34 research outputs found
The impact of a consultant led inreach service on patient transfer to respiratory wards: A Quality Improvement Project
No full textExposure to welding fumes and lower airway infection with Streptococcus pneumoniae
No full textBackgroundWelders are at increased risk of pneumococcal pneumonia. The mechanism for this association is not known. The capacity of pneumococci to adhere to and infect lower airway cells is mediated by host-expressed platelet-activating factor receptor (PAFR).ObjectiveWe sought to assess the effect of mild steel welding fumes (MS-WF) on PAFR-dependent pneumococcal adhesion and infection to human airway cells in vitro and on pneumococcal airway infection in a mouse model.MethodsThe oxidative potential of MS-WF was assessed by their capacity to reduce antioxidants in vitro. Pneumococcal adhesion and infection of A549, BEAS-2B, and primary human bronchial airway cells were assessed by means of quantitative bacterial culture and expressed as colony-forming units (CFU). After intranasal instillation of MS-WF, mice were infected with Streptococcus pneumoniae, and bronchoalveolar lavage fluid (BALF) and lung CFU values were determined. PAFR protein levels were assessed by using immunofluorescence and immunohistochemistry, and PAFR mRNA expression was assessed by using quantitative PCR. PAFR was blocked by CV-3988, and oxidative stress was attenuated by N-acetylcysteine.ResultsMS-WF exhibited high oxidative potential. In A549 and BEAS-2B cells MS-WF increased pneumococcal adhesion and infection and PAFR protein expression. Both CV-3988 and N-acetylcysteine reduced MS-WF–stimulated pneumococcal adhesion and infection of airway cells. MS-WF increased mouse lung PAFR mRNA expression and increased BALF and lung pneumococcal CFU values. In MS-WF–exposed mice CV-3988 reduced BALF CFU values.ConclusionsHypersusceptibility of welders to pneumococcal pneumonia is in part mediated by the capacity of welding fumes to increase PAFR-dependent pneumococcal adhesion and infection of lower airway cells
Breaking the mould, a first parse at natural language processing in aspergillosis diagnosis
No full textOpportunistic bacterial, viral and fungal infections of the lung
No full textRespiratory opportunistic infections are a major cause of morbidity and mortality in severely immunocompromised patients, such as those treated with biological therapies, chemotherapy and solid organ or stem cell transplants, and those with haematological malignancy, aplastic anaemia or HIV infection. The type and degree of immune defect dictates the profile of potential opportunistic pathogens; T-cell-mediated defects increase the risk of viral (cytomegalovirus, respiratory viruses) and Pneumocystis jirovecii infections, whereas neutrophil defects are associated with bacterial pneumonia and invasive aspergillosis. However, patients often have combinations of immune defects, and a wide range of other opportunistic infections can cause pneumonia. Importantly, conventional non-opportunistic pathogens are also frequently encountered in immunocompromised hosts and should not be overlooked. The radiological pattern of disease (best assessed by computed tomography) and speed of onset help identify the likely pathogen(s); this can then be supported by targeted investigation including early use of bronchoscopy in selected patients. Rapid and expert clinical assessment can help identify the most likely pathogens, allowing timely appropriate therapy
Pneumonia
No full textPneumonia is a common lung infection that causes significant mortality and morbidity worldwide, particularly in children and elderly individuals. The diagnosis is confirmed by radiographic evidence of new consolidation. Pneumonia can be caused by a variety of microorganisms, with the dominant pathogens varying across the globe and between community- or hospital-acquired infections. Bacterial causes are usually acquired by microaspiration of organisms colonizing the nasopharynx. Microbes reaching the distal airways and alveoli induce local and systemic inflammatory responses and can disseminate beyond the lung. Although most cases of pneumonia occur in the community, a significant subset develop in hospital, often caused by multidrug-resistant bacteria, which are associated with higher mortality. Microbiological investigations are required to identify the pathogenic organism but lack sensitivity. Severity scoring systems can be used to predict outcome and identify patients who can be safely managed in outpatient settings. The mainstay of treatment is early antibiotics and, if appropriate, supportive therapies such as oxygen and intravenous fluids. Large vaccination programmes have proven effective in reducing the incidence of some of the causative organisms; however, the overall incidence of pneumonia remains high, and further research is required to improve care in at-risk groups such as the elderly
Pulmonary immune response to Streptococcus pneumoniae
No full textStreptococcus pneumoniae is a common cause of respiratory infection associated with significant morbidity and mortality. The immune response to S. pneumoniae is complex, multi-layered and incompletely understood. The lung has
non-specific defence mechanisms that include cellular and secreted components. The initial response to bacteria that adhere to or breach the epithelium is mediated by the innate immune system and recognition of non-specific motifs common to many pathogens. This stimulates the inflammatory response and subsequently the development of the more specific adaptive immune system. Better understanding of the immune response to S. pneumoniae will underpin future progress in both the prevention of infection and adjuvants to existing treatments
Rising incidence of Pneumocystis pneumonia: A population-level descriptive ecological study in England
No full textObjectives: Pneumocystis pneumonia (PCP) is an opportunistic infection that causes significant morbidity and mortality in the immunocompromised population. This population is growing and diversifying, yet contemporary epidemiology is lacking. We investigated the population-level incidence of PCP over the past decade. Methods: We conducted a descriptive study of all hospital admissions in England from April 2012 to March 2022. PCP episodes, age, median length of stay, gender and episodes of other respiratory fungal infections were collected. Consumption of Trimethoprim-Sulfamethoxazole was obtained between January 2019 and May 2022. Results: The incidence of PCP increased from 2·2–4·5/100,000 population between 2012/2013 and 2019/2020 (p < 0·0001). There was a drop in 2020/2021 to 2·7/100,000 before returning to 3.9/100,000 in 2021/2022. PCP episodes rose as a proportion of all-cause admissions as well as a proportion of episodes due to other fungal infections. The proportion of PCP patients aged 75+ increased from 14% to 26%. The median length of stay was 13.5 days. Consumption of intravenous Trimethoprim-Sulfamethoxazole increased from 0.24 × 100,000 to 0.30 × 100,000 defined daily doses. Conclusions: The incidence of PCP is rising rapidly and represents a significant burden to the healthcare system. Further study into who is at risk of PCP is needed to better determine who should be given prophylaxis.</p
LSC Abstract – The inflammatory response to streptococcus pneumoniae is exaggerated by the polysaccharide capsule
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