Search results
Results from the WOW.Com Content Network
Enterotoxins have a particularly marked effect upon the gastrointestinal tract, causing traveler's diarrhea and food poisoning. The action of enterotoxins leads to increased chloride ion permeability of the apical membrane of intestinal mucosal cells.
The binding site is between beta sheets eight and nine. This allows the human claudin-3,4,6,7,8 and 14 to bind but not 1,2,5, and 10. The way the protein work is it destroys the cell membrane structure of animals by binding to claudin family proteins. These are components of tight junctions of the epithelial cell membrane.
Heat-stable enterotoxins (STs) are secretory peptides produced by some bacterial strains, such as enterotoxigenic Escherichia coli [2] which are in general toxic to animals. These peptides keep their 3D structure and remain active at temperatures as high as 100 °C.
A type of aflatoxin, AFB1, is the most common mycotoxin that is found in human food and animal feed. [38] AFB1 targets the liver of both humans and animals. [38] Acute aflatoxicosis can make humans and animals have symptoms like abdominal pain, vomiting, and even death. [38]
Enterotoxins are chromosomally encoded exotoxins that are produced and secreted from several bacterial organisms. It is a heat stable toxin and is resistant to digestive protease. [5] [6] It is the ingestion of the toxin that causes the inflammation and swelling of the intestine. [citation needed]
Koch's postulation was proven correct by Indian microbiologist Sambhu Nath De, who in 1951 studied and documented the effects of injecting rabbits with heat-killed cholera bacteria. [5] He concluded from this experiment that an endotoxin liberated upon disintegration of the bacteria was the cause of the symptoms of cholera. [ 5 ]
This means that cows cause 2 0 times the human fatalities as sharks, alligators, and bears which are perceived as the most ferocious animals but only claim a victim a year each.
Antibiotics are of questionable value and have not shown to be of clear clinical benefit. Antibiotics that interfere with DNA synthesis, such as fluoroquinolones, have been shown to induce the Stx-bearing bacteriophage and cause increased production of toxins. [9]