Clinical Findings of Shiga Toxin-Producing E. coli (STEC) Infection
STEC infections present with a spectrum of gastrointestinal manifestations ranging from acute watery diarrhea to life-threatening hemorrhagic colitis and hemolytic uremic syndrome, with approximately 8% of O157 STEC infections progressing to HUS characterized by thrombocytopenia, hemolytic anemia, and acute renal failure. 1
Gastrointestinal Manifestations
Primary Symptoms
- Acute onset of diarrhea is the hallmark presentation, which may initially be watery but frequently progresses to bloody diarrhea (hemorrhagic colitis) 2, 3
- Severe crampy abdominal pain is a prominent feature that can be severe enough to mimic surgical emergencies 4
- Both bloody and non-bloody diarrhea patterns occur; the absence of visible blood does not rule out STEC infection, as both O157 and non-O157 strains have been isolated from patients with nonbloody diarrhea 5
Colonic Pathology
- Severe mucosal damage occurs through Shiga toxin-mediated mechanisms, including inhibition of water absorption, surface epithelial necrosis with detachment, mononuclear inflammatory infiltrate, and loss of goblet cells 6
- Hemorrhagic colitis develops due to the direct cytotoxic effects of Shiga toxins on the colonic mucosa 2, 4
Important Clinical Caveat
White blood cells are often but not always detected in stools of STEC-infected patients and should not be used as a criterion for testing or diagnosis 5. This is a common pitfall—many infections are missed when testing is restricted only to bloody stools or those with fecal leukocytes 5.
Hemolytic Uremic Syndrome (HUS)
Incidence and Characteristics
- Approximately 8% of patients with O157 STEC infection develop HUS, representing the most severe complication 1
- HUS is characterized by the classic triad: thrombocytopenia, hemolytic anemia, and acute renal failure 1, 2
Extraintestinal Complications
- Acute renal failure is the defining feature of HUS, with extreme nephrotoxicity mediated by Shiga toxins 2
- Neurologic impairment can occur, particularly in infected patients under 9 years of age 2
- These complications are associated with severe outcomes and potential long-term sequelae 2
Pathophysiologic Mechanism
The toxins are taken up by recipient cells such as toxin-sensitive renal proximal tubular epithelial cells through Shiga toxin-containing extracellular vesicles secreted by intoxicated macrophages, contributing to the spreading of toxins within the host and exacerbating kidney dysfunction 3.
Epidemiologic and Demographic Patterns
Age Distribution
- While STEC bacteria are isolated more frequently from children, almost half of all STEC isolates are from persons of all ages 5
- Patients under 9 years of age are at particular risk for severe complications including HUS with neurologic impairment 2
Seasonal Variation
- Infections are more common during summer months but can occur throughout the year 1
- Selective testing based only on season results in missed infections 5
Detection Frequency
STEC are detected in 0%-4.1% of stools submitted for testing at clinical laboratories, with rates similar to other bacterial pathogens: Salmonella (1.9%-4.8%), Shigella (0.2%-3.1%), and Campylobacter (0.9%-9.3%) 5. In northern states, O157 STEC are more commonly isolated than some other enteric pathogens 5.
Critical Timing for Diagnosis
Specimens must be collected as soon as possible after symptom onset, ideally within the first week of illness, as bacteria become difficult or impossible to detect after 7 days and Shiga toxin genes may be lost 7. This narrow diagnostic window makes early clinical suspicion essential 7.
Treatment Implications Based on Clinical Findings
What to Avoid
- Antibiotics increase the risk of HUS, particularly with O157 strains, and should not be used 7
- Antidiarrheal medications worsen illness and must be avoided 5, 7