Recent Implications of Intrauterine and Postnatal Rubella

Abstract

Many new facets of rubella virus infection, both natural and congenital, have been recently exposed. In its intrauterine role, the virus is curiously selective and it is possible that the genes of the fetus are important in determining both the occurrence and severity of infection. The risk to the fetus is highest if infection occurs in early pregnancy, but there is some risk up to 24 weeks gestation. Multiplicity of defects and chronic persistence of fetal infection are characteristic features of congenital rubella infection. The clinical manifestations, diagnosis and management of congenital rubella are discussed, with emphasis on the long term sequelae. Postnatal rubella may be difficult to diagnose, since many cases are subclinical and history is unreliable:— serological diagnosis is therefore critical during pregnancy. Vaccination programmes designed to prevent congenital rubella are evaluated; while these show promise, the ideal vaccine is yet to become available.

Comparison of passive haemagglutination and haemagglutination-inhibition techniques for detection of antibodies to rubella virus.

“…In the absence of reliable clinical data, it is not possible to distinguish between this group and patients who have had a recent infection; in both cases there will be no PHA antibody detectable. In view of the teratogenic potential of rubella virus (Dudgeon, 1967;Forrest and Menser, 1975) the distinction is very important, and all sera negative by PHA would also have to be tested by HI to separate the two groups irrespective of available clinical information. Owing to the urgency of rapid diagnosis of rubella infection in pregnant women, demonstration of seroconversion by PHA is impractical.…”

“…The typical HI response of three children is shown in Figure 1. (Dudgeon, 1967;Forrest and Menser, 1975) Although realising that the antigens used in the HI and PHA tests were probably not the same, it was thought that the delay in the development of PHA antibody may have been due to the presence of rubella-specific IgM in the serum which, in an unknown fashion, inhibited the PHA reaction. To test this hypothesis, sera negative by PHA but positive by HI and known to contain rubellaspecific IgG and IgM were treated with 2-mercaptoethanol or centrifuged through sucrose gradients to separate the IgG and IgM components.…”