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l Zidovudine (ZDV) short course 1 страница
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Table 29
(PACTG) 076 Zidovudine (ZDV) Regimen
| Time of ZDV administration | Regimen |
| Antepartum | Oral administration of 100 mg ZDV five times daily, initiated at 14-34 weeks' gestation and continued throughout the pregnancy |
| Intrapartum | During labor, intravenous administration of ZDV in a 1-hour initial dose of 2 mg/kg body weight, followed by a continuous infusion of 1 mg/kg body weight/hour until delivery |
| Postpartum | Oral administration of ZDV to the newborn (ZDV syrup at 2 mg/kg body weight/dose every 6 hours) for the first 6 weeks of life, beginning at 8-12 hours after birth. (Note: intravenous dosage for infants who can not tolerate oral intake is 1. 5 mg/kg body weight intravenously every 6 hours. ) |
l Zidovudine (ZDV) short course
The regimen is 300 mg ZDV orally twice daily from 36 weeks gestation until the onset of labour and 300 mg every three hours from the onset of labour until delivery. During the intrapartum period, ZDV infusion at the rate of 2 mg/kg wmay be administered within the first hour and then continuously infused at the rate of 1 mg/kg/h until delivery. Patients should abandon breastfeeding and use the infant formula.
The scheme of ART different in different countries, while principles are similar. Thus, Royal College of Obstetricians and Gynaecologists proposed the following scheme of ART in pregnancy (Green-top Guideline # 39 (2010):
a) For women who require HIV treatment for their own health, their prescribed ART regimen should be continued throughout pregnancy and postpartum.
b) For women who do not require HIV treatment for their own health, ART should be initiated between 20 and 28 weeks and discontinued at delivery.
c) For women who do not require HIV treatment for their own health, have a viral load less than 10 000 copies/ml and are prepared to be delivered by elective caesarean section, an acceptable alternative to ART is zidovudine monotherapy initiated between 20 and 28 weeks, given orally twice daily, intravenously at delivery and discontinued immediately thereafter.
Combination drug regimens are also used for treatment of HIV infection and for prevention of perinatal HIV transmission. In general, women who are receiving ART for HIV infection should continue the same regimen during pregnancy if it is well tolerated and yields effective HIV virologic suppression. If the regimen contains stavudine, didanosine, or full-dose ritonavir, a regimen change should be considered. In 2015, the World Health Organization (WHO) revised its guidelines to recommend initiation of lifelong antiretroviral therapy (ART) for all HIV-infected individuals regardless of CD4 cell count, including pregnant and breastfeeding women. Thus, ART should be initiated as early as possible in all HIV-infected pregnant women and continued lifelong. In addition, all infants born to HIV-infected mothers should receive post-exposure antiretroviral prophylaxis.
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• Combination therapy and other antiretroviral drugs
Protease inhibitor based regimen
Lopinavir (LPV) 400 mg plus ritonavir (RTV) 100 mg PO BID if no lopinavir-associated mutations: Insufficient data for any dosage recommendations in the presence of any lopinavir-associated resistance substitution; some authors increase dose to 600 mg/150 mg twice a day in second and third trimester of pregnancy; once-daily LPV/RTV dosing is not recommended during pregnancy; oral solution should not be used in pregnancy because of its high alcohol content
Non-nucleoside reverse transcriptase inhibitors based regimen
Regimens include the following:
· Efavirenz (EFV) 600 mg PO daily: Although there are concerns of potential neural tube defects in women of childbearing age before pregnancy is detected, increasing data in pregnancy are reassuring or
· Rilpivirine (RPV) 25 mg PO daily if pretreatment HIV viral load is less than 100, 000 copies/mL and CD4 exceeds 200 cells/µL: Limited pregnancy data with highly variable pharmacokinetics.
Mode of delivery
Because of increased fetal exposure to infected maternal blood and secretions, increased transmission may come from:
• Amniotomy
• Fetal scalp electrode/sampling
• Forceps/vacuum extractor
• Episiotomy
• Vaginal tears
Cesarean section before labor and/or rupture of membranes reduces risk of mother-to-child transmission by 50–80% compared with other modes of delivery in women on no antiretroviral therapy or on ZDV alone.
Delivery by elective caesarean section at 38 weeks to prevent labour and/or ruptured membranes is recommended for:
• women taking ART who have a plasma viral load greater than 50 copies/ml;
• women taking ZDV monotherapy as an alternative to ART;
• women with HIV and hepatitis C virus co-infection.
Delivery by elective caesarean section for obstetric indications or maternal request should be delayed until after 39 completed weeks of gestation in women with plasma viral loads of less than 50 copies/ml, to reduce the risk of transient tachypnoea of the newborn.
Optimally, IV ZDV should be instituted at least 3 hours prior to surgery. Prophylactic antibiotics should be considered because of the increased infectious morbidity. Amniocentesis, application of a fetal scalp electrode, and other invasive procedures should be avoided whenever possible.
Only women with plasma viral loads of less than 50 copies/ml should be offered a planned vaginal delivery. In the absence of a documented mode of delivery plan or, in the event of uncertainty about viral load results, urgent advice should be sought from the HIV physicians.
Opportunistic Infection Prophylaxis
Pneumocystis carinii pneumonia (PCP) prophylaxis: when the CD4 count is less than 200/ml, trimethoprim-sulfamethoxazole double strength (TMP/SMX-DS), once daily, is recommended. Alternatively, dapsone may be used. In the first trimester of pregnancy, TMP/SMX should be avoided; aerosolized pentamidine isethionate may be substituted.
Mycobacterium avium complex (MAC) prophylaxis: Azithromycin, 1200 mg once weekly, is recommended for MAC prophylaxis when the CD4 count is less than 100/ml.
Toxoplasmosis prophylaxis should be given when the CD4 count is less than 100/ml; it is provided adequately by TMP/SMX, as given for PCP prophylaxis.
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Previously, patients who were started on prophylaxis for opportunistic infections were kept on their regimens even when their CD4 counts increased or viral loads decreased; it has been postulated that the risk of these illnesses remains high because less effective CD4 cells form after HIV infection. There is less evidence to support the safety of discontinuing toxoplasmosis prophylaxis, however, so it should be continued indefinitely.
Women with HIV may be taking systemic antifungal medications for candidiasis prophylaxis; this prophylaxis should be discontinued in pregnancy due to the potential for azole-induced teratogenicity. Similarly, cytomegalovirus (CMV) prophylaxis with ganciclovir is not recommended in pregnancy. Women with positive results on tuberculin skin tests should be treated after a chest radiograph has been obtained to rule out active disease. Treatment may be deferred until the second trimester. Isoniazid, either daily or twice weekly, is the treatment of choice. Pyridoxine hydrochloride should be administered as well to minimize the risk of neuropathy.
Routine vaccinations include the hepatitis B virus (HBV) series, one-time pneumonia vaccine, and an annual influenza vaccine. Rubella vaccine may be safely administered as indicated. Severely immunocompromised patients may fail to mount an appropriate response to vaccines, however. Studies of nonpregnant adults have shown transient bursts of viremia after vaccination. The effect of transient postvaccination viremia on vertical transmission rates is unknown. It is reasonable to defer vaccination in pregnancy until antiretroviral therapy has been established.
Serum monitoring of HIV-infected patients includes obtaining a baseline CD4 count, HIV RNA polymerase chain reaction (PCR) quantification, CBC, and liver function tests, and assessing CMV infection and toxoplasmosis status. If the CMV test results are positive, an ophthalmologic evaluation is indicated. The risk of CMV retinitis is present in patients with a CD4 count of less than 50/ml. Toxoplasmosis in HIV-infected patients is usually caused by reactivation of latent disease (seroprevalence of 10–30%). Toxoplasmosis risk is increased in patients with a CD4 count of less than 100/mL (75% of cases occur in those with a CD4 count of less than 50/mL); prophylaxis is provided by TMP/SMX-DS.
After a patient is started on antiretroviral therapy, a set of laboratory studies should be repeated on a monthly basis for 2 months, then every 2 or 3 months, or after any changes in her medical therapy, depending on her response to therapy. An effective therapeutic regimen should result in an increase in the patient's CD4 count and a substantial decrease in her viral load; undetectable viral levels are to be expected on the triple-drug regimen. Failure to achieve such an effect warrants a reevaluation of the regimen.
Patients requiring only ZDV for fetal indications must be informed of the possibility that their risk of drug resistance will increase with one-drug therapy. Pregnancy is the only indication for such therapy at this point. Our practice is to administer zidovudine in combination with lamivudine (3TC, Epivir) in an attempt to decrease the risk that resistant viral serotypes will arise.
CYTOMEGALOVIRUS (CMV)
Epidemiology
CMV infection is the most common congenital infection affecting 0. 4–2. 3% of neonates. CMV is a ubiquitous DNA herpesvirus. The virus has been isolated from saliva, cervical secretions, semen, and urine. Infection can also be contracted by exposure to infected breast milk or blood products. Transmission can occur from mother to child both in utero and postpartum. An estimated 40, 000 infants are born infected with CMV infection. By school age, 30–60% of children are infected.
Clinical Manifestations
Maternal infection. In immunocompetent adults, CMV infection is silent; symptoms appear in only 1–5% of cases. These symptoms include low-grade fever, malaise, arthralgias, and, occasionally, pharyngitis with lymphadenopathy. As in other herpesvirus infections, after primary infection, cytomegalovirus becomes latent, with periodic episodes of reactivation and shedding of virus. Mothers determined to be seronegative for CMV before conception or early in gestation have a 1–4% risk of acquiring the infection during pregnancy, with a 30–40% rate of fetal transmission. Fetal infection also can result from recurrent maternal CMV infection. In fact, most fetal infections are due to recurrent maternal infection. These infections rarely lead to congenital abnormalities. Previously acquired immunity confers a decreased likelihood of clinically apparent disease, because partial protection to the fetus is provided by maternal antibodies. Acquired immunity does not impede transmission, but evidently prevents the serious sequelae that develop with primary maternal infection.
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Congenital infection. Ten percent to 15% of infected infants have clinically apparent disease, with 90% developing sequelae. Of the remaining 85–90% with asymptomatic infection, 5–15% develop long-term sequelae. A higher risk of sequelae is seen in fetuses infected earlier in gestation than in those infected later. Preterm neonates are at greatest risk of infection. Manifestations of CMV in the neonate may include focal or generalized organ involvement. Common clinical findings in fetal infection include the presence of petechiae, hepatosplenomegaly, jaundice, microcephaly with periventricular calcifications, oligohydramnios, intrauterine growth retardation, premature delivery, inguinal hernias in boys, and chorioretinitis. Nonimmune hydrops has also been reported. A severely affected infant may present with purpura, “blueberry muffin skin, ” and “salt and pepper skin. ” Approximately one-third of neonates with symptomatic infection die from severe disease, generally with cerebral involvement. Infants who survive symptomatic CMV are at high risk of significant developmental and neurologic problems. Sixty percent to 70% of these survivors suffer hearing loss; visual disturbances, motor impairments, language and learning disabilities, and mental retardation are also common.
Diagnosis
Maternal infection currently can be reliably detected only by documenting maternal seroconversion using serial Immunoglobulin G (IgG) measurements during pregnancy. If seropositivity is detected at least several months before conception, symptomatic fetal infection is unlikely. In practice, however, this testing does not occur. Most primary infections are clinically silent, so the majority are undiagnosed. Screening of asymptomatic pregnant women for seroconversion is not recommended because distinguishing primary from secondary CMV infection is frequently difficult using CMV serology. The CMV IgM test result is positive in only 75% of primary infections and in 10% of secondary infections. Screening is also of limited value due to the lack of a CMV vaccine and the inability to predict severity of sequelae of primary infection.
Fetal infection. Ultrasonography may enable the detection of the fetal anomalies that characterize CMV infection. Amniocentesis and cordocentesis have also been used to diagnose fetal infection using measurement of total and specific IgM antibodies and viral culture.
Management
Effective in utero CMV therapy for the fetus does not exist. Given the difficulty in distinguishing primary from secondary maternal CMV infection, counseling patients about pregnancy termination is problematic because most infected fetuses do not suffer serious sequelae. Breast feeding is discouraged in women with active infection.
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VARICELLA ZOSTER VIRUS
Epidemiology
The incidence of varicella in pregnancy is approximately 0. 7: 1000 pregnancies. Herpes zoster is also uncommon in women of childbearing age.
The major mode of transmission is respiratory, although direct contact with vesicular or pustular lesions may also result in disease. Nearly all persons are infected before adulthood, 90% before the age of 10.
Varicella outbreaks occur most frequently during winter and spring. The incubation period is 13–17 days. Infectivity is greatest 24–48 hours before the onset of rash and lasts 3–4 days to the rash. The virus is rarely isolated from crusted lesions.
Clinical Manifestations
Maternal infection. Primary varicella infection tends to be more severe in adults than in children. Infection is especially severe in pregnancy. The risk of varicella pneumonia appears to increase in pregnancy, starting several days after the onset of the characteristic rash. When varicella pneumonia occurs in pregnancy, maternal mortality may reach 40% in the absence of specific antiviral therapy. Early signs and symptoms of varicella pneumonia should be managed aggressively. Herpes zoster infection, or reactivation of varicella, is more common in older and immunocompromised patients. Zoster is not more prevalent or severe in pregnancy.
Congenital infection. Of fetuses born to mothers who had active disease during the first 20 weeks of pregnancy, 20–40% are infected. The risk of congenital malformation after fetal exposure to primary maternal varicella before 20 weeks' gestation is estimated to be approximately 5%. Fetal infection with varicella zoster virus can lead to one of three major outcomes: intrauterine infection, which infrequently causes congenital abnormalities; postnatal disease, ranging from typical varicella with a benign course to fatal disseminated infection; and shingles, appearing months or years after birth. The sequelae of congenital varicella syndrome have been attributed to the occurrence of infection before 20 weeks' gestation. Those afflicted may exhibit a variety of abnormalities, including cutaneous scars, limb-reduction anomalies, malformed digits, muscle atrophy, growth restriction, cataracts, chorioretinitis, microphthalmia, cortical atrophy, microcephaly, and psychomotor retardation. The risk of this syndrome is estimated to be around 2%. Infection after 20 weeks' gestation may lead to postnatal disease. If maternal infection occurs within 5 days of delivery, hematogenous transplacental viral transfer may cause significant infant morbidity, incurring infant mortality rates between 10% and 30%. Sufficient antibody transfer to protect the fetus apparently requires at least 5 days after the onset of the maternal rash. Women who develop chickenpox, especially near term, should be observed for and educated about signs and symptoms of labor; they should receive tocolytic therapy if labor begins before the 5th day of the maternal infection. Neonatal therapy is also important when a mother develops signs of chickenpox less than 3 days postpartum.
Herpes zoster is not associated with fetal sequelae.
Diagnosis
Clinical Picture. The diagnosis of acute varicella zoster in the mother can usually be established by the characteristic clinical cutaneous manifestations described as chickenpox. The generalized vesicular rash of chickenpox usually appears on the head and ears, then spreads to the face, trunk, and extremities. Mucous membrane involvement is common. Lesions in different areas will be in different stages of evolution. Vesicles and pustules evolve into crusted lesions, which then heal and may leave scars. Herpes zoster, or shingles, demonstrates a unilateral vesicular eruption, usually in a dermatomal distribution.
Laboratory studies. Confirmation of the diagnosis may be obtained by examining scrapings of lesions, which may reveal multinucleated giant cells. For rapid diagnosis, varicella zoster antigen may be demonstrated in exfoliated cells from lesions by immunofluorescent antibody staining.
Ultrasonography. Detailed ultrasonographic examination is probably the best means for assessing a fetus for major limb and growth disturbances. Other abnormalities that have been detected before 20 weeks' gestation include polyhydramnios, hydrops fetalis, multiple hyperechogenic foci within the liver, limb defects, and hydrocephaly. Although ultrasonography can be offered in pregnancies with maternal varicella, it is less likely to be helpful in cases of zoster due to the very low risk of fetal sequelae.
Management
Exposure of a previously uninfected woman during pregnancy
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An IgG titer should be obtained within 24–48 hours of a patient's exposure to a person with noncrusted lesions. The presence of IgG within a few days of exposure reflects prior immunity. Absence of IgG indicates susceptibility.
· Varicella zoster immune globulin. To prevent maternal infection in patients without IgG, some advocate administering varicella zoster immune globulin (VZIG) within 96–144 hours of exposure, in a dosage of 125 U/10 kg up to a maximum of 625 units, or five vials, intramuscularly (IM). Because it is difficult to obtain serologic test results in a timely manner, and because no proven benefit results from administration of VZIG for the prevention of maternal-fetal transmission or amelioration of maternal symptoms and sequelae, many experts do not currently recommend VZIG administration to pregnant women who have been exposed to varicella. If the mother becomes infected, a risk exists of fetal infection and the potential sequelae. Pregnant women with varicella, however, may be advised to continue with the pregnancy because the risk of congenital varicella is small.
· Maternal illness. Generally, the disease course in pregnant patients is similar to that in nonpregnant patients and requires no specific treatment. Most patients require only supportive care with fluids and analgesics. If evidence of pneumonia or disseminated disease appears, the patient should be admitted to the hospital for treatment with intravenous acyclovir. A decrease in maternal morbidity and mortality occurs in pregnant women afflicted with varicella pneumonia who are treated with acyclovir during the last two trimesters, and the drug is safe to use at this stage of gestation. The dosage of acyclovir is 10–15 mg/kg intravenously (IV) every 8 hours for 7 days, or 800 mg by mouth (PO) five times per day.
· Vaccination. An attenuated live vaccine was approved by the FDA in 1995. One dose is recommended for all children between ages 1 and 12, which results in a 97% seroconversion rate. Two doses, given 4–8 weeks apart, are recommended for adolescents and adults without a history of varicella infection. Use of the vaccine during pregnancy is not recommended.
PARVOVIRUS B19
Epidemiology
Thirty percent to 60% of adults have acquired immunity to human parvovirus B19. Most clinical infections, which are known as erythema infectiosum or fifth disease, occur in school-aged children. The virus is spread primarily by the respiratory route. Outbreaks usually occur in the midwinter to spring months.
Clinical Manifestations
Maternal infection. Adults may present with the typical clinical features of fifth disease, particularly a red, macular rash and erythroderma affecting the face, which gives a characteristic “slapped cheek” appearance. Sixty percent of infected adults have acute joint swelling, usually with symmetrical involvement of peripheral joints; the arthritis may be severe and chronic. Some adults have completely asymptomatic infection. Parvovirus B19 may cause aplastic crises in patients with hemolytic anemia (i. e., sickle cell disease). The course of the infection is unchanged in pregnancy.
Fetal infection. Approximately one-third of maternal infections are associated with fetal infection. On transplacental transfer of the virus, fetal red blood cell precursors may be infected. Infection of fetal red blood cell precursors can result in fetal anemia, which, if severe, leads to nonimmune hydrops fetalis. The likelihood of severe fetal disease is increased if maternal infection occurs during the first 18 weeks of pregnancy, but the risk of hydrops fetalis persists even when infection occurs in the late third trimester. Fetal immunoglobulin M (IgM) production after 18 weeks' gestation probably contributes to the resolution of infection in fetuses who survive. Fetal demise may occur at any stage of pregnancy. Studies suggest that the overall risk of fetal death after maternal parvovirus B19 infection is lower than 10%, and the risk is lower still in the second half of pregnancy. Although no direct evidence exists that parvovirus B19 causes congenital anomalies, there is some evidence that possible damage to the fetal myocardium results from infection.
Diagnosis
The illness may be suspected on epidemiologic grounds if a regional outbreak is ongoing or if a family member is known to be affected.
Clinical Picture. Children, the most common transmitters of parvovirus B19 infection, present with systemic symptoms such as fever, malaise, myalgia, and headaches as well as with a confluent, indurated facial rash that imparts the characteristic “slapped-cheek” appearance of fifth disease. The rash spreads over 1–2 days to other areas, especially exposed surfaces such as the arms and legs, and is usually macular and reticular in appearance.
A pregnant woman who has been exposed to a child with fifth disease, who presents with an unexplained morbilliform or purpuric rash, or who has a known history of chronic hemolytic anemia and presents with an aplastic crisis should be evaluated for parvovirus B19 virus by measuring IgG and IgM titers. For patients who have had contact with an infected individual, titers should be drawn 10 days after exposure. Parvovirus B19 IgM appears 3 days after the onset of illness, peaks in 30–60 days, and may persist for 4 months. Parvovirus B19 IgG usually is detected by the seventh day of illness and persists for years.
Management
No specific antiviral therapy exists for parvovirus B19 infection.
Prophylaxis. Intravenous gamma globulin should be administered on an empiric basis to immunocompromised patients with known exposure to parvovirus B19 and should be used for treatment of women in aplastic crisis with viremia.
Detection of fetal hydrops. When maternal infection is identified, serial sonographic studies should be performed. Although hydrops fetalis usually develops within 6 weeks of maternal infection, it can appear as late as 10 weeks after maternal infection. Weekly or biweekly ultrasonographic scans can be performed.
Intrauterine blood transfusion has been demonstrated to be a successful therapeutic measure for correcting the fetal anemia in fetal hydrops. Single or serial intrauterine transfusions may be undertaken.
RUBELLA VIRUS
Epidemiology
The number of reported cases of congenital rubella syndrome is now at an all-time low. Transmission results from direct contact with the nasopharyngeal secretions of an infected person. The most contagious period is a few days before the onset of a maculopapular rash. The disease is communicable, however, for 1 week before and for 4 days after the onset of the rash. The incubation period ranges from 14 to 21 days.
Clinical Manifestations
Maternal infection. Rubella is symptomatic in 50–70% of those who contract the virus. The illness is usually mild, with a maculopapular rash that generally persists for 3 days; generalized lymphadenopathy (especially postauricular and occipital), which may precede the rash; and transient arthritis. Rubella follows the same mild course in pregnancy. The disease is often asymptomatic. Up to 50% of women with affected infants report no history of a rash during their pregnancies.
Fetal infection after maternal viremia leads to a state of chronic infection. At least 50% of all fetuses are infected when primary maternal rubella infection occurs in the first trimester, when the greatest risk of congenital anomalies exists. Multiple organ system involvement can occur. Permanent congenital defects include ocular defects such as cataracts, microphthalmia, and glaucoma; heart abnormalities, especially patent ductus arteriosus, pulmonary artery stenosis, and atrioventricular septal defects; sensorineural deafness; occasional microcephaly; and encephalopathy that culminates in mental retardation or profound motor impairment. As many as one-third of infants asymptomatic at birth may develop late manifestations, including diabetes mellitus, thyroid disorders, and precocious puberty. The extended rubella syndrome (progressive panencephalitis and type I diabetes mellitus) may develop as late as the second or third decade of life. Infants born with congenital rubella may shed the virus for many months.
Mortality. Spontaneous abortion occurs in 4–9% and stillbirth in 2–3% of pregnancies complicated by maternal rubella. The overall mortality of infants with congenital rubella syndrome is 5–35%.
Diagnosis
Serology. Diagnosis is usually confirmed by serology because viral isolation is technically difficult; moreover, results from tissue culture may take up to 6 weeks to obtain. Many rubella antibody detection methods exist, including hemagglutination inhibition and radioimmunoassay, and latex agglutination. Specimens should be obtained as soon as possible after exposure, 2 weeks later, and, if necessary, 4 weeks after exposure. Serum specimens from both acute and convalescent phases should be tested; a fourfold or greater increase in titer or seroconversion indicates acute infection. If the patient is seropositive on the first titer, no risk to the fetus is apparent. Primary rubella confers lifelong immunity; protection, however, may be incomplete. Antirubella IgM can be found in both primary and reinfection rubella. Reinfection rubella is usually subclinical, rarely associated with viremia, and infrequently results in a congenitally infected infant.
Prenatal diagnosis is made by identification of IgM in fetal blood obtained by direct puncture under ultrasonographic guidance at 22 weeks' gestation or later. The presence of rubella-specific IgM antibody in blood obtained by cordocentesis indicates congenital rubella infection, because IgM does not cross the placenta.
Management
Pregnant women should undergo rubella serum evaluation as part of routine prenatal care. A clinical history of rubella is unreliable. The rubella vaccine is an attenuated live virus, and if the patient is nonimmune, she should receive rubella vaccine after delivery. Contraception should be used for a minimum of 3 months after vaccination. There is a theoretical risk of teratogenicity if the vaccine is used during pregnancy. The CDC has maintained a registry since 1971 to monitor fetal effects of vaccination, however, and there have been no reported cases of vaccine-induced malformations.
If a pregnant woman is exposed to rubella, immediate serologic evaluation is mandatory. If primary rubella is diagnosed, the mother should be informed about the implications of the infection for the fetus. If acute infection is diagnosed during the first trimester, the option of therapeutic abortion should be considered. Women who decline this option may be given immune globulin because it may modify clinical rubella in the mother. Immune globulin, however, does not prevent infection or viremia and affords no protection to the fetus.
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