Medscape is available in 5 Language Editions – Choose your Edition here.



  • Author: Stefano Guandalini, MD; Chief Editor: Carmen Cuffari, MD  more...
Updated: Aug 19, 2015

Practice Essentials

Diarrhea is the reversal of the normal net absorptive status of water and electrolyte absorption to secretion. The augmented water content in the stools (above the normal value of approximately 10 mL/kg/d in the infant and young child, or 200 g/d in the teenager and adult) is due to an imbalance in the physiology of the small and large intestinal processes involved in the absorption of ions, organic substrates, and thus water.

Essential update: Children with diarrhea may benefit from green tea and pomegranate extract

Research conducted in a community clinic in Nicaragua demonstrates that green tea and pomegranate extract combined with a standard oral rehydration solution help children with diarrhea improve faster.[1]

The study involved 61 children, 2 to 17 years of age, who had uncontrolled diarrhea in the previous 48 hours. All patients received an oral rehydration solution for 2 days. In addition, 30 patients received the extract on day 1. The remaining 31 children, serving as the control group, received the extract on day 2. Researchers observed patients in the first 24 hours and rated their bowel movements on the Bristol Stool Scale (BSS).

Results showed the average time to achieve a BSS score of 4 or less was significantly shorter in the extract group than in the control group (3.1 vs 9.2 hours; P = .002).

In addition, a BSS score of 4 or less in the first bowel movement after treatment was achieved by more patients in the extract group than the control group (60% vs 29%). BSS scores in the extract group were maintained on day 2.[1]

Signs and symptoms

Acute diarrhea is defined as the abrupt onset of 3 or more loose stools per day and lasts no longer than 14 days; chronic or persistent diarrhea is defined as an episode that lasts longer than 14 days. The distinction has implications not only for classification and epidemiologic studies but also from a practical standpoint, because protracted diarrhea often has different etiologies, poses different management problems, and has a different prognosis.

The clinical presentation and course of diarrhea therefore depend on its cause and on the host. Consider the following to determine the source/cause of the patient’s diarrhea:

  • Stool characteristics (eg, consistency, color, volume, frequency)
  • Presence of associated enteric symptoms (eg, nausea/vomiting, fever, abdominal pain)
  • Use of child daycare (common pathogens: rotavirus, astrovirus, calicivirus; Campylobacter, Shigella, Giardia, and Cryptosporidium species [spp])
  • Food ingestion history (eg, raw/contaminated foods, food poisoning)
  • Water exposure (eg, swimming pools, marine environment)
  • Camping history (possible exposure to contaminated water sources)
  • Travel history (common pathogens affect specific regions; also consider rotavirus and Shigella, Salmonella, and Campylobacter spp regardless of specific travel history, as these organisms are prevalent worldwide)
  • Animal exposure (eg, young dogs/cats: Campylobacter spp; turtles: Salmonella spp)
  • Predisposing conditions (eg, hospitalization, antibiotic use, immunocompromised state)

Signs and symptoms of diarrhea may include the following:

  • Dehydration: Lethargy, depressed consciousness, sunken anterior fontanel, dry mucous membranes, sunken eyes, lack of tears, poor skin turgor, delayed capillary refill
  • Failure to thrive and malnutrition: Reduced muscle/fat mass or peripheral edema
  • Abdominal pain/cramping
  • Borborygmi
  • Perianal erythema

See Clinical Presentation for more detail.


Fecal laboratory studies include the following:

  • Examination for ova and parasites
  • Leukocyte count
  • pH level: A pH level of 5.5 or less or the presence of reducing substances indicates carbohydrate intolerance, which is usually secondary to viral illness
  • Examination of exudates for presence/absence of leukocytes
  • Cultures: Always culture for Salmonella, Shigella, and Campylobacter spp and Y enterocolitica in the presence of clinical signs of colitis or if fecal leukocytes are present; look for Clostridium difficile in those with diarrhea characterized by colitis and/or bloody stools; assess for Escherichia coli, particularly O157:H7, with bloody diarrhea and a history of eating ground beef; screen for Vibrio and Plesiomonas spp with a history of eating raw seafood or foreign travel
  • Enzyme immunoassay for rotavirus or adenovirus antigens
  • Latex agglutination assay for rotavirus

Other laboratory studies may include the following:

  • Serum albumin levels: Low in protein-losing enteropathies from enteroinvasive intestinal infections (eg, Salmonella spp, enteroinvasive E coli)
  • Fecal alpha1-antitrypsin levels: High in enteroinvasive intestinal infections
  • Anion gap to determine nature of the diarrhea (ie, osmolar vs secretory)
  • Intestinal biopsy: May be indicated in the presence of chronic or protracted diarrhea, as well as in cases in which a search for a cause is believed to be mandatory (eg, in patients with acquired immunodeficiency syndrome [AIDS] or patients who are otherwise severely immunocompromised)

See Workup for more detail.


Acute-onset diarrhea is usually self-limited; however, an acute infection can have a protracted course. Management is generally supportive: In most cases, the best option for treatment of acute-onset diarrhea is the early use of oral rehydration therapy (ORT).[2]


Vaccines (eg, rotavirus) can help increase resistance to infection. Antimicrobial and antiparasitic agents may be used to treat diarrhea caused by specific organisms and/or clinical circumstances. Such medications include the following:

  • Cefixime
  • Ceftriaxone
  • Cefotaxime
  • Erythromycin
  • Furazolidone
  • Iodoquinol
  • Metronidazole
  • Paromomycin
  • Quinacrine
  • Sulfamethoxazole and trimethoprim
  • Vancomycin
  • Tetracycline
  • Nitazoxanide
  • Rifaximin

See Treatment and Medication for more detail.



Acute diarrhea is defined as the abrupt onset of 3 or more loose stools per day. The augmented water content in the stools (above the normal value of approximately 10 mL/kg/d in the infant and young child, or 200 g/d in the teenager and adult) is due to an imbalance in the physiology of the small and large intestinal processes involved in the absorption of ions, organic substrates, and thus water. A common disorder in its acute form, diarrhea has many causes and may be mild to severe.

Childhood acute diarrhea is usually caused by infection of the small and/or large intestine; however, numerous disorders may result in diarrhea, including a malabsorption syndrome and various enteropathies. Acute-onset diarrhea is usually self-limited; however, an acute infection can have a protracted course. By far, the most common complication of acute diarrhea is dehydration.

Although the term "acute gastroenteritis" is commonly used synonymously with "acute diarrhea," the former term is a misnomer. The term gastroenteritis implies inflammation of both the stomach and the small intestine, whereas, in reality, gastric involvement is rarely if ever seen in acute diarrhea (including diarrhea with an infectious origin); in addition, enteritis is also not consistently present. Examples of infectious acute diarrhea syndromes that do not cause enteritis include Vibrio cholerae– induced diarrhea and Shigella -induced diarrhea. Thus, the term acute diarrhea is preferable to acute gastroenteritis.

Diarrheal episodes are classically distinguished into acute and chronic (or persistent) based on their duration. Acute diarrhea is thus defined as an episode that has an acute onset and lasts no longer than 14 days; chronic or persistent diarrhea is defined as an episode that lasts longer than 14 days. The distinction, supported by the World Health Organization (WHO), has implications not only for classification and epidemiological studies but also from a practical standpoint because protracted diarrhea often has a different set of causes, poses different problems of management, and has a different prognosis.



Diarrhea is the reversal of the normal net absorptive status of water and electrolyte absorption to secretion. Such a derangement can be the result of either an osmotic force that acts in the lumen to drive water into the gut or the result of an active secre­tory state induced in the enterocytes. In the former case, diarrhea is osmolar in nature, as is observed after the ingestion of nonabsorbable sugars such as lactulose or lactose in lactose malabsorbers. Instead, in the typical active secretory state, enhanced anion secretion (mostly by the crypt cell compartment) is best exemplified by enterotoxin-­induced diarrhea.

In osmotic diarrhea, stool output is proportional to the intake of the unabsorbable substrate and is usually not massive; diarrheal stools promptly regress with discontinuation of the offending nutrient, and the stool ion gap is high, exceeding 100 mOsm/kg. In fact, the fecal osmolality in this circumstance is accounted for not only by the electrolytes but also by the unabsorbed nutrient(s) and their degradation products. The ion gap is obtained by subtracting the concentration of the elec­trolytes from total osmolality (assumed to be 290 mOsm/kg), according to the formula: ion gap = 290 – [(Na + K) × 2].

In secretory diarrhea, the epithelial cells’ ion transport processes are turned into a state of active secretion. The most common cause of acute-onset secretory diarrhea is a bacterial infection of the gut. Several mechanisms may be at work. After colonization, enteric pathogens may adhere to or invade the epithelium; they may produce enterotoxins (exotoxins that elicit secretion by increasing an intracellular second messenger) or cytotoxins. They may also trigger release of cytokines attracting inflammatory cells, which, in turn, contribute to the acti­vated secretion by inducing the release of agents such as prostaglandins or platelet-activating factor. Features of secretory diarrhea include a high purg­ing rate, a lack of response to fasting, and a normal stool ion gap (ie, 100 mOsm/kg or less), indicating that nutrient absorption is intact.



United States

In the United States, one estimate before the introduction of specific antirotavirus immunization in 2006 assumed a cumulative incidence of 1 hospitalization for diarrhea per 23-27 children by age 5 years, with more than 50,000 hospitalizations. By these estimates, rotavirus was associated with 4-5% of all childhood hospitalizations and a cost of nearly $ 1 billion.[3] Furthermore, acute diarrhea is responsible for 20% of physician referrals in children younger than 2 years and for 10% in children younger than 3 years.

The impact of vaccination on rotavirus morbidity has been remarkable, with significant reduction of diarrhea-associated hospitalizations and visits to emergency departments in children in the years 2007-2008 compared with the prevaccine period.[4]


In developing countries, an average of 3 episodes per child per year in children younger than 5 years is reported; however, some areas report 6-8 episodes per year per child. In these settings, malnutrition is an important additional risk factor for diarrhea, and recurrent episodes of diarrhea lead to growth faltering and substantially increased mortality.[5] Childhood mortality associated with diarrhea has constantly but slowly declined during the past 2 decades, mostly because of the widespread use of oral rehydration solutions; however, it appears to have plateaued over the past several years.

Because the single most common cause of infectious diarrhea worldwide is rotavirus, and because a vaccine has been in use for over 3 years now, a reduction in the overall frequency of diarrheal episodes is hoped for in the near future.



Mortality from acute diarrhea is overall globally declining but remains high. Most estimates have diarrhea as the second cause of childhood mortality, with 18% of the 10.6 million yearly deaths in children younger than age 5 years.

Despite a progressive reduction in global diarrheal disease mortality over the past 2 decades, diarrhea morbidity in published reports from 1990-2000 slightly increased worldwide compared with previous reports. In the United States, an average of 369 diarrhea-associated deaths/year occurred among children aged 1-59 months during 1992-1998 and 2005-2006.[6] The vast majority of diarrhea-associated infant deaths were reported in 2005-2007, with 86% of deaths occurring among low-birthweight (< 2500 g) infants.[7]

Furthermore, in countries in which the toll of diarrhea is highest, poverty also adds an enormous additional burden, and long-term consequences of the vicious cycle of enteric infections, diarrhea, and malnutrition are devastating.[5]


Most cases of infectious diarrhea are not sex specific. Females have a higher incidence of Campylobacter species infections and hemolytic uremic syndrome (HUS).


Viral diarrhea is most common in young children. Rotavirus and adenovirus are particularly prevalent in children younger than 2 years. Astrovirus and norovirus usually infect children younger than 5 years. Yersinia enterocolitis typically infects children younger than 1 year, and the Aeromonas organism is a significant cause of diarrhea in young children.

Very young children are particularly susceptible to secondary dehydration and secondary nutrient malabsorption. Age and nutritional status appear to be the most important host factors in determining the severity and the duration of diarrhea. In fact, the younger the child, the higher is the risk for severe, life-threatening dehydration as a result of the high body-water turnover and limited renal compensatory capacity of very young children. Whether younger age also means a risk of run­ning a prolonged course is an unsettled issue. In developing countries, persis­tent postenteritis diarrhea has a strong inverse correlation with age.

Contributor Information and Disclosures

Stefano Guandalini, MD Founder and Medical Director, Celiac Disease Center, Chief, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, University of Chicago Medical Center; Professor, Department of Pediatrics, Section of Gastroenterology, Hepatology and Nutrition, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

Stefano Guandalini, MD is a member of the following medical societies: American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, European Society for Paediatric Gastroenterology, Hepatology & Nutrition, North American Society for the Study of Celiac Disease

Disclosure: Received consulting fee from AbbVie for consulting.


Richard E Frye, MD, PhD Associate Professor, Department of Pediatrics, University of Arkansas for Medical Sciences

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

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.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Carmen Cuffari, MD Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine

Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, Royal College of Physicians and Surgeons of Canada

Disclosure: Received honoraria from Prometheus Laboratories for speaking and teaching; Received honoraria from Abbott Nutritionals for speaking and teaching.

Additional Contributors

Chris A Liacouras, MD Director of Pediatric Endoscopy, Division of Gastroenterology and Nutrition, Children's Hospital of Philadelphia; Associate Professor of Pediatrics, University of Pennsylvania School of Medicine

Chris A Liacouras, MD is a member of the following medical societies: American Gastroenterological Association

Disclosure: Nothing to disclose.

  1. Kling J. Green Tea and Pomegranate Extract Help Fight Diarrhea in Children. Medscape Medical News. Available at Accessed: October 24, 2014.

  2. King CK, Glass R, Bresee JS, Duggan C. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003 Nov 21. 52:1-16. [Medline].

  3. Fischer TK, Viboud C, Parashar U, Malek M, Steiner C, Glass R, et al. Hospitalizations and deaths from diarrhea and rotavirus among children 111111111J Infect Dis</i>. 2007 Apr 15. 195(8):1117-25. [Medline].

  4. Cortese MM, Tate JE, Simonsen L, Edelman L, Parashar UD. Reduction in gastroenteritis in United States children and correlation with early rotavirus vaccine uptake from national medical claims databases. Pediatr Infect Dis J. 2010 Jun. 29(6):489-94. [Medline].

  5. Talbert A, Thuo N, Karisa J, Chesaro C, Ohuma E, Ignas J, et al. Diarrhoea complicating severe acute malnutrition in kenyan children: a prospective descriptive study of risk factors and outcome. PLoS One. 2012. 7(6):e38321. [Medline]. [Full Text].

  6. Esposito DH, Holman RC, Haberling DL, Tate JE, Podewils LJ, Glass RI, et al. Baseline estimates of diarrhea-associated mortality among United States children before rotavirus vaccine introduction. Pediatr Infect Dis J. 2011 Nov. 30(11):942-7. [Medline].

  7. Mehal JM, Esposito DH, Holman RC, Tate JE, Sinden LL, Parashar UD. Risk Factors for Diarrhea-Associated Infant Mortality in the United States, 2005-2007. Pediatr Infect Dis J. 2012 Mar 9. [Medline].

  8. Vernacchio L, Vezina RM, Mitchell AA, Lesko SM, Plaut AG, Acheson DW. Diarrhea in American infants and young children in the community setting: incidence, clinical presentation and microbiology. Pediatr Infect Dis J. 2006 Jan. 25(1):2-7. [Medline].

  9. Guarino A, Albano F, Ashkenazi S, et al. European Society for Paediatric Gastroenterology, Hepatology, and Nutrition/European Society for Paediatric Infectious Diseases evidence-based guidelines for the management of acute gastroenteritis in children in Europe: executive summary. J Pediatr Gastroenterol Nutr. 2008 May. 46(5):619-21. [Medline].

  10. [Guideline] Atia AN, Buchman AL. Oral rehydration solutions in non-cholera diarrhea: a review. Am J Gastroenterol. 2009 Oct. 104(10):2596-604; quiz 2605. [Medline].

  11. Guandalini S. Probiotics for prevention and treatment of diarrhea. J Clin Gastroenterol. 2011 Nov. 45 Suppl:S149-53. [Medline].

  12. Ruiz-Palacios GM, Perez-Schael I, Velazquez FR, et al. Safety and efficacy of an attenuated vaccine against severe rotavirus gastroenteritis. N Engl J Med. 2006 Jan 5. 354(1):11-22. [Medline]. [Full Text].

  13. Soares-Weiser K, MacLehose H, Bergman H, Ben-Aharon I, Nagpal S, Goldberg E, et al. Vaccines for preventing rotavirus diarrhoea: vaccines in use. Cochrane Database of Systematic Reviews. 2012.

  14. Platts-Mills JA, Babji S, Bodhidatta L, et al. Pathogen-specific burdens of community diarrhoea in developing countries: a multisite birth cohort study (MAL-ED). Lancet Glob Health. 2015 Sep. 3 (9):e564-75. [Medline].

  15. Abubakar I, Aliyu SH, Arumugam C, Usman NK, Hunter PR. Treatment of cryptosporidiosis in immunocompromised individuals: systematic review and meta-analysis. Br J Clin Pharmacol. 2007 Apr. 63(4):387-93. [Medline].

  16. Barclay L. Zinc supplements reduce diarrhea in children. Medscape Medical News. May 15, 2014. [Full Text].

  17. Bellemare S, Hartling L, Wiebe N, et al. Oral rehydration versus intravenous therapy for treating dehydration due to gastroenteritis in children: a meta-analysis of randomised controlled trials. BMC Med. 2004 Apr 15. 2:11. [Medline]. [Full Text].

  18. Bryce J, Boschi-Pinto C, Shibuya K, Black RE,. WHO estimates of the causes of death in children. Lancet. 2005 Mar 26-Apr 1. 365(9465):1147-52. [Medline].

  19. Charles MD, Holman RC, Curns AT, et al. Hospitalizations associated with rotavirus gastroenteritis in the United States, 1993-2002. Pediatr Infect Dis J. 2006 Jun. 25(6):489-93. [Medline].

  20. Coffin SE, Elser J, Marchant C, et al. Impact of acute rotavirus gastroenteritis on pediatric outpatient practices in the United States. Pediatr Infect Dis J. 2006 Jul. 25(7):584-9. [Medline].

  21. Girard MP, Steele D, Chaignat CL, Kieny MP. A review of vaccine research and development: human enteric infections. Vaccine. 2006 Apr 5. 24(15):2732-50. [Medline].

  22. Guandalini S. Treatment of acute diarrhea in the new millennium. J Pediatr Gastroenterol Nutr. 2000 May. 30(5):486-9. [Medline].

  23. Guandalini S, Dincer AP. Nutritional management in diarrhoeal disease. Baillieres Clin Gastroenterol. 1998 Dec. 12(4):697-717. [Medline].

  24. Guandalini S, Kahn S. Acute diarrhea. Walker A, Goulet O, Kleinman J, et al eds. Pediatric Gastrointestinal Disease. Ontario, Canada: Brian C. Decker; 2008. Vol 1: 252-64/Chapter 15.

  25. Matson DO, Staat MA, Azimi P, Itzler R, Bernstein DI, Ward RL, et al. Burden of rotavirus hospitalisations in young children in three paediatric hospitals in the United States determined by active surveillance compared to standard indirect methods. J Paediatr Child Health. 2012 Apr 25. [Medline].

  26. Mayo-Wilson E, Junior JA, Imdad A, Dean S, Chan XH, Chan ES, et al. Zinc supplementation for preventing mortality, morbidity, and growth failure in children aged 6 months to 12 years of age. Cochrane Database Syst Rev. 2014 May 15. 5:CD009384. [Medline].

  27. Miller RC, Petereit DG, Sloan JA, et al. A phase III randomized study of sulfasalazine versus placebo in the prevention of acute diarrhea in patients receiving pelvic radiation therapy [abstract LBA2]. Presented at American Society for Radiation Oncology (ASTRO) 55th Annual Meeting; September 22, 2013; Atlanta, Georgia.

  28. Mulcahy N. Recommended drug may cause diarrhea with radiation. October 3, 2013. Medscape Medical News. Available at Accessed: October 7, 2013.

  29. Sandhu BK, Isolauri E, Walker-Smith JA, et al. A multicentre study on behalf of the European Society of Paediatric Gastroenterology and Nutrition Working Group on Acute Diarrhoea. Early feeding in childhood gastroenteritis. J Pediatr Gastroenterol Nutr. 1997 May. 24(5):522-7. [Medline].

  30. Sullivan PB. Nutritional management of acute diarrhea. Nutrition. 1998 Oct. 14(10):758-62. [Medline].

  31. [Guideline] Walker-Smith JA, Sandhu BK, Isolauri E, et al. Guidelines prepared by the ESPGAN Working Group on Acute Diarrhoea. Recommendations for feeding in childhood gastroenteritis. European Society of Pediatric Gastroenterology and Nutrition. J Pediatr Gastroenterol Nutr. 1997 May. 24(5):619-20. [Medline].

Table 1. Stool Characteristics and Determining Their Source
Stool Characteristics Small Bowel Large Bowel
Appearance Watery Mucoid and/or bloody
Volume Large Small
Frequency Increased Highly increased
Blood Possibly positive but never gross blood Commonly grossly bloody
pH Possibly < 5.5 >5.5
Reducing substances Possibly positive Negative
WBCs < 5/high power field Commonly >10/high power field
Serum WBCs Normal Possible leukocytosis, bandemia
Organisms Viral
  • Rotavirus
  • Adenovirus
  • Calicivirus
  • Astrovirus
  • Norovirus
Invasive bacteria
  • Escherichia Coli (enteroinvasive, enterohemorrhagic)
  • Shigella species
  • Salmonella species
  • Campylobacter species
  • Yersinia species
  • Aeromonas species
  • Plesiomonas species
Enterotoxigenic bacteria
  • E coli
  • Klebsiella
  • Clostridium perfringens
  • Cholera species
  • Vibrio species
Toxic bacteria
  • Clostridium difficile
  • Giardia species
  • Cryptosporidium species
  • Entamoeba organisms
Table 2. Organisms and Frequency of Symptoms
Organism Incubation Duration Vomiting Fever Abdominal Pain
Rotavirus 1-7 d 4-8 d Yes Low No
Adenovirus 8-10 d 5-12 d Delayed Low No
Norovirus 1-2 d 2 d Yes No No
Astrovirus 1-2 d 4-8 d +/- +/- No
Calicivirus 1-4 d 4-8 d Yes +/- No
Aeromonas species None 0-2 wk +/- +/- No
Campylobacter species 2-4 d 5-7 d No Yes Yes
C difficile Variable Variable No Few Few
C perfringens Minimal 1 d Mild No Yes
Enterohemorrhagic E coli 1-8 d 3-6 d No +/- Yes
Enterotoxigenic E coli 1-3 d 3-5 d Yes Low Yes
Plesiomonas species None 0-2 wk +/- +/- +/-
Salmonella species 0-3 d 2-7 d Yes Yes Yes
Shigella species 0-2 d 2-5 d No High Yes
Vibrio species 0-1 d 5-7 d Yes No Yes
Y enterocolitica None 1-46 d Yes Yes Yes
Giardia species 2 wk 1+ wk No No Yes
Cryptosporidium species 5-21 d Months No Low Yes
Entamoeba species 5-7 d 1-2+ wk No Yes No
Table 3. Dehydration Severity, Signs, and Symptoms
Hydration 0-5% Dehydration


5-10% Dehydration


10% or More


General Well Restless Lethargic
Eyes Normal Sunken Very sunken
Tears Present Absent Absent
Mouth Moist Dry Very dry
Thirst Drinks normally Thirsty Drinks poorly
Skin Pinch retracts immediately Pinch retracts slowly Pinch stays folded
Table 4. Common Bacteria and Optimum Culture Mediums
Organism Detection Method Microbiologic Characteristics
Aeromonas species Blood agar Oxidase-positive flagellated gram-negative bacillus (GNB)
Campylobacter species Skirrow agar Rapidly motile curved gram-negative rod (GNR); Campylobacter jejuni 90% and Campylobacter coli 5% of infections
C difficile Cycloserine-cefoxitin-fructose-egg (CCFE) agar; enzyme immunoassay (EIA) for toxin; latex agglutination (LA) for protein Anaerobic spore-forming gram-positive rod (GPR); toxin-mediated diarrhea; produces pseudomembranous colitis
C perfringens None available Anaerobic spore-forming GPR; toxin-mediated diarrhea
E coli MacConkey eosin-methylene blue (EMB) or Sorbitol-MacConkey (SM) agar Lactose-producing GNR
Plesiomonas species Blood agar Oxidase-positive GNR
Salmonella species Blood, MacConkey EMB, xylose-lysine-deoxycholate (XLD), or Hektoen enteric (HE) agar Nonlactose non–H2S-producing GNR
Table 5. Probiotic Efficacy in Diarrhea
Condition Patients and Controls Most-Studied Probiotics Evidence of Efficacy

(- to +++)

Prevention of Daycare Diarrhea 2000 Lactobacillus GG

Bifidobacterium lactis

Lactobacillus reuteri

Lactobacillus casei

Bifidobacterium bifidum + Streptococcus thermophilus

Prevention of Nosocomial Diarrhea 1000 Lactobacillus GG ++
Prevention of Antibiotic-Associated Diarrhea 2000 Lactobacillus GG

Saccharomyces boulardii

Infectious Diarrhea 3500 Lactobacillus GG

Saccharomyces boulardii

Persistent Diarrhea 460 Lactobacillus GG +
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.