The pneumococcus, Streptococcus pneumoniae is the most common etiologic cause in acute otitis media as well as the primary cause of bacterial sepsis, non-epidemic bacterial meningitis, and community-attained pneumonia. The pneumococcal illness gets anteceded by colonization that is especially common among children who have more than a single serotype recurrently colonizing the nasopharynx of the same patient simultaneously (Yamamoto et al., 2014). More importantly, linear bacterial movement from the nasopharynx to the capillaries, by and large, regarded as occult bacteremia, is a well-established complication of pneumococcal carriage, especially within the early infantile period. Pneumococcal colonization entails bacterium binding to the surface of carbohydrate cells such as N-acetyl-glucosamine present on the respirational epithelium, and this operation is gets facilitated through the cell-wall linked superficial proteins (Yamamoto et al., 2014). Concerning the presence of the inflammatory response, studies relating to the inflammatory as well as microbial incidences which describe death or survival upon intranasal immunization of mice containing an LD50 Streptococcus pneumoniae got explored. The survival got linked with low inflammation and bacterial clearance even though no lung tissue injury or neutrophil recruitment got observed.
Correspondingly, COPD persons are susceptible to bacterial colonization as well as exacerbations which are typically caused by respiratory infections of bacterial etiology. Studies similarly report the association between the common exacerbator phenotype with increased systematic inflammation as well as poor quality of life (Vlahos &Bozinovski, 2014). However, contrary to Streptococcus pneumoniae, alveolar macrophages function is crucial to high rates of colonization as well as augmented vulnerability to exacerbations reported in chronic obstructive pulmonary disease. Furthermore, acute cigarette smoke disclosure is the prime cause of the chronic obstructive pulmonary disease that exhausts intracellular glutathione stores. The oxidative stress results in interference of glutathione metabolism that gets measured as the main vulnerability component of lung illnesses. The resulting systematic inflammation associated with COPD leads to increased risk of lung cancer as well as other cardiovascular diseases especially the coronary artery disease (Bourbeau& Bartlett, 2008). As the health practitioner, I am capable of playing a fundamental role in assisting patients to recognize the nature of COPD and the possible merits of medication, to address issues concerning probable adverse events and impacts as well as inspire patients to cultivate the self-management abilities. This is attainable through the exploration of the patient's concerns and beliefs vis-a-vis the benefits and safety of treatments since studies indicate that most patients harbor assumed doubts.
Yamamoto, K., Ahyi, A. N. N., Pepper-Cunningham, Z. A., Ferrari, J. D., Wilson, A. A., Jones, M. R., ... &Mizgerd, J. P. (2014). Roles of lung epithelium in neutrophil recruitment during pneumococcal pneumonia. American journal of respiratory cell and molecular biology, 50(2), 253-262. https://www.ncbi.nlm.nih.gov/pubmed/24010952
Vlahos, R., &Bozinovski, S. (2014). Role of alveolar macrophages in chronic obstructive pulmonary disease. Frontiers in immunology, 5, 435. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4160089/
Bourbeau, J., & Bartlett, S. J. (2008). Patient adherence to COPD. Thorax, 63(9), 831-838. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4747423/
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