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Gastrointestinal Infections

Gastrointestinal Infections

Gastrointestinal Infections

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Introduction to GI Infections - Gut Invaders 101

  • Overview: Infections targeting stomach, small & large intestines.
  • Transmission: Primarily fecal-oral route; contaminated food/water.
  • Host Defenses:
    • Gastric acid (pH <4)
    • Mucus barrier
    • Peristalsis
    • Normal gut flora (competitive inhibition)
    • Gut-Associated Lymphoid Tissue (GALT) - Secretory IgA.
  • Pathogen Mechanisms:
    • Adherence to mucosa
    • Toxin production: Enterotoxins (watery diarrhea), Cytotoxins (cell damage, dysentery)
    • Mucosal invasion & inflammation (e.g., Shigella, invasive E. coli)
  • Clinical Patterns:
    • Watery diarrhea: Small bowel; non-inflammatory; high volume.
    • Dysentery: Large bowel; inflammatory; blood, mucus, pus; lower volume. Host defense mechanisms in the GI tract

⭐ Most GI infections are acquired via the fecal-oral route, often through contaminated food or water sources (e.g., Vibrio cholerae, Rotavirus).

Bacterial GI Infections - The Nasty Bugs

  • Escherichia coli

    • ETEC: Traveler's diarrhea (watery). LT (↑cAMP), ST (↑cGMP) toxins.
    • EHEC (O157:H7): Hemorrhagic colitis, HUS. Shiga-like toxin. 📌 "Hamburger HUS"
    • EPEC: Infantile diarrhea. Adherence, microvilli effacement.
    • EIEC: Invasive, dysentery. Resembles Shigella.
  • Salmonella

    • Non-typhoidal: Gastroenteritis (poultry, eggs).
    • Typhoidal (S. typhi): Typhoid fever (rose spots, step-ladder fever).

      S. typhi gallbladder colonization causes chronic carrier state.

  • Shigella spp. (S. dysenteriae)

    • Bacillary dysentery (bloody, mucoid). Shiga toxin. Low infective dose (10-100 organisms). Invades M cells.
  • Vibrio cholerae

    • Profuse "rice-water" stools. Cholera toxin (↑cAMP). Severe dehydration. TCBS agar.
  • Campylobacter jejuni

    • Common cause of bloody diarrhea. Guillain-Barré syndrome. Grows 42°C (microaerophilic). 📌 "Campy likes it hot (42°C)"
  • Clostridioides difficile

    • Antibiotic-associated diarrhea, pseudomembranous colitis. Toxins A & B.
  • Toxin-mediated (Preformed):

    • Staphylococcus aureus: Rapid vomiting (meats, custards).
    • Bacillus cereus: Emetic (fried rice) / diarrheal types.
  • Yersinia enterocolitica

    • Pseudoappendicitis (pork, milk). Cold enrichment.

Viral & Parasitic GI Infections - Tiny Troublemakers

  • Viral Agents:

    • Rotavirus: MCC severe childhood diarrhea (watery); villous blunting. Oral vaccine.
    • Norovirus: Highly contagious; epidemic non-bacterial gastroenteritis (cruise ships); abrupt V/D.
    • Adenovirus (enteric 40, 41): Pediatric diarrhea, can be prolonged.
    • Astrovirus: Star-shaped (EM); diarrhea in children, immunocompromised.
  • Parasitic Agents:

    • Giardia lamblia: Flagellated protozoan; foul steatorrhea, malabsorption. Cysts in contaminated water.
      • 📌 Giardia: Greasy, Gassy, Giardiasis.
    • Entamoeba histolytica: Amebiasis: dysentery (bloody); liver abscess. Ingested RBCs in trophozoites.

      Entamoeba histolytica causes flask-shaped colonic ulcers & "anchovy paste" liver abscesses.

    • Cryptosporidium parvum: Severe watery diarrhea in AIDS (CD4 < 100); oocysts acid-fast.
    • Cyclospora cayetanensis: Prolonged watery diarrhea; oocysts acid-fast (larger); contaminated produce.
    • Isospora belli (Cystoisospora): Chronic watery diarrhea in immunocompromised; oocysts oval, acid-fast.

Micrographs of parasitic GI infections

Diagnosis & Complications - Spotting & Stopping Sickness

  • Diagnosis (Spotting):
    • Stool analysis: Key for pathogens (microscopy, culture, antigen tests like C. diff toxin, PCR).
    • Endoscopy & Biopsy: For severe, persistent, or diagnostically challenging cases (e.g., CMV colitis, pseudomembranes).
    • Blood tests: Assess severity (CBC, electrolytes, renal function). Serology rarely for acute.
  • Complications (Stopping Sickness):
    • Immediate: Dehydration & electrolyte imbalance (priority: ORS/IV fluids).
    • Severe GI: Hemorrhage, perforation (e.g., typhoid ulcers), toxic megacolon.
    • Extra-intestinal: HUS (EHEC O157:H7), GBS (Campylobacter), Reactive Arthritis (📌 CRYSY: Campylobacter, Reactive arthritis, Yersinia, Salmonella, Shigella).

Campylobacter jejuni infection is the most frequent antecedent of Guillain-Barré Syndrome (GBS).

High‑Yield Points - ⚡ Biggest Takeaways

  • Vibrio cholerae: Rice-water stools, cholera toxin (↑cAMP).
  • Salmonella typhi: Enteric fever, rose spots, pea soup diarrhea.
  • Shigella: Bacillary dysentery (bloody, mucoid), Shiga toxin, invasive.
  • EHEC (O157:H7): Hemorrhagic colitis, risk of HUS.
  • Campylobacter jejuni: Common bacterial cause, linked to Guillain-Barré syndrome.
  • Clostridium difficile: Pseudomembranous colitis, antibiotic-associated.
  • Rotavirus: Major cause of severe childhood diarrhea.

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