Intestinal Tract Infection with E.Coli

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The first step is the adherence of the organism to the cells of the jejunum and ileum by means of pili that protrude from the bacterial surface. Once attached, the bacteria synthesize enterotoxins (exotoxins that act in the enteric tract), which act on the cells of the jejunum and ileum to cause diarrhea. The toxins are strikingly cell-specific; the cells of the colon are not susceptible, probably because they lack receptors for the toxin. Enterotoxigenic strains of E coli (ETEC) can produce either or both of two
enterotoxins.
(1) The heat-labile toxin (LT) acts by stimulating adenylate cyclase. Both LT and cholera toxin act by catalyzing the addition of adenosine diphosphate-ribose (a process called ADP-ribosylation) to the G protein that stimulates the cyclase. This irreversibly activates the cyclase. The resultant increase in intracellular cyclic adenosine monophosphate (AMP) concentration stimulates cyclic AMP– dependent protein kinase, which phosphorylates ion transporters in the membrane. The transporters export ions, which cause an outpouring of fluid, potassium, and chloride from the enterocytes into the lumen of the gut, resulting in watery diarrhea. Note that cholera toxin has the same mode of action.
(2) The other enterotoxin is a low-molecular-weight, heat-stable toxin (ST), which stimulates guanylate cyclase. The enterotoxin-producing strains do not cause inflammation, do not invade the intestinal mucosa, and cause a watery, nonbloody diarrhea However, certain strains of E. coli are enteropathic (enteroinvasive) and cause disease not by enterotoxin formation but by invasion of the epithelium of the large intestine, causing bloody diarrhea (dysentery) accompanied by inflammatory cells (neutrophils) in the stool.
Certain enterohemorrhagic strains of E. coli (i.e., those with the O157:H7 serotype) (STEC) also cause bloody diarrhea by producing an exotoxin called Shiga toxin, so called because it is very similar to that produced by Shigella species. Shiga toxin acts by removing an adenine from the large (28S) ribosomal RNA, thereby stopping protein synthesis. Shiga toxin is encoded by temperate (lysogenic) bacteriophages. Shiga toxin is also called verotoxin because it has a cytopathic effect on Vero (monkey) cells in culture.
These O157:H7 strains are associated with outbreaks of bloody diarrhea following ingestion of undercooked hamburger, often at fast-food restaurants. The bacteria on the surface of the hamburger are killed by the cooking, but those in the interior, which is undercooked, survive. Also, direct contact with animals (e.g., visits to farms and petting zoos) has resulted in bloody diarrhea caused by O157:H7
strains. E. coli O157 has a low ID50 of approximately 100 organisms.
Some patients with bloody diarrhea caused by O157:H7 strains also have a life-threatening complication called hemolytic–uremic syndrome (HUS), which occurs when Shiga toxin enters the bloodstream. This syndrome consists of hemolytic anemia, thrombocytopenia, and acute renal failure. The hemolytic anemia and renal failure occur because there are receptors for Shiga toxin on the surface of the endothelium of small blood vessels and on the surface of kidney epithelium. Death of the endothelial cells of small blood vessels results in a microangiopathic hemolytic anemia in which the red cells passing through the damaged area become grossly distorted (schistocytes) and then lyse.
Thrombocytopenia occurs because platelets adhere to the damaged endothelial surface. Death of the kidney epithelial cells leads to renal failure. Treatment of diarrhea caused by O157:H7 strains with antibiotics, such as ciprofloxacin, increases the risk of developing HUS by increasing the amount of Shiga toxin released by the dying bacteria.

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Hello! I am Dukagjin Zeqiraj from Kosovo. I have finished Medical Faculty in Prishtina ( capital city of Kosovo). Now I live in Pristina and I work in QKMF Podujeve (family medicine center). Tel: +38344311154