Acute Diarrhea

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2] Sudarshana Datta, MD [3]

The term ‘diarrhea’ is derived from the Greek term “to flow through.” It is characterized by the passage of unformed or abnormally liquid stools at an increased frequency. Acute diarrhea has a duration of <2 weeks. Infectious agents responsible for majority of cases include Norovirus, Salmonella, Shigella, Clostridium perfringens, Staphylococcus aureus, Rotavirus, Shigella, Enterotoxigenic E.coli (ETEC), Campylobacter and Cryptosporidium parvum. Risk factors may be classified based on travel history, epidemics, outbreaks, food history, animal contact, hospitalization and immunosupression. The pathophysiology of acute diarrhea includes osmotic, secretory, inflammatory types, and diarrhea due to altered motility. Acute diarrhea due to an osmotic causes includes osmotic laxatives such as lactose intolerance, antacids, fructose, lactulose, laxatives magnesium, phosphate, and sorbitol, which induce a secretory state. Bacterial infection of the intestine leads to activation of epithelial ion channels with increased secretion of anions. Invasion of the epithelium by various pathogens lead to exotoxin production and enhancement of enterocyte secretion by cytotoxins or intracellular signalling. The mortality rate due to acute diarrhea has been estimated for all ages to be 17.8 deaths per 100 000 of population. There is no established diagnostic study of choice for acute diarrhea as it is generally self-limited. Specific diagnostic studies are performed if symptoms last >7 days, in moderate-to-severe cases, dysentery, and to determine etiology in order to enable directed pathogen-specific therapy. Symptomatic treatment for diarrhea includes consumption of adequate amounts of water, mixed with electrolytes to replace water and salt depletion. According to the ACG Clinical Guideline, use of balanced electrolyte rehydration is recommended in patients with traveller’s diarrhea, excessively watery and severe diarrhea. Medical supervision is required in infants with diarrhea, moderate or severe diarrhea in young children, bloody diarrhea, diarrhea for more than two weeks and diarrhea associated with non-cramping abdominal pain, fever and weight loss. Empiric therapy is used as an initial treatment for diagnostic testing, after testing has failed to confirm a diagnosis, when there is no specific treatment or when specific treatment fails to effect a cure. Pharmacotherapy for acute diarrhea includes the use of antibiotics, anticholinergics, antimotility agents and other nonspecific antidiarrheal agents (probiotics).

The word “diarrhea” was coined by Hippocrates. ‘Diarrhea’ is derived from the Greek term “to flow through.” Diarrhea is a common manifestation of the gastrointestinal disease.

Diarrhea is defined as the passage of unformed or abnormally liquid stools at an increased frequency. Acute diarrhea has a duration of <2 weeks and may be classified on the basis of etiology and presentation. On the basis of etiology, acute diarrhea may be classified into infectious and non-infectious subtypes. Based on the type of presentation, acute diarrhea may be classified into watery and inflammatory types. Watery diarrhea may further be classified into secretory and osmotic types of diarrhea.

Diarrhea is a condition of altered intestinal water and electrolyte transport. The pathophysiology of acute diarrhea includes osmotic, secretory, inflammatory types, and diarrhea due to altered motility. Acute diarrhea due to an osmotic causes includes osmotic laxatives such as lactose intolerance, antacids, fructose, lactulose, laxatives magnesium, phosphate, and sorbitol, which induce a secretory state. Bacterial infection of the intestine leads to activation of epithelial ion channels with increased secretion of anions. Invasion of the epithelium by various pathogens lead to exotoxin production and enhancement of enterocyte secretion by cytotoxins or intracellular signalling. In case of motility disorders of the gut, rapid transit time delivers fluid secreted during digestion to the distal small bowel or colon. This prevents reabsorption of normally secreted fluid in the small bowel, overwhelming the reabsorptive capacity of the colon.

Common causes of acute diarrhea in both developing and developed nations are infections. Infectious agents responsible for majority of cases include Norovirus, Salmonella, Shigella, Clostridium perfringens, Staphylococcus aureus, Rotavirus, Shigella, Enterotoxigenic E.coli (ETEC), Campylobacter and Cryptosporidium parvum. Less commonly, acute diarrhea may be be caused by Norwalk viruses or may be associated with systemic infections including influenza, urinary tract infections, and HIV infection. Other common causes of acute diarrhea include food allergies and drug side effects. Less commonly, acute diarrhea can be a symptom in the initial stages of systemic conditions including Ischemic colitis, Hyperthyroidism, Tropical sprue and with disorders of digestion and the absorption process.

The differentials of acute diarrhea include Ischemic colitis, Lactose intolerance, Tropical sprue, Pseudomembranous enterocolitis, Campylobacteriosis, Salmonellosis, Shigellosis, Escherichia coli enteritis, Yersinia enterocolitica, Vibrio cholera, Aeromonas, Plesiomonas, Staphylococcus aureus, Bacillus cereus, Clostridium perfringens, Rotavirus, Norovirus, Adenovirus, Entamoeba histolytica, medications, Short bowel syndrome, Organophosphate poisoning, Radiation enteritis and Opium withdrawal.

In the US, the overall weighted prevalence for acute diarrheal illness corresponded to 0·6 episodes per person per year from 1996 to 2003. It has been found that approximately 179 million cases of acute gastroenteritis including 47.8 million cases of food-borne illness, occur each year in the US. The mortality rate due to acute diarrhea has been estimated for all ages to be 17.8 deaths per 100 000 of population. Global mortality rate for children (<5 years) is much higher, with a figure of 74·3 deaths per 100 000 of population. Morbidity and mortality of diarrhea differs by location, with the highest rates of under-5 mortality noted in sub-Saharan Africa and South Asia, in particular in Chad (594 deaths per 100 000) and Niger (485 deaths per 100 000).

The risk factors of acute diarrhea may be assessed based on the epidemiologic associations and the patient exposure histories. Risk factors may be classified based on travel history, epidemics, outbreaks, food history, animal contact, hospitalization and immunosupression. The 2017 Infectious Diseases Society of America Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea lists the risk factors of diarrhea along with their causative pathogens.

There is insufficient evidence to recommend routine screening for acute diarrhea.

Untreated cases of acute diarrhea may progress to develop symptoms of fluid depletion including altered mental status, electrolyte imbalances, dehydration, metabolic acidosis and malnutrition. Common complications of acute diarrhea include confusion, convulsions, sepsis, and death. Prognosis is generally good when the underlying cause is identified and treated early.

There is no established diagnostic study of choice for acute diarrhea as it is generally self-limited. Specific diagnostic studies are performed if symptoms last >7 days, in moderate-to-severe cases, dysentery, and to determine etiology in order to enable directed pathogen-specific therapy.

The hallmark of acute diarrhea is the sudden onset of 3 or more stools per day, lasting less than 2 weeks. The most common symptoms of acute diarrhea include increased frequency of bowel movements, abdominal pain, elevation of body temperature, symptoms of fluid loss (dark or scant urine, excessive thirst, dizziness, fatigue).

Patients with acute diarrhea usually appear ill, dehydrated or lethargic. Common physical examination findings of acute diarrhea include hypotension and other signs of volume depletion (depressed consciousness, sunken anterior fontanel, dry mucous membranes, sunken eyes, poor skin turgor and delayed capillary refill), abdominal tenderness and distension, increased peristaltic activity (borborygmi).

Laboratory investigations performed in the evaluation of patients with acute diarrhea include spot stool analysis, detection of occult blood, white blood cells, stool culture, quantitative stool analysis, fecal weight, stool osmotic gap, fecal pH, fecal fat concentration and analysis for laxative abuse. According to the ACG guidelines, stool culture is done only in cases where the patient is at high risk of spreading the disease to others. Stool diagnostic studies are performed when symptoms last for >7 days, patient has dysentery or moderate-to-severe diarrhea and to determine etiology to enable directed pathogen-specific therapy. Antibiotic sensitivity testing for management of acute diarrhea is not advised.

There are no ECG findings associated with acute diarrhea.

An x-ray may be helpful in the diagnosis of some of the rare causes of acute diarrhea. Findings on an x-ray suggestive of organic causes acute diarrhea include intestinal dilation, irregular mucosal surface and increased luminal fluid.

There are no ultrasound findings associated with acute diarrhea.

CT scan is not routinely performed for cases of acute diarrhea. However, it may help in the detection of certain rare causes of acute diarrhea such as inflammatory bowel disease, intestinal lymphoma, carcinoid syndrome, and other neuroendocrine tumors.

There are no MRI findings associated with acute diarrhea.

There are no other imaging findings associated with acute diarrhea.

Sigmoidoscopy and colonoscopy may help in the diagnosis of conditions such as melanosis coli due to laxative abuse, amebiasis, polyps, ulceration, Crohn’s disease, and ulcerative colitis. Upper GI endoscopy and biopsy help in the diagnosis of Crohn’s disease, giardiasis, intestinal lymphoma, lymphangiectasia, eosinophilic gastroenteritis, Whipple’s disease, mastocytosis, abetalipoproteinemia, fungal and protozoal infections.

The majority of cases of acute diarrhea are self-limited and require only supportive care. Symptomatic treatment for diarrhea includes consumption of adequate amounts of water, mixed with electrolytes to replace water and salt depletion. According to the ACG Clinical Guideline, use of balanced electrolyte rehydration is recommended in patients with traveller’s diarrhea, excessively watery and severe diarrhea. Medical supervision is required in infants with diarrhea, moderate or severe diarrhea in young children, bloody diarrhea, diarrhea for more than two weeks and diarrhea associated with non-cramping abdominal pain, fever and weight loss. Empiric therapy is used as an initial treatment for diagnostic testing, after testing has failed to confirm a diagnosis, when there is no specific treatment or when specific treatment fails to effect a cure. Pharmacotherapy for acute diarrhea includes the use of antibiotics, anticholinergics, antimotility agents and other nonspecific antidiarrheal agents (probiotics).

Surgical intervention is not recommended for the management of acute diarrhea.

Primary prevention of acute diarrhea includes measures such as counseling in patients and their close contacts. In addition, counseling prior to travel and hand washing using alcohol-based sanitizers are other recommended practices. Hand washing is particularly important for prevention of community-acquired diarrhea outbreaks in cruise ships or institutions.

There are no established measures for the secondary prevention of acute diarrhea.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ajay Gade MD[2]]

The word “diarrhea” was coined by Hippocrates. Diarrhea is derived from the Greek term “to flow through”. Diarrhea is a common manifestation of gastrointestinal disease.

The historical perspective of the acute diarrhea is as follows:^{[1][2][3][4][5][6][7][8][9]}

• The word “diarrhea” was coined by Hippocrates.
• Diarrhea is derived from the Greek term “to flow through.” Diarrhea is a common manifestation of gastrointestinal disease.
• In 1898, Kioshi Shiga provided the first description of Shigella dysenteriae type 1, the bacteria responsible for bacterial dysentery.
• In 1903, Conradi reported that extracts of Shiga’s bacillus are found in paralyzed and killed rabbits.
• Similar findings were published independently by Neisser and Shiga.
• The research in the next 70 years showed the following:
  • The endotoxic activity associated with Shiga’s bacillus from the activity of the protein Stx
  • The partial purification of Stx
  • The discovery that high iron concentrations inhibit Stx synthesis
  • The seminal observation by Bridgwater et al. and Howard that Stx appears to target vascular endothelium in the brain
  • The discovery by Vicari et al. that Stx is lethal for certain epithelial cells in culture

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Diarrhea is defined as the passage of unformed or abnormally fluid stools at an increased frequency. Acute diarrhea has a duration of < 4 weeks and may be classified on the basis of etiology and presentation. On the basis of etiology, acute diarrhea may be classified into infectious and non-infectious sub-types. Based on the type of presentation, acute diarrhea may be classified into watery and inflammatory types. Watery diarrhea may be further classified into secretory and osmotic types of diarrhea.

• Acute diarrhea may be classified according to etiology into infectious and non-infectious subtypes/groups. The infectious group may further be classified into bacterial, viral, fungal and protozoal subgroups. The non-infectious group is further classified into diarrhea due to medications, poisoning and systemic illnesses.

• Based on the type of presentation, acute diarrhea may be classified into watery and inflammatory types. Watery diarrhea may further be classified into secretory and osmotic types of diarrhea.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

Diarrhea is a condition of altered intestinal water and electrolyte transport. The pathophysiology of acute diarrhea includes osmotic, secretory, inflammatory types, and diarrhea due to altered motility. Acute diarrhea due to osmotic causes includes osmotic laxatives such as lactose intolerance, antacids, fructose, lactulose, and increased concentration of magnesium, phosphate, and sorbitol, which induce a secretory state. Bacterial infection of the intestine leads to activation of epithelial ion channels with increased secretion of anions. Invasion of the epithelium by various pathogens lead to exotoxin production and enhancement of enterocyte secretion by cytotoxins or intracellular signalling. In case of motility disorders of the gut, rapid transit time delivers fluid secreted during digestion to the distal small bowel or colon. This prevents reabsorption of normally secreted fluid in the small bowel, overwhelming the reabsorptive capacity of the colon.

The exact pathogenesis of acute diarrhea is different for infectious and non-infectious causes. Diarrhea is a condition of altered intestinal water and electrolyte transport. The pathophysiology of acute diarrhea includes osmotic, secretory, inflammatory types, and diarrhea due to altered motility.^[1]

Stool osmotic gap in cases of osmotic diarrhea is characterized by osmotic gap >125 mOsm/kg. In case of osmotic diarrhea, fasting leads to cessation of diarrhea.

• Acute diarrhea due to an osmotic causes includes osmotic laxatives such as lactose intolerance, antacids, fructose, lactulose, laxatives and high concentration of magnesium, phosphate, and sorbitol, which induce a secretory state.^[2][3]
• Maldigestion syndromes such as disaccharidase deficiency may also result in chronic osmotic diarrhea.

Secretory diarrhea results from disordered electrolyte transport and is the result of alteration of the absorptive role of the gut and increased secretory capacity. In secretory diarrheas, stool osmotic gap is <50 mOsm/kg and fasting does not lead to diarrhea cessation.

• Bacterial infection of the intestine leads to activation of epithelial ion channels with increased secretion of anions.
• Invasion of the epithelium by various pathogens lead to exotoxin production and enhancement of enterocyte secretion by cytotoxins or intracellular signalling.
• Cytokines activate the release of inflammatory mediators such as platelet activating factor and prostaglandins which stimulate secretion.

Disruption of the normal colonic epithelial barrier by microorganisms is mainly responsible for inflammatory diarrhea. This disruption may lead to exudative, secretory, or malabsorptive components of inflammatory diarrhea.

• Inflammatory causes of diarrhea might present with features that suggest malabsorption or rectal bleeding.
• The nature of the malabsorption depends on the regions affected (e.g., proximal vs. distal small bowel), and rectal bleeding is usually a manifestation of colonic or rectal ulcerations.^[4]

Both rapid and slow transit time are associated with motility disorders causing diarrhea.

• Rapid transit time delivers fluid secreted during digestion to the distal small bowel or colon. This prevents reabsorption of normally secreted fluid in the small bowel, overwhelming the reabsorptive capacity of the colon.
• Slow transit time results in bacterial overgrowth with bile acid deconjugation, poor micelle formation, and steatorrhea.
• Delayed transit time may lead to symptoms such as steatorrhea, usually up to 14 g per day.^[5]

For the details of the genetics, associated conditions, gross and microscopic pathology of the following causes of acute diarrhea, click the links below.

• Rotavirus
• Traveler’s diarrhea
• Ulcerative colitis
• Crohn’s disease
• Lactose intolerance
• Cholera
• Microsporidiosis
• Giardiasis
• Cryptosporidiosis
• Hyperthyroidism

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2] Sudarshana Datta, MD [3]

Common causes of acute diarrhea in both developing and developed nations are infections. Infectious agents responsible for majority of cases include Norovirus, Salmonella, Shigella, Clostridium perfringens, Staphylococcus aureus, Rotavirus, Shigella, Enterotoxigenic E.coli (ETEC), Campylobacter and Cryptosporidium parvum. Less commonly, acute diarrhea may be be caused by Norwalk viruses or may be associated with systemic infections including influenza, urinary tract infections, and HIV infection. Other common causes of acute diarrhea include food allergies and drug side effects. Less commonly, acute diarrhea can be a symptom of the initial stages of systemic conditions including Ischemic colitis, hyperthyroidism, tropical sprue and with disorders of digestion and the absorption.

Causes of acute diarrhea based on infectious agents are enlisted below. Common causes of diarrhea differ based on geographical location, food hygiene standards, sanitation, water supply, and the season. The causes include the following:^{[1][2][3][4][5][6][7][8][9][10]}

• Shigella species ( S.dysentriae, S.flexneri, S.sonneii, S.boydii)
• Vibrio cholerae
• Non-typhoidal Salmonella: S.typhimurium, S.enterica
• Campylobacter jejuni
• Clostridium difficile: Antibiotic associated diarrhea (eg: Amoxicillin with clavulanic acid, Clindamycin, Cephalosporins)
• Yersinia enterocolitica
• Aeromonas
• Sepsis:
  • Staphylococcus aureus (staphylococcal toxic shock syndrome [TSS])
  • Salmonella septicemia
• Hemolytic uraemic syndrome (Shiga toxin producing E. coli ETEC)
• Shigella species
• Clostridium difficile
• Campylobacter jejuni
• Escherichia coli:
  • ETEC
  • EPEC
  • EHEC
  • EIEC
  • EAEC
• Vibrio parahemolyticus
• Aeromonas
• Plesiomonas shigelloides
• Mycobacterium Avium complex
• Bacillus cereus
• Clostridium perfringens
• Listeria monocytogenes

Viral causes of diarrhea

• Rotavirus
• Norovirus
• Adenovirus
• Astrovirus
• Calcivirus
• Influenza virus
• Human immunodeficiency virus
• CMV
• Astrovirus
• Norwalk virus

Protozoa

• Entamoeba histolytica
• Cryptosporidium parvum

• Entamoeba histolytica
• Giardia lamblia
• Microsporidia
• Isospora

• Sepsis
• Urinary tract infection
• Appendicitis
• Intussusception
• Short bowel syndrome
• Radiation enteritis
• Chemotherapy induced enteritis
• Hyperthyroidism
• Irritable bowel syndrome
• Tropical sprue
• Ischemic colitis
• VIPoma
• Infectious colitis

Disorders of digestive/absorptive processes

• Glucose-galactose malabsorption
• Sucrase-isomaltase deficiency
• Late-onset (adult-type) hypolactasia, leads to lactose intolerance

Medications

• Antibiotics, mostly with Cephalosporins
• Magnesium containing antacids
• Laxatives
• Antiretroviral agents
• Chemotherapeutic agents
• Antifungals
• Digoxin
• Lactulose

Ingestion of plants (eg, hyacinths, daffodils, Amanita species mushrooms)

Food allergies

• Cow’s milk protein allergy
• Soy protein allergy

Organophosphate poisoning

Opium withdrawal

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

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]

The differentials of acute diarrhea include Ischemic colitis, Lactose intolerance, Tropical sprue, Pseudomembranous enterocolitis, Campylobacteriosis, Salmonellosis, Shigellosis, Escherichia coli enteritis, Yersinia enterocolitica, Vibrio cholera, Aeromonas, Plesiomonas, Staphylococcus aureus, Bacillus cereus, Clostridium perfringens, Rotavirus, Norovirus, Adenovirus, Entamoeba histolytica, medications, Short bowel syndrome, Organophosphate poisoning, Radiation enteritis and Opium withdrawal.

To review the differential diagnosis of diarrhea, click here.

To review the differential diagnosis of traveler’s diarrhea, click here.

To review the differential diagnosis of acute watery diarrhea, click here.

To review the differential diagnosis of acute bloody diarrhea, click here.

To review the differential diagnosis of acute fatty diarrhea, click here.

To review the differential diagnosis of acute diarrhea and fever, click here.

To review the differential diagnosis of acute diarrhea and abdominal pain, click here.

To review the differential diagnosis of acute diarrhea and weight loss, click here.

To review the differential diagnosis of acute diarrhea, fever, and abdominal pain, click here.

To review the differential diagnosis of acute diarrhea, abdominal pain, and weight loss, click here. The following table outlines the major differential diagnoses of acute 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

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

In the US, the overall weighted prevalence for acute diarrheal illness corresponded to 0·6 episodes per person per year from 1996 to 2003. It has been found that approximately 179 million cases of acute gastroenteritis including 47.8 million cases of food-borne illness, occur each year in the US. The mortality rate due to acute diarrhea has been estimated for all ages to be 17.8 deaths per 100 000 of population. Global mortality rate for children (<5 years) is much higher, with a figure of 74·3 deaths per 100 000 of population. Morbidity and mortality of diarrhea differs by location, with the highest rates of under-5 mortality noted in sub-Saharan Africa and South Asia, in particular in Chad (594 deaths per 100 000) and Niger (485 deaths per 100 000).

In the US:

• From 1996 to 2003, Center for Disease Control’s Foodborne Diseases Active Surveillance Network (FoodNet) conducted four 12-month random population-based surveys. A total of 52 840 interviews were completed. The overall weighted prevalence for acute diarrheal illness corresponded to 0·6 episodes per person per year. ^[1]

International:

• A systematic analysis for the Global Burden of Disease Study 2015 estimated that there were 2.39 billion episodes of diarrhea for the year 2015, of which 957.5 million occurred in children younger than 5 years.^[2]
• It also reported that from 2005 to 2015, diarrhea incidence decreased by 10.4% in children under-5 and by 5.9% among all ages and both rates of change were less than the declines in mortality rates.^[3]

• In the US, approximately 179 million cases of acute gastroenteritis including 47.8 million cases of food-borne illness, occur each year.^[4][5]

• In 2015, diarrhea was responsible for 1.31 million deaths across the globe.
• The mortality rate estimated for all ages was 17.8 deaths per 100 000 of population.^[6]

• Children under 5 year of age are affected predominantly when compared to all other age groups.
• Global mortality rate for children (<5 years) in 2015 was 74·3 deaths per 100 000 of population.^[7]

• In general there is no racial predilection to acute diarrhea.

• In children (age < 5 years) mortality rate was noted to be slightly different for the two genders. Mortality rate for boys was 74·1 deaths per 100 000, and for girls it was 74.5 deaths per 100 000. ^[8]

• Morbidity and mortality of diarrhea differs by location. The figure below shows all age mortality by geography.

• The highest rates of under-5 mortality was noted in sub-Saharan Africa and South Asia, in particular in Chad (594 deaths per 100 000) and Niger (485 deaths per 100 000). However, due to their moderate-to-high burden and large populations, India (105 000 deaths) and Nigeria (103 000 deaths) combined had 42% of the 499 000 global under-5 deaths in 2015 due to diarrhea.^[9]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2] Sudarshana Datta, MD [3]

The risk factors of acute diarrhea may be assessed based on the epidemiologic associations and the patient exposure histories. Risk factors may be classified based on travel history, epidemics, outbreaks, food history, animal contact, hospitalization and immunosupression. The 2017 Infectious Diseases Society of America Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea lists the risk factors of diarrhea along with their causative pathogens.

According to the 2017 Infectious Diseases Society of America Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea, common risk factors along with causative pathogens of diarrhea include the following:^[1]

• Foodborne outbreaks in hotels, cruise ships, resorts, restaurants, catered events^[2]
  • Shigella, Vibrio cholerae, Bacillus cereus, Staphylococcus aureus, nontyphoidal Salmonella, Clostridium perfringens, Campylobacter, ETEC, Listeria, Norovirus, Rotavirus, Cryptosporidium, Cyclospora cayetanensis
• Consumption of unpasteurized milk or dairy products^[3]
  • Salmonella, Campylobacter, Brucella (goat milk cheese), Coxiella burnetii, Yersinia enterocolitica, S. aureus toxin, Cryptosporidium, Listeria, Mycobacterium bovis
• Consumption of raw or undercooked meat or poultry^[4]
  • C. perfringens (beef, poultry), EHEC (ground beef), Salmonella (poultry), Calcivirus (oysters), Campylobacter (poultry), Vibrio (oysters),Yersinia (pork, chitterlings), S. aureus (poultry), and Trichinella (pork, wild game meat)
• Consumption of fruits or unpasteurized fruit juices, vegetables, leafy greens, and sprouts
  • Hepatitis A, Listeria monocytogenes, Nontyphoidal Salmonella, Cyclospora, Cryptosporidium, Norovirus
• Consumption of undercooked eggs
  • Salmonella, Shigella (egg salad)
• Consumption of raw shellfish
  • Hepatitis A, Vibrio species, Plesiomonas, Norovirus

• Swimming in or drinking untreated fresh water^[5]
  • Giardia, Campylobacter, Cryptosporidium, Salmonella, Shigella, Plesiomonas shigelloides, Aeromonas
• Swimming in recreational water facility with treated water^[5][6]
  • Cryptosporidium
• Exposure to house pets with diarrhea
  • Campylobacter, Yersinia
• Exposure to pig feces in certain parts of the world
  • Balantidium coli
• Contact with young poultry or reptiles
  • Nontyphoidal Salmonella
• Visiting a farm or petting zoo
  • Cryptosporidium, Campylobacter

• Age group
  • Birth- 3 months: Nontyphoidal Salmonella
  • 6–18 months: Rotavirus
  • 1–7 years: Shigella
  • Young adults: Campylobacter
  • Adults >50 years with a history of atherosclerosis: Nontyphoidal Salmonella

• Immunocompromised individuals
  • Nontyphoidal Salmonella, Yersinia, Shigella, Cryptosporidium, Campylobacter
• Hemochromatosis or hemoglobinopathy
  • Salmonella, Y. enterocolitica
• AIDS, immunosuppressive therapies, homosexual men, transplant recipients
  • Cytomegalovirus, Mycobacterium avium–intercellulare complex, Cryptosporidium, Cyclospora, Cystoisospora, Microsporidia, HIV

• Drug side effects^[7]
  • Broad spectrum antibiotics
  • Immunosuppressants
  • Antifungals

• Recent antimicrobial therapy and hospitalization^[7]
  • C. difficile
  • Multidrug-resistant Salmonella
  • Rotavirus

• Anal–genital, oral-anal, or digital-anal contact
  • Shigella, Giardia lamblia, Campylobacter, E. histolytica, Cryptosporidium and sexually transmitted infections, Salmonella
• Healthcare, long-term care, prison exposure, or employment
  • Norovirus, Clostridium difficile, Shigella, Cryptosporidium, Giardia, Rotavirus
• Day care
  • Rotavirus, Cryptosporidium, Giardia, Shigella, Norovirus, Calcivirus, Campylobacter
• Travel to endemic areas, poor sanitation and crowding^[8]
  • Escherichia coli (enteroaggregative, enterotoxigenic, enteroinvasive), Shigella, Typhi and nontyphoidal Salmonella, Campylobacter, Vibrio cholerae, Aeromonas, Plesiomonas, Rotavirus, Norovirus (Cruise ship diarrhea), enteric Adenovirus, Entamoeba histolytica, Cryptosporidium, Blastocystis, Giardia, Cyclospora, Cystoisospora