Prevalence of stx Genes in Enteropathogenic Escherichia coli (EPEC)
Enteropathogenic Escherichia coli (EPEC) strains do not typically harbor Shiga toxin (stx) genes, as the presence of stx genes would classify them as Shiga toxin-producing E. coli (STEC) rather than EPEC. This fundamental distinction is critical for proper classification and clinical management.
Classification and Definitions
EPEC and STEC are distinguished primarily by their virulence gene profiles:
- EPEC: Defined by the presence of the eae gene (encoding intimin) and the ability to form attaching and effacing (A/E) lesions on intestinal cells, but lacking Shiga toxin genes 1
- STEC: Defined by the presence of Shiga toxin genes (stx1 and/or stx2) 2
- Atypical EPEC: Possess the eae gene but lack both the bundle-forming pilus (bfpA) gene and stx genes 3
Evolutionary Relationship
The relationship between EPEC and STEC is evolutionarily significant:
- STEC O26 is believed to have evolved from EPEC O26 strains through the acquisition of stx genes 4
- Some stx-negative E. coli O157:H7 isolates may represent either:
- STEC strains that have lost the Stx-encoding bacteriophage during infection or culturing
- Progenitors of STEC strains that have not yet acquired the Stx phage 5
Prevalence Data
The prevalence of stx genes in strains classified as EPEC is effectively zero by definition, as:
- The CDC and IDSA guidelines clearly define EPEC as eae-positive but stx-negative 2
- When an E. coli strain acquires stx genes, it is reclassified as STEC regardless of its other characteristics 1
Diagnostic Implications
This distinction has important diagnostic implications:
- Simultaneous testing for both O157 STEC and non-O157 STEC is recommended by the CDC 2
- Laboratory methods should detect both LEE-positive and LEE-negative STEC strains, including culture, EIA, and PCR for detecting stx1 and stx2 genes 1
- The IDSA recommends that "STEC O157 should be assessed by culture and non-O157 STEC should be detected by Shiga toxin or genomic assays" 2
Clinical Significance
The distinction between EPEC and STEC has significant clinical implications:
- STEC infections, particularly those with stx2 genes, are associated with increased risk of hemolytic uremic syndrome (HUS) 2, 1
- Antibiotic therapy in patients with STEC infections might be associated with more severe disease 2
- Early identification of STEC is crucial for appropriate management, including parenteral volume expansion to reduce renal damage 2
Common Pitfalls in Classification
A key pitfall in clinical practice is the misclassification of EPEC and STEC:
- Some strains may lose stx genes during culturing or infection, leading to misclassification as EPEC 5
- Relying solely on stx gene detection without culture confirmation may miss important pathogenic E. coli strains 2
- Some atypical EPEC strains may represent former STEC that have lost their stx genes 5
In summary, by definition, true EPEC strains do not harbor stx genes. When stx genes are detected, the strain should be classified as STEC, not EPEC, regardless of other virulence factors present.