Achievable logoAchievable logo
USMLE/1
Sign in
Sign up
Purchase
Textbook
Support
How it works
Resources
Exam catalog
Mountain with a flag at the peak
Textbook
Introduction
1. Anatomy
2. Microbiology
2.1 General bacteriology
2.2 Introduction to systemic bacteriology
2.3 Gram positive cocci
2.4 Gram negative cocci
2.5 Gram positive bacilli
2.6 Gram negative bacilli
2.6.1 Introduction
2.6.2 E.coli
2.6.3 Klebsiella pneumoniae
2.6.4 Proteus
2.6.5 Vibrio cholerae
2.6.6 Other Vibrios
2.6.7 Salmonella
2.6.8 Pseudomonas
2.6.9 Minor pathogens
2.7 Other important bacteria
2.8 Virology
2.9 Parasitology
2.10 Mycology
3. Physiology
4. Pathology
5. Pharmacology
6. Immunology
7. Biochemistry
8. Cell and molecular biology
9. Biostatistics and epidemiology
10. Genetics
11. Behavioral science
Wrapping up
Achievable logoAchievable logo
2.6.2 E.coli
Achievable USMLE/1
2. Microbiology
2.6. Gram negative bacilli

E.coli

3 min read
Font
Discuss
Share
Feedback

The factors important in pathogenicity are pili (for initial adhesion to cells), enterotoxins (heat stable and heat labile toxins), endotoxin (as in all Gram negative bacteria), and capsule (seen in invasive strains causing systemic infections and septicaemia).

Heat labile toxin: Like cholera toxin and the enterotoxin of Bacillus cereus, the heat labile toxin of E.coli causes ADP ribosylation and activation of Gs. This stimulates adenylate cyclase, increasing cAMP. The result is loss of Na, Cl, and water from intestinal cells, which presents as watery diarrhea. The toxin has two subunits, A and B:

  • Subunit B binds to Gm ganglioside receptors on the small intestinal epithelium.
  • Subunit A is the active (enzymatic) unit.

Heat stable toxin: This is a polypeptide not inactivated by boiling for 30 minutes. It stimulates guanylate cyclase to increase cGMP, inhibiting the reabsorption of sodium and causing diarrhoea.

Verotoxin or Shiga-like toxin: This toxin is produced by EHEC (enterohemorrhagic E.coli) or STEC, especially strains such as E. coli O 157:H7. It inactivates protein synthesis by removing adenine from 28 S rRNA. It binds to receptors on the kidney and the endothelium of small vessels, causing hemolytic uremic syndrome and bloody diarrhea.

Human pathology:

E.coli is a common cause of UTI and diarrhea.

UTI: E.coli is the leading cause of community acquired UTI. It presents as dysuria (pain and burning sensation during micturition), increased frequency, and rarely fever. Pili help the bacteria adhere to the urothelium and cause UTI. Some strains carrying the “K” antigen are also prone to cause UTI.

Diarrhea: Five types of E.coli cause diarrhea and/or dysentery (blood in stools). These are as follows:

EPEC (Enteropathogenic E.coli) - Seen in cases of diarrhea in children. Causes disruption of the brush border in the small intestine.

ETEC (Enterotoxigenic E.coli) - Cause of “traveller’s diarrhea”. Produces heat labile and heat stable toxins.

EIEC (Enteroinvasive E.coli) - Causes bloody stools due to invasion of the intestinal mucosa. It is peculiar in being non lactose fermenting and non motile. Keep this in mind in the differential of bloody diarrhea (dysentery).

EHEC (Enterohemorrhagic E.coli) - New terminology is STEC (shiga toxin producing E.coli). It may cause mild diarrhea to severe HUS, especially in small children, older adults, and immunodeficient individuals. Common implicated foods include raw (or undercooked) meat, lettuce, alfalfa sprouts, salami, or raw (unpasteurized) milk, juice, or cider. E.coli O157 diarrhea should NOT be treated with antibiotics, especially beta lactams and fluoroquinolones, as they have been shown to be associated with the development of HUS.

EAEC (Enteroaggregative E.coli) - Causes diarrhea due to production of heat stable enterotoxin.

Other infections caused by E.coli include meningitis and sepsis in infants and older adults, peritonitis, and wound infections.

Laboratory diagnosis of E.coli infections

Samples include urine, stool, blood, CSF, wound discharge, etc., depending on the clinical findings. Isolation by culture is not essential, since empiric treatment is typically started based on clinical features and history alone. Culture is important in cases showing resistance to antibiotics, septicaemia, meningitis, and suspected E.coli O 157 diarrhea.

Lactose fermenting
colonies E.coli
Lactose fermenting colonies E.coli

Gram stain shows Gram negative bacilli. MacConkey’s agar shows pink lactose fermenting colonies, except in EIEC. EMB agar shows colonies with a green metallic sheen. E.coli O 157 H7 can be identified by its inability to ferment sorbitol, which is characteristic.

Factors in Pathogenicity

  • Pili: initial adhesion to host cells
  • Enterotoxins: heat labile (LT) and heat stable (ST) toxins
  • Endotoxin: present in all Gram negative bacteria
  • Capsule: seen in invasive, systemic, and septicemic strains

Heat Labile Toxin (LT)

  • ADP ribosylation → activates Gs protein → ↑ adenylate cyclase → ↑ cAMP
  • Causes loss of Na, Cl, water → watery diarrhea
  • Two subunits:
    • B: binds Gm ganglioside receptors
    • A: enzymatic activity

Heat Stable Toxin (ST)

  • Not inactivated by boiling
  • Stimulates guanylate cyclase → ↑ cGMP
  • Inhibits sodium reabsorption → diarrhea

Verotoxin (Shiga-like Toxin)

  • Produced by EHEC/STEC (e.g., O157:H7)
  • Inactivates 28S rRNA → inhibits protein synthesis
  • Binds kidney/endothelial receptors → hemolytic uremic syndrome (HUS), bloody diarrhea

Human Pathology

  • Common causes: UTI, diarrhea
  • UTI:
    • Leading cause of community-acquired UTI
    • Symptoms: dysuria, frequency, rarely fever
    • Pili and K antigen aid in pathogenesis
  • Diarrhea: five types of diarrheagenic E.coli
    • EPEC: disrupts brush border, pediatric diarrhea
    • ETEC: “traveller’s diarrhea,” produces LT and ST toxins
    • EIEC: invasive, bloody stools, non-lactose fermenting, non-motile
    • EHEC/STEC: shiga toxin, HUS, avoid antibiotics (esp. beta lactams, fluoroquinolones)
    • EAEC: heat stable enterotoxin, persistent diarrhea

Other Infections

  • Meningitis and sepsis (infants, elderly)
  • Peritonitis, wound infections

Laboratory Diagnosis

  • Samples: urine, stool, blood, CSF, wound discharge
  • Culture not always essential; important for resistant cases, sepsis, meningitis, suspected O157
  • Gram stain: Gram negative bacilli
  • MacConkey agar: pink lactose fermenting colonies (except EIEC)
  • EMB agar: green metallic sheen
  • O157:H7: does not ferment sorbitol (diagnostic feature)

Sign up for free to take 1 quiz question on this topic

All rights reserved ©2016 - 2026 Achievable, Inc.

E.coli

The factors important in pathogenicity are pili (for initial adhesion to cells), enterotoxins (heat stable and heat labile toxins), endotoxin (as in all Gram negative bacteria), and capsule (seen in invasive strains causing systemic infections and septicaemia).

Heat labile toxin: Like cholera toxin and the enterotoxin of Bacillus cereus, the heat labile toxin of E.coli causes ADP ribosylation and activation of Gs. This stimulates adenylate cyclase, increasing cAMP. The result is loss of Na, Cl, and water from intestinal cells, which presents as watery diarrhea. The toxin has two subunits, A and B:

  • Subunit B binds to Gm ganglioside receptors on the small intestinal epithelium.
  • Subunit A is the active (enzymatic) unit.

Heat stable toxin: This is a polypeptide not inactivated by boiling for 30 minutes. It stimulates guanylate cyclase to increase cGMP, inhibiting the reabsorption of sodium and causing diarrhoea.

Verotoxin or Shiga-like toxin: This toxin is produced by EHEC (enterohemorrhagic E.coli) or STEC, especially strains such as E. coli O 157:H7. It inactivates protein synthesis by removing adenine from 28 S rRNA. It binds to receptors on the kidney and the endothelium of small vessels, causing hemolytic uremic syndrome and bloody diarrhea.

Human pathology:

E.coli is a common cause of UTI and diarrhea.

UTI: E.coli is the leading cause of community acquired UTI. It presents as dysuria (pain and burning sensation during micturition), increased frequency, and rarely fever. Pili help the bacteria adhere to the urothelium and cause UTI. Some strains carrying the “K” antigen are also prone to cause UTI.

Diarrhea: Five types of E.coli cause diarrhea and/or dysentery (blood in stools). These are as follows:

EPEC (Enteropathogenic E.coli) - Seen in cases of diarrhea in children. Causes disruption of the brush border in the small intestine.

ETEC (Enterotoxigenic E.coli) - Cause of “traveller’s diarrhea”. Produces heat labile and heat stable toxins.

EIEC (Enteroinvasive E.coli) - Causes bloody stools due to invasion of the intestinal mucosa. It is peculiar in being non lactose fermenting and non motile. Keep this in mind in the differential of bloody diarrhea (dysentery).

EHEC (Enterohemorrhagic E.coli) - New terminology is STEC (shiga toxin producing E.coli). It may cause mild diarrhea to severe HUS, especially in small children, older adults, and immunodeficient individuals. Common implicated foods include raw (or undercooked) meat, lettuce, alfalfa sprouts, salami, or raw (unpasteurized) milk, juice, or cider. E.coli O157 diarrhea should NOT be treated with antibiotics, especially beta lactams and fluoroquinolones, as they have been shown to be associated with the development of HUS.

EAEC (Enteroaggregative E.coli) - Causes diarrhea due to production of heat stable enterotoxin.

Other infections caused by E.coli include meningitis and sepsis in infants and older adults, peritonitis, and wound infections.

Laboratory diagnosis of E.coli infections

Samples include urine, stool, blood, CSF, wound discharge, etc., depending on the clinical findings. Isolation by culture is not essential, since empiric treatment is typically started based on clinical features and history alone. Culture is important in cases showing resistance to antibiotics, septicaemia, meningitis, and suspected E.coli O 157 diarrhea.

Gram stain shows Gram negative bacilli. MacConkey’s agar shows pink lactose fermenting colonies, except in EIEC. EMB agar shows colonies with a green metallic sheen. E.coli O 157 H7 can be identified by its inability to ferment sorbitol, which is characteristic.

Key points

Factors in Pathogenicity

  • Pili: initial adhesion to host cells
  • Enterotoxins: heat labile (LT) and heat stable (ST) toxins
  • Endotoxin: present in all Gram negative bacteria
  • Capsule: seen in invasive, systemic, and septicemic strains

Heat Labile Toxin (LT)

  • ADP ribosylation → activates Gs protein → ↑ adenylate cyclase → ↑ cAMP
  • Causes loss of Na, Cl, water → watery diarrhea
  • Two subunits:
    • B: binds Gm ganglioside receptors
    • A: enzymatic activity

Heat Stable Toxin (ST)

  • Not inactivated by boiling
  • Stimulates guanylate cyclase → ↑ cGMP
  • Inhibits sodium reabsorption → diarrhea

Verotoxin (Shiga-like Toxin)

  • Produced by EHEC/STEC (e.g., O157:H7)
  • Inactivates 28S rRNA → inhibits protein synthesis
  • Binds kidney/endothelial receptors → hemolytic uremic syndrome (HUS), bloody diarrhea

Human Pathology

  • Common causes: UTI, diarrhea
  • UTI:
    • Leading cause of community-acquired UTI
    • Symptoms: dysuria, frequency, rarely fever
    • Pili and K antigen aid in pathogenesis
  • Diarrhea: five types of diarrheagenic E.coli
    • EPEC: disrupts brush border, pediatric diarrhea
    • ETEC: “traveller’s diarrhea,” produces LT and ST toxins
    • EIEC: invasive, bloody stools, non-lactose fermenting, non-motile
    • EHEC/STEC: shiga toxin, HUS, avoid antibiotics (esp. beta lactams, fluoroquinolones)
    • EAEC: heat stable enterotoxin, persistent diarrhea

Other Infections

  • Meningitis and sepsis (infants, elderly)
  • Peritonitis, wound infections

Laboratory Diagnosis

  • Samples: urine, stool, blood, CSF, wound discharge
  • Culture not always essential; important for resistant cases, sepsis, meningitis, suspected O157
  • Gram stain: Gram negative bacilli
  • MacConkey agar: pink lactose fermenting colonies (except EIEC)
  • EMB agar: green metallic sheen
  • O157:H7: does not ferment sorbitol (diagnostic feature)