Pak Prijanto,
ini ada artikel dari the merck manual, semoga berguna. Semoga anak bapak
bisa tumbuh baik dan dijauhkanNya dari hal2 yg. tidak kita inginkan.
Salam,
Rien.
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CONGENITAL AND PERINATAL CYTOMEGALOVIRUS INFECTION
Infection with cytomegalovirus acquired prenatally or perinatally.
(See also Cytomegalovirus Infection under Herpesvirus Infections in Ch.
162.)
Cytomegalovirus (CMV) is frequently isolated from newborns at birth.
Although most infants
shedding this virus are asymptomatic, others have life-threatening
illness and devastating long-term
sequelae.
Many questions regarding transmission of CMV and risk to the fetus
remain unanswered. For
example, it is not known when a woman with primary CMV can safely
conceive. Because risk to
the fetus is difficult to assess, women who develop primary CMV during
pregnancy should be
counseled. Many authorities do not recommend routine serologic testing
for CMV before or
during pregnancy in healthy women.
Etiology, Epidemiology, and Pathogenesis
CMV, a DNA virus belonging to the Herpesviridae family, is named after
the characteristic large
cells containing intranuclear and cytoplasmic inclusions often seen in
histologic specimens.
Although differences among CMV isolates can be detected with
restriction endonuclease analysis
of viral DNA, the similarities are greater; therefore, only one
serotype of CMV is recognized. Like
other herpesviruses, CMV is capable of latency and reactivation. CMV
has been isolated from
various sites, including saliva, urine, breast milk, semen, cervical
secretions, amniotic fluid, and
buffy coat. Acquiring CMV at an early age appears to be related to
various factors, such as low
socioeconomic status, high rates of breastfeeding, and increased
exposure to other young children
(eg, in day care centers). CMV is also thought to be transmitted
sexually.
Congenital CMV infection, which occurs in 0.2 to 2.2% of all live
births worldwide, is thought
to result from transplacental acquisition of a primary or recurrent
maternal infection. Clinically
apparent disease in the newborn is much more likely to occur after a
primary maternal exposure,
particularly in the first half of pregnancy. In some higher
socioeconomic groups in the USA, 50%
of young women lack antibody to CMV, making them susceptible to primary
infection.
Perinatal CMV infection is acquired by exposure to infected cervical
secretions, breast milk, or
blood products. Maternal antibody is thought to be protective, and most
of these term newborns
are asymptomatic or are not affected by contact with the virus. In
contrast, preterm infants lacking
antibody to CMV who receive seropositive blood can develop significant
illness.
Transfusion with CMV-positive blood can result in serious infection or
death in premature
infants born to CMV-seronegative mothers. Efforts should be made to
transfuse these infants with
only CMV-negative blood or components (see Prophylaxis and Treatment,
below).
Symptoms and Signs
Many women who become infected with CMV during pregnancy are
asymptomatic, but some
develop a mononucleosis-like illness.
About 10% of infants with congenital CMV infection are symptomatic at
birth; manifestations
include intrauterine growth retardation, prematurity, microcephaly,
jaundice, petechiae,
hepatosplenomegaly, periventricular calcifications, chorioretinitis,
and pneumonitis. Infants who
acquire CMV after birth may develop pneumonia, hepatosplenomegaly,
hepatitis,
thrombocytopenia, and atypical lymphocytosis.
Diagnosis
Laboratory diagnosis of CMV is made by virus isolation or serologic
tests.
A primary maternal infection is more frequently diagnosed by serologic
tests than by culture; a
positive culture may be due to reactivation of the virus.
Seroconversion from a negative to a
positive CMV-specific titer strongly suggests infection. A fourfold or
greater rise in CMV-specific
IgG levels between specimens from acute and convalescent stages and an
elevated CMV-specific
IgM level in tests performed by a reliable laboratory may also indicate
newly acquired infection.
However, results should be interpreted with caution because IgM may be
produced during
reactivation, may exist for a prolonged period of time, or may not be
detectable in primary
infection. IgG levels can be measured by complement fixation,
immunofluorescence, indirect
hemagglutination, radioimmunoassay, or ELISA. IgM levels are most
reliably measured by
radioimmunoassay or ELISA.
In newborns, viral culture is the primary diagnostic tool. Culture
specimens should be kept
refrigerated before inoculation on fibroblast cells. Congenital CMV can
be diagnosed if the virus is
isolated from urine or other body fluids obtained within the first 2 wk
of life. After 2 wk, positive
cultures may indicate perinatal or congenital infection. Infants may
shed CMV for several years
after both types of infection.
A CBC and differential and liver function tests may be helpful.
Radiologic examination of the
infant's head and an ophthalmologic evaluation should also be
performed.
Symptomatic congenital CMV infection must be distinguished from other
congenital infections,
including toxoplasmosis, rubella, herpes simplex, and syphilis.
Symptomatic newborns have a mortality rate of up to 30%, and 70 to 90%
of the survivors have
some neurologic impairment, including hearing loss, mental retardation,
and visual disturbances. In
addition, 10% of asymptomatic infants also eventually develop
neurologic sequelae. Since hearing
defects are a concern, close monitoring after the neonatal period is
needed.
Prophylaxis and Treatment
Although CMV is ubiquitous and reactivation is common, the nonimmune
pregnant woman may be
able to limit her exposure to the virus. For instance, since CMV
infection is common in children
attending day care centers, pregnant women should always wash their
hands thoroughly after
exposure to urine and respiratory secretions of such children.
Transfusion-associated perinatal
CMV disease can be avoided by giving preterm seronegative infants blood
products from CMV
seronegative donors or products that have been treated to make them
noninfectious. Development
of a vaccine against CMV is under investigation.
No specific therapy for congenital or perinatal CMV infections is
available. Ganciclovir has been
shown to decrease viral shedding in infants with congenital CMV.
However, when therapy stops,
the virus is again shed. Therefore, its role in the treatment of
infants with congenital CMV infection
is uncertain.
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