Master the board step 3

Obstetrics
Management
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Test for toxoplasma IgG and IgM levels.
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Give pyrimethamine and sulfadiazine for the treatment of serologically
confirmed fetal/neonatal infection via amniocentesis.
Varicella
Varicella is in the family Herpesviridae, human herpesvirus type 3.
Primary infection causes varicella. After clinical symptoms disappear, the virus
lies dormant in the dorsal root ganglia. It may reactivate late in life, causing
shingles. Herpesvirus commonly reactivates in immunocompromised patients.
Transplacental infection results from primary varicella infection in the
mother (25–40 percent infection rate).
The greatest risk to the fetus is if a rash appears in the mother between 5 days
antepartum and 2 days postpartum.
Neonatal infection presents with “zigzag” skin lesions, limb hypoplasia, microcephaly,
microphthalmia, chorioretinitis, and cataracts.
Prevention
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Vaccination: Live-attenuated varicella virus to nonpregnant women.
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Postexposure prophylaxis: VariZIG (purified human immunoglobulin
with high levels of antivaricella antibodies) within 10 days of exposure.
VariZIG does not prevent infection but only attenuates the clinical effects of
the virus. (Note: VZIG is no longer available.)
Treatment
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Maternal varicella (uncomplicated): Oral acyclovir to mother plus VariZIG
to mother and neonate
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Congenital varicella: VariZIG and IV acyclovir to the neonate
Rubella
Rubella is a single-stranded RNA virus of the family Togaviridae.
Vertical transmission of rubella virus (causative virus of German measles)
occurs with primary infection during pregnancy (70–90 percent).
Neonates with congenital rubella present with congenital deafness (most
common sequelae), congenital heart disease (e.g., patent ductus arteriosus, or
PDA), cataracts, mental retardation, hepatosplenomegaly, thrombocytopenia,
and “blueberry muffin” rash. Adverse effects occur with primary infection
in the first 10 weeks of gestation.
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