Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning¶
Chapter 138 | Part 5: Infectious Diseases · Part 5 – Infectious Diseases: Bacterial · Chapter 138
Key Clinical Points¶
- Diarrhea is defined as the passage of loose or watery stools conforming to the shape of a container three or more times in a 24-h period.
- Symptoms of severe dehydration include lethargy, obtundation, feeble pulse, hypotension, and shock; these require IV fluids (e.g., Ringer's lactate).
- Bloody stools without fecal leukocytes should alert the laboratory to the possibility of infection with Shiga toxin–producing enterohemorrhagic Escherichia coli (EHEC).
- Loperamide should not be used by patients with fever or dysentery; its use may prolong diarrhea in patients with infection due to Shigella or other invasive organisms.
- Antibacterial agents should not be administered to individuals in whom enterohemorrhagic E. coli infection is suspected, as antibiotics may increase the risk of hemolytic-uremic syndrome (HUS) and renal failure.
- Traveler's diarrhea is most commonly caused by enterotoxigenic Escherichia coli (10–45%) and enteroaggregative E. coli (5–35%).
- Staphylococcal food poisoning has the shortest incubation period (1–6 h) and is associated with contaminated foods like ham, poultry, potato salad, and mayonnaise.
- Campylobacter jejuri is especially common in areas of Asia and is a major cause of reactive arthritis following infection with invasive organisms.
- Oral rehydration solution (ORS) is the mainstay of treatment for acute diarrheal diseases; WHO recommends reduced-osmolarity/reduced-salt ORS.
- Prophylactic antimicrobial agents are not generally recommended for the prevention of traveler's diarrhea except when travelers are immunocompromised or have underlying illness.
1. DEFINITION & OVERVIEW¶
• Definition: Diarrhea is the passage of loose or watery stools that conform to the shape of a container three or more times in a 24-h period.
• Global Impact: Acute diarrheal disease is a leading cause of illness globally, associated with an estimated 1.57 million deaths per year.
• Pediatric Risk: In low- and middle-income countries, one in ten deaths among children <5 years of age is attributable to diarrhea.
• Long-term Consequences: Recurrent intestinal infections are associated with physical and mental stunting, wasting, micronutrient deficiencies, and malnutrition.
2. EPIDEMIOLOGY¶
• General Trends: Diarrhea mortality has decreased substantially in the past three decades.
• Traveler's Diarrhea: Most common travel-related infectious illness, affecting 20–50% of people traveling from temperate industrialized countries to tropical regions of Asia, Africa, and Central and South America.
• Timeline: Onset is usually 3 days to 2 weeks after arrival; most cases begin within the first 3–5 days. The illness is generally self-limited, lasting 1–5 days.
• Outbreak Settings: Closed and semi-closed communities (day-care centers, schools, cruise ships) are important settings for outbreaks of enteric infections.
• Key Pathogens by Setting: ◦ Norovirus: Most common etiologic agent associated with outbreaks in these settings. ◦ Clostridioides difficile: Predominant cause of nosocomial diarrhea among adults in the United States.
Table 138-3 Causes of Traveler's Diarrhea
| ETIOLOGIC AGENT | APPROXIMATE PERCENTAGE OF CASES | COMMENTS |
|---|---|---|
| Bacteria | 50–75 | |
| Enterotoxigenic Escherichia coli | 10–45 | Single most important agent |
| Enteroaggregative E. coli | 5–35 | Emerging enteric pathogen with worldwide distribution |
| Campylobacter jejuri | 5–25 | More common in Asia |
| Shigella | 0–15 | Major cause of dysentery |
| Salmonella | 0–15 | |
| Others | 0–5 | Including Aeromonas, Plesiomonas, and Vibrio cholerae |
| Viruses | 0–20 | |
| Norovirus | 0–10 | Associated with cruise ships |
| Rotavirus | 0–5 | Particularly common among children |
| Parasites | 0–10 | |
| Giardia lamblia | 0–5 | Affects hikers and campers who drink from freshwater streams |
| Cryptosporidium | 0–5 | Resistant to chlorine treatment of water sources |
| Entamoeba histolytica | <1 | |
| Cyclospora | <1 | |
| Other | 0–10 | |
| Acute food poisoning | 0–5 | |
| No pathogen identified | 10–50 |
2.1 Travel History¶
• 20–50% of travelers to tropical regions experience sudden onset of abdominal cramps, anorexia, and watery diarrhea.
• Enterotoxigenic and enteroaggregative E. coli are the most common pathogens in classic secretory traveler's diarrhea syndrome.
• Campylobacter jejuni is especially common in Asia.
• Norovirus is highly contagious and associated with outbreaks on cruise ships.
• Rotavirus is rarely a cause of pediatric diarrheal outbreaks in the US since 2006 vaccination.
2.2 Location¶
• Closed communities (day-care centers, cruise ships) are key settings for enteric infections.
• C. difficile is the predominant cause of nosocomial diarrhea in adults.
• Norovirus outbreaks are common in healthcare settings.
• Klebsiella oxytoca causes antibiotic-associated hemorrhagic colitis.
• Enteropathogenic E. coli outbreaks occur in newborn nurseries.
• One-third of elderly patients in chronic-care institutions develop significant diarrheal illness annually.
2.3 Age¶
• Children <5 years account for most global morbidity/mortality from enteric pathogens.
• Breast-fed infants are protected until solid foods are introduced.
• Rotavirus infection is universal in unvaccinated children (first or second year of life).
• Norovirus infections are more common in older children and adults.
• Enterotoxigenic, enteropathogenic, and enterohemorrhagic E. coli; Shigella; C. jejuni; and Giardia lamblia have higher attack rates in children.
2.4 Host Immune Status¶
• Immunocompromised hosts are at elevated risk of acute/chronic infectious diarrhea.
• Cell-mediated immunity defects (AIDS) increase risk of invasive enteropathies (salmonellosis, listeriosis, cryptosporidiosis).
• Hypogammaglobulinemia increases risk of C. difficile colitis and giardiasis.
• Cancer patients are more likely to develop C. difficile due to antibiotic exposure/hospitalizations.
• Infectious diarrhea can be life-threatening in immunocompromised hosts with complications like persistent infection, bacteremia, and metastatic seeding.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
• Enteric pathogens use multiple mechanisms to overcome host defenses: inoculum size, adherence, toxin production, invasion, intestinal motility, mucin disruption, immunity, and genetic determinants.
• Understanding virulence factors is critical for diagnosis/treatment.
Table 138-1 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 jejuri, 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 |
3.1 Inoculum Size¶
• Shigella, EHEC, Giardia, Entamoeba: 10–100 organisms needed to cause infection.
• Vibrio cholerae: 10^5–10^8 organisms required.
• Salmonella inoculum varies by species, host, and food vehicle.
• Shigella, EHEC, Giardia, Entamoeba can spread via person-to-person contact.
• Salmonella may require growth in food before reaching infectious dose.
3.2 Adherence¶
• Pathogens must adhere to gastrointestinal mucosa to initiate infection.
• V. cholerae uses toxin-coregulated pilus for adherence.
• Enterotoxigenic E. coli requires colonization factor antigen for upper small intestine colonization.
• EPEC and EHEC produce virulence determinants that allow attachment/effacement of intestinal epithelium.
3.3 Toxin Production¶
• Enterotoxins (cholera toxin, LT, ST) cause watery diarrhea via secretory mechanisms.
• Cytotoxins (Shigella dysenteriae type 1, V. parahaemolyticus, C. difficile) cause dysentery with bloody stools.
• Neurotoxins (staphylococcal, B. cereus) act on CNS to produce vomiting.
3.4 Invasion¶
• Shigella and EIEC invade mucosal epithelial cells, causing dysentery.
• Salmonella invades bowel mucosa but generally does not cause full dysentery syndrome.
• S. Typhi and Y. enterocolitica penetrate intestinal mucosa, multiply in Peyer patches, and disseminate via bloodstream to cause enteric fever.
3.5 Intestinal Motility¶
• Impaired motility (opioids, anatomic abnormalities) increases small bowel infection risk.
• Lomotil treatment for Shigella may prolong fever/organism shedding.
• Opioid use in Salmonella gastroenteritis increases bacteremia risk.
3.6 Intestinal Mucin¶
• Mucus barrier separates commensal microbiota from epithelium.
• Pathogens overcome mucus via enzyme secretion, flagella-mediated motility, or toxin diffusion.
• Shigella toxins disrupt mucus production to reach cell surface.
3.7 Immunity¶
• Humoral immunity (IgG, IgM, secretory IgA) and mucosal immune responses protect against enteric pathogens.
• M cells in distal small bowel bind bacterial antigens, leading to lymphocyte proliferation and IgA-secreting plasma cell formation.
3.8 Genetic Determinants¶
• Blood group O increases susceptibility to V. cholerae, Shigella, E. coli O157, norovirus.
• Polymorphisms in inflammatory mediator genes affect outcomes for EAggEC, STEC, Salmonella, C. difficile, and V. cholerae.
3.9 Host Defenses¶
• Intestinal microbiota provide colonization resistance via geographic/nutritional exclusion.
• Patients with fewer intestinal bacteria (infants, antibiotic users) are at higher infection risk.
• Acidic pH of stomach and volatile fatty acids from colonic microbiota inhibit pathogen colonization.
• Gastric surgery/achlorhydria increase infection risk with Salmonella, G. lamblia, helminths.
• Rotavirus and Shigella are resistant to gastric acidity.
4. CLINICAL MANIFESTATIONS¶
• Definition: Diarrhea is the passage of loose or watery stools that conform to the shape of a container three or more times in a 24-h period.
• Key Discriminators: ◦ Blood/mucus in stool → indicates ulceration. ◦ Rice-water stools → suggests cholera or similar toxigenic process. ◦ Tenesmus → feature of shigellosis or amebiasis. ◦ Abdominal pain severity → reflects inflammatory processes (e.g., Shigella, Campylobacter). ◦ Vomiting patterns → distinguish toxin-mediated vs. systemic illness.
• Dehydration Assessment: ◦ Mild: thirst, dry mouth, decreased urine output. ◦ Moderate: orthostatic fall in BP, sunken eyes. ◦ Severe: lethery, obtundation, feeble pulse, hypotension, and shock.
Table 138-1 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 jejuri, 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 |
4.1 Physical Examination¶
• Signs of dehydration: ◦ Mild: thirst, dry mouth, decreased urine output. ◦ Moderate: orthostatic fall in BP, sunken eyes. ◦ Severe: lethargy, obtundation, feeble pulse, hypotension.
4.2 Diagnostic Approach¶
• Distinguish inflammatory vs noninflammatory diarrhea using history/epidemiology.
• Fecal leukocytes/lactoferrin tests identify inflammatory disease.
• Stool culture/molecular testing for specific pathogens in severe cases/high-risk patients.
• Table 138-1 categorizes causes of acute infectious diarrhea.
5. DIFFERENTIAL DIAGNOSIS¶
• Noninflammatory: Watery stools without fecal leukocytes (enterotoxins).
• Inflammatory: Dysentery with fecal polymorphonuclear leukocytes (invasion/cytotoxins).
• Penetrating: Enteric fever with fecal mononuclear leukocytes.
• Table 138-1 provides examples of pathogens in each category.
6. INVESTIGATIONS & DIAGNOSIS¶
• Noninflammatory diarrhea is often self-limited and may not require specific etiology determination.
• Fecal leukocyte/lactoferrin tests help distinguish inflammatory vs noninflammatory disease.
• Stool culture/molecular testing identifies causative organisms in severe cases/high-risk patients.
6.1 Laboratory Evaluation¶
• Fecal leukocytes: thin smear with methylene blue, examine wet mount.
• Fecal lactoferrin: more sensitive than fecal leukocyte tests (latex agglutination/ELISA formats).
• Stool culture/molecular testing for specific pathogens in severe cases/high-risk patients.
7. MANAGEMENT & TREATMENT¶
• Rehydration is the mainstay of treatment (WHO-recommended reduced-osmolarity ORS).
• Avoid loperamide in fever/dysentery; may prolong Shigella infection.
• Antibiotics contraindicated in suspected EHEC infection (risk of HUS).
7.1 Rehydration¶
• Oral rehydration solution (ORS) is the mainstay for acute diarrheal diseases.
• WHO recommends reduced-osmolarity/reduced-salt ORS.
• IV fluids (e.g., Ringer's lactate) required for severe dehydration.
7.2 Antimicrobial Therapy¶
• Avoid antibiotics in suspected EHEC infection (risk of hemolytic-uremic syndrome).
• Empirical antimicrobials may be used in inflammatory diarrhea (e.g., ciprofloxacin for Shigella, azithromycin for C. difficile).
7.3 Prophylaxis¶
• Not generally recommended for traveler's diarrhea except in immunocompromised patients.
• Bismuth subsalicylate may reduce risk in travelers.
7.4 Drug Therapy¶
• Loperamide contraindicated in fever/dysentery (may prolong Shigella infection).
• Racecadotril may be used for noninflammatory diarrhea.
• Antimicrobials: ciprofloxacin, azithromycin, metronidazole, etc., based on pathogen and severity.
8. PROGNOSIS & COMPLICATIONS¶
• Most cases are self-limited but can lead to dehydration, malnutrition, or complications like HUS.
• Postdiarrhea complications: reactive arthritis (C. jejuri), chronic carriage (Salmonella), C. difficile recurrence.
Table 138-2 Postdiarrhea Complications of Acute Infectious Diarrheal Illness
| COMPLICATION | DETAILS |
|---|---|
| Chronic diarrhea (diarrhea lasting >4 weeks) | • Lactase deficiency • Small-bowel bacterial overgrowth • Malabsorption syndromes (tropical and celiac sprue) (Occurs in ~1% of travelers with acute diarrhea; Protozoa account for approximately one-third of cases) |
| Irritable bowel syndrome | Occurs in ~10% of travelers with traveler's diarrhea |
| Hemolytic-uremic syndrome (hemolytic anemia, thrombocytopynea, and renal failure) | Follows infection with Shiga toxin–producing bacteria (Shigella dysenteriae type 1 and enterohemorrhagic Escherichia coli) |
8.1 Postdiarrhea Complications¶
• Reactive arthritis following C. jejuri infection.
• Chronic intestinal carriage after Salmonella gastroenteritis.
• Recurrent C. difficile infections.
9. SPECIAL POPULATIONS¶
• Immunocompromised Hosts: - Higher risk of acute/chronic infectious diarrhea. - Increased risk of invasive enteropathies (salmonellosis, listeriosis, cryptosporidiosis). - Hypogammaglobulinemia increases risk of C. difficile colitis and giardiasis. - Risk of persistent infection, bacteremia, and metastatic seeding.
• Travelers: - Prophylaxis not generally recommended unless immunocompromised. - Bismuth subsalicylate may be used to reduce risk.
10. CLINICAL DECISION PATHWAY (FIGURE 138-1)¶
- Initial Assessment: Presenting with diarrhea, nausea, or vomiting.
- Action: Initiate symptomatic/oral rehydration therapy.
- Evaluation of Severity & Duration:
- Is duration >1 day and is the illness severe?
- NO → Resolution.
- YES → Obtain history and stool for WBCs.
- Assessment of Inflammatory Status (based on WBC count):
- Noninflammatory (No WBCs present) → Continue symptomatic therapy; further evaluation if no resolution.
- Inflammatory (WBCs present) → Culture for Shigella, Salmonella, Campylobacter jejuri; Consider Clostridioides difficile toxin → Consider: Empirical antimicrobial therapy.
- Extended Duration Check:
- If duration >10 days → Examine stool for parasites → Specific antiparasitic therapy.
11. KEY PEARLS & HIGH-YIELD POINTS¶
• EHEC Warning: Bloody stools without fecal leukocytes → Alert lab for EHEC. Antibiotics are contraindicated here due to HUS risk.
• Loperamide Rule: Never use in patients with fever or dysentery (risk of prolongs Shigella infection).
• Norovirus: Highly contagious and robust on surfaces; common in cruise ships/healthcare settings.
• C. difficile: Leading cause of nosocomial diarrhea in adults.
• Clinical Distinction: - Noninflammatory → Watery, no WBCs. - Inflammatory → Dysentery, WBCs present. - Penetrating → Enteric fever, mononuclear leukocytes.
12. ADDITIONAL TABLES¶
• Table 138-4 Bacterial Food Poisoning: - 1–6 h: Staphylococcus aureus (Nausea, vomiting, diarrhea; Ham, poultry, potato/egg salad, mayonnaise) and Bacillus cereus (Fried rice). - 8–16 h: Abdominal cramps, diarrhea (vomiting rare). - >16 h: - E. coli: Watery diarrhea (Salads, cheese, meats, water). - EHEC: Bloody diarrhea (Ground beef, roast beef, salami, raw milk, raw vegetables, apple juice). - Salmonella spp.: Inflammatory diarrhea (Beef, poultry, eggs, dairy products). - Campylobacter jejuri: Inflammatory diarrhea (Poultry, raw milk). - Shigella spp.: Dysentery (Potato or egg salad, lettuce, raw vegetables). - Vibrio parahaemolyticus: Dysentery (Mollusks, crustaceans).
• Table 138-5 Treatment of Traveler's Diarrhea: - Watery diarrhea (no blood, no fever), 1–2 unformed stools/day without distressing symptoms → ORS, Pedialyte, Lytren, or flavored mineral water + saltine crackers. - Dysentery (blood) or fever (>37.8°C) → Antibacterial drug. - Infants (<2 years old) → Fluids/electrolytes; continue feeding (especially breast milk); seek medical attention for moderate dehydration, fever >24 h, bloody stools, or diarrhea lasting several days.
Reference Tables¶
TABLE 138-1 Gastrointestinal Pathogens Causing Acute Diarrhea MECHANISM Noninflammatory (enterotoxin)¶
Harrison's 22e, p.1077
| 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 |
| Colon or distal small bowel |
Dysentery or inflammatory diarrhea |
Fecal polymorphonuclear leukocytes; substantial increase in fecal lactoferrin |
||
| Penetrating | Distal small bowel |
Enteric fever | Fecal mononuclear leukocytes |
Salmonella Typhi, Y. enterocolitica |
TABLE 138-3 Causes of Traveler’s Diarrhea¶
Harrison's 22e, p.1079
| ETIOLOGIC AGENT | APPROXIMATE PERCENTAGE OF CASES |
COMMENTS |
|---|---|---|
| Bacteria | 50–75 | |
| Enterotoxigenic Escherichia coli |
10–45 | Single most important agent |
| Enteroaggregative E. coli | 5–35 | Emerging enteric pathogen with worldwide distribution |
| Campylobacter jejuni | 5–25 | More common in Asia |
| Shigella | 0–15 | Major cause of dysentery |
| Salmonella | 0–15 | — |
| Others | 0–5 | Including Aeromonas, Plesiomonas, and Vibrio cholerae |
| Viruses | 0–20 | |
| 0–10 | ||
| 0–5 | ||
| Parasites | 0–10 | |
| Giardia lamblia | 0–5 | Affects hikers and campers who drink from freshwater streams |
| Cryptosporidium | 0–5 | Resistant to chlorine treatment of water sources |
| Entamoeba histolytica | <1 | — |
| Cyclospora | <1 | — |
| Other | 0–10 | |
| 0–5 | ||
| 10–50 |
TABLE 138-2 Postdiarrhea Complications of Acute Infectious Diarrheal Illness COMPLICATION Chronic diarrhea (diarrhea…¶
Harrison's 22e, p.1079
| COMPLICATION | COMMENTS |
|---|---|
| Chronic diarrhea (diarrhea lasting >4 weeks) • Lactase deficiency • Small-bowel bacterial overgrowth • Malabsorption syndromes (tropical and celiac sprue) |
Occurs in ~1% of travelers with acute diarrhea Protozoa account for approximately one-third of cases |
| Irritable bowel syndrome | Occurs in ~10% of travelers with traveler’s diarrhea |
| Hemolytic-uremic syndrome (hemolytic anemia, thrombocytopenia, and renal failure) |
Follows infection with Shiga toxin–producing bacteria (Shigella dysenteriae type 1 and enterohemorrhagic Escherichia coli) |
TABLE 138-4 Bacterial Food Poisoning¶
Harrison's 22e, p.1080
| INCUBATION PERIOD, ORGANISM |
SYMPTOMS | COMMON FOOD SOURCES |
|---|---|---|
| 1–6 h | ||
| Staphylococcus aureus | Nausea, vomiting, diarrhea |
Ham, poultry, potato or egg salad, mayonnaise, cream pastries |
| Bacillus cereus | Nausea, vomiting, diarrhea |
Fried rice |
| 8–16 h | ||
| Abdominal cramps, diarrhea (vomiting rare) |
||
| Abdominal cramps, diarrhea (vomiting rare) |
||
| >16 h | ||
| Watery diarrhea | ||
| Enterotoxigenic Escherichia coli |
Watery diarrhea | Salads, cheese, meats, water |
| Enterohemorrhagic E. coli |
Bloody diarrhea | Ground beef, roast beef, salami, raw milk, raw vegetables, apple juice |
| Salmonella spp. | Inflammatory diarrhea | Beef, poultry, eggs, dairy products |
| Campylobacter jejuni | Inflammatory diarrhea | Poultry, raw milk |
| Shigella spp. | Dysentery | Potato or egg salad, lettuce, raw vegetables |
| Vibrio parahaemolyticus | Dysentery | Mollusks, crustaceans |
TABLE 138-5 Treatment of Traveler’s Diarrhea on the Basis of Clinical Features a¶
Harrison's 22e, p.1081
| CLINICAL SYNDROME | SUGGESTED THERAPY |
|---|---|
| Watery diarrhea (no blood in stool, no fever), 1 or 2 unformed stools per day without distressing enteric symptoms |
Oral fluids (oral rehydration solution, Pedialyte, Lytren, or flavored mineral water) and saltine crackers |
| Dysentery (passage of bloody stools) or fever (>37.8°C) |
Antibacterial drugc |
| Diarrhea in infants (<2 years old) | Fluids and electrolytes (oral rehydration solution, Pedialyte, Lytren); continue feeding, especially with breast milk; seek medical attention for moderate dehydration, fever lasting >24 h, bloody stools, or diarrhea lasting more than several days |