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Traveler's diarrhea pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.

Overview

The transmission and pathogenesis of traveler’s diarrhea is dependent on the infectious agent. The majority of organisms associated with traveler’s diarrhea are transmitted by the fecal-oral route and by contaminated food (meat, unpasteurized milk, cheese, vegetables, and fruits). The pathogenesis and mechanism of infection depends on the infectious agent. In E. coli traveler’s diarrhea (most common), the organism secretes 2 endotoxins, heat-labile toxin (LT) and heat-stable toxin (ST), to induce clinical manifestations.

Pathophysiology

  • The transmission and pathogenesis of traveler’s diarrhea is dependent on the infectious agent.
  • The following table summarizes the natural reservoir, transmission, and pathogenesis of common infectious agents associated with traveler’s diarrhea:
Infectious Agent Characteristics Reservoir Common Mode of Transmission Pathogenesis
Bacteria
E. coli (ETEC)
  • Gram-negative rod
  • Humans and animals
  • Fecal-oral route
  • Contaminated ground beef, unpasteurized milk, cheese, vegetables, or water
  • Enterotoxin-mediated: secretion of heat-labile toxin (LT) and heat-stable toxin (ST)
Campylobacter jejuni
  • Gram-negative rod
  • Humans and animals
  • Fecal-oral route
  • Contaminated meat, unpasteurized milk, cheese, vegetables, or water
  • Exposure to infected animals
  • Enterotoxin-mediated: secretion of Cholera-like enterotoxin
Shigella spp.
  • Gram-negative rod
  • Humans only
  • Fecal-oral route
  • Contaminated meat and pork, unpasteurized milk, cheese, vegetables, or water
  • Low inoculum sufficient for infection (resistant to gastric acid)
  • Enterotoxin-mediated: secretion of Shiga toxin
  • Invasion of macrophages and induction of cellular apoptosis
  • Intracellular spread by actin polymerization processes (rocket propulsion)
Salmonella spp.
  • Gram-negative rod
  • S. typhi: Humans only
  • Other Salmonella spp.: Humans and animals
  • Fecal-oral route
  • Contaminated raw egg shells, poultry, unpasteurized milk, cheese, vegetables, or water
  • High inoculum sufficient for infection (inactivated by gastric acid)
  • Vi capsule endotoxin prevents opsonization and lysis
  • Spread through the reticuloendothelial system
Viruses
Norovirus
  • Positive-sense, single-stranded RNA virus
  • Humans and animals
  • Fecal-oral route
  • Contaminated food, vegetables, and water
  • Fomites
  • Aerosol exposure
  • Virus uses P2 subdomain for binding and HBGA for attachment on host cell
Rotavirus
  • Double-stranded RNA virus
  • Humans and animals
  • Fecal-oral route
  • Fomites
  • Poorly understood pathogenesis
  • Viral replication in villous epithelium of host small intestine
Protozoa
Giardia lamblia
  • Anerobic, flagellated protozoan parasite
  • Humans and animals
  • Ingestion of cysts in water or uncooked foods
  • Fecal-oral route
  • Attaches to the epithelium by a ventral adhesive disc, and reproduces via binary fission
  • Usually luminal infection, no hematogenous spread
Entamoeba histolytica
  • Anaerobic parasitic protozoa with pseudopods
  • Humans
  • Rare (but present) in animals
  • Ingestion of cysts in water
  • Fecal-oral route
  • Excystation in the small intestine and migration to the large intestine
  • Luminal and extraluminal infection, hematogenous spread common
Cryptosporidium spp.
  • Spore-forming parasite
  • Humans and animals
  • Ingestion of oocytes in water
  • Fecal-oral route
  • Minimally invasive, surface-level mucosal inflammation
  • Usually luminal infection, potential to infect biliary tree

References

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