Sections

Overview

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 Presentation for more details.

Diagnosis

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.

Management

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.

Next: Background

Background

Bacterial gastroenteritis 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 may include viral infections, improper diet, malabsorption syndromes, various enteropathies, and inflammatory bowel disease. (See Etiology, Presentation, Workup, and Treatment.)

Gastroenteritis can be classified in many ways; according to the duration of symptoms it is described as acute, persistent, chronic, or recurrent, as follows^{[4, 5]}:

Acute: Duration of 14 days or less
Persistent: More than 14 days but fewer than 30 days in duration
Chronic: Duration greater than 30 days
Recurrent: Diarrhea that recurs after 7 days without diarrhea

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.)^{[6, 7, 8, 9]}

Next: Background

Etiology

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

Shigella infection has a higher incidence in summer and fall. Campylobacter infection similarly 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, is a major cause of gastroenteritis in Japan and appears to be an emerging foodborne pathogen in North America. In 2016, the CDC reported 0.45 cases per 100,000.^{[10, 11]}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.^[10]

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.^[12]

PPI therapy has also been suggested to be an independent risk factor for the development and recurrence of C difficile colitis^[13]as well as increases the risk Campylobacter gastroenteritis.^[14]

Next: Background

Epidemiology

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.^{[8, 9]}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.^{[9, 15, 16]}

From 2000 to 2009, the number of hospitalized patients with any Clostridioides difficile (formerly 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.^[17]

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.^[17]

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.^{[7, 9, 15, 16, 18]}

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%).^[19]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.^[20]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.^{[21, 22]}

Next: Background

Prognosis

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.

Once malnutrition from secondary malabsorption begins, the prognosis becomes less favorable 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.

The mortality rate from bacterial gastroenteritis is low in industrialized countries. 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).^[23]

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.

Complications

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.

Hemolytic uremic syndrome

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.

Reactive arthritis (formerly known as Reiter syndrome)

Reactive arthritis is a form of inflammatory arthritis that develops in response to an infection in another part of the body. Arthritis, urethritis, conjunctivitis, and mucocutaneous lesions are characteristic. Affected individuals usually do not demonstrate all the features.

Dehydration

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.^[24]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.

Next: Background

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.

Dietary 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.

Clinical Presentation

Guandalini S, Pensabene L, Zikri MA, et al. Lactobacillus GG administered in oral rehydration solution to children with acute diarrhea: a multicenter European trial. J Pediatr Gastroenterol Nutr. 2000 Jan. 30(1):54-60. [QxMD MEDLINE Link].
Simakachorn N, Pichaipat V, Rithipornpaisarn P, et al. Clinical evaluation of the addition of lyophilized, heat-killed Lactobacillus acidophilus LB to oral rehydration therapy in the treatment of acute diarrhea in children. J Pediatr Gastroenterol Nutr. 2000 Jan. 30(1):68-72. [QxMD MEDLINE Link].
Duggan C, Nurko S. "Feeding the gut": the scientific basis for continued enteral nutrition during acute diarrhea. J Pediatr. 1997 Dec. 131(6):801-8. [QxMD MEDLINE Link].
Hiyoshi H, Tiffany CR, Bronner DN, Baumler AJ. Typhoidal Salmonella serovars: ecological opportunity and the evolution of a new pathovar. FEMS Microbiol Rev. 2018 Jul 1. 42(4):527-41. [QxMD MEDLINE Link]. [Full Text].
Sattar SBA, Singh S. Bacterial gastroenteritis. StatPearls [Internet]. 2023 Aug 8. [QxMD MEDLINE Link]. [Full Text].
Salminen S, Isolauri E, Onnela T. Gut flora in normal and disordered states. Chemotherapy. 1995. 41 suppl 1:5-15. [QxMD MEDLINE Link].
Marks MI. Infectious diarrhea: introduction and commentary. Pediatr Ann. 1994 Oct. 23(10):526-7. [QxMD MEDLINE Link].
Liebelt EL. Clinical and laboratory evaluation and management of children with vomiting, diarrhea, and dehydration. Curr Opin Pediatr. 1998 Oct. 10(5):461-9. [QxMD MEDLINE Link].
Hamer DH, Gorbach SL. Infectious diarrhea and bacterial food poisoning. Feldman M, Scharschmidt BF, Sleisenger MH, eds. Sleisinger and Fordtran’s Gastrointestinaland Liver Disease. 6th ed. Philadelphia, Pa: WB Saunders; 1998. 1594-632.
Xu F, Gonzalez-Escalona N, Haendiges J, et al. Sequence type 631 Vibrio parahaemolyticus, an emerging foodborne pathogen in North America. J Clin Microbiol. 2017 Feb. 55(2):645-8. [QxMD MEDLINE Link]. [Full Text].
Rezny BR, Evans DS. Vibrio parahaemolyticus infection. StatPearls [Internet]. 2023 Jun 26. [QxMD MEDLINE Link]. [Full Text].
Chen Y, Liu B, Glass K, Du W, Banks E, Kirk M. Use of proton pump inhibitors and the risk of hospitalization for infectious gastroenteritis. PLoS One. 2016. 11(12):e0168618. [QxMD MEDLINE Link]. [Full Text].
Cadle RM, Mansouri MD, Logan N, Kudva DR, Musher DM. Association of proton-pump inhibitors with outcomes in Clostridium difficile colitis. Am J Health Syst Pharm. 2007 Nov 15. 64(22):2359-63. [QxMD MEDLINE Link].
Wei L, Ratnayake L, Phillips G, et al. Acid suppression medications and bacterial gastroenteritis: a population-based cohort study. Br J Clin Pharmacol. 2017 Jan 5. 27(1):40-51. [QxMD MEDLINE Link]. [Full Text].
Steffen R, Collard F, Tornieporth N, et al. Epidemiology, etiology, and impact of traveler's diarrhea in Jamaica. JAMA. 1999 Mar 3. 281(9):811-7. [QxMD MEDLINE Link]. [Full Text].
Streit JM, Jones RN, Toleman MA, Stratchounski LS, Fritsche TR. Prevalence and antimicrobial susceptibility patterns among gastroenteritis-causing pathogens recovered in Europe and Latin America and Salmonella isolates recovered from bloodstream infections in North America and Latin America: report from the SENTRY Antimicrobial Surveillance Program (2003). Int J Antimicrob Agents. 2006 May. 27(5):367-75. [QxMD MEDLINE Link].
Centers for Disease Control and Prevention (CDC). Vital signs: preventing Clostridium difficile infections. MMWR Morb Mortal Wkly Rep. 2012 Mar 9. 61(9):157-62. [QxMD MEDLINE Link]. [Full Text].
World Health Organization. Cholera: fact sheet no. 107. November 2008. Available at https://www.who.int/mediacentre/factsheets/fs107/en/. Accessed: February 19, 2009.
May FJ, Polkinghorne BG, Fearnley EJ. Epidemiology of bacterial toxin-mediated foodborne gastroenteritis outbreaks in Australia, 2001 to 2013. Commun Dis Intell Q Rep. 2016 Dec 24. 40(4):E460-E469. [QxMD MEDLINE Link].
Campylobacter (Campylobacteriosis). Centers for Disease Control and Prevention (CDC). Available at https://www.cdc.gov/campylobacter/technical.html. Accessed: February 15, 2018.
Lee LA, Gerber AR, Lonsway DR, et al. Yersinia enterocolitica O:3 infections in infants and children, associated with the household preparation of chitterlings. N Engl J Med. 1990 Apr 5. 322(14):984-7. [QxMD MEDLINE Link].
Centers for Disease Control and Prevention. Yersinia enterocolitica. October 25, 2005. Available at https://www.cdc.gov/ncidod/dbmd/diseaseinfo/yersinia_g.htm. Accessed: February 18, 2009.
Centers for Disease Control and Prevention (CDC). Deaths from gastroenteritis double. Available at https://www.cdc.gov/media/releases/2012/p0314_gastroenteritis.html.
Garcia Rodriguez LA, Ruigomez A, Panes J. Acute gastroenteritis is followed by an increased risk of inflammatory bowel disease. Gastroenterology. 2006 May. 130(6):1588-94. [QxMD MEDLINE Link].
Calbo E, Freixas N, Xercavins M, et al. Foodborne nosocomial outbreak of SHV1 and CTX-M-15-producing Klebsiella pneumoniae: epidemiology and control. Clin Infect Dis. 2011 Mar. 52(6):743-9. [QxMD MEDLINE Link].
Biswas JS, Al-Ali A, Rajput P, Smith D, Goldenberg SD. A parallel diagnostic accuracy study of three molecular panels for the detection of bacterial gastroenteritis. Eur J Clin Microbiol Infect Dis. 2014 Nov. 33(11):2075-81. [QxMD MEDLINE Link].
Calderaro A, Martinelli M, Buttrini M, et al. Contribution of the FilmArray(R) Gastrointestinal Panel in the laboratory diagnosis of gastroenteritis in a cohort of children: a two-year prospective study. Int J Med Microbiol. 2018 Jul. 308(5):514-21. [QxMD MEDLINE Link].
Humphries RM, Linscott AJ. Laboratory diagnosis of bacterial gastroenteritis. Clin Microbiol Rev. 2015 Jan. 28(1):3-31. [QxMD MEDLINE Link]. [Full Text].
Cody SH, Abbott SL, Marfin AA, et al. Two outbreaks of multidrug-resistant Salmonella serotype typhimurium DT104 infections linked to raw-milk cheese in Northern California. JAMA. 1999 May 19. 281(19):1805-10. [QxMD MEDLINE Link]. [Full Text].
World Health Organization. Drug-resistant Salmonella: fact sheet no. 139. Revised April 2005. Available at https://www.who.int/mediacentre/factsheets/fs139/en/. Accessed: February 19, 2009.
Mylius M, Dreesman J, Pulz M, et al. Shiga toxin-producing Escherichia coli O103:H2 outbreak in Germany after school trip to Austria due to raw cow milk, 2017 - The important role of international collaboration for outbreak investigations. Int J Med Microbiol. 2018 Jul. 308(5):539-44. [QxMD MEDLINE Link].
Goldenberg JZ, Yap C, Lytvyn L, et al. Probiotics for the prevention of Clostridium difficile-associated diarrhea in adults and children. Cochrane Database Syst Rev. 2017 Dec 19. 12:CD006095. [QxMD MEDLINE Link].
Guandalini S, Dincer AP. Nutritional management in diarrhoeal disease. Baillieres Clin Gastroenterol. 1998 Dec. 12(4):697-717. [QxMD MEDLINE Link].
Sullivan PB. Nutritional management of acute diarrhea. Nutrition. 1998 Oct. 14(10):758-62. [QxMD MEDLINE Link].
Ruiz-Palacios GM, Perez-Schael I, Velazquez FR, et al, for the Human Rotavirus Vaccine Study Group. Safety and efficacy of an attenuated vaccine against severe rotavirus gastroenteritis. N Engl J Med. 2006 Jan 5. 354(1):11-22. [QxMD MEDLINE Link]. [Full Text].
[Guideline] Shane AL, Mody RK, Crump JA, et al. 2017 Infectious Diseases Society of America clinical practice guidelines for the diagnosis and management of infectious diarrhea. Clin Infect Dis. 2017 Nov 29. 65(12):1963-73. [QxMD MEDLINE Link]. [Full Text].
Cuypers WL, Jacobs J, Wong V, Klemm EJ, Deborggraeve S, Van Puyvelde S. Fluoroquinolone resistance in Salmonella: insights by whole-genome sequencing. Microb Genom. 2018 Jul. 4(7):e000195. [QxMD MEDLINE Link]. [Full Text].
US Food and Drug Administration. FDA updates warnings for fluoroquinolone antibiotics on risks of mental health and low blood sugar adverse reactions. July 10, 2018. Available at https://www.fda.gov/news-events/press-announcements/fda-updates-warnings-fluoroquinolone-antibiotics-risks-mental-health-and-low-blood-sugar-adverse. Accessed: July 18, 2018.
Frellick M. FDA: Stronger fluoroquinolone warnings for mental health, hypoglycemia. Medscape Medical News from WebMD. July 10, 2018. Available at https://www.medscape.com/viewarticle/899142. Accessed: July 18, 2018.
Brooks M. FDA clears novel test for infectious gastroenteritis. Medscape Medical News. January 15, 2013. Available at https://www.medscape.com/viewarticle/777671. Accessed: February 9, 2013.
[Guideline] DuPont HL, The Practice Parameters Committee of the American College of Gastroenterology. Guidelines on acute infectious diarrhea in adults. Am J Gastroenterol. 1997 Nov. 92(11):1962-75. [QxMD MEDLINE Link].
Garcia Rodriguez LA, Ruigomez A, Panes J. Use of acid-suppressing drugs and the risk of bacterial gastroenteritis. Clin Gastroenterol Hepatol. 2007 Dec. 5(12):1418-23. [QxMD MEDLINE Link].
Gibreel A, Taylor DE. Macrolide resistance in Campylobacter jejuni and Campylobacter coli. J Antimicrob Chemother. 2006 Aug. 58(2):243-55. [QxMD MEDLINE Link]. [Full Text].
Kaur S, Vaishnavi C, Prasad KK, Ray P, Kochhar R. Comparative role of antibiotic and proton pump inhibitor in experimental Clostridium difficile infection in mice. Microbiol Immunol. 2007. 51(12):1209-14. [QxMD MEDLINE Link]. [Full Text].
Mines D, Stahmer S, Shepherd SM. Poisonings: food, fish, shellfish. Emerg Med Clin North Am. 1997 Feb. 15(1):157-77. [QxMD MEDLINE Link].
Nataro JP, Steiner T, Guerrant RL. Enteroaggregative Escherichia coli. Emerg Infect Dis. 1998 Apr-Jun. 4(2):251-61. [QxMD MEDLINE Link].
Paterson DL. Resistance in gram-negative bacteria: Enterobacteriaceae. Am J Med. 2006 Jun. 119(6 suppl 1):S20-8; discussion S62-70. [QxMD MEDLINE Link].
Rodriguez LA, Ruigomez A. Increased risk of irritable bowel syndrome after bacterial gastroenteritis: cohort study. BMJ. 1999 Feb 27. 318(7183):565-6. [QxMD MEDLINE Link]. [Full Text].
Trachtman H, Christen E. Pathogenesis, treatment, and therapeutic trials in hemolytic uremic syndrome. Curr Opin Pediatr. 1999 Apr. 11(2):162-8. [QxMD MEDLINE Link].
Wong CS, Jelacic S, Habeeb RL, Watkins SL, Tarr PI. The risk of the hemolytic-uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 infections. N Engl J Med. 2000 Jun 29. 342(26):1930-6. [QxMD MEDLINE Link]. [Full Text].
Surana NK, Kasper DL. Moving beyond microbiome-wide associations to causal microbe identification. Nature. 2017 Dec 14. 552(7684):244-7. [QxMD MEDLINE Link]. [Full Text].
[Guideline] Berenger B, Chui L, Reimer AR, et al, for the Canadian Public Health Laboratory Network. Canadian Public Health Laboratory Network position statement: Non-culture based diagnostics for gastroenteritis and implications for public health investigations. Can Commun Dis Rep. 2017 Dec 7. 43(12):279-81. [QxMD MEDLINE Link]. [Full Text].
Lee H, Ku HJ, Lee DH, et al. Characterization and genomic study of the novel bacteriophage HY01 infecting both Escherichia coli O157:H7 and Shigella flexneri: potential as a biocontrol agent in food. PLoS One. 2016. 11(12):e0168985. [QxMD MEDLINE Link]. [Full Text].

Media Gallery

of 0

Table 1. Stool Characteristics and Sources

Stool Characteristics	Small Bowel	Large Bowel
Appearance	Watery	Mucus and/or blood
Volume	Large	Small
Frequency	Increased	Increased
Blood	Possibly heme-positive but never gross blood	Possibly grossly bloody
pH	Possibly < 5.5	> 5.5
Reducing substances	Possibly positive	Negative
White blood cell (WBC) count	< 5/high-power field (HPF)	Possibly > 10/HPF
Serum WBC count	Normal	Possible leukocytosis, bandemia
Organisms	Preformed 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

Table 2. Symptoms and Their Characteristics

Organism	Incubation	Duration	Vomiting	Fever	Abdominal Pain
Aeromonas species	None	0-2 weeks	+/-	+/-	No
Bacillus species	1-16 hours	1-2 days	Yes	No	Yes
Campylobacter species	2-4 days	5-7 days	No	Yes	Yes
C difficile	Variable	Variable	No	Few	Few
C perfringens	0-1	1 day	Mild	No	Yes
Enterohemorrhagic E coli	1-8 days	3-6 days	No	+/-	Yes
Enterotoxigenic E coli	1-3 days	3-5 days	Yes	Low	Yes
Listeria species	20 hours	2 days	Few	Yes	+/-
Plesiomonas species	None	0-2 weeks	+/-	+/-	+/-
Salmonella species	0-3 days	2-7 days	Yes	Yes	Yes
Shigella species	0-2 days	2-7 days	No	High	Yes
S aureus	2-6 hours	1 day	Yes	No	Yes
Vibrio species	0-1 days	5-7 days	Yes	No	Yes
Y enterocolitica	0-6	1-46 days	Yes	Yes	Yes

Table 3. Common Bacteria and Optimum Culture Media

Organism	Detection Method	Microbiologic Characteristics
Aeromonas species	Blood agar	Oxidase-positive, flagellated GNB
Bacillus species	Blood agar	Facultatively aerobic, spore-forming GPR; beta hemolytic; reduces nitrates; ferments carbohydrates
Campylobacter species	Skirrow agar	Rapidly motile, curved GNR; Campylobacter jejuni 90% of infections, Campylobacter coli 5% of infections
C difficile	CCFE agar, EIA for toxin, LA for protein	Anaerobic, spore-forming GPR; toxin-mediated diarrhea; produces pseudomembranous colitis
C perfringens	None available	Anaerobic, spore-forming GPR; toxin-mediated diarrhea
E coli	MacConkey, EMB, or SM agar	Lactose-producing GNR
Listeria species	Blood agar	Flagellated GPB
Plesiomonas species	Blood agar	Oxidase-positive GNR
Salmonella species	Blood, MacConkey, EMB, XLD, or HE agar	Nonlactose, non–H2S-producing GNR
Shigella species	Blood, MacConkey, EMB, XLD, or HE agar	Nonlactose and H2S-producing GNR; verotoxin (neurotoxin)
Staphylococcus species	Blood agar	Heat-stable, preformed toxin-mediated GPC
Vibrio species	Blood or TCBS agar	Oxidase-positive, motile, curved GNB
Y enterocolitica	CIN agar	Nonlactose-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.

Back to List

#author-disclosures{display:block}#author-disclosures.modal-layer{position:relative}#author-disclosures .modal-content{max-height:none}#author-disclosures .close-modal{display:none}

Author

Jennifer Lynn Bonheur, MD Attending Gastroenterologist

Jennifer Lynn Bonheur, MD is a member of the following medical societies: American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, New York Academy of Sciences, New York Society for Gastrointestinal Endoscopy, Sigma Xi, The Scientific Research Honor Society

Disclosure: Nothing to disclose.

Coauthor(s)

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

Mukul Arya, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

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

M Akram Tamer, MD is a member of the following medical societies: American Medical Association, Florida Medical Association

Disclosure: Nothing to disclose.

Chief Editor

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

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

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

TOP PICKS FOR YOU

Bacterial Gastroenteritis

Practice Essentials

Signs and symptoms

Diagnosis

Management

Background

Etiology

Risk factors

Epidemiology

Occurrence in the United States

International occurrence

Race-, sex-, and age-related demographics

Prognosis

Morbidity and mortality

Complications

Patient Education

References

Tables

Contributor Information and Disclosures

What would you like to print?