Gastroenteritis is inflammation of the stomach and intestines, commonly caused by infections from bacteria, viruses, or parasites. Transmission may be foodborne, fecal-oral, or through animal contact. Common clinical features include abdominal pain, diarrhea, vomiting, fever, and dehydration. Diagnostic testing with stool analysis or culture is not always required, but can help determine the etiology in certain circumstances. The majority of cases of gastroenteritis are self-limited; therefore, the only required treatment is supportive therapy (fluids). However, antibiotics are indicated in severe cases.

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  • The 2nd leading cause of morbidity and mortality worldwide
  • 3 million deaths annually (> 8,400 per day)
  • Mostly affects young children in developing countries
  • International travelers are particularly susceptible.
  • In the United States:
    • 179 million cases per year (17 million cases are foodborne)
    • Approximately 2 million hospitalizations


  • Viral:
    • Norovirus (common)
    • Rotavirus (common)
    • Enteric adenovirus
    • Astrovirus
    • Immunocompromised patients:
      • Cytomegalovirus
      • Enterovirus
  • Bacterial:
    • Salmonella (common)
    • Campylobacter (common)
    • Shigella
    • Escherichia coli (E. coli)
    • Clostridium
    • Yersinia
  • Parasitic:
    • Giardia lamblia
    • Entamoeba histolytica
    • Cryptosporidium
    • Cyclospora


  • Modes of infection:
    • Foodborne (toxin accumulation in food products)
    • Fecal-oral (bacterial contamination)
    • Direct or indirect animal transmission
  • Mechanism of diarrhea, associated findings, and etiology are described in the table below.
Mechanism of diarrheaNon-inflammatory (adhesion, enterotoxin)Inflammatory (invasion, cytotoxin)Penetrating (invades lymphatics)
PresentationWatery diarrheaDysentery (blood or mucus) or inflammatory diarrheaEnteric fever
Stool findings
  • No fecal white blood cells (WBCs)
  • Mild or no increase in fecal lactoferrin
  • Fecal polymorphonuclear leukocytes
  • Increased fecal lactoferrin
Fecal mononuclear leukocytes
Pathogen involved
  • Vibrio cholerae
  • Enterotoxigenic E. coli
  • Enteroaggregative
  • E. coli
  • Clostridium perfringens
  • Bacillus cereus
  • Staphylococcus aureus
  • Rotavirus
  • Norovirus
  • Enteric adenoviruses
  • Giardia lamblia
  • Cryptosporidium
  • Cyclospora
  • Shigella
  • Salmonella
  • Campylobacter jejuni
  • Enterohemorrhagic E. coli
  • Enteroinvasive E. coli
  • Yersinia enterocolitica
  • Listeria monocytogenes
  • Vibrio parahaemolyticus
  • Clostridioides difficile*
  • Entamoeba histolytica
  • Klebsiella oxytoca
  • Salmonella typhi
  • Y. enterocolitica
*Note: C. difficile produces a cytotoxin and enterotoxin, which leads to watery diarrhea, but fecal leukocytes can be seen due to inflammation of the inner lining of the bowel (pseudomembranous colitis).

Clinical presentation

  • Common symptoms:
    • Abdominal pain and cramps
    • Diarrhea (watery, mucoid, or bloody)
    • Vomiting 
    • Fever
    • Anorexia
    • Headache
    • Myalgia
  • Evidence of severe dehydration: 
    • Tachycardia
    • Hypotension
Gastroenteritis symptoms

Summary of common symptoms and incubation periods based on the pathogen: Bacillus cereus is listed twice since it produces two types of food-borne illness due to different enterotoxins. Emetic-type illness has an incubation of around 1‒6 hours, and diarrheal-type illness has an incubation period of 8‒16 hours.
Note: this is a generalization, and patient presentation can vary.
ETEC: Enterotoxigenic E. coli
EHEC: Enterohemorrhagic E. coli

Image by Lecturio.
Table: Characteristic features of important organisms associated with gastroenteritis
OrganismCharacteristic features
Bacillus cereus
  • Diarrhea, vomiting, abdominal cramping
  • Ingestion of preformed toxins in foods, such as fried rice
Staphylococcus aureus
  • Vomiting, abdominal pain
  • Diarrhea is not typical but may occur.
  • Caused by a preformed toxin in foods, such as ham, poultry, potato, egg salad, mayonnaise
  • Rapid onset of symptoms
Clostridioides difficile
  • Abdominal pain, watery diarrhea, possible fever
  • Associated with antibiotic exposure
  • Watery diarrhea, frequent fever, abdominal pain, and vomiting
  • Associated with undercooked foods, especially poultry, beef, and eggs
  • Antibiotic treatment needed only for severe disease or immunocompromised patients
Vibrio vulnificus
  • Vomiting, diarrhea, and abdominal pain
  • Associated with raw or undercooked shellfish
  • May cause invasive, life-threatening disease in immunocompromised patients or those with liver disease (hemochromatosis)
Clostridium perfringens
  • Watery diarrhea, cramps, and fever
  • Associated with undercooked or unrefrigerated food
Escherichia coli
  • Watery diarrhea, may be bloody if associated with enterohemorrhagic (Shiga toxin–producing) strain
  • Associated with undercooked beef or foods contaminated with bovine feces
  • Bloody diarrhea with fever
  • Bacteremia can occur.
  • Associated with contaminated food or water, especially during international travel
Campylobacter species
  • Abdominal pain, bloody diarrhea
  • Highest incidence in children and young adults
  • Associated with raw or undercooked meats
  • “Pseudoappendicitis”
  • Cryptosporidium
  • Cystoisospora (formerly Isospora)
  • Microsporidia species
Chronic watery diarrhea in immunosuppressed patients
  • Common in the wilderness and rural areas of the United States
  • Asymptomatic patients may continue to shed the organisms for months.
Rotavirus and norovirus
  • Brief illness
  • Vomiting common
  • Commonly seen in cruise ship buffets (norovirus)


  • Stool testing:
    • Most patients do not require stool testing.
    • Guided by clinical history and findings:
      • Blood or pus in the stool
      • Persistent fever
      • Severe symptoms
      • Prolonged course
      • High-risk patients
    • Fecal leukocytes or lactoferrin → inflammatory diarrhea
    • Stool culture and polymerase chain reaction (PCR) panel
    • Stool ova and parasites 
    • Direct viral antigen (rarely indicated)
    • C. difficile toxin enzyme immunoassay
  • General testing:
    • Generally only done in severe disease with evidence of dehydration
    • Basic metabolic panel → assesses for acute kidney injury and electrolyte abnormalities
    • Complete blood count → leukocytosis may be seen; eosinophilia may signal a parasitic infection

The following algorithm summarizes the workup of gastroenteritis:

Diagnostic workup of community acquired infectious diarrhea

Workup of gastroenteritis

Image by Lecturio.


  • Supportive care:
    • Most infections are self-limiting and only require oral rehydration therapy.
    • Intravenous (IV) fluid hydration may be required for severe disease.
    • Oral and IV solutions should contain replacement electrolytes.
  • Antidiarrheal agents (loperamide, bismuth salicylate): 
    • Reduce the duration of diarrhea
    • Can delay the excretion of the causative pathogens or toxins, and are contraindicated in:
      • Diarrhea with fever
      • Bloody or mucoid stool
      • Diarrhea caused by C. difficile and Shigella
  • Antibiotic therapy:
    • Not routinely used
    • The decision to use antibiotics is often empirical, because enteric pathogen testing is not always expedient.
    • Possible indications: 
      • Dysentery (passage of bloody stools)
      • Fever > 38°C (100.4°F)
      • Severe symptoms and hospitalization
      • High-risk population group (infants, elderly, immunocompromised, patients with comorbidities)
      • C. difficile infection
    • Contraindicated if Shiga toxin–producing E. coli is suspected (risk of hemolytic-uremic syndrome (HUS))
    • Frequently used antibiotics:
      • Fluoroquinolones
      • Azithromycin
      • Trimethoprim-sulfamethoxazole (TMP-SMX)
      • 3rd-generation cephalosporins


  • During the infection:
    • Hypovolemic shock
    • Severe dehydration
    • Acute kidney injury 
    • Metabolic acidosis
    • Electrolyte imbalances
    • Death
  • Post-diarrheal complications are summarized in the table below:
Table: Post-diarrheal complications
ComplicationDescriptionOrganism responsible
Chronic diarrhea (lasting more than 2 weeks)
  • Lactase deficiency
  • Small-bowel bacterial overgrowth
  • Malabsorption syndromes (tropical and celiac sprue)
Can occur with any type of acute diarrhea, especially protozoal
Initial presentation or exacerbation of inflammatory bowel diseaseDue to triggering of the inflammatory responseCan occur with any type of acute diarrhea, especially C. difficile
Reactive arthritis
  • Asymmetric oligoarthritis of the large joints
  • Enthesopathy
  • Shigella
  • Salmonella
  • Campylobacter
  • Yersinia
  • Hemolytic anemia
  • Thrombocytopenia
  • Renal failure
Follows infection with Shiga toxin-producing bacteria (Shigella and enterohemorrhagic E. coli)
Guillain-Barré syndromeAcute immune-mediated polyneuropathiesCampylobacter



  • Campylobacter jejuni are curved, gram-negative, oxidase-positive rods with polar flagella.
  • Distinguishing features: 
    • Require a CO2-rich environment
    • Grow at 42.0°C (107.6°F)
    • May appear S-shaped or like seagull wings due to their helical structure
  • The most common pathogen responsible for foodborne gastroenteritis in the United States
  • Highly contagious
Campylobacter species

Image showing the characteristic S-shaped or seagull wing-shaped Campylobacter

Image: “F0001” by the Department of Microbiology/Immunology, Catholic University of Health and Allied Sciences, Mwanza, Tanzania. License: CC BY 2.0.


  • Fecal-oral
  • Foodborne (undercooked poultry and unpasteurized milk) and contaminated water
  • Direct contact with infected animals (cats, dogs, pigs) or animal products


  • Invades the mucosa of the intestines → produces endotoxins, enterotoxins, and cytotoxins → destroys mucosal surfaces → blood and pus in stools (inflammatory diarrhea)
  • Rarely penetrates to cause septicemia

Clinical presentation

  • Acute watery and bloody diarrhea
  • Fever
  • Severe right lower quadrant abdominal pain resembling appendicitis (“pseudoappendicitis”)
  • Headache
  • Myalgias


  • Most cases will have a spontaneous resolution.
  • Macrolides and fluoroquinolones
  • A 3rd-generation cephalosporin, imipenem, ampicillin, or gentamicin can be given for extraintestinal infections.


  • Guillain-Barré syndrome (cross-reaction between C. jejuni antibodies and human gangliosides)
  • Reactive arthritis (in HLA-B27–positive patients)
  • Hemolytic anemia
  • Endocarditis and myopericarditis
  • Meningitis

Non-typhoidal Salmonella


  • S. enteritidis and S. typhimurium are gram-negative, non–lactose fermenting bacteria.
  • Produce hydrogen sulfide and are motile (unlike Shigella)
  • The 2nd most common pathogen responsible for bacterial foodborne gastroenteritis


  • Foodborne bacterial infection (poultry, raw eggs, milk)
  • Reservoir: enteric tracts of humans and domestic animals (turtles, reptiles, chickens)
  • Salmonella is sensitive to stomach acid. Lowered stomach acidity (antacids or gastrectomy) increases the risk for infection.
  • Other risk factors: 
    • Hemolytic conditions (sickle cell anemia, malaria)
    • Splenectomy
    • Cirrhosis
    • Leukemia and lymphoma
    • HIV infection


  • Bacteria invade the mucosa in the ileocecal region and are released into the lamina propria → influx of neutrophils → inflammation → ↑ prostaglandins and cAMP → loose diarrhea and necrosis of the upper mucosa
  • Septicemia is not common (< 5%) with S. enteritidis, but may occur with other subtypes.

Clinical presentation

  • Incubation period of 8–72 hours, lasts 3–7 days
  • Inflammatory watery diarrhea (occasionally bloody) 
  • Fever, chills
  • Headache
  • Myalgias
  • Severe vomiting 
  • Abdominal cramping


  • Supportive care
  • Antibiotics:
    • Not required for most uncomplicated cases
    • Prolongs fecal excretion of the pathogen
    • Only indicated for systemic manifestations or severe diarrhea:
      • Fluoroquinolones (ciprofloxacin) 
      • TMP-SMX 
      • Azithromycin
      • 3rd-generation cephalosporins (ceftriaxone)


  • Bacteremia
  • Reactive arthritis
  • Osteomyelitis (particularly in sickle cell patients)
  • Meningitis 
  • Myocarditis, endocarditis


Shigella causes bacilliary dysentery, also known as shigellosis.


  • S. dysenteriae, S. flexneri, S. sonnei, and S. boydii are gram-negative rods.
  • Gastric acid resistant
  • S. dysenteriae type 1 produces Shiga toxin (enterotoxin).


  • Fecal-oral
  • Humans are the only natural reservoir.
  • Flies are vectors.
  • Foodborne (unpasteurized milk products and raw, unwashed vegetables)
  • Contaminated water
  • Highly contagious


  • Shigella invades M cells through macropinocytosis → taken up by macrophages → escapes its phagosome → reaches epithelial cytoplasm and replicates → induces inflammatory response → epithelial and immune cell death
  • Polymerized actin filaments are used to spread cell-to-cell without needing to re-enter the extracellular milieu.
  • Shiga toxin release by S. dysenteriae:
    • Has 3 properties: neurotoxic, cytotoxic, enterotoxic
    • Causes intestinal secretion of solutes and water
    • Can induce HUS
  • Resulting effects:
    • Watery diarrhea
    • Mucus secretion
    • Leukocyte infiltration 
    • Superficial ulcers 
    • Rarely causes invasion of blood vessels

Clinical presentation

  • Incubation period of 0–48 hours, lasts 2–7 days
  • Fever
  • Abdominal cramping
  • Tenesmus (urgency to defecate)
  • Inflammatory diarrhea with mucus, pus, and blood


  • Usually resolves spontaneously
  • Rehydration and electrolyte replacement may be needed.
  • Antibiotics shorten the duration of symptoms and pathogen shedding in the stool:
    • Fluoroquinolones
    • Azithromycin
    • 3rd-generation cephalosporins
  • Avoid antimotility medications, because they can worsen symptoms and may lead to toxic megacolon.


  • HUS → due to Shiga toxin, often seen in children
  • Acute blood loss → mucosal ulcerations
  • Intestinal complications: 
    • Toxic megacolon
    • Colonic perforation
    • Intestinal obstruction 
    • Proctitis
    • Rectal prolapse → due to tenesmus
  • Reactive arthritis 
  • Though invasive, Shigella only rarely causes septicemia.

Vibrio cholerae

Cholera is a severe form of gastroenteritis caused by Vibrio cholerae (V. cholerae).


  • V. cholerae is a gram-negative, oxidase-positive, curved rod with polar flagella.
  • Grows on alkaline media
  • Distinguishing feature: “shooting star” motility inactivated by specific serum
  • Produces the cholera toxin


  • Inhabitant of coastal estuarine waters
  • Fecal-oral spread
  • Undercooked seafood or contaminated water
  • Sensitive to stomach acid; requires a high dose for infection
  • Outbreaks tend to occur during warm months.
  • Endemic in areas of Asia, Africa, the Middle East, Central and South America, and the U.S. Gulf Coast
  • Susceptibility is increased in:
    • Patients with type O blood
    • Antacid, antihistamine, or proton pump inhibitor use


  • Motility, mucinase, and toxin-coregulated pili (TCP) aid in attachment to the intestinal mucosa.
  • Leads to colonization of the intestinal lining without invasion of the intestinal wall
  • Cholera enterotoxin is released: activates adenylate cyclase → ↑ cAMP → efflux of electrolytes and water by the small bowel mucosa in the duodenum and jejunum

Clinical presentation

  • Incubation period is 1–3 days.
  • Some patients may be asymptomatic or have only mild symptoms.
  • Profuse “rice-water” stools 
  • Abdominal pain and nausea are less prominent than other forms of gastroenteritis.
  • Can quickly lead to severe dehydration and electrolyte depletion within hours:
    • Thirst
    • Oliguria
    • Muscle cramping
    • ↓ skin turgor
  • Severe cases can lead to altered mental status, renal tubular necrosis, and circulatory collapse.


  • Urgent fluid and electrolyte replacement is the 1st priority.
  • Antibiotics are used for severe disease, and can decrease diarrhea and shedding:
    • Doxycycline
    • Azithromycin (erythromycin in children)
    • Ciprofloxacin


  • Severe dehydration
  • Renal failure
  • Hypovolemic shock

Non-cholera V. cholerae infections

The following table briefly summarizes the milder form of gastroenteritis caused by non-cholera V. cholerae:

Vibrio parahaemolyticusVibrio mimicusVibrio vulnificus
Distinguishing feature
  • Non-lactose fermenter
  • Does not produce enterotoxin
  • “Mimics” V. cholerae in biochemical tests
  • Can produce cholera-like enterotoxin
  • Lactose fermenter
  • Iron-dependent growth
TransmissionConsumption of undercooked or raw seafoodConsumption of undercooked or raw seafood
  • Gastroenteritis: consumption of undercooked or raw seafood
  • Skin infections: swimming in brackish water, shucking oysters
  • Gastroenteritis (less common)
  • Cellulitis or necrotizing fasciitis (common in patients with liver disease, especially hemochromatosis)
Clinical presentationWatery diarrhea with cramping and abdominal painWatery diarrhea, nausea, abdominal cramping
  • Gastroenteritis: watery diarrhea with cramping and abdominal pain (for gastroenteritis)
  • Skin infection: rapidly spreading, difficult to treat cellulitis that may progress to necrotizing fasciitis and eventually sepsis
  • Gastroenteritis: self-limiting
  • Cellulitis/necrotizing fasciitis: tetracycline or 3rd-generation cephalosporins



  • Yersinia enterocolitica are gram-negative, oxidase-negative coccobacilli.
  • Facultative anaerobes
  • Pleomorphic bacterium that belongs to Enterobacteriaceae
  • Obligate pathogen
  • Distinguishing features:
    • Motile at 25.0°C (77°F), nonmotile at 37.0°C (98.6°F)
    • Cold growth


  • Foodborne (raw or undercooked pork, unpasteurized milk)
  • Blood products
  • Contaminated water
  • Direct or indirect contact with an infected animal (livestock, rabbits, rodents)


  • Adheres to epithelial cells in the ileum → invades the intestinal wall, likely through M cells → colonizes lymphoid tissue (Peyer’s patches)
  • Can invade mesenteric lymph nodes and disseminate
  • Enterotoxin production similar to ETEC
  • Leads to mucosal ulceration in the terminal ileum
  • Iron overload states increase the pathogenicity.

Clinical presentation

  • Incubation period is around 4–6 days; the duration is 1–2 weeks.
  • Inflammatory bloody diarrhea
  • Fever
  • Nausea and vomiting
  • Abdominal pain
  • Pharyngitis (approximately 20%)


  • Generally only requires supportive care
  • Antibiotics may be used based on severity, but there is questionable clinical benefit:
    • Fluoroquinolones 
    • TMP-SMX
    • 3rd-generation cephalosporins


  • Reactive arthritis
  • Erythema nodosum
  • Systemic infection
  • Abdominal (rare): 
    • Mesenteric lymphadenitis (“pseudoappendicitis” with right lower quadrant pain)
    • Mesenteric vein thrombosis (can lead to bowel necrosis)
    • Bowel perforation
    • Toxic megacolon
    • Cholangitis
    • Peritonitis


Clostridium perfringens enterocolitis will be discussed here.


  • Clostridium perfringens type A are gram-positive, anaerobic, spore-forming rods.
  • Distinguishing features:
    • Non-motile
    • Anaerobic: “stormy fermentation” in milk media
    • Double zone of hemolysis on blood agar


  • Foodborne (undercooked or poorly refrigerated meat, reheated meat dishes, legumes)
  • Spores can survive cooking temperatures.
  • Proliferates on foods that are improperly stored


  • Spores germinate under anaerobic conditions.
  • Enterotoxin is produced in the intestines → disrupts ion transport → watery diarrhea, cramps

Clinical presentation

  • Incubation period of 6–24 hours, resolves within 24–48 hours (usually < 24 hours)
  • Severe abdominal cramping
  • Non-inflammatory, watery diarrhea
  • Vomiting and fever are uncommon.


  • Supportive care 
  • Usually a self-limited disease

Other pathologic manifestations

  • Gas gangrene
  • Cellulitis and fasciitis
  • Necrotizing enterocolitis (from type C strains):
    • Beta-toxin produces segmental necrosis of the intestine.
    • Presents with bloody diarrhea, abdominal pain, and vomiting
    • Treatment:
      • Antibiotics (penicillin G, metronidazole)
      • Possible surgery for failure to respond, perforation, or obstruction

Related videos



  • Rotavirus is a non-enveloped, segmented, double-stranded RNA reovirus.
  • The most common cause of severe diarrhea among infants and children worldwide
Rotavirus particles

Transmission electron micrograph of rotavirus particles

Image by CDC/Dr. Erskine Palmer, PD.


  • Fecal-oral route
  • Only a small inoculum is required for transmission.
  • Common during the winter months


  • Penetrates cells of the small intestinal villi → cholera toxin–like protein production → destruction and blunting of the microvilli → disrupts electrolyte and water absorption
  • ↓ disaccharidase activity → malabsorption of lactose and D-xylose → osmotic influx into the intestine 
  • Watery stools develop due to active water secretion and impaired absorption.

Clinical presentation

  • Incubation period is < 48 hours, and the duration is 4–5 days.
  • Fever
  • Malaise
  • Abdominal pain
  • Vomiting
  • Non-inflammatory, non-bloody, watery diarrhea: can be severe and lead to serious dehydration

Management and prevention

  • Disease is self-limited.
  • Oral rehydration
  • IV fluids in patients with severe dehydration
  • Live attenuated vaccine: 
    • Given to all children before 8 months of age 
    • Contraindications:
      • Severe combined immunodeficiency disease (SCID)
      • History of intussusception


  • Seizures
  • Encephalopathy
  • Encephalitis


Pathogen and epidemiology

  • Norovirus (also known as Norwalk virus) is a non‑enveloped RNA calicivirus.
  • Community outbreaks (nursing homes, hospitals, cruise ships, etc.) are common. 
  • Causes the most common type of adult gastroenteritis
Transmission electron microscope image of untreated murine norovirus

Electron microscopy of norovirus

Image: “Norovirus” by Department of Food Science and Technology, Faculty of Marine Science, Tokyo University of Marine Science and Technology, 4 -5-7, Konan, Minato-ku, Tokyo, 108-8477 Japan. License: CC BY 4.0, edited by Lecturio


  • The virus is highly virulent.
  • Fecal-oral route through contaminated food, water, or contaminated surfaces
  • Person‑to‑person contact
  • Aerosolized


  • Mechanism is not entirely understood.
  • Delayed gastric emptying leads to nausea and vomiting.
  • Jejunal biopsy shows blunting of microvilli, but the mucosa is otherwise intact.
  • Cytoplasmic vacuolization is seen along with mononuclear infiltrates of tissue.
  • The virus appears to decrease brush border enzymes, causing malabsorption.
Recombinant porcine norovirus identified from piglet with diarrhea

Hematoxylin and eosin stain:
A: Normal-appearing, long villi of the duodenum
B: Villi of the duodenum showing mild villous atrophy from a norovirus infection
C: Normal-appearing, long villi of the jejunum
D: Villi of the jejunum showing mild villous atrophy from a norovirus infection

Image: “F3” by the Key Laboratory of Veterinary Biotechnology, School of Agriculture and Biology, Shanghai JiaoTong University, 800 Dongchuan Road, Shanghai, People’s Republic of China. License: CC BY 2.0.

Clinical presentation

  • Incubation period is 24–60 hours.
  • Abrupt onset of nausea and vomiting
  • Watery, non-bloody diarrhea
  • Abdominal cramps
  • Headache
  • Myalgias
  • Malaise

Diagnosis and management

  • Diagnosis is usually based on clinical suspicion.
  • Management includes rehydration with oral or IV fluids.


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