ENTEROHEMORRHAGIC E.COLI (EHEC)

Shiga toxin-producing e.coli (STEC) and Verocytotoxin-producing E.coli(VTEC)

key pathogenic mechanism

1. Bundle Forming Pili

2. initimin

3. Shiga toxin 1 and 2

• acquired by lysogenic bacteriophage

clinical manifestation and complication

1. dysenteric diarrhea

2. mild diarrhea which can lead to hemorrhagic collitis

3. severe abdominal pain with bloody diarrhea

4. causing Hemolytic Uremic Syndrome

- characterized by:

• thrombocytopenia

• microangiopathic hemolytic anemia

• acute renal failure

• produce Shiga toxin 1 and 2

• common serotype = O157 : H7

• some are LEE positive, produce A/E cyrtopathology

• low infective dose , can cause disease

pathogenesis

1. B subunit of Stx bind to host cell Gb3 glycolipid

2. A subunit get internalized

3. cleaves into A1 and A2 fragment

4. A1 interact with 28s rRNA

5. lead cessation of protein synthesis

6. cell death

• Gb3 present on intestinal villi and renal endothelium

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PATHOGENESIS OF HEMOLYTIC UREMIC SYNDROME (HUS)

1. translocation of Stx across intestinal lumen into bloodstream

2. damage to endothelium

3. platelet activation and thrombin deposition

4. decrease glomerular filtration

5. acute renal failure

• Stx also stimulate expression of inflammatory cytokine

• enhance expression of B subunit receptor for Gb3

diagnosis

1. Sorbitol MacConkey Agar

• no fermentation of sorbitol

• produces pale colonies

2. Rainbow Agar

• O157 appear as black colonies

• -ve for glucuronidase

3. toxin detection

• cell cytotoxicity assay → demonstration of cytotoxicity in Vero cell line (gold standard)

• immunoassay / rapid test → fecal toxin Stx1 and Stx2 detection by ELISA / LFA

• molecular method : PCR → detect gene coding for Stx1 and Stx2

management

• antibiotic therapy is contraindicated as it will increase released of toxin exacerbate

• monitor possibilities for HUS

• avoid anti peristaltic agent