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Immune defense mechanisms of Digestive System
Low ph of stomach
Peristalsis
Mucus production
Normal microbiota
Peyers patches (with M cells)
Gastritis
Stomach inflammation
Enteritis
Intestinal mucosa inflammation
Gastroenteritis
Inflammation of both stomach and intestines
Hepatitis
Liver inflammation
Colitis
Colon inflammation
Dysentery
Severe colon damage causing blood, mucus-filled stool
Staphylococcus aureus food poisoning
Ingestion of heat-stable exotoxins from contaminated food
Rapid onset vomiting, diarrhea (resolves in 24 hrs)
Cause: often undercooked foods or kept below 60 degrees C
Toxin survives stomach acid and damages GI cells
Lower Digestive Tract Infection
Diarrhea, nausea, vomiting, sometimes fever
Fecal-oral, contaminated food, water
Invasion, toxin production (enterotoxins cause fluid loss; cytotoxins kill cells
Salmonellosis
Symptoms: Diarrhea, nausea, vomiting fever (lasts day-weeks)
invasion of small intestine, inflammation causes diarrhea
Cause: undercooked poultry, eggs, reptiles
Children and immunocompromised people are more susceptible
Treatment: often resolves on its own; antibiotics for severe cases
Causative agent: Salmonella enterica (S. Typhi)
Virulence factors of Salmonella
Adhesion to epithelial cells
Capsule (Typhi)
Intracellular survival
Prevention of Salmonella
Proper cooking
Hygiene
Typhoid vaccine
E. Coli characteristics
Gram-negative rod
Some pathogenic strains
E. Coli
Symptoms: Ranges from watery to blood diarrhea, cramps
Pathology: Adhesion (fimbriae), enterotoxins
Transmission: contaminated food and water; unpasteurized drinks
Susceptible: Infants, travelers
Prevention: Hygiene, pasteurization
Pathogenic groups of E. Coli
ETEC – Traveler’s diarrhea
EHEC/STEC – Bloody diarrhea, HUS
EPEC – Pediatric diarrhea
EIEC – Invasive, dysentery-like illness
E. Coli virulence factors
Toxins (e.g., Shiga), adhesion molecules
Treatment: Rehydration; avoid antibiotics in EHEC (can worsen HUS)
Shigella
Characteristics: Non-motile Gram-negative rods; four species
Symptoms: Dysentery, fever, cramps, vomiting, possibly HUS
Pathology: Invades M cells, escapes macrophages, invades epithelial cells
Virulence: Shiga toxin (S. dysenteriae), cell invasion
Transmission: Fecal-oral; low infectious dose
Susceptible: Infants, developing countries
Treatment: Rehydration; antibiotics (some resistance); no vaccine
Helicobacter pylori
Characteristics: Spiral Gram-negative, motile, microaerophile
Survival: Produces urease to neutralize stomach acid
Disease: Gastritis, peptic ulcers, possibly cancer
Pathogenesis: Invades mucosa, reduces mucus protection
Treatment: Antibiotic combo therapy
Clostridium difficile
Characteristics: Gram-positive anaerobe, spore-forming
Symptoms: Diarrhea, colitis, pseudomembranous colitis, toxic megacolon
Transmission: Fecal-oral; spores resist disinfectants
Susceptible: Elderly, hospitalized, recent antibiotics
Virulence: TcdA (enterotoxin), TcdB (cytotoxin)
Treatment: Stop antibiotics if possible, rehydration, vancomycin or metronidazole, fecal transplants in severe cases
Prevention: Hand hygiene, careful antibiotic use
Vibrio cholera
Characteristics: Curved, Gram-negative rod; salt and alkaline tolerant
Symptoms: Severe watery diarrhea, up to 20L/day, vomiting, cramps
Transmission: Contaminated water, seafood, vegetables
Virulence: Cholera toxin (A-B toxin increases Cl⁻ secretion)
Treatment: Rapid rehydration, antibiotics if needed
Prevention: Clean water, sanitation, oral vaccine for travelers
What cells are does hepatitis infect
Hepatocytes
A: Fecal-oral; acute; vaccine available
B: Blood/body fluids; chronic; cancer risk; vaccine available
C: Bloodborne; often chronic; no vaccine
D: Requires HBV co-infection
E: Fecal-oral; rare in U.S.
Rotavirus
Severe in children; fecal-oral; vaccine available
Norovirus
Very contagious; common in enclosed spaces; self-limiting