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Cholera is caused by a number of types of Vibrio cholerae, with some types producing more severe disease than others. [2] It is spread mostly by unsafe water and unsafe food that has been contaminated with human feces containing the bacteria. [2] Undercooked shellfish is a common source. [9] Humans are the only known host for the bacteria. [2]
Sambhu Nath De isolated the cholera toxin and demonstrated the toxin as the cause of cholera in 1959. The bacterium has a flagellum (a tail like structure) at one pole and several pili throughout its cell surface. It undergoes respiratory and fermentative metabolism.
Quorum sensing is essentially the intercommunication between cells to interact and respond to its environment.V. cholerae uses two autoinducers: cholera autoinducer-1 (CAI-1) and autoinducer-2 (AI-2). CAI-1 is the major quorum-sensing signal. Quorum sensing is the cell to cell communication that allows organisms to share information.
The daily cycle of carbohydrate build-up from photosynthesis and carbohydrate catabolism during dark hours is enough to fine-tune the cell's position in the water column, bring it up toward the surface when its carbohydrate levels are low and it needs to photosynthesis, and allowing it to sink away from the harmful UV radiation when the cell's ...
One of the most important aspects of cholera toxin is the retrograde traffic mechanism that transports the toxin from the cell membrane back to the trans-Golgi network and the endoplasmic reticulum. Since both cholera toxin and GM1 species can be tagged with a fluorescent tags, the mechanism of retrograde traffic can be monitored.
BEIJING (Reuters) -Detection in the Chinese city of Wuhan of a bacteria that caused cholera in a student and was separately found in samples from softshell turtles at a food market has struck a ...
A representation by Robert Seymour of the cholera epidemic depicts the spread of the disease in the form of poisonous air.. The miasma theory was the predominant theory of disease transmission before the germ theory took hold towards the end of the 19th century; it is no longer accepted as a correct explanation for disease by the scientific community.
Formation of the pre-replication complex during late M and early G1 phase is required for genome replication, but after the genome has been replicated the pre-RC must not form again until the next cell cycle. In prokaryotes, various studies have demonstrated that the pre-RC is a complex that is only present for a fraction of the cell cycle.