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Traveler's diarrhea

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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


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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

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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)
  • Gram-negative rod
  • Humans and animals
  • Fecal-oral route
  • Contaminated ground beef, unpasteurized milk, cheese, vegetables, or water
  • Enterotoxin-mediated: secretion of heat-labile toxin (LT) and heat-stable toxin (ST)
Campylobacter jejuni
  • Gram-negative rod
  • Humans and animals
  • Fecal-oral route
  • Contaminated meat, unpasteurized milk, cheese, vegetables, or water
  • Exposure to infected animals
  • Enterotoxin-mediated: secretion of Cholera-like enterotoxin
Shigella spp.
  • Gram-negative rod
  • Humans only
  • Fecal-oral route
  • Contaminated meat and pork, unpasteurized milk, cheese, vegetables, or water
  • Low inoculum sufficient for infection (resistant to gastric acid)
  • Enterotoxin-mediated: secretion of Shiga toxin
  • Invasion of macrophages and induction of cellular apoptosis
  • Intracellular spread by actin polymerization processes (rocket propulsion)
Salmonella spp.
  • Gram-negative rod
  • S. typhi: Humans only
  • Other Salmonella spp.: Humans and animals
  • Fecal-oral route
  • Contaminated raw egg shells, poultry, unpasteurized milk, cheese, vegetables, or water
  • High inoculum sufficient for infection (inactivated by gastric acid)
  • Vi capsule endotoxin prevents opsonization and lysis
  • Spread through the reticuloendothelial system
Viruses
Norovirus
  • Positive-sense, single-stranded RNA virus
  • Humans and animals
  • Fecal-oral route
  • Contaminated food, vegetables, and water
  • Fomites
  • Aerosol exposure
  • Virus uses P2 subdomain for binding and HBGA for attachment on host cell
Rotavirus
  • Double-stranded RNA virus
  • Humans and animals
  • Fecal-oral route
  • Fomites
  • Poorly understood pathogenesis
  • Viral replication in villous epithelium of host small intestine
Protozoa
Giardia lamblia
  • Anerobic, flagellated protozoan parasite
  • Humans and animals
  • Ingestion of cysts in water or uncooked foods
  • Fecal-oral route
  • Attaches to the epithelium by a ventral adhesive disc, and reproduces via binary fission
  • Usually luminal infection, no hematogenous spread
Entamoeba histolytica
  • Anaerobic parasitic protozoa with pseudopods
  • Humans
  • Rare (but present) in animals
  • Ingestion of cysts in water
  • Fecal-oral route
  • Excystation in the small intestine and migration to the large intestine
  • Luminal and extraluminal infection, hematogenous spread common
Cryptosporidium spp.
  • Spore-forming parasite
  • Humans and animals
  • Ingestion of oocytes in water
  • Fecal-oral route
  • Minimally invasive, surface-level mucosal inflammation
  • Usually luminal infection, potential to infect biliary tree

References

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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

Causes by Organ System

Cardiovascular Gangrene, kawasaki disease, superior mesenteric artery occlusion, organophosphates,abetalipoproteinaemia, viral haemorrhagic fever, autonomic neuropathy, selenium
Chemical / poisoning No underlying causes
Dermatologic Kawasaki disease, mercury, pellagra, celiac disease, acrodermatitis enteropathica, staphylococcal toxic shock syndrome, systemic sclerosis, Degos’ disease, kwashiorkor
Drug Side Effect No underlying causes
Ear Nose Throat No underlying causes
Endocrine Autoimmune adrenalitis, glucagonoma, hyperthyroidism, selenium
Environmental Arsenicals, carbon monoxide toxicity, organophosphates
Gastroenterologic Superior mesenteric artery occlusion, organophosphates, glucagonoma, bacterial overgrowth of small intestine, bile acid malabsorption syndrome,Brainerd diarrhea, celiac disease, cholestatic jaundice, collagenous colitis, colonic villous adenomata, colorectal cancer, crohn disease, faecal impaction, faecal incontinence, graft versus host disease, hirschsprung disease, intususception of intestine, irritable bowel syndrome, Large bowel obstruction, Laxative abuse, Lymphocytic colitis, Malabsorption syndrome, Postgastrectomy syndrome, protein losing enteropathy,short bowel syndrome, sucrase-isomaltase deficiency, ulcerative colitis, acrodermatitis enteropathica, lactase deficiency, abetalipoproteinaemia,meckel diverticulitis, pernicious anaemia, bacillary dysentery, bacillus cereus, campylobacter jejuni, cytomegalovirus, entamoeba histolytica, enterotoxigenic escherichia coli, escherichia coli, giardia lamblia, isosporiasis, legionella pneumophila, trichuriasis, tropical sprue, systemic sclerosis, whipple disease, autonomic neuropathy, Degos’ disease, kwashiorkor
Genetic Pancreatitis, chronic, acrodermatitis enteropathica, iduronate-2-sulfatase deficiency, lactase deficiency, Rapadilino syndrome
Hematologic Celiac disease, abetalipoproteinaemia, meckel diverticulitis, pernicious anaemia, viral haemorrhagic fever, entamoeba histolytica,HIV-1 disease, vitamin B12 deficiency, somatostatinoma
Iatrogenic No underlying causes
Infectious Disease Bacillus cereus, balantidiasis, campylobacter jejuni, capillaria, clostridium welchii, cryptosporidiosis,cyclospora cayetanensis, cyclosporiasis, cytomegalovirus, dengue fever, dientamoeba fragilis, dysentery, entamoeba histolytica, enterotoxigenic escherichia coli, escherichia coli, giardia lamblia, HIV-1 disease, hymenolepiasis, isosporiasis, legionella pneumophila, microsporidiasis,penicillium marneffei, pneumatosis cystoides intestinalis, pseudomembranous colitis, rotavirus, salmonella, sapporo-like virus, shigellosis, small round structured virus, staphylococcal toxic shock syndrome, staphylococcus aureus, streptococcus suis, strongyloidiasis, trichinella spiralis,trichuriasis, tropical sprue, typhoid fever, vibrio parahaemolyticus, visceral leishmaniasis, yersinia enterocolitica, adenovirus
Musculoskeletal / Ortho Rapadilino syndrome, Viral haemorrhagic fever, Dengue fever, Systemic sclerosis, Whipple disease
Neurologic Mercury, pellagra, hirschsprung disease, pernicious anaemia, staphylococcal toxic shock syndrome, autonomic neuropathy, Degos’ disease, ethylmalonic encephalopathy, vitamin B12 deficiency, zinc deficiency
Nutritional / Metabolic No underlying causes
Obstetric/Gynecologic No underlying causes
Oncologic Colorectal cancer, large bowel obstruction, small bowel lymphoma, somatostatinoma
Opthalmologic Hyperthyroidism, adenovirus
Overdose / Toxicity Arsenicals, carbon monoxide toxicity, mercury, organophosphates, pancreatitis, chronic, paraquat, thallium
Psychiatric Irritable bowel syndrome
Pulmonary Systemic sclerosis, severe acute respiratory syndrome
Renal / Electrolyte Autoimmune adrenalitis, laxative abuse, legionella pneumophila, staphylococcal toxic shock syndrome, systemic sclerosis
Rheum / Immune / Allergy No underlying causes
Sexual HIV-1 disease, zinc deficiency
Trauma Pancreatitis, chronic
Urologic Organophosphates, malakoplakia
Dental No underlying causes
Miscellaneous Brainerd diarrhea, complement 5 deficiency, copper salts, functional disorders

Causes in Alphabetical Order


References


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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 phosphokinasePCR: 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

(Traveler’s diarrhea)

+ + + + 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
  • Clinical diagnosis
Rotavirus + + + + Nl Nl Nl Nl
  • Stool immune–based assays
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
  • Antigen testing
  • Serology 
Giardia + + + + + + Nl Nl Nl Nl
  • Antigen detection assays
Cryptosporidium + + + + + Nl
  • Positive stool microscopy
Nl Nl Nl
  • Polymerase chain reaction

References

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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. 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.
  2. 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.

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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


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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
  • 1 day to 10 days
  • Excellent
Campylobacter jejuni
  • 1 day to 7 days
  • Excellent
Shigella
  • 1 day to 3 days
  • Excellent
Salmonella
  • 6 hrs to 3 days
  • Excellent
Viruses
Norovirus
  • 12 hrs to 2 days
  • Excellent
Rotavirus
  • 12 hrs to 2 days
  • Excellent
Protozoa
Giardia
  • 7 days to 21 days
  • Excellent
Entamoeba histolytica
  • 7 days to 21 days
  • Extraluminal complications common
  • Excellent
Cryptosporidium
  • 2 days to 10 days
  • Excellent

References


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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

Case Studies

Case Studies

Case #1

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