Bacterial Gastroenteritis

Updated: Jul 17, 2018
  • Author: Jennifer Lynn Bonheur, MD; Chief Editor: BS Anand, MD  more...
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Practice Essentials

Bacterial gastroenteritis has many causes, can range from mild to severe, and typically manifests with symptoms of vomiting, diarrhea, and abdominal discomfort. It is usually self-limited, but improper management of an acute infection can lead to a protracted course.

Signs and symptoms

An index of suspicion can be generated for a specific set of potential causative pathogens by considering the following stool characteristics:

  • Appearance

  • Volume

  • Frequency

  • Presence or absence of blood

  • pH

  • Presence or absence of reducing substances

  • White blood cell (WBC) count

  • Serum WBC count

Diarrhea is defined as daily stools with a mass greater than 15 g/kg for children younger than 2 years and greater than 200 g for children 2 years or older. Adult stool patterns vary from 1 stool every 3 days to 3 stools per day; therefore, consider individual stool patterns.

Systemic features that can guide empiric therapy and help narrow the differential diagnosis of the causative organism include the following:

  • Onset and duration of symptoms

  • Presence or absence of vomiting

  • Presence or absence of fever

  • Presence or absence of abdominal pain

Specific bacterial pathogens may be associated with the following:

  • Ingestion of particular foods

  • Exposure to water

  • Exposure to animals

  • Travel to particular countries

  • Preexisting conditions

Physical findings may include the following:

  • Dehydration (primary cause of morbidity and mortality)

  • Malnutrition (typically a sign of a chronic process)

  • Abdominal pain

  • Borborygmi

  • Perianal erythema

See Clinical Presentation for more details.


Diagnostic approaches may include the following assessments:

  • Stool pH

  • Presence of reducing substances in stool

  • Fecal leukocytes

  • Antilisteriolysin O (ALLO)

  • Identification of pseudomembranes in the colon by direct visualization (diagnostic for C difficile)

  • Stool culture

A high index of suspicion is needed to choose the appropriate culture medium. Media used to isolate bacteria responsible for gastroenteritis include the following:

  • Blood agar: All aerobic bacteria and yeast; detects cytochrome oxidase production

  • MacConkey EMB agar: Inhibits gram-positive organisms; permits lactose fermentation

  • XLD agar and HE agar: Inhibit gram-positive organisms and nonpathogenic gram-negative bacilli; permit lactose fermentation and H2S production

  • Skirrow agar: Selective for Campylobacter species

  • SM agar: Selective for enterohemorrhagic E coli

  • CIN agar: Selective for Yersinia enterocolitica

  • Thiosulfate-citrate-bile-sucrose (TCBS) agar: Selective for Vibrio species

  • CCFE agar: Selective for C difficile

See Workup for more detail.


Because most infectious diarrheas are self-limited, medical care is primarily supportive and may include the following:

  • Oral rehydration: Live Lactobacillus GG and heat-killed Lactobacillus LB reduce the duration of diarrhea in children when added to oral rehydration solution [1, 2]

  • When oral rehydration is unsuccessful, intravenous (IV) rehydration should be provided

  • Close monitoring for secondary complications

  • For some bacterial gastroenteritis infections, antimicrobial therapy is required

  • For refractory cases of Cryptosporidium infection, antimotility agents are useful

Standard antimicrobial therapies for bacterial gastroenteritis include the following:

  • Aeromonas species: Cefixime and most third- and fourth-generation cephalosporins

  • Bacillus species: None necessary for self-limited gastroenteritis; vancomycin and clindamycin for severe disease

  • Campylobacter species: Erythromycin; therapy started more than 4 days after onset of symptoms appears to produce no clinical benefit

  • C difficile: Discontinuance of the potential causative antibiotics; if this is impossible or ineffective, oral metronidazole or (in seriously ill patients who do not respond to metronidazole) vancomycin

  • Clostridium perfringens: None

  • Listeria species: None necessary unless invasive disease occurs; ampicillin and trimethoprim-sulfamethoxazole (TMP-SMX) for invasive disease

  • Plesiomonas species: TMP-SMX or any cephalosporin

  • Vibrio cholerae: Tetracycline; in resistant cases, TMP-SMX, erythromycin, doxycycline, chloramphenicol, or furazolidone

  • Yersinia species: TMP-SMX, fluoroquinolones, or aminoglycosides; reserved for complicated cases

  • E coli: TMP-SMX if diarrhea is moderate or severe; for systemic complications, a parenteral second-generation or third-generation cephalosporin

  • Salmonella species: None necessary for nontyphoid, uncomplicated diarrhea but may be considered for infants younger than 3 months and for high-risk patients (eg, those who are immunocompromised or have sickle cell disease); for drug-sensitive strains, ampicillin or, alternatively, TMP-SMX, fluoroquinolones, or third-generation cephalosporins

  • Shigella species: None necessary for most mild infections; for moderate-to-severe cases, ampicillin for drug-sensitive strains and TMP-SMX for ampicillin-resistant strains or in cases of penicillin allergy; fluoroquinolones may be considered in patients with highly resistant organisms

Dietary measures include the following:

  • Begin with the BRAT diet (ie, bananas, rice, applesauce, toast)

  • Introduce lean meats and clear fluids as soon as possible [3]

  • When giving lactose-containing dairy products, be alert for signs of malabsorption

  • For infants, continue breastfeeding throughout the illness

See Treatment and Medication for more detail.



Bacterial gastroenteritis is a very common disorder. It has many causes, can range from mild to severe, and usually manifests with symptoms of vomiting, diarrhea, and abdominal discomfort. Other causes of some of these symptoms include viral infections, improper diet, malabsorption syndromes, various enteropathies, and inflammatory bowel disease. (See Etiology,Presentation, Workup, and Treatment.)

Bacterial gastroenteritis is usually self-limited, but improper management of an acute infection can lead to a protracted course. By far, the most common complication is dehydration. (See Prognosis and Presentation.) [4, 5, 6, 7]



Salmonella, Shigella, and Campylobacter species are the top three leading causes of bacterial diarrhea worldwide, followed closely by Aeromonas species.

Aeromonas and Shigella infection have a higher incidence in summer and fall, and Campylobacter infection usually occurs in summer months. Yersinia infection occurs most frequently in winter months and in colder climates.

Bacteria employ several mechanisms to invoke a pathologic response. Invasive bacteria cause mucosal ulceration and abscess formation with a subsequent inflammatory cascade. Bacterial toxins control enteral and extraenteral cellular processes. For example, the heat-labile and heat-stable enterotoxins of Escherichia coli activate enteral adenylate cyclase and guanylate cyclase signaling systems.

Verotoxin, which enterohemorrhagic E coli and Shigella species produce, causes systemic disorders such as seizures and hemolytic-uremic syndrome (HUS). Other noninvasive bacteria adhere to the gut wall, causing inflammation.

Organisms such as E coli and Clostridium species are normal enteric flora, pathogenic strains of which can cause gastroenteritis.

Vibrio parahaemolyticus, a seafood-transmitted bacterium, appears to be an emerging foodborne pathogen in North America, with over 45,000 cases every year in the United States alone. [8]  The rise in incidence may be attributed in part to the climate change effects on the quantity and distribution of this pathogen. A new lineage of V parahaemolyticus has been identified (sequence type 631) that may rapidly become the predominant type endemic to the Atlantic coast of North America. [8]

Risk factors

Studies have suggested that the use of acid-suppressing medications (proton pump inhibitors [PPIs], although not H2 receptor antagonists [H2RAs]) may increase the risk of developing gastroenteritis by reducing the acidic environment that serves as an initial defense mechanism against gastrointestinal infections. This effect has also been noted to be dose dependent (ie, an increased dose of PPI therapy is associated with an increased risk of infection). PPI use has also been associated with a higher risk of gastroenteritis hospitalization. [49]

PPI therapy has also been suggested to be an independent risk factor for the development and recurrence of C difficilecolitis [9]  as well as increases the risk Campylobacter gastroenteritis. [10]



Occurrence in the United States

Bacterial gastroenteritis is a very common problem in primary care and emergency department settings, especially in children younger than 5 years. [6, 7] Diarrhea accounts for as many as 5% of pediatric office visits and 10% of hospitalizations in this age group.

Very often, gastroenteritis is underreported in the adult population. Each year, gastroenteritis in adults accounts for 8 million doctor visits and 250,000 hospitalizations. Episodes of gastroenteritis do not occur at random but usually take place in outbreaks. Traveler's diarrhea affects 20-50% of people traveling from industrialized to developing countries. [7, 11, 12]

From 2000 to 2009, the number of hospitalized patients with any Clostridium difficile infection (CDI) discharge diagnoses more than doubled, from approximately 139,000 to 336,600, and the number with a primary CDI diagnosis more than tripled, from 33,000 to 111,000. [13]

Among CDIs identified in the Center for Disease Control and Prevention’s (CDC’s) Emerging Infections Program data in 2010, 94% were associated with receiving health care; of these, 75% had onset among persons not currently hospitalized, including recently discharged patients, outpatients, and nursing home residents. [13]

International occurrence

Worldwide, millions of children and adults are affected by diarrhea each year. In developing countries, where sanitation is suboptimal, epidemics of bacterial gastroenteritis can develop and cause significant mortality. [5, 7, 11, 12, 14]

In a retrospective Australian study (2001-2013), investigators analyzing bacterial toxin-mediated foodborne outbreaks found that Clostridium perfringens was the most common cause (76%), and that the most common settings were commercial preparation food services (48%) and elderly care facilities (39%). [15] The main contributing factor across all outbreaks was inadequate temperature control of the food.

Race-, sex-, and age-related demographics

Most infectious diarrheas do not affect one sex more than the other. [39]  Aeromonas species are a significant cause of bacterial gastroenteritis in young children. Very young children are particularly susceptible to secondary dehydration and malabsorption. Yersinia species infect children younger than 1 year almost exclusively, though it has been reported that the preparation and ingestion of chitterlings (the small intestine of pigs) may pose an increased risk of infection with Yersinia enterocolitica serotype O:3. [16, 17]



With proper management, the prognosis for bacterial gastroenteritis is very good, especially in industrialized countries. Mortality predominantly is due to dehydration and secondary malnutrition from a protracted course. Treat severe dehydration with parenteral fluids.

Once malnutrition from secondary malabsorption begins, prognosis becomes grim unless the patient is hospitalized and supplemental parenteral nutrition is started. Neonates and young infants are at particular risk for dehydration, malnutrition, and malabsorption syndromes.

Even though the mortality rate from bacterial gastroenteritis is low in industrialized countries, people can, and do, die from complications. Prognosis in countries without modern medical care or for patients with serious preexisting medical conditions is more guarded.

Morbidity and mortality

Diarrhea and vomiting are so commonplace that nonphysicians usually underappreciate the potential mortality and morbidity of bacterial gastroenteritis. In the United States each year, several hundred people die from complications of bacterial gastroenteritis; the majority are elderly persons.

The CDC reported that enteritis deaths more than doubled in the United States between 1999 and 2007, from about 7,000 to 17,000. Adults older than 65 years accounted for 83% of deaths. C difficile was the most common bacterial infectious cause of gastroenteritis-associated deaths, being tied to 14,500 of them (up from 2700 in 1999). [18]

Gastroenteritis-causing pathogens are the second leading cause of morbidity and mortality worldwide. Many developing countries do not have the resources to properly treat diarrhea and vomiting associated with bacterial gastroenteritis, leading to a disproportionately high mortality rate.


Common complications that can occur with various organisms in cases of bacterial gastroenteritis are as follows:

  • Aeromonas caviae - Intussusception, gram-negative sepsis, and hemolytic uremic syndrome (HUS)

  • Bacillus species - Fulminant liver failure (very rare) and rhabdomyolysis (very rare)

  • Campylobacter species - Bacteremia, meningitis, cholecystitis, urinary tract infection, pancreatitis, and Reiter syndrome

  • C difficile - Chronic diarrhea, toxic megacolon, and ileus

  • C perfringens serotype C - Enteritis necroticans

  • Enterohemorrhagic E coli - Hemorrhagic colitis

  • Enterohemorrhagic E coli O157:H7 - HUS

  • Listeria species - Bacteremia and meningitis

  • Plesiomonas species - Septicemia

  • Salmonella species - Enteric fever, bacteremia, meningitis, osteomyelitis, myocarditis, and Reiter syndrome

  • Shigella species - Seizures, HUS, bowel perforation, and Reiter syndrome

  • Vibrio species - Rapid dehydration

  • Yersinia enterocolitica - Appendicitis, bowel perforation, intussusception, peritonitis, toxic megacolon, cholangitis, bacteremia, and Reiter syndrome

Enteric fever

S typhi causes enteric fever. This syndrome has an insidious onset of malaise, fever, abdominal pain, and bradycardia. Diarrhea and rash (rose spots) appear after 1 week of symptoms. Bacteria may have disseminated at that time, and treatment is required to prevent systemic complications such as hepatitis, myocarditis, cholecystitis, and gastrointestinal bleeding.


Damage to the vascular endothelial cells by verotoxin causes HUS. Thrombocytopenia, microangiopathic hemolytic anemia, and acute renal failure are characteristic of HUS. Symptoms usually develop 1 week after the onset of diarrhea, when organisms may be absent.

Reiter syndrome

Reiter syndrome can complicate acute infections. Arthritis, urethritis, conjunctivitis, and mucocutaneous lesions are characteristic. Affected individuals usually do not demonstrate all the features.


Dehydration is the most common complication from gastroenteritis in the United States. Continuing fluid losses without compensatory intake can result in severe dehydration. Hyponatremic seizures can be avoided by rehydrating with oral rehydration solution instead of free water.

Inflammatory bowel disease

A study suggested that infectious gastroenteritis may play a role in the initiation and/or exacerbation of inflammatory bowel disease. [19] Similarly, irritable bowel syndrome may develop more often following bacterial gastroenteritis. This topic is highly controversial, and no conclusive evidence currently exists to support or refute this hypothesis.

Carrier states

Carrier states are observed after some bacterial gastroenteritis infections. After Salmonella diarrhea, 1-4% of individuals with nontyphoid and enteric fever infections become carriers. The carrier stage for Salmonella species is more likely to develop in females, infants, and individuals with biliary tract disease. Asymptomatic C difficile carriage may be seen in many hospitalized patients receiving antibiotics and in 50% of infants.


Patient Education

Education is most important for the prevention and treatment of bacterial gastroenteritis. Proper oral rehydration therapy helps to prevent dehydration and hastens recovery of the intestinal mucosa.

Diet restrictions that prevent secondary malabsorption are extremely important; relapse typically occurs due to dietary noncompliance.

Emphasize proper hygiene and food preparation practices to caretakers in order to prevent future infections and spread of bacterial gastroenteritis.

For patient education information, see Gastroenteritis (Stomach Flu) and Foreign Travel.