Bacterial Gastroenteritis 

  • Author: Jennifer Lynn Bonheur, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: Apr 15, 2011
 

Background

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. 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.[1, 2, 3, 4]

For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center and Public Health Center. Also, see eMedicine's patient education articles Gastroenteritis and Foreign Travel.

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Pathophysiology

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.

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.

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Epidemiology

Frequency

United States

Bacterial gastroenteritis is a very common problem in primary care and emergency department settings, especially for children younger than 5 years.[3, 4] 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 affects adults and accounts for 8 million doctor visits and 250,000 hospitalizations. Episodes of gastroenteritis do not occur at random but usually occur in outbreaks. Traveler's diarrhea affects 20-50% of people traveling from industrialized to developing countries.[4, 5, 6]

International

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.[2, 4, 5, 6, 7]

Mortality/Morbidity

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 people.

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. Gastroenteritis-causing pathogens are the second leading cause of morbidity and mortality worldwide.

Race

It has been reported that the preparation and ingestion of chitterlings, common among some blacks, especially during the holiday season, may pose an increased risk of infection with Yersinia enterocolitica serotype O:3.[8, 9]

Sex

Most infectious diarrheas do not affect one sex more than the other; however, females have a higher incidence of Campylobacter infections and hemolytic-uremic syndrome (HUS).

Age

Yersinia species infect children younger than 1 year almost exclusively, and Aeromonas species are a significant cause of bacterial gastroenteritis in young children. Very young children are particularly susceptible to secondary dehydration and malabsorption.

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Contributor Information and Disclosures
Author

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

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, and Sigma Xi

Disclosure: Nothing to disclose.

Coauthor(s)

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

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, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Richard E Frye, MD, PhD  Assistant Professor, Departments of Pediatrics and Neurology, University of Texas Health Science Center 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.

M Akram Tamer, MD  Program Director, Professor, Department of Pediatrics, University of Miami

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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; Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

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.

Alex J Mechaber, MD, FACP  Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD  Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

References
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Table 1. Stool Characteristics and Determining Their Source
Stool CharacteristicsSmall BowelLarge Bowel
AppearanceWateryMucus and/or blood
VolumeLargeSmall
FrequencyIncreasedIncreased
BloodPossibly heme-positive but never gross bloodPossibly grossly bloody
pHPossibly < 5.5>5.5
Reducing SubstancesPossibly positiveNegative
WBC count< 5/HPFPossibly >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, Giardia and Cryptosporidium species



Other causes:



Entamoeba species



Table 2. Organisms and Frequency of Symptoms
OrganismIncubationDurationVomitingFeverAbdominal Pain
Aeromonas speciesNone0-2 weeks+/-+/-No
Bacillus species1-16 hours1-2 daysYesNoYes
Campylobacter species2-4 days5-7 daysNoYesYes
C difficileVariableVariableNoFewFew
C perfringens0-11 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 aureus2-6 hours1 dayYesNoYes
Vibrio species0-1 days5-7 daysYesNoYes
Y enterocolitica0-61-46 daysYesYesYes
Table 3. Common Bacteria and Optimum Culture Media
OrganismDetection MethodMicrobiological 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 difficileCCFE agar, EIA for toxin, LA for proteinAnaerobic, spore-forming GPR; toxin-mediated diarrhea; produces pseudomembranous colitis
C perfringensNone availableAnaerobic, spore-forming GPR; toxin-mediated diarrhea
E coliMacConkey, 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 enterocoliticaCIN agarNonlactose-producing, oval GNR
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