Today in intern report, Monica presented a case of a young woman with acute bloody diarrhea and CT scan findings of pancolitis, who developed HUS. The story is still evolving, but one way we potentially explained this case was the precipitation of HUS in a patient with possible EHEC infection and antibiotic therapy. Wow!
- Antibiotics in the context of EHEC (E coli O157:H7) can precipitate HUS!
- A helpful way of thinking about acute, bloody diarrhea is infectious (Shigella, Salmonella, EHEC, etc) vs non-infectious causes (inflammatory such as IBD, ischemic, malignancy)
- Not all community cases of acute diarrhea require stool testing – there are specific circumstances that warrant stool cultures (see below).
Stool Culture in Acute Diarrhea
- It is reasonable to continue supportive management without performing stool cultures for MOST patients who present with acute, community-acquired diarrhea.
- In general, we obtain standard stool cultures in patients with acute community-acquired diarrhea with the following features:
- Severe illness (hypovolemia, > 6 stools per 24 hours, severe abd pain)
- Concerning inflammatory features (bloody diarrhea, T > 38.5)
- Other high-risk factors: elderly age, immunocompromised patients, history of IBD, pregnancy
- Persistent symptoms > 1 week
- Public health concerns – food handlers, healthcare workers, day care center workers
- What is included in a standard stool culture?
- Salmonella, Campylobacter, Shigella, E. coli O157:H7 (isolated on sorbitol-MacConkey agar and ID’ed with antigen testing)
- What additional testing should we send for bloody diarrhea?
- When we suspect EHEC: Check Shiga toxin, as certain strains of the Shiga toxin producing E. coli cannot be identified by our routine sorbitol-MacConkey agar testing
- Consider testing for intestinal amebiasis: extended travelers, patients from endemic areas, MSM, institutionalized patients
Hemolytic Uremic Syndrome associated with E. Coli O157:H7 infection
- Characterized by MAHA, thrombocytopenia, and acute renal injury. Rare neurologic complications can also occur.
- 6-9% of STEC (Shiga-Toxin secreting E. Coli) infections
- Pathophysiology 1) Shiga toxin released by E. coli binds to globotriaosylceramide (Gb3) on surface of vascular endothelial cells, particularly in the kidney and brain à inhibits protein synthesis à induces broad inflammatory response à releases cytokines and chemokines à thrombosis and organ damage! 2) Shiga toxin also activates alternative pathway of complement system by binding to factor H proteins!
- Best approach: Basic supportive care
- Under investigation but not standard-of-care:
- PLEX: remove Shiga-like toxin and prothrombotic factors and replace them with coagulation, tissue, and complement factors
- Oral Shiga toxin-binding agent
- Eculizumab: Monoclonal antibody to C5 complement factor blocking complement activation. There are case series demonstrating the benefit of using eculizumab in children with STEC-HUS