Traveler’s diarrhea is a common infectious disease that affects approximately 10-20 million travelers each year. It is defined as the passage of ≥3 unformed stools per day plus ≥1 associated enteric symptoms, such as abdominal pain or cramps, occurring in a traveler after arrival, usually in a resource-limited destination. Traveler’s diarrhea may be classified according to the agent responsible the disease into either bacterial (most common), viral, or protozoal traveler’s diarrhea. The most common cause of traveler’s diarrhea is enterotoxigenic E. coli, responsible for approximately 70% to 80% of cases in adults. The most potent risk factor in the development of traveler’s diarrhea is history of recent travel to a developing country in the past month (required for the diagnosis of traveler’s diarrhea). Other risk factors include immunocompromised status, pregnancy, recent ingestion of uncooked or poorly handled vegetables, meat, poultry, raw milk, drinking from untreated water, exposure to infected individuals, daycare, and healthcare settings, concomitant administration of H2-receptor antagonists, and recent sexual history of receptive anal or oral-anal contact. In the general population, traveler’s diarrhea is usually self-limited with an excellent prognosis. Common symptoms include diarrhea (either watery or bloody), nausea, vomiting, abdominal pain, and bloating with or without fever. In bacterial and viral traveler’s diarrhea, symptoms typically last a few hours to several days. In protozoal traveler’s diarrhea, however, symptoms may persist for several weeks or months. Traveler’s diarrhea is a clinical diagnosis, and additional laboratory testing is usually not required in acute, non-complicated cases. The mainstay of therapy for traveler’s diarrhea is rehydration and antimicrobial therapy. Since the majority of cases of traveler’s diarrhea are caused by bacterial pathogens, empiric antibiotic monotherapy using either fluoroquinolone or azithromycin is usually recommended in both adult and pediatric patients diagnosed with traveler’s diarrhea. At this time, prophylactic antibiotics should not be recommended for most travelers. Prophylactic antibiotics using fluoroquinolones for 1 to 3 days may be effective in the prevention of some cases of traveler’s diarrhea (e.g. for short-term travelers who are high-risk hosts (such as those who are immunosuppressed) or who are taking critical trips (such as engaging in a sporting event) during which even a short bout of diarrhea could affect the trip).

Traveler’s diarrhea may be classified according to the agent responsible the disease into either bacterial (most common), viral, or protozoal traveler’s diarrhea.

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.

Traveler’s diarrhea is an infectious disease caused by either bacteria (most common), viruses, or protoza. The most common cause of traveler’s diarrhea is enterotoxigenic E. coli (ETEC), which is responsible for up to 80% of all cases. Other common bacterial causes include other E. coli strains, Campylobacter, Shigella, and Salmonella. Common viral causes include norovirus, rotavirus, or astrovirus infection. Common protozoal causes include Giardia, Entamoeba histolytica, and Cryptoosporidium.

Traveler’s diarrhea must be differentiated from other causes of fever, abdominal pain, and diarrhea, such as acute pancreatitis, appendicitis, bowel obstruction, diverticulitis, drug reaction, hyperthyroidism, inflammatory bowel disease, mesenteric ischemia, peritonitis, and pneumonia.

The worldwide annual incidence of traveler’s diarrhea is estimated to be approximately 10-20 million cases. Individuals of all age groups are affected by traveler’s diarrhea, and pediatric patients are more likely to develop viral traveler’s diarrhea. There is no gender or racial predilection for the development of traveler’s diarrhea. Generally, traveler’s diarrhea is more common in developing countries during Summer and early Fall (July to October).

The most potent risk factor in the development of traveler’s diarrhea is history of recent travel to a developing country in the past month (required for the diagnosis of traveler’s diarrhea). Other risk factors include immunocompromised status, pregnancy, recent ingestion of uncooked or poorly handled vegetables, meat (e.g. hamburgers), poultry, raw milk, or poorly stored foods that require refrigeration (e.g. mayonnaise), drinking from untreated water, exposure to infected individuals, daycare, and healthcare settings, origin of traveler being a developed country, concomitant administration of H2-receptor antagonists, and recent sexual history of receptive anal or oral-anal contact.

In the general population, traveler’s diarrhea is usually self-limited with an excellent prognosis in the majority of cases. In bacterial and viral traveler’s diarrhea, symptoms typically last a few hours to several days after exposure. In protozoal traveler’s diarrhea, symptoms may persist for several weeks / months. Complications of traveler’s diarrhea are generally related to the dehydration associated with severe diarrhea. Other complications are related to the infectious agent responsible for the disease.

Traveler’s diarrhea is a clinical diagnosis. It is diagnosed when the following criteria are met: passage of ≥3 unformed stools per day plus ≥1 associated enteric symptoms, such as abdominal pain or cramps, occurring in a traveler after arrival, usually in a resource-limited destination. History-taking should focus on the presence of risk factors for the development of traveler’s diarrhea. A positive history of recent travel to a developing country within the past month is required for the diagnosis of traveler’s diarrhea. Symptoms of traveler’s diarrhea include diarrhea (either watery or bloody), nausea, vomiting, abdominal pain, and bloating with or without fever. Less common symptoms may be related to complications of traveler’s diarrhea and may include spontaneous bruising, oliguria/anuria, and painless gross hematuria.

Physical examination of patients with traveler’s diarrhea may be remarkable for abdominal tenderness, fever (occasionally), and signs of dehydration, such as abnormal orthostatic vital signs, reduced skin turgor, slow capillary refill, and dry mucous membranes. Physical examination among patients with severe dehydration may be remarkable for altered mental status. Physical examination may also be remarkable for findings suggestive of complications of the traveler’s diarrhea (e.g. hemolytic uremic syndrome, abscess formation, cognitive dysfunction, ocular disease).

In acute non-complicated cases of traveler’s diarrhea, identification of the agent responsible for traveler’s diarrhea is usually not necessary. Diagnostic laboratory tests for traveler’s diarrhea usually include either stool culture, ELISA, or polymerase chain reaction (PCR). Other laboratory findings in traveler’s diarrhea are usually non-specific and may include increased white blood cell count and elevated inflammatory markers. Laboratory findings suggestive of dehydration may include relative polycythemia, metabolic alkalosis, elevated BUN and serum creatinine (suggestive of pre-renal acute kidney injury). When hospitalized, patients should also be monitored for laboratory findings that may suggest development of complications associated with traveler’s diarrhea.

Other diagnostic studies are not required for the diagnosis of traveler’s diarrhea.

The mainstay of therapy for traveler’s diarrhea is rehydration and antimicrobial therapy. Since the majority of cases of traveler’s diarrhea are caused by bacterial pathogens, empiric antibiotic therapy is usually recommended among both adult and pediatric patients diagnosed with traveler’s diarrhea. Travelers who develop three or more loose stools in a 24-hour period — especially if associated with nausea, vomiting, abdominal cramps, fever, or blood in stools — benefit from antimicrobial therapy. Antibiotics usually are given for 3–5 days, but single dose or 1-day regimen are also effective among adults and children. Antimicrobial monotherapy typically includes oral administration of either levofloxacin 500 mg qd, norfloxacin 400 mg bid, ciprofloxacin 500 mg bid, Ofloxacin 200 mg bid, or azithromycin 500 mg qd (3-5 days) or 1000 mg (single dose). Symptomatic management of abdominal cramps and vomiting may also be required.

Prophylactic antibiotics should not be recommended for most travelers. Prophylactic antibiotics using fluoroquinolones for 1 to 3 days may be effective in the prevention of some cases of traveler’s diarrhea (e.g. for short-term travelers who are high-risk hosts (such as those who are immunosuppressed) or who are taking critical trips (such as engaging in a sporting event) during which even a short bout of diarrhea could affect the trip). A traveler relying on prophylactic antibiotics will need to carry an alternative antibiotic to use in case diarrhea develops despite prophylaxis. Other preventive measures include maintaining good hygiene, drinking safe water, and proper food handling during travel.

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Traveler’s diarrhea may be classified according to the agent responsible the disease into either bacterial, viral, or protozoal traveler’s diarrhea.

Traveler’s diarrhea may be classified according to the agent responsible the disease:

• Bacterial (80% of cases, usually E. coli)
• Viral
• Protozoal

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.

• 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:

Traveler’s diarrhea is an infectious disease caused by either bacteria (most common), viruses, or protoza. The most common cause of traveler’s diarrhea is enterotoxigenic E. coli (ETEC), which is responsible for up to 80% of all cases. Other common bacterial causes include other E. coli strains, Campylobacter, Shigella, and Salmonella. Common viral causes include norovirus, rotavirus, or astrovirus infection. Common protozoal causes include Giardia, Entamoeba histolytica, Cryptoosporidium, and Cyclospora.

• The most common causative agent associated with traveler’s diarrhea is enterotoxigenic Escherichia coli (ETEC).
• In infants and children, it is estimated that nearly 70% of diarrhea is due to viruses.

Common causes of traveler’s diarrhea are shown below:

• Campylobacter jejuni
• Cryptosporidiosis
• Entamoeba histolytica
• Enterotoxigenic Escherichia coli
• Escherichia coli
• Giardia lamblia
• Rotavirus
• Salmonella
• Shigellosis
• Staphylococcus aureus
• Vibrio parahaemolyticus
• Viral haemorrhagic fever
• Visceral leishmaniasis
• Yersinia enterocolitica

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To review the differential diagnosis of diarrhea, click here.

The following table outlines the major differential diagnoses of traveler’s diarrhea.^{[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30]}

Abbreviations: GI: Gastrointestinal, CBC: Complete blood count, WBC: White blood cell, RBC: Red blood cell, Plt: Platelet, Hgb: Hemoglobin, ESR: Erythrocyte sedimentation rate, CRP: C–reactive protein, IgE: Immunoglobulin E, IgA: Immunoglobulin A, ETEC: Escherichia coli enteritis, EPEC: Enteropathogenic Escherichia coli, EIEC: Enteroinvasive Escherichia coli, EHEC: Enterohemorrhagic Escherichia coli, EAEC: Enteroaggregative Escherichia coli, Nl: Normal, ASCA: Anti saccharomyces cerevisiae antibodies, ANCA: Anti–neutrophil cytoplasmic antibody, DNA: Deoxyribonucleic acid, CFTR: Cystic fibrosis transmembrane conductance regulator, SLC10A2: Solute carrier family 10 member 2, SeHCAT: Selenium homocholic acid taurine or tauroselcholic acid, IEL: Intraepithelial lymphocytes, MRCP: Magnetic resonance cholangiopancreatography, ANA: Antinuclear antibodies, AMA: Anti-mitochondrial antibody, LDH: Lactate dehydrogenase, CPK: Creatine phosphokinase, PCR: Polymerase chain reaction, ELISA: Enzyme–linked immunosorbent assay, LT: Heat–labile enterotoxin, ST: Heat–stable enterotoxin, RT-PCR: Reverse–transcriptase polymerase chain reaction, CD4: Cluster of differentiation 4, HIV: Human immunodeficiency virus, RUQ: Right-upper quadrant, VIP: Vasoactive intestinal peptide, GI: Gastrointestinal, FAP: Familial adenomatous polyposis, HNPCC: Hereditary nonpolyposis colorectal cancer, MTP: Microsomal triglyceride transfer protein, Scl‑70: Anti–topoisomerase I, TSH: Thyroid-stimulating hormone, T4: Thyroxine, T3: Triiodothyronine, DTR: Deep tendon reflex, RNA: Ribonucleic acid

The worldwide annual incidence of traveler’s diarrhea is estimated to be approximately 10-20 million cases. Individuals of all age groups are affected by traveler’s diarrhea, and pediatric patients are more likely to develop viral traveler’s diarrhea. There is no gender or racial predilection for the development of traveler’s diarrhea. Generally, traveler’s diarrhea is more common in developing countries during Summer and early Fall (July to October).

• The worldwide annual incidence of traveler’s diarrhea is estimated to be approximately 10-20 million cases.^[1]

• Individuals of all age groups are affected by traveler’s diarrhea.
• Pediatric patients are more likely to develop viral traveler’s diarrhea than adults.

• There is no gender predilection for the development of traveler’s diarrhea.

• There is no racial predilection for the development of traveler’s diarrhea.

• Traveler’s diarrhea is more common during Summer and early Fall (July to October).^[2]

• Traveler’s diarrhea is commonly associated with travel to developing countries.^[1]
• The incidence of traveler’s diarrhea in developing countries ranges from 20% to 90% per a 2-week stay.^[1]

• Compared with developing countries, the incidence of traveler’s diarrhea is much less common in developed countries.^[1]

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The most potent risk factor in the development of traveler’s diarrhea is history of recent travel to a developing country in the past month (required for the diagnosis of traveler’s diarrhea). Other risk factors include immunocompromised status, pregnancy, recent ingestion of uncooked or poorly handled vegetables, meat (e.g. hamburgers), poultry, raw milk, or poorly stored foods that require refrigeration (e.g. mayonnaise), drinking from untreated water, exposure to infected individuals, daycare, and healthcare settings, origin of traveler being a developed country, concomitant administration of H2-receptor antagonists, and recent sexual history of receptive anal or oral-anal contact.

The most potent risk factor in the development of traveler’s diarrhea is history of recent travel to a developing country in the past month (recent travel is required for diagnosis of traveler’s diarrhea).

Other risk factors include the following:

• Immunocompromised status
• Pregnancy
• Recent ingestion of uncooked or poorly handled vegetables, meat / poultry, raw milk, or poorly stored foods that require refrigeration (e.g. mayonnaise)
• Recent drinking from untreated water (e.g. stream or well)
• Exposure to daycare
• Exposure to healthcare settings (e.g. nursing homes or hospitals)
• Exposure to contacts with similar symptoms
• Origin of traveler is a developed country (i.e. individuals traveling from developing countries are at lower risk)
• Concomitant administration of H2 receptor antagonist
• Recent sexual history of receptive anal or oral-anal contact

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In the general population, traveler’s diarrhea is usually self-limited with an excellent prognosis in the majority of cases. In bacterial and viral traveler’s diarrhea, symptoms typically last a few hours to several days after exposure. In protozoal traveler’s diarrhea, symptoms may persist for several weeks / months. Complications of traveler’s diarrhea are generally related to the dehydration associated with severe diarrhea. Other complications are related to the infectious agent responsible for the disease.

• In the general population, traveler’s diarrhea is usually self-limited with an excellent prognosis in the majority of cases.
• The following table summarizes, the natural history, complications, and prognosis of the common infectious agents responsible for traveler’s diarrhea.

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