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Microbiology

Organism Pathogenicity

Understanding the pathogenicity of gastrointestinal (GI) pathogens is crucial for effective diagnosis, treatment, and prevention of diarrheal illnesses. Pathogenicity is the ability of a microorganism to cause disease, and it is determined by the pathogen’s capacity to:

  1. Colonize: the host
  2. Invade: tissues
  3. Evade: the host’s immune defenses
  4. Produce: toxins or other harmful substances

Organism Pathogenicity in Gastrointestinal Infections

Salmonella spp.

  • Etiology: Gram-negative rods
  • Transmission: Fecal-oral route, contaminated food (e.g., poultry, eggs, meat)
  • Virulence Mechanisms
    • Adherence and Invasion: Invades intestinal epithelial cells
    • Type III Secretion System (T3SS): Delivers effector proteins into host cells, disrupting cellular functions
    • Survival in Macrophages: Survives inside macrophages
  • Pathogenicity
    • Salmonellosis (gastroenteritis)
    • Typhoid fever (caused by S. Typhi)
    • Diarrhea, abdominal cramps, fever
  • Pathogenesis: Ingestion, invasion of intestinal cells, inflammation, and toxin production

Shigella spp.

  • Etiology: Gram-negative rods
  • Transmission: Fecal-oral route, contaminated food or water
  • Virulence Mechanisms
    • Adherence and Invasion: Invades intestinal epithelial cells
    • Type III Secretion System (T3SS): Delivers effector proteins
    • Shiga Toxin (Stx) (in S. dysenteriae): Inhibits protein synthesis
  • Pathogenicity
    • Shigellosis (bacillary dysentery)
    • Bloody diarrhea, abdominal cramps, fever
  • Pathogenesis: Ingestion, invasion of intestinal cells, inflammation, and toxin production

Escherichia coli (Toxigenic)

  • Etiology: Gram-negative rods
  • Transmission: Fecal-oral route, contaminated food or water
  • Virulence Mechanisms
    • Enterotoxigenic E. coli (ETEC): Produces heat-labile (LT) and/or heat-stable (ST) toxins
    • Shiga Toxin-Producing E. coli (STEC): Produces Shiga toxins (Stx1 and/or Stx2)
    • Enteropathogenic E. coli (EPEC): Attaching and effacing (A/E) lesions in the gut
  • Pathogenicity
    • ETEC: Traveler’s diarrhea
    • STEC: Hemorrhagic colitis, hemolytic uremic syndrome (HUS)
    • EPEC: Diarrhea in infants
  • Pathogenesis: Various mechanisms depending on the E. coli type. Toxin production, destruction

Campylobacter spp.

  • Etiology: Gram-negative, curved or S-shaped rods
  • Transmission: Fecal-oral route, contaminated food (e.g., poultry, undercooked meat)
  • Virulence Mechanisms
    • Adherence and Invasion: Adheres to and invades intestinal epithelial cells
    • Toxins: Produce toxins
  • Pathogenicity
    • Campylobacteriosis (gastroenteritis)
    • Diarrhea, abdominal cramps, fever
  • Pathogenesis: Ingestion, invasion of intestinal cells, and toxin production

Vibrio spp. (e.g., V. cholerae, V. parahaemolyticus)

  • Etiology: Gram-negative rods (curved)
  • Transmission: Ingestion of contaminated food or water, especially seafood
  • Virulence Mechanisms
    • V. cholerae: Cholera toxin (CT) causes massive fluid secretion
    • V. parahaemolyticus: Produces hemolysins
  • Pathogenicity
    • V. cholerae: Cholera (severe watery diarrhea)
    • V. parahaemolyticus: Gastroenteritis
  • Pathogenesis: Toxin production leading to fluid secretion, or damage

Yersinia enterocolitica

  • Etiology: Gram-negative rods
  • Transmission: Fecal-oral route, contaminated food (e.g., pork)
  • Virulence Mechanisms
    • Adherence and Invasion: Invades intestinal epithelial cells
    • Type III Secretion System (T3SS): Deliver effector proteins
  • Pathogenicity
    • Yersiniosis (gastroenteritis)
    • Diarrhea, abdominal pain, fever. Can mimic appendicitis
  • Pathogenesis: Ingestion, invasion of intestinal cells, and inflammation

Aeromonas spp.

  • Etiology: Gram-negative rods
  • Transmission: Ingestion of contaminated food or water
  • Virulence Mechanisms
    • Adherence: Promotes attachment
    • Toxins: Produces toxins
  • Pathogenicity
    • Gastroenteritis, wound infections
    • Diarrhea, abdominal pain
  • Pathogenesis: Ingestion, invasion of intestinal cells, and toxin production

Plesiomonas shigelloides

  • Etiology: Gram-negative rods
  • Transmission: Ingestion of contaminated food or water
  • Virulence Mechanisms
    • Adherence and Invasion: Invades intestinal epithelial cells
  • Pathogenicity
    • Gastroenteritis
    • Diarrhea, abdominal pain
  • Pathogenesis: Ingestion, invasion of intestinal cells, and inflammation

Additional Considerations

  • Foodborne Illness: Many of these pathogens are spread through contaminated food
  • Outbreak Investigations: Serotyping is essential in tracking outbreaks
  • Antibiotic Resistance: Resistance is possible in many of these organisms
  • Host Factors: The severity of illness depends on the host’s immune status

Key Terms

  • Pathogenicity: The ability of a microorganism to cause disease
  • Virulence: The degree of pathogenicity
  • Etiology: The cause of a disease
  • Transmission: The spread of a pathogen
  • Adherence: Attachment to host cells
  • Invasion: Entry into host tissues
  • Toxins: Harmful substances produced by pathogens
  • Type III Secretion System (T3SS): A mechanism used by some bacteria to inject proteins into host cells
  • Enterotoxigenic E. coli (ETEC): Produces heat-labile (LT) and heat-stable (ST) toxins
  • Shiga Toxin-Producing E. coli (STEC): Produces Shiga toxins
  • Hemolytic Uremic Syndrome (HUS): A serious complication of STEC infections
  • Plesiomonas shigelloides: Gram-negative rods
  • Fecal-oral route: Transmission through the ingestion of fecal matter
  • Toxin: A poisonous substance