Rotavirus infection pathophysiology: Difference between revisions
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Latest revision as of 00:03, 30 July 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]
Overview
Rotavirus is transmitted by the feco-oral route. It is transmitted from the infected children to other individuals before and after the occurance of the diarrhea. It can also spread through infected hands, food and objects like toys. Pathogenesis of the rotavirus takes place in the intestine where virus replication takes place and severe watery diarrhea takes place. Rotavirus protein number 4 plays an important role in causing the diarrhea and the rotavirus clinical manifestations. The infection destroys number of the intestinal digestive enzymes and malabsorption takes place leading to diarrhea. Rotavirus infection is not limited to the intestine only. It can affects the central nervous system causing meningitis.
Pathophysiology
Pathogenesis
- After entrance the virus to the body through the mouth, replication takes place in the small intestine where it can cause severe watery diarrhea.
- The pathogenesis of the rotavirus infection depends on the enzymes destruction and the enterotoxins of the virus itself.
- Virus virulence factors have a significant role in the pathogenesis of the rotavirus infections. The rotavirus has 11 genes at which each gene plays a role in the pathogenesis e.g. gene 3 helps in the virus replication, genes 4 and 9 help in the infection initiation, and gene 5 is responsible for the protein coding resulting in interfering the action of the antiviral drugs.[1]
- The main site of infection to the rotavirus are the intestinal villi. By the help of the viral protein number 4, rotavirus can bind its receptors initiating its infection. After the infection, replication takes place releasing viruses into the intestinal lumen. Proceeding from the virus replication, rotavirus produces the enterotoxins e.g. non structural protein 4 which will have a significant effect in causing the watery diarrhea.
- Rotavirus diarrhea is a watery diarrhea, not like the bacterial diarrhea, which occurs via many mechanisms dicussed as the following:
- The non-structural protein 4 stimulate free calcium ions
- The infection by the virus destroys the intestinal digestive enzymes like the maltase which is responsible for the carbohydrates digestion. This enzyme destruction increases the fluids in the lumen and causes malabsorption which leads to diarrhea.[2]
- Rotavirus infection is not limited to the intestine only. It can affects the central nervous system causing meningitis.
Transmission
- Rotavirus spreads easily among infants and young children. Children can spread the virus both before and after they become sick with diarrhea. They can also pass rotavirus to family members and other people with whom they have close contact.[3]
- People who are infected with rotavirus shed rotavirus in their stool - this is often how the virus spreads from a person’s body to other people and into the environment. They shed the virus most when they are sick and during the first 3 days after they recover.
- The virus spreads by the fecal-oral route; this means the virus is shed by an infected person and then enters a susceptible person’s mouth to cause infection. Rotavirus can be spread by the following:
- Hands
- Objects (toys, surfaces)
- Food
- Water
Associated conditions
Rotavirus may be associated with the following diseases:[4]
References
- ↑ Greenberg HB, Estes MK (2009). "Rotaviruses: from pathogenesis to vaccination". Gastroenterology. 136 (6): 1939–51. doi:10.1053/j.gastro.2009.02.076. PMC 3690811. PMID 19457420.
- ↑ Sack DA, Rhoads M, Molla A, Molla AM, Wahed MA (1982). "Carbohydrate malabsorption in infants with rotavirus diarrhea". Am J Clin Nutr. 36 (6): 1112–8. PMID 7148733.
- ↑ CDC https://www.cdc.gov/rotavirus/about/transmission.html Accessed on April 27, 2017
- ↑ Parashar UD, Nelson EA, Kang G (2013). "Diagnosis, management, and prevention of rotavirus gastroenteritis in children". BMJ. 347: f7204. doi:10.1136/bmj.f7204. PMID 24379214.