Overview
Epidemiology
- 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
Etiology
- 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
Pathogenesis
- 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 diarrhea | Non-inflammatory (adhesion, enterotoxin) | Inflammatory (invasion, cytotoxin) | Penetrating (invades lymphatics) |
---|---|---|---|
Presentation | Watery diarrhea | Dysentery (blood or mucus) or inflammatory diarrhea | Enteric fever |
Stool findings |
|
| Fecal mononuclear leukocytes |
Pathogen involved |
|
|
|
Clinical presentation
- Common symptoms:
- Abdominal pain and cramps
- Diarrhea (watery, mucoid, or bloody)
- Vomiting
- Fever
- Anorexia
- Headache
- Myalgia
- Evidence of severe dehydration:
- Tachycardia
- Hypotension
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
Organism | Characteristic features |
---|---|
Bacillus cereus |
|
Staphylococcus aureus |
|
Clostridioides difficile |
|
Salmonella |
|
Vibrio vulnificus |
|
Clostridium perfringens |
|
Escherichia coli |
|
Shigella |
|
Campylobacter species |
|
| Chronic watery diarrhea in immunosuppressed patients |
Giardia |
|
Rotavirus and norovirus |
|
Diagnosis
- 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:
Management
- 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
Complications
- During the infection:
- Hypovolemic shock
- Severe dehydration
- Acute kidney injury
- Metabolic acidosis
- Electrolyte imbalances
- Death
- Post-diarrheal complications are summarized in the table below:
Complication | Description | Organism responsible |
---|---|---|
Chronic diarrhea (lasting more than 2 weeks) |
| Can occur with any type of acute diarrhea, especially protozoal |
Initial presentation or exacerbation of inflammatory bowel disease | Due to triggering of the inflammatory response | Can occur with any type of acute diarrhea, especially C. difficile |
Reactive arthritis |
|
|
HUS |
| Follows infection with Shiga toxin-producing bacteria (Shigella and enterohemorrhagic E. coli) |
Guillain-Barré syndrome | Acute immune-mediated polyneuropathies | Campylobacter |
Campylobacter
Pathogen
- 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
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.Transmission
- Fecal-oral
- Foodborne (undercooked poultry and unpasteurized milk) and contaminated water
- Direct contact with infected animals (cats, dogs, pigs) or animal products
Pathogenesis
- 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
Management
- Most cases will have a spontaneous resolution.
- Macrolides and fluoroquinolones
- A 3rd-generation cephalosporin, imipenem, ampicillin, or gentamicin can be given for extraintestinal infections.
Complications
- 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
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Non-typhoidal Salmonella
Pathogen
- 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
Transmission
- 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
Pathogenesis
- 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
Management
- 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)
Complications
- Bacteremia
- Reactive arthritis
- Osteomyelitis (particularly in sickle cell patients)
- Meningitis
- Myocarditis, endocarditis
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Shigella
Shigella causes bacilliary dysentery, also known as shigellosis.
Pathogen
- S. dysenteriae, S. flexneri, S. sonnei, and S. boydii are gram-negative rods.
- Gastric acid resistant
- S. dysenteriae type 1 produces Shiga toxin (enterotoxin).
Transmission
- Fecal-oral
- Humans are the only natural reservoir.
- Flies are vectors.
- Foodborne (unpasteurized milk products and raw, unwashed vegetables)
- Contaminated water
- Highly contagious
Pathogenesis
- 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
Antibiotics
- 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.
Complications
- 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.
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Vibrio cholerae
Cholera is a severe form of gastroenteritis caused by Vibrio cholerae (V. cholerae).
Pathogen
- 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
Transmission
- 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
Pathogenesis
- 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.
Management
- 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
Complications
- 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 parahaemolyticus | Vibrio mimicus | Vibrio vulnificus | |
---|---|---|---|
Distinguishing feature |
|
|
|
Transmission | Consumption of undercooked or raw seafood | Consumption of undercooked or raw seafood |
|
Disease | Gastroenteritis | Gastroenteritis |
|
Clinical presentation | Watery diarrhea with cramping and abdominal pain | Watery diarrhea, nausea, abdominal cramping |
|
Management | Self-limiting | Self-limiting |
|
Yersinia
Pathogen
- 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
Transmission
- Foodborne (raw or undercooked pork, unpasteurized milk)
- Blood products
- Contaminated water
- Direct or indirect contact with an infected animal (livestock, rabbits, rodents)
Pathogenesis
- 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%)
Management
- Generally only requires supportive care
- Antibiotics may be used based on severity, but there is questionable clinical benefit:
- Fluoroquinolones
- TMP-SMX
- 3rd-generation cephalosporins
Complications
- 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
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Clostridium
Clostridium perfringens enterocolitis will be discussed here.
Pathogen
- 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
Transmission
- Foodborne (undercooked or poorly refrigerated meat, reheated meat dishes, legumes)
- Spores can survive cooking temperatures.
- Proliferates on foods that are improperly stored
Pathogenesis
- 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.
Management
- 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
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Rotavirus
Pathogen
- Rotavirus is a non-enveloped, segmented, double-stranded RNA reovirus.
- The most common cause of severe diarrhea among infants and children worldwide
Transmission
- Fecal-oral route
- Only a small inoculum is required for transmission.
- Common during the winter months
Pathophysiology
- 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
Complications
- Seizures
- Encephalopathy
- Encephalitis
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Norovirus
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
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 LecturioTransmission
- The virus is highly virulent.
- Fecal-oral route through contaminated food, water, or contaminated surfaces
- Person‑to‑person contact
- Aerosolized
Pathogenesis
- 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.
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
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.
References
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