Pathogenesis

Cholera and Body Function

Vibrio Cholerae have the ability to secrete an enterotoxin (known as cholera toxin) that enters the intestinal cells.

Cholera toxin increases the production and activity of enzymes that regulate the pumping mechanism of the body. This pumping controls the movement of fluids and electrolytes in both your intestinal and circulatory system.

By increasing the enzymes produced, cholera toxin leaves the pump on, causing an enormous outflow of fluid and leading to extreme dehydration. This can lead to the outflow of up to 1 liter of fluid per hour.

Life-threatening cases of cholera are all caused by the loss of water and electrolytes in the body. (11)

Cholera Toxin (CT)

Cholera toxin is an A-B type toxin as well as an enterotoxin. It affects the internal cell functions of the body

CT B subunits bind to the receptors of a protein (G protein) found on intestinal cells. Endocytosis of the CT occurs, and the toxin is taken into the endoplasmic reticulum, where it's transported to the cytoplasm.

The CT A subunit alters the G protein to control its activity, increasing the production of a monophosphate that regulates hormones known as cyclic AMPs. By doing so, it inhibits the regulatory functions of the G protein.

As many chloride ions and other ions are released out of the cell, water leaves as well in order to equilibrate the osmolarity. This leads to dehydration as water is released. (11)(18)

A picture of Cholera Toxin invading an intestinal cell

A Video on Cholera Toxin

This is a video describing in detail how cholera toxin invades and effects an intestinal cell, disrupting the cells internal functions and quickly ruining the hosts internal mechanisms. (18)

The Immune System Response

Innate Immune Response

The innate immune system is virtually non-responsive to bacterial invasion of cholera. Cholera is a rapidly progressive disease that is typically non-inflammatory because of its ability to suppress the immune system.

By also releasing a toxin called MARTX (multifunctional auto-processing repeats-in-toxin), it can inhibit the inflammatory response of the innate immune system by blocking pro-inflammatory cytokines, prohibiting the intestinal cells from calling more immune cells to the scene. (12)

Adaptive Immune Response

Cellular Immune Response

If the patient survives the initial stages of infection, eventually through antigen presentation in the gastrointestinal mucosa, antigen-specific B cells will migrate to lymph nodes and will start proliferating. Levels of T cells and B cells increase significantly around a week into the infection. Studies also show that the immune response to cholera is T cell-dependent, relying on helper T cells. (11)

Humoral Immune Response

Production of antibodies for cholera is stimulated once detected. Because the infections is primarily in the intestinal mucosal system, the amount of IgA specific antibodies increases. As antibodies are made to combat V. cholera LPS, cholera toxin, and colonization factors, one infection of cholera provides long-term protection against another infection from the bacteria. (11)

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