Viral Respiratory Conditions
Pathophysiology
Pathogenesis of viral respiratory conditions
- Viruses are the cause of most URIs, with most cases associated with rhinovirus, parainfluenza virus, coronavirus, adenovirus, respiratory syncytial virus, coxsackievirus, and influenza virus1
- Pathogens enter the respiratory tract, invading the mucosa, via direct contact of an infected subject or by inhalation of droplets1,2
- Symptoms may include redness, edema, secretions of the respiratory tract, and fever2
- Excess or viscous mucus may cause a degenerative cycle to occur that arrests cilia and clogs sinus ostia3,4
Pathogenesis of the common cold5
- Viruses seem to invade epithelial cells in the respiratory mucosa
- Destruction and throwing off of these cells or loss of ciliary activity is dependent on the specific virus
- Increase in leuykocyte infiltration and nasal secretions, including large amounts of protein and immunoglobulin, suggest cytokines and immune mechanisms may be responsible for some common cold manifestations
Pathogenesis of hay fever and upper respiratory allergies
- Since the nose is the most common point of entry for allergens, patients with upper respiratory allergies often complain of signs and symptoms of allergic rhinitis
- After the first exposure to an antigen, macrophages present processed peptides to T helper cells
- After more exposure to the same antigen, these cells are stimulated to differentiate into either more T helper cells or B cells
- - B cells may then differentiate into plasma cells and produce immunoglobulin E (IgE) specific to that antigen
- Allergen-specific IgE molecules will bind to the surface of mast cells, sensitizing them
- - Further exposures lead to the binding of adjacent IgE molecules
- - This leads to the release of preformed mediators from mast cell granules
- Histamine, leukotrienes, and kinins cause early phase symptoms, such as sneezing, rhinorrhea, and congestion
- Late-phase reactions start 2 to 4 hours later and are caused by newly arrived inflammatory cells
- Mediators released by these cells prolong the earlier reactions and lead to chronic inflammation
References: 1. Mossad SB. Upper respiratory tract infections. Cleveland Clinic Web site. Revised July 29, 2005. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/infectiousdisease/urti/urti.htm . Accessed July 17, 2008. 2. Meneghetti A. Upper respiratory tract infection. Updated Dec 13, 2007. eMedicine Web site. http://www.emedicine.com/med/topic2339.htm. Accessed July 11, 2008. 3. Becker DG. Sinusitis. J Long Term Eff Med Implants. 2003;13(3):175-194. 4. Taghizadeh F, Hadley JA, Osguthorpe JD. Pharmacological treatments for rhinosinusitis. Expert Opin Pharmacother. 2002;3(3):305-313. 5. Dasaraju PV, Liu C. Infections of the respiratory system. Graduate School of Biomedical Sciences of University of Texas Medical Branch Web site. http://gsbs.utmb.edu/microbook/ch093.htm. Accessed July 11, 2008. 6. Nguyen QA. Allergic rhinitis. http://www.emedicine.com/ent/TOPIC194.htm. Accessed November 21, 2008.
