Acute viral nasopharyngitis pathophysiology
Acute viral nasopharyngitis Microchapters |
Differentiating acute viral nasopharyngitis from other diseases |
---|
Diagnosis |
Treatment |
Case Studies |
Acute viral nasopharyngitis pathophysiology On the Web |
American Roentgen Ray Society Images of Acute viral nasopharyngitis pathophysiology |
Risk calculators and risk factors for Acute viral nasopharyngitis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]
Overview
Rhinovirus (the most common cause of common cold) is usually transmitted via aerosol generated by coughing or sneezing.Following transmission, the virus invades the epithelial cells and causes the release of inflammatory cytokines that leads to the various symptoms of cold.
Pathophysiology
Virus
Common colds are most often caused by infection by one of the more than 100 serotypes of rhinovirus, a type of picornavirus. Other viruses causing colds are coronavirus, human parainfluenza viruses, human respiratory syncytial virus, adenoviruses, enteroviruses, or metapneumovirus.[1][2][3]
Transmission
The common cold virus is transmitted between people by one of two ways:
- In aerosol form generated by coughing, sneezing, or
- From contact with the saliva or nasal secretions of an infected person, either directly or from contaminated surfaces.
- Symptoms are not necessary for viral shedding or transmission, as a percentage of asymptomatic subjects exhibit viruses in nasal swabs.[4]
- The infectious period (time during which an infected person can infect others) begins about one day before symptoms begin, and continues for the first five days of the illness.
- The virus enters the cells of the lining of the nasopharynx (the area between the nose and throat) and rapidly multiplies.
- The major entry point is normally the nose, but can also be the eyes (in this case drainage into the nasopharynx would occur through the Nasolacrimal duct).
{{#ev:youtube|GoRhRJXp0j8}}
Pathogenesis
- Viruses undergo frequent changes in their antigenic coat. This helps the viruses to evade the immune system and enables them to cause recurrent infections.
- Rhinovirus binds to ICAM-1 receptors on epithelial cells. Binding to ICAM-1 receptors releases inflammatory cytokines but does not cause damage to epithelial cells.
- Respiratory syncytial virus does not cause any release of cytokines. Instead, it replicates in the nose and pharynx. In many occasions, it can spread to the lower respiratory tract.[5]
- Human parainfluenza virus causes inflammation of the tract and subsequently, parainfluenza infection is much more severe than other viruses.
- The body responds using both humoral immunity (IgA in the epithelium) and cellular immunity (different inflammatory cells in the adenoids and tonsils) to fight the offending virus.[3]
- Normal flora inhabitants in the nasopharynx also play an important role in eliminating the infection.
References
- ↑ "Common Cold (Upper Respiratory Infection)". The Merck Manual Online. Merck & Co. November 2005.
- ↑ CKS (2007). "Common Cold (Topic Review)". Clinical Knowledge Summaries Service.
- ↑ 3.0 3.1 van Kempen M, Bachert C, Van Cauwenberge P (1999). "An update on the pathophysiology of rhinovirus upper respiratory tract infections". Rhinology. 37 (3): 97–103. PMID 10567986.
- ↑ "Common Cold" (PDF) (pdf). Department of Health, Government of South Australia. 2005.
- ↑ Blaas D, Fuchs R (2016). "Mechanism of human rhinovirus infections". Mol Cell Pediatr. 3 (1): 21. doi:10.1186/s40348-016-0049-3. PMC 4889530. PMID 27251607.