Bronchiectasis can develop in association with cystic fibrosis, intralobar sequestration, postinfectious conditions from TB/Staph, and autoimmune disorders.

• A. Cystic fibrosis
• B. Intralobar sequestration
• C. Postinfectious TB/Staph
• D. All of the above

Answer: (D)

Bronchiectasis results from a harmful cycle where infection and inflammation destroy the bronchial wall, leading to irreversible dilation. Any condition that promotes recurrent infection or impairs airway defenses can start this process. In cystic fibrosis, thick, sticky mucus traps bacteria and drives repeated infections with prominent neutrophilic inflammation, gradually eroding the bronchial walls. Intralobar sequestration is a congenital area of lung tissue with abnormal drainage and blood supply that frequently becomes the site of recurrent infections, causing localized bronchial damage and bronchiectasis in adjacent airways. Postinfectious bronchiectasis follows severe infections, such as TB or Staphylococcus aureus, where scarring and sustained inflammation chronically weaken the bronchial walls. Autoimmune disorders can also cause chronic airway inflammation and remodeling, contributing to bronchial dilation over time. Since each scenario can initiate the destructive cycle, all of the above can be associated with bronchiectasis.