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Epidemiology, pathogenesis, clinical presentation and diagnosis of viral

gastroenteritis in children
David O Matson, MD, PhD
Section Editors
Morven S Edwards, MD
George D Ferry, MD
Deputy Editor
Mary M Torchia, MD

Last literature review version 19.3: Fri Sep 30 00:00:00 GMT 2011 | This topic last
updated: Thu Mar 17 00:00:00 GMT 2011(More)

INTRODUCTION — Gastroenteritis ranks with respiratory tract infection as the most

common infectious disease syndrome of humans. Approximately five billion episodes of
diarrhea occur worldwide annually, accounting for 15 to 30 percent of all deaths in some
countries [1].

Bacterial and parasitic gastrointestinal infections have decreased in frequency as a result of

improvements in public health infrastructure from the treatment, piping, and proper delivery
of drinking water and disposal of sewage. However, viral gastroenteritis has not declined in
a comparable fashion from these interventions.

The epidemiology, pathogenesis, clinical features, and diagnosis of viral gastroenteritis in

children will be reviewed here. Mass immunization with rotavirus vaccines has changed the
epidemiology of that infection and of acute infectious gastroenteritis overall. The prevention
and treatment of this infection are discussed separately. (See "Prevention and treatment of
viral gastroenteritis in children".)

ETIOLOGIC AGENTS — Many microbial pathogens cause acute gastroenteritis [2]. In

addition, a number of non-infectious conditions can present with symptoms
indistinguishable from those of infectious gastroenteritis (table 1). (See "Evaluation of
diarrhea in children", section on 'Causes'.)

Microbes generally are called "enteritis pathogens" when their infection results in intestinal
symptoms. Enteritis pathogens newly recognized since 1970 include viruses (table 2),
parasitic agents (eg, Isospora belli, Cryptosporidium, Giardia), and bacterial agents (eg,
Campylobacter jejuni, C. upsaliensis, Clostridium difficile, some Escherichia coli, Salmonella
strains, Mycobacteria such as M. avium complex). The illness caused by enteritis pathogens
varies but generally includes a combination of diarrhea, vomiting, and fever, of differing
duration and severity.

The viral gastroenteritis pathogens all infect the intestine and induce gastrointestinal
symptoms. This shared ability contrasts with so-called "enteric viruses" that may infect the
intestine but predominantly produce manifestations at extraintestinal sites. For example,
many picornaviruses (echoviruses, coxsackieviruses, and polioviruses) and the SARS
coronavirus cause mild gastroenteritis, but the illnesses for which they are recognized are
extraintestinal (eg, pleuritis, myocarditis, and neuritis or pneumonia).
The proven pathogens of viral gastroenteritis are (table 2):

 Rotaviruses
 Caliciviruses
 Astroviruses
 Enteric adenovirus serotypes 40 and 41 (group F)
 Some picornaviruses (eg, Aichi virus)

Commercial assays are available for rotaviruses, astroviruses, adenoviruses 40 and 41, and
Norovirus caliciviruses.

Additional viruses, including non-group F adenoviruses, coronaviruses, pestiviruses, Breda

virus, parvoviruses, toroviruses, and picobirnaviruses and other picornaviruses (eg,
echovirus 22) have been linked to human gastroenteritis with varying degrees of certainty
[3-5]. Most of these viruses cause gastroenteritis in animals, a factor that directed interest
to their role in human illness. Animal-to-human transmission certainly has occurred for
many of these agents, although the likelihood and frequency of cross-species infections are

EPIDEMIOLOGY — Viral gastroenteritis occurs in both developed and developing countries.

The epidemiology presented here generally pertains to developed countries.

 Burden of illness — Approximately 1 in 50 children born each year in developed

nations is hospitalized for acute gastroenteritis sometime during childhood (<18
years of age). Viral gastroenteritis accounts for approximately 3 to 5 percent of all
hospital days and 7 to 10 percent of hospitalizations each year for children younger
than 18 years [1,6].

More than 95 percent of viral gastroenteritis hospitalizations occur in children

younger than five years. The highest rate of illness occurs in children between 3 and
24 months of age, increased risk resulting from clearance of transplacental antibody
and weaning, and decreased risk with acquisition of protective immunity [7,8].

Among children younger than five years, the average rate of illness ranges from one
to five episodes per child-year, resulting in a total of 15 to 25 million episodes of
acute gastroenteritis per year in the US [6,9,10]. Approximately 3 to 5 million of
these episodes result in clinician visits, and 200,000 in hospitalization.
 Etiology — Before rotavirus immunization, approximately one-half of hospitalizations
for acute, nonbacterial gastroenteritis in children in the United States were caused by
rotavirus, and 5 to 15 percent each by caliciviruses, astroviruses, and enteric
adenoviruses. The remaining one-fourth to one-third of cases cannot be linked to
any of these pathogens, but probably represent underdiagnosis of the common
pathogens [11-13]. Rotavirus also accounts for the majority of cases of severe viral
gastroenteritis in developing countries [14-16]. Rotavirus immunization is discussed
separately. (See "Rotavirus vaccines".)
 Season — Hospitalizations for viral gastroenteritis peak in the winter; 70 to 90
percent of viral gastroenteritis-related hospitalizations occur during the winter.
During the peak month, which varies from region to region, viral gastroenteritis may
account for 20 to 25 percent of pediatric hospitalizations.
 Transmission — The fecal-oral route is the major mechanism of transmission of the
viral enteropathogens. However, the possibility of respiratory tract inoculation has
been suggested by the explosiveness of some outbreaks of rotavirus and calicivirus
infection in situations apparently precluding fecal-oral spread [17,18].

PATHOGENESIS — The predominant clinical manifestations of rotaviral gastroenteritis

result from intestinal infection [19-22]. The first day after exposure, the virus infects
enterocytes within the villous epithelium of the jejunum and ileum, leading to destruction of
the cells of this layer. Destruction of enterocytes results in a transudation of fluid into the
intestinal lumen and net loss of fluid and salt in feces. During days two to five after
infection, adjacent villi fuse, reducing the surface area of injury and improving integrity of
the barrier against fluid loss. From days 6 to 10 after infection, normal villous architecture is

Intestinal injuries lead to a loss of the ability to digest food (especially complex sugars) and
to absorb digested food across the intestinal mucosa. This inability to digest complex sugars
manifests as transient lactose intolerance.

In addition, rotaviruses may cause secretory diarrhea via the nonstructural glycoprotein
(NSP4) enterotoxin, which alters intracellular Ca+2 mobilization in GI epithelial cells
[23,24]. Elevation of ionized Ca+2 leads to age-dependent halide ion movement across the
plasma membrane. Altered Ca+2 mobilization may signal other Ca+2-sensitive cellular
processes, such as cation channels and ion and solute transporters to increase fluid
secretion while curtailing fluid absorption [25]. These primary Ca+2-dependent steps
appear to be cyclic nucleotide-independent. A secondary component appears to involve the
enteric nervous system and may be cyclic nucleotide-dependent [26].

CLINICAL PRESENTATION — The clinical manifestations of viral gastroenteritis include

diarrhea, vomiting, fever, anorexia, headache, abdominal cramps, and myalgia. None of
these symptoms clearly distinguishes among the viral pathogens or viral gastroenteritis
from diarrheal illness due to bacterial or parasitic organisms. However, there are some
clinical and epidemiologic clues that favor viral over other causes of gastroenteritis.
(See 'Differential diagnosis' below.)

Viral gastroenteritis generally manifests with loose, watery stools that can be normal in
color or relatively pale colored. As many as 20 episodes of vomiting and 20 episodes of
diarrhea can occur during a single day. Stools may be odorless or foul-smelling.

The constellation of symptoms varies from day to day and from person to person. Illness
usually begins 12 hours to 4 days after exposure and generally lasts for three to seven days
[19,21,22]. Children may have only diarrhea or vomiting at first, but with progression
become sufficiently ill to require hospitalization. Other symptoms may develop as the
disease evolves; approximately 10 percent of children hospitalized for rotavirus infection
have only fever and/or vomiting at the time of admission [12].
Although viral gastroenteritis is common, and virtually every child has more than one
symptomatic episode, most viral enteric infections are asymptomatic, but the asymptomatic
patient may transmit the virus to others [7,27].

Factors associated with severe or prolonged clinical manifestations include:

 First infection with a particular pathogen

 Malnutrition or an immunocompromised host
 Lack of maternally acquired immunity (eg, antibody acquired transplacentally or in
human milk)
 Change in serotype of the infecting strain
 Large inoculum size
 Strain virulence

Except for Aichi virus, each of the enteric viruses causing gastroenteritis includes multiple
serotypes. No differences in clinical outcome have been attributed specifically to serotype or
to differences in age at time of infection.

INITIAL EVALUATION — The initial evaluation of children with symptoms of acute

gastroenteritis focuses on assessment of severity of illness and exclusion of causes of
vomiting and/or diarrhea that require definitive therapy (eg, meningitis, acute abdominal
processes, diabetes mellitus, and toxic ingestions). A complete blood count (for evidence of
anemia or hemolysis; elevated white blood cell or band count that may indicate bacterial
infection), serum electrolytes, and stool studies (eg, fecal leukocytes, pH, reducing
substances) may be helpful.

The disease severity is reflected by the degree of hypovolemia [2]. Weight loss, prolonged
capillary refill time, loss of skin turgor, and abnormal respiratory pattern are the best
individual signs of hypovolemia. Other important signs include elevated temperature and
pulse, diminished systolic and/or diastolic blood pressure, sunken fontanel (in children
whose fontanel remains open), and dry mucus membranes (table 3). (See "Clinical
assessment and diagnosis of hypovolemia (dehydration) in children", section on 'clinical

Laboratory studies to evaluate the severity of hypovolemia are discussed separately.

Measurement of serum electrolytes is generally indicated for children who require
intravenous fluid repletion, for these values will guide rehydration approaches. (See "Clinical
assessment and diagnosis of hypovolemia (dehydration) in children", section on 'Laboratory

DIFFERENTIAL DIAGNOSIS — The clinical presentation may provide clues to suggest a

particular gastroenteritis pathogen.

Viral versus other pathogens

Clinical features — The age of the child, associated findings, appearance of the stool, and
history of exposures may provide clues to distinguish viral from other pathogens.
 Age — Bacterial and parasitic agents generally cause gastroenteritis in children at an
older age (eg, two to four years), whereas viral pathogens tend to cause serious
gastroenteritis in those younger than two years.
 Presence of blood or mucus — The presence of gross blood or mucus in the stool
suggests bacterial or parasitic infection; these almost never occur with viral
gastroenteritis. Blood detected in the stool only by guaiac test is not a useful
 Exposures — Bacterial or parasitic acute gastroenteritis may be associated with
foreign travel, exposure to poultry or other farm animals, or consumption of
processed meat.

Stool studies — Several stool studies also may provide clues that distinguish viral from
other pathogens:

 Fecal leukocytes — Presence of fecal leukocytes suggests a bacterial or parasitic

etiology (table 4). Fecal leukocytes are appreciated by examining a fecal smear
stained with a Wright stain. Fecal leukocytes indicate inflammation in the bowel wall
but do not distinguish between infectious and non-infectious inflammatory processes.
If the cause is infectious, viral agents are unlikely. Most bacteria cause a
polymorphonuclear inflammation, although Salmonella typhi and Entamoeba
histolytica frequently cause a mononuclear reaction.
 Stool pH and reducing substances — Stool pH <6 and the presence of reducing
substances are indicative of hydrocarbon intolerance (which is frequently present in
viral gastroenteritis)

Viral pathogens — Attempts to distinguish among the viral causes of a gastroenteritis

episode by history generally are discouraging. However, clinical features and the pattern of
illness may help to implicate a particular virus (table 5).

Rotaviruses — Rotaviruses are the most important cause of viral gastroenteritis because
rotaviruses are detected more frequently as the severity of illness increases. Before
rotavirus immunization, rotaviruses accounted for approximately 10 percent of diarrhea
episodes that required medical treatment, and 50 percent of those that required
hospitalization. At the peak of the winter gastroenteritis season, a child with dehydration
requiring medical intervention had a 70 to 90 percent chance of having rotavirus infection
[6]. The effects of rotavirus immunization on these statistics continue to be evaluated.
(See "Rotavirus vaccines", section on 'Efficacy/effectiveness'.)

The clinical characteristics of children hospitalized with acute gastroenteritis in whom

rotavirus was and was not detected were described in two studies (table 6) [11,12].

 In the first study, in which diarrhea was a criterion for enrollment, vomiting and
isotonic dehydration were more frequent among children with rotavirus infection.
 In the second study, which enrolled patients with diarrhea or vomiting not associated
with a respiratory or structural cause (eg, pyloric stenosis), diarrhea was the most
common presenting symptom and was more common among children hospitalized
with rotavirus gastroenteritis than with other etiologies (table 6). Children with
rotavirus infection also were more likely to have vomiting and high fever (>39ºC)
than those with acute gastroenteritis of other causes.

During the first five years of life, the frequency of rotavirus detection varies according to
age and symptoms at the time of admission (table 7) [12]. Rotavirus is detected in one-
quarter to one-third of preschool-age children who require hospitalization for diarrhea,
vomiting, and/or fever (in any combination). The clinical spectrum narrows with increasing
age, as illustrated below:

 At zero to two months of age, rotavirus is detected in 5 to 20 percent of patients

who present with diarrhea, vomiting, or fever, alone or in combination
 After five months, rotavirus detection is unlikely in the absence of diarrhea and

Other viruses — The majority of the viral gastroenteritis episodes requiring hospitalization
that are not associated with rotavirus are caused by astrovirus or calicivirus, which also
occur predominantly in the winter months [28-30].

Vomiting tends to be more prominent in caliciviral gastroenteritis than in other types of viral
gastroenteritis. Astrovirus, calicivirus, and adenovirus gastroenteritis is consistently milder
than rotavirus gastroenteritis.

Astrovirus and calicivirus episodes usually are of shorter duration than rotavirus
gastroenteritis [29,31-33]. In contrast, children admitted to the hospital with enteric
adenovirus infection are more likely than those with rotavirus infection to have diarrhea that
persists for more than five days [34-36].

Outbreaks that include a large (>30 percent) proportion of cases in patients older than two
years probably are caused by caliciviruses and astroviruses. A teenager or adult with severe
acute gastroenteritis is more likely to have calicivirus infection, especially as part of a
common-source outbreak, particularly if the outbreak is linked to water or food
contamination [37-41].


Clinical diagnosis — The diagnosis of acute viral gastroenteritis is made clinically. Clinical
features suggestive of viral gastroenteritis include: age younger than two years; watery
diarrhea; absence of gross blood, mucus, and fecal leukocytes; stool pH <6; and the
presence of reducing substances. (See 'Clinical presentation' above and 'Differential
diagnosis' above.)

Etiologic diagnosis — Viral gastroenteritis pathogens are excreted in the stool and can be
detected one to two days before symptoms begin through several days after symptoms
have resolved [42]. Testing for specific viruses usually is not necessary in
immunocompetent hosts with routine gastroenteritis. However, it may be indicated during
outbreaks of gastroenteritis, to make decisions about specific therapy, and for cohorting and
isolation of hospitalized patients.
Submission of a sample (or samples) for viral testing should occur when outbreaks of
gastroenteritis occur in a healthcare institution, when specific antiviral measures (eg,
immunoglobulin or colostrum) are considered, and when identification of a particular virus is
needed to assess success of control measures, such as cohorting. (See "Prevention and
treatment of viral gastroenteritis in children".)

Stool cultures and/or stool examination for ova and parasites may be indicated in cases of
persistent diarrhea, in immunocompromised hosts, when infectious etiology must be
excluded to verify another diagnosis (eg, inflammatory bowel disease), in the setting of an
outbreak, and when immunosuppressive therapy may be initiated (eg, inflammatory
disease, transplantation) [2].

Specific viral assays — Viral gastroenteritis pathogens can be detected by specific assays
for single agents or broadly reactive assays. Commercial assays are available for
rotaviruses, astroviruses, adenoviruses 40 and 41, and Norovirus caliciviruses. The widely
available assays for detection of single agents are enzyme immunoassays (EIAs), latex
agglutination (LA), and reverse transcription-polymerase chain reaction (RT-PCR).

The RT-PCR genomic detection method is needed for astrovirus and calicivirus detection
because antigen detection methods (EIA and LA) are not yet mature for these viruses, and
RT-PCR is more sensitive than EIA or LA in most situations. (See "Epidemiology, clinical
manifestations, and diagnosis of noroviruses, astroviruses and sapoviruses", section on

Aichi virus is little studied; in general, picornaviruses are detected by inoculation in cell

Electron microscopy (EM) is the only method that can simultaneously identify the presence
and type of several viral enteropathogens, although the method is fairly insensitive. EM is
the first method used at some centers.

Sample collection — For all of the assays described above, fresh, bulk unfrozen stool (a
soiled diaper may be used) should be sent to the laboratory. The assays can be performed
with less than 0.1 g of stool, although a greater quantity improves sensitivity (from
approximately 70 to >90 percent).

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education

materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are
written in plain language, at the 5th to 6th grade reading level, and they answer the four or
five key questions a patient might have about a given condition. These articles are best for
patients who want a general overview and who prefer short, easy-to-read materials. Beyond
the Basics patient education pieces are longer, more sophisticated, and more detailed.
These articles are written at the 10th to 12th grade reading level and are best for patients
who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)
 Basics topics (see "Patient information: Diarrhea in children (The Basics)")
 Beyond the Basics topics (see "Patient information: Acute diarrhea in children")


 Proven pathogens of viral gastroenteritis include rotaviruses, caliciviruses,

astroviruses, enteric adenovirus serotypes 40 and 41, and some picornaviruses
(table 2). Rotaviruses are the most important cause. (See 'Etiologic agents' above.)
 Clinical manifestations of viral gastroenteritis include diarrhea, vomiting, fever,
anorexia, headache, abdominal cramps, and myalgia. (See 'Clinical
presentation' above.)
 The initial evaluation focuses on assessing severity of illness and excluding causes of
vomiting and diarrhea that require definitive therapy (eg, meningitis, acute
abdominal processes, diabetes mellitus, and toxic ingestions). (See 'Initial
evaluation' above.)
 Laboratory tests in the initial evaluation may include a complete blood count (for
evidence of anemia or hemolysis), serum electrolytes, and stool studies (eg, fecal
leukocytes, pH, reducing substances). (See 'Initial evaluation' above and "Clinical
assessment and diagnosis of hypovolemia (dehydration) in children", section on
'Laboratory testing' and 'Differential diagnosis' above.)
 Clinical features may suggest a particular pathogen. (See 'Differential
diagnosis' above.)

 Viral gastroenteritis is suggested by watery stools without blood or mucus, the

absence of fecal leukocytes, stool pH <6, and the presence of reducing substances.
The pattern of illness may help to implicate a particular virus (table 5).
 Bacterial or parasitic gastroenteritis is suggested by fecal leukocytes, gross blood, or
mucus in the stool. Bacterial or parasitic gastroenteritis tends to occur in children
two to four years of age and may be associated with foreign travel, exposure to
poultry or other farm animals, and consumption of processed meat.

 The diagnosis of acute viral gastroenteritis is made clinically. (See 'Clinical

diagnosis' above.)
 Clinical indications for specific viral assays may include outbreaks of gastroenteritis
in a healthcare institution; consideration of treatment with specific antiviral measures
(eg, immunoglobulin or colostrum); and to evaluate the success of various infection
control measures (eg, cohorting). (See 'Etiologic diagnosis' above.)
 The treatment of viral gastroenteritis in children is discussed separately.
(See "Prevention and treatment of viral gastroenteritis in children".)

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