Abstract

diovascular defects or cataracts or simply the presence of a lymphocyte transforming agent in the cord blood of an otherwise asymptomatic neonate. • 4 This report documents severe, multiple congenital anomalies in an infant exposed to the EBV from conception to delivery. It differs from previously reported cases in its widespread tissue involvement, possibly representing the congenital infection in its severest form. The EBV may cause a spectrum of involvement in the congenitally infected offspring ranging from the subclinical type to severe deformity and death. Its incidence is difficult to define, but it is probably an uncommon cause of congenital malformation. The absence of cord blood IgM levels in our patient is consistent with the report of Chang and Blankenshipa in that infection occurred prior to the development of immunocompetency in the fetus. Also, congenitally infected infants with low cord blood lgM levels were stillborn or died in utero with significantly greater frequency. The place of the EB V in perinatal infections is strongly implied both by its close physical relationship to other known viral teratogens and by the spectrum of perinatal involvement just described. The question of its importance and prevalence as a teratogen cannot be answered at this time.

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