Gastroenteritis Overview and Pathogenesis

Study Notes

Gastroenteritis is inflammation of the stomach and intestines.
The digestive tract's anatomy includes the small intestine, large intestine, stomach, sigmoid colon, rectum, and anus.

Gastroenteritis can be acute, persistent, or chronic.
Etiology (causes) include viruses (Norovirus, Rotavirus, E. coli, C. difficile, C. perfringens, Shigella, Salmonella, Giardia, Entamoeba, Cryptosporidium) and non-infectious causes.
Transmission can occur through contaminated food, water, surfaces, or person-to-person contact, including aerosolized vomitus.
Epidemiology studies the distribution and patterns of acute, persistent, and chronic gastroenteritis.

Pathogens can cause gastroenteritis in three ways:
- Producing toxins in food before consumption (e.g., S. aureus, B. cereus)
- Producing toxins within the GI tract (e.g., Clostridium perfringens, Enterotoxigenic E. coli)
- Invading the intestinal wall (e.g., Enterohemorrhagic E. coli) causing inflammation and diarrhea.

Viruses impact enterocytes (intestinal cells):
- Disrupt brush border enzyme production (e.g., maltase, lactase) leading to malabsorption and osmotic diarrhea.
- Viral toxins cause cell lysis, leading to fluid loss and electrolyte abnormalities.
Viral shedding occurs in feces and sometimes vomit.
Symptoms typically peak 24 to 48 hours after exposure.

Most cases are self-limiting.
Complications can include:
- Dehydration and electrolyte imbalances (hypovolemia, metabolic acidosis)
- Hemolytic uremic syndrome (HUS) in some cases, particularly with E. coli strains producing Shiga toxins.

Management mainly focuses on supportive care (rehydration) for most cases
Antibiotics may be necessary for certain bacterial cases.
Proper food handling, sanitation, hygiene measures, and vaccinations are crucial preventative strategies.

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