Chapter 85: Infectious Diarrheas and Bacterial Food Poisoning

Acute diarrheal disease, which is associated with ∼1.7 million deaths per year, is the second most common infectious cause of death worldwide among children <5 years old (after lower respiratory tract infection). The wide range of clinical manifestations is matched by the wide variety of infectious agents involved (Table 85-1). An approach to pts with infectious diarrhea is presented in Fig. 85-1.

TABLE 85-1: Gastrointestinal Pathogens Causing Acute Diarrhea
Noninflammatory (enterotoxin)Proximal small bowelWatery diarrheaNo fecal leukocytes; mild or no increase in fecal lactoferrinVibrio 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 bowelDysentery or inflammatory diarrheaFecal polymorphonuclear leukocytes; substantial increase in fecal lactoferrinShigella 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
PenetratingDistal small bowelEnteric feverFecal mononuclear leukocytesSalmonella Typhi, Y. enterocolitica
Abbreviations: LT, heat-labile enterotoxin; ST, heat-stable enterotoxin.
Clinical algorithm for the approach to pts with community-acquired infectious diarrhea or bacterial food poisoning. Key to superscripts: 1. Diarrhea lasting >2 weeks is generally defined as chronic; in such cases, many of the causes of acute diarrhea are much less likely, and a new spectrum of causes needs to be considered. 2. Fever often implies invasive disease, although fever and diarrhea may also result from infection outside the gastrointestinal tract, as in malaria. 3. Stools that contain blood or mucus indicate ulceration of the large bowel. Bloody stools without fecal leukocytes should alert the laboratory to the possibility of infection with Shiga toxin–producing enterohemorrhagic Escherichia coli. Bulky white stools suggest a small-intestinal process that is causing malabsorption. Profuse “rice-water” stools suggest cholera or a similar toxigenic process. 4. Frequent stools over a given period can provide the first warning of impending dehydration. 5. Abdominal pain may be most severe in inflammatory processes like those due to Shigella, Campylobacter, and necrotizing toxins. Painful abdominal muscle cramps, caused by electrolyte loss, can develop in severe cases of cholera. Bloating is common in giardiasis. An appendicitis-like syndrome should prompt a culture for Yersinia enterocolitica with cold enrichment. 6. Tenesmus (painful rectal spasms with a strong urge to defecate but little passage of stool) may be a feature of cases with proctitis, as in shigellosis or amebiasis. 7. Vomiting implies an acute infection (e.g., a toxin-mediated illness or food poisoning) but can also be prominent in a variety of systemic illnesses (e.g., malaria) and in intestinal obstruction. 8. Asking pts whether anyone else they know is sick is a more efficient means of identifying a common source than is constructing a list of recently eaten foods. If a common source seems likely, specific foods can be investigated. See text for a discussion of bacterial food poisoning. 9. Current antibiotic therapy or a recent history of treatment suggests Clostridium difficile diarrhea. Stop antibiotic treatment if possible and consider tests for C. difficile toxins. Antibiotic use may increase the risk of chronic intestinal carriage following salmonellosis. (From Steiner TS, Guerrant RL: Principles and syndromes of enteric infection, in Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases, 7th ed, Mandell GL et al [eds]. Philadelphia, Churchill Livingstone, 2010, pp 1335–1351; Guerrant RL, Bobak DA: N Engl J Med 325:327, 1991.)

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