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Digestive tract immune defense mechanisms
Low pH of the stomach
Peristalsis
Mucous production
Normal microbiota
Peyer’s 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 bloody, mucous-filled stool
Food Poisoning (Staphylococcus aureus)
Cause: Ingestion of heat-stable exotoxins from contaminated food
Symptoms: Rapid onset vomiting, diarrhea (within hours); resolves in 24 hrs
Foods: Often undercooked or kept below 60°C
Pathogenesis: Toxin survives stomach acid and damages GI cells
Lower digestive tract infection
Symptoms: Diarrhea, nausea, vomiting, sometimes fever
Transmission: Fecal-oral; contaminated food, water
Mechanisms: Invasion, toxin production (enterotoxins cause fluid loss; cytotoxins kill cells)
Salmonellosis Characteristics
Agent: Salmonella enterica (e.g., Enteritidis, Typhi)
Symptoms: Diarrhea, nausea, vomiting, fever (lasts days–weeks)
Pathology: Invasion of small intestine, inflammation causes diarrhea
Transmission: Undercooked poultry, eggs, reptiles
Salmonella
Susceptible Groups: Children, immunocompromised
Virulence Factors: Adhesion to epithelial cells, capsule (Typhi), intracellular survival
Prevention: Proper cooking, hygiene; typhoid vaccine
Treatment: Often self-limiting; antibiotics in severe cases
E. Coli Characteristics
Gram-negative rod, some strains pathogenic
Symptoms: Ranges from watery to bloody diarrhea, cramps
Pathology: Adhesion (fimbriae), enterotoxins
Transmission: Contaminated food, water; unpasteurized drinks
E. Coli
Susceptible: Infants, travelers
Pathogenic Groups:
ETEC – Traveler’s diarrhea
EHEC/STEC – Bloody diarrhea, HUS
EPEC – Pediatric diarrhea
EIEC – Invasive, dysentery-like illness
Virulence: Toxins (e.g., Shiga), adhesion molecules
Prevention: Hygiene, pasteurization
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
Shigella
Susceptible: Infants, developing countries
Treatment: Rehydration; antibiotics (some resistance); no vaccine
Helicobacter pylori
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 difficle characteristics
Gram-positive anaerobe, spore-forming
Symptoms: Diarrhea, colitis, pseudomembranous colitis, toxic megacolon
Transmission: Fecal-oral; spores resist disinfectants
Clostridium difficile
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 Cholerae characteristics
Curved, Gram-negative rod; salt and alkaline tolerant
Symptoms: Severe watery diarrhea, up to 20L/day, vomiting, cramps
Transmission: Contaminated water, seafood, vegetables
Vibrio Cholerae
Virulence: Cholera toxin (A-B toxin increases Cl⁻ secretion)
Treatment: Rapid rehydration, antibiotics if needed
Prevention: Clean water, sanitation, oral vaccine for travelers
Hepatic Viruses
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