A 32-year-old Indian male presents with acute onset bloody diarrhea, abdominal cramps, and fever after consuming contaminated ground beef at a wedding. Stool culture grows sorbitol-fermenting E. coli. Regarding non-motile Shiga-toxigenic E. coli (STEC) O157:H⁻, all of the following are true EXCEPT:

Explanation

## Shiga-Toxigenic E. coli (STEC) O157:H⁻ — Epidemiology and Pathogenesis ### Clinical Context The patient's presentation of **bloody diarrhea** (hemorrhagic colitis) following contaminated beef consumption is classic for **STEC O157:H⁻** infection. The sorbitol-fermenting isolate confirms this is NOT the typical sorbitol-negative O157:H⁻ strain, but the question tests knowledge of O157:H⁻ characteristics. ### Correct Statements (Options 0, 1, 2) **Key Point:** STEC O157:H⁻ identification and pathogenesis: | Feature | Details | |---------|----------| | **Sorbitol fermentation** | O157:H⁻ is sorbitol-**negative** (unlike commensal E. coli); used for differential diagnosis on MacConkey agar | | **Shiga toxin genes** | Encoded by **lysogenic bacteriophages** (Stx1 and/or Stx2); not chromosomal | | **HUS incidence** | Occurs in 5–10% of STEC infections; mortality ~1–2% in children | | **Pathophysiology** | Toxin absorption → thrombotic microangiopathy → hemolysis, thrombocytopenia, acute kidney injury | **High-Yield:** Sorbitol-MacConkey agar is the **gold standard** for presumptive STEC screening. O157:H⁻ colonies appear **colorless** (sorbitol-negative), while commensal E. coli appear **pink/red** (sorbitol-positive). **Clinical Pearl:** HUS is a medical emergency in children <5 years. Early recognition and fluid management (avoid antibiotics and antimotility agents, which increase toxin absorption) are critical. ### Why Option 3 is Wrong **Warning:** The designation **H⁻** means **non-motile** — the strain lacks flagella and does NOT express H antigen. This is the defining characteristic of O157:H⁻. **Mnemonic:** **O157:H⁻** = **O**-antigen 157 (somatic), **H⁻** = **H**-antigen **absent** (non-motile). Do not confuse with motile strains like O157:H7. **Key Point:** Lack of motility does NOT impair pathogenesis; Shiga toxin and lipopolysaccharide (LPS) are the primary virulence factors. Intestinal invasion occurs via direct epithelial damage and toxin-mediated effects, not motility-driven penetration. [cite:Jawetz, Melnick & Adelberg's Medical Microbiology 28e Ch 16; Park Textbook of Preventive and Social Medicine 26e Ch 7] ## Pathogenic Cascade ```mermaid flowchart TD A[STEC O157:H⁻ ingestion]:::outcome --> B[Adherence to colonic epithelium]:::action B --> C[Shiga toxin secretion]:::action C --> D{Local vs. systemic?}:::decision D -->|Local| E[Hemorrhagic colitis]:::outcome D -->|Systemic absorption| F[Toxin enters bloodstream]:::action F --> G[Endothelial damage + thrombosis]:::action G --> H{HUS develops?}:::decision H -->|Yes 5-10%| I[Hemolytic uremic syndrome]:::urgent H -->|No| J[Recovery]:::outcome ```