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Escherichia coli Infections

by Larry M. Bush, MD, Maria T. Perez, MD

Escherichia coli are the most numerous aerobic commensal inhabitants of the large intestine. Certain strains cause diarrhea, and all can cause infection when they invade sterile sites (eg, the urinary tract). Diagnosis is by standard culture techniques. Toxin assays may help identify the cause of diarrhea. Treatment with antibiotics is guided by susceptibility testing.

Diseases caused by E. coli

  • UTI (most common)

  • Enteric infection (certain strains)

  • Invasive infection (rare, except in neonates)

Most commonly, E. coli cause UTIs, which usually represent ascending infection (ie, from the perineum via the urethra).

E. coli normally inhabit the GI tract; however, some strains have acquired genes that enable them to cause intestinal infection. When ingested, the following strains can cause diarrhea:

  • Enterohemorrhagic: These strains (including serotype O157:H7 and others—see Infection by Escherichia coli O157:H7 and Other Enterohemorrhagic E. coli (EHEC)) produce several cytotoxins, neurotoxins, and enterotoxins, including Shiga toxin (verotoxin), and cause bloody diarrhea; hemolytic-uremic syndrome develops in 2 to 7% of cases (see Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic-Uremic Syndrome (HUS)). Such strains have most often been acquired from undercooked ground beef but may also be acquired from infected people by the fecal-oral route when hygiene is inadequate.

  • Enterotoxigenic: These strains can cause watery diarrhea, particularly in infants and travelers (see Traveler’s Diarrhea).

  • Enteroinvasive: These strains can cause inflammatory diarrhea.

  • Enteropathogenic: These strains can cause watery diarrhea, particularly in infants.

  • Enteroaggregative: Some strains are emerging as potentially important causes of persistent diarrhea in patients with AIDS and in children in tropical areas.

Other strains are capable of causing extraintestinal infection if normal intestinal anatomic barriers are disrupted (eg, by ischemia, inflammatory bowel disease, or trauma), in which case the organism may spread to adjacent structures or invade the bloodstream. Hepatobiliary, peritoneal, cutaneous, and pulmonary infections also occur. E. coli bacteremia may also occur without an evident portal of entry.

In neonates, particularly preterm infants, E. coli bacteremia and meningitis (caused by strains with the K1 capsule, a marker for neuroinvasiveness) are common (see Neonatal Bacterial Meningitis and Neonatal Sepsis).


  • Culture

Samples of blood, stool, or other clinical material are sent for culture. If an enterohemorrhagic strain is suspected, the laboratory must be notified because special culture media are required.


  • Various antibiotics depending on site of infection and susceptibility testing

Treatment must be started empirically based on the site and severity of infection (eg, mild bladder infection, urosepsis) and then modified based on antibiotic susceptibility testing. Many strains are resistant to ampicillin and tetracyclines, so other drugs should be used; they include ticarcillin, piperacillin, cephalosporins, aminoglycosides, trimethoprim/sulfamethoxazole (TMP/SMX), and fluoroquinolones.

Surgery may be required to drain pus, debride necrotic lesions, or remove foreign bodies.

Drug resistance

Besides being resistant to ampicillin and tetracycline, E. coli have become increasingly resistant to TMP/SMX and fluoroquinolones. Also, multidrug-resistant strains that produce extended-spectrum β-lactamases (ESBLs) have emerged as an important cause of community-acquired UTI and sepsis. ESBLs can hydrolyze most β-lactams, including penicillins and broad-spectrum cephalosporins and monobactams, but not carbapenems (imipenem, meropenem, doripenem, ertapenem); carbapenems should be used for ESBL-producing E. coli.

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