Bronchiolitis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alonso Alvarado, M.D. [2]
Overview
Bronchiolitis is transmitted by air droplets. It is caused by RSV which leads to infection of nasopharyngeal mucosa. After the infection, the virus will spread to the lower airway tracts till it reaches the bronchioles where the viral replication takes place. The viral infection induces inflammation which leads to edema and necrosis of the bronchiolar epithelium. Cough reflex occurs due to exposure of the subepithelial tissue and nerve fibers. Vascular permeablity increases leading to edema and swelling. Histopathologically, bronchiolitis obliterans shows intraluminal polyps, inflammatory infiltration and macrophages. Constrictive bronchiolitis shows thickening of the airways and interluminal narrowing.
Pathophysiology
Transmission
- Bronchiolitis is not transmissible among individuals. However, when bronchiolitis is caused by respiratory syncytial virus (RSV) it may be transmitted by air droplets.
- Air droplets containing respiratory syncytial virus (RSV) leads to infection of nasopharyngeal mucosa and subsequent bronchiolitis.
Pathogenesis
Bronchiolitis is caused by a viral replication process and inflammation as the following:[1]
- Starting from the nasopharyngeal mucosa, respiratory syncytial virus (RSV) spreads to the lower airway tracts. It spreads till it reaches the bronchioles where viral replication takes place.
- The respiratory syncytial virus (RSV) infection induces an inflammatory response. It leads to infiltration of inflammatory cells (RSV-specific lymphocytes), edema and necrosis of the epithelium in the bronchioles. The epithelium is then sloughed into the lumina, causing proliferation of cuboidal epithelial cells without cilia.[2]
- Respiratory syncytial virus (RSV) causes lysis of the epithelial tissue which leads to the exposure of the subepithelial tissue and nerve fibers so inducing a cough reflex.
- The vascular permeability increases which result in edema and swelling.
- This inflammation process leads to complete or partial obstruction from reduction in bronchiolar lumina. Accumulation of necrotic tissue produce a valve mechanism, leading to hyperinflation.
- By this mechanism, air flow can increase into the lungs by increased negative pressure during inspiration but is unable to flow out of the lung as the airway's diameter is smaller during expiration.[2] Obstructed areas can evolve to atelectasis. In children, Kohn channels are not well developed, therefore atelectasis and hyperinflation can be greater.
Microscopic pathology
Bronchiolitis shows histopathological findings that differ between different types of the bronchiolitis.[3]
- Bronchiolitis obliterans:
- Intraluminal polyps (protrusions inside the bronchioles with fibroblastic proliferation)
- Inflammatory infiltration
- Type two pneumocytes lining the alveoli
- Macrophages
- Constrictive bronchiolitis:
- Scars leading to interluminal narrowing and obstruction.
- Thickening of the airways due to submucosal collagen and fibrosis.
- Proliferative bronchiolitis:
- Histopathology shows Masson bodies (fibrotic buds extending into alveoli).
References
- ↑ Garibaldi BT, Illei P, Danoff SK (2012). "Bronchiolitis". Immunol Allergy Clin North Am. 32 (4): 601–19. doi:10.1016/j.iac.2012.08.002. PMID 23102068.
- ↑ 2.0 2.1 Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier.
- ↑ Couture C, Colby TV (2003). "Histopathology of bronchiolar disorders". Semin Respir Crit Care Med. 24 (5): 489–98. doi:10.1055/s-2004-815600. PMID 16088569.