Dysentery pathophysiology
|
Dysentery Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Dysentery pathophysiology On the Web |
|
American Roentgen Ray Society Images of Dysentery pathophysiology |
|
Risk calculators and risk factors for Dysentery pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2]
Pathophysiology
Dysentery results from viral infections, bacterial infections, or parasitic infestations. These pathogens typically reach the large intestine after entering orally, through ingestion of contaminated food or water, oral contact with contaminated objects or hands, and so on.
Each specific pathogen has its own mechanism or pathogenesis, but in general the result is damage to the intestinal lining, leading to the inflammatory immune response. This can cause elevated temperature, painful spasms of the intestinal muscles (cramping), swelling due to water leaking from capillaries of the intestine (edema), and further tissue damage by the body's immune cells and the chemicals, called cytokines, they release to fight the infection. The result can be impaired nutrient absorption, excessive water and mineral loss through the stools due to breakdown of the control mechanisms in the intestinal tissue that normally remove water from the stools, and in severe cases the entry of pathogenic organisms into the bloodstream.
Some microorganisms – for example, bacteria of the genus Shigella – secrete substances known as cytotoxins, which kill and damage intestinal tissue on contact. Viruses directly attack the intestinal cells, taking over their metabolic machinery to make copies of themselves, which leads to cell death.