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 spreads 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 bronchioles epithelium. Cough reflex occurs due to exposure of the sub-epithelial tissue and nerve fibers. Vascular permeability 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 transmitted between individuals but when it is infected by RSV it may be transmitted by air droplets.
- This air droplets lead to infection of the nasopharyngeal mucosa.
Pathogenesis
Bronchiolitis is caused by a viral replication process and inflammation as the following:[1]
- Starting from the nasopharyngeal mucosa the RSV spreads to the lower airway tracts. It spreads till it reaches the bronchioles where viral replication takes place.
- The viral infection induces an inflammatory response which leads to infiltration of inflammatory cells (RSV-specific lymphocytes), edema and necrosis of the epithelium in the bronchioles which is then sloughed into the lumina causing proliferation of cuboidal epithelial cells without cilia.[2][3]
- 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 due to reduction of the bronchiolar lumina and necrotic tissue accumulation producing a valve mechanism, leading to hyperinflation.
- By this mechanism, air can flow 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.[4]
- 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 which are fibrotic buds extend to the 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.
- ↑ Wright M, Mullett CJ, Piedimonte G (2008). "Pharmacological management of acute bronchiolitis". Ther Clin Risk Manag. 4 (5): 895–903. PMC 2621418. PMID 19209271.
- ↑ 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.