eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Gastroenteritis

Randy P Prescilla, MD, Instructor in Anesthesia, Harvard Medical School; Assistant in Perioperative Anesthesia, Children's Hospital Boston

Updated: Jan 5, 2009

Introduction

Background

Gastroenteritis is a very common pediatric condition and is second only to respiratory infections as the most common reason for unscheduled visits to pediatricians.

Pathophysiology

Gastroenteritis is a clinical syndrome caused by various viral, bacterial, and parasitic enteropathogens. The mechanisms potentially responsible for viral diarrhea include lysis of enterocytes, interference with the brush border function that leads to malabsorption of electrolytes, stimulation of cyclic adenosine monophosphate (cAMP), and carbohydrate malabsorption. The proposed pathophysiology of bacterial gastroenteritis involves the elaboration of toxin by enterotoxigenic pathogens and the invasion and inflammation of mucosa by invasive pathogens. Parasitic organisms invade epithelial cells and cause villus atrophy and eventual malabsorption.

Frequency

United States

Incidence rates for diarrhea are 1-2.5 episodes per child per year, which annually leads to approximately 38 million cases, 2-3.7 million physician visits, 320,000 hospitalizations, and 325-425 deaths.

International

More than 1 billion cases and at least 4 million deaths per year are attributed to diarrhea worldwide.

Mortality/Morbidity

Mortality and morbidity from diarrhea relate to the degree of dehydration. Most deaths in the United States correlate to lower maternal socioeconomic factors and prematurity.

Age

Dehydration risk in children relates to age, and infants are most susceptible.

Clinical

History

  • Pertinent information in individuals with suspected gastroenteritis includes the following:
    • Presence or absence of vomiting
    • Frequency, duration, and character of diarrhea
    • Travel history
    • Contacts with sick individuals
    • Antibiotic use
    • Seafood ingestion
    • Possible ingestion of toxic substances
    • Chronic illness
  • Determine the amount and type of fluids ingested for the past 24 hours and the child's urine output.
  • Seizures in a patient with diarrhea should raise the possibility of gastroenteritis caused by Shigella species, enterohemorrhagic Escherichia coli, or an electrolyte imbalance. Hyponatremia is more common than hypernatremia.
    • Consider hyponatremic dehydration in children who have been fed bland and dilute fluids (eg, tea, rice water, dilute formula).
    • Consider hypernatremic dehydration in patients who have been drinking mainly salt solutions and other hypertonic solutions, who have been losing hypotonic fluids (eg, profuse watery diarrhea), and who present with a depressed sensorium beyond what would be expected from the apparently mild signs of dehydration.

Physical

  • The criterion standard and most accurate clinical indicator of the extent of dehydration is the percentage loss of body weight during the illness, which represents the child's fluid deficit.
  • Other vital clinical findings include the following:
    • Thirst
    • Listlessness
    • Dry mucous membranes
    • Sunken fontanelles
    • Sunken eyes
    • Absence of tears
    • Decreased skin turgor
    • Decreased capillary filling time
    • Tachycardia
    • Weak pulse
    • Reduced blood pressure
  • Examine the stools to check for mucus, blood streaks, or gross blood.
  • Tenting or loss of skin turgor (eg, when pinched skin does not return to the original flat shape) usually occurs in moderate-to-severe cases of dehydration yet is not always present in dehydration. Tenting or skin turgor loss seldom occurs with hypernatremic dehydration, a condition in which doughy skin is more common.

Causes

  • Bacterial infections cause most gastroenteritis cases in less affluent nations.
    • The most important causal agent in these countries is diarrhea-causing E coli (eg, enteropathogenic [EPEC], enterotoxigenic [ETEC], enteroaggregative [EAEC], enteroinvasive [EIEC], enterohemorrhagic [EHEC]).
    • Other bacteria that cause gastroenteritis less often include Campylobacter, Aeromonas, Shigella, and Salmonella species.
    • Vibrios species, especially Vibrios cholerae, play major roles in epidemics. In seafood poisoning, Vibrio parahaemolyticus is associated with gastroenteritis.
  • Viral infections cause 30-40% of gastroenteritis cases in affluent countries.
    • Rotavirus accounts for about 3.5 million cases per year and as many as 110,000 hospital admissions for diarrhea.
      • Rotavirus is the single most important cause of dehydrating diarrhea in both developed and developing countries. It produces severe diarrhea, accounting for most episodes in children younger than 2 years who require hospitalization for diarrhea and dehydration.1
      • Rotavirus incidence has a distinct seasonal pattern.
      • Rotavirus infection occurs most frequently in children aged 3-15 months and may occur in children as old as 24 months, although the vast majority of children have acquired antibodies by that age.
      • Rotavirus is transmitted by fecal oral spread with secondary spread via respiratory route.
      • A rotavirus vaccine has been available in the United States since 2006 (see Deterrence/Prevention).
    • Norwalk virus is responsible for outbreaks of gastroenteritis in older children and adults. Unlike rotavirus, which affects mainly children, the Norwalk virus causes illness in all age groups.
    • Enteric adenoviruses account for 5-20% of hospitalizations for acute diarrhea. Compared to rotavirus and Norwalk virus, enteric adenoviruses have a longer incubation period (ie, 8-10 d compared with 1-3 d), and the diarrhea associated with adenoviruses lasts longer (ie, 5-12 d compared with 5-7 d for rotavirus and 1-2 d for Norwalk). Astroviruses and caliciviruses each account for 3-5% hospitalizations for acute diarrhea.
    • Additional information about viral gastroenteritis can be obtained from The Centers for Disease Control and Prevention (CDC).
  • The most common bacterial agents in the United States are Salmonella, Shigella, Campylobacter, and Yersinia species and E coli. Enteroaggregative E coli has recently been shown to be an unrecognized cause of community-acquired diarrhea in infants in the United States. Campylobacter jejuni affects approximately 2 million people in the United States annually. Clostridium difficile is the most common cause of pseudomembranous colitis, a condition often observed in patients who develop severe diarrhea during or following a course of antibiotics. Clindamycin is the most common antibiotic identified, although almost all antibiotics have been implicated.
    • In patients with sickle cell disease, Salmonella species are the most frequent cause of gastroenteritis.
    • Giardia lamblia is the only parasite frequently isolated from patients with diarrhea. Other parasites include Cryptosporidium parvum and Cyclospora cayetanensis.
    • Nonpathogenic isolates include Entamoeba coli, Endolimax nana, Iodamoeba butschlii, and Blastocystis hominis.
    • In patients with human immunodeficiency virus (HIV) or acquired immunodeficiency syndrome (AIDS), Mycobacterium avium is another causative agent, in addition to the other bacteria mentioned above. Protozoal agents include Cryptosporidium species, Isospora belli, G lamblia, Entamoeba histolytica, Cyclospora species, and microsporidia. Viral causes include cytomegalovirus and rotavirus.
    • Persistent infectious diarrhea may be caused by Shigella, Giardia, and Cryptosporidium species, EPEC, EAEC, and Entamoeba histolytica.
    • Additional information on bacterial foodborne and diarrheal diseases is available from the CDC.

Differential Diagnoses

Crohn Disease
Cystic Fibrosis
Hemolytic-Uremic Syndrome
Lactose Intolerance

Other Problems to Be Considered

Chronic nonspecific diarrhea of childhood (toddler diarrhea)

Workup

Laboratory Studies

  • Most cases of children with mild-to-moderate dehydration require no laboratory tests. Electrolyte, BUN, serum creatinine, and glucose levels may be obtained for severely dehydrated children or those with atypical or inconsistent histories and physical examination results. Other laboratory tests may be performed to assess hydration status, including hematocrit and urine specific gravity tests.
  • Fecal leukocytes are usually observed in infections caused by invasive E coli and Shigella and Campylobacter species. This test's predictive value varies, as does that of occult blood testing.
  • Gram stain of the stools may help differentiate infectious from noninfectious diarrhea. Gram-negative seagull-shaped bacteria visible with Gram stain strongly suggest campylobacteriosis. An ova and parasite examination and specialized staining procedures are necessary to diagnose a parasitic etiology.
  • Stool cultures are usually reserved for cases of children with bloody diarrhea and those who are severely dehydrated, chronically ill or immunocompromised, or who have the appearance of toxemia.
  • Metabolic acidosis with a normal anion gap occurs with loss of bicarbonate, including the following conditions:
    • Ureterostomy
    • Small bowel fistula
    • Extra chloride
    • Diarrhea
    • Carbonic anhydrase inhibitors
    • Early chronic renal failure
    • Addison disease
    • Renal tubular acidosis
    • Pancreatic fistula
    • Parenteral nutrition

Imaging Studies

  • Although imaging studies are not routine for gastroenteritis, anatomical abnormalities (eg, obstruction) should be excluded in cases involving vomiting without diarrhea. Consider the possibility of intussusception in very young patients. Exclude appendicitis in patients who have abdominal pain greater than diarrhea.

Histologic Findings

  • Stool examination for patients whose gastroenteritis is caused by invasive enteropathogens usually reveals small amounts of mucoid stools containing leukocytes, RBCs, and/or gross blood. Both tests, however, have low specificity and are better used for their negative predictive value (ie, up to 95%).
  • The probability of an invasive bacterial pathogen is very low when both test results are negative.

Treatment

Medical Care

The American Academy of Pediatrics (AAP) states, "oral rehydration therapy is the preferred treatment of fluid and electrolytes lost by diarrhea in children with mild-to-moderate dehydration."2 In addition, both the AAP and the European Society for Paediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) recommend rapid rehydration over 3-4 hours.2,3 A useful method is to administer 100 mL/kg/d for the first 10 kg of body weight (BW), 50 mL/kg for the next 10 kg BW, and 20 mL/kg for each additional kg BW.

The latest CDC recommendations for managing acute gastroenteritis in children can be viewed online at Managing Acute Gastroenteritis Among Children.4

  • Oral rehydration therapy in the home environment
    • Several oral rehydration solutions (ORSs) and pediatric maintenance solutions are available commercially (eg, Pedialyte, Rehydralyte, Kaolectrolyte, CeraLyte, Infalyte, Equalyte).
    • A general guideline is to provide 4-8 oz for every episode of loose or watery stools until the diarrhea resolves.
    • These fluids are not recommended for rehydration: tea, juices, pop, Kool-Aid, Gatorade (or similar sport drinks), boiled rice water, or boiled skim milk.
  • Rehydration therapy in healthcare settings
    • Oral rehydration is possible in a doctor's office with available space for at least 4 hours monitoring, adequately trained staff, and adequate mechanisms for billing this service. Intravenous rehydration also is feasible in these settings for mildly dehydrated patients who do not tolerate oral rehydration.
    • Provide rapid intravenous rehydration for patients with the following conditions:
      • Severe dehydration with cardiovascular involvement (ie, hypotension or shock)
      • Failure of oral rehydration because of persistent vomiting
      • High stool output (ie, usually >10 mL/kg BW/h)
      • Monosaccharide malabsorption, evidenced by the presence of glucose or reducing substances in the stool and a significant increase in the stool volume following administration of the ORS
    • Cerebral edema is the most serious potential consequence of rapidly infusing hypotonic fluids in a patient with hypernatremic dehydration.
  • Medications
    • Loperamide, opiates, opiate-and-atropine combination drugs, anticholinergic drugs, and absorbents are not recommended to treat diarrhea in children. No evidence exists that these are effective, and use may lead to possible adverse events.
    • Similarly, routine use of bismuth subsalicylate and lactobacillus-containing compounds is not recommended.
    • Most authorities do not recommend routine antiemetic use for children. Clinical evidence is currently insufficient to justify the use of ondansetron or metoclopramide in children with acute viral gastroenteritis.
    • Although antibiotic treatment clearly shortens the clinical illness and duration of pathogen excretion in dysentery caused by Shigella species, routine antibiotic use provides no clear advantage to treat gastroenteritis caused by Campylobacter jejuni, Yersinia enterocolitica, E coli, and Salmonella species.
    • Antibiotic administration may be considered for very young patients with Salmonella- caused gastroenteritis, for patients who are immunocompromised, and for patients who are systemically ill.
    • Evidence suggests that antibiotic treatment of enterohemorrhagic E coli infection may increase the risk for developing hemolytic uremic syndrome.
    • Rifaximin has excellent antibacterial activity and was approved in 2004 for the treatment for traveler's diarrhea caused by noninvasive strains of E coli.

Diet

  • Rapidly reintroducing normal feeding is the optimal rehydration method for children who are mildly to moderately dehydrated.
  • For infants, the AAP, ESPGHAN, and other groups currently recommend full-strength formula. The recommended rehydration method for breastfed infants is to continue to receive mother's milk.
  • For older children, the usual advice is to eat bananas, rice cereals, applesauce, and toast (ie, BRAT diet). Also on the recommended list are complex carbohydrates (eg, rice, wheat, bread, cereals), lean meats, yogurt, fruits, and vegetables.

Medication

Antibiotics

In cases of Shigella enteritis, antibiotic treatment provides more rapid resolution of symptoms and faster fecal shedding of the organism. Trimethoprim-sulfamethoxazole (TMP-SMZ) is the drug of choice. In uncomplicated enteritis caused by nontyphoidal Salmonella species, antibiotics have no beneficial effect and may prolong the carrier state. The role of antimicrobials to treat enteritis caused by Campylobacter species, Y enterocolitica, and E coli remains controversial. Metronidazole is the recommended medication for G lamblia.


Sulfamethoxazole and Trimethoprim (Bactrim, Cotrim, Septra)

An antibacterial combination that may be used to treat enteritis caused by susceptible strains of Shigella flexneri and Shigella sonnei when antibacterial therapy is indicated.

Dosing

Adult

160 mg (based on trimethoprim component)/800 mg (based on sulfamethoxazole component) PO bid for 5 d (ie, 1 double-strength tab bid)

Pediatric

8 mg/kg/d (based on trimethoprim component) PO divided bid for 5 d

Interactions

May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine

Contraindications

Documented hypersensitivity; documented megaloblastic anemia from folate deficiency; pregnant and nursing mothers; infants <2 mo; marked hepatic damage and renal insufficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue at first appearance of rash or sign of adverse reaction; obtain CBC counts regularly when used for more than 5 d; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; caution in folate deficiency (eg, patients with chronic alcoholism, older patients, patients receiving anticonvulsant therapy, patients with malabsorption syndrome); hemolysis may occur in patients with G-6-PD deficiency; patients with AIDS may not tolerate or respond to TMP-SMZ; caution in patients with renal or hepatic impairment (perform urinalyses and renal function tests during therapy); administer fluids to prevent crystalluria and stone formation


Metronidazole (Flagyl)

Appears to be absorbed into cells where intermediate-metabolized compounds are formed that bind DNA and inhibit protein synthesis.

Dosing

Adult

250 mg PO tid for 5 d

Pediatric

5 mg/kg PO tid for 5 d

Interactions

Cimetidine may increase toxicity; may increase effects of anticoagulants; may increase toxicity of lithium and phenytoin; disulfiramlike reaction may occur with PO-ingested ethanol

Contraindications

Documented hypersensitivity; first trimester of pregnancy

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Contraindicated in pregnancy during first trimester; adjust dose in patients with hepatic disease; monitor for seizures and development of peripheral neuropathy


Rifaximin (Xifaxan, RedActiv, Flonorm)

Nonabsorbed (<0.4%), broad-spectrum antibiotic specific for enteric pathogens of the gastrointestinal tract (ie, Gram-positive, Gram-negative, aerobic and anaerobic). Rifampin structural analog. Binds to beta-subunit of bacterial DNA-dependent RNA polymerase, thereby inhibiting RNA synthesis. Indicated for E coli (enterotoxigenic and enteroaggregative strains) associated with travelers' diarrhea.

Dosing

Adult

200 mg PO tid

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

Induces CYP450 3A4 in vitro; limited data available; no significant interactions shown in single dose studies with midazolam and PO contraceptives

Contraindications

Documented hypersensitivity to rifaximin or rifamycin antimicrobial agents (eg, rifampin)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May promote intestinal bacterial overgrowth and cause superinfection; discontinue if diarrhea persists more than 24-48 h or worsens; seek immediate medical care if fever and/or bloody stools emerge (tablets not effective); not effective for travelers' diarrhea due to suspected pathogens other than E coli; postmarketing reports include allergic dermatitis, rash, angioneurotic edema, urticaria, and pruritus

Vaccines

These agents elicit active immunization to increase resistance to infection. Vaccines consist of microorganisms or cellular components, which act as antigens. Administration of the vaccine stimulates the production of antibodies with specific protective properties.


Rotavirus vaccine (RotaTeq, Rotarix)

Currently, 2 orally administered live-virus vaccine are available.
RotaTeq contains 5 live human-bovine reassortant rotaviruses and is administered as a 3-dose regimen against G1, G2, G3, and G4 serotypes, the 4 most common rotavirus group A serotypes. It also contains attachment protein P1A (genotype P[8]).
Rotarix contains an attenuated human strain and is effective against rotavirus G1, G3, G4, and G9 strains and is administered as a 2-dose series in infants aged 6-24 wk.

Dosing

Adult

Not indicated

Pediatric

RotaTeq:
First dose: 2 mL PO administered between age 6-12 wk
Second and third doses: 2 mL PO administered at 4-10 wk intervals; complete third dose by age 32 wk

Rotarix:
First dose: 1 mL PO administered at age 6 wk
Second dose: 1 mL PO at least 4 wk after the first dose and before age 24 wk

Interactions

Immunosuppressive therapies (eg, irradiation, antimetabolites, alkylating agents, cytotoxic drugs, high-dose corticosteroids) may decrease the immune response

RotaTeq:
In clinical trials, RotaTeq was administered concomitantly with DTaP, IPV, Hib, hepatitis B vaccine, and pneumococcal conjugate vaccine; no evidence of reduced antibody responses to the vaccines that were concomitantly administered with RotaTeq

Rotarix:
In 484 infants, no evidence of interference in the immune responses to any of the antigens when Pediarix and a US-licensed Hib conjugate vaccine were coadministered with Rotarix as compared with separate administration of Rotarix

Contraindications

RotaTeq: Documented hypersensitivity

Rotarix: History of uncorrected congenital malformation of the GI tract (such as Meckel diverticulum) that would predispose the infant for intussusception

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Common adverse effects include diarrhea, vomiting, otitis media, inflamed nasal passages, and bronchospasm; refrigerate and protect from light; handle and discard empty tube according to biological waste procedures; do not mix in same syringe with other vaccines or solutions

Intussusception
Previously marketed rotavirus vaccine (RotaShield) was associated with intussusception and removed from the market

RotaTeq did not show an increased risk compared with placebo in clinical trials (monitor for signs of intestinal blockage); in the Rotavirus Efficacy and Safety Trial [REST] (n=69,625), the data did not show an increased risk of intussusception for RotaTeq when compared with placebo; in postmarketing experience, cases of intussusception have been reported in temporal association with RotaTeq

Rotarix did not show an increase in intussusception when evaluated in a safety study (including 63,225 infants) conducted in Latin America and Finland; 31,673 infants received Rotarix compared with 31,552 infants who received placebo; no increased risk of intussusception was observed in this clinical trial

Immunocompromised patients
No safety or efficacy data are available for either vaccine regarding administration to infants who may be immunocompromised because of coexisting disease, neoplasia, or infection, or who have received immunosuppressive drugs or biologicals

History of GI disorders
No safety or efficacy data are available for administration to infants with history of or chronic GI disorders including active acute GI illness, chronic diarrhea resulting in failure to thrive, congenital abdominal disorders, abdominal surgery, or intussusception

Viral shedding and transmission
The live vaccine virus may be transmitted to nonvaccinated contacts; potential for viral transmission following vaccination should be weighed against the possibility of acquiring and transmitting natural rotavirus; caution is advised when considering whether to administer rotavirus vaccine to individuals with immunodeficient close contacts

RotaTeq: Shedding was evaluated among a subset of subjects in REST 4-6 d after each dose and among all subjects who submitted a stool antigen rotavirus positive sample at any time; RotaTeq was shed in the stools of 32 of 360 (8.9%; 95% CI, 6.2%, 12.3%) vaccine recipients tested after dose 1; 0 of 249 (0.0%; 95% CI, 0.0%, 1.5%) vaccine recipients tested after dose 2; and in 1 of 385 (0.3%, 95% CI, <0.1%, 1.4%) vaccine recipients after dose 3; in phase 3 studies, shedding was observed as early as day 1 and as late as day 15 after a dose; transmission was not evaluated

Rotarix: Rotavirus shedding in stool occurs after vaccination with peak excretion occurring around day 7 after dose 1; live rotavirus shedding was evaluated in 2 studies among a subset of infants at day 7 after dose 1; in these studies, estimated percentages of recipients of Rotarix who shed live rotavirus were 25.6% (95% CI, 10.2, 41.1) and 26.5% (95% CI, 15.5, 37.5), respectively; transmission of virus was not evaluated

Follow-up

Transfer

  • Transfer by emergency medical service unit any patient with gastroenteritis who has moderate-to-severe dehydration to the nearest emergency department for intravenous rehydration.

Deterrence/Prevention

  • Rotavirus vaccines: Currently, 2 rotavirus vaccines are approved in the United States (ie, RotaTeq [Merck & Co, Inc] and Rotarix [GlaxoSmithKline]). See Medication.

Prognosis

  • Prognosis is excellent because gastroenteritis is usually self-limited.
  • Children usually improve after an intravenous bolus.
  • Patients who receive oral rehydration solutions (ORSs) gradually improve.

Patient Education

  • For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center. Also, see eMedicine's patient education article, Gastroenteritis.

Miscellaneous

Medicolegal Pitfalls

  • Failure to assess the extent of dehydration (sometimes due to insufficient information provided by parents who have telephoned the physician for advice)
  • Failure by parents/patients to understand instructions
  • Failure to schedule a follow-up visit
  • Failure to diagnose ingestion(s)
  • Failure to diagnose renal or acid-base abnormalities
  • Failure to exclude anatomical abnormalities (eg, obstruction, abdominal infections)

Special Concerns

  • Manage dehydration aggressively in patients who have sickle cell disease to prevent sequelae (eg, infarction, stroke, splenic sequestration). Administration of 1.5 times the normal rate of maintenance fluid infusion is a routine practice.

References

  1. Rotavirus surveillance--worldwide, 2001-2008. MMWR Morb Mortal Wkly Rep. Nov 21 2008;57(46):1255-7. [Medline][Full Text].

  2. AAP. Practice parameter: the management of acute gastroenteritis in young children. Pediatrics. Mar 1996;97(3):424-35. [Medline].

  3. Szajewska H, Hoekstra JH, Sandhu B. Management of acute gastroenteritis in Europe and the impact of the new recommendations: a multicenter study. The Working Group on acute diarrhea of the European Society for Paediatric Gastroenterology, Hepatology, and Nutrition. J Pediatr Gastroenterol Nutr. May 2000;30(5):522-7. [Medline].

  4. King CK, Glass R, Bresee JS, et al. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. Nov 21 2003;52(RR-16):1-16. [Medline].

  5. Amieva MR. Important bacterial gastrointestinal pathogens in children: a pathogenesis perspective. Pediatr Clin North Am. Jun 2005;52(3):749-77, vi. [Medline].

  6. CDC. Foodborne and Diarrheal Diseases Branch. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/foodborne/. Accessed April 24, 2006.

  7. CDC. Viral Gastroenteritis. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/ncidod/dvrd/revb/gastro/faq.htm. Accessed April 24, 2006.

  8. DeWitt TG, Humphrey KF, McCarthy P. Clinical predictors of acute bacterial diarrhea in young children. Pediatrics. Oct 1985;76(4):551-6. [Medline].

  9. DuPont HL. What's new in enteric infectious diseases at home and abroad. Curr Opin Infect Dis. Oct 2005;18(5):407-12. [Medline].

  10. Ericsson CD, DuPont HL. Rifaximin in the treatment of infectious diarrhea. Chemotherapy. 2005;51 Suppl 1:73-80. [Medline].

  11. Gastanaduy AS, Begue RE. Acute gastroenteritis. Clin Pediatr. Jan 1999;38(1):1-12. Review. [Medline].

  12. Gorelick MH, Shaw KN, Murphy KO. Validity and reliability of clinical signs in the diagnosis of dehydration in children. Pediatrics. May 1997;99(5):E6. [Medline][Full Text].

  13. Huicho L, Sanchez D, Contreras M, et al. Occult blood and fecal leukocytes as screening tests in childhood infectious diarrhea: an old problem revisited. Pediatr Infect Dis J. Jun 1993;12(6):474-7. [Medline].

  14. Jimenez SG, Heine RG, Ward PB, Robins-Browne RM. Campylobacter upsaliensis gastroenteritis in childhood. Pediatr Infect Dis J. Nov 1999;18(11):988-92. [Medline].

  15. Lasche J, Duggan C. Managing acute diarrhea: what every pediatrician needs to know. Contemp Pediatr. 1999;16(2):74-82.

  16. Liebelt EL. Clinical and laboratory evaluation and management of children with vomiting, diarrhea, and dehydration. Curr Opin Pediatr. Oct 1998;10(5):461-9. [Medline].

  17. Murphy MS. Guidelines for managing acute gastroenteritis based on a systematic review of published research. Arch Dis Child. Sep 1998;79(3):279-84. [Medline].

  18. Nataro JP. Treatment of bacterial enteritis. Pediatr Infect Dis J. May 1998;17(5):420-1. [Medline].

  19. Powell EC, Hampers LC. Physician variation in test ordering in the management of gastroenteritis in children. Arch Pediatr Adolesc Med. Oct 2003;157(10):978-83. [Medline].

  20. US Food and Drug Administration. Rotarix Product Information. FDA.gov. Available at http://www.fda.gov/cber/label/rotarixLB.pdf. Accessed 11/27/2008.

  21. US Food and Drug Administration. RotaTeq Product Information. FDA.gov. Available at http://www.fda.gov/cber/label/rotateqlb.pdf. Accessed 11/27/08.

Keywords

gastroenteritis, enterogastritis, viral diarrhea, prematurity, dehydration, Shigella, enterohemorrhagic Escherichia coli, electrolyte imbalance, hyponatremia, hypernatremia, hypernatremic dehydration, rotavirus, dehydrating diarrhea, Norwalk virus, enteric adenovirus, calicivirus, sickle cell disease, Giardia lamblia, Cryptosporidium parvum, Cyclospora cayetanesis, Entamoeba coli, Endolimax nana, Iodamoeba butschlii, Blastocystis hominis, HIV, AIDS, cytomegalovirus

Contributor Information and Disclosures

Author

Randy P Prescilla, MD, Instructor in Anesthesia, Harvard Medical School; Assistant in Perioperative Anesthesia, Children's Hospital Boston
Disclosure: Nothing to disclose.

Medical Editor

Ashir Kumar, MBBS, MD, FAAP, Professor, Department of Pediatrics and Human Development, College of Human Medicine, Michigan State University; Consulting Staff, Department of Pediatrics, EW Sparrow Hospital
Ashir Kumar, MBBS, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association of Physicians of Indian Origin, American Federation for Clinical Research, American Society for Microbiology, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Joseph Domachowske, MD, Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York-Upstate Medical University
Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Consulting; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching; sanofi pasteur Grant/research funds Unrestricted research grant; sanofi pasteur  Consulting; sanofi pasteur Honoraria Speaking and teaching; Tap Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association
Disclosure: None None None

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