Thin-section computed tomography detects long-term pulmonary sequelae 3 years after novel influenza A virus-associated pneumonia.

BACKGROUND: The aim of this research was to evaluate long-term pulmonary sequelae on paired inspiration-expiration thin-section computed tomography (CT) scans 3 years after influenza A (H1N1) virus-associated pneumonia, and to analyze the affecting factors on pulmonary fibrosis. METHODS: Twenty-four patients hospitalized with H1N1 virus-associated pneumonia at our hospital between September 2009 and January 2010 were included. The patients underwent thin-section CT 3 years after recovery. Abnormal pulmonary lesion patterns (ground-glass opacity, consolidation, parenchymal bands, air trapping, and reticulation) and evidence of fibrosis (architectural distortion, traction bronchiectasis, or honeycombing) were evaluated on follow-up thin-section CT. Patients were assigned to Group 1 (with CT evidence of fibrosis) and Group 2 (without CT evidence of fibrosis). Demographics, rate of mechanical ventilation therapy, rate of intensive care unit admission, cumulative prednisolone-equivalent dose, laboratory tests results (maximum levels of alanine aminotransferase, aspartate transaminase [AST], lactate dehydrogenase [LDH], and creatine kinase [CK]), and peak radiographic opacification of 24 patients during the course of their illness in the hospital were compared between two groups. RESULTS: Parenchymal abnormality was present in 17 of 24 (70.8%) patients and fibrosis occurred in 10 of 24 (41.7%) patients. Patients in Group 1 (10/24; 41.7%) had a higher rate of mechanical ventilation therapy (Z = -2.340, P = 0.019), higher number of doses of cumulative prednisolone-equivalent (Z = -2.579, P = 0.010), higher maximum level of laboratory tests results (AST [Z = -2.140, P = 0.032], LDH [Z = -3.227, P = 0.001], and CK [Z = -3.345, P = 0.019]), and higher peak opacification on chest radiographs (Z = -2.743, P = 0.006) than patients in group 2 (14/24; 58.3%). CONCLUSIONS: H1N1 virus-associated pneumonia frequently is followed by long-term pulmonary sequelae, including fibrotic changes, in lung parenchyma. Patients who need more steroid therapy, need more mechanical ventilation therapy, had higher laboratory tests results (maximum levels of AST, LDH, and CK), and had higher peak opacification on chest radiographs during treatment are more likely to develop lung fibrosis.

[Severe pneumonia caused by Aeromonas veronii biovar sobria: a case report and review of the literature].

OBJECTIVE: To describe the clinical features of severe pneumonitis with Aeromonas veronii biovar sobria. METHOD: Case report and review of the related literatures. The clinical symptoms, laboratory tests, radiographic patterns, diagnosis, and therapeutic management of a case of severe pneumonia caused by A. veronii biovar sobria were described. RESULTS: The clinical symptoms of this patient included cough and sputum production with high fever, followed by acute respiratory distress symptom associated with septic shock. Progressive infiltration of lungs was evident in chest radiography, changes suggestive of interstitial pneumonia. Oxygenation was improved by mechanical ventilation and anti-shock therapy was administered. A. veronii biovar sobria was grown in three consecutive cultures of airway secretions by fiberoptic bronchoscopy. Mild interstitial inflammation was revealed by pathology of transbronchial lung biopsy specimens. The clinical symptoms and the chest infiltrates improved significantly after therapy with antibiotics and glucocorticoids. CONCLUSIONS: A. veronii biovar sobria, an intestinal bacterial pathogen, can cause severe pneumonia, which is often underestimated and inadequately understood. Appropriate antibiotics, glucocorticoids and nutritional support are effective treatments.