Microbiologists have studied the genetic mechanisms by which the V. cholerae bacteria turn off the production of some proteins and turn on the production of other proteins as they respond to the series of chemical environments they encounter, passing through the stomach, through the mucous layer of the small intestine, and on to the intestinal wall. Of particular interest have been the genetic mechanisms by which cholera bacteria turn on the protein production of the toxins that interact with host cell mechanisms to pump chloride ions into the small intestine, creating an ionic pressure which prevents sodium ions from entering the cell. The chloride and sodium ions create a salt-water environment in the small intestines, which through osmosis can pull up to six liters of water per day through the intestinal cells, creating the massive amounts of diarrhea. The host can become rapidly dehydrated unless treated properly.By inserting separate, successive sections of V. cholerae DNA into the DNA of other bacteria, such as E. coli that would not naturally produce the protein toxins, researchers have investigated the mechanisms by which V. cholerae responds to the changing chemical environments of the stomach, mucous layers, and intestinal wall. Researchers have discovered a complex cascade of regulatory proteins controls expression of V. cholerae virulence determinants. In responding to the chemical environment at the intestinal wall, the V. cholerae bacteria produce the TcpP/TcpH proteins, which, together with the ToxR/ToxS proteins, activate the expression of the ToxT regulatory protein.
In humans
In humans, enteroliths are rare and may be difficult to distinguish from gall stones. Their chemical composition is diverse, and rarely can a nidus be found. A differential diagnosis of an enterolith requires the enterolith, a normal gallbladder, and a diverticulum.An enterolith typically forms within a diverticulum. An enterolith formed in a Meckels diverticulum sometimes is known as a Meckels enterolith. Improper use of magnesium oxide as a long-term laxative has been reported to cause enteroliths and/or medication bezoars.Most enteroliths are not apparent and cause no complications. However, any complications that do occur are likely to be severe. Of these, bowel obstruction is most common, followed by ileus and perforation. Bowel obstruction and ileus typically occur when a large enterolith is expelled from a diverticulum into the lumen. Perforation typically occurs within the diverticulum.On plain X-rays,the visibility of the enterolith depends on its calcium content. Calcium-rich stones usually demonstrate a radiodense rim and a relatively radioluscent core. Choleic acid stones are almost always radiolucent. They sometimes can be visualized on CT scans without contrast;  presence of contrast in the lumen may reveal the enterolith as a void. Most often, they are visualized using ultrasound. Although recent surveys of enterolith composition are lacking, one early review notes struvite (as in equines), calcium phosphate, and calcium carbonate and reports choleic acid. Deoxycholic acid and cholic acid have also been reported. Treatment
In simple cases of obstruction, where there are no complications, a variety of non-surgical and surgical techniques are used to remove the enterolith.