Acute Gastroenteritis

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Kliegman: Nelson Textbook of Pediatrics, 18th ed.
Copyright © 2007 Saunders, An Imprint of Elsevier Chapter 337 – Acute Gastroenteritis in Children Zulfiqar Ahmed Bhutta The term gastroenteritis denotes infections of the gastrointestinal tract caused by bacterial, viral, or parasitic pathogens (Tables 337-1 to 337-3 [1] [2] [3]). Many of these infections are food-borne illnesses. The most common manifestations are diarrhea and vomiting, which may also be associated with systemic features such as abdominal pain and fever. The term gastroenteritis captures the bulk of infectious cases of diarrhea. The term diarrheal disorders is more commonly used to denote infectious diarrhea in public health settings, although several noninfectious causes of gastrointestinal illness with vomiting and/or diarrhea are well recognized ( Table 337-4 ).

TABLE 337-1 -- Food-borne Illnesses (Bacterial) DURAT INCUBA ION OF ASSOCIA LABORAT ETIOLOG TION SIGNS AND ILLNES TED ORY TREATMEN Y PERIOD SYMPTOMS S FOODS TESTING T Bacillus anthracis 2 days to weeks Nausea, Weeks vomiting, malaise, bloody diarrhea, acute abdominal pain Insufficien Blood tly cooked contamina ted meat Penicillin is first choice for naturally acquired gastrointe stinal anthrax. Ciproflox acin is second option. Bacillus 1–6 hr cereus (preformed enterotoxin) Sudden onset of severe nausea and vomiting. Diarrhea may be present. 24 hr Improperl y refrigerate d cooked or fried rice, meats Normally a Supportive clinical care diagnosis. Clinical laboratories do not routinely identify this organism. If indicated, send stool


DURAT INCUBA ION OF ASSOCIA LABORAT TION SIGNS AND ILLNES TED ORY TREATMEN PERIOD SYMPTOMS S FOODS TESTING T and food specimens to reference laboratory for culture and toxin identificatio n.

Bacillus cereus (diarrheal toxin)

10–16 hours

Abdominal 24–48 hr cramps, watery diarrhea, nausea.

Meats, stews, gravies, vanilla sauce

Testing not Supportive necessary, care selflimiting (consider testing food and stool for toxin in outbreaks). Blood culture and positive serology Acute: Rifampin and doxycycline daily for ≥6 wk. Infections with complications require combination therapy with rifampin, tetracycline, and an aminoglycosid e. Supportive care. For severe cases, antibiotics such as erythromycin and quinolones may be indicated early in the diarrheal

Brucella abortus, B. melitensis, and B. suis

7–21 days Fever, chills, sweating, weakness, headache, muscle and joint pain, diarrhea, bloody stools during acute phase


Raw milk, goat cheese made from unpasteuri zed milk, contamina ted meats

Campylobac 2–5 days ter jejuni

Diarrhea, cramps, fever, and vomiting; diarrhea may be bloody.

2–10 days

Raw and undercook ed poultry, unpasturiz ed milk, contamina ted water

Routine stool culture; Campyloba cter requires special media and incubation at 42°C to grow.



Clostridium 12–72 hr botulinum— children and adults (preformed toxin)

Vomiting, diarrhea, blurred vision, diplopia, dysphagia, and descending muscle weakness

Variable (from days to months). Can be complic ated by respirato ry failure and death.

Homecanned foods with a low acid content, improperl y canned commerci al foods, homecanned or fermented fish, herbinfused oils, baked potatoes in aluminium foil, cheese sauce, bottled garlic, foods held warm for extended periods of time (e.g., in a warm oven)

Stool, serum, and food can be tested for toxin. Stool and food can also be cultured for the organism. These tests can be performed at some state health department laboratories and CDC.

Supportive care. Botulism antitoxin is helpful if given early in the course of the illness. Contact the state health department. The 24-hour number for state health departments to call is (700) 488–7100.

Clostridium 3–30 days In infants <12 botulinum— mo, lethargy, infants weakness, poor feeding, constipation, hypotonia, poor head control, poor gag and sucking reflex

Variable Honey, homecanned vegetables and fruits, corn syrup

Stool, serum, and food can be tested for toxin. Stool and food can also be cultured for the organism.

Supportive care. Botulism immune globulin can be obtained from the Infant Botulism Prevention Program,


DURAT INCUBA ION OF ASSOCIA LABORAT TION SIGNS AND ILLNES TED ORY TREATMEN PERIOD SYMPTOMS S FOODS TESTING T These tests can be performed at some state health department laboratories and CDC. Health and Human Services, California (510-5402646), Botulinum antitoxin is generally not recommended for infants. Supportive care. Antibiotics not indicated.

Clostridium perfringens toxin

8–16 hr

Watery diarrhea, nausea, abdominal cramps; fever is rare.

24–48 hr Meats, poultry, gravy, dried or precooked foods, timeand/or temperatur e-abused food

Stools can be tested for enterotoxin and cultured for organism. Because Clostridium perfringens can normally be found in stool, quantitative cultures must be done. Stool culture; E. coli O157 : H7 requires special media to grow. If E. coli O157 : H7 is suspected, specific testing must be requested. Shiga toxin

Enterohemor 1–8 days rhagic E. coli (EHEC) including E. coli O157 : H7 and other Shiga toxin– producing E. coli (STEC)

Severe 5–10 diarrhea that is days often bloody, abdominal pain and vomiting. Usually, little or no fever is present. More common in children <4 yr old.

Undercoo ked beef especially hamburger , unpasteuri zed milk and juice, raw fruits and vegetables (e.g., sprouts), salami (rarely),

Supportive care, monitor renal function, hemoglobin, and platelets closely. E. coli O157 : H7 infection is also associated with hemolytic uremic syndrome (HUS), which


DURAT INCUBA ION OF ASSOCIA LABORAT TION SIGNS AND ILLNES TED ORY TREATMEN PERIOD SYMPTOMS S FOODS TESTING T and testing may contamina be done ted water using commercial kits; positive isolates should be forwarded to public health laboratories for confirmatio n and serotyping. can cause lifelong complications. Studies indicate that antibiotics may promote the development of HUS.

Enterotoxige 1–3 days nic E. coli (ETEC)

Watery diarrhea, abdominal cramps, some vomiting

3 to >7 days

Water or food contamina ted with human feces

Stool culture. ETEC requires special laboratory techniques for identificatio n. If suspected, must request specific testing. Blood or cerebrospin al fluid cultures. Asymptom atic fecal carriage occurs; therefore, stool culture usually not helpful.

Supportive care. Antibiotics are rarely needed except in severe cases. Recommende d antibiotics include TMPSMX and quinolones.

Listeria 9–48 hr monocytoge for nes gastrointes tinal symptoms , 2–6 wk for invasive disease

Fever, muscle aches, and nausea or diarrhea. Pregnant women may have mild flulike illness, and infection can lead to premature delivery or stillbirth.

Variable Fresh soft cheeses, unpasteuri zed milk, inadequate ly pasteurize d milk, ready-toeat deli meats, hot dogs

Supportive care and antibiotics; Intravenous ampicillin, penicillin, or TMP-SMX are recommended for invasive disease.


DURAT INCUBA ION OF ASSOCIA LABORAT TION SIGNS AND ILLNES TED ORY TREATMEN PERIOD SYMPTOMS S FOODS TESTING T Elderly or immunocompr omised patients may have bacteremia or meningitis. At birth and infancy Infants infected from mother at risk for sepsis or meningitis. Diarrhea, 4–7 days fever, abdominal cramps, vomiting. S. typhi and S. paratyphi produce typhoid with insidious onset characterized by fever, headache, constipation, malaise, chills, and myalgia; diarrhea is uncommon, and vomiting is not usually severe. Contamin Routine ated eggs, stool poultry, cultures unpasteuri zed milk or juice, cheese, contamina ted raw fruits and vegetables (alfalfa sprouts, melons). S. typhi epidemics are often related to fecal contamina tion of water supplies or streetvended foods. Supportive care. Other than for S. typhi and S. paratyphi, antibiotics are not indicated unless there is extraintestinal spread, or the risk of extraintestinal spread, of the infection. Consider ampicillin, gentamicin, TMP-SMX, or quinolones if indicated. A vaccine exists for S. typhi. Antibody to listerolysin O may be helpful to identify outbreak retrospectiv ely.

Salmonella spp.

1–3 days

Shigella spp. 24–48 hr

Abdominal cramps, fever, and diarrhea. Stools may contain blood

4–7 days Food or Routine water stool contamina cultures ted with human

Supportive care. TMPSMX recommended in the U. S. if


DURAT INCUBA ION OF ASSOCIA LABORAT TION SIGNS AND ILLNES TED ORY TREATMEN PERIOD SYMPTOMS S FOODS TESTING T and mucus. fecal material. Usually person-toperson spread, fecal-oral transmissi on. Ready-toeat foods touched by infected food workers, e.g., raw vegetables , salads, sandwiche s. 24–48 hrs Unrefriger ated or improperl y refrigerate d meats, potato and egg salads, cream pastries. Contamin ated water, fish, shellfish, streetvended food typically from Latin America or Asia organism is susceptible; nalidixic acid or other quinolones may be indicated if organism is resistant, especially in developing countries.

Staphylococ 1–6 hr cus aureus (preformed enterotoxin)

Sudden onset of severe nausea and vomiting. Abdominal cramps. Diarrhea and fever may be present.

Normally a Supportive clinical care. diagnosis. Stool, vomitus, and food can be tested for toxin and cultured if indicated. Stool culture; Vibrio cholerae requires special media to grow. If V. cholerae is suspected, must request Supportive care with aggressive oral and intravenous rehydration. In cases of confirmed cholera, tetracycline or doxycycline is recommended

Vibrio cholerae (toxin)

24–72 hr

Profuse watery diarrhea and vomiting, which can lead to severe dehydration and death within hours

3–7 days. Causes lifethreateni ng dehydrat ion.


DURAT INCUBA ION OF ASSOCIA LABORAT TION SIGNS AND ILLNES TED ORY TREATMEN PERIOD SYMPTOMS S FOODS TESTING T specific testing. for adults, and TMP-SMX for children (<8 yr). Supportive care. Antibiotics are recommended in severe cases: tetracycline, doxycycline, gentamicin, and cefotaxime.

Vibrio 2–48 hr parahaemol yticus

Watery diarrhea, abdominal cramps, nausea, vomiting.

2–5 days Undercoo ked or raw seafood, such as fish, shellfish

Stool cultures. Vibrio parahaemol yticus requires special media to grow. If V. parahaemol yticus is suspected, must request specific testing. Stool, wound, or blood cultures. Vibrio vulnificus requires special media to grow. If V. vulnificus is suspected, must request specific testing.

Vibrio vulnificus

1–7 days

Vomiting, 2–8 days diarrhea, abdominal pain, bactermia, and wound infections. More common in the immunocompr omised, or in patients with chronic liver disease (presenting with bullous skin lesions). Can be fatal in patients with liver disease and the immunocompr omised. Appendicitis-

Undercoo ked or raw shellfish, especially oysters, other contamina ted seafood, and open wounds exposed to seawater

Supportive care and antibiotics; tetracycline, doxycycline, and ceftazidime are recommended .


24–48 hr

1–3 wk, Undercoo Stool,


ETIOLOG Y enterocolytic a and Y. pseudotuber culosis

DURAT INCUBA ION OF ASSOCIA LABORAT TION SIGNS AND ILLNES TED ORY TREATMEN PERIOD SYMPTOMS S FOODS TESTING T like symptoms usually (diarrhea and selfvomiting, limiting fever, and abdominal pain) occur primarily in older children and young adults. May have a scarlitiniform rash or erythema nodosum with Y. pseudotubercu losis. ked pork, unpasteuri zed milk, tofu, contamina ted water. Infection has occurred in infants whose caregivers handled chitterling s.

vomitus, or care. If blood septicemia or culture. other invasive Yersinia disease requires occurs, special antibiotic media to therapy with grow. If gentamicin or suspected, cefotaxime must (doxycycline request and specific ciprofloxacin testing. also Serology is effective). available in research and reference laboratories . From: Department of Health and Human Services, Centers for Disease Control and Prevention: Diagnosis and management of foodbourne illnesses. MMWR 2004:53:7–9. CDC, Centers for Disease Control and Prevention;TMP-SMX, trimethoprimsulfamethoxazole.

TABLE 337-2 -- Food-borne Illnesses (Viral) DURATI INCUBAT ON OF ASSOCIA LABORAT ETIOLO ION SIGNS AND ILLNES TED ORY TREATM GY PERIOD SYMPTOMS S FOODS TESTING ENT Hepatitis A 28 days average (15–50 days) Diarrhea, dark Variable, Shellfish urine, jaundice, 2 wk–3 harvested and flu-like mo from symptoms, i.e., contaminat fever, headache, ed waters, nausea, and raw abdominal pain produce, contaminat ed nated drinking water, Increase in ALT, billirubin. Positive IgM and anti– hepatitis A antibodies. Supportive care. Prevention with immunizati on.


DURATI ON OF ASSOCIA LABORAT ILLNES TED ORY TREATM S FOODS TESTING ENT uncooked foods and cooked foods that are not reheated after contact with infected food handler

Norovirus 12–48 hr es (and other caliciviru ses)

Nausea, 12–60 hr vomiting, abdominal cramping, diarrhea, fever, myalgia, and some headache. Diarrhea is more prevalent in adults and vomiting is more prevalent in children. Prolonged asymptomatic excretion possible. Vomiting, 4–8 days watery diarrhea, low-grade fever. Temporary lactose intolerance may occur. Infants and children, elderly, and immunocompro mised are especially vulnerable. Nausea, vomiting,

Shellfish, fecally contaminat ed foods, ready-toeat foods touched by infected food workers (salads, sandwiches , ice, cookies, fruit)

Routine RTPCR and EM on fresh unpreserved stool samples. Clinical diagnosis, negative bacterial cultures. Stool is negative for WBCs.

Supportive care such as rehydration . Good hygiene.

Rotavirus 1–3 days

Fecally contaminat ed foods. Ready-toeat foods touched by infected food workers (salads, fruits).

Identificatio n of virus in stool via immunoassa y

Supportive care. Severe diarrhea may require fluid and electrolyte replacemen t.

Other viral

10–70 hr

2–9 days Fecally Identificatio Supportive contaminat n of the virus care,

INCUBAT ETIOLO ION SIGNS AND GY PERIOD SYMPTOMS agents (astroviru ses, adenoviru ses, parvoviru ses) diarrhea, malaise, abdominal pain, headache, fever

DURATI ON OF ASSOCIA LABORAT ILLNES TED ORY TREATM S FOODS TESTING ENT ed foods. Ready-toeat foods touched by infected food workers. Some shellfish.

in early usually acute stool mild, selfsamples. limiting. Serology. Good Commercial hygiene. ELISA kits are now available for adenoviruses and astroviruses. From: Department of Health and Human Services, Centers for Disease Control and Prevention: Diagnosis and management of foodbourne illnesses. MMWR 2004:53:9. ALT, alanine aminotransferase; ELISA, enzyme linked immunoserbent assay; EM, electron microscopy; IgM, immunoglobulin M;RT-PCR, reverse transcriptose polymerase chain reaction; WBCs, white blood cells.

TABLE 337-3 -- Food-borne Illnesses (Parasitic) DURAT INCUBA ION OF ASSOCIA LABORAT ETIOLOG TION SIGNS AND ILLNES TED ORY TREATMEN Y PERIOD SYMPTOMS S FOODS TESTING T Angiostron 1 wk to ≥1 Severe gylus mo headaches, cantonensis nausea, vomiting, neck stiffness, paresthesias, hyperesthesias, seizures, and other neurologic abnormalities Several weeks to several months Raw or undercook ed intermedia te hosts (e.g., snails or slugs), infected paratenic (transport) hosts (e.g., crabs, freshwater shrimp), fresh produce contamina ted with Examinatio n of CSF for elevated pressure, protein, leukocytes, and eosinophils; serologic testing using ELISA to detect antibodies to Angiostron gylus cantonensis Supportive care. Repeat lumbar punctures and use of corticosteroid therapy may be used for more severely ill patients.



Cryptospor 2–10 days Diarrhea idium (usually watery), stomach cramps, upset stomach, slight fever

May be remitting and relapsing over weeks to months

Any uncooked food or food contamina ted by an ill food handler after cooking; drinking water Various types of fresh produce (imported berries, lettuce)

Request specific examinatio n of the stool for Cryptospori dium. May need to examine water or food.

Supportive care, selflimited. If severe consider paromomycin for 7 days. For children aged 1–11 yr, consider nitazoxanide for 3 days.

Cyclospora 1–14 days, Diarrhea cayetanensi usually at (usually s least 1 wk watery), loss of appetite, substantial loss of weight, stomach cramps, nausea, vomiting, fatigue Entamoeba 2–3 days Diarrhea histolytica to 1–4 wk (often bloody), frequent bowel movements, lower abdominal pain

May be remitting and relapsing over weeks to months

Request TMP-SMX for specific 7 days. examinatio n of the stool for Cyclospora. May need to examine water or food. Examinatio n of stool for cysts and parasites— may need at least 3 samples. Serology for longterm infections. Metronidazole and a luminal agent (iodoquinol or paromomycin)

May be protracte d (several weeks to several months)

Any uncooked food or food contamina ted by an ill food handler after cooking; drinking water Any uncooked food or food contamina

Giardia lamblia

1–2 wk

Diarrhea, stomach cramps, gas, weight loss

Days to weeks

Examinatio Metronidazole n of stool for ova and parasites— may need at


DURAT ION OF ASSOCIA LABORAT SIGNS AND ILLNES TED ORY TREATMEN SYMPTOMS S FOODS TESTING T ted by an ill food handler after cooking; drinking water. least 3 samples.

Toxoplasm 5–23 days Generally Months a gondii asymptomatic, 20% may develop cervical lymphadenopa thy and/or a flu-like illness. In immunocompr omised patients: central nervous system (CNS) disease, myocarditis, or pneumonitis is often seen.

Accidental ingestion of contamina ted substances (e.g., soil contamina ted with cat feces on fruits and vegetables ), raw or partly cooked meat (especially pork, lamb, or venison)

Isolation of parasites from blood or other body fluids; observation of parasites in patient specimens via microscopy or histology. Detection of organisms is rare; serology (reference laboratory needed) can be a useful adjunct in diagnosing toxoplasmo sis. However, IgM antibodies may persist for 6–18 mo and thus may not necessarily indicate recent infection. PCR of

Asymptomatic healthy, but infected, persons do not require treatment. Spiramycin or pyrimethamine plus sulfadiazine may be used for pregnant women. Pyrimethamine plus sulfadiazine may be used for immunocompr omised persons, in specific cases. Pyrimethamine plus sulfadiazine (with or without steroids) may be given for ocular disease when indicated. Folinic acid is given with pyrimethamine plus sulfadiazine to counteract


DURAT ION OF ASSOCIA LABORAT SIGNS AND ILLNES TED ORY TREATMEN SYMPTOMS S FOODS TESTING T bodily bone marrow fluids. For suppression. congenital infection: isolation of T. gondii from placenta, umbilical cord, or infant blood. PCR of white blood cells, CSF, or amniotic fluid, or IgM and IgA serology, performed by a reference laboratory.

Toxoplasm In infants a gondii at birth (congenital infection)

Treatment of Months the mother may reduce severity and/or incidence of congenital infection. Most infected infants have few symptoms at birth. Later, they will generally develop signs of congenital toxoplasmosis (mental retardation, severely impaired eyesight,

Passed from mother (who acquired acute infection during pregnancy ) to child


DURAT ION OF ASSOCIA LABORAT SIGNS AND ILLNES TED ORY TREATMEN SYMPTOMS S FOODS TESTING T cerebral palsy, seizures), unless the infection is treated

Acute:nausea, Months Raw or Positive Supportive diarrhea, undercook serology or care plus vomiting, ed demonstrati mebendazole fatigue, fever, contamina on of larvae or albendazole abdominal ted meat, via muscle discomfort usually biopsy. followed by pork or Increase in muscle wild game eosinophils. soreness, meat (e.g., weakness, and bear or occasional moose) cardiac and neurologic complications From: Department of Health and Human Services, Centers for Disease Control and Prevention: Diagnosis and management of foodbourne illnesses. MMWR 2004:53:9–10. CSF, cerebrospinal fluid; ELISA, enzyme linked immunoserbent assay; IgM, immunoglobulin M;PCR, polymerase chain reaction; TMP-SMX, trimethoprimsulfamethoxazole.

Trichinella 1–2 days spiralis for initial symptoms; others begin 2–8 wk after infection

TABLE 337-4 -- Food-borne Illnesses (Noninfectious) DURAT INCUBA ION OF ASSOCIA LABORAT ETIOLOG TION SIGNS AND ILLNES TED ORY TREATM Y PERIOD SYMPTOMS S FOODS TESTING ENT Antimony 5 min–8 Vomiting, metallic Usually hr usually taste self<1 hr limited Few hours Vomiting, colic, diarrhea Several days Metallic container Identificati Supportiv on of metal e care in beverage or food Gastric lavage, BAL (dimercap rol)


Contamin Urine. May ated food cause eosinophili a

INCUBA ETIOLOG TION SIGNS AND Y PERIOD SYMPTOMS Cadmium 5 min–8 Nausea, vomiting, hr usually myalgia, increase <1 hr in salivation, stomach pain

DURAT ION OF ASSOCIA LABORAT ILLNES TED ORY TREATM S FOODS TESTING ENT Usually selflimited Seafood, oysters, clams, lobster, grains, peanuts Identificati Supportiv on of metal e care in food

Ciguatera fish poisoning (ciguatera toxin)

2–6 hr

Gl:abdominal pain, Days to A variety nausea, vomiting, weeks to of large diarrhea months reef fish: grouper, red snapper, amberjack , and barracuda (most common) Neurologic:paresth esias, reversal of hot or cold, pain, weakness Cardiovascular:bra dycardia, hypotension, increase in T wave abnormalities Usually selflimited Metallic container

Radioassay for toxin in fish or a consistent history

Supportiv e care, IV mannitol. Children more vulnerable .

3 hr

2–5 days


5 min–8 Nausea, vomiting, hr usually blue or green <1 hr vomitus 1 wk or longer

Identificati Supportiv on of metal e care in beverage or food


Numbness, May be weakness of legs, protracte spastic paralysis, d impaired vision, blindness, coma. Pregnant women and the developing fetus are especially vulnerable. Vomiting, diarrhea, confusion, visual disturbance, Selflimited

Fish Analysis of Supportiv exposed to blood, hair e care organic mercury, grains treated with mercury fungicides Wild mushroom s (cooking may not Typical syndrome and mushroom Supportiv e care

Mushroom <2 hr toxins, short-acting (museinol,

INCUBA ETIOLOG TION SIGNS AND Y PERIOD SYMPTOMS muscarine, psilocybin, Coprius artemetaris, ibotenic acid) Mushroom toxins, longacting (amanitin) 4–8 hr diarrhea; 24–48 hr liver failure salivation, diaphoresis, hallucinations, disulfiram-like reaction, confusion, visual disturbance.

DURAT ION OF ASSOCIA LABORAT ILLNES TED ORY TREATM S FOODS TESTING ENT destroy these toxins) identified or demonstrati on of the toxin

Diarrhea, Often abdominal cramps, fatal leading to hepatic and renal failure

Mushroo ms

Typical syndrome and mushroom identified and/or demonstrati on of the toxin

Supportiv e care, lifethreatenin g, may need life support

Nitrite poisoning

1–2 hr

Nausea, vomiting, cyanosis, headache, dizziness, weakness, loss of consciousness, chocolate-brown colored blood

Usually selflimited

Cured Analysis of meats, any the food, contamina blood ted foods, spinach exposed to excessive nitrificatio n

Supportiv e care, methylene blue

Pesticides Few min (organophos to few phates or hours carbamates

Nausea, vomiting, Usually abdominal cramps, selfdiarrhea, headache, limited nervousness, blurred vision, twitching, convulsions, salivation and meiosis

Any Analysis of Atropine; contamina the food, 2-PAM ted food blood (Pralidoxi me) is used when atropine is not able to control symptoms and is rarely necessary in carbamate poisoning. Detection of tetrodotoxi n in fish Lifethreatenin g, may need

Puffer fish (tetrodotoxi n)

<30 min

Parasthesias, Death Puffer fish vomiting, diarrhea, usually abdominal pain, in 4–6 hr ascending

INCUBA ETIOLOG TION SIGNS AND Y PERIOD SYMPTOMS paralysis, respiratory failure Scombroid (histamine) 1 min–3 hr

DURAT ION OF ASSOCIA LABORAT ILLNES TED ORY TREATM S FOODS TESTING ENT respirator y support Fish:bluefi n, tuna, skipjack, mackerel, marlin, escolar, and mahi mahi Demonstrat ion of histamine in food or clinical diagnosis Supportiv e care, antihistam ines

Flushing, rash, 3–6 hr burning sensation of skin, mouth and throat, dizziness, urticaria, parasthesias

Shellfish toxins (diarrheic, neurotoxic, amnesic)

Diarrheic shellfish poisoning (DSP)— 30 min to 2 hr

Nausea, vomiting, diarrhea, and abdominal pain accompanied by chills, headache, and fever

Hours to A variety 2–3 days of shellfish, primarily mussels, oysters, scallops, and shellfish from the Florida coast and the Gulf of Mexico

Detection of the toxin in shellfish; highpressure liquid chromatogr aphy

Supportiv e care, generally selflimiting. Elderly are especially sensitive to ASP

Neurotoxi c shellfish poisoning (NSP)— few min to hours

Tingling and numbness of lips, tongue, and throat, muscular aches, dizziness, reversal of the sensations of hot and cold, diarrhea, and vomiting Vomiting, diarrhea, abdominal pain and neurologic problems such as confusion, memory loss, disorientation, seizure, coma Diarrhea, nausea, Days Scallops, Detection Life-

Amnesic shellfish poisoning (ASP)— 24–48 hr


30 min–3

INCUBA ETIOLOG TION SIGNS AND Y PERIOD SYMPTOMS toxins (paralytic shellfish poisoning) hr vomiting leading to parasthesias of mouth, lips, weakness, dysphasia, dysphonia, respiratory paralysis

DURAT ION OF ASSOCIA LABORAT ILLNES TED ORY TREATM S FOODS TESTING ENT mussels, clams, cockles of toxin in food or water where fish are located; highpressure liquid chromatogr aphy threatenin g, may need respirator y support

Sodium fluoride

Few min to 2 hr

Salty or soapy Usually taste, numbness of selfmouth, vomiting, limited diarrhea, dilated pupils, spasms, pallor, shock, collapse

Dry foods (e.g., dry milk, flour, baking powder, cake mixes) contamina ted with sodium fluoride– containing insecticide s and rodenticid es

Testing of Supportiv vomitus or e care gastric washings. Analysis of the food.


Few hours Nausea, vomiting, Several diarrhea, painful days parathesias, motor polyneuropathy, hair loss 5 min–8 Nausea, vomiting, hr usually diarrhea <1 hr Few min to 3 hr Usually selflimited

Contamin Urine, hair ated food

Supportiv e care


Metallic container Grains such as wheat, corn, barley Metallic container

Analysis of Supportiv the food e care Analysis of Supportiv the food e care


Nausea, headache, Usually abdominal pain, selfvomiting limited


Few hours Stomach cramps, Usually nausea, vomiting, selfdiarrhea, myalgias limited

Analysis of Supportiv the food, e care blood and



feces, saliva or urine From: Department of Health and Human Services, Centers for Disease Control and Prevention: Diagnosis and management of foodbourne illnesses. MMWR 2004:53:11–12.


Diarrheal disorders in childhood account for a large proportion (18%) of childhood deaths, with an estimated 1.8 million deaths per year globally. The World Health Organization (WHO) suspects that there are >700 million episodes of diarrhea annually in children <5 yr of age in developing countries. While global mortality may be declining, the overall incidence of diarrhea remains unchanged at about 3.2 episodes per child year ( Fig. 337-1 ). In the United States, there are ≈1.5 million outpatient visits for gastroenteritis, 200,000 hospitalizations, and 300 deaths annually.

Figure 337-1 Global trends in diarrhea incidence.

Globally, it was estimated in 1999 that Shigella infections may lead to 600,000 deaths per year of children <5 yr of age, or a quarter to a third of all diarrhea-related mortality in this age

group. Rates of hospitalization and deaths due to Shigella infections, especially S. dysenteriae type 1, the most severe form of shigellosis, may be declining; recent estimates are 160,000 deaths. Rotavirus infections (the most common identifiable viral cause of gastroenteritis in all children) account for at least 35% of severe and potentially fatal watery diarrhea episodes, with an estimated 500,000 deaths per year worldwide due to rotavirus infections. The decline in diarrheal mortality, despite the lack of significant changes in incidence, is the result of improved case management of diarrhea, as well as improved nutrition of infants and children. These interventions have included widespread home- and hospital-based oral rehydration therapy, as well as improved nutritional management of children with diarrhea. Persistently high rates of diarrhea among young children, despite intensive efforts at control, are of particular concern. There is very little information on the long-term consequences of diarrheal diseases, especially persistent or prolonged diarrhea and malnutrition. Diarrheal illnesses may have a significant impact on psychomotor and cognitive development in young children. Early and repeated episodes of childhood diarrhea during periods of critical development, especially when associated with malnutrition, co-infections, and anemia may have long-term effects on linear growth, as well as on physical and cognitive functions.

Gastroenteritis is due to infection acquired through the feco-oral route or by ingestion of contaminated food or water. Gastroenteritis is associated with poverty, poor environmental hygiene, and development indices. Enteropathogens that are infectious in a small inoculum (Shigella, Escherichia coli, noroviruses, rotavirus, Giardia lamblia, Cryptosporidium parvum, Entamoeba histolytica) can be transmitted by person-to-person contact, whereas others such as cholera are generally a consequence of contamination of food or water supply (see Tables 337-1 to 337-3 [1] [2] [3]). In the United States, rotavirus and the noroviruses (small round viruses such as Norwalk-like virus and caliciviruses) are the most common viral agents, followed by enteric adenoviruses and astroviruses (see Table 337-2 ). Food-borne outbreaks of diarrhea in the United States are most commonly due to Salmonella and Campylobacter species, followed much less often by Shigella, Cryptosporidium, E. coli 0157: H7, Yersinia, Listeria, Vibrio, and Cyclospora species, in that order. Salmonella, Shigella, and, most notably, the various diarrhea-producing E. coli organisms are the most common pathogens in developing countries (see Table 337-1 ). Clostridium difficile (by toxin production) is linked to antibiotic-associated diarrhea and pseudomembranous colitis, although most cases of antibiotic-associated diarrhea in children are not due to C. difficile. C. difficile negative antibiotic associated hemorrhagic colitis in adults may be due to cytotoxin-producing Klebsiella oxytoca. In developed countries, episodes of infectious diarrhea can occur through seasonal exposure to organisms such as rotavirus or exposure to pathogens in settings of close contact (e.g., daycare centers). Children in developing countries become infected with a diverse group of bacterial and parasitic pathogens, whereas all children in developed as well as developing countries acquire rotavirus and, in many cases, other viral enteropathogens as well as G. lamblia and C. parvum in their 1st 5 yr of life.

Pathogenesis and severity of bacterial disease depend on whether organisms have preformed toxins (Staphylococcus aureus, Bacillus cereus), produce toxins, or are invasive and on whether they replicate in food. Enteropathogens can lead to either an inflammatory or noninflammatory response in the intestinal mucosa. Enteropathogens elicit noninflammatory diarrhea through enterotoxin production by some bacteria, destruction of villus (surface) cells by viruses, adherence by parasites, and adherence and/or translocation by bacteria. Inflammatory diarrhea is usually caused by bacteria that directly invade the intestine or produce cytotoxins with consequent fluid, protein, and cells (erythrocytes, leukocytes) that enter the intestinal lumen. Some enteropathogens possess more than one virulence property. Some viruses, such as rotavirus, target the microvillous tips of the enterocytes and can enter the cells by either direct invasion or calcium-dependent endocytosis. This can result in villus shortening and loss of enterocyte absorptive surface through cell shortening and loss of microvilli ( Fig. 337-2 ).

Figure 337-2 Pathogenesis of rotavirus infection and diarrhea. ER, endoplasmic reticulum; TJ, tight junction. (Adapted from Ramig RF: Pathogenesis of intestinal and systemic rotavirus infection. J Virol 2004;78:10213–10220.)

Most bacterial pathogens elaborate enterotoxins; the rotavirus protein NSP4 acts as a viral enterotoxin. Bacterial enterotoxins can selectively activate enterocyte intracellular signal transduction, and can also affect cytoskeletal rearrangements with subsequent alterations in the water and electrolyte fluxes across enterocytes. Upregulation of these pathways results in inhibition of NaCl-coupled transport and increased efflux of chloride, resulting, in turn, in net secretion and loss of water into the intestinal lumen ( Fig. 337-3 ). Coupled transport of sodium to glucose and amino acids is largely unaffected. The nitric oxide pathway can also be involved, as endogenous nitric oxide production is significantly higher in infectious compared with noninfectious diarrhea.

Figure 337-3 Mechanism of cholera toxin. (Adapted from Thapar M, Sanderson IR: Diarrhoea in children: An interface between developing and developed countries. Lancet 2004;363:641–653; and Montes M, DuPont HL: Enteritis, enterocolitis and infectious diarrhea syndromes. In Cohen J, Powderly WG, Opal SM, et al [editors]: Infections Diseases, 2nd ed. London, Mosby, 2004, pp 31–52.)

Enterotoxigenic E. Coli (ETEC) colonizes and adheres to enterocytes of the small bowel via its surface fimbriae (pili) and induces hypersecretion of fluids and electrolytes into the small intestine through one of two toxins: the heat-labile enterotoxin (LT) or the heat-stable enterotoxin. LT is structurally similar to the Vibrio cholera toxin, and activates adenylate cyclase, resulting in an increase in intracellular cyclic guanosine monophosphate (cGMP) (see Fig. 337-3 ). In contrast, Shigella spp. cause gastroenteritis via a superficial invasion of colonic mucosa, which they invade through M cells located over Peyer patches. After phagocytosis, a series of events occurs, including apoptosis of macrophages, multiplication and spread of bacteria into adjacent cells, release of inflammatory mediators (interleukin [IL]1 and IL-8), transmigration of neutrophils into the lumen of the colon, neutrophil necrosis and degranulation, further breach of the epithelial barrier, and mucosal destruction ( Fig. 337-4 ).

Figure 337-4 Pathogenesis of Shigella infection and diarrhea. (Adapted from Opal SM, Keusch GT: Host responses to infection. In Cohen J, Powderly WG, Opal SM, et al [editors]: Infections Diseases, 2nd ed. London, Mosby, 2004, pp 31–52.)


Major risks include environmental contamination and increased exposure to enteropathogens. Additional risks include young age, immune deficiency, measles, malnutrition, and lack of exclusive or predominant breast-feeding. Malnutrition increases severalfold the risk of diarrhea and associated mortality. The fraction of such infectious diarrhea deaths that are attributable to nutritional deficiencies varies with the prevalence of deficiencies; the highest attributable fractions are in sub-Saharan Africa, south Asia, and Andean Latin America. The risks are particularly higher with micronutrient malnutrition; in children with vitamin A deficiency, the risk of dying from diarrhea, measles, and malaria is increased by 20–24%.

Zinc deficiency increases the risk of mortality from diarrhea, pneumonia, and malaria by 13– 21%. The majority of cases of diarrhea resolve within the 1st wk of the illness. A smaller proportion of diarrheal illnesses fail to resolve and persist for >2 wk. Persistent diarrhea is defined as episodes that began acutely but last for at least 14 days. Such episodes account for between 3% and 20% of all diarrheal episodes in children <5 yr of age and up to 50% of all diarrhearelated deaths. Many children (especially infants and toddlers) in developing countries have frequent episodes of acute diarrhea. Although few individual episodes persist beyond 14 days, frequent episodes of acute diarrhea can result in nutritional compromise and may predispose these children to develop persistent diarrhea, protein-calorie malnutrition, and secondary infections.

Most of the clinical manifestations and clinical syndromes of diarrhea are related to the infecting pathogen and the dose/inoculum (see Tables 337-1 to 337-3 [1] [2] [3]). Additional manifestations depend on the development of complications (such as dehydration and electrolyte imbalance) and the nature of the infecting pathogen (see Chapter 55.1 ). Usually the ingestion of preformed toxins (such as those of Staphylococcus aureus) is associated with the rapid onset of nausea and vomiting within 6 hr, with possible fever, abdominal cramps, and diarrhea within 8–72 hr. Watery diarrhea and abdominal cramps after an 8–16 hr incubation period are associated with enterotoxin-producing Clostridium perfringens and Bacillus cereus. Abdominal cramps and watery diarrhea after a 16–48 hr incubation period can be associated with noroviruses, several enterotoxin-producing bacteria, Cryptosporidium, and Cyclospora. Several organisms, including Salmonella, Shigella, Campylobacter jejuni, Yersinia enterocolitica, enteroinvasive E. coli, and Vibrio parahaemolyticus, produce diarrhea that can contain blood as well as fecal leukocytes in association with abdominal cramps, tenesmus, and fever; these features suggest bacterial dysentery and fever. Bloody diarrhea and abdominal cramps after a 72–120 hr incubation period are associated with infections due to Shigella and also Shiga toxin–producing E. coli, such as E. coli 0157 : H7. Organisms associated with dysentery or hemorrhagic diarrhea can also cause watery diarrhea alone without fever or that precedes a more complicated course that results in dysentery. Although many of the manifestations of acute gastroenteritis in children are nonspecific, some clinical features can help identify major categories of diarrhea and allow rapid triage for antibiotic or specific dietary therapy (see Tables 337-1 to 337-3 [1] [2] [3]). There is considerable overlap in the symptomatology. The positive predictive values for the features of dysentery are very poor; however, the negative predictability for bacterial pathogens is much better in the absence of signs of dysentery. If warranted and if facilities and resources permit, the etiology can be verified by appropriate laboratory testing.

Most of the complications associated with gastroenteritis are related to delays in diagnosis and delays in the institution of appropriate therapy. Without early and appropriate rehydration, many children with acute diarrhea would develop dehydration with associated complications (see Chapters 53 , 54 , 55 , and 68 ). These can be life-threatening in infants and young children. Inappropriate therapy can lead to prolongation of the diarrheal episodes, with consequent malnutrition and complications such as secondary infections and micronutrient

deficiencies (iron, zinc). In developing countries, associated bacteremias are well-recognized complications in malnourished children with diarrhea. Specific pathogens are associated with extra-intestinal manifestations and complications. These are not pathognomonic of the infection nor do they always occur in close temporal association with the diarrheal episode ( Table 337-5 ).

TABLE 337-5 -- Extraintestinal Manifestations of Enteric Infections ASSOCIATED ENTERIC MANIFESTATION PATHOGEN(S) ONSET AND PROGNOSIS Focal infections due to systemic spread of bacterial pathogens, including vulvovaginitis, urinary tract infection, endocarditis, osteomyelitis, meningitis, pneumonia, hepatitis, peritonitis, chorioamnionitis, soft tissue infection, and septic thrombophlebitis All major pathogens can cause such direct extraintestinal infections, including Salmonella, Onset usually during the acute infection, but may present subsequently. Prognosis depends on infection site.

Shigella, Yersinia, Campylobacter, Clostridium difficile Reactive arthritis Salmonella, Shigella, Yersinia, Campylobacter, Cryptosporidium, Clostridium difficile Campylobacter Typically occurs about 1–3 wk after infection. Relapses after reinfection may develop in 15– 50% of people but most children recover fully within 2–6 mo after the 1st symptoms appear. Usually occurs a few weeks after the original infection. Prognosis good although 15–20% may have sequelae. Can be of sudden onset in acute, referring to a sudden attack of inflammation, or chronic, which comes on gradually. In most cases, the kidneys heal with time. Characterized by recurrent episodes of blood in the urine, this condition results from deposits of the protein immunoglobulin A (IgA) in the glomeruli. IgA nephropathy can progress for years with no noticeable symptoms. Men seem

Guillain-Barré syndrome


Shigella, Campylobacter, Yersinia

IgA nephropathy




ONSET AND PROGNOSIS more likely to develop this disorder than are women.

Erythema nodosum

Yersinia, Campylobacter, Salmonella Shigella dysenteriae 1, Escherichia coli 0157: H7, others

Although painful, is usually benign and more commonly seen in adolescents. Resolves with 4– 6 weeks. Sudden onset, short-term renal failure. In severe cases, renal failure requires several sessions of dialysis to take over the kidney function, but most children recover without permanent damage to their health.

Hemolytic uremia syndrome

Campylobacter, Relatively rare complication and Yersinia may have a chronic course. From: Department of Health and Human Services, Centers for Disease Control and Prevention: Managing acute gastroenteritis among children. MMWR Recomm Rep 2004;53:1–33.

Hemolytic anemia


The diagnosis of gastroenteritis is based on clinical recognition, an evaluation of its severity by rapid assessment, and confirmation by appropriate laboratory investigations, if indicated.

The most common manifestation of gastrointestinal tract infection in children is diarrhea, abdominal cramps, and vomiting. Systemic manifestations are varied and associated with a variety of causes. The evaluation of a child with acute diarrhea includes: Assess the degree of dehydration and acidosis and provide rapid resuscitation and rehydration with oral or intravenous fluids as required ( Table 337-6 and Table 337-7 ). Obtain appropriate contact or exposure history. This includes information on exposure to contacts with similar symptoms, intake of contaminated foods or water, child-care center attendance, recent travel to a diarrhea-endemic area, and use of antimicrobial agents. Clinically determine the etiology of diarrhea for institution of prompt antibiotic therapy, if indicated. Although nausea and vomiting are nonspecific symptoms, they are indicative of infection in the upper intestine. Fever is suggestive of an inflammatory process but also occurs as a result of dehydration or co-infection

(e.g., urinary tract infection, otitis media). Fever is common in patients with inflammatory diarrhea. Severe abdominal pain and tenesmus are indicative of involvement of the large intestine and rectum. Features such as nausea and vomiting and absent or low-grade fever with mild to moderate periumbilical pain and watery diarrhea are indicative of small intestine involvement and also reduce the likelihood of a serious bacterial infection. This clinical approach to the diagnosis and management of diarrhea in young children is a critical component of the integrated management of childhood illness (IMCI) package that is being implemented in developing countries with high burden of diarrhea mortality ( Fig. 337-5 ).

TABLE 337-6 -- Symptoms Associated with Dehydration MILD TO MINIMAL OR NO MODERATE DEHYDRATION DEHYDRATION (3– (<3% LOSS OF BODY 9% LOSS OF BODY SYMPTOM WEIGHT) WEIGHT) Mental status Thirst Heart rate Well;alert Normal, fatigued or restless, irritable

SEVERE DEHYDRATION (>9% LOSS OF BODY WEIGHT) Apathetic, lethargic, unconscious Drinks poorly; unable to drink Tachycardia, with bradycardia in most severe cases Weak, thready, or impalpable Deep Deeply sunken Absent Parched Recoil in >2 sec Prolonged;minimal Cold;mottled;cyanotic

Drinks normally; might Thirsty;eager to drink refuse liquids Normal Normal to increased

Quality of pulses Breathing Eyes Tears Mouth and tongue Skinfold Capillary refill Extremities

Normal Normal Normal Present Moist Instant recoil Normal Warm

Normal to decreased Normal;fast Slightly sunken Decreased Dry Recoil in <2 sec Prolonged Cool

Urine output Normal to decreased Decreased Minimal From: Department of Health and Human Services, Centers for Disease Control and Prevention: Diagnosis and management of foodbourne illnesses. MMWR 2004:52;5. Sources: Adapted from Duggan C, Santosham M, Glass RI: The management of acute diarrhea in children: Oral rehydration, maintenance, and nutritional therapy.MMWR 1992;41 (No. RR-16):1–20;and World Health Organization: The treatment of diarrhoea: a manual for physicians and other senior health workers. Geneva, Switzerland: World Health Organization,

1995. Available at


TABLE 337-7 -- Summary of Treatment Based on Degree of Dehydration DEGREE OF REHYDRATION REPLACEMENT OF DEHYDRATION THERAPY LOSSES NUTRITION Minimal or no dehydration Not applicable <10 kg body weight: 60–120 mL oral rehydration solution (ORS) for each diarrheal stool or vomiting episode; >10 kg body weight: 120–240 mL ORS for each diarrheal stool or vomiting episode Continue breastfeeding, or resume age-appropriate normal diet after initial hydration, including adequate caloric intake for maintenance[*] Same

Mild to moderate dehydration Severe dehydration

ORS, 50–100 mL/kg body Same weight over 3–4 hr

Lactated Ringer solution Same;if unable to drink, Same or normal saline in 20 administer through mL/kg body weight nasogastric tube or intravenous amounts until administer 5% dextrose perfusion and mental ¼ normal saline with 20 status improve; then mEq/L potassium administer 100 mL/kg chloride intravenously body weight ORS over 4 hr or 5% dextrose ½ normal saline intravenously at twice maintenance fluid rates From: Department of Health and Human Services, Centers for Disease Control and Prevention: Diagnosis and management of foodbourne illnesses. MMWR 2004;52:1–33.
* Overly restricted diets should be avoided during acute diarrheal episodes. Breast-fed infants should continue to nurse ad libitum

even during acute rehydration. Infants too weak to eat can be given milk or formula through a nasogastric tube. Lactosecontaining formulas are usually well tolerated. If lactose malabsorption appears clinically substantial, lactose-free formulas can be used. Complex carbohydrates, fresh fruits, lean meats, yogurt, and vegetables are all recommended. Carbonated drinks or commercial juices with a high concentration of simple carbohydrates should be avoided.

Figure 337-5 Integrated management of the sick child (IMCI) protocol for the recognition and management of diarrhea in developing countries.


Microscopic examination of the stool and cultures can yield important information on the etiology of diarrhea. Stool specimens should be examined for mucus, blood, and leukocytes. Fecal leukocytes are indicative of bacterial invasion of colonic mucosa, although some patients with shigellosis have minimal leukocytes at an early stage of infection, as do patients infected with Shiga toxin–producing E. coli and E. histolytica. In endemic areas, stool microscopy must include examination for parasites causing diarrhea, such as G. lamblia and E. histolytica. Stool cultures should be obtained as early in the course of disease as possible from children with bloody diarrhea in whom stool microscopy indicates fecal leukocytes; in outbreaks with suspected hemolytic-uremic syndrome (HUS); and in immunosuppressed children with diarrhea. Stool specimens for culture need to be transported and plated quickly; if the latter is not quickly available, specimens may need to be transported in special media. The yield and diagnosis of bacterial diarrhea can be significantly improved by using molecular diagnostic procedures such as PCR. In most previously healthy children with uncomplicated watery diarrhea, no laboratory evaluation is needed except for epidemiologic purposes.

The broad principles of management of acute gastroenteritis in children include oral rehydration therapy, enteral feeding and diet selection, zinc supplementation, and additional therapies such as probiotics.

Children, especially infants, are more susceptible than adults to dehydration because of the greater basal fluid and electrolyte requirements per kg and because they are dependent on others to meet these demands. Dehydration must be evaluated rapidly and corrected in 4–6 hr

according to the degree of dehydration and estimated daily requirements. A small minority of children, especially those in shock or unable to tolerate oral fluids, require initial intravenous rehydration, but oral rehydration is the preferred mode of rehydration and replacement of ongoing losses ( Table 337-7 and Table 337-8 ). Risks associated with severe dehydration that may necessitate intravenous resuscitation include: age <6 mo, prematurity, chronic illness, fever >38°C if < 3 mo or >39°C if 3–36 mo, bloody diarrhea, persistent emesis, poor urine output, sunken eyes, and a depressed level of consciousness. Although, in general, the standard WHO oral rehydration solution (ORS) is adequate, lower osmolality oral rehydration fluids can be more effective in reducing stool output. Compared with standard ORS, lower sodium and glucose ORS (containing 75 mEq of sodium and 75 mmol of glucose per liter, with total osmolarity of 245 mOsm per liter) reduces stool output, vomiting, and the need for intravenous fluids without substantially increasing the risk of hyponatremia.

TABLE 337-8 -- Composition of Commercial Oral Rehydration Solutions (ORS) and Commonly Consumed Beverages SODIU POTASSI CHLORI M UM DE BASE[*] OSMOLARI CARBOHYDR (MMOL/ (MMOL/L (MMOL/ (MMOL/ TY SOLUTION ATE (G/L) L) ) L) L) (MOSM/L) ORS World Health 13.5 Organization (WHO) [2005] WHO [2002] 13.5 WHO (1975) 20 European Society of Paediatric Gastroenterol 16 ogy, Hepatology and Nutrition Enfalyte[†] Pedialyte
[§] [¶]






75 90

20 20

65 80

30 30

245 311






30 25 25 40

50 45 75 50–90

25 20 20 20

45 35 65 NA[††]

34 30 30 30

200 250 305 220

Rehydralyte CeraLyte[**]

COMMONLY USED BEVERAGES (NOT APPROPRIATE FOR DIARRHEA TREATMENT) Apple juice[§§] 120 Coca-Cola[¶¶] 112 Classic 0.4 1.6 44 N/A 45 N/A N/A 13.4 730 650

From: Department of Health and Human Services, Centers for Disease Control and Prevention: Diagnosis and management of foodbourne illnesses. MMWR 2004;52:1–33.
* †

Actual or potential bicarbonate (e.g., lactate, citrate, or acetate). Mead-Johnson Laboratories, Princeton, New Jersey. Additional information is available at .


Ross Laboratories (Abbott Laboratories), Columbus, Ohio. Data regarding Flavored and Freezer Pop Pedialyte are identical. Additional information is available at .

Ross Laboratories (Abbott Laboratories), Columbus, Ohio. Additional information is available at 7546E5?OpenDocument . .

* * † † § § ¶ ¶

Cera Products, L. L. C., Jessup, Maryland. Additional information is available at Not applicable.

Meeting U. S. Department of Agriculture minimum requirements.

Coca-Cola Corporation, Atlanta, Georgia. Figures do not include electrolytes that might be present in local water used for bottling. Base = phosphate.

Cereal-based oral rehydration fluids can also be advantageous in malnourished children and can be prepared at home. Home remedies including decarbonated soda beverages, fruit juices, and tea are not suitable for rehydration or maintenance therapy as they have inappropriately high osmolalities and low sodium concentrations. A clinical evaluation plan and management strategy for children with moderate to severe diarrhea is outlined in Figure 337-5 and Table 337-7 . Oral rehydration should be given to infants and children slowly, especially if they have emesis. It can be given initially by a dropper, teaspoon, or syringe, beginning with as little as 5 mL at a time. The volume is increased as tolerated. Replacement for emesis or stool losses is noted in Table 337-7 . Oral rehydration can also be given by a nasogastric tube if needed; this is not the usual route. Limitations to oral rehydration therapy include shock, an ileus, intussusception, carbohydrate intolerance (rare), severe emesis, and high stool output (>10 mL/kg/hr).

Continued enteral feeding in diarrhea aids in recovery from the episode and a continued ageappropriate diet after rehydration is the norm. Although intestinal brush border surface and luminal enzymes can be affected in children with prolonged diarrhea, there is evidence that satisfactory carbohydrate, protein, and fat absorption can take place on a variety of diets. Once rehydration is complete, food should be reintroduced while oral rehydration can be continued to replace ongoing losses from emesis or stools and for maintenance. Breastfeeding or nondiluted regular formula should be resumed as soon as possible. Foods with complex carbohydrates (rice, wheat, potatoes, bread, and cereals), lean meats, yogurt, fruits, and vegetables are also tolerated. Fatty foods or foods high in simple sugars (juices, carbonated sodas) should be avoided. The usual energy density of any diet used for the

therapy of diarrhea should be around 1 kcal/g, aiming to provide an energy intake of a minimum of 100 kcal/kg/day and a protein intake of between 2 and 3 g/kg/day. In selected circumstances when adequate intake of energy-dense food is problematic, the addition of amylase to the diet through germination techniques can also be helpful. With the exception of acute lactose intolerance in a small subgroup, most children with diarrhea are able to tolerate milk and lactose-containing diets. Withdrawal of milk and replacement with specialized (and expensive) lactose-free formulations are unnecessary. Although children with persistent diarrhea are not lactose intolerant, administration of a lactose load exceeding 5 g/kg/day may be associated with higher purging rates and treatment failure. Alternative strategies for reducing the lactose load while feeding malnourished children with prolonged diarrhea include addition of milk to cereals as well as replacement of milk with fermented milk products such as yogurt. Rarely, when dietary intolerance precludes the administration of cow's milk–based formulations or milk it may be necessary to administer specialized milk-free diets such as a comminuted or blenderized chicken-based diet or an elemental formulation. Although effective in some settings, the latter are unaffordable in most developing countries. In addition to rice-lentil formulations, the addition of green banana or pectin to the diet has also been shown to be effective in the treatment of persistent diarrhea. Figure 337-6 indicates a suggestive algorithm for the management of children with prolonged diarrhea in developing countries.

Figure 337-6 Persistent diarrhea. NG, nasogastric tube; ORS, oral rehydration solution.


There is strong evidence that zinc supplementation in children with diarrhea in developing countries leads to reduced duration and severity of diarrhea and could potentially prevent 300,000 deaths. WHO and UNICEF recommend that all children with acute diarrhea in at-risk areas should receive oral zinc in some form for 10–14 days during and after diarrhea (10 mg/day for infants <6 mo of age and 20 mg/day for those >6 mo). In addition to improving diarrhea, administration of zinc in community settings leads to increased use of ORS and reduction in the use of antimicrobials.

The use of probiotic nonpathogenic bacteria for prevention and therapy of diarrhea has been successful in developing countries. There are a variety of organisms (Lactobacillus,

Bifidobacterium) that have a good safety record; therapy has not been standardized and the most effective (and safe) organism has not been identified. Antimotility agents (loperamide) are contraindicated in children with dysentery and probably have no role in the management of acute watery diarrhea in otherwise healthy children. Similarly, antiemetic agents such as the phenothiazines are of little value and are associated with potentially serious side effects (lethargy, dystonia, malignant hyperpyrexia). Nonetheless, ondansetron is an effective and less toxic antiemetic agent. Because persistent vomiting may limit oral rehydration therapy, a single sublingual dose of an oral dissolvable tablet of ondansetron (2 mg children 8–15 kg; 4 mg children <15–30 kg; 8 mg children >30 kg) may be given. However, most children do not require specific antiemetic therapy; careful oral rehydration therapy is usually sufficient (see Chapter 55.1 ). Racecadotril, an enkephalinse inhibitor, has been shown to reduce stool output in patients with diarrhea. Experience with this drug in children is limited, and for the average child with acute diarrhea it may be unnecessary.

Timely antibiotic therapy in select cases of diarrhea may reduce the duration and severity of diarrhea and prevent complications ( Table 337-9 ). While these agents are important to use in specific cases, their widespread and indiscriminate use leads to the development of antimicrobial resistance. Nitazoxanide, an anti-infective agent, has been effective in the treatment of a wide variety of pathogens including Cryptosporidum parvum, Giardia lamblia, Entamoeba histolytica, Blastocystis hominis, C. difficile, and rotavirus.

TABLE 337-9 -- Antibiotic Therapy for Infectious Diarrhea DOSE AND DURATION OF TREATMENT Ceftriaxone IV, IM 50–100 mg/kg/d qd, bid × 7 d Ciprofloxacin PO 20–30 mg/kg/d bid × 7–10 d 10 mg/kg/d of TMP and 50 mg/kg/d of SMX bid × 5 d Ampicillin PO, IV 50–100 mg/kg/d qid × 7 d EPEC, ETEC, EIEC TMP-SMX or ciprofloxacin 10 mg/kg/d of TMP and 50 mg/kg/d of SMX bid × 5 d



Shigella (severe dysentery Ciprofloxacin, ampicillin, ceftriaxone, or and EIEC dysentery) trimethoprim-sulfamethoxazole (TMPSMX). Most strains are resistant to many antibiotics.



DOSE AND DURATION OF TREATMENT Ciprofloxacin PO 20–30 mg/kg/d qid for 5–10 d


No antibiotics for uncomplicated gastroenteritis in normal hosts caused by non-typhoidal species. Treatment indicated in infants <3 mo, and patients with malignancy, chronic GI disease, severe colitis hemoglobinopathies, or HIV infection, and other immunoincompetent patients. Most strains have become resistant to multiple antibiotics.

See treatment of Shigella



10 mg/kg/d of TMP and 50 mg/kg/d of SMX bid for 5 d Ciprofloxacin PO 20–30 mg/kg/d divided bid × 7–10 d


Yersinia spp.

Antibiotics are not usually required for diarrhea. Deferoxamine therapy should be withheld for severe infections or associated bacteremia. Treat sepsis as for immunocompromised hosts, using combination therapy with parenteral doxycycline, aminoglycoside, TMP-SMX, or fluoroquinolone.

Campylobacter jejuni

Erythromycin or azithromycin

Erythromycin PO, 50 mg/kg/d divided tid × 5 d Azithromycin PO, 5–10 mg/kg/d qid × 5d

Clostridium difficile

Metronidazole (first line) Discontinue initiating antibiotic Vancomycin (2nd line)

PO 30 mg/kg/d divided tid × 5 d PO 40 mg/kg/d qid ×7d

ORGANISM Entamoeba histolytica

DRUG OF CHOICE Metronidazole followed by iodoquinol or paromomycin

DOSE AND DURATION OF TREATMENT PO 30–40 mg/kg/d tid × 7–10 d PO 30–40 mg/kg/d tid × 20 d PO 25–35 mg/kg/d tid × 7 d

Giardia lamblia

Furazolidone or metronidazole or albendazole or quinacrine

Furazolidone PO 25 mg/kg/d qid for 5–7 d Metronidazole PO 30–40 mg/kg/d tid ×7d Albendazole PO 200 mg bid × 10 d

Cryptosporidium spp.

Nitazoxanide PO treatment may not be Children 1–3 yr: needed in normal hosts. In 100 mg bid × 3 d immunocompromised, PO immunoglobulin Children 4–11 yr: + aggressively treat HIV, etc. 200 mg bid Adults: 500 mg bid TMP-SMX PO 5 mg/kg/d and 25 mg/kg/d, respectively, bid × 7–10 d PO 5 mg/kg/d and 25 mg/kg/d respectively, bid × 7d Metronidazole PO 30–40 mg/kg/d tid × 7–10 d Iodoquinol PO 40 mg/kg/d tid × 20 d

Isospora spp.

Cyclospora spp.


Blastocystis hominis

Metronidazole or iodoquinol

bid, 2 times a day; EIEC, Enteroinvasive Escherichia coli;EPEC, Enteropathogenic E. coli; ETEC, Enterotoxigenic E. coli; IM, intramuscular; IV, intravenous; PO, oral; qd, daily; qid, 4 times a day, SMX, sulfamethoxazole; tid, 3 times a day; TMP, trimethoprim.


In many developed countries, diarrhea due to pathogens such as Clostridum botulinum, E. coli 0157 : H7, Salmonella, Shigella, V. cholerae, Cryptosporidium, and Cyclospora is a notifiable disease and, thus, contact tracing and source identification is important in preventing outbreaks. Many developing countries struggle with huge disease burdens of diarrhea where a wider approach to diarrhea prevention may be required. Preventive strategies may be of relevance to both developed and developing countries.

Exclusive breast-feeding (administration of no other fluids or foods for the 1st 6 mo of life) is not common. Exclusive breast-feeding protects very young infants from diarrheal disease through the promotion of passive immunity (see Chapters 42 and 94 ) and through reduction in the intake of potentially contaminated food and water. Breast milk contains all the nutrients needed in early infancy, and when continued during diarrhea, also diminishes the adverse impact on nutritional status.

There is a strong inverse association between appropriate, safe complementary feeding and mortality in children age 6–11 mo; malnutrition is an independent risk for the frequency and severity of diarrheal illness. Complementary foods should be introduced at 6 mo of age while breast-feeding should continue for up to 1 yr (longer period for developing countries). Complementary foods in developing countries are generally poor in quality and frequently heavily contaminated, thus predisposing to diarrhea. Contamination of complementary foods can be potentially reduced through caregivers' education and improving home food storage. Vitamin A supplementation reduces childhood mortality by 34%; improved vitamin A status reduces the frequency of severe diarrhea.

Most infants acquire rotavirus diarrhea early in life; an effective rotavirus vaccine would have a major effect on reducing diarrhea mortality in developing countries. In 1998, a quadrivalent Rhesus rotavirus–derived vaccine was licensed in the United States but subsequently withdrawn due to an increased risk of intussusception. Newer vaccines are approved for both developed and developing countries and significantly reduce diarrhea mortality (see Chapters 170 , 262 ). Other vaccines that could potentially reduce the burden of severe diarrhea and mortality in young children are vaccines against Shigella and ETEC.

Much of the reduction in diarrhea prevalence in the developed world is the result of improvement in standards of hygiene, sanitation, and water supply. In addition, routine handwashing with plain soap in the home can reduce the incidence of diarrhea in all environments. Behavioral change strategies through promotion of handwashing indicate that handwashing promotion and access to soap reduces the burden of diarrhea in developing countries.


Improved management of diarrhea through prompt identification and appropriate therapy significantly reduces diarrhea duration, its nutritional penalty, and risk of death in childhood. Improved management of acute diarrhea is a key factor in reducing the burden of prolonged episodes and persistent diarrhea. The WHO/UNICEF recommendations to use low osmolality ORS and zinc supplementation for the management of diarrhea, coupled with selective and appropriate use of antibiotics, have the potential to reduce the number of diarrheal deaths among children. Email to Colleague Print Version Copyright © 2008 Elsevier Inc. All rights reserved. -

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