Acute gastroenteritis in children

• Acute gastroenteritis in children is a sudden illness with diarrhoea and/or vomiting, usually from an infection picked up from stool, food or a contaminated surface.
• The illness itself is usually self-limited, but dehydration is the threat, especially under five and especially under six months of age.
• Most cases are viral (rotavirus, norovirus, adenovirus, astrovirus) or of unknown cause; bacterial causes are a minority, but they are the ones that usually explain blood in the stool.
• Treatment is supportive: give oral rehydration solution (ORS) early and in small amounts, keep feeding, add zinc, and escalate to intravenous fluid when shock, red flags or persistent vomiting appear.
• Red flags for something other than gastroenteritis include fever with specific age cut-offs, blood or mucus in stool, bilious vomit, severe or localised abdominal pain, altered consciousness, neck stiffness, non-blanching rash, and signs of shock or dehydration. ^[2]
• Rotavirus vaccination has transformed severe disease in infants; it is given by mouth in two or three doses before eight months of age, so every eligible infant should be offered it. ^[3]

By the end of this page you should be able to:

1. Define acute gastroenteritis in children and separate it from persistent, chronic and functional diarrhoea.
2. Recognise the common viral, bacterial and parasitic causes, and the clinical clues that point to each.
3. Assess dehydration using the WHO clinical categories, and identify children at high risk of it.
4. Choose the right rehydration route and volume, including oral, nasogastric and intravenous therapy, and explain why reduced-osmolarity ORS and zinc are used.
5. Apply the red-flag list to avoid missing surgical, neurological or systemic diagnoses.
6. Know when antibiotics help in childhood gastroenteritis and when they are withheld, including the special case of Shiga-toxin-producing E. coli.
7. Outline the schedule, efficacy, contraindications and precautions of the two rotavirus vaccines licensed in most English-speaking countries.

Gastroenteritis describes inflammation of the stomach and intestines; in practice the term is used for the syndrome even when the intestine is not biopsied. Diarrhoea, in the WHO definition, is the passage of three or more loose or liquid stools per day, or more frequent stools than the child's own normal pattern. ^[1] Vomiting alone without abnormal stools, for example in a viral upper airway infection, is not gastroenteritis.

Classification of diarrhoea by duration guides both cause and management. ^[5] Acute watery or acute bloody diarrhoea lasts fewer than seven days. Prolonged diarrhoea lasts seven to thirteen days. Persistent diarrhoea lasts fourteen to twenty-nine days and is a forerunner of malnutrition. Chronic diarrhoea lasts thirty days or more and raises questions of non-infectious causes such as coeliac disease, inflammatory bowel disease or carbohydrate intolerance. In children, the acute form is what this page is about.

Two further distinctions matter for assessment. Watery diarrhoea suggests a secretory or proximal small-bowel process, with many large stools and little fever or blood. Dysentery means frequent small stools, mucus and blood, fever and tenesmus, indicating colonic inflammation. Toxin-mediated food poisoning is very abrupt, often within hours of a meal, with vomiting dominant and the organism never replicating in the gut.

Diarrhoeal disease is the third leading cause of death in children aged one to fifty-nine months worldwide; it is both preventable and treatable. ^[1] Each year diarrhoea kills around 443,832 children under five and a further 50,851 children aged five to nine, and there are nearly 1.7 billion cases of childhood diarrhoeal disease every year. ^[1] Children who are malnourished or have impaired immunity, including children living with HIV, are at the greatest risk of life-threatening illness, and diarrhoea is itself a leading cause of malnutrition in children under five. ^{[1] [2]}

The cause mix changes with age and with where the child lives. In high-resource settings norovirus has become the dominant cause of medically attended acute gastroenteritis, and nontyphoidal Salmonella the leading bacterial one; rotavirus dominated before vaccine introduction. In low-resource settings the common agents include enterotoxigenic, enteropathogenic and enteroaggregative E. coli, Shigella, typhoidal and nontyphoidal Salmonella, Campylobacter, Vibrio cholerae, Entamoeba histolytica, Giardia, Blastocystis, Cyclospora, Cystoisospora and Cryptosporidium. ^{[1] [5]} Among children under five, the most common viral pathogens are rotavirus, norovirus, adenovirus and astrovirus. ^{[1] [3] [4]}

Rotavirus shows how epidemiology and vaccination interact. Before vaccine introduction roughly 2.7 million rotavirus infections occurred every year in the United States, ninety-five percent of children had been infected by five years of age, and the infection caused 410,000 physician visits, more than 200,000 emergency department visits, 55,000 to 70,000 hospitalisations and 20 to 60 deaths annually. ^[3] In the pre-vaccine era the proportion of severe diarrhoea in children under five that was due to rotavirus was similar (about 35 to 40 percent) in developed and developing countries, showing that clean water and sanitation alone cannot prevent infection. ^[3] Worldwide, before the vaccine, rotavirus was responsible for up to 500,000 diarrheal deaths a year. ^{[3] [4]}

Viruses cause most acute gastroenteritis. They infect enterocytes of the small intestine, producing watery diarrhoea with vomiting, and they are highly transmissible by the faecal-oral route, on hands and surfaces, and through aerosols after vomiting.

Rotavirus is a double-stranded RNA virus (family Reoviridae) with VP7 (G) and VP4 (P) outer proteins that define serotype and induce neutralising antibody. ^[3] The incubation period is short, usually less than 48 hours. ^[3] Illness ranges from asymptomatic to severe dehydrating diarrhoea with fever and vomiting; up to one-third of infected children have a temperature over 39 degrees Celsius. ^[3] Symptoms usually resolve in three to seven days. ^[3] The first infection after three months of age is the most severe; infants under three months are partly protected by maternal antibody and breastfeeding. ^[3] Rotavirus is resistant to environmental inactivation and may remain viable for weeks or months if not disinfected. ^[3] Children who are immunocompromised may have more severe or persistent disease. ^{[3] [4]}

Norovirus is a very contagious virus and the leading cause of vomiting and diarrhoea, and of foodborne illness, in the United States. ^[4] It causes acute gastroenteritis (an inflammation of the stomach or intestines). ^[4] Symptoms appear 12 to 48 hours after exposure. ^[4] Diarrhoea, vomiting, nausea and stomach pain are the most common features, with fever, headache and body aches also seen. ^[4] Most people get better in one to three days, but the virus can still be spread for two weeks or more after recovery. ^[4] There are many norovirus types, so infection does not give lasting protection. ^[4] Raw or undercooked shellfish, especially oysters, are a common vehicle. ^[4] There is no specific drug; antibiotics do not work against norovirus. ^[4]

Adenovirus (types 40 and 41) and astrovirus cause milder, longer watery diarrhoea, especially in winter, and are common in young children. They share the same supportive management.

Bacteria cause a smaller share of childhood gastroenteritis, but they are the organisms that usually require a change in management. They are worth knowing in three groups: those that invade the bowel and cause dysentery (Shigella, Salmonella, Campylobacter, Yersinia, enteroinvasive E. coli), those that secrete enterotoxins without invasion (Vibrio cholerae, enterotoxigenic E. coli), and those that cause haemorrhagic colitis and the haemolytic uraemic syndrome (Shiga-toxin-producing E. coli, STEC). A practical rule is that bacterial infection is likelier when the stool contains blood or mucus, or when fever and systemic signs are prominent. ^[5]

The infectious diarrhoea topic for adults and children covers the organisms, their sources and their clinching investigations in detail. In brief:

• Salmonella (nontyphoidal) is linked to eggs, poultry, reptiles and pets; it causes fever and abdominal pain, and hospitalisation or bacteraemia risk rises in infants, immunocompromised children, malnourished children and those with haemoglobinopathy. ^[5]
• Shigella passes with a very low inoculum person to person; it produces fever, tenesmus and frequent small bloody stools. Seizures in children are recognised, often with fever or electrolyte disturbance. ^[5]
• Campylobacter is a common cause of bloody diarrhoea in resource-rich settings and is linked to undercooked poultry. It is the commonest antecedent of Guillain-Barre syndrome. ^[5]
• Yersinia enterocolitica causes fever and diarrhoea followed by right-lower-quadrant pain from mesenteric adenitis that can mimic appendicitis, and it is dangerous in iron overload or liver disease. ^[5]
• STEC (including E. coli O157:H7) produces haemorrhagic colitis with little or no fever after undercooked beef, raw milk, sprouts or farm contact. Antibiotics and antimotility drugs are deliberately avoided, because antibacterial therapy may increase the risk of the haemolytic uraemic syndrome. ^[5]
• Vibrio cholerae causes massive isotonic "rice-water" diarrhoea with rapid dehydration; it is afebrile and waterborne. ^[5]
• Clostridioides difficile causes antibiotic-associated diarrhoea and pseudomembranous colitis.

Very short incubation food poisoning is toxin, not infection: Staphylococcus aureus enterotoxin within 30 minutes to eight hours; Bacillus cereus in emetic or diarrhoeal forms; and Clostridium perfringens 6 to 24 hours after reheated meat. ^[5] These illnesses settle on their own and do not benefit from antibiotics.

Parasites more often cause persistent than acute diarrhoea. Cryptosporidium, Giardia, Entamoeba histolytica, Cyclospora and Cystoisospora should be considered in persistent, travel-related or immunocompromised presentations. ^[5] Low inocula and easy secondary transmission characterise the viral and certain bacterial and parasitic agents, which is why hand hygiene and exclusion from childcare matter. ^[5]

A pathogen has to survive stomach acid, colonise the small bowel or colon, and then cause diarrhoea by one of two broad mechanisms (or both).

Secretory diarrhoea. The enterocyte secretes chloride and water faster than it absorbs them. Rotavirus and norovirus damage mature small-bowel villous tips and reduce absorption, while cholera toxin and enterotoxigenic E. coli (heat-labile and heat-stable toxins) lock adenylyl cyclase activation in place, producing large-volume isotonic losses. The result is frequent watery stools without blood, with the danger lying in volume loss and electrolyte depletion, including potassium and bicarbonate loss leading to metabolic acidosis.

Inflammatory or invasive diarrhoea. The organism crosses or disrupts the mucosa of the distal ileum or colon, producing a dysentery syndrome: fever, tenesmus, small frequent stools with mucus and blood. Mucosal invasion releases interleukins and recruits neutrophils, which is why stool microscopy may show leukocytes and why antibiotics change the course in specific cases.

Toxin-forming disease. Shiga toxin from STEC and from Shigella dysenteriae serotype 1 enters the circulation and damages endothelium, producing the haemolytic uraemic syndrome: microangiopathic haemolysis, thrombocytopenia and acute kidney injury. ^[5] Antibacterial therapy may increase Shiga-toxin release, which is why it is deliberately withheld in these infections. ^[5]

Rotavirus also shows why "benign but dehydrating" is the right phrase: it replicates in the small-bowel villous epithelium, damages absorptive surface, activates the enteric nervous system, and its non-structural NSP4 protein has enterotoxin-like effects. ^[3] The clinical result is vomiting early, then watery diarrhoea from day two, with the highest dehydration risk in children aged three to thirty-five months. ^[3]

The diagnosis usually rests on the story. Useful questions are:

• onset and duration, whether the stool is loose and how many in twenty-four hours;
• whether there is vomiting and when it started;
• the colour (whether there is blood, mucus or black stool), the volume and whether water is all the child can pass;
• fever and its height;
• urine output, whether tears are present, lethargy, thirst, and any unresponsiveness;
• oral intake, last feed, whether fluids were tried, and medicines already given;
• sick contacts, childcare or school, recent travel, food eaten, swimming, animal or farm contact, recent antibiotics, and birth and growth history.

NICE gives the typical course: diarrhoea usually lasts five to seven days and in most children stops within two weeks; vomiting usually lasts one to two days and stops in most within three days. ^[2] Parents need not rush to a doctor for a child who remains playful and hydrated.

Compare what is usual with the red flags that suggest a diagnosis other than gastroenteritis. ^[2]

Start with general appearance. A dehydrated child looks irritable then lethargic, with sunken eyes, a dry mouth, absent tears, and cold, mottled extremities; a well child is alert and playful. Count pulses and capillary refill, check body temperature, heart rate and respiration, inspect the abdomen, and establish recent weight if available.

The WHO/primary-care classification of dehydration in children rests on clinical signs and is the one used in both resource-rich and resource-poor settings. ^[1]

The full severe category requires at least two of its signs, including a skin pinch that returns very slowly (at least two seconds), inability to drink or drink poorly, lethargy or unconsciousness, or sunken eyes. ^[1]

NICE identifies risk factors for dehydration beyond the clinical assessment: ^[2]

• age younger than one year (especially younger than six months);
• low birth weight;
• more than five diarrhoeal stools in the previous twenty-four hours; ^[2]
• vomiting more than twice in the previous twenty-four hours; ^[2]
• inability to tolerate fluids before presentation;
• stopping breastfeeding during the illness;
• signs of malnutrition.

A small baby who vomits and passes loose stools can lose weight fast because body water makes up a large proportion of body mass and the margin for error is small. That is why early ORS at home matters most in this group.

The main differential lies between gastroenteritis and the conditions in the red-flag table, particularly intussusception in an infant, appendicitis in an older child, diabetic ketoacidosis, and sepsis. Enteritis from Yersinia can mimic appendicitis from right-lower-quadrant pain and fever. ^[5]

Within gastroenteritis itself, the pattern of stool and fever gives clues.

The great majority of children with acute watery diarrhoea who are otherwise well need no tests; the illness is self-limited and investigation does not change treatment. ^[5] Testing is considered when there are blood or mucus in the stool, fever, severe or dehydration-prone illness, very young or older age, hospital or antibiotic exposure, travel, immunocompromise, outbreak potential, or symptoms lasting more than a few days. ^[5]

When indicated:

• Selective stool culture as the default for many laboratories, covering Salmonella, Shigella, Campylobacter and E. coli O157 or Shiga-toxin producers; tell the laboratory if Yersinia, Vibrio or special pathogens are suspected, because media differ. ^[5]
• Shiga-toxin testing (immunoassay or PCR) to detect non-O157 STEC; monitor haemoglobin, platelets, urea and creatinine once STEC is diagnosed, because HUS can appear days later, with a peripheral smear for fragmented red cells if HUS is suspected. ^[5]
• Multiplex PCR panels detect many viral, bacterial and parasitic targets simultaneously. A positive nucleic-acid test detects DNA or RNA, not necessarily living organisms, so interpret in clinical context. ^[5]
• Blood cultures in infants under three months, in sepsis or suspected enteric fever, and with systemic manifestations, immunocompromise or travel exposure. ^[5]
• C. difficile testing only in people over two years with antibiotic or healthcare association, or in relevant travellers. ^[5]
• Parasite tests (ova and parasites, including Cryptosporidium, Cyclospora and Cystoisospora when specifically requested) in persistent diarrhoea of fourteen days or more, travel, or immunocompromise. ^[5]
• Metabolic panel (electrolytes, urea, creatinine) and blood count in dehydrated or unwell children.
• Rotavirus antigen or PCR in stool is available but, in settings with high vaccination coverage, use it thoughtfully because the positive predictive value falls when disease is rare. ^[3]

For the purposes of clinical management, the diagnosis of acute gastroenteritis is clinical: sudden change in stool consistency to loose or watery, with or without vomiting, and without another explanation. ^[2] No laboratory test is required in uncomplicated cases. Severity classification exists for two purposes: grading dehydration (as in the table above) and deciding who needs investigating for other causes.

• No dehydration or some dehydration: oral management.
• Severe dehydration or shock: intravenous or nasogastric rescue. ^[2]
• Severity of the episode in research settings is graded by composite scores such as the Vesikari score, used mainly in vaccine and research settings rather than in everyday practice. ^[3]

For parent-facing safety, parents should know the expected course and when to seek help: diarrhoea for five to seven days up to two weeks and vomiting for one to two days up to three. ^[2]

The management algorithm below collects the principles. The single most useful phrase is "rehydrate, feed, add zinc, watch for red flags."

Assess before treating. Check the hydration category, the red flags, and the risk factors. Remote assessment is acceptable only with a reliable safety net; children with shock, an alternative serious diagnosis, high risk of dehydration, clinical dehydration, or unreliable social circumstances need face-to-face care. ^[2]

Rehydration comes first. The most important therapy is replacing water and electrolytes.

• No clinical dehydration and no increased risk: continue usual feeds including breast or other milk feeds, encourage the child to drink, and discourage fruit juice and carbonated drinks. ^[2]
• No dehydration but increased risk (under one year, low birth weight, over five stools or over two vomits in twenty-four hours, inadequate intake before presentation, stopped breastfeeding, or malnutrition): as above, plus oral rehydration solution as supplemental fluid. ^[2]
• Clinical dehydration: low-osmolarity ORS solution (240 to 250 mOsm per litre) for oral rehydration therapy; give 50 ml per kilogram for fluid deficit replacement over four hours, in addition to maintenance fluid; give it frequently and in small amounts; and consider giving it via nasogastric tube if the child cannot drink or vomits persistently. ^[2] Continue breast or milk feeds where tolerated, and discourage fruit juices and carbonated drinks in children at risk. ^[2]
• Shock: rapid intravenous infusion of 10 ml per kilogram of 0.9 percent sodium chloride solution, repeated if there is inadequate response, with reassessment. ^[2] The bolus volume was changed from 20 ml per kilogram to 10 ml per kilogram in the 2022 exceptional surveillance update. ^[2] Switch back to ORS as soon as the child can drink. ^[2]
• After rehydration: continue or restart usual feeds, and give 5 ml per kilogram of ORS after each large watery stool in children at high risk of recurrence. ^[2]

Reduced-osmolarity ORS (240 to 250 mOsm per litre) is recommended as first-line therapy for mild to moderate dehydration of any cause, because the low osmolarity reduces stool volume and vomiting. ^{[5] [2]} WHO also supports its use in children with acute watery diarrhoea and dehydration. ^[7]

Feeding continues. From NICE: continue breastfeeding and other milk feeds; after rehydration, encourage normal eating and drinking. Early feeding shortens the illness. The old practice of starving a child until diarrhoea stops has no place in modern care. ^[2]

Zinc is the one nutrient that shortens the episode. WHO recommends adjunctive oral zinc for children with acute watery diarrhoea and with persistent diarrhoea. ^[7] The dose is 10 mg daily (half a dispersible tablet) for children under six months, and 20 mg daily (one tablet) for older children, for ten to fourteen days. ^{[6] [1]} Zinc cuts episode duration by 25 percent, reduces stool volume by 30 percent and can shorten subsequent episodes, and it is given between meals with the dose repeated if the child vomits within thirty minutes. ^{[6] [1]} It is a core part of treatment in resource-challenged settings, where deficiency is common. ^{[1] [6]}

Where guidelines differ on zinc. A more recent WHO guideline changes the dose, on the grounds of vomiting and tolerability: in children with acute watery or persistent diarrhoea it suggests a 5 mg daily dose for up to fourteen days, noting more vomiting at 20 mg and comparable diarrhoeal outcomes, and duodenal formulations showing less vomiting. ^{[7] [6]} The older 10 and 20 mg regimen therefore still stands where local formularies stock it and supply it; the important message is to give zinc for ten to fourteen days at whatever standard the infant or child will tolerate. ^{[6] [7]}

Antibiotics. NICE and WHO agree on the general rule: do not routinely give antibiotics to children with gastroenteritis. ^{[2] [7]} Antibiotics are reserved for: ^{[2] [5]}

• suspected or confirmed septicaemia or extra-intestinal spread of infection; ^[2]
• children under six months with Salmonella gastroenteritis; ^[2]
• children who are malnourished or immunocompromised with Salmonella gastroenteritis; ^[2]
• Clostridioides difficile pseudomembranous enterocolitis, giardiasis, dysenteric shigellosis, dysenteric amoebiasis or cholera; ^[2]
• bloody diarrhoea with systemic illness or dehydration, where management includes selected investigations and empiric therapy guided by local microbial susceptibility. ^[5]

Empiric regimens differ by organism and by age; NICE and WHO stress that any antibiotic is guided by local susceptibility, the clinical picture and the culture result rather than by a single drug class. ^{[2] [7]}

Equally important are the deliberate avoidances:

• Do not give antibiotics in STEC infection, especially O157:H7 or any strain producing Shiga toxin 2 (or an unknown toxin genotype), because antibacterial therapy may increase the risk of HUS. Monitoring and hydration matter more than drugs. ^[5]
• Do not use antimotility agents (loperamide) in children under eighteen. Loperamide may be used in immunocompetent adults with acute watery diarrhoea but must be avoided at any age in inflammatory or febrile diarrhoea and in suspected or proven pseudomembranous colitis. ^[5]

Dysentery and invasive disease need precise treatment. Shigella usually warrants an antimicrobial chosen by local susceptibility; typhoid and paratyphoid need culture-guided therapy; Campylobacter is treated when severe, bloody or in a high-risk patient; and cholera receives an antimicrobial as an adjunct to, never in place of, rehydration. ^[5]

• ORS by nasogastric tube. Use when vomiting persists or intake remains poor despite repeated small oral volumes. ^[2]
• Hypernatraemic dehydration. Still use oral rehydration therapy with low-osmolarity ORS; do not switch to free water faster than the gut can handle, and monitor carefully. ^[2]
• Persistent vomiting of ORS. Admit or extend observation; intravenous fluid becomes necessary. ^[2]

Few children with infective gastroenteritis need surgery, but red flags (bilious vomiting, severe localised abdominal pain, ileus, an abdominal mass) demand exclusion of intussusception and obstruction. Suspected or confirmed septicaemia, extra-intestinal spread, or a child who is unwell despite fluids all need hospital care. ^[2]

Advise parents and carers on the expected course and the safety net: seek reassessment if the child is getting more unwell, responsiveness changes (irritability or lethargy), urine output falls, skin becomes pale or mottled, or symptoms are not resolved within the expected window. ^[2] Resume full diet, extra fluids and normal activities as the child improves. School or childcare exclusion should last until at least 48 hours after the last episode of diarrhoea or vomiting, and swimming avoidance until two weeks after the last episode. ^[2] Family handwashing with soap in warm running water, not sharing towels, and not preparing food while symptomatic are the main transmission controls. ^[2]

• Dehydration and shock, the commonest serious complication, especially under one year.
• Electrolyte imbalance and acidosis from secretory diarrhoea; hypokalaemia and metabolic acidosis are both common in severe rotavirus disease. ^[3]
• Severe dehydration leading to organ hypoperfusion if treatment is delayed.
• Haemolytic uraemic syndrome in STEC infection and Shigella dysenteriae serotype 1: microangiopathic haemolysis, thrombocytopenia, and acute kidney injury. About 10 percent of laboratory-confirmed STEC patients who develop HUS do not have bloody diarrhoea, and frequent haemoglobin, platelet, urea and creatinine monitoring after diagnosis is essential. ^[5]
• Guillain-Barre syndrome after Campylobacter. ^[5]
• Reactive arthritis after Salmonella, Shigella, Campylobacter and Yersinia. ^[5]
• Post-infectious irritable bowel syndrome. ^[5]
• Malnutrition and growth faltering after persistent diarrhoea. ^[1]
• Rotavirus complications include metabolic acidosis and severe dehydration; treatment is supportive with continued feeding. ^[3] Immunocompromised children can develop multi-organ involvement. ^[3]
• Norovirus dehydration is a risk in the very young, older adults and immunocompromised people. ^[4]

Prognosis is excellent in otherwise healthy children once dehydration is corrected. Most children recover fully within one to two weeks. Death and long-term morbidity arise overwhelmingly from dehydration in children under five, from malnutrition and from invasive disease in immunocompromised children. ^[1] Children who survive dysentery usually recover completely; acute kidney injury from HUS carries a different prognosis and is managed by a nephrology team.

Rotavirus vaccination is the standout preventive measure for severe childhood gastroenteritis. Two oral vaccines are licensed for infants in the United States and widely used elsewhere. ^{[3] [1]}

• RotaTeq (RV5) is a bovine-human reassortant vaccine given in three doses at two, four and six months of age. ^[3]
• Rotarix (RV1) is a live attenuated human rotavirus vaccine given in two doses at two and four months of age. ^[3]
• The first dose may be started as early as six weeks; the first dose must not be started at fifteen weeks or older in routine use; the maximum age for any dose is eight months and zero days; and the minimum interval between doses is four weeks. ^[3]
• In large clinical trials RotaTeq gave 98 percent protection against severe rotavirus gastroenteritis and 74 percent protection against gastroenteritis of any severity, and reduced emergency department visits by 94 percent and hospitalisation by 96 percent through the first two years. ^[3]
• Rotarix showed 85 percent protection against severe rotavirus gastroenteritis to 1 year in a Latin American trial and 96 percent protection through the first rotavirus season in a European trial, and a 96 percent reduction in hospitalisation for rotavirus gastroenteritis through the second season. ^[3]
• Both vaccines protect 74 to 87 percent against any rotavirus gastroenteritis and 85 to 98 percent against severe disease; a meta-analysis through 2017 found 84 and 83 percent effectiveness respectively against emergency department visit or hospitalisation. ^[3]
• Protection has been shown through the first two to three years of life in high-income settings and is lower in the second year in low-income settings. ^[3]

Both vaccines are given by placing drops in the infant's mouth; they should not be injected. ^[3] Contraindications and precautions matter: ^[3]

• severe (anaphylactic) allergy to a component of the vaccine, or a severe reaction to a previous dose;
• a history of intussusception;
• severe combined immunodeficiency (SCID);
• the Rotarix applicator contains latex, so infants with severe latex allergy should receive RotaTeq instead; ^[3]
• defer vaccination in infants with moderate or severe acute illness including gastroenteritis until recovery, although infants living in immunocompromised or pregnant households are vaccinated on the routine schedule; ^[3]
• preterm infants may be vaccinated if at least six weeks of chronological age, clinically stable, and vaccinated at or after discharge from the neonatal unit. ^[3]

Post-licensure surveillance in high- and middle-income countries detected an increased risk of intussusception: about one extra case per 20,000 to 100,000 vaccinated infants, mainly within the first week (extending up to 21 days after the first dose) following the first or second dose. Parents and clinicians should be aware of this rare risk so that possible intussusception is evaluated promptly. ^[3]

Other prevention rests on all the practical measures in the parent-facing section: exclusive breastfeeding for the first six months, handwashing, safe water, food safety (cooking shellfish, separating raw and cooked foods), rotavirus vaccination, and clean reporting of notifiable disease such as Salmonella, STEC O157, Shigella and Listeria. ^{[1] [5]}

There is no vaccine against norovirus in routine use. ^[4]

• Children under six months and under three months in particular are at high risk. Any Salmonella gastroenteritis under six months is an antibiotic indication, and blood cultures are taken in infants under three months. ^{[2] [5]}
• Malnourished children need refeeding as well as rehydration and are more likely to need antibiotics when Salmonella is involved. ^{[1] [2]}
• Immunocompromised children have a wider differential, including Cryptosporidium, Cyclospora, Cystoisospora, and may have prolonged or severe rotavirus or norovirus disease; see the low-resource and immunocompromise sections of the infectious diarrhoea topic. ^{[3] [5]}
• Children with known or suspected immune deficiency need specialist consultation before rotavirus vaccination. ^[3]
• Children with chronic gastrointestinal conditions (for example Hirschsprung disease or short-gut syndrome) are not contraindicated from rotavirus vaccination and should benefit from it. ^[3]

Low-resource guidance is drawn most directly from WHO and from the dehydration guidance. ^{[1] [2]}

• Identify dehydration by ability to drink, skin pinch and sunken eyes.
• Rehydrate with reduced-osmolarity ORS made up from a standard packet in one litre of safe water; give small frequent amounts; intravenous therapy only for severe dehydration or shock. ^{[1] [2]}
• Continue feeding and breastfeeding during and after rehydration. ^[2]
• Give zinc for 10 to 14 days (10 mg under six months, 20 mg thereafter). ^{[1] [6]}
• Promote exclusive breastfeeding for the first six months and rotavirus vaccination. ^[1]
• Handwashing, safe water and sanitation reduce the annual burden that in low-income countries reaches about three episodes a year in children under three. ^[1]
• Report bloody diarrhoea and give antibiotics when appropriate, including dysentery and cholera.
• Cholera outbreaks need rapid volume replacement. ^[5]
• Refer early if a cardiac or surgical diagnosis (intussusception, appendicitis) is possible and local surgical capacity is not available.

• Acute gastroenteritis is a sudden syndrome of loose or watery stools and/or vomiting; diarrhoea of fewer than seven days is acute, fourteen to twenty-nine days is persistent, and thirty days or more is chronic. ^[5]
• Most illness is viral and self-limited; dehydration is the real danger, especially under one year. ^{[1] [2]}
• NICE red flags (specific fever cut-offs by age, blood or mucus in stool, bilious vomit, severe localised abdominal pain, altered consciousness, neck stiffness, non-blanching rash, dehydration) keep serious diagnoses from being missed. ^[2]
• Reduced-osmolarity ORS (240 to 250 mOsm per litre) is first-line for clinical dehydration, at 50 ml per kilogram over four hours plus maintenance fluids, with intravenous 0.9 percent saline 10 ml per kilogram rapidly for shock. ^{[2] [5]}
• Zinc works: it reduces episode duration by 25 percent and stool volume by 30 percent, given for 10 to 14 days. ^[1]
• Breastfeeding and other feeds should continue throughout; starving a child has no place in management. ^[2]
• NICE calls for exclusion from school or childcare until 48 hours after the last symptom, and from swimming pools for two weeks. ^[2]
• Antibiotics are withheld in most cases, and are specifically avoided in STEC because of HUS risk. ^{[2] [5]}
• Antimotility drugs are not used in children under eighteen. ^[5]
• Rotavirus vaccination (two-dose Rotarix or three-dose RotaTeq, by mouth, before eight months) prevents most severe rotavirus disease and hospitalisation, with a small risk of intussusception in the week after dosing. ^[3]
• Norovirus has no vaccine; handwashing and exclusion are the main controls. ^[4]
• Cross-check the gastroenterology page on infectious diarrhoea and foodborne illness for the adult and organism-by-organism detail; dehydration and paediatric fluids is closely related.

Infectious diarrhoea and foodborne illness; dehydration and paediatric fluids; enteric fever and typhoid; cholera; Shigella infection; rotavirus immunisation; infant feeding; acute abdomen in children; intussusception.