In the 1970s, Stella Chess found a high prevalence of autism in children with congenital rubella syndrome (CRS), 200 times that of the general population at the time. Many researchers quote this fact to add proof to the current theory that maternal infection with immune system activation in pregnancy leads to autism in the offspring. This rubella and autism association is presented with the notion that rubella has been eliminated in today’s world. CRS cases are no longer typically seen; yet, autistic children often share findings of CRS including deafness, congenital heart defects, and to a lesser extent visual changes. Autistic children commonly have hyperactivity and spasticity, as do CRS children. Both autistic and CRS individuals may develop type 1 diabetes as young adults. Neuropathology of CRS infants may reveal cerebral vasculitis with narrowed lumens and cerebral necrosis. Neuroradiological findings of children with CRS show calcifications, periventricular leukomalacia, and dilated perivascular spaces. Neuroradiology of autism has also demonstrated hyperintensities, leukomalacia, and prominent perivascular spaces. PET studies of autistic individuals exhibit decreased perfusion to areas of the brain similarly affected by rubella. In both autism and CRS, certain changes in the brain have implicated the immune system. Several children with autism lack antibodies to rubella, as do children with CRS. These numerous similarities increase the probability of an association between rubella virus and autism. Rubella and autism cross many ethnicities in many countries. Contrary to current belief, rubella has not been eradicated and globally affects up to 5% of pregnant women. Susceptibility continues as vaccines are not given worldwide and are not fully protective. Rubella might still cause autism, even in vaccinated populations.
Objective: Autism may arise from any of several categories of harm, including genetic, environmental, perinatal, and drug exposures. Rubella has been examined as one of the viral causes of autism. We designed a study to determine whether antenatal susceptibility to rubella, shown by low or no immunity when tested in the antepartum, was associated with child autism spectrum disorders. Study Design: Children ages 2.5 years to 7.5 years with autism spectrum disorder were identified, and matched on age and sex with children having no such diagnosis. To identify mothers who were rubella-susceptible, we noted those with pregnancy rubella IgG values under 10 IU/mL; since low-immunity might also pose a risk, we analyzed those with IgG values under 20 IU/mL. Exclusion criteria included preterm delivery, child brain injury or genetic disorder, and maternal use of anti-epileptic or illicit drugs. Results: For the years 2007 to 2011, we identified 56 children with autism meeting study criteria, and identified suitable children as matched controls. Of the 56 autism-case mothers, one had a rubella IgG value under 10 IU/mL, while 6 of the control mothers had an IgG value under 10 IU/mL. For the low-immunity group, 19 of the autism-case mothers had an IgG value under 20 IU/mL, while 18 of the control mothers had an IgG value under 20 IU/mL. These associations were tested with McNemar's exact (binomial) test. There was no statistical relationship between the presence of an autism diagnosis and mother's rubella susceptibility at the <10 IU/mL level (p=0.13), and at the <20 IU/mL level (p=0.85). Conclusions: We failed to find evidence supporting the concept that antenatal rubella susceptibility was associated with child autism. Results are not conclusive since this exploratory study was under-powered. We believe that the hypothesis warrants more investigation, including studies with greater power and complementary approaches.
ObjectiveThe objectives are to estimate the vertical transmission rate in twins relative to singleton pregnancies, to evaluate whether discordance within twin pairs is rare, and to characterize concordance within monozygotic and dizygotic twin pairs in relation to hereditability.MethodsWe first sought to estimate the vertical transmission rate of congenital CMV infection in twins by gathering cohort-based studies of congenital CMV in which vertical transmission in both singleton and twin pregnancies was reported. This also allowed us to compare singleton and twin infection rates. From the above studies and other large cohorts of congenitally infected infants, the percentage of discordantly infected twin pairs determined whether this is a rare phenomenon. Theorizing discordance is not rare, we then analyzed data from cases with twin outcomes for congenital CMV infection, according to whether the twins were monozygotic or dizygotic, and calculated their corresponding concordance rates to estimate the broad-sense heritability. Lastly, we described other factors that might affect vertical transmission.ResultsFrom five articles following at-risk pregnancies, the rate of vertical transmission in twin pregnancies is 58.7% (95% CI 43.3-72.3%) whereas in singleton pregnancies it is 31.4% (95% CI: 29.0-34.0%) p = 0.0002. Of ten studies of larger cohorts of infants with congenital CMV infection, 21 of 42 twin pairs with at least one twin infected were discordant for congenital CMV (50.0%, 95% CI: 34.4–65.6%) indicating discordance of congenital CMV infection in twin pairs is not rare. Of 28 studies covering 37 twin pairs where at least one twin had congenital CMV, and zygosity was known, eleven of thirteen monozygotic twin pairs (84.6%; 95% CI: 53.7-97.3%) were concordant for CMV infection, and nine of twenty-four dizygotic twin pairs (37.5%; 95% CI: 19.6-59.2%) were concordant for infection giving an estimated hereditability of 94.2%. Within these 37 twin pairs, factors such as primary or recurrent maternal infection, prematurity, growth discordance, and sex are described; however, in many of these cases these factors are unknown.ConclusionThe rate of vertical transmission of congenital CMV is higher for twins than singletons. Discordance of congenital CMV in twins is not rare and suggests a possible genetic susceptibility to congenital CMV.
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