Cystic fibrosis is believed to arise from a biochemical genetic defect that reduces the ability to fight infections (gene therapy is currently being tested, at a proposed cost of $311,000 per year). Frequent lung infections are the hallmark of cystic fibrosis, without consideration of whether a lung infection is the disease; and the infection is causing an altered immune system, genetic defects, and endothelial damage. Cystic fibrosis is treated symptomatically, and patients suffer for a lifetime, may require a lung transplant, and have a shortened lifespan.
Chlamydia pneumonia and psittacosis infections can produce copious thick mucus, pus, and sputum clogging the lung; consolidation of pus in the lower lung; inclusion cyst formation; low oxygen levels; and scarring of the lung. Chlamydia pneumonia can attack endothelial cells in the lung; and has been “associated” with acute respiratory exacerbation. When the patients first acquire chlamydia pneumonia—in utero or after birth, is unknown. Chlamydia pneumonia is common in the community, and the rate of chlamydia psittacosis is unknown. Other pathogens, such as pseudomonas and streptococcus have also been found in cystic fibrosis patients.
Cystic fibrosis is caused by immortal pathogens acquired in utero or as a young child. Significant benefit was observed with continuous macrolide therapy; however, macrolide therapy was only beneficial when continued long-term, suggesting the underlying immortal infection is difficult to treat. Diagnosing chlamydia and other pathogens, and adding therapies that treat these pathogens and improve penetration of the macrolide will improve the effectiveness of treatment.
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