ROTAVIRUS
INFECTIONS
Etiologic Agent
 Rotaviruses are members of the family Reoviridae. The viral
genome consists of 11 segments of double-strand RNA that are
enclosed in a triple-layered, nonenveloped, icosahedral capsid
75 nm in diameter. Viral protein 6 (VP6), the major structural
protein, is the target of commercial immunoassays and
determines the group specificity of rotaviruses.
 There are seven major groups of rotavirus (A through G);
human illness is caused primarily by group A and, to a much
lesser extent, by groups B and C. Two outer-capsid proteins,
VP7 (G-protein) and VP4 (P-protein), determine serotype
specificity, induce neutralizing antibodies, and form the basis
for binary classification of rotaviruses (G and P types).
 The segmented genome of rotavirus allows genetic
reassortment (i.e., exchange of genome segments between
viruses) during co-infection—a property that may play a role in
viral evolution and has been utilized in the development of
reassortant animal-human rotavirus–based vaccines.
Epidemiology
 Worldwide, nearly all children are infected with rotavirus by 3–5
years of age. Neonatal infections are common but are often
asymptomatic or mild, presumably because of protection from
maternal antibody or breast-feeding.
 First infections after 3 months of age are likely to be
symptomatic, and the incidence of disease peaks among
children 4–23 months of age.
 Reinfections are common, but the severity of disease
decreases with each repeat infection. Therefore, severe
rotavirus infections are relatively uncommon among older
children and adults.
 Nevertheless, rotavirus can cause illness in parents and
caretakers of children with rotavirus diarrhea,
immunocompromised persons, travelers, and elderly individuals
and should be considered in the differential diagnosis of
gastroenteritis among adults.
Epidemiology
 In temperate climates, rotavirus disease occurs
predominantly during the cooler fall and winter
months. In the United States, the rotavirus
season each year begins in the Southwest
during the autumn (October through
December) and migrates across the continent,
peaking in the Northeast during the spring
(March through May); the reasons for this
characteristic pattern are not clear. In tropical
settings, rotavirus disease occurs year-round,
with less pronounced seasonal peaks.
PATHOGENESIS
 Rotavirus-induced diarrhea appears to be due
to decreased absorption of salt and water
related to selective infection of the absorptive
intestinal villus cells, which results in net fluid
secretion.
 Depressed levels of disaccharidases and
impaired D-xylose absorption have been
observed.
 Intestinal fluid loss may also be due to
activation of the enteric nervous system.
CLINIC
 Common clinical findings usually include
vomiting, abdominal distress, diarrhea, and
mild dehydration. Fever and vomiting
frequently precede diarrhea.
 Stools are typically watery and usually do not
contain blood or leukocytes.
 Dehydration and associated electrolyte
imbalance may occur in severe cases,
requiring hospitalization.
CLINIC
 The course of rotavirus disease is
generally 3 to 9 days, and the mean time
of hospitalization when required is 4
days.
 Asymptomatic rotavirus infections are
common, especially in newborn children,
and the association of illness with
rotavirus infection increases with the age
of the child up to the age of 2 years.
DIAGNOSIS
 Several tests have been developed for
diagnosis of rotavirus infection, but
antigen detection by enzyme-linked
immunosorbent assay (ELISA) is now
the preferred method.
TREATMENT
 There is presently no specific antiviral therapy
for rotavirus infections.
 Treatment is usually directed at prevention of
severe dehydration and electrolyte imbalance.
 Use of oral rehydration salt solutions
containing glucose or sucrose has been shown
to be as effective as intravenous fluid therapy
for mild to moderately severe dehydrating
rotavirus gastroenteritis.
PREVENTION
 Because the morbidity in developed countries
is similar to that in developing countries, it is
thought that diarrhea in developing countries is
not likely to be reduced by improved sanitation
and water supplies; thus, control measures will
require effective vaccines. The principal
approach taken in the past as well as in more
recent years has been active immunization
with live, attenuated rotavirus.

ROTAVIRUS-INFECTIONS-slides.pdf

  • 1.
  • 2.
    Etiologic Agent  Rotavirusesare members of the family Reoviridae. The viral genome consists of 11 segments of double-strand RNA that are enclosed in a triple-layered, nonenveloped, icosahedral capsid 75 nm in diameter. Viral protein 6 (VP6), the major structural protein, is the target of commercial immunoassays and determines the group specificity of rotaviruses.  There are seven major groups of rotavirus (A through G); human illness is caused primarily by group A and, to a much lesser extent, by groups B and C. Two outer-capsid proteins, VP7 (G-protein) and VP4 (P-protein), determine serotype specificity, induce neutralizing antibodies, and form the basis for binary classification of rotaviruses (G and P types).  The segmented genome of rotavirus allows genetic reassortment (i.e., exchange of genome segments between viruses) during co-infection—a property that may play a role in viral evolution and has been utilized in the development of reassortant animal-human rotavirus–based vaccines.
  • 3.
    Epidemiology  Worldwide, nearlyall children are infected with rotavirus by 3–5 years of age. Neonatal infections are common but are often asymptomatic or mild, presumably because of protection from maternal antibody or breast-feeding.  First infections after 3 months of age are likely to be symptomatic, and the incidence of disease peaks among children 4–23 months of age.  Reinfections are common, but the severity of disease decreases with each repeat infection. Therefore, severe rotavirus infections are relatively uncommon among older children and adults.  Nevertheless, rotavirus can cause illness in parents and caretakers of children with rotavirus diarrhea, immunocompromised persons, travelers, and elderly individuals and should be considered in the differential diagnosis of gastroenteritis among adults.
  • 4.
    Epidemiology  In temperateclimates, rotavirus disease occurs predominantly during the cooler fall and winter months. In the United States, the rotavirus season each year begins in the Southwest during the autumn (October through December) and migrates across the continent, peaking in the Northeast during the spring (March through May); the reasons for this characteristic pattern are not clear. In tropical settings, rotavirus disease occurs year-round, with less pronounced seasonal peaks.
  • 9.
    PATHOGENESIS  Rotavirus-induced diarrheaappears to be due to decreased absorption of salt and water related to selective infection of the absorptive intestinal villus cells, which results in net fluid secretion.  Depressed levels of disaccharidases and impaired D-xylose absorption have been observed.  Intestinal fluid loss may also be due to activation of the enteric nervous system.
  • 10.
    CLINIC  Common clinicalfindings usually include vomiting, abdominal distress, diarrhea, and mild dehydration. Fever and vomiting frequently precede diarrhea.  Stools are typically watery and usually do not contain blood or leukocytes.  Dehydration and associated electrolyte imbalance may occur in severe cases, requiring hospitalization.
  • 11.
    CLINIC  The courseof rotavirus disease is generally 3 to 9 days, and the mean time of hospitalization when required is 4 days.  Asymptomatic rotavirus infections are common, especially in newborn children, and the association of illness with rotavirus infection increases with the age of the child up to the age of 2 years.
  • 12.
    DIAGNOSIS  Several testshave been developed for diagnosis of rotavirus infection, but antigen detection by enzyme-linked immunosorbent assay (ELISA) is now the preferred method.
  • 13.
    TREATMENT  There ispresently no specific antiviral therapy for rotavirus infections.  Treatment is usually directed at prevention of severe dehydration and electrolyte imbalance.  Use of oral rehydration salt solutions containing glucose or sucrose has been shown to be as effective as intravenous fluid therapy for mild to moderately severe dehydrating rotavirus gastroenteritis.
  • 14.
    PREVENTION  Because themorbidity in developed countries is similar to that in developing countries, it is thought that diarrhea in developing countries is not likely to be reduced by improved sanitation and water supplies; thus, control measures will require effective vaccines. The principal approach taken in the past as well as in more recent years has been active immunization with live, attenuated rotavirus.