Ranging from a mild annoyance to a devastating dehydrating illness, acute diarrheal disease is a leading cause of illness globally, with an estimated 4.6 billion episodes worldwide per year. Diarrheal disease ranks second only to lower respiratory infection as the most common infectious cause of death worldwide. Among children <5 years old, diarrheal disease is a particularly important cause of death. Every year nearly 2 million children in this age group die of diarrheal disease; the majority of these young children are impoverished and live in resource-poor areas. By contributing to malnutrition and thereby reducing resistance to other infectious agents, diarrheal disease is also an indirect factor in a far greater burden of disease.
The wide range of clinical manifestations of acute gastrointestinal illnesses is matched by the wide variety of infectious agents involved, including viruses, bacteria, and parasitic pathogens (Table 128–1). This chapter discusses factors that enable gastrointestinal pathogens to cause disease, reviews host defense mechanisms, and delineates an approach to the evaluation and treatment of patients presenting with acute diarrhea. Individual organisms causing acute gastrointestinal illnesses are discussed in detail in subsequent chapters.
Table 128–1 Gastrointestinal Pathogens Causing Acute Diarrhea |Favorite Table|Download (.pdf)
Table 128–1 Gastrointestinal Pathogens Causing Acute Diarrhea
|Mechanism||Location||Illness||Stool Findings||Examples of Pathogens Involved|
|Noninflammatory (enterotoxin)||Proximal small bowel||Watery diarrhea||No fecal leukocytes; mild or no increase in fecal lactoferrin||Vibrio cholerae, enterotoxigenic Escherichia coli (LT and/or ST), enteroaggregative E. coli, Clostridium perfringens, Bacillus cereus, Staphylococcus aureus, Aeromonas hydrophila, Plesiomonas shigelloides, rotavirus, norovirus, enteric adenoviruses, Giardia lamblia, Cryptosporidium spp., Cyclospora spp., microsporidia|
|Inflammatory (invasion or cytotoxin)||Colon or distal small bowel||Dysentery or inflammatory diarrhea||Fecal polymorphonuclear leukocytes; substantial increase in fecal lactoferrin||Shigella spp., Salmonella spp., Campylobacter jejuni, enterohemorrhagic E. coli, enteroinvasive E. coli, Yersinia enterocolitica, Listeria monocytogenes, Vibrio parahaemolyticus, Clostridium difficile, A. hydrophila, P. shigelloides, Entamoeba histolytica, Klebsiella oxytoca|
|Penetrating||Distal small bowel||Enteric fever||Fecal mononuclear leukocytes||Salmonella typhi, Y. enterocolitica|
Enteric pathogens have developed a variety of tactics to overcome host defenses. Understanding the virulence factors employed by these organisms is important in the diagnosis and treatment of clinical disease.
The number of microorganisms that must be ingested to cause disease varies considerably from species to species. For Shigella, enterohemorrhagic Escherichia coli, Giardia lamblia, or Entamoeba, as few as 10–100 bacteria or cysts can produce infection, while 105−108Vibrio cholerae organisms must be ingested orally to cause disease. The infective dose of Salmonella varies widely, depending on the species, host, and food vehicle. The ability of organisms to overcome host defenses has important implications for transmission; Shigella, enterohemorrhagic E. coli, Entamoeba, and Giardia can spread by person-to-person contact, whereas under some circumstances Salmonella may have to grow in food for several hours before reaching an effective infectious dose.
Many organisms must adhere to the gastrointestinal mucosa as an initial step in the pathogenic process; thus, organisms that can compete with the normal bowel flora and colonize the mucosa have an important advantage in causing disease. Specific cell-surface ...