Escherichia coli

Escherichia coli 
Pathophysiology
Intestinal illness caused by E coli results from the ingestion of bacteria and the innate ability of E coli to overcome host defenses. Gram-negative bacteria are characterized by their cell envelope, which comprises an inner cytoplasmic cell membrane, peptidoglycan cell wall, and outer membrane. The outer membrane is composed of a lipid bilayer, associated proteins, and lipopolysaccharide, and causes a toxic reaction if lysed. Pathogenic E coli strains each have distinctive virulence factors encoded on plasmids, transposons, and bacteriophages.

Intestinal Infections

Enterotoxigenic E coli pathophysiology

Colonizing fimbriae expressed by ETEC enable the bacteria to attach to the intestinal wall. Once connected, ETEC expresses either a heat-labile toxin or a heat-stable toxin, both of which are secretory toxins encoded on plasmids. Heat-labile toxin stimulates adenylate cyclase, leading to increased intracellular cyclic adenosine monophosphate (cAMP) and subsequent chloride secretion from intestinal crypt cells. This mechanism also inhibits intestinal villi from absorbing sodium chloride.

The resulting increase in electrolytes leads to the secretion of free water into the intestinal lumen, thus producing watery diarrhea. The heat-stable toxin stimulates guanylate cyclase, leading to increased intracellular cyclic guanosine monophosphate. This results in subsequent chloride secretion and inhibition of sodium chloride absorption in the intestinal lumen, thereby producing watery diarrhea.

Enteropathogenic E coli pathophysiology

A bundle-forming pilus is encoded by the plasmid (pEAF), enabling EPEC to form a localized attachment to enterocytes in the small intestine. Once bound, the outer membrane protein colonization factor, intimin, facilitates enhanced adherence. Intimin is an outer membrane protein colonization factor encoded on the eae gene within the locus of enterocyte effacement (LEE) chromosomal island.[24] The LEE chromosomal island elaborates approximately 20 secretory toxins that are injected into the enterocyte by a type III injectisome. These toxins trigger a series of events that ultimately lead to the characteristic effacement of microvilli, increased permeability of tight junctions, and alterations in water and electrolyte secretion and absorption.

EspF is a LEE-secreted protein that is not involved with attaching and effacing. EspF appears to disrupt the intestinal barrier function by altering electrical resistance, thereby increasing monolayer permeability. This LEE-secreted protein has several protein-protein interaction domains that may function by interacting with endocytic regulation. EspG and EspG2 are 2 other secreted proteins that inhibit luminal membrane chloride absorption by decreasing surface expression of the Cl-/OH-exchanger via disruption of microtubules.

Enteroaggregative E coli pathophysiology

EAEC exhibits a stacked brick pattern of adherence to epithelial cells.[28] The virulence plasmid encodes the transcriptional activator AggR, which activates several virulence factors, although the scientific understanding of this process is incomplete. AggR likely induces aggregative adherence fimbriae, adhesin, surface protein dispersin, and the enterotoxins Pet, EAST-1, ShET1, and ShET2. Dispersin likely promotes aggregative adherence fimbriae-mediated colonization.

Enterohemorrhagic/Shiga toxin-producing E coli pathophysiology

EHEC/STEC produces bloody diarrhea due to its ability to express Shiga toxin 1 (Stx1) and Shiga toxin 2 (Stx2). Stx1 and Stx2 are closely related to Shiga toxin (Stx) produced by Shigella dysenteriae. EHEC/STEC, which expresses Stx2, results in bloody diarrhea and may also express Stx1, while bacteria that do not express Stx2 do not induce bloody diarrhea. These toxins inhibit protein synthesis, leading to enterocyte cell death and inflammatory colitis.

EHEC/STEC is also known for its ability to induce hemolytic uremic syndrome (HUS). The classic triad of microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency characterizes HUS.[35] Please see StatPearls' companion resource, "Enterohemorrhagic Escherichia coli," for further information on the pathophysiology and toxicokinetics of EHEC/STEC.

Enteroinvasive E coli

Like EHEC, enterotoxins induce secretory diarrhea. Subsequent colonization and invasion of the colonic mucosa, along with replication and cell-to-cell spread, result in inflammatory colitis.

Extraintestinal Infections

Extraintestinal infections caused by E coli are generally the result of the translocation of commensal E coli outside of the intestine. The urinary tract is the most common extraintestinal site of infection caused by E coli.[37] UTIs are a significant reason for ambulatory care visits in the United States and are the second most common cause of hospitalization after pneumonia.[38][39] UTIs from E coli result from bacteria ascending the urethra and are more common in women than men, given the proximity of the urethra.

E coli is also a frequent cause of ventilator-associated pneumonia, a major life-threatening hospital-acquired infection with a suspected pathogenesis as a result of aspiration of gastric contents. In contrast, E coli rarely causes community-acquired pneumonia, but is associated with severe outcomes when it does cause this infection.[42] E coli bacteremia is typically the result of spread from a primary E coli infection at another site.
https://www.ncbi.nlm.nih.gov/books/NBK564298/

https://www.ncbi.nlm.nih.gov/books/NBK564298/

Escherichia coli

You may need to right click on the area showing the instructions and select "Automatically Resize" depending upon the browser.