Bacterial Gastroenteritis


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:

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:

Specific bacterial pathogens may be associated with the following:

Physical findings may include the following:

See Clinical Presentation for more details.


Diagnostic approaches may include the following assessments:

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

See Workup for more detail.


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

Standard antimicrobial therapies for bacterial gastroenteritis include the following:

Dietary measures include the following:

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:

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.


Stool characteristics

Diarrhea is defined as daily stools with a mass greater than 15g/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.

Consistency, color, volume, and frequency are very important in determining whether the stool source is from the small or large bowel. Table 1, below, outlines these characteristics and demonstrates that an index of suspicion can be generated easily for a specific set of organisms.

Table 1. Stool Characteristics and Sources

View Table

See Table

Systemic symptoms

Associated systemic symptoms can guide empiric therapy. Some enteric infections have characteristic systemic symptoms, whereas the associated systemic features of others do not occur reliably. Table 2, below, outlines the frequency of these symptoms with various organisms.

The characteristics of symptom onset and symptom duration can narrow the differential diagnosis of the organism. The onset of symptoms within 6 hours of exposure to the bacterial source indicates a preformed toxin, probably produced by a species of Staphylococcus or Bacillus. Table 2 outlines the incubation periods and duration of common bacteria.

Table 2. Symptoms and Their Characteristics

View Table

See Table

Food-borne bacteria

Particular foods are associated with certain bacterial infections. Ingestion of raw or contaminated food, particularly raw milk and meat, is a common cause of bacterial gastroenteritis. The following list outlines organisms that cause food poisoning:

A study by Calbo et al reported a foodborne nosocomial outbreak due to extended-spectrum β-lactamase (ESBL)–producing Klebsiella pneumoniae.[20] This may be the first reported hospital outbreak that provides evidence that food can be a transmission vector for ESBL K pneumoniae.

Water-borne bacteria

Water is a major reservoir for many organisms that cause diarrhea. Swimming pools have been associated with outbreaks of Shigella organisms, and Aeromonas species are associated with exposure to the marine environment.

Animal-borne bacteria

Animals can transmit particular bacteria. Exposure to young dogs or cats is associated with Campylobacter transmission. Exposure to turtles is associated with Salmonella transmission.

Travel-associated infections

Travel history is an important and a useful clue in determining bacterial etiology. Enterotoxigenic E coli is the leading cause of traveler's diarrhea. RotavirusShigella, Salmonella, and Campylobacter species are prevalent worldwide and need to be considered, regardless of specific travel history.

The risk of contracting diarrhea while traveling is the highest in Africa. Travel to Portugal, Spain, and Eastern European countries is also associated with a relatively high risk. Organisms associated with travel to particular locations are as follows:

Bacteria associated with preexisting conditions

Preexisting medical conditions can predispose patients to infections with particular organisms. The following list outlines such medical conditions and their associated organisms:


Outbreaks are caused by particular bacteria, including enterohemorrhagic E coli O157:H7, Listeria monocytogenes, C perfringens, and Salmonella species.

Physical Examination

Dehydration is the primary cause of morbidity and mortality in cases of gastroenteritis. Assess every patient for signs, symptoms, and severity of dehydration. Lethargy, depressed consciousness, dry mucous membranes, sunken eyes, poor skin turgor, and delayed capillary refill should raise the suspicion for dehydration.

Malnutrition is typically a sign of a chronic process. Reduced muscle and fat mass is found. This is usually due to the development of secondary carbohydrate intolerance.

Abdominal pain is a common symptom in gastroenteritis. Nonspecific, nonfocal abdominal pain and cramping are common with some organisms. This pain usually does not increase with palpation. Focal abdominal pain worsened by palpation, rebound tenderness, or guarding should alert the clinician to possible complications or to another noninfectious gastrointestinal diagnosis.

Borborygmi, defined as a significant increase in peristaltic activity with small bowel diarrhea, can cause an audible and/or palpable increase in bowel activity.

Perianal erythema results from the passage of many stools causing a constantly wet area. Failure to properly dry the buttocks and perianal area results in erythema and skin breakdown.

Approach Considerations

A stool pH of 5.5 or below or the presence of reducing substances indicates carbohydrate intolerance. This is usually transient in nature.

Enteroinvasive infections of the large bowel cause leukocytes, predominantly neutrophils, to accumulate in the lumen which are then shed into stool. The absence of fecal leukocytes does not eliminate the possibility of enteroinvasive organisms; however, the presence of fecal leukocytes eliminates consideration of enterotoxigenic E coli, Vibrio species, and viruses. Shigella characteristically causes marked bandemia with variable total white blood cell (WBC) count.

Examine any exudate found in the stool for leukocytes. Such exudates are highly suggestive of inflammatory bowel disease, which could be infectious or of another origin.

Antilisteriolysin O (ALLO) is positive during the convalescent phase of bacterial gastroenteritis and when invasive disease has occurred.

Commercially available multiplex molecular panels may be more sensitive and provide more rapid results (< 3 hours) than stool cultures, which are labor intensive and whose results may take longer than 1 day (66.5 hours).[21, 44]


Identification of pseudomembranes in the colon by direct visualization is diagnostic for C difficile; however, the yield may be low.

Bacterial Cultures

Identifying the causative agent underlying the gastroenteritis is important in the management of patients with severe or prolonged diarrhea, symptoms consistent with invasive disease, or a history that may predict a complicated disease course.[22] Moreover, stool culture findings are a means for public health officials to identify and track outbreaks of bacterial gastroenteritis.

Table 3, below, lists common bacteria and the optimal culture media for their growth.

Table 3. Common Bacteria and Optimum Culture Media

View Table

See Table

The following is a list of the different culture media used to isolate bacteria. A high index of suspicion is needed to choose the appropriate medium.

Stool cultures are useful when positive, but the yield is usually low. Refrigerate stool that is not cultured at 4°C within 2 hours of collection, or place it in a transport medium. Always culture stool for Campylobacter, Salmonella, and Shigella species, especially if stool leukocytes or gross blood is found in the stool.

Serotype Salmonella for S typhimurium DT104, particularly if the gastroenteritis is associated with raw milk or cheese ingestion. S typhimurium DT104 is a multidrug-resistant organism, and antibiotic sensitivities are crucial to guide therapy.[23, 24]  

Preformed toxin from Bacillus or Staphylococcus species may cause rapid-onset gastroenteritis. In such cases, the bacteria may not exist in the gastrointestinal tract; therefore, culture the food ingested by the person.

Bloody diarrhea with a history of ground beef ingestion should raise the suspicion for enterohemorrhagic E coli. If E coli is found in the stool, type it to determine if it is O157:H7. Report cases of E coli O157:E7 gastroenteritis (and other infectious problems) to the state health department. Shiga toxin-producing Escherichia coli (STEC) O103:H2 has also been detected in raw cow milk and dairy farm cattle.[43]

History of raw seafood ingestion or foreign travel should prompt additional screening for Vibrio and Plesiomonas species.

Approach Considerations

Because most infectious diarrhea is self-limited, medical care is primarily supportive in nature. Oral rehydration therapy is the cornerstone of diarrhea treatment, especially for small bowel infections that produce a large volume of watery stool output. Studies confirm that early refeeding hastens recovery. Many commercial oral rehydration formulas are available and have been designed to promote optimal absorption of nutrients.

Young infants and neonates are at a high risk for secondary complications and require close monitoring, as do older individuals.

Consider intravenous rehydration when oral rehydration is unsuccessful. Particular attention must be paid to repletion of potassium as needed.

Administer maintenance fluids plus replacement of losses to ill children. Administer small amounts of fluid at frequent intervals in order to minimize discomfort and vomiting. A 5 or 10cc syringe without a needle is a very useful tool. The syringe can be used to place small amounts of fluid in the mouth quickly. Once the patient becomes better hydrated, cooperation improves enough for the patient to take small sips from a cup. This method is time intensive and requires dedication. Encouragement from the physician is necessary to promote compliance.

Live Lactobacillus GG and heat-killed Lactobacillus LB reduce the duration of diarrhea in children when they are added to oral rehydration solution.[1, 2]  A systematic review and meta-analysis of 31 randomized-controlled trials comprising 8672 children and adults suggests with moderate certainty that probiotics are effective for preventing C difficile-associated diarrhea and that short-term use of probiotics in conjunction with antibiotics appears to be safe in those who are immunocompetent and those who aren't severely debilitated.[45] Adverse effects appeared in 32 trials assessed, but they were more common in the control groups.

Antimicrobial therapy is indicated for some bacterial gastroenteritis infections. However, many conditions are self-limited and do not require therapy.

Antimotility agents are not indicated routinely for infectious diarrhea (except for refractory cases of Cryptosporidium infection).

Inpatient care

Admit neonates or young infants with moderate dehydration, suspected infection with enterohemorrhagic E coli, or bloody diarrhea.

Oral rehydration in cases of gastroenteritis is a time-consuming task that requires vigilance. Evaluate the caretaker of a child who requires oral rehydration for compliance. Consider admission if any doubt exists regarding potential compliance.

Older patients, often with other illnesses, require careful observation and consideration for admission.


Certain organisms cause abdominal pain and bloody stools. Symptoms resembling appendicitis, hemorrhagic colitis, intussusception, or toxic megacolon may be observed. In such cases, obtain a consultation with a surgeon.

Consider consultation with an infectious disease specialist, especially for any patient who is immunocompromised due to human immunodeficiency virus (HIV) infection, chemotherapy, or immunosuppressive drugs, because atypical organisms are more likely and complications can be more serious and can fulminate.


Although some claim that changes in dietary regimen are not necessary, improper diet can result in prolonged recovery or development of carbohydrate malabsorption, especially if the acute episode is overshadowed by an undiagnosed chronic bacterial or malabsorption syndrome.

Thus, a prolonged course of diarrhea should prompt investigation of complicating factors. Results from tests such as stool acidity and reducing substances can indicate carbohydrate malabsorption. Failure to recognize this complication can result in significant rapid weight loss with wasting of fat and muscle mass.

Dietary considerations

The BRAT diet (ie, bananas, rice, applesauce, toast) has been recommended for years in cases of gastroenteritis. This diet is adequate during early convalescence, but, as the patient tolerates solid food, advance the diet to provide adequate protein and caloric intake.[3, 25, 26]

Introduce lean meats and clear fluids as soon as possible.[3] Dairy products are said to be better absorbed when given with proteins or complex carbohydrates.

When feeding lactose-containing dairy products, carefully monitor the patient for signs of malabsorption.

Breast milk contains many substances that promote bowel growth and antagonize bacteria; thus, continue breastfeeding throughout the illness for infants.


Follow-up care in cases of bacterial gastroenteritis depends on the severity of the infection and the age of the patient. Uncomplicated diarrhea may not require follow-up if the patient or caretaker is reliable and has adequate access to medical care if needed.

Monitor young children, elderly patients, and debilitated individuals closely to ensure that complications do not occur. Monitor patients requiring labor-intensive oral rehydration to ensure that the proper diet has been reintroduced.

Neonates require strict follow-up care within a few days of the illness to ensure that malabsorption and dehydration do not occur.

Deterrence and Prevention

Avoidance of undercooked meats and seafood, as well as contaminated water supplies, when traveling may help to reduce the risk of transmission of food and water-borne infectious causes of gastroenteritis and associated symptoms.


Salmonella typhi vaccine is recommended for travelers to countries with a high incidence of this infection, persons with intimate exposure to a documented typhoid fever carrier, and workers with frequent exposure to these bacteria. Live attenuated, killed whole-cell, and capsular polysaccharide vaccines are available.

Vibrio vaccine is available but only protects 50% of immunized persons for 3-6 months. It is not indicated for widespread use.

In February 2006, the US Food and Drug Administration (FDA) approved an oral vaccine for rotavirus (RotaTeq) for use in infants. On Feb 21, 2006, the American Academy of Pediatrics (AAP) and the Advisory Committee on Immunization Practices (ACIP) recommended that RotaTeq be part of regularly scheduled childhood immunizations. The vaccine is administered in a 3-dose series starting between ages 6 and 12 weeks and ending before age 32 weeks.

Clinical trials of RotaTeq demonstrated prevention of 74% of all rotavirus gastroenteritis cases, of nearly all severe rotavirus gastroenteritis cases, and of nearly all hospitalizations. A previously marketed rotavirus vaccine (RotaShield) was associated with intussusception, but RotaTeq did not show an increased risk compared with placebo in clinical trials.

In April 2008, the FDA approved Rotarix, another oral vaccine, for prevention of rotavirus gastroenteritis. It is currently recommended that Rotarix be administered in 2 separate doses to patients between ages 6 and 24 weeks. Rotarix was efficacious in a large study, which showed that it protected patients with severe rotavirus gastroenteritis and also decreased the rate of severe diarrhea or gastroenteritis from any cause.[27]

Medication Summary

The goals of pharmacotherapy in cases of gastroenteritis are to reduce morbidity and to prevent complications. The following is a list of standard antimicrobial therapies for bacterial gastroenteritis (although, as previously stated, many conditions are self-limited and require no therapy):

* Note that fluoroquinolone resistance in Salmonella is increasingly being reported worldwide, with several molecular mechanisms described.[40]

Antibiotic treatment appears to increase the likelihood of developing HUS. Consider antibiotics if diarrhea is moderate or severe. Trimethoprim-sulfamethoxazole is a first-line drug, but a parenteral second-generation or third-generation cephalosporin for systemic complications should be used.

Antibiotic treatment prolongs the carrier state and is associated with relapse; thus, treatment is not indicated for nontyphoid, uncomplicated diarrhea. Consider treatment for infants younger than 3 months and for high-risk patients, such as patients who are immunocompromised or who have sickle cell disease.

Ampicillin is recommended for drug-sensitive strains. Trimethoprim-sulfamethoxazole, fluoroquinolones,* or third-generation cephalosporins (fluoroquinolones are not recommended for use in children) are also acceptable alternatives. S typhimurium T104 is a multidrug-resistant organism. Sensitivities from the cultured specimens are important to guide therapy.

In July 2018, the FDA ordered ordered label changes for fluoroquinolones to strengthen warnings about the antibiotics' risks for mental health side effects and serious blood sugar disturbances.[41, 42]

Shigella species

Antibiotic treatment may shorten illness duration and shedding but does not prevent complications. Most mild infections will recover without antibiotics. Moderate to severe cases should be treated with antibiotics. Ampicillin is preferred for drug-sensitive strains. For ampicillin-resistant strains or in cases of penicillin allergy, trimethoprim-sulfamethoxazole is the drug of choice, although resistance does occur. Fluoroquinolones* may be considered in patients with highly resistant organisms.

Cefixime (Suprax)

Clinical Context:  Cefixime is a potent, long-acting oral cephalosporin with increased gram-negative coverage. It arrests bacterial growth by binding to 1 or more penicillin-binding proteins.

Ceftriaxone (Rocephin)

Clinical Context:  Ceftriaxone is a third-generation parenteral antibiotic with wide coverage, including of gram-negative bacilli. It arrests bacterial growth by binding to 1 or more penicillin-binding proteins.

Cefotaxime (Claforan)

Clinical Context:  Cefotaxime is a third-generation parenteral antibiotic with wide coverage, including of gram-negative bacilli. It arrests bacterial cell wall synthesis, which, in turn, inhibits bacterial growth.

Erythromycin (E.E.S., EryPed, Erythrocin, Ery-Tab)

Clinical Context:  Erythromycin is an old bacteriostatic macrolide with activity against most gram-positive organisms and atypical respiratory organisms. It is useful for Campylobacter and Vibrio enteritis. Nausea is a common adverse effect and may be tolerated poorly by some patients. Enteric-coated tablets are associated with less nausea.

Trimethoprim-sulfamethoxazole (Bactrim, Bactrim DS, Septra DS)

Clinical Context:  This is a folate synthesis blocker that has wide antibiotic coverage.

Vancomycin (Vancocin)

Clinical Context:  Vancomycin therapy is a powerful treatment for antibiotic-associated colitis. Vancomycin is indicated for patients who cannot receive or whose condition has not responded to penicillins and cephalosporins or who are infected with resistant staphylococci.

To avoid toxicity, the current recommendation is to assay trough levels after the third dose drawn 0.5 hour before the next dosing. Use creatinine clearance to adjust the dose in patients diagnosed with renal impairment.

Vancomycin is used in conjunction with gentamicin for prophylaxis in patients allergic to penicillin who are undergoing a gastrointestinal or genitourinary procedure.

Rifaximin (Xifaxan)

Clinical Context:  Rifaximin is a nonabsorbed (< 0.4%), broad-spectrum antibiotic specific for enteric pathogens of the gastrointestinal tract (ie, gram-positive, gram-negative, aerobic, anaerobic). Rifampin is a structural analogue. It binds to the beta subunit of bacterial deoxyribonucleic acid (DNA)-dependent ribonucleic acid (RNA) polymerase, thereby inhibiting RNA synthesis. It is indicated for E coli (enterotoxigenic and enteroaggregative strains) associated with travelers' diarrhea.

Rifamycin (Aemcolo, Rifamycin SV MMX)

Clinical Context:  Oral nonabsorbable antibiotic which can be used for the treatment of bacterial infections of the colon. Belongs to the ansamycin antibacterial drug class and acts by inhibiting the beta-subunit of bacterial DNA-dependent RNA polymerase, blocking 1 of the DNA transcription steps, which results in bacterial synthesis inhibition and consequently bacterial growth. It is indicated for traveler’s diarrhea caused by noninvasive strains of E coli, not complicated by fever or blood in the stool.

Class Summary

Along with the immune system, antibiotics help to destroy offending organisms.

What is bacterial gastroenteritis?What stool characteristics should be considered in the evaluation of suspected bacterial gastroenteritis?How is diarrhea defined in bacterial gastroenteritis?Which systemic features should be considered in the evaluation of bacterial gastroenteritis?Which factors are associated with specific pathogens in bacterial gastroenteritis?Which physical findings are characteristic of bacterial gastroenteritis?Which assessments may be included in the workup of bacterial gastroenteritis?How are culture media selected in the workup of bacterial gastroenteritis?What is included in medical care for bacterial gastroenteritis?What are antimicrobial treatment options for bacterial gastroenteritis?What are dietary modifications for management of bacterial gastroenteritis?What is the manifestation of bacterial gastroenteritis?What are the leading causes of bacterial gastroenteritis?How does the season influence the likely etiology of bacterial gastroenteritis?What is the pathophysiology of bacterial gastroenteritis?What is the role of verotoxin in the etiology of bacterial gastroenteritis?Which normal enteric flora have pathogenic strains that cause gastroenteritis?What is the role of Vibrio parahaemolyticus in the etiology of bacterial gastroenteritis?What are the risk factors for bacterial gastroenteritis?What is the prevalence of bacterial gastroenteritis in the US?What is the global prevalence of bacterial gastroenteritis?How does the prevalence of bacterial gastroenteritis vary by sex?How does the prevalence of bacterial gastroenteritis vary by age?What is the prognosis of bacterial gastroenteritis?What is the morbidity and mortality of bacterial gastroenteritis?What are common complications of bacterial gastroenteritis?What is enteric fever in bacterial gastroenteritis?What causes HUS in bacterial gastroenteritis?What is Reiter syndrome in bacterial gastroenteritis?How does dehydration occur in bacterial gastroenteritis?What is the role of bacterial gastroenteritis in the etiology of inflammatory bowel disease (IBD)?What is the prevalence of carrier states in bacterial gastroenteritis?What information about bacterial gastroenteritis should patients be given?How is diarrhea defined and stool assessed in the evaluation of bacterial gastroenteritis?What are systemic symptoms of bacterial gastroenteritis?Which food-borne pathogens cause bacterial gastroenteritis?Which water-borne pathogens cause bacterial gastroenteritis?Which animal-borne pathogens cause bacterial gastroenteritis?What is the role of travel history in determining etiology in bacterial gastroenteritis?Which pathogens are associated with particular locations in the etiology of bacterial gastroenteritis?Which medical conditions can predispose patients to bacterial infections causing gastroenteritis?What pathogens are associated with outbreaks of bacterial gastroenteritis?What are the physical findings characteristic of bacterial gastroenteritis?What are the physical findings of malnutrition in bacterial gastroenteritis and what do they signify?How is abdominal pain characterized in bacterial gastroenteritis?What is borborygmi in bacterial gastroenteritis?What causes perianal erythema in bacterial gastroenteritis?Which conditions should be considered in the differential diagnoses of bacterial gastroenteritis?What are the differential diagnoses for Bacterial Gastroenteritis?What is the initial approach to the workup for bacterial gastroenteritis?How is C difficile infection diagnosed in bacterial gastroenteritis?What is the role of bacterial cultures in the diagnostic assessment of bacterial gastroenteritis?Which culture media are used in the workup of bacterial gastroenteritis?What is the role of stool cultures in the diagnosis of bacterial gastroenteritis?Why is it important to test for S typhimurium DT104 in bacterial gastroenteritis?When is ingested food cultured for bacteria in the workup of gastroenteritis?What raises the suspicion of enterohemorrhagic E coli in bacterial gastroenteritis?What should prompt additional screening for Vibrio and Plesiomonas in the workup of bacterial gastroenteritis?What are the treatment options for bacterial gastroenteritis?When is inpatient care indicated for the treatment of bacterial gastroenteritis?Which specialist consultations are needed for the treatment of bacterial gastroenteritis?When are dietary modifications indicated in the treatment of bacterial gastroenteritis?Which dietary modifications are used in the treatment of bacterial gastroenteritis?What is included in follow-up care for bacterial gastroenteritis?What may reduce the risk of transmission of food and water-borne infections causing bacterial gastroenteritis?Which vaccines are used to prevent bacterial gastroenteritis?Which vaccines should infants receive to prevent bacterial gastroenteritis?What is the role of RotaTeq in the prevention of bacterial gastroenteritis?What is the role of Rotarix in the prevention of bacterial gastroenteritis?What are the goals of drug treatment for bacterial gastroenteritis?What are the risks and benefits of antibiotic treatment for bacterial gastroenteritis?Which medications in the drug class Antibiotics are used in the treatment of Bacterial Gastroenteritis?


Jennifer Lynn Bonheur, MD, Attending Physician, Division of Gastroenterology, Lenox Hill Hospital

Disclosure: Nothing to disclose.


M Akram Tamer, MD, Professor, Program Director, Department of Pediatrics, University of Miami, Leonard M Miller School of Medicine

Disclosure: Nothing to disclose.

Mukul Arya, MD, Associate Professor of Internal Medicine, Weill Cornell Medical College; Assistant Director of Therapeutic Endoscopy, Department of Gastroenterology and Internal Medicine, Wyckoff Heights Medical Center

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD, Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

Disclosure: Nothing to disclose.


Simmy Bank, MD Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.

Richard E Frye, MD, PhD Assistant Professor, Departments of Pediatrics and Neurology, University of Texas Medical School at Houston

Richard E Frye, MD, PhD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, Child Neurology Society, and International Neuropsychological Society

Disclosure: Nothing to disclose.

John Gunn Lee, MD Director of Pancreaticobiliary Service, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, University of California at Irvine School of Medicine

John Gunn Lee, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment


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Stool Characteristics Small Bowel Large Bowel
AppearanceWateryMucus and/or blood
BloodPossibly heme-positive but never gross bloodPossibly grossly bloody
pHPossibly < 5.5>5.5
Reducing substancesPossibly positiveNegative
White blood cell (WBC) count< 5/high-power field (HPF)Possibly >10/HPF
Serum WBC countNormalPossible leukocytosis, bandemia
OrganismsPreformed toxins:

Bacillus species, Staphylococcus aureus

Invasive bacteria:

E coli and Shigella, Salmonella, Campylobacter, Yersinia, Aeromonas, and Plesiomonas species

Toxic bacteria:

E coli, cholera, C perfringens, Vibrio species, Listeria monocytogenes

Toxic bacteria:

C difficile

Other causes:

rotavirus, adenovirus, calicivirus, astrovirus, Norwalk virus, and Giardia and Cryptosporidium species

Other causes:

Entamoeba species

Organism Incubation Duration Vomiting Fever Abdominal Pain
Aeromonas speciesNone0-2 weeks+/-+/-No
Bacillus species1-16 hours1-2 daysYesNoYes
Campylobacter species2-4 days5-7 daysNoYesYes
C difficile VariableVariableNoFewFew
C perfringens 0-11 dayMildNoYes
Enterohemorrhagic E coli1-8 days3-6 daysNo+/-Yes
Enterotoxigenic E coli1-3 days3-5 daysYesLowYes
Listeria species20 hours2 daysFewYes+/-
Plesiomonas speciesNone0-2 weeks+/-+/-+/-
Salmonella species0-3 days2-7 daysYesYesYes
Shigella species0-2 days2-7 daysNoHighYes
S aureus 2-6 hours1 dayYesNoYes
Vibrio species0-1 days5-7 daysYesNoYes
Y enterocolitica 0-61-46 daysYesYesYes
Organism Detection Method Microbiologic Characteristics
Aeromonas speciesBlood agarOxidase-positive, flagellated GNB
Bacillus speciesBlood agarFacultatively aerobic, spore-forming GPR; beta hemolytic; reduces nitrates; ferments carbohydrates
Campylobacter speciesSkirrow agarRapidly motile, curved GNR; Campylobacter jejuni 90% of infections, Campylobacter coli 5% of infections
C difficile CCFE agar, EIA for toxin, LA for proteinAnaerobic, spore-forming GPR; toxin-mediated diarrhea; produces pseudomembranous colitis
C perfringens None availableAnaerobic, spore-forming GPR; toxin-mediated diarrhea
E coli MacConkey, EMB, or SM agarLactose-producing GNR
Listeria speciesBlood agarFlagellated GPB
Plesiomonas speciesBlood agarOxidase-positive GNR
Salmonella speciesBlood, MacConkey, EMB, XLD, or HE agarNonlactose, non–H2S-producing GNR
Shigella speciesBlood, MacConkey, EMB, XLD, or HE agarNonlactose and H2S-producing GNR; verotoxin (neurotoxin)
Staphylococcus speciesBlood agarHeat-stable, preformed toxin-mediated GPC
Vibrio speciesBlood or TCBS agarOxidase-positive, motile, curved GNB
Y enterocolitica CIN agarNonlactose-producing, oval GNR
CCFE = cycloserine-cefoxitin-fructose-egg; CIN = cefsulodin-irgasan-novobiocin; EIA= enzyme immunoassay; EMB = e-methylene blue; GNB = gram-negative bacillus; GNR = gram-negative rod; GPB = gram-positive bacillus; GPC = gram-positive cocci; GPR = gram-positive rod; H2S = hydrogen sulfide; HE = Hektoen enteric; LA = latex agglutination; SM = Sorbitol-MacConkey; TCBS = thiosulfate-citrate-bile-sucrose; XLD = xylose-lysine-deoxycholate.