Cmv in Pregnancy-Ak Februari 2013

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    A. Kurdi Syamsuri

    Department of Obstetrics and GynaecologyUniversity of Sriwijaya / dr. M. Hoesin Hospital

    Palembang - Indonesia

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    Congenital CMV infection

    2007

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    2007

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    2007

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    95% clinically inapparent

    35% transmitted to fetus

    No clear relationship between gestational ageand transmission

    Fetal damage more likely in first 26 weeks, (32%)than later (15%)

    Pongjitsiri S, Congenital CMV Infection, 2007

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    Primary maternal infection leads to fetal infectionin 30-50% of cases--10-15% of these have overtclinical disease

    Secondary maternal infection less likely to lead tofetal infection (1-2% ) but can do so and may leadto severe disease (Boppana et al, NEJM 2001, 344: 1366)

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    Rates of primary CMV infection

    during pregnancy

    Study (Location) Rate as % of Rate as % of % cong CMV,Pregnancies Seronegatives primary mat infStern 1.1 4.1 45

    (London)Grant (Scotland) 0.29 0.71 38

    Stagno (USA, 0.57 1.4 47

    mid-income)

    Ahlfors (Sweden) 0.32 1.4 43

    Griffiths (London) 0.30 0.86 20

    Pongjitsiri S, Congenital CMV Infection, 2007

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    Factors Associated With Delivering a Newborn

    With Congenital CMV Infection

    in Multiparous Women

    JAMA. 2003;289:1008-1011

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    Following a diagnosis of fetal CMV infection,

    serial ultrasound examinations should be

    performed every 2 to 4 weeks to detect

    sonographic abnormalities, which may aid indetermining the prognosis of the fetus, although it

    is important to be aware that the absence of

    sonographic findings does not guarantee a

    normal outcome. (II-2B)

    J Obstet Gynaecol Can 2010;32(4):348354

    SOGC CLINICAL PRACTICE GUIDELINE

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    Jaundice (67%) Petechiae (76%)

    Hepatosplenomegaly (60%) Microcephaly (53%) Chorioretinitis (20%) Seizure (7%) Fatal outcome (10%)

    Boppana et al. (1999) Pediatrics 104:55Pongjitsiri S, Congenital CMV Infection, 2007

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    IUGR Cerebral ventriculomegaly

    Microcephaly Intracranial calcifications Ascites/pleural effusion Hydrop fetalis Oligohydramnios/polyhydramnios Hyperechogenic bowel Liver calcifications

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    Neurological sequelae are the most common, and mostsevere: >90% of newborns with symptomatic congenital CMV

    infection have visual, audiologic and/or other neurologicalsequelae

    - 5-17% of newborns with asymptomatic congenitalCMV infection develop neurological sequelae (esp.hearing loss)

    Pongjitsiri S, Congenital CMV Infection, 2007

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    In case of primary maternal infection, parents

    should be informed about a 30% to 40% risk or

    intrauterine transmission and fetal infection, anda risk of 20% to 25% for development of

    sequelae postnatally if the fetus is infected.

    (II-2A)

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    Seizures

    Chorioretinitis

    Periventricular calcifications

    Sensorineural hearing loss motor deficits

    Pongjitsiri S, Congenital CMV Infection, 2007

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    Primary maternal infection

    Symptomatic congenital CMV infection

    Presence of neonatal neurologicalabnormalities

    Abnormal head CT scan

    Chorioretinitis in the newborn

    Pongjitsiri S, Congenital CMV Infection, 2007

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    Frequency of sequelae

    Symptomatic (7%) Asymptomatic (93%)

    Infant death 10% 0

    Hearing loss 60% 715%

    Mental retardation 45% 210%

    Cerebral palsy 35%

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    Isolation of CMV from urine or other body fluid(CSF, blood, saliva) in the first 21 days of life isconsidered proof of congenital infection

    Serologic tests are unreliable; IgM tests currentlyavailable have both false positive and false negativeresults

    PCR may be useful in selected cases

    Pongjitsiri S, Congenital CMV Infection, 2007

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    Detection: screening formaternalCMV infection

    CMV IgG antibody sensitive and specific

    screen for past infection

    CMV IgM antibody variable sensitivity and

    specificity

    Antibody avidity testing can increase accuracy

    of detection of primary infection No test for immune mothers who will transmit

    Pongjitsiri S, Congenital CMV Infection, 2007

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    Pongjitsiri S, Congenital CMV Infection, 2007

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    Advanced CMV diagnosis

    IgM confirmation by Western blot

    Determination of the IgG avidity

    index

    Isolation of the virus from urine,saliva and blood

    Pongjitsiri S, Congenital CMV Infection, 2007

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    Evaluation of mothers at risk of

    transmitting CMV to the fetus

    Negative,no further testing

    Positive =primary infection

    Test for IgM Antibody

    Positive

    IgG Positive =Seroconversion

    Negative,no further tests

    Retest later

    Negative

    Test for IgG antibody

    at first prenatal visit

    Refer for prenatal diagnosis

    Pongjitsiri S, Congenital CMV Infection, 2007

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    Diagnosis of primary maternal cytomegalovirus

    (CMV) infection in pregnancy should be based on

    de-novo appearance of virus-specific IgG in the

    serum of a pregnant woman who was previouslyseronegative, or on detection of specific IgM

    antibody associated with low IgG avidity. (II-2A)

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    The prenatal diagnosis of fetal CMV infection

    should be based on amniocentesis, which should

    be done at least 7 weeks after presumed time of

    maternal infection and after 21 weeks ofgestation. This interval is important because it

    takes 5 to 7 weeks following fetal infection and

    subsequent replication of the virus in the kidney

    for a detectable quantity of the virus to besecreted to the amniotic fluid. (II-2A)

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    The diagnosis of secondary infection should be

    based on a significant rise of IgG antibody titre

    with or without the presence of IgM and high IgG

    avidity.

    In cases of proven secondary infection,

    amniocentesis may be considered, but the risk

    benefit ratio is different because of the lowtransmission rate. (III-C)

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    ALGO

    RITHMF

    OR

    PRENATAL

    DIAGNO

    SISOFCONGENITALCMV

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    Ganciclovir has been shown to be effective therapy

    for certain CMV infections in immunocompromisedhosts (e.g., retinitis or enterocolitis in HIV-infected

    patients) Neonatal experience with ganciclovir is limited, the

    toxicity of the drug is considerable (e.g., platelets,

    neutrophils), and oral bioavailability unreliable

    Pongjitsiri S, Congenital CMV Infection, 2007

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    A six week course of IV ganciclovir may reduce therate of long-term hearing loss in neonates withsymptomatic CMV infection

    However, this regimen is associated with significanttoxicity, long-term followup data are lacking, andthe optimal duration of therapy (if any) is unknown

    Potential benefits of antiviral therapy for

    asymptomatically infected neonates may begreater

    Pongjitsiri S, Congenital CMV Infection, 2007

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    A vaccine to prevent CMV infections is

    desperately needed Trials of candidate vaccines are underway CMV Vaccine development a Level One

    priority !!

    Pongjitsiri S, Congenital CMV Infection, 2007

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    Many different ways toprevent CMV

    Our approach:

    Hygiene

    Avoiding intimate contact with salivarysecretions and urine from young children

    Careful hand washing after changing diapersand wiping secretions.

    Education about CMV and how to prevent it

    through hygiene

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