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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.
The eukaryotic cell cycle consists of four distinct phases: G 1 phase, S phase (synthesis), G 2 phase (collectively known as interphase) and M phase (mitosis and cytokinesis). M phase is itself composed of two tightly coupled processes: mitosis, in which the cell's nucleus divides, and cytokinesis, in which the cell's cytoplasm and cell membrane divides forming two daughter cells.
A 2002 study showed that Chlorella cell walls contain lipopolysaccharides, endotoxins found in Gram-negative bacteria that affect the immune system and may cause inflammation. [ 19 ] [ 20 ] [ 21 ] However, more recent studies have found that the lipopolysaccharides in organisms other than Gram-negative bacteria, for example in cyanobacteria ...
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.
Bacteria can reduce their susceptibility by changing their surface receptors and preventing phage adsorption. In the case of V. cholerae, the changed receptor gene expression is due to an alteration in cell-density during its infection cycle, a process called quorum sensing (QS). The stool samples collected from patients contain clumps of ...
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.