Most E. coli strains are harmless, but pathogenic varieties cause serious food poisoning, septic shock, meningitis, or urinary tract infections in humans.

[3] E. coli and related bacteria constitute about 0.1% of gut flora,[4] and fecal–oral transmission is the major route through which pathogenic strains of the bacterium cause disease.

Cells are able to survive outside the body for only a limited amount of time, which makes them ideal indicator organisms to test environmental samples for fecal contamination.

[9] Group II K antigens closely resemble those in gram-positive bacteria and greatly differ in composition and are further subdivided according to their acidic components, generally 20–50% of the CPS chains are bound to phospholipids.

Antibiotic and supportive treatment protocols for it are not as well-developed, as it has the ability to be very enterohemorrhagic like O157:H7, causing bloody diarrhea, but also is more enteroaggregative, meaning it adheres well and clumps to intestinal membranes.

[citation needed] Earlier, poor hygienic methods of preparing meat in Scotland killed seven people in 1996 due to E. coli poisoning, and left hundreds more infected.

[12] If E. coli bacteria escape the intestinal tract through a perforation (for example from an ulcer, a ruptured appendix, or due to a surgical error) and enter the abdomen, they usually cause peritonitis that can be fatal without prompt treatment.

Recent research suggests treatment of enteropathogenic E. coli with antibiotics may significantly increase the chance of developing haemolytic-uremic syndrome.

[15] Gastrointestinal infections can cause the body to develop memory T cells to attack gut microbes that are in the intestinal tract.

Uropathogenic E. coli (UPEC) is responsible for approximately 90% of urinary tract infections (UTI) seen in individuals with ordinary anatomy.

[11] In ascending infections, fecal bacteria colonize the urethra and spread up the urinary tract to the bladder as well as to the kidneys (causing pyelonephritis),[37] or the prostate in males.

[11] Approximately 1% of the human population lacks this receptor, [citation needed] and its presence or absence dictates an individual's susceptibility or non-susceptibility, respectively, to E. coli urinary tract infections.

[citation needed] Another virulence factor commonly present in UPEC is the Dr family of adhesins, which are particularly associated with cystitis and pregnancy-associated pyelonephritis.

[38] UPEC can evade the body's innate immune defences (e.g. the complement system) by invading superficial umbrella cells to form intracellular bacterial communities (IBCs).

Biofilm-producing E. coli are recalcitrant to immune factors and antibiotic therapy, and are often responsible for chronic urinary tract infections.

[11] Descending infections, though relatively rare, occur when E. coli cells enter the upper urinary tract organs (kidneys, bladder or ureters) from the blood stream.

[41] And because of the absence of the IgM antibodies from the mother (these do not cross the placenta because FcRn only mediates the transfer of IgG), plus the fact that the body recognizes as self the K1 antigen, as it resembles the cerebral glycopeptides, this leads to a severe meningitis in the neonates.

[citation needed] Some E. coli strains contain a polyketide synthase genomic island (pks), which encodes a multi-enzymatic machinery that produces colibactin, a substance that damages DNA.

[48] Diagnosis of infectious diarrhea and identification of antimicrobial resistance is performed using a stool culture with subsequent antibiotic sensitivity testing.

The U.S. Centers for Disease Control and Prevention recommend that "all stools submitted for routine testing from patients with acute community-acquired diarrhea (regardless of patient age, season of the year, or presence or absence of blood in the stool) be simultaneously cultured for E. coli O157:H7 (O157 STEC) and tested with an assay that detects Shiga toxins to detect non-O157 STEC".

Antibiotics which may be used to treat E. coli infection include amoxicillin, as well as other semisynthetic penicillins, many cephalosporins, carbapenems, aztreonam, trimethoprim-sulfamethoxazole, ciprofloxacin, nitrofurantoin and the aminoglycosides.

[54] Resistance to beta-lactam antibiotics has become a particular problem in recent decades, as strains of bacteria that produce extended-spectrum beta-lactamases have become more common.

In 2009, a gene called New Delhi metallo-beta-lactamase (shortened NDM-1) that even gives resistance to intravenous antibiotic carbapenem, were discovered in India and Pakistan on E. coli bacteria.

[citation needed] Increased concern about the prevalence of this form of "superbug" in the United Kingdom has led to calls for further monitoring and a UK-wide strategy to deal with infections and the deaths.

[citation needed] Phage therapy—viruses that specifically target pathogenic bacteria—has been developed over the last 80 years, primarily in the former Soviet Union, where it was used to prevent diarrhea caused by E.

[58] However, on January 2, 2007, the United States FDA gave Omnilytics approval to apply its E. coli O157:H7 killing phage in a mist, spray or wash on live animals that will be slaughtered for human consumption.

[citation needed] Researchers have actively been working to develop safe, effective vaccines to lower the worldwide incidence of E. coli infection.

[61] In March 2006, a vaccine eliciting an immune response against the E. coli O157:H7 O-specific polysaccharide conjugated to recombinant exotoxin A of Pseudomonas aeruginosa (O157-rEPA) was reported to be safe in children two to five years old.

[62] In 2006, Fort Dodge Animal Health (Wyeth) introduced an effective, live, attenuated vaccine to control airsacculitis and peritonitis in chickens.

[68] Results of the study showed that "the bacterium is more likely to cause severe diarrhea in people with type A blood," and this finding may aid current and future efforts to develop an effective vaccine against the pathogenic strains of E.