![]() ![]() aeruginosa evolves in CF lungs to adopt a mucoid phenotype (attributable to release of alginate exoproduct) that confers selective advantage for the pathogen and poor prognosis for the host. aeruginosa exhibit a stereotypic mode of pathogenesis a sentinel and early colonization event often engenders lifelong pulmonary infection by the same genetic strain. ![]() The Cystic Fibrosis Trust has information on lung transplants in cystic fibrosis. If you do have CF, thick mucus clogs the airways and makes it difficult to. If you don’t have CF, the mucus that lines organs and body cavities, such as your lungs and nose, is slippery and watery. It’s estimated that up to 9 out of 10 people will survive for at least a year after a transplant. Cystic fibrosis (CF) is a genetic (inherited) disease that causes sticky, thick mucus to build up in organs, including your lungs and pancreas. Robust pulmonary inflammation in the setting of inspissated mucus and chronic bacterial infection leads to collateral tissue injury and further aggravates respiratory decline. The outlook for people with cystic fibrosis is often better than for many transplant patients, as they’re often younger and in better general health. Microbiome analysis has identified dozens of other bacterial species in CF lungs, although a relationship of these less well-characterized organisms to disease progression has not been determined. CF respiratory secretions are exceedingly difficult to clear, and a complex bacterial flora that includes Staphylococcus aureus, Haemophilus influenzae, and Pseudomonas aeruginosa (among other pathogens, see below) is routinely cultured from CF sputum. The major morbidity and mortality associated with CF is attributable to pulmonary compromise, characterized by copious hyperviscous and adherent secretions that obstruct small and medium-sized airways. ![]()
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