The Modern Diagnostic Approach to Community-Acquired Pneumonia in Adults

Respiratory tract infections, the majority of which are community acquired, are among the leading causes of death worldwide and a leading indication for hospital admission. The burden of disease demonstrates a "U"-shaped distribution, primarily affecting young children as the immune system matures, and older adults as the process of immunosenescence and accumulation of comorbidities leads to increased susceptibility to infection. Diagnosis of community-acquired pneumonia (CAP) is traditionally based on demonstration of a new infiltrate on a chest radiograph in a patient presenting with an acute respiratory illness or sepsis. Advances in diagnosis have been slow, and although there are increasing data on the value of computed tomography or lung ultrasound as more sensitive diagnostic methodologies, they are not widely used as initial diagnostic tests. There are a wide range of differential diagnoses and pneumonia "mimics" which should be considered in patients presenting with CAP. Once the diagnosis of CAP has been made, identifying the causative microorganism is the next stage in the diagnostic process. Traditional culture-based approaches are relatively insensitive and achieve a positive diagnosis in only 30 to 70% of cases, even when rigorously applied. Urinary antigen tests, polymerase chain reaction assays, and even next-generation sequencing technologies have become available and are increasing the rates of positive diagnosis. In an era of increasing antimicrobial resistance, the accurate diagnosis of CAP and determining the causative pathogen are ever more important. Getting these both right is key in reducing both morbidity and mortality from CAP, and appropriate antimicrobial stewardship which is now an international healthcare priority.</p

Management of chronic airway diseases:What can we learn from real-life data?

Chronic obstructive pulmonary disease (COPD), alpha-1 antitrypsin deficiency (AATD) and non-cystic fibrosis bronchiectasis (hereafter referred to as bronchiectasis) are distinct but related airway diseases: COPD is characterised by persistent and usually progressive airflow limitation associated with an enhanced chronic inflammatory response in the airways and lung to noxious particles or gases (1). COPD is a clinical and physiological diagnosis. AATD is a genetic disorder that causes defective production of alpha-1-antitrypsin (AAT), leading to decreased AAT activity in the blood and lungs and deposition of excessive abnormal AAT protein in liver cells (2). AATD is a laboratory diagnosis. Bronchiectasis is characterised by the presence of airway dilatation and wall thickening on imaging (e.g. computed tomography [CT]), with persistent or recurrent bronchial infection (3). Bronchiectasis is a pathological or radiological diagnosis. Despite differences in the pathobiology of these conditions, they share many of the same clinical features and many of the same challenges. A definitive diagnosis is often complicated by symptom non-specificity as illustrated in a case study

Advances in bronchiectasis:endotyping, genetics, microbiome, and disease heterogeneity

Bronchiectasis is characterised by pathological dilation of the airways. More specifically, the radiographic demonstration of airway enlargement is the common feature of a heterogeneous set of conditions and clinical presentations. No approved therapies exist for the condition other than for bronchiectasis caused by cystic fibrosis. The heterogeneity of bronchiectasis is a major challenge in clinical practice and the main reason for difficulty in achieving endpoints in clinical trials. Recent observations of the past 2 years have improved the understanding of physicians regarding bronchiectasis, and have indicated that it might be more effective to classify patients in a different way. Patients could be categorised according to a heterogeneous group of endotypes (defined by a distinct functional or pathobiological mechanism) or by clinical phenotypes (defined by relevant and common features of the disease). In doing so, more specific therapies needed to effectively treat patients might finally be developed. Here, we describe some of the recent advances in endotyping, genetics, and disease heterogeneity of bronchiectasis including observations related to the microbiome.</p

Utility of routine screening for alpha-1 antitrypsin deficiency in patients with bronchiectasis

Alpha-1 antitrypsin deficiency (AATD) is a cause of bronchiectasis. Guidelines for bronchiectasis from the British Thoracic Society do not recommend to routinely test patients for AATD. In contrast, guidelines for AATD recommend routine screening. This contradiction, in part, results from the lack of data from large studies performing comprehensive screening. We screened 1600 patients with bronchiectasis at two centres in the UK from 2012 to 2016. In total, only eight individuals with AATD were identified representing 0.5% of the overall population. We conclude that routine screening for AATD in bronchiectasis in the UK has a low rate of detection. Further studies are required in different geographical regions, which may have a higher prevalence of AATD.info:eu-repo/semantics/publishedVersio

Review of the British Thoracic Society Winter Meeting 2015, 2-4 December, London, UK

The British Thoracic Society Winter Meeting 2015 is reviewed in this article. Over 3 days in December, this annual scientific meeting attracted over 2300 delegates and up-to-date respiratory research was presented by leading UK and international speakers. This article reviews a number of symposia and selected abstract presentations from the meeting.</p