Traveler's diarrhea
For patient information click here
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.
Synonyms and keywords: Traveller’s diarrhoea; Tourist diarrhea; Traveler’s dysentery; TD; Montezuma’s revenge; Wilderness diarrhea; WD; Wilderness-acquired diarrhea; WAD; Backcountry diarrhea
Overview
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
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).
Classification
Traveler’s diarrhea may be classified according to the agent responsible the disease into either bacterial (most common), viral, or protozoal traveler’s diarrhea.
Pathophysiology
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.
Causes
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.
Differential Diagnosis
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.
Epidemiology and Demographics
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).
Risk Factors
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.
Natural History, Complications and Prognosis
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.
Diagnosis
History and Symptoms
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
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).
Laboratory Findings
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
Other diagnostic studies are not required for the diagnosis of traveler’s diarrhea.
Treatment
Medical Therapy
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.
Prevention
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.
References
Classification
Overview
Traveler’s diarrhea may be classified according to the agent responsible the disease into either bacterial, viral, or protozoal traveler’s diarrhea.
Classification
Traveler’s diarrhea may be classified according to the agent responsible the disease:
- Bacterial (80% of cases, usually E. coli)
- Viral
- Protozoal
References
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) |
|
|
|
|
| Campylobacter jejuni |
|
|
|
|
| Shigella spp. |
|
|
|
|
| Salmonella spp. |
|
|
|
|
| Viruses | ||||
| Norovirus |
|
|
|
|
| Rotavirus |
|
|
|
|
| Protozoa | ||||
| Giardia lamblia |
|
|
|
|
| Entamoeba histolytica |
|
|
|
|
| Cryptosporidium spp. |
|
|
|
|
References
Causes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
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.
Causes
- 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:
| E. coli, enterotoxigenic | 20-80% |
| E. coli, enteroaggregative | 0-20% |
| E. coli, enteroinvasive | 0-6% |
| Shigella spp | 2-30% |
| Salmonella spp | 0-33% |
| Campylobacter jejuni | 3-17% |
| Vibrio parahemolyticus | 0-31% |
| Aeromonas hydrophila | 0-30% |
| Giardia lamblia | 0 to less than 20% |
| Entamoeba histolytica | 0-5% |
| Cryptosporidium sp | 0 to less than 20% |
| Rotavirus | 0-36% |
| Norwalk virus | 0-10% |
Common Causes
- 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
Causes by Organ System
Causes in Alphabetical Order
References
Differentiating Traveler’s Diarrhea from other Diseases
To review the differential diagnosis of diarrhea, click here.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2], Seyedmahdi Pahlavani, M.D. [3]
Traveler’s Diarrhea Differential Diagnosis
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
| Cause | Clinical manifestation | Lab findings | Extra intestinal findings | Cause/Pathogenesis | Gold standard diagnosis | |||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Symptoms | GI signs | |||||||||||||||||||||
| Duration | Diarrhea | Fever | Abdominal pain | Weight loss | ||||||||||||||||||
| Stool exam | CBC | Other lab findings | ||||||||||||||||||||
| Acute | Chronic | Watery | Bloody | Fatty | WBC | RBC | Ova/Parasite | Osmotic gap | Other | WBC | Hgb | Plt | ||||||||||
| Cause | Duration | Diarrhea | Fever | Abdominal pain | Weight loss | GI signs | Stool exam | CBC | Other lab findings | Extra intestinal findings | Cause/Pathogenesis | Gold standard diagnosis | ||||||||||
| Acute | Chronic | Watery | Bloody | Fatty | WBC | RBC | Ova/Parasite | Osmotic gap | Other | WBC | Hgb | Plt | ||||||||||
| Campylobacteriosis | + | – | + | + | – | + | + | – |
|
+ | + | – | Nl |
|
↑ | Nl | Nl | Nl | ||||
| Salmonellosis | + | + | + | + | – | + | + | – | + | + | – | Nl |
|
↑ | Nl | ↑ | ||||||
| Shigellosis | + | – | + | + | – | + | + | – |
|
+ | + | – | Nl |
|
↑/↓ | ↓ | ↓ |
|
||||
| Cause | Duration | Diarrhea | Fever | Abdominal pain | Weight loss | GI signs | Stool exam | CBC | Other lab findings | Extra intestinal findings | Cause/Pathogenesis | Gold standard diagnosis | ||||||||||
| Acute | Chronic | Watery | Bloody | Fatty | WBC | RBC | Ova/Parasite | Osmotic gap | Other | WBC | Hgb | Plt | ||||||||||
| Escherichia coli enteritis | ETEC | + | – | + | – | – | + | – | – |
|
+ | – | – | Nl |
|
↑ | Nl | Nl | – | – |
|
|
| EIEC | + | – | + | + | – | + | + | – |
|
+ | + | – | Nl |
|
↑ | Nl | Nl | – | – | |||
| EAEC | + | + | + | + | – | – | + | – |
|
+ | + | – | Nl |
|
↑ | ↓ | ↓ | – |
|
|||
| Yersinia enterocolitica | + | – | + | + | – | + | + | – |
|
+ | + | – | Nl |
|
↑ | Nl | Nl | – | ||||
| Cause | Duration | Diarrhea | Fever | Abdominal pain | Weight loss | GI signs | Stool exam | CBC | Other lab findings | Extra intestinal findings | Cause/Pathogenesis | Gold standard diagnosis | ||||||||||
| Acute | Chronic | Watery | Bloody | Fatty | WBC | RBC | Ova/Parasite | Osmotic gap | Other | WBC | Hgb | Plt | ||||||||||
| Vibrio cholera | + | – | + | – | – | – | + | – | + | – | – | Nl |
|
↑ | Nl | Nl |
|
|||||
| Aeromonas | + | + | + | + | – | + | + | – |
|
+ | + | – | Nl |
|
↑ | Nl | Nl | – |
|
| ||
| Norovirus | + | – | + | – | – | + | + | – | – | – | – | Nl |
|
↓ | Nl | Nl | – |
| ||||
| Rotavirus | + | – | + | – | – | + | – | – |
|
+ | – | – | Nl | – | Nl | Nl | Nl |
| ||||
| Cause | Duration | Diarrhea | Fever | Abdominal pain | Weight loss | GI signs | Stool exam | CBC | Other lab findings | Extra intestinal findings | Cause/Pathogenesis | Gold standard diagnosis | ||||||||||
| Acute | Chronic | Watery | Bloody | Fatty | WBC | RBC | Ova/Parasite | Osmotic gap | Other | WBC | Hgb | Plt | ||||||||||
| Entamoeba histolytica | + | + | + | + | – | + | + | – | + | + | + | Nl | – | ↑ | Nl | Nl | – |
|
| |||
| Giardia | – | + | + | – | + | – | + | + | – | – | + | Nl | – | Nl | Nl | Nl | – |
| ||||
| Cryptosporidium | – | + | + | – | – | – | + | + | – | – | + | Nl |
|
Nl | Nl | Nl |
|
|
| |||
References
- ↑ Casburn-Jones, Anna C; Farthing, Michael Jg (2004). “Traveler’s diarrhea”. Journal of Gastroenterology and Hepatology. 19 (6): 610–618. doi:10.1111/j.1440-1746.2003.03287.x. ISSN 0815-9319.
- ↑ Kamat, Deepak; Mathur, Ambika (2006). “Prevention and Management of Travelers’ Diarrhea”. Disease-a-Month. 52 (7): 289–302. doi:10.1016/j.disamonth.2006.08.003. ISSN 0011-5029.
- ↑ Pfeiffer, Margaret L.; DuPont, Herbert L.; Ochoa, Theresa J. (2012). “The patient presenting with acute dysentery – A systematic review”. Journal of Infection. 64 (4): 374–386. doi:10.1016/j.jinf.2012.01.006. ISSN 0163-4453.
- ↑ Barr W, Smith A (2014). “Acute diarrhea”. Am Fam Physician. 89 (3): 180–9. PMID 24506120.
- ↑ Amil Dias J (2017). “Celiac Disease: What Do We Know in 2017?”. GE Port J Gastroenterol. 24 (6): 275–278. doi:10.1159/000479881. PMID 29255768.
- ↑ Kotloff KL, Riddle MS, Platts-Mills JA, Pavlinac P, Zaidi A (2017). “Shigellosis”. Lancet. doi:10.1016/S0140-6736(17)33296-8. PMID 29254859. Vancouver style error: initials (help)
- ↑ Yamamoto-Furusho, J.K.; Bosques-Padilla, F.; de-Paula, J.; Galiano, M.T.; Ibañez, P.; Juliao, F.; Kotze, P.G.; Rocha, J.L.; Steinwurz, F.; Veitia, G.; Zaltman, C. (2017). “Diagnóstico y tratamiento de la enfermedad inflamatoria intestinal: Primer Consenso Latinoamericano de la Pan American Crohn’s and Colitis Organisation”. Revista de Gastroenterología de México. 82 (1): 46–84. doi:10.1016/j.rgmx.2016.07.003. ISSN 0375-0906.
- ↑ Borbély, Yves M; Osterwalder, Alice; Kröll, Dino; Nett, Philipp C; Inglin, Roman A (2017). “Diarrhea after bariatric procedures: Diagnosis and therapy”. World Journal of Gastroenterology. 23 (26): 4689. doi:10.3748/wjg.v23.i26.4689. ISSN 1007-9327.
- ↑ Crawford, Sue E.; Ramani, Sasirekha; Tate, Jacqueline E.; Parashar, Umesh D.; Svensson, Lennart; Hagbom, Marie; Franco, Manuel A.; Greenberg, Harry B.; O’Ryan, Miguel; Kang, Gagandeep; Desselberger, Ulrich; Estes, Mary K. (2017). “Rotavirus infection”. Nature Reviews Disease Primers. 3: 17083. doi:10.1038/nrdp.2017.83. ISSN 2056-676X.
- ↑ Kist M (2000). “[Chronic diarrhea: value of microbiology in diagnosis]”. Praxis (Bern 1994) (in German). 89 (39): 1559–65. PMID 11068510.
- ↑ Guerrant RL, Shields DS, Thorson SM, Schorling JB, Gröschel DH (1985). “Evaluation and diagnosis of acute infectious diarrhea”. Am. J. Med. 78 (6B): 91–8. PMID 4014291.
- ↑ López-Vélez R, Turrientes MC, Garrón C, Montilla P, Navajas R, Fenoy S, del Aguila C (1999). “Microsporidiosis in travelers with diarrhea from the tropics”. J Travel Med. 6 (4): 223–7. PMID 10575169.
- ↑ Wahnschaffe, Ulrich; Ignatius, Ralf; Loddenkemper, Christoph; Liesenfeld, Oliver; Muehlen, Marion; Jelinek, Thomas; Burchard, Gerd Dieter; Weinke, Thomas; Harms, Gundel; Stein, Harald; Zeitz, Martin; Ullrich, Reiner; Schneider, Thomas (2009). “Diagnostic value of endoscopy for the diagnosis of giardiasis and other intestinal diseases in patients with persistent diarrhea from tropical or subtropical areas”. Scandinavian Journal of Gastroenterology. 42 (3): 391–396. doi:10.1080/00365520600881193. ISSN 0036-5521.
- ↑ Mena Bares LM, Carmona Asenjo E, García Sánchez MV, Moreno Ortega E, Maza Muret FR, Guiote Moreno MV, Santos Bueno AM, Iglesias Flores E, Benítez Cantero JM, Vallejo Casas JA (2017). “75SeHCAT scan in bile acid malabsorption in chronic diarrhoea”. Rev Esp Med Nucl Imagen Mol. 36 (1): 37–47. doi:10.1016/j.remn.2016.08.005. PMID 27765536.
- ↑ Gibson RJ, Stringer AM (2009). “Chemotherapy-induced diarrhoea”. Curr Opin Support Palliat Care. 3 (1): 31–5. doi:10.1097/SPC.0b013e32832531bb. PMID 19365159.
- ↑ Abraham BP, Sellin JH (2012). “Drug-induced, factitious, & idiopathic diarrhoea”. Best Pract Res Clin Gastroenterol. 26 (5): 633–48. doi:10.1016/j.bpg.2012.11.007. PMID 23384808.
- ↑ Reintam Blaser A, Deane AM, Fruhwald S (2015). “Diarrhoea in the critically ill”. Curr Opin Crit Care. 21 (2): 142–53. doi:10.1097/MCC.0000000000000188. PMID 25692805.
- ↑ McMahan ZH, DuPont HL (2007). “Review article: the history of acute infectious diarrhoea management–from poorly focused empiricism to fluid therapy and modern pharmacotherapy”. Aliment. Pharmacol. Ther. 25 (7): 759–69. doi:10.1111/j.1365-2036.2007.03261.x. PMID 17373914.
- ↑ Schiller LR (2012). “Definitions, pathophysiology, and evaluation of chronic diarrhoea”. Best Pract Res Clin Gastroenterol. 26 (5): 551–62. doi:10.1016/j.bpg.2012.11.011. PMID 23384801.
- ↑ Giannella RA (1986). “Chronic diarrhea in travelers: diagnostic and therapeutic considerations”. Rev. Infect. Dis. 8 Suppl 2: S223–6. PMID 3523719.
- ↑ Silverberg MS, Satsangi J, Ahmad T, Arnott ID, Bernstein CN, Brant SR; et al. (2005). “Toward an integrated clinical, molecular and serological classification of inflammatory bowel disease: report of a Working Party of the 2005 Montreal World Congress of Gastroenterology”. Can J Gastroenterol. 19 Suppl A: 5A–36A. PMID 16151544.
- ↑ Sauter GH, Moussavian AC, Meyer G, Steitz HO, Parhofer KG, Jüngst D (2002). “Bowel habits and bile acid malabsorption in the months after cholecystectomy”. Am J Gastroenterol. 97 (7): 1732–5. doi:10.1111/j.1572-0241.2002.05779.x. PMID 12135027.
- ↑ Maiuri L, Raia V, Potter J, Swallow D, Ho MW, Fiocca R; et al. (1991). “Mosaic pattern of lactase expression by villous enterocytes in human adult-type hypolactasia”. Gastroenterology. 100 (2): 359–69. PMID 1702075.
- ↑ RUBIN CE, BRANDBORG LL, PHELPS PC, TAYLOR HC (1960). “Studies of celiac disease. I. The apparent identical and specific nature of the duodenal and proximal jejunal lesion in celiac disease and idiopathic sprue”. Gastroenterology. 38: 28–49. PMID 14439871.
- ↑ Konvolinka CW (1994). “Acute diverticulitis under age forty”. Am J Surg. 167 (6): 562–5. PMID 8209928.
- ↑ Satsangi J, Silverberg MS, Vermeire S, Colombel JF (2006). “The Montreal classification of inflammatory bowel disease: controversies, consensus, and implications”. Gut. 55 (6): 749–53. doi:10.1136/gut.2005.082909. PMC 1856208. PMID 16698746.
- ↑ Haque R, Huston CD, Hughes M, Houpt E, Petri WA (2003). “Amebiasis”. N Engl J Med. 348 (16): 1565–73. doi:10.1056/NEJMra022710. PMID 12700377.
- ↑ Hertzler SR, Savaiano DA (1996). “Colonic adaptation to daily lactose feeding in lactose maldigesters reduces lactose intolerance”. Am J Clin Nutr. 64 (2): 232–6. PMID 8694025.
- ↑ Briet F, Pochart P, Marteau P, Flourie B, Arrigoni E, Rambaud JC (1997). “Improved clinical tolerance to chronic lactose ingestion in subjects with lactose intolerance: a placebo effect?”. Gut. 41 (5): 632–5. PMC 1891556. PMID 9414969.
- ↑ BLACK-SCHAFFER B (1949). “The tinctoral demonstration of a glycoprotein in Whipple’s disease”. Proc Soc Exp Biol Med. 72 (1): 225–7. PMID 15391722.
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.
Overview
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).
Incidence
- The worldwide annual incidence of traveler’s diarrhea is estimated to be approximately 10-20 million cases.[1]
Age
- Individuals of all age groups are affected by traveler’s diarrhea.
- Pediatric patients are more likely to develop viral traveler’s diarrhea than adults.
Gender
- There is no gender predilection for the development of traveler’s diarrhea.
Race
- There is no racial predilection for the development of traveler’s diarrhea.
Seasonal Variation
- Traveler’s diarrhea is more common during Summer and early Fall (July to October).[2]
Developing Countries
- 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]
Developed Countries
- Compared with developing countries, the incidence of traveler’s diarrhea is much less common in developed countries.[1]
References
- ↑ 1.0 1.1 1.2 1.3 Steffen R (2005). “Epidemiology of traveler’s diarrhea”. Clin Infect Dis. 41 Suppl 8: S536–40. doi:10.1086/432948. PMID 16267715.
- ↑ Evans MR, Shickle D, Morgan MZ (2001). “Travel illness in British package holiday tourists: prospective cohort study”. J Infect. 43 (2): 140–7. doi:10.1053/jinf.2001.0876. PMID 11676522.
Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.
Overview
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.
Risk Factors
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
References
Natural History, Complications and Prognosis
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
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.
Natural History, Complications and Prognosis
- 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.
| Agent | Incubation Period | Natural History | Common Complications | Prognosis in the General Population |
| Bacteria | ||||
| E. coli |
|
|
| |
| Campylobacter jejuni |
|
|
| |
| Shigella |
|
|
| |
| Salmonella |
|
|
|
|
| Viruses | ||||
| Norovirus |
|
|
| |
| Rotavirus |
|
|
| |
| Protozoa | ||||
| Giardia |
|
|
|
|
| Entamoeba histolytica |
|
|
|
|
| Cryptosporidium |
|
|
|
|
References
Diagnosis
Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | Other Diagnostic Studies
Treatment
Treatment
Medical Therapy | Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Looking for the patient version?
© 2026 MyEClinic – IFTM Institut für Telematik in der Medizin GmbH
