Bacterial gastroenteritis Last updated: 

May 25, 2021

QBANK SESSION CLINICAL SCIENCES CLINICIAN LEARNED

Summary

Bacterial gastroenteritis is caused by a variety of organisms,

including Campylobacter, Salmonella, Shigella, Yersinia, Vibrio cholerae, Staphylococcus
aureus, diarrheagenic Escherichia coli, Clostridium difficile, Clostridium perfringens, and
noncholera Vibrio species. Infection may be foodborne, fecal-oral, or involve direct or indirect
animal transmission. Clinical features can be mild, manifesting as abdominal pain and diarrhea,
or severe, including vomiting and watery or inflammatory diarrhea, fever, and hypotension. Stool
analysis may reveal leukocytes or blood in certain cases. Stool cultures may be considered in
severe gastroenteritis. Bacterial gastroenteritisis usually self-limiting and only requires supportive
therapy. However, antibiotics are indicated when supportive therapy does not suffice or
in immunosuppressed patients. Adequate food and water hygiene is crucial for preventing
disease.

NOTES FEEDBACK

Overview

Clinical features
Mild–moderate: abdominal pain, diarrhea
Severe: tachycardia, hypotension, fever, bloody or profuse watery diarrhea, and metabolic
acidosis

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Overview of bacterial gastroenteritis [1]

Pathogen Pathophysiology Associations

Secretory diarrhea

Bacillus cereus Enterotoxin or bacterial Rice, vomiting

invasion shifts water and
electrolyte Recent travel (e.g., Asia, Africa, the Middle East, Mexico, C
ETEC
excretion/absorption and South America) [2]

in proximal small
Clostridium perfringens Undercooked meat and raw legumes
intestine → watery diarrhea

Inadequately refrigerated food

Staphylococcus aureus
Poor hand hygiene among food preparers
 Poor hand hygiene among food preparers
Overview of bacterial gastroenteritis [1]
Vibrio cholerae Profuse secretory diarrhea
Pathogen Pathophysiology Associations
Invasive diarrhea

Milk/pork
Yersinia
Pathogens penetrate May manifest as pseudoappendicitis
the mucosa and invade
the reticuloendothelial Recent travel (e.g., Asia, Africa, Central, and South Americ
Salmonella typhi or systemof the distal small Typically manifests in three
paratyphi intestine→ enteric fever stages: fever with relative bradycardia; rose-colored exa
the lower chest and abdomen; and hepatosplenomegaly

Inflammatory diarrhea

Most common bacterial organism pathogen responsible f

Campylobacter
foodborne gastroenteritis in the US

Undercooked meat; most common association

EHEC
with hemolytic-uremic syndrome (HUS)
Bacteria or cytotoxins
Clostridium difficile damage Recent antibiotic use
the colonic mucosa→ blood
in stool and fever Second most common association
Shigella
with hemolytic-uremic syndrome (HUS)

NoncholeraVibrio species Shellfish

Salmonella(non-typhoidal) Poultry/eggs

Diagnosis: stool analysis [3]
Leukocytes, occult blood, and/or lactoferrin (best initial tests) 
Stool culture (confirmatory test): indicated in suspected invasive bacterial enteritis, severe illness,
or fever (> 38.5 degrees), required hospitalization, or stool tests positive for leukocytes/occult
blood/lactoferrin
Clostridium difficile toxin: if patient has a recent history of antibiotic use
Stool microscopy in certain cases (e.g., ova and parasites)
Endoscopy (colonscopy) showing signs of inflammation (infectious colitis) 
Differential diagnosis: See “Overview of bacterial gastroenteritis“ and “Food poisoning.”
Treatment
Usually self-limiting: supportive therapy (see diarrhea)
Antibiotic therapy is not routinely indicated in bacterial gastroenteritis.
Indications for antibiotic therapy 
Complicated diarrhea with high-grade fever and severe symptoms
High-risk population group (e.g., infants, patients with comorbidities such as sickle cell disease)
Confirmed C. difficile infection  [3]
Contraindicated for EHEC! 
Complications
Dehydration (most common; especially severe in shigellosis, cholera)
Malnutrition
Permanent carrier status (chronic Salmonella carrier)
Prevention
Food and water hygiene
Report diseases according to
the CDC guidelines: salmonellosis, shigellosis, yersiniosis, cholera, shiga toxin-
producing Escherichia coli (EHEC) colitis, non-cholera Vibrio species
infections, vancomycin-resistant Staphylococcus aureus food poisoning [4][5]
Cholera vaccination 
See also the overview of diarrhea and food poisoning.

[1][2][3][4][5][6][7][8][9][10]

NOTES FEEDBACK

Campylobacter enteritis (campylobacteriosis)

Pathogen
Campylobacter jejuni, Campylobacter coli [11]
Curved, gram-negative, oxidase-positive rods with polar flagella 
Optimal growth temperature: 37–42°C [12]
Most common pathogen responsible for foodborne gastroenteritis in the US [13]
Highly contagious: low infective dose required (> 500 pathogens)
Transmission
Fecal-oral
Foodborne (undercooked meat and unpasteurized milk) and contaminated water
Direct contact with infected animals (cats, dogs, pigs) or animal products [11]
Incubation period: 2–4 days
Clinical features
Duration: up to a week
High fever, aches, dizziness
Inflammatory (bloody) diarrhea, especially in children
Severe abdominal pain may present as pseudoappendicitis or colitis
Treatment: (in severe cases) macrolides (e.g., erythromycin or azithromycin) [11]
Complications (more common and severe in HIV-positive patients)
Guillain-Barré syndrome
Reactive arthritis
Acute abdomen: cholecystitis, pancreatitis
Bacteremia
 To remember that Campylobacter jejuni grows best at hot temperatures, think:
“There's no camping without a campfire.”

NOTES FEEDBACK

Salmonellosis (Salmonella gastroenteritis)

Pathogen: Salmonella enterica serotype Enteritidis, Salmonella enterica serotype Typhimurium

Gram-negative bacteria, obligate pathogen
Produces hydrogen sulfide
Does not ferment lactose
2nd most common pathogen responsible for bacterial foodborne gastroenteritis
Transmission: foodborne (poultry, raw eggs, and milk)
Incubation period: 0–3 days
Clinical features
Duration: 3–7 days
Fever (usually resolves within 2 days), chills, headaches, myalgia
Severe vomiting and inflammatory (watery-bloody) diarrhea 
Treatment (antibiotic therapy in severe cases)
Fluoroquinolones (e.g., ciprofloxacin)
Alternative: TMP-SMX or cephalosporins (e.g., ceftriaxone), depending on the antimicrobial
susceptibility test
Antibiotic treatment prolongs fecal excretion of the pathogen; only indicated for systemic
manifestations or diarrhea > 9/day
Complications: (especially in immunocompromised patients, e.g., HIV)
Bacteremia
Reactive arthritis
Systemic disease: osteomyelitis, meningitis, myocarditis
Special variant of salmonella infections: enteric fever (see typhoid fever) 
References:[14][15][16][17][18][19][20][21]

NOTES FEEDBACK

Shigellosis (bacillary dysentery)

Pathogens: Shigella dysenteriae, Shigella flexneri, Shigella sonnei [22]

Gram-negative rods
Produce Shiga toxin (enterotoxin) and endotoxin
Invade M cells via pinocytosis and travel from cell to cell via actin filaments (no hematogenous
spread) 
Transmission
Fecal-oral (especially a concern in areas with poor sanitation)
Oral-anal sexual contact
Foodborne (unpasteurized milk products and raw, unwashed vegetables)
Contaminated water
Incubation period: 0–2 days
Infectivity: highly contagious; very low infective dose required (10 or more bacteria) 
Clinical features
Duration: 2–7 days
High fever
Tenesmus, abdominal cramps
Profuse inflammatory, mucoid-bloody diarrhea
Treatment: in severe cases, antibiotic therapy with fluoroquinolones or 3rd generation
cephalosporins  [23]
Complications
HUS 
Intestinal complications (e.g., toxic megacolon, colonic perforation, intestinal
obstruction, proctitis, rectal prolapse) [23]
Febrile seizures 
Reactive arthritis
Prevention: no vaccine available
[22][23][24][25]

NOTES FEEDBACK

Cholera

Pathogen: Vibrio cholerae
Rare in developed countries
Gram-negative, oxidase positive, curved bacterium with a single
polar flagellum → produces cholera toxin
Cholera toxin stimulates adenylate cyclase via activation of Gs → increased cyclic AMP →
increased ion secretion (mainly chloride)
Transmission
Fecal-oral
Undercooked seafood or contaminated water (e.g., non-segregated drinking water and sewage
systems)
Incubation period: 0–2 days
Infectivity
Acid-labile (grows well in an alkaline medium)  → High infective dose required (over
108pathogens)
Clinical features
Low-grade fever, vomiting
Profuse 'rice-water' stools 
Diagnosis: dipstick (rapid test; initial test)  and stool culture (confirmatory)
Treatment
Urgent fluid replacement 
Antibiotic therapy in severe cases: doxycycline; alternatively, erythromycin in children
Complications
Severe dehydration
Pneumonia may occur in children.
References:[10][16][26][27][28]

NOTES FEEDBACK

Yersiniosis

Pathogen: Yersinia enterocolitica, Yersinia pseudotuberculosis

Gram-negative, rod-shaped, pleomorphic bacterium; obligate pathogen
Transmission
Foodborne (e.g., raw/undercooked pork, unpasteurized milk products)
Contaminated water
Direct/indirect contact with infected animal (e.g., dogs, pigs, rodents, and their feces)
Incubation period: 4–6 days
Clinical features
Duration: 1–46 days
Low-grade fever, vomiting
Inflammatory diarrhea (may be bloody in severe cases)
Pseudoappendicitis → mesenteric lymphadenitis, particularly in the ileum, with typical signs of
appendicitis 
Diagnosis: direct pathogen detection in culture or cold enrichment 
Treatment: in severe cases, antibiotic therapy with fluoroquinolones or 3rd generation
cephalosporins (depends on susceptibility to the drug) 
Complications: particularly in patients with HLA-B27
Reactive arthritis
Erythema nodosum
Acute abdomen: appendicitis, bowel perforation, toxic megacolon, cholangitis
Bacteremia
References:[29][30][31][32][33][34][35]

NOTES FEEDBACK

Clostridium perfringens enterocolitis

Pathogen: Clostridium perfringens
Gram-positive, anaerobic, spore-forming rod-shaped bacterium → produce exotoxins
Also causes gas gangrene
Transmission: foodborne (undercooked or poorly refrigerated meat, legumes)
Incubation period: 6–24 hours
Clinical features
Duration: < 24 hours
Severe abdominal cramping
Watery diarrhea
Diagnosis: toxin detection in stool cultures
Treatment: supportive therapy only
Complications: clostridial necrotizing enteritis
Requires antibiotic therapy: penicillin, metronidazole
Surgery may be required for complicated and/or refractory disease (e.g., perforation)
References:[16][26][36][37][38]

NOTES FEEDBACK

Noncholera Vibrio infection

Pathogen
Vibrio parahaemolyticus  : non-lactose fermenter, gram-negative bacilli
Vibrio vulnificus: lactose fermenter, gram-negative bacilli
Transmission
Foodborne (raw or undercooked shellfish)
Wounds infected by contaminated sea water
Incubation period: 12–52 hours
Clinical features
Inflammatory diarrhea
Low-grade fever, vomiting, abdominal pain
Cellulitis, bullous skin lesions
Treatment: In severe wound infection
Doxycycline or fluoroquinolone (e.g., ciprofloxacin)
Surgical debridement
Complications
Complications of noncholera Vibrio infection are common in patients with high levels of
free iron (e.g., liver disease, hemochromatosis) or immunocompromized state.
Septic shock and necrotizing fasciitis associated with Vibrio vulnificus infection (rare)