Diare

1854 Part XVIII The Digestive System
and astroviruses (see Table 340-2). Foodborne outbreaks in the United

States are mostly caused by norovirus, accounting for 58% of all epi-
sodes, and by bacterial causes, which are most commonly Salmonella,
Clostridium perfringens, Campylobacter, and Staphylococcus aureus,
followed much less often by E. coli, Clostridium botulinum, Shigella,
Cryptosporidium, Yersinia, Listeria, Vibrio, and Cyclospora species, in
that order. Food sources include poultry, leafy vegetables, beef, fruits
and nuts, vine-stalk vegetables, and many other foods.
Direct person-to-person contact outbreaks of gastroenteritis are
Chapter 340 usually caused by norovirus and Shigella species. Unknown agents are
seen in 30-40%; other pathogens include Salmonella, rotavirus, Giardia,
Acute Gastroenteritis in Cryptosporidium, Clostridium difficile, and C. jejuni.
The exact etiologic fractions of diarrhea among children in develop-
Children ing countries are a subject of much research, and our knowledge of the
various pathogens that cause moderate to severe childhood diarrhea
has grown considerably (Fig. 340-1; Table 340-5). There are indications
Zulfiqar Ahmed Bhutta that rates of hospitalization and deaths caused by Shigella infections,
especially Shigella dysenteriae type 1, the most severe form of shigel-
losis, may be declining; however, it accounts for nearly 28,000 deaths
The term gastroenteritis denotes infections of the gastrointestinal tract annually. Enteropathogenic E. coli is responsible for 79,000 and entero-
caused by bacterial, viral, or parasitic pathogens (Tables 340-1 to 340- toxigenic E. coli (ETEC) may be responsible for 42,000 deaths annually
3). Many of these infections are foodborne illnesses. The most common among children younger than 5yr. Rotavirus infections (the most
manifestations are diarrhea and vomiting, which can also be associated common identifiable viral cause of gastroenteritis in all children)
with systemic features such as abdominal pain and fever. The term account for 197,000 deaths annually or 28% of all deaths caused by
gastroenteritis captures the bulk of infectious cases of diarrhea. The diarrhea among children younger than 5yr of age.
term diarrheal disorders is more commonly used to denote infectious
diarrhea in public health settings, although several noninfectious PATHOGENESIS OF INFECTIOUS DIARRHEA
causes of gastrointestinal illness with vomiting and/or diarrhea are well Pathogenesis and severity of bacterial disease depend on whether
recognized (Table 340-4). organisms have preformed toxins (S. aureus, Bacillus cereus), produce
secretory (cholera, E. coli, Salmonella, Shigella) or cytotoxic (Shigella,
EPIDEMIOLOGY OF CHILDHOOD DIARRHEA S. aureus, Vibrio parahaemolyticus, C. difficile, E. coli, C. jejuni) toxins,
Diarrheal disorders in childhood account for a large proportion (9%) or are invasive, and on whether they replicate in food. Enteropathogens
of childhood deaths, with an estimated 0.71 million deaths per year can lead to either an inflammatory or noninflammatory response in
globally, making it the second most common cause of child deaths the intestinal mucosa (Table 340-6).
worldwide. Almost 1.731 billion episodes of diarrhea occurred in Enteropathogens elicit noninflammatory diarrhea through entero-
2010 in children younger than 5yr of age in developing countries, with toxin production by some bacteria, destruction of villus (surface) cells
more than 80% of the episodes occurring in Africa and South Asia by viruses, adherence by parasites, and adherence and/or translocation
(50.5% and 32.5%, respectively) and 36 million of the total episodes by bacteria. Inflammatory diarrhea is usually caused by bacteria that
progress to severe episodes. Global mortality may be declining rapidly, directly invade the intestine or produce cytotoxins with consequent
but the overall incidence of diarrhea has only declined from 3.4 to fluid, protein, and cells (erythrocytes, leukocytes) that enter the intes-
approximately 2.9 episodes per child-year in the past 2 decades, and tinal lumen. Some enteropathogens possess more than 1 virulence
it is estimated to account for 23 million childhood disability-adjusted property. Some viruses, such as rotavirus, target the microvillus tips of
life years. the enterocytes and can enter the cells by direct invasion or calcium-
The decline in diarrheal mortality, despite the lack of significant dependent endocytosis. This can result in villus shortening and loss of
changes in incidence, is the result of preventive rotavirus vaccination enterocyte absorptive surface through cell shortening and loss of
and improved case management of diarrhea, as well as improved nutri- microvilli (Fig. 340-2).
tion of infants and children. These interventions have included wide- Most bacterial pathogens elaborate enterotoxins; the rotavirus
spread home- and hospital-based oral rehydration therapy and protein NSP4 acts as a viral enterotoxin. Bacterial enterotoxins can
improved nutritional management of children with diarrhea. selectively activate enterocyte intracellular signal transduction and can
In addition to the risk of mortality, persistently high rates of diar- also affect cytoskeletal rearrangements with subsequent alterations in
rhea, especially prolonged and persistent diarrhea among young chil- the water and electrolyte fluxes across enterocytes. In toxigenic diar-
dren may be associated with long-term adverse outcomes. Diarrheal rhea, enterotoxin produced by Vibrio cholerae, increased mucosal
illnesses, especially early and repeated episodes among young children levels of cyclic adenosine monophosphate, inhibit electroneutral NaCl
can be associated with malnutrition, micronutrient deficiencies, and absorption but have no effect on glucose-stimulated Na+ absorption.
significant deficits in psychomotor and cognitive development. In inflammatory diarrhea (e.g., Shigella spp. or Salmonella spp.) there
is extensive histologic damage, resulting in altered cell morphology and
ETIOLOGY OF DIARRHEA reduced glucose-stimulated Na+ and electroneutral NaCl absorption.
Gastroenteritis is the result of infection acquired through the fecaloral The role of 1 or more cytokines in this inflammatory response is criti-
route or by ingestion of contaminated food or water. Gastroenteritis is cal. In secretory cells from crypts, Cl secretion is minimal in normal
associated with poverty, poor environmental hygiene, and develop- subjects and is activated by cyclic adenosine monophosphate in toxi-
ment indices. Enteropathogens that are infectious in a small inoculum genic and inflammatory diarrhea (Fig. 340-3).
(Shigella, enterohemorrhagic Escherichia coli, Campylobacter jejuni, ETEC colonizes and adheres to enterocytes of the small bowel via
noroviruses, rotavirus, Giardia lamblia, Cryptosporidium parvum, Ent- its surface fimbriae (pili) and induces hypersecretion of fluids and
amoeba histolytica) can be transmitted by person-to-person contact, electrolytes into the small intestine through 1 of 2 toxins: the heat-
whereas others, such as cholera, are generally a consequence of con- labile enterotoxin or the heat-stable enterotoxin. Heat-labile entero-
tamination of food or water supply (see Tables 340-1 to 340-3). toxin is structurally similar to the V. cholerae toxin, and activates
In the United States, rotavirus and the noroviruses (small round adenylate cyclase, resulting in an increase in intracellular cyclic gua-
viruses such as Norwalk-like virus and caliciviruses) are the most nosine monophosphate (Fig. 340-4). In contrast, Shigella spp. cause
common viral agents, followed by sapoviruses, enteric adenoviruses, Text continued on p. 1864
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Table 340-1 Foodborne Bacterial Illnesses
INCUBATION SIGNS AND DURATION OF
ETIOLOGY PERIOD SYMPTOMS ILLNESS ASSOCIATED FOODS LABORATORY TESTING TREATMENT
Bacillus anthracis 2 days to weeks Nausea, vomiting, Weeks Insufficiently cooked Blood Penicillin is first choice for naturally
malaise, bloody contaminated meat acquired GI anthrax but use beta
diarrhea, acute lactams with high index of
abdominal pain suspicion for resistance
Ciprofloxacin is second option
Bacillus cereus 1-6hr Sudden onset of severe 24hr Improperly refrigerated Normally a clinical diagnosis Supportive care
(preformed nausea and vomiting cooked or fried rice, meats Clinical laboratories do not
enterotoxin) Diarrhea may be routinely identify this
present organism
If indicated, send stool and
food specimens to reference
laboratory for culture and
toxin identification
Bacillus cereus 10-16hr Abdominal cramps, 24-48hr Meats, stews, gravies, vanilla Testing not necessary, Supportive care
(diarrheal toxin) watery diarrhea, sauce self-limiting
nausea Consider testing food and
stool for toxin in outbreaks
Brucella abortus, 7-21 days Fever, chills, sweating, Weeks Raw milk, goat cheese made Blood culture and positive Acute: Rifampin and doxycycline
Brucella melitensis, weakness, headache, from unpasteurized milk, serology daily for 6wk
and Brucella suis muscle and joint pain, contaminated meats Infections with complications
diarrhea, bloody require combination therapy with
stools during acute rifampin, tetracycline, and an
phase aminoglycoside
Campylobacter jejuni 2-5 days Diarrhea, cramps, fever, 2-10 days Raw and undercooked Routine stool culture; Supportive care
and vomiting; poultry, unpasteurized milk, Campylobacter requires For severe cases, antibiotics, such
diarrhea may be contaminated water special media and incubation as azithromycin and quinolones,
bloody at 42C (107.6F) to grow may be indicated early in the
diarrheal disease
Guillain-Barr syndrome can be a
sequela
Clostridium 12-72hr Vomiting, diarrhea, Variable (days to Home-canned foods with a Stool, serum, and food can be Supportive care
botulinum: children blurred vision, months) low acid content, improperly tested for toxin Botulism antitoxin is helpful if

and adults diplopia, dysphagia, Can be canned commercial foods, Stool and food can also be given early in the course of the
(preformed toxin) descending muscle complicated by home-canned or fermented cultured for the organism illness. Antitoxin for children and
weakness respiratory fish, herb-infused oils, baked These tests can be performed adults is available through CDC
failure and potatoes in aluminium foil, at some state health Contact the state health
death cheese sauce, bottled department laboratories and department. The 24-hr number
garlic, foods held warm for CDC for CDC is (800) 232-4636
extended periods (e.g., in a (800-CDC-INFO)
warm oven)
Clostridium 3-30 days In infants <12mo, Variable Honey, home-canned Stool, serum, and food can be Supportive care
botulinum: infants lethargy, weakness, vegetables and fruits, corn tested for toxin Botulinum antitoxin for infants can
poor feeding, syrup Stool and food can also be be obtained from the Infant
constipation, cultured for the organism Botulism Prevention Program,
hypotonia, poor head These tests can be performed Health and Human Services,
control, poor gag and at some state health California (510-540-2646)
sucking reflex department laboratories and
CDC
Chapter 340 Acute Gastroenteritis in Children 1855
Continued
Table 340-1 Foodborne Bacterial Illnessescontd
Clostridium 8-16hr Watery diarrhea, 24-48hr Meats, poultry, gravy, dried or Stools can be tested for Supportive care
perfringens toxin nausea, abdominal precooked foods, time- enterotoxin and cultured for Antibiotics not indicated
cramps; fever is rare and/or temperature-abused organism
food Because Clostridium
perfringens can normally be
found in stool, quantitative

cultures must be done: A
count of at least 106 C.
perfringens spores per gram
of stool within 48hr of when
illness began is required to
diagnose infection
Enterohemorrhagic 1-8 days Severe diarrhea that is 5-10 days Undercooked beef especially Stool culture; E. coli O157:H7 Supportive care, monitor renal
Escherichia coli often bloody, hamburger, unpasteurized requires special media to function, hemoglobin, and
(EHEC) including E. abdominal pain and milk and juice, raw fruits and grow. If E. coli O157:H7 is platelets closely. E. coli O157:H7
coli O157:H7 and vomiting vegetables (e.g., sprouts), suspected, specific testing infection is also associated with
other Shiga Usually, little or no salami (rarely), contaminated must be requested. Shiga hemolytic uremic syndrome
toxinproducing E. fever is present water toxin testing may be done (HUS), which can cause lifelong
coli (STEC) More common in using commercial kits; complications
children <4yr old positive isolates should be Studies indicate that antibiotics
forwarded to public health might promote the development
laboratories for confirmation of HUS. Antidiarrheal agents like
and serotyping Imodium may also increase the
risk of developing HUS
Enterotoxigenic E. 1-3 days Watery diarrhea, 3 to >7 days Water or food contaminated Stool culture Supportive care
coli (ETEC) abdominal cramps, with human feces ETEC requires special Antibiotics are rarely needed

some vomiting laboratory techniques for except in severe cases
identification that may not Recommended antibiotics include
be widely available; quinolones although these are
consequently, physicians rarely required unless there is
may make the diagnosis severe infection and should be
based on a patients history administered early. Antimotility
and symptoms medications should be avoided
If ETEC is suspected, must by persons with high fevers or
alert microbiology laboratory bloody diarrhea, and should be
that is testing the specimen discontinued if diarrhea
symptoms persist more than
48hr. Bismuth subsalicylate
compounds (e.g., Pepto-Bismol)
can help reduce the number of
bowel movements
Listeria 9-48hr for GI Fever, muscle aches, Variable Fresh soft cheeses, Blood or cerebrospinal fluid Supportive care and antibiotics;
monocytogenes symptoms, and nausea or unpasteurized milk, cultures. Selective intravenous ampicillin, penicillin
2-6wk for diarrhea inadequately pasteurized enrichment media improve G, or TMP-SMX is recommended
invasive Pregnant women might milk, ready-to-eat deli rates of isolation from for invasive disease
disease have mild flu-like meats, hot dogs contaminated specimens
illness, and infection Asymptomatic fecal carriage
can lead to occurs; therefore, stool
premature delivery or culture usually not helpful
stillbirth Antibody to listeriolysin O may
Elderly or be helpful to identify
immunocompromised outbreak retrospectively
patients can have
bacteremia or
meningitis
At birth and Infants infected from Higher dosages of ampicillin
infancy mother at risk for recommended for neonatal
sepsis or meningitis sepsis or meningitis
Salmonella spp. 1-3 days Diarrhea, fever, 4-7 days Contaminated eggs, poultry, Routine stool cultures Supportive care
abdominal cramps, unpasteurized milk or juice, Other than for S. typhi and
vomiting cheese, contaminated raw S. paratyphi, antibiotics are not
S. typhi and S. fruits and vegetables (alfalfa indicated unless there is
paratyphi produce sprouts, melons) extraintestinal spread, or the risk
typhoid with insidious S. typhi epidemics are often of extraintestinal spread of the
onset characterized related to fecal infection
by fever, headache, contamination of water Consider ampicillin, third-
constipation, malaise, supplies or street-vended generation cephalosporins, or
chills, and myalgia; foods quinolones if indicated
diarrhea is A vaccine exists for S. typhi but is
uncommon, and not completely effective.
vomiting is not Washing hands and avoiding
usually severe suspicious foods is equally useful
at preventing disease as
vaccination
Shigella spp. 24-48hr Abdominal cramps, 4-7 days Food or water contaminated Routine stool cultures Supportive care. Antibiotics are
fever, diarrhea with human fecal material recommended for severe
Stools might contain Usually person-to-person disease, bloody diarrhea, or
blood and mucus spread, fecaloral compromised immune systems.
transmission Resistance to traditional first-line
Ready-to-eat foods touched drugs like ampicillin and

by infected food workers, TMP-SMX is common. When
e.g., raw vegetables, salads, susceptibility is unknown or when
sandwiches an ampicillin- or TMP-SMX
resistant strain is isolated,
choices for therapy include
fluoroquinolones, ceftriaxone,
and azithromycin. Antidiarrheal
agents such as Imodium or
Lomotil can worsen the illness
and should be avoided
Staphylococcus 1-6hr Sudden onset of severe 24-48hr Unrefrigerated or improperly Normally a clinical diagnosis Supportive care
aureus (preformed nausea and vomiting refrigerated meats, potato Stool, vomitus, and food can
enterotoxin) Abdominal cramps and egg salads, cream be tested for toxin and
Diarrhea and fever may pastries cultured if indicated
be present
Continued
Table 340-1 Foodborne Bacterial Illnessescontd
Vibrio cholerae 24-72hr Profuse watery diarrhea 3-7 days Contaminated water, fish, Stool culture Supportive care with aggressive
(toxin) and vomiting, which Causes life- shellfish, street-vended food V. cholerae requires special oral and intravenous rehydration
can lead to severe threatening typically from Latin America media to grow: Cary-Blair Doxycycline is recommended as
dehydration and dehydration or Asia media is ideal for transport, first-line treatment for adults,
death within hours and the selective thiosulfate whereas azithromycin is
citratebile salts agar (TCBS) recommended as first-line
is ideal for isolation and treatment for children and
identification. ; if V. cholerae pregnant women. Ciprofloxacin
is suspected, must request and doxycycline recommended
specific testing. as second-line drugs for children
Commercially available rapid
test kits (e.g., Crystal VC
dipstick) are useful in
epidemic settings but do not
test susceptibility or subtype
so should not be used for
routine diagnosis
Vibrio 2-48hr Watery diarrhea, 2-5 days Undercooked or raw seafood, Stool cultures. V. Supportive care
parahaemolyticus abdominal cramps, such as fish, shellfish parahaemolyticus requires There is no evidence that
nausea, vomiting special media (TCBS agar) to antibiotic treatment decreases
grow; must request specific the severity or the length of the
testing illness. Antibiotics are
recommended in severe or
prolonged cases: tetracycline or
ciprofloxacin can be used
Vibrio vulnificus 1-7 days Vomiting, diarrhea, 2-8 days Undercooked or raw shellfish, Stool, wound, or blood Supportive care and antibiotics:
abdominal pain, especially oysters, other cultures doxycycline, and a third-
bacteremia, and contaminated seafood, and V. vulnificus requires special generation cephalosporin such
wound infections open wounds exposed to media (TCBS agar) to grow; as ceftazidime is recommended
More common and seawater if V. vulnificus is suspected,
potentially fatal in the must request specific testing
immunocompromised
or in patients with
chronic liver disease
(presenting with
septic shock and
hemorrhagic bullous

skin lesions)
Yersinia 24-48hr Appendicitis-like 1-3wk, usually Undercooked pork, Stool, vomitus, or blood Supportive care
enterocolitica symptoms (diarrhea self-limiting unpasteurized milk, tofu, culture, throat, lymph nodes, If septicemia or other invasive
and Yersinia and vomiting, fever, contaminated water joint fluid, urine, and bile disease occurs, antibiotic therapy
pseudotuberculosis abdominal pain) Infection has occurred in Yersinia requires special media with aminoglycosides,
occur primarily in infants whose caregivers to grow; must request doxycycline, TMP-SMX, or
older children and handled chitterlings specific testing fluoroquinolones may be useful
young adults Serology is available in
Might have a research and reference
scarlatiniform laboratories
rash or erythema
nodosum with Y.
pseudotuberculosis
CDC, Centers for Disease Control and Prevention; GI, gastrointestinal; TMP-SMX, trimethoprim-sulfamethoxazole.
From Centers for Disease Control and Prevention: Diagnosis and management of foodborne illnesses, MMWR 53(RR-4):1-33, 2004.
Table 340-2 Foodborne Viral Illnesses
INCUBATION SIGNS AND DURATION
ETIOLOGY PERIOD SYMPTOMS OF ILLNESS ASSOCIATED FOODS LABORATORY TESTING TREATMENT
Hepatitis A 28 days average Diarrhea, dark urine, Variable, Shellfish harvested from Increase in ALT, bilirubin Supportive care
(15-50 days) jaundice, and flu-like 2wk-3mo contaminated waters, raw Positive IgM and antihepatitis A antibodies Prevention with immunization
symptoms, i.e., fever, produce, contaminated (vaccine available for persons
headache, nausea, drinking water, uncooked 1 year and older)
and abdominal pain foods, and cooked foods
that are not reheated after
contact with infected food
handler
Caliciviruses 12-48hr Nausea, vomiting, 12-60hr Shellfish, fecally Routine RT-PCR. RT-PCR assays are the Supportive care such as
(including abdominal cramping, contaminated foods, preferred laboratory method for detecting rehydration. Avoid giving
noroviruses and diarrhea, fever, ready-to-eat foods touched norovirus. Conventional RT-PCR followed antimotility agents to
sapoviruses) myalgia, and some by infected food workers by sequence analysis of the RT-PCR children younger than 3yr
headache (salads, sandwiches, ice, products is used for norovirus genotyping. old. However, these agents
Diarrhea is more cookies, fruit) Rapid commercial assays, such as enzyme may be helpful in older
prevalent in adults immunoassays (EIAs), have poor sensitivity children and adults,
and vomiting is more and are not recommended for establishing particularly when used along
prevalent in children diagnosis with rehydration treatment
Prolonged Clinical diagnosis, negative bacterial cultures Good hygiene
asymptomatic Stool is negative for WBCs
excretion possible
Rotavirus (groups 1-3 days Vomiting, watery 4-8 days Fecally contaminated foods Diagnosis may be made by rapid antigen Supportive care
A-C) diarrhea, low-grade Ready-to-eat foods touched detection of rotavirus in stool specimens. Severe diarrhea can require
fever by infected food workers fluid and electrolyte
Temporary lactose (salads, fruits) replacement
intolerance can occur
Infants and children,
elderly, and

immunocompromised
are especially
vulnerable
Other viral agents 10-70hr Nausea, vomiting, 2-9 days Fecally contaminated foods Identification of the virus in early acute stool Supportive care, usually mild,
(astroviruses, diarrhea, malaise, Ready-to-eat foods touched samples self-limiting
adenoviruses, abdominal pain, by infected food workers Serology Good hygiene
parvoviruses) headache, fever Some shellfish Commercial ELISA kits are available for
adenoviruses and astroviruses
ALT, alanine aminotransferase; ELISA, enzyme-linked immunosorbent assay; IgM, immunoglobulin M; RT-PCR, reverse transcriptase polymerase chain reaction; WBCs, white blood cells.
From Centers for Disease Control and Prevention: Diagnosis and management of foodborne illnesses. MMWR 53(RR-4):1-33, 2004.
Table 340-3 Foodborne Parasitic Illnesses
Angiostrongylus 1wk-1mo Severe headaches, Several weeks to Raw or undercooked No readily available blood tests. Supportive care. There is no specific
cantonensis nausea, vomiting, neck several months intermediate hosts (e.g., History is major guide to treatment. Repeat lumbar punctures
stiffness, paresthesias, snails or slugs), infected diagnosis. Examination of CSF and use of corticosteroid therapy
hyperesthesias, paratenic (transport) for elevated pressure, protein, may be used for more severely ill
seizures, and other hosts (e.g., crabs, leukocytes, and eosinophils; patients
neurologic freshwater shrimp), fresh serologic testing using ELISA
abnormalities produce contaminated to detect antibodies to
with intermediate or Angiostrongylus cantonensis
transport hosts
Cryptosporidium 2-10 days Diarrhea (usually May be remitting Any uncooked food or Request specific examination of Supportive care, self-limited
watery), stomach and relapsing food contaminated by the stool for Cryptosporidium. If severe, nitazoxanide can be
cramps, upset over weeks to an ill food handler after Most often, stool specimens prescribed for all patients 1yr of age
stomach, slight fever months cooking; drinking water are examined microscopically or older
using different techniques
(e.g., acid-fast staining, direct
fluorescent antibody [DFA],
and/or enzyme immunoassays
for detection of
Cryptosporidium sp. antigens)
May need to examine water or
food
Cyclospora 1-14 days, usually Diarrhea (usually May be remitting Various types of fresh Request specific examination of TMP-SMX for 7 days

cayetanensis at 1wk watery), loss of and relapsing produce (imported the stool for Cyclospora
appetite, substantial over weeks to berries, lettuce) May need to examine water or
loss of weight, months food
stomach cramps,
nausea, vomiting,
fatigue
Entamoeba 2-3 days1-4wk Diarrhea (often bloody), May be protracted Any uncooked food or Examination of fresh stool for For asymptomatic infections,
histolytica frequent bowel (several weeks to food contaminated by cysts and parasites; may need paromomycin and iodoquinol are the
movements, lower several months) an ill food handler after at least 3 samples drugs of choice. For symptomatic
abdominal pain cooking; drinking water Serology for long-term infections intestinal disease or extraintestinal
infections (e.g., hepatic abscess), the
drugs of choice are metronidazole
and tinidazole, immediately followed
by treatment with paromomycin or
iodoquinol
Giardia lamblia 1-2wk Diarrhea, stomach Days to weeks Any uncooked food or Examination of stool for ova and Metronidazole, tinidazole, or
cramps, gas, weight food contaminated by parasites; may need at least 3 nitazoxanide. Alternatives to these
loss an ill food handler after samples medications include paromomycin,
cooking; drinking water quinacrine, and furazolidone
Toxoplasma 5-23 days Generally asymptomatic, Months Accidental ingestion of The diagnosis of toxoplasmosis Asymptomatic healthy, but infected,
gondii 20% develop cervical contaminated is typically made by serologic persons do not require treatment
lymphadenopathy substances (e.g., soil testing. however, IgM Spiramycin or pyrimethamine plus
and/or a flu-like illness contaminated with cat antibodies can persist for sulfadiazine may be used for
In immunocompromised feces on fruits and 6-18mo and thus do not pregnant women
patients: CNS disease, vegetables), raw or necessarily indicate recent Pyrimethamine plus sulfadiazine may
myocarditis, or partially cooked meat infection be used for immunocompromised
pneumonitis is often (especially pork, lamb, PCR of bodily fluids persons, in specific cases
seen and venison) Diagnosis can also be made by Pyrimethamine plus sulfadiazine (with
isolation of parasites from or without steroids) may be given for
blood or other body fluids; ocular disease when indicated
observation of parasites in Folinic acid is given with
patient specimens via pyrimethamine plus sulfadiazine to
microscopy or histology counteract bone marrow suppression
Detection of organisms is rare
Toxoplasma In infants at birth Treatment of the Months Passed from mother (who Isolation of T. gondii from
gondii mother can reduce acquired acute infection placenta, umbilical cord, or
(congenital severity and/or during pregnancy) to infant blood; PCR of white
infection) incidence of child blood cells, CSF, or amniotic
congenital infection fluid, or IgM and IgA serology,
Most infected infants performed by a reference
have few symptoms at laboratory
birth; later, they
generally develop
signs of congenital
toxoplasmosis (mental
retardation, severely
impaired eyesight,
cerebral palsy,
seizures), unless the
infection is treated
Trichinella 1-2 days for Acute: nausea, diarrhea, Months Raw or undercooked Positive serology or Supportive care plus mebendazole
spiralis initial vomiting, fatigue, contaminated meat, demonstration of larvae via or albendazole. In addition to
symptoms; fever, abdominal usually pork or wild muscle biopsy; increase in antiparasitic medication, treatment

others begin discomfort followed game meat (e.g., bear eosinophils with steroids is sometimes required
2-8wk after by muscle soreness, or moose) in more severe cases
infection weakness, and
occasional cardiac and
neurologic
complications
CNS, central nervous system; CSF, cerebrospinal fluid; ELISA, enzyme-linked immunosorbent assay; IgA, immunoglobulin A; IgM, immunoglobulin M; PCR, polymerase chain reaction; TMP-SMX,
trimethoprim-sulfamethoxazole.
From Centers for Disease Control and Prevention: Diagnosis and management of foodborne illnesses. MMWR 53(RR-4):1-33, 2004.
Table 340-4 Foodborne Noninfectious Illnesses
INCUBATION DURATION OF LABORATORY
ETIOLOGY PERIOD SIGNS AND SYMPTOMS ILLNESS ASSOCIATED FOODS TESTING TREATMENT
Antimony 5min8hr usually Vomiting, metallic taste Usually self- Metallic container Identification of Supportive care
<1hr limited metal in beverage
or food
Arsenic Few hours Vomiting, colic, diarrhea Several days Contaminated food Urine Gastric lavage, BAL
Can cause (dimercaprol)
eosinophilia
Cadmium 5min8hr usually Nausea, vomiting, myalgia, increase in Usually self- Seafood, oysters, clams, Identification of Supportive care
<1hr salivation, stomach pain limited lobster, grains, peanuts metal in food
Ciguatera fish 2-6hr GI: abdominal pain, nausea, vomiting, Days to weeks to A variety of large reef fish: Radioassay for toxin Supportive care, IV
poisoning diarrhea months grouper, red snapper, in fish or a mannitol
(ciguatera toxin) amberjack, and barracuda consistent history Children more
(most common) vulnerable
3hr Neurologic: paresthesias, reversal of
hot or cold, pain, weakness
2-5 days Cardiovascular: bradycardia,
hypotension, increase in T-wave
abnormalities
Copper 5min8hr usually Nausea, vomiting, blue or green Usually self- Metallic container Identification of Supportive care
<1hr vomitus limited metal in beverage
or food
Mercury 1wk or longer Numbness, weakness of legs, spastic May be protracted Fish exposed to organic Analysis of blood, Supportive care
paralysis, impaired vision, blindness, mercury, grains treated hair
coma with mercury fungicides
Pregnant women and the developing
fetus are especially vulnerable
Mushroom toxins, <2hr Vomiting, diarrhea, confusion, visual Self-limited Wild mushrooms (cooking Typical syndrome Supportive care
short-acting disturbance, salivation, diaphoresis, might not destroy these and mushroom
(muscimol, hallucinations, disulfiram-like toxins) identified or

muscarine, reaction, confusion, visual demonstration of
psilocybin, disturbance the toxin
Coprinus
atramentaria,
ibotenic acid)
Mushroom toxins, 4-8hr diarrhea; Diarrhea, abdominal cramps, leading Often fatal Mushrooms Typical syndrome Supportive care,
long-acting 24-48hr liver to hepatic and renal failure and mushroom life-threatening, may
(amanitin) failure identified and/or need life support
demonstration of
the toxin
Nitrite poisoning 1-2hr Nausea, vomiting, cyanosis, headache, Usually self- Cured meats, any Analysis of the food, Supportive care,
dizziness, weakness, loss of limited contaminated foods, blood methylene blue
consciousness, chocolate-brown spinach exposed to
blood excessive nitrification
Pesticides Few minutes to Nausea, vomiting, abdominal cramps, Usually self- Any contaminated food Analysis of the food, Atropine; 2-PAM
(organophosphates few hours diarrhea, headache, nervousness, limited blood (pralidoxime) is used
or carbamates) blurred vision, twitching, convulsions, when atropine is not
salivation, meiosis able to control
symptoms; rarely
necessary in
carbamate poisoning
Puffer fish <30min Paresthesias, vomiting, diarrhea, Death usually in Puffer fish Detection of Life-threatening, may
(tetrodotoxin) abdominal pain, ascending paralysis, 4-6hr tetrodotoxin in fish need respiratory
respiratory failure support
Scombroid 1min-3hr Flushing, rash, burning sensation of 3-6hr Fish: bluefin, tuna, skipjack, Demonstration of Supportive care,
(histamine) skin, mouth and throat, dizziness, mackerel, marlin, escolar, histamine in food antihistamines
urticaria, paresthesias and mahi mahi or clinical diagnosis
Shellfish toxins Diarrheic shellfish Nausea, vomiting, diarrhea, and hr to 2-3 days A variety of shellfish, Detection of the Supportive care,
(diarrheic, poisoning: abdominal pain accompanied by primarily mussels, oysters, toxin in shellfish; generally self-limiting
neurotoxic, 30min-2hr chills, headache, and fever scallops, and shellfish from high-pressure
amnesic) the Florida coast and the liquid
Gulf of Mexico chromatography
Neurotoxic Tingling and numbness of lips, tongue,
shellfish and throat, muscular aches, dizziness,
poisoning: few reversal of the sensations of hot and
minutes to hours cold, diarrhea, and vomiting
Amnesic shellfish Vomiting, diarrhea, abdominal pain Elderly are especially
poisoning: and neurologic problems such as sensitive to amnesic
24-48hr confusion, memory loss, shellfish poisoning
disorientation, seizure, coma
Shellfish toxins 30min-3hr Diarrhea, nausea, vomiting leading to Days Scallops, mussels, clams, Detection of toxin in Life-threatening, may
(paralytic shellfish paresthesias of mouth and lips, cockles food or water need respiratory
poisoning) weakness, dysphasia, dysphonia, where fish are support
respiratory paralysis located; high-
pressure liquid
chromatography
Sodium fluoride Few minutes to Salty or soapy taste, numbness of Usually self- Dry foods (e.g., dry milk, Testing of vomitus or Supportive care
2hr mouth, vomiting, diarrhea, dilated limited flour, baking powder, cake gastric washings
pupils, spasms, pallor, shock, mixes) contaminated with Analysis of the food
collapse NaF-containing insecticides
and rodenticides

Thallium Few hours Nausea, vomiting, diarrhea, painful Several days Contaminated food Urine, hair Supportive care
paresthesias, motor polyneuropathy,
hair loss
Tin 5min-8hr usually Nausea, vomiting, diarrhea Usually self- Metallic container Analysis of the food Supportive care
<1hr limited
Vomitoxin Few minutes to Nausea, headache, abdominal pain, Usually self- Grains such as wheat, corn, Analysis of the food Supportive care
3hr vomiting limited barley
Zinc Few hours Stomach cramps, nausea, vomiting, Usually self- Metallic container Analysis of the food, Supportive care
diarrhea, myalgias limited blood and feces,
saliva or urine
BAL, bronchoalveolar lavage; GI, gastrointestinal.
Figure 340-1 Attributable incidence of pathogen-specific moderate-to-severe diarrhea per 100 child-yr by age stratum, all sites combined. The
bars show the incidence rates and the error bars show the 95% confidence intervals. (From Kotloff KL, Nataro JP, Blackwelder WC, etal. Burden
and aetiology of diarrhoeal disease in infants and young children in developing countries [the Global Enteric Multicenter Study, GEMS]: a prospec-
tive, case-control study. Lancet 382(9888):209222, 2013, Fig. 4.)
gastroenteritis via a superficial invasion of colonic mucosa, which vitamin A deficiency, and accounts for 157,000 deaths from diarrhea,
they invade through M cells located over Peyer patches. After phago- measles, and malaria. Zinc deficiency is estimated to cause 116,000
cytosis, a series of events occurs, including apoptosis of macrophages, deaths from diarrhea and pneumonia. Table 340-7 summarizes some
multiplication and spread of bacteria into adjacent cells, release of of the key risk factors associated with childhood diarrhea globally.
inflammatory mediators (interleukin-1 and -8), transmigration of neu- The majority of cases of diarrhea resolve within the 1st wk of the
trophils into the lumen of the colon, neutrophil necrosis and degranu- illness. A smaller proportion of diarrheal illnesses fail to resolve and
lation, further breach of the epithelial barrier, and mucosal destruction persist for longer than 2wk. Persistent diarrhea is defined as episodes
(Fig. 340-5). that began acutely but last for 14 or more days. Such episodes account
for 3-19% of all diarrheal episodes in children younger than 5yr of age
RISK FACTORS FOR GASTROENTERITIS and up to 50% of all diarrhea-related deaths; persistent diarrhea has a
In developed countries, episodes of infectious diarrhea can occur case fatality rate of 60%. Many children (especially infants and tod-
through seasonal exposure to organisms such as rotavirus, or exposure dlers) in developing countries have frequent episodes of acute diarrhea.
to pathogens in settings of close contact (e.g., daycare centers). Major Although few individual episodes persist beyond 14 days, frequent
risks include environmental contamination and increased exposure to episodes of acute diarrhea, as well as prolonged diarrhea (lasting
enteropathogens. Additional risks include young age, immunodefi- between 7-13 days of age), can result in nutritional compromise and
ciency, measles, malnutrition, and lack of exclusive or predominant can predispose these children to develop persistent diarrhea, protein-
breastfeeding. Malnutrition increases the risk of diarrhea and associ- calorie malnutrition, and secondary infections.
ated mortality, and moderate to severe stunting increases the odds of
diarrhea-associated mortality. The fraction of such infectious diarrhea CLINICAL MANIFESTATION OF DIARRHEA
deaths that are attributable to nutritional deficiencies varies with the Most of the clinical manifestations and clinical syndromes of diarrhea
prevalence of deficiencies; the highest attributable fractions are in sub- are related to the infecting pathogen and the dose or inoculum (see
Saharan Africa, south Asia, and Andean Latin America. The risks are Tables 340-1 to 340-3). Additional manifestations depend on the devel-
particularly higher with micronutrient malnutrition; in children with opment of complications (e.g., dehydration and electrolyte imbalance)

Table 340-5 Weighted Annual Incidence (Per 100 Child-Years) of Moderate-to-Severe Diarrhea Attributable to a Specific
Pathogen, with 95% Confidence Interval, By Age Stratum and Country
AGE
GROUP PATHOGEN GAMBIA MALI MOZAMBIQUE KENYA INDIA BANGLADESH PAKISTAN
<12mo VIRUSES
Rotavirus 3.2 (1.7-4.6) 8.4 (3.5-13.3) 3.5 (1.5-5.4) 10.1 (5.4-14.8) 25.4 (14.7-36.2) 2.1 (1.0-3.2) 5.5 (2.6-8.5)
Norovirus GII 1.2 (0.4-2.0)
Adenovirus 40/41 0.3 (0.1-0.6) 0.7 (0.1-1.3) 0.3 (0.0-0.5) 3.7 (1.6-5.9) 0.5 (0.2-0.8) 0.5 (0.1-0.8)
BACTERIA
ST-ETEC (ST-only 0.7 (0.1-1.2) 1.4 (0.3-2.5) 3.6 (1.4-5.8) 2.8 (0.9-4.8) 0.2 (0.0-0.4) 1.7 (0.6-2.8)
or LT/ST)
Shigella 0.5 (0.2-0.9) 2.3 (0.8-3.8) 1.9 (0.4-3.3) 1.7 (0.8-2.6) 1.9 (0.8-2.9)
Aeromonas 1.2 (0.3-2.2) 2.8 (1.0-4.5)
Campylobacter 1.1 (0.1-2.2) 1.7(0.0-3.3)
jejuni
Typical EPEC 2.7 (0.6-4.7)
Nontyphoidal 0.5 (0.2-0.9)
Salmonella
Vibrio cholerae 0.8 (0.2-1.3)
O1
PROTOZOA
Cryptosporidium 1.6 (0.7-2.4) 5.4 (2.1-8.8) 1.8 (0.7-3.0) 4.6 (2.0-7.2) 11.1 (5.4-16.9) 0.7 (0.2-1.2) 1.4 (0.1-2.6)
Entamoeba 0.5 (0.0-0.9)
histolytica
12-23mo VIRUSES
Rotavirus 3.3 (1.3-5.2) 4.1 (1.0-7.1) 3.0 (1.6-4.3) 12.4 (7.1-17.7) 3.0 (1.1-4.9) 1.6 (0.6-2.7)
Norovirus GII 1.7 (0.5-2.8) 2.3 (0.4-4.2)
Adenovirus 40/41 0.4 (0.0-0.8) 2.2 (0.9-3.4) 0.4 (0.0-0.7)
BACTERIA
ST-ETEC (ST-only 1.5 (0.3-2.8) 0.8 (0.0-1.7) 0.7 (0.2-1.2) 1.5 (0.6-2.5) 2.8 (1.1-4.6) 0.9 (0.2-1.7)
or LT/ST)
EAEC 1.6 (0.0-3.2)
Shigella 2.5 (0.9-4.1) 0.8 (0.0-1.6) 0.5 (0.1-0.9) 1.0 (0.3-1.8) 3.5 (1.7-5.4) 8.5 (3.3-13.7) 2.1 (0.7-3.4)
Aeromonas 1.9 (0.2-3.7) 1.6 (0.2-2.9)
Campylobacter
jejuni
Typical EPEC 0.8 (0.0-1.5)
Salmonella
Vibrio cholerae 1.6 (0.6-2.7) 0.2 (0.0-0.5) 1.3 (0.4-2.1)
O1
PROTOZOA
Cryptosporidium 1.5 (0.4-2.5) 1.6 (0.0-3.3) 2.0 (0.9-3.0) 4.1 (1.2-6.9) 1.4 (0.4-2.4)
Entamoeba
histolytica
2459mo VIRUSES
Rotavirus 0.4 (0.1-0.6) 0.4 (0.0-3.2) 0.3 (0.1-0.4) 3.5 (0.0-7.1)
Norovirus GII 0.3 (0.0-0.5)
Sapovirus 0.8 (0.0-1.8)
Adenovirus 40/41
BACTERIA
ST-ETEC (ST-only 0.3 (0.0-0.5) 0.4 (0.1-0.6) 1.5 (0.0-3.1) 0.1 (0.0-0.3)
or LT/ST)
EAEC
Shigella 0.4 (0.1-0.7) 0.3 (0.0-2.9) 0.4 (0.0-0.9) 0.7 (0.4-1.1) 2.9 (0.0-5.9) 3.1 (0.0-6.3) 0.2 (0.0-0.4)
Aeromonas 0.8 (0.0-1.8) 0.5 (0.2-0.9)
Campylobacter 2.4 (0.0-5.0) 0.4 (0.0-0.7)
jejuni
Typical EPEC
Salmonella
Vibrio cholerae 0.2 (0.0-0.5) 1.8 (0.0-3.8) 0.1 (0.0-0.3)
O1
PROTOZOA
Cryptosporidium 0.2 (0.0-0.4)
Entamoeba 0.3 (0.0-2.7)
histolytica
EAEC, enteroadherent Escherichia coli; EPEC, enteropathogenic Escherichia coli; ETEC, enterotoxigenic Escherichia coli; LT, heat-labile; ST, heat stable.

Table 340-6 Comparison of 3 Types of Enteric Infection

TYPE OF INFECTION
PARAMETER I II III
Mechanism Noninflammatory (enterotoxin or Inflammatory (invasion, cytotoxin) Penetrating
adherence/superficial invasion)
Location Proximal small bowel Colon Distal small bowel
Illness Watery diarrhea Dysentery Enteric fever
Stool examination No fecal leukocytes Fecal polymorphonuclear Fecal mononuclear leukocytes
Mild or no lactoferrin leukocytes
Lactoferrin
Examples Vibrio cholerae Shigella Salmonella typhi
Escherichia coli (ETEC, LT, ST) E. coli (EIEC, EHEC) Yersinia enterocolitica
Clostridium perfringens Salmonella enteritidis ?Campylobacter fetus
Bacillus cereus Vibrio parahaemolyticus
Staphylococcus aureus Clostridium difficile
Also: Campylobacter jejuni
Giardia lamblia Entamoeba histolytica*
Rotavirus
Norwalk-like viruses
Cryptosporidium parvum
E. coli (EPEC, EAEC)
Microsporidia
Cyclospora cayetanensis
*Although amebic dysentery involves tissue inflammation, the leukocytes are characteristically pyknotic or absent, having been destroyed by the virulent amebae.

Although not typically enterotoxic, these pathogens alter bowel physiology via adherence, superficial cell entry, cytokine induction, or toxins that inhibit cell
function.
EAEC, enteroaggregative E. coli; EHEC, enterohemorrhagic E. coli; EIEC, enteroinvasive E. coli; EPEC, enteropathogenic E. coli; ETEC, enterotoxigenic E. coli;
LT, heat-labile; ST, heat-stable.
From Mandell GL, Bennett JE, Dolin R, editors: Principles and practices of infectious diseases, ed 7, Philadelphia, 2010, Churchill Livingstone.
NSP4 STa
EAST1
Guanylin
Para-cellular Cl Zinc Uroguanylin
Ca2 disrupts
water flow secretion
Rota- cytoskeleton Increased
Baterial from CFTR
virus Cl secretion
toxins CT Yersinia spp.
(Cholera, LT
E. coli)
Replication
Disrupts
G
PLC TJ GC-C
M
YoPs
IP3
NSP4 PK
Ca2 from cGMP
ER stores cAMP
Ca2 from
ER stores
Crypt cell
Enterocyte
Adenylate
Directly or via cyclase
NSP4 ENS activation
Figure 340-3 Mechanism of cholera toxin. (Adapted from Thapar M,
Figure 340-2 Pathogenesis of rotavirus infection and diarrhea. ENS, Sanderson IR: Diarrhoea in children: an interface between developing
enteric nervous system; ER, endoplasmic reticulum; PLC, phospholi- and developed countries, Lancet 363:641653, 2004; and Montes M,
pase C; TJ, tight junction. (Adapted from Ramig RF: Pathogenesis of DuPont HL: Enteritis, enterocolitis and infectious diarrhea syndromes.
intestinal and systemic rotavirus infection, J Virol 78:1021310220, In Cohen J, Powderly WG, Opal SM, etal, editors: Infectious diseases,
2004.) ed 2, London, 2004, Mosby, pp. 3152.)

Toxigenic Inflammatory
Lumen of
small
intestine Glucose Glucose Glucose
Na Na Na
cAMP
Glucose Glucose Glucose
Na Na Na

Na Na Na
Na Na Na Na Na Na
H H H H H H
cAMP
HCO3 HCO3 HCO3 HCO3 HCO3 HCO3
Cl Cl Cl Cl Cl Cl

Inflammatory
cell
Villus Lumen of
small intestine
Crypt
Cl 2Cl cAMP Cl 2Cl Cl 2Cl

K K K K K K
Na Na Na Na Na Na
Cl Cl
A B
Figure 340-4 Movement of Na and Cl in the small intestine. A, Movement in normal subjects. Na+ is absorbed by 2 different mechanisms in
+
absorptive cells from villi: glucose-stimulated absorption and electroneutral absorption (which represents the coupling of Na+/H+ and Cl/HCO3
exchanges). B, Movement during diarrhea caused by a toxin and inflammation. (From Petri WA, Miller M, Binder HJ, etal: Enteric infections,
diarrhea and their impact on function and development, J Clin Invest 118:12771290, 2008.)
Shigella bacilli
M cell
Epithelial barrier
damage and more
Shigella enter
Colon
enterocyte
Neutrophils
IL-8, attraction and
other transmigration
mediators
Cell-cell and
basolateral
invasion Macrophage to
undergo apoptosis
Figure 340-5 Pathogenesis of Shigella infection and diarrhea. IL-8, Interleukin-8. (Adapted from Opal SM, Keusch GT: Host responses to infec-
tion. In Cohen J, Powderly WG, Opal SM, etal, editors: Infectious diseases, ed 2, London, 2004, Mosby, pp. 3152.)

Table 340-7 Proven Risk Factors with Direct Biologic Links to Diarrhea: Relative Risks (RR) or Odds Ratios (OR) and 95%
Confidence Intervals
DIARRHEA
MORBIDITY MORTALITY
No breastfeeding (0-5mo) RR = 2.65 (1.72-4.07) compared to RR = 10.52 (2.79-39.6) compared to exclusively
exclusively breastfed infants breastfed infants
No breastfeeding (6-23mo) RR = 1.32 (1.06-1.63) RR = 2.18 (1.14-4.16)
Underweight (<2WAZ) RR = 1.23 (1.12-1.35)
2 to <1WAZ OR = 2.1 (1.6-2.7)
3 to <2WAZ RR 1.23 (1.12-1.35) OR = 3.4 (2.7-16.5)
<3WAZ OR = 9.5 (5.5-16.5)
Stunted
2 to <1HAZ OR = 1.2 (0.9-1.7)
3 to <2HAZ OR = 1.6 (1.1-2.5)
<3HAZ OR = 4.6 (2.7-8.1)
Wasted
2 to <1WHZ OR = 1.2 (0.7-1.9)
3 to <2WHZ OR = 2.9 (1.8-4.5)
<3WHZ OR = 6.3 (2.7-14.7)
Vitamin A deficiency Inconsistent evidence RR = 1.47 (1.25-175)
Zinc deficiency RR = 1.15 (1.06-1.23) RR = 0.82
Crowding (>8 persons/kitchen)
Indoor air pollution
Unwashed hands RR = 0.58 (0.490.69) Risk relationship suggested but studies of poor
methodologic quality
Poor water quality (at source) RR = 0.73 (0.53-1.01) Inconsistent evidence Relationship suggested but few studies of sufficient
from blinded studies quality
Inappropriate excreta disposal Limited evidence suggests risk relationship
HAZ, height-for-age Z-score; WAZ, weight-for-age Z score; WHZ, weight-for-height Z-score.
Adapted from Walker CL, Rudan I, Liu L, etal: Global burden of childhood pneumonia and diarrhoea. Lancet 381:14051416, 2013.
and the nature of the infecting pathogen (Table 340-8). Usually the features of dysentery are very poor; the negative predictability for
ingestion of preformed toxins (e.g., those of S. aureus) is associated bacterial pathogens is much better in the absence of signs of dysentery.
with the rapid onset of nausea and vomiting within 6hr, with possible If warranted and if facilities and resources permit, the etiology can be
fever, abdominal cramps, and diarrhea within 8-72hr. Watery diarrhea verified by appropriate laboratory testing.
and abdominal cramps after an 8-16hr incubation period are associ-
ated with enterotoxin-producing C. perfringens and B. cereus. Abdomi- COMPLICATIONS
nal cramps and watery diarrhea after a 16-48hr incubation period can Most of the complications associated with gastroenteritis are related to
be associated with noroviruses, several enterotoxin-producing bacte- delays in diagnosis and delays in the institution of appropriate therapy.
ria, Cryptosporidium, and Cyclospora, and also have been a notable Without early and appropriate rehydration, many children with acute
feature of influenza virus H1N1 infections. Several organisms, includ- diarrhea would develop dehydration with associated complications
ing Salmonella, Shigella, C. jejuni, Yersinia enterocolitica, enteroinvasive (see Chapter 57). These can be life-threatening in infants and young
or hemorrhagic (Shigatoxin-producing) E. coli, and V. parahaemolyti- children. Inappropriate therapy can lead to prolongation of the diar-
cus, produce diarrhea that can contain blood as well as fecal leukocytes rheal episodes, with consequent malnutrition and complications such
in association with abdominal cramps, tenesmus, and fever; these fea- as secondary infections and micronutrient deficiencies (iron, zinc,
tures suggest bacterial dysentery and fever (Table 340-8). Bloody diar- vitamin A). In developing countries and HIV-infected populations,
rhea and abdominal cramps after a 72-120hr incubation period are associated bacteremias are well-recognized complications in malnour-
associated with infections from Shigella and also Shigatoxin-producing ished children with diarrhea.
E. coli, such as E. coli O157:H7. Organisms associated with dysentery Specific pathogens are associated with extraintestinal manifestations
or hemorrhagic diarrhea can also cause watery diarrhea alone without and complications. These are not pathognomonic of the infection, nor
fever or that precedes a more complicated course that results in do they always occur in close temporal association with the diarrheal
dysentery. episode (Table 340-9).
Although many of the manifestations of acute gastroenteritis in chil-
dren are nonspecific, some clinical features can help identify major DIAGNOSIS
categories of diarrhea and allow rapid triage for antibiotic or specific The diagnosis of gastroenteritis is based on clinical recognition, an
dietary therapy (see Tables 340-1 to 340-4). There is considerable evaluation of its severity by rapid assessment and by confirmation by
overlap in the symptomatology. The positive predictive values for the appropriate laboratory investigations, if indicated.

ment of Childhood Illnesses package that is being implemented in

Table 340-8 Differential Diagnosis of Acute Dysentery developing countries that have a high burden of diarrhea mortality
and Inflammatory Enterocolitis (Figs. 340-6 and 340-7).
SPECIFIC INFECTIOUS PROCESSES
Bacillary dysentery (Shigella dysenteriae, Shigella flexneri, Shigella Stool Examination
sonnei, Shigella boydii; invasive Escherichia coli) Microscopic examination of the stool and cultures can yield important
Campylobacteriosis (Campylobacter jejuni) information on the etiology of diarrhea. Stool specimens could be
Amebic dysentery (Entamoeba histolytica) examined for mucus, blood, and leukocytes. Fecal leukocytes indicate
Ciliary dysentery (Balantidium coli) bacterial invasion of colonic mucosa, although some patients with
Bilharzial dysentery (Schistosoma japonicum, Schistosoma mansoni) shigellosis have minimal leukocytes at an early stage of infection, as do
Other parasitic infections (Trichinella spiralis) patients infected with Shigatoxin-producing E. coli and E. histolytica.
Vibriosis (Vibrio parahaemolyticus) Recent advances in rapid molecular methods of diagnosis for bacterial
Salmonellosis (Salmonella typhimurium)
and parasitic infections have made the role of traditional microscopy
Typhoid fever (Salmonella typhi)
Enteric fever (Salmonella choleraesuis, Salmonella paratyphi) less important; however, this is still a useful test in developing coun-
Yersiniosis (Yersinia enterocolitica) tries. XTAG GPP is an FDA-approved gastrointestinal pathogen panel
Spirillar dysentery (Spirillum spp.) using multiplexed nucleic acid technology that detects Campylobacter,
C. difficile, toxin A/B, E. coli 0157, enterotoxigenic E. coli, Salmonella,
PROCTITIS
Shigella, Shiga-like toxin E. coli, norovirus, rotavirus A, Giardia, and
Gonococcal (Neisseria gonorrhoeae)
Herpetic (herpes simplex virus) Cryptosporidium. Stool cultures should be obtained as early in the
Chlamydial (Chlamydia trachomatis) course of disease as possible from children with bloody diarrhea in
Syphilitic (Treponema pallidum) whom stool microscopy indicates fecal leukocytes, in outbreaks with
suspected hemolytic-uremic syndrome, and in immunosuppressed
OTHER SYNDROMES
children with diarrhea. Stool specimens for culture need to be trans-
Necrotizing enterocolitis of the newborn
Enteritis necroticans
ported and plated quickly; if the latter is not quickly available, speci-
Pseudomembranous enterocolitis (Clostridium difficile) mens might need to be transported in special transport media. The
Typhlitis yield and diagnosis of bacterial diarrhea is improved by using molecu-
lar diagnostic procedures such as real-time polymerase chain reaction.
CHRONIC INFLAMMATORY PROCESSES In most previously healthy children with uncomplicated watery diar-
Enteropathogenic and enteroaggregative E. coli
Gastrointestinal tuberculosis
rhea, no laboratory evaluation is needed except for epidemiologic
Gastrointestinal mycosis purposes.
Parasitic enteritis
TREATMENT
SYNDROMES WITHOUT KNOWN INFECTIOUS CAUSE The broad principles of management of acute gastroenteritis in
Idiopathic ulcerative colitis
Crohn disease
children include oral rehydration therapy, enteral feeding and diet
Radiation enteritis selection, zinc supplementation, and additional therapies such as
Ischemic colitis probiotics.
Allergic enteritis
Oral Rehydration Therapy
From Mandell GL, Bennett JE, Dolin R, editors: Principles and practices of
infectious diseases, ed 7, Philadelphia, 2010, Churchill Livingstone.
Children, especially infants, are more susceptible than adults to dehy-
dration 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
Clinical Evaluation of Diarrhea 4-6hr according to the degree of dehydration and estimated daily
The most common manifestations of gastrointestinal tract infection in requirements. A small minority of children, especially those in shock
children are diarrhea, abdominal cramps, and vomiting. Systemic or unable to tolerate oral fluids, require initial intravenous rehydration,
manifestations are varied and associated with a variety of causes. The but oral rehydration is the preferred mode of rehydration and replace-
evaluation of a child with acute diarrhea includes: ment of ongoing losses (see Tables 340-8 and 340-9). Risks associated
Assessing the degree of dehydration and acidosis and provide with severe dehydration that might necessitate intravenous resuscita-
rapid resuscitation and rehydration with oral or intravenous fluids tion include: age <6mo; prematurity; chronic illness; fever >38C
as required (Tables 340-10 and 340-11). (100.4F) if younger than 3mo or >39C (102.2F) if 3-36mo of age;
Obtaining appropriate contact, travel, or exposure history. This bloody diarrhea; persistent emesis; poor urine output; sunken eyes;
includes information on exposure to contacts with similar and a depressed level of consciousness. The low-osmolality World
symptoms, intake of contaminated foods or water, child-care Health Organization (WHO) oral rehydration solution (ORS) contain-
center attendance, recent travel of patient or contact with a person ing 75mEq of sodium, 64mEq of chloride, 20mEq of potassium, and
who traveled to a diarrhea-endemic area, and use of antimicrobial 75mmol of glucose per liter, with total osmolarity of 245mOsm/L, is
agents. now the global standard of care and more effective than home fluids,
Clinically determining the etiology of diarrhea for institution of including decarbonated soda beverages, fruit juices, and tea. These are
prompt antibiotic therapy, if indicated. not suitable for rehydration or maintenance therapy because they have
Although nausea and vomiting are nonspecific symptoms, they indi- inappropriately high osmolalities and low sodium concentrations.
cate infection in the upper intestine. Fever suggests an inflammatory Figure 340-7 and Tables 340-10 and 340-11 outline a clinical evaluation
process but also occurs as a result of dehydration or coinfection (e.g., plan and management strategy for children with moderate to severe
urinary tract infection, otitis media). Fever is common in patients with diarrhea. Oral rehydration should be given to infants and children
inflammatory diarrhea. Severe abdominal pain and tenesmus indicate slowly, especially if they have emesis. It can be given initially by a
involvement of the large intestine and rectum. Features such as nausea dropper, teaspoon, or syringe, beginning with as little as 5mL at a time.
and vomiting and absent or low-grade fever with mild to moderate The volume is increased as tolerated. Replacement for emesis or stool
periumbilical pain and watery diarrhea indicate small intestine involve- losses is noted in Table 340-11. Oral rehydration can also be given by
ment and also reduce the likelihood of a serious bacterial infection. a nasogastric tube if needed; this is not the usual route.
This clinical approach to the diagnosis and management of diarrhea Limitations to oral rehydration therapy include shock, an ileus,
in young children is a critical component of the Integrated Manage- intussusception, carbohydrate intolerance (rare), severe emesis, and

Table 340-9 Extraintestinal Manifestations of Enteric Infections

MANIFESTATION ASSOCIATED ENTERIC PATHOGEN(S) ONSET AND PROGNOSIS
Focal infections from systemic spread of All major pathogens can cause such Onset usually during the acute infection but can occur
bacterial pathogens, including direct extraintestinal infections, subsequently
vulvovaginitis, urinary tract infection, including Salmonella, Shigella, Yersinia, Prognosis depends on infection site
endocarditis, osteomyelitis, meningitis, Campylobacter, Clostridium difficile
pneumonia, hepatitis, peritonitis,
chorioamnionitis, soft-tissue infection,
and septic thrombophlebitis
Reactive arthritis Salmonella, Shigella, Yersinia, Typically occurs 1-3wk after infection
Campylobacter, Cryptosporidium, Relapses after reinfection can develop in 15-50% of
C. difficile people, but most children recover fully within 2-6mo
after the first symptoms appear
Guillain-Barr syndrome Campylobacter Usually occurs a few weeks after the original infection
Prognosis is good although 15-20% may have sequelae
Glomerulonephritis Shigella, Campylobacter, Yersinia 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
Immunoglobulin A (IgA) nephropathy Campylobacter Characterized by recurrent episodes of blood in the
urine, this condition results from deposits of the
protein IgA in the glomeruli. IgA nephropathy can
progress for years with no noticeable symptoms
Men seem more likely to develop this disorder than
women
Erythema nodosum Yersinia, Campylobacter, Salmonella Although painful, is usually benign and more commonly
seen in adolescents
Resolves with 4-6wk
Hemolytic uremic syndrome Shigella dysenteriae 1, Escherichia coli Sudden onset, short-term renal failure
O157:H7, others 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 anemia Campylobacter, Yersinia Relatively rare complication and can have a chronic
course
From Centers for Disease Control and Prevention: Managing acute gastroenteritis among children, MMWR Recomm Rep 53:133, 2004.
Table 340-10 Symptoms Associated with Dehydration

MINIMAL OR NO MILD TO MODERATE
DEHYDRATION DEHYDRATION SEVERE DEHYDRATION
SYMPTOM (<3% LOSS OF BODY WEIGHT) (3-9% LOSS OF BODY WEIGHT) (>9% LOSS OF BODY WEIGHT)
Mental status Well; alert Normal, fatigued or restless, irritable Apathetic, lethargic, unconscious
Thirst Drinks normally; might refuse Thirsty; eager to drink Drinks poorly; unable to drink
liquids
Heart rate Normal Normal to increased Tachycardia, with bradycardia in
most severe cases
Quality of pulses Normal Normal to decreased Weak, thready, or impalpable
Breathing Normal Normal; fast Deep
Eyes Normal Slightly sunken Deeply sunken
Tears Present Decreased Absent
Mouth and tongue Moist Dry Parched
Skinfold Instant recoil Recoil in <2sec Recoil in >2sec
Capillary refill Normal Prolonged Prolonged; minimal
Extremities Warm Cool Cold; mottled; cyanotic
Urine output Normal to decreased Decreased Minimal
Adapted from Duggan C, Santosham M, Glass RI: The management of acute diarrhea in children: oral rehydration, maintenance, and nutritional therapy, MMWR
Recomm Rep 41(RR-16):120, 1992; and World Health Organization: The treatment of diarrhoea: a manual for physicians and other senior health workers, Geneva,
1995, World Health Organization; Centers for Disease Control and Prevention: Diagnosis and management of foodborne illnesses, MMWR 53(RR-4):1-33, 2004.

high stool output (>10mL/kg/hr). Ondansetron (oral mucosal absorp- can be affected in children with prolonged diarrhea, there is evidence
tion preparation) reduces the incidence of emesis, thus permitting that satisfactory carbohydrate, protein, and fat absorption can take
more effective oral rehydration and is well established in emergency place on a variety of diets. Once rehydration is complete, food should
management of acute gastroenteritis in developed countries. be reintroduced while oral rehydration is continued to replace ongoing
losses from emesis or stools and for maintenance. Breastfeeding or
Enteral Feeding and Diet Selection nondiluted regular formula should be resumed as soon as possible.
Continued enteral feeding in diarrhea aids in recovery from the Foods with complex carbohydrates (rice, wheat, potatoes, bread, and
episode, and a continued age-appropriate diet after rehydration is the cereals), lean meats, yogurt, fruits, and vegetables are also tolerated.
norm. Although intestinal brush-border surface and luminal enzymes Fatty foods or foods high in simple sugars (juices, carbonated sodas)
Table 340-11 Summary of Treatment Based on Degree of Dehydration

DEGREE OF DEHYDRATION REHYDRATION THERAPY REPLACEMENT OF LOSSES NUTRITION
Minimal or no dehydration Not applicable <10kg body weight: 60-120mL ORS Continue breastfeeding or
for each diarrheal stool or vomiting resume age-appropriate
episode >10kg body weight: normal diet after initial
120-240mL ORS for each diarrheal hydration, including adequate
stool or vomiting episode caloric intake for maintenance*
Mild to moderate dehydration ORS, 50-100mL/kg body weight Same Same
over 3-4hr
Severe dehydration Lactated Ringer solution or normal Same; if unable to drink, administer Same
saline in 20mL/kg body weight through nasogastric tube or
IV until perfusion and mental administer 5% dextrose in normal
status improve; then administer saline with 20mEq/L potassium
100mL/kg body weight ORS chloride IV
over 4hr or 5% dextrose normal
saline IV at twice maintenance
fluid rates
*Overly restricted diets should be avoided during acute diarrheal episodes. Breastfed 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. Lactose-containing 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.
ORS, oral rehydration solution.
Two of the following signs: If child has no other severe classification:

Does the child have diarrhea? -Give fluid for severe dehydration (Plan C).
Lethargic or unconscious OR
If yes, ask: Look and feel: Sunken eyes If child also has another severe classification:
Not able to drink or drinking Severe - Refer URGENTLY to hospital with mother
For how long? Look at the childs general poorly dehydration giving frequent sips of ORS on the way.
condition. Skin pinch goes back very Advise the mother to continue breastfeeding.
Is there blood
Is the child: slowly.
in the stool?
Lethargic or unconscious? If child is two years or older and there is cholera
Restless and irritable? in your area, give antibiotic for cholera.
Look for sunken eyes. Two of the following signs: Give fluid and food for some dehydration (Plan B).
For dehydration
Offer the child fluid. Is the child: Restless irritable If child also has a severe classification:
Not able to drink or drinking poorly? Sunken eyes Some - Refer URGENTLY to hospital with mother
Drinking eagerly, thirsty? Drinks eagerly, thirsty dehydration giving frequent sips of ORS on the way.
Skin pinch goes back slowly. Advise the mother to continue breastfeeding.
Pinch the skin of the abdomen.
Does it go back: Advise mother when to return immediately.
Classify Follow-up in 2 days if not improving.
Very slowly (longer than 2
seconds)? diarrhea Not enough signs to classify Give fluid and food to treat diarrhea at home (Plan A).
Slowly? No
as some or severe Advise mother when to return immediately.
dehydration
dehydration Follow-up in 2 days if not improving.
Dehydration present Severe Treat dehydration before referral unless the child has
persistent another severe classification.
diarrhea Refer to hospital.
And if diarrhea
14 days or more No dehydration Advise the mother on feeding a child who has
PERSISTENT DIARRHEA.
Persistent
Give multivitamin, mineral supplement for two weeks
diarrhea
Advise mother when to return immediately
Follow-up in 5 days.
Blood in the stool Treat for 5 days with an oral antibiotic

And if blood Dysentery recommended for Shigella.
in stool Advise mother when to return immediately
Follow-up in 5 days.
Figure 340-6 Integrated Management of Childhood Illnesses (IMCI) protocol for the recognition and management of diarrhea in developing
countries. ORS, Oral rehydration solution.

Persistent diarrhea
(diarrhea 14 days with malnutrition)
Assessment, resuscitation, and early stabilization

SUSPECTED Intravenous and/or oral rehydration (hypo-osmolar ORS)
SEVERE Treat electrolyte imbalance
DEHYDRATION Screen and treat associated systemic infections
Continued breastfeeding
Reduced lactose load by
Milk-cereal (usually rice-based) diet or
Replacement of milk with yogurt
Micronutrient supplementation (zinc, vitamin A, folate)
Recovery Continued or recurrent diarrhea

Poor weight gain
Follow-up for growth Reinvestigate for infections

Second-line dietary therapy (comminuted chicken or elemental diets)
Continued diarrhea and dehydration
Refer URGENTLY to Reinvestigate to exclude intractable diarrhea of infancy

hospital for IV or NG Intravenous hyperalimentation plus
treatment Slow or continuous enteral alimentation
DANGER SIGNS, COUGH

DIARRHEA
ASSESS AND CLASSIFY
Figure 340-7 Management of persistent diarrhea. IV, Intravenous; NG, nasogastric tube; ORS, oral rehydration solution.
should be avoided. The usual energy density of any diet used for the algorithm for managing children with prolonged diarrhea in develop-
therapy of diarrhea should be around 1kcal/g, aiming to provide an ing countries.
energy intake of a minimum of 100kcal/kg/day and a protein intake Among children in low- and middle-income countries, where the
of 2-3g/kg/day. In selected circumstances when adequate intake of dual burden of diarrhea and malnutrition is greatest and where access
energy-dense food is problematic, the addition of amylase to the diet to proprietary formulas and specialized ingredients is limited, the use
through germination techniques can also be helpful. of locally available age-appropriate foods should be promoted for the
With the exception of acute lactose intolerance in a small subgroup, majority of acute diarrhea cases. Lactose intolerance is an important
most children with diarrhea are able to tolerate milk and lactose- complication in some cases, but even among those children for whom
containing diets. Withdrawal of milk and replacement with specialized lactose avoidance may be necessary, nutritionally complete diets com-
(and expensive) lactose-free formulations are unnecessary. Although prised of locally available ingredients can be used at least as effectively
children with persistent diarrhea are not lactose intolerant, administra- as commercial preparations or specialized ingredients. These same
tion of a lactose load exceeding 5g/kg/day may be associated with conclusions may also apply to the dietary management of children with
higher purging rates and treatment failure. Alternative strategies for persistent diarrhea, but the evidence remains limited.
reducing the lactose load while feeding malnourished children who
have prolonged diarrhea include addition of milk to cereals and Zinc Supplementation
replacement of milk with fermented milk products such as yogurt. Zinc supplementation in children with diarrhea in developing coun-
Rarely, when dietary intolerance precludes the administration of tries leads to reduced duration and severity of diarrhea and could
cows milkbased formulations or whole milk it may be necessary to potentially prevent a large proportion of cases from recurring. Zinc
administer specialized milk-free diets such as a comminuted or blend- administration for diarrhea management can significantly reduce all-
erized chicken-based diet or an elemental formulation. Although cause mortality by 46% and hospital admission by 23%. In addition to
effective in some settings, the latter are unaffordable in most develop- improving diarrhea recovery rates, administration of zinc in commu-
ing countries. In addition to rice-lentil formulations, the addition of nity settings leads to increased use of ORS and reduction in the inap-
green banana or pectin to the diet has also been shown to be effective propriate use of antimicrobials. All children older than 6mo of age
in the treatment of persistent diarrhea. Figure 340-7 gives an with acute diarrhea in at-risk areas should receive oral zinc (20mg/

day) in some form for 10-14 days during and continued after diarrhea. interventions to reduce the risk of premature childhood mortality and
The role of zinc in well nourished, zinc replete populations in devel- the potential to prevent 12% of all deaths of children younger than
oped countries is less certain. 5yr of age.
Additional Therapies Improved Complementary Feeding Practices

The use of probiotic nonpathogenic bacteria for prevention and therapy There is a strong inverse association between appropriate, safe comple-
of diarrhea has been successful in some settings although the evidence mentary feeding and mortality in children age 6-11mo; malnutrition
is inconclusive to recommend their use in all settings. In addition to is an independent risk for the frequency and severity of diarrheal
restoring beneficial intestinal flora, probiotics can enhance host protec- illness. Complementary foods should be introduced at 6mo of age, and
tive immunity such as downregulation of proinflammatory cytokines breastfeeding should continue for up to 2yr. Complementary foods in
and upregulation of anti inflammatory cytokines. A variety of organ- developing countries are generally poor in quality and often are heavily
isms (Lactobacillus, Bifidobacterium) have a good safety record; therapy contaminated, thus predisposing to diarrhea. Contamination of com-
has not been standardized and the most effective (and safe) organism plementary foods can be potentially reduced through caregivers edu-
has not been identified. Saccharomyces boulardii is effective in cation and improving home food storage. Improved vitamin A status
antibiotic-associated and in C. difficile diarrhea, and there is some has been shown to reduce the frequency of severe diarrhea. Vitamin A
evidence that it might prevent diarrhea in daycare centers. Lactobacil- supplementation reduces all-cause childhood mortality by 25% (95%
lus rhamnosus GG is associated with reduced diarrheal duration and confidence interval [CI], 12-36%) and diarrhea-specific mortality by
severity, which reduction is more evident in cases of childhood rota- 30% (95% CI, 14-42%).
virus diarrhea.
Antimotility agents (loperamide) are contraindicated in children Rotavirus Immunization
with dysentery and probably have no role in the management of acute Most infants acquire rotavirus diarrhea early in life; an effective rota-
watery diarrhea in otherwise healthy children. Similarly, antiemetic virus vaccine would have a major effect on reducing diarrhea mortality
agents, such as the phenothiazines, are of little value and are associated in developing countries. In 1998, a quadrivalent Rhesus rotavirus-
with potentially serious side effects (lethargy, dystonia, malignant derived vaccine was licensed in the United States but subsequently
hyperpyrexia). Nonetheless, ondansetron is an effective and less-toxic withdrawn because of an increased risk of intussusception. Subsequent
antiemetic agent and as indicated previously, is a useful adjunct to the development and testing of newer rotavirus vaccines have led to their
treatment of vomiting in ambulatory settings with reduced risk of introduction in most developed countries and approval by the WHO
intravenous fluid requirements and hospitalization. Because persistent in 2009 for widespread use in developing countries. It is now clear
vomiting can limit oral rehydration therapy, a single sublingual dose that the introduction of these vaccines is associated with a significant
of an oral dissolvable tablet of ondansetron (4mg 4-11yr and 8mg reduction in severe diarrhea and associated mortality.
for children older than 11yr [generally 0.2mg/kg]) may be given. The institution of large-scale rotavirus vaccination programs has led
However, most children do not require specific antiemetic therapy; to major reduction in the burden of disease and associated mortality.
careful oral rehydration therapy is usually sufficient. In an evaluation of large-scale rotavirus vaccine introduction, coverage
Racecadotril, an enkephalins inhibitor, has inconsistently been rate of 74% was achieved in infants younger than 12mo of age, with
shown to reduce stool output in patients with diarrhea. Experience 41% reduction (95% CI, 36-47%) in diarrhea-related mortality. In an
with this drug in children is limited, and for the average child with evaluation of the vaccine in Africa, overall protective efficacy against
acute diarrhea it may be unnecessary. rotavirus gastroenteritis ranged from 49-61%, with 30% protective effi-
cacy against all-cause severe gastroenteritis in infancy. Vaccine (live
Antibiotic Therapy virus) associated rotavirus infection has been reported in children with
Timely antibiotic therapy in select cases of diarrhea related to bacterial severe combined immunodeficiency disease, but the vaccine has been
infections can reduce the duration and severity of illness and prevent shown to be safe in HIV-infected populations.
complications (Table 340-12). Although these agents are important to Other vaccines that could potentially reduce the burden of severe
use in specific cases, their widespread and indiscriminate use leads to diarrhea and mortality in young children are vaccines against cholera,
the development of antimicrobial resistance. Nitazoxanide, an antiin- Shigella, and ETEC. Preventive use of cholera vaccines in endemic
fective agent, is effective in the treatment of a wide variety of patho- countries can reduce the risk of developing cholera by 52% (95% CI,
gens, including C. parvum, G. lamblia, E. histolytica, Blastocystis 36-65%).
hominis, C. difficile, and rotavirus.
Improved Water and Sanitary Facilities and
PREVENTION Promotion of Personal and Domestic Hygiene
In many developed countries, diarrhea caused by pathogens such as Much of the reduction in diarrhea prevalence in the developed world
C. botulinum, E. coli O157:H7, Salmonella, Shigella, V. cholerae, is the result of improvement in standards of hygiene, sanitation, and
Cryptosporidium, and Cyclospora is a notifiable disease and, thus, water supply. Strikingly, an estimated 88% of all diarrheal deaths
contact tracing and source identification is important in preventing worldwide can be attributed to unsafe water, inadequate sanitation, and
outbreaks. poor hygiene. Improving water quality can reduce the risk of diarrhea
Many developing countries struggle with huge disease burdens of by 17%, whereas hand washing with soap and safe excreta disposal
diarrhea where a wider approach to diarrhea prevention may be reduce the risk of diarrhea by 48% and 36%, respectively. Behavioral
required. Preventive strategies may be of relevance to both developed change strategies through promotion of handwashing indicate that
and developing countries. handwashing promotion and access to soap reduces the burden of
diarrhea in developing countries.
Promotion of Exclusive Breastfeeding
Exclusive breastfeeding (administration of no other fluids or foods for Improved Case Management of Diarrhea
the 1st 6mo of life) is not common, especially in many developed Improved management of diarrhea through prompt identification and
countries. Exclusive breastfeeding protects very young infants from appropriate therapy significantly reduces diarrhea duration, its nutri-
diarrheal disease through the promotion of passive immunity and tional penalty, and risk of death in childhood. Improved management
through reduction in the intake of potentially contaminated food of acute diarrhea is a key factor in reducing the burden of prolonged
and water. Breast milk contains all the nutrients needed in early episodes and persistent diarrhea. The WHO/UNICEF recommenda-
infancy, and when continued during diarrhea, it also diminishes the tions to use low-osmolality ORS and zinc supplementation for the
adverse impact on nutritional status. Exclusive breastfeeding for the management of diarrhea, coupled with selective and appropriate use
1st 6mo of life is widely regarded as one of the most effective of antibiotics, have the potential to reduce the number of diarrheal

Table 340-12 Antibiotic Therapy for Infectious Diarrhea

ORGANISM DRUG OF CHOICE DOSAGE AND DURATION OF TREATMENT
Shigella (severe dysentery Ciprofloxacin, ampicillin, ceftriaxone, azithromycin, or Ceftriaxone 50-100mg/kg/day IV or IM, qd or bid 7 days
and EIEC dysentery) TMP-SMX Ciprofloxacin 20-30mg/kg/day PO bid 7-10 days
Most strains are resistant to several antibiotics Ampicillin PO, IV 50-100mg/kg/day qid 7 days
EPEC, ETEC, EIEC TMP-SMX or ciprofloxacin TMP 10mg/kg/day and SMX 50mg/kg/day bid 5 days
Ciprofloxacin PO 20-30mg/kg/day qid for 5-10 days
Salmonella No antibiotics for uncomplicated gastroenteritis in See treatment of Shigella
normal hosts caused by nontyphoidal species
Treatment indicated in infants younger than 3mo,
and patients with malignancy, chronic GI disease,
severe colitis hemoglobinopathies, or HIV infection,
and other immunocompromised patients
Most strains are resistant to multiple antibiotics
Aeromonas/Plesiomonas TMP-SMX TMP 10mg/kg/day and SMX 50mg/kg/day bid for 5 days
Ciprofloxacin Ciprofloxacin PO 20-30mg/kg/day divided bid 7-10 days
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 50mg/kg/day divided tid 5 days
Azithromycin PO 5-10mg/kg/day qid 5 days
Clostridium difficile Metronidazole (first line) PO 30mg/kg/day divided qid 5 days; max 2g
Discontinue initiating antibiotic
Vancomycin (second line) PO 40mg/kg/day qid 7 days, max 125mg
Entamoeba histolytica Metronidazole followed by iodoquinol or Metronidazole PO 30-40mg/kg/day tid 7-10 days
paromomycin Iodoquinol PO 30-40mg/kg/day tid 20 days
Paromomycin PO 25-35mg/kg/day tid 7 days
Giardia lamblia Furazolidone or metronidazole or albendazole or Furazolidone PO 25mg/kg/day qid 5-7 days
quinacrine Metronidazole PO 30-40mg/kg/day tid 7 days
Albendazole PO 200mg bid 10 days
Cryptosporidium spp. Nitazoxanide PO treatment may not be needed in Children 1-3yr: 100mg bid 3 days
normal hosts Children 4-11yr: 200mg bid
In immunocompromised, PO immunoglobulin +
aggressively treat HIV, etc.
Isospora spp. TMP-SMX PO TMP 5mg/kg/day and SMX 25mg/kg/day, bid 7-10
days
Cyclospora spp. TMP/SMX PO TMP 5mg/kg/day and SMX 25mg/kg/day bid 7
days
Blastocystis hominis Metronidazole or iodoquinol Metronidazole PO 30-40mg/kg/day tid 7-10 days
Iodoquinol PO 40mg/kg/day tid 20 days
EIEC, Enteroinvasive Escherichia coli; EPEC, enteropathogenic E. coli; ETEC, enterotoxigenic E. coli; GI, gastrointestinal; max, maximum; SMX, sulfamethoxazole;
TMP, trimethoprim.
deaths among children through Community Case Management and on the season and the region visited (see Table 340-12). Travelers diar-
Integrated Management of Childhood Illnesses. rhea has a high attack rate among travelers from higher-income coun-
Community-based interventions to diagnose and treat childhood tries visiting, during the summer, countries in a warmer climate that
diarrhea through community health workers leads to a significant rise have a high prevalence of indigenous infectious diarrhea. Travelers
in care seeking behaviors for diarrhea and are associated with signifi- diarrhea can manifest with watery diarrhea or as dysentery. Without
cantly increased use of ORS and zinc at household level as well as treatment, 90% will have resolved within a week and 98% within a
reduction in the unnecessary use of antibiotics for diarrhea by 75%. month of onset. Some individuals develop more severe diarrhea and
become dehydrated or unwell and may experience systemic complica-
Bibliography is available at Expert Consult. tions that warrant further attention. Most cases of travelers diarrhea
resolve spontaneously and a simple stool culture may be the only
investigation required. For those individuals with ongoing symptoms,
further tests should be requested depending on the history and clinical
340.1 Travelers Diarrhea presentation.
Zulfiqar Ahmed Bhutta
TREATMENT
Travelers diarrhea is a common complication of visitors to developing Travelers diarrhea is often self-limiting but requires particular atten-
countries and is caused by a variety of pathogens, in part depending tion to avoid dehydration. For infants and children, rehydration, as

Chapter 340 Acute Gastroenteritis in Children 1874.e1
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Centers for Disease Control and Prevention: Cryptosporidiosis surveillance disease in infants and young children in developing countries (the Global
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discussed in Chapter 340, is appropriate, followed by a standard diet.
Adolescents and adults should increase their intake of electrolyte-rich
fluids. Kaolin-pectin, anticholinergic agents, Lactobacillus, and bismuth
salicylate have not been effective therapies. Loperamide, an antimotil-
ity and antisecretory agent, reduces the number of stools in older
children with watery diarrhea and improves outcomes when used in
combination with antibiotics in travelers diarrhea. However, loper-
amide should be used with great caution or not at all in febrile or toxic
patients with dysentery and in those with bloody diarrhea.
Antibiotics, with or without loperamide, can also reduce the number
of unformed stools. Short-duration (3 days) therapy with fluoroquino-
lones, trimethoprim-sulfamethoxazole, azithromycin, or rifaximin is
effective; the choice of antibiotic depends on the age of the patient, the
potential organism, and the organisms local resistance patterns.
However, antibiotics often have a negative risk-benefit ratio when
weighing potential side effects vs treatment need for a short-lasting and
self-limiting disease such as travelers diarrhea. Azithromycin has
several advantages over other antibiotics. It is taken only once
(1,000mg), the rate of antimicrobial resistance is low, and it has a good
safety profile. Furthermore, in contrast to rifaximin, it can be used in
severe cases of diarrhea with fever or bloody stools and can even be
administered in children. Optionally, azithromycin can be combined
with antimotility medications such as loperamide. Travelers should be
reminded that diarrhea can be a symptom of other severe diseases,
such as malaria. Therefore, if diarrhea persists or additional symptoms
such as fever occur, travelers should seek medical advice. For up-to-
date information on local pathogens and resistant patterns, see
www.cdc.gov/travel.
PREVENTION
Travelers should drink bottled or canned beverages or boiled water.
They should avoid ice, salads, and fruit they did not peel them-
selves. Food should be eaten hot, if possible. Raw or poorly cooked
seafood is a risk, as is eating in a restaurant rather than a private
home. Swimming pools and other recreational water sites can also be
contaminated.
Chemoprophylaxis is not routinely recommended for previously
healthy children or adults. Nonetheless, travelers should bring azithro-
mycin (younger than 16yr of age) or ciprofloxacin (older than 16yr
of age) and begin antimicrobial therapy if diarrhea develops.
Bibliography is available at Expert Consult.

Bibliography Hill DR, Ryan ET: Management of travellers diarrhoea, BMJ 337:863867, 2008.
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Clin North Am 60(2):507527, 2013. 2006.
Gascn J: Epidemiology, etiology and pathophysiology of travelers diarrhea, Paulke-Korinek M, Kollaritsch H: Treatment of travelers diarrhea, Curr Opin Infect
Digestion 73(Suppl 1):102108, 2006. Dis 17, 2013.
Hearn P, Doherty T: Diarrhoea in travellers, Medicine (Baltimore) 42(2):8488,
2014.


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1854 Part XVIII The Digestive System

and astroviruses (see Table 340-2). Foodborne outbreaks in the United

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found in stool, quantitative

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Table 340-6 Comparison of 3 Types of Enteric Infection

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ment of Childhood Illnesses package that is being implemented in

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Table 340-9 Extraintestinal Manifestations of Enteric Infections

Table 340-10 Symptoms Associated with Dehydration

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Table 340-11 Summary of Treatment Based on Degree of Dehydration

Two of the following signs: If child has no other severe classification:

Blood in the stool Treat for 5 days with an oral antibiotic

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Assessment, resuscitation, and early stabilization

Recovery Continued or recurrent diarrhea

Follow-up for growth Reinvestigate for infections

Refer URGENTLY to Reinvestigate to exclude intractable diarrhea of infancy

DANGER SIGNS, COUGH

ASSESS AND CLASSIFY

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Additional Therapies Improved Complementary Feeding Practices

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Table 340-12 Antibiotic Therapy for Infectious Diarrhea

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Bibliography is available at Expert Consult.

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