Rubella and pregnancy.

Maternal rubella infection during pregnancy can induce more or less severe congenital defects. In France in 1989, 43 rubella infections in pregnant women were recorded by the National Laboratory of Health. Diagnosis of primary rubella infection rests on detection of specific IgM antibodies. The most reliable technique for detection of IgM antibody is the antibody-capture immunoassay. Presence of rubella-specific IgM antibodies must be interpreted with caution: specific IgM antibodies may occur following reinfection and there have also been reports of rubella-specific reactivity in sera collected after infections with other viruses. In some cases, presence of rubella-specific IgM antibodies cannot be ascribed to any of the reasons above and remains completely unexplained. Fetal infection can be demonstrated by detecting rubella-specific IgM antibodies in fetal blood. However, very sensitive techniques must be used in order to obtain reliable results. Today, widespread immunization is still essential. Immunization of all seronegative pregnant women immediately after delivery is especially important since most mothers of babies with congenital rubella were multiparous. Women exposed to rubella may be offered normal human immunoglobulins as soon as possible after the exposure; if delayed, this treatment may be ineffective.     

Rubella in pregnancy: intrauterine transmission and perinatal outcome during a Brazilian epidemic.

Sixty pregnant women with clinical signs of rubella and specific rubella antibodies were studied between January 1999 and December 2002 in order to determine the intrauterine rubella transmission rate and the presence of the virus in amniotic fluid and fetal tissues by nested PCR. Thirty-three patients presented rubella before 12 weeks of gestation and 27 after 12 weeks. Gestational age at the time of acute rubella was determined on the basis of the date of last menstruation and the first trimester ultrasound scan. Thirteen patients with clinical features of rubella before 12 weeks of gestation were submitted to amniocentesis. Three products of conception were analyzed. The presence of the rubella virus was determined by nested PCR. IgM and IgG antibodies were analyzed in neonatal samples at birth and at 3 months of age using a capture immunoassay. Newborn follow-up was based on the presence of congenital rubella syndrome-compatible defects, anti-rubella antibodies, echocardiographic alterations, brainstem evoked response audiometry, and ophthalmological pathology. Five miscarriages and four fetal deaths were observed in the group of patients presenting clinical features before 12 weeks of gestation. IgM antibodies were detected in seven neonates at birth and at 3 months of age. Deafness was observed in three cases and pigmentary retinopathy in one case. Fourteen of the 16 samples (13 amniotic fluid and 3 fetal tissue samples) submitted to virological analysis tested positive. Four fetal deaths, five miscarriages (one with negative virology) and seven newborns with anti-rubella IgM at birth and/or at 3 months age were observed in the group with rubella before 12 weeks of gestation. There were three cases in which virological analysis of the amniotic fluid samples was positive (infected) while the newborn showed no signs of congenital rubella syndrome and anti-rubella IgM were absent. When maternal rubella occurred after 12 weeks of gestation, no fetal or neonatal rubella signs were observed. Eradication of congenital rubella syndrome is possible since vaccination campaigns continue and all services related to the health care of children, adolescents and women have become aware of the significance of the problem and are collaborating. All pregnant women in Brazil should be screened for the rubella antibody and the susceptible group should be vaccinated after giving birth.     

Impaired Cellular Immunity to Rubella Virus in Congenital Rubella

Specific cell-mediated immunity (CMI) responses to rubella virus were studied in 12 children with documented congenital rubella syndrome employing a ⁵¹Cr lymphocytotoxicity microassay. Hemagglutination inhibition antibody was detected in 11 of the 12 children, with titers ranging from 1:4 to 1:128. CMI to rubella virus was demonstrated in only 3 of the 11 antibody-positive children. The 12th child was negative for both hemagglutination inhibition and CMI. Of the three children with a positive CMI response, two had histories of reinfection with rubella virus. These data suggest that congenital rubella infection produces an impaired CMI response which subsequently may be altered by reinfection with rubella virus. The lack of CMI in the presence of antibody and concurrent excretion of live virus in the child with documented congenital rubella infection suggest a factor to be explored in the pathogenesis of this disease.     

Rubella virosomes: Preparation and ultrastructure

Rubella virosomes were prepared from preformed liposomes and detergent solubilized viral hemagglutinin. The liposomes were made from lecithin/dicetyl phosphate (3.5: 1) films resuspended in NTE buffer and sonicated. Viral hemagglutinin was prepared from purified virus after solubilization with Triton X-100 and centrifugation through a sucrose gradient containing β-d-octylglucoside. Electron microscopy of the rate zonal purified virosomes, showed virus-like structures of 40–80 nm. The virosomes retained the biological activity of the hemagglutinin and had a buoyant density of 1.2 g/cm³.     

Rubella screening: organization and incentive

Women aged 15-44 in a total population of 13,300 were screened for rubella immunity. Seventy-one per cent of the women at risk responded to a letter asking them to attend for a blood test, and of these nearly two thirds were screened. Practice expenditure on the programme was three times greater than income. We suggest a simpler, cheaper way of screening which involves minimal extra work and where an age-sex register is not required. We propose the introduction of a higher item-of-service payment for rubella vaccination.