cohort (M = 20 & F = 10) had a median age of 37 (range 16–85 yrs); were predominantly foreign born (27/30); HIV-negative (29/30) individuals with strongly positive TST's (mean 18 + 5 mm). Induced-sputum cultures were negative for M-TB in all patients after a full 60-day incubation period. BAL was culture positive for M-TB in 3/30 cases (10%) with 2 strains being pan-sensitive and the third being INH resistant. BAL microscopy with acid-fast smear ( n = 30) and BAL Gen-probe ( n = 23) were negative in all cases. A third of the patients (9/27, 33%) with negative bronchoscopy results were treated for culture negative TB. Treatment for latent TB was initiated in 5/27 (18%) individuals whereas 13/27 (48%) received no further treatment. Conclusion Bronchoscopy provided diagnostic confirmation of pulmonary TB in 10% of subjects at least 2 negative induced-sputum samples by smear microscopy and NAA testing.

Summary Background Sarcoidosis is characterised by a T-lymphocytic alveolitis with a typically increased T4/T8 ratio. The diagnostic value of this ratio is under debate. Aim of the work We prospectively evaluated the influence of BAL pre-lavage and the impact of bronchial contamination on BAL differential cell count in 108 BAL specimens obtained from patients with histologically confirmed sarcoidosis. Methods BAL was performed by instilling 150–300ml normal saline either in the middle lobe or the lingula. Fifty-one patients (47%) underwent additional pre-lavage with 50ml normal saline. Bronchial contamination was assessed by semi-quantitative analysis of mucus, ciliated and squamous cells in the untreated BAL recovery. Results Pre-lavage did neither influence the lavage cellularity nor extend of contamination of the BAL. Content of mucus and ciliated cells, indicating bronchial contamination, showed a high correlation (Kendal's tau=0.61). Presence of either mucus or ciliated cells in the BAL recovery was associated with a significant lower T4/T8 ratio (mucus: 4.9 vs. 8.0, p =0.009; ciliated cells: 4.1vs.7.4, p =0.001). Squamous cells in the BAL recovery representing oropharyngeal contamination did not significantly influence the T4/T8 ratio (7.7 vs. 5.6, p =0.10). Conclusion Bronchial contamination of BAL as determined by the presence of mucus and ciliated cells in the recovery decreases the T4/T8 ratio of BAL in sarcoidosis.

Pulmonary infection by Nocardia is an uncommon opportunistic infection in humans. Thirty-five patients with pulmonary nocardiosis were identified in two tertiary referral hospitals. A retrospective review of the patient characteristics, clinical and laboratory features including antimicrobial susceptibility at diagnosis was carried out. Radiological features derived from chest radiographs and CT scans were also documented. In our population, the predominant risk factors were immuno-compromised state, corticosteroid therapy, and underlying pulmonary pathology. The presenting features were similar to those previously described but disseminated infection was not common. The radiological changes were diverse and non-specific.Nocardia asteroides was the commonest species. Most Nocardia isolates were susceptible to imipenem, ceftriaxone, amikacin, and cotrimoxazole. Co-existing microbial agents are common and reflect the underlying complex disorders.

Summary Introduction Smoking can cause a variety of pulmonary interstitial diseases. Pulmonary fibrosis has traditionally been considered a non-smoking-related disease. Recently, however, evidence of smoking-induced fibrosis has emerged. Subjects and methods A group of eight patients from the pulmonary clinic in Rabin Medical Center with a combine presentation of fibrosis and emphysema was identified retrospectively. All patients underwent chest computed tomography and pulmonary function tests. One patient underwent lung–heart transplantation and a complete review of his lung pathology was obtained. Transbronchial biopsy was performed in 3 additional patients and echocardiography was performed to evaluate the pulmonary vasculature. Results Upper-lobe emphysema with bulluos changes was found in all patients. In addition, a basal interstitial process was recognized, ranging from ground glass opacities to severe pulmonary fibrosis, with honeycombing. The radiological findings matched the pathological results of combined emphysema and usual interstitial pneumonia. Pulmonary function tests were also in accord, showing severe hypoxemia with mild obstruction, normal-to-mildly reduced lung volumes and a severe decrease in diffusion capacity. Most of the patients had moderate-to-severe pulmonary hypertension as well as diffuse coronary artery disease. Conclusion Our findings are in line with emerging evidence that the spectrum of interstitial damage caused by smoke includes not only Langerhans cell hystiocytosis, respiratory bronchiolitis or desquamative interstitial pneumonia but also advanced usual interstitial pneumonitis as well. We believe that in some patients smoking plays a destructive role by a variety of mechanisms and can cause emphysema, lung fibrosis as well as pulmonary vasculopathy and hypertension. Future studies are needed to define the genetics and pathophysiology of this uncommonly reported clinical syndrome.

In the endemic area of tuberculosis, there are many cases that present tuberculosis as a solitary pulmonary nodule (SPN) on chest radiographs. The objective of this study is to evaluate the diagnostic yield of transbronchial lung biopsy (TBLB) under fluoroscopic guidance in SPNs such as lung cancer or pulmonary tuberculoma in areas with high prevalence of tuberculosis.One hundred and seventy patients with SPNs on chest radiographs were included in the study; all had negative sputum smears for tubercle bacilli and no malignancy by sputum cytology before bronchoscopy. Transbronchial lung biopsy and brushing were performed, routinely, under fluoroscopic guidance.Of 170 patients, 120 (70·6%) had lung cancer (including three with metastatic cancer), 40 (23·5%) patients had pulmonary tuberculosis (Tb), and the remaining 10 (5·9%) patients had other benign pulmonary lesions. The overall diagnostic rate in SPNs was 62·4% (106 of 170). Transbronchial lung biopsy and brushing revealed a diagnostic sensitivity of 70·0% in lung cancer (84 of 120) and a sensitivity of 55% in Tb (22 of 40). In addition, TBLB and brushing also provided rapid microscopic identification of Tb in 18 of 40 patients (45%, including 15 by TBLB, one by brushing smear, and two by postbronchoscopic sputum). The percentage of positive diagnosis correlated with diameter of the SPN. Solitary pulmonary nodules with diameter less than 2 cm were diagnosed in only 35·3% of cases (6 of 17; cancer 40% vs. Tb 29%). In contrast, the diagnostic rates in SPNs with diameters 2–4 cm and greater than 4 cm were 64·5% (78 of 121; cancer 72·0% vs. Tb 62·5%) and 68·8% of cases (22 of 32), respectively.Diagnostic bronchoscopy under fluoroscopic guidance is a useful tool in evaluation of patients with a peripheral pulmonary nodule since it may provide additional information to minimize unnecessary thoracotomy and give way for proper medication as early as possible.

Fiberoptic bronchoscopy with bronchoalveolar lavage (BAL) and transbronchial biopsy (TBB) was performed in 40 patients suspected to have pulmonary tuberculosis, in whom chest roentgenogram revealed minimal infiltration and sputum smears were negative for acid-fast bacilli. Bronchoscopic procedures provided overall diagnostic yields in 47·5% (1940) of patients. The diagnostic yield of overall bronchoscopic procedures for tuberculosis in this study was 32·5% (1340) of patients. It consisted of positive BAL smear in 7·5% (340) of patients, positive for mycobacterial culture in 15% (640) of patients and TBB revealing granuloma in 17·5% (740) of patients. Non-tuberculosis conditions were diagnosed by the bronchoscopic method in six patients (15%). These results suggest that in an area with a high prevalence of tuberculosis, bronchoscopic procedures should be performed in those cases in which other diagnoses such as malignancy must be ruled out. Transbronchial biopsy has a major role for early diagnosis and should be performed in all cases, if possible.

SummaryBackgroundAssessing inflammatory activity is useful in the management of persistent symptomatic sarcoidosis patients. 18F-FDG PET (PET) has been shown to be a sensitive technique to assess inflammatory activity in sarcoidosis. The aim of this study was to evaluate whether the severity of pulmonary involvement is associated with PET activity in persistent symptomatic sarcoidosis patients.MethodsOver a 5-year period, relevant clinical data including laboratory and lung function test results were gathered from the medical records of 95 sarcoidosis patients with persistent disabling symptoms who underwent both a PET and HRCT. HRCT scans were classified using a semiquantitative scoring system and PET findings as positive or negative, respectively.ResultsPET was positive in 77/95 patients, of whom 56 demonstrated pulmonary PET-positivity. HRCT scores were high (7.1 ± 3.6) in patients with positive pulmonary PET findings (n = 56) compared to patients with negative pulmonary PET findings (n = 39; 3.0 ± 2.9; p