Zusammenfassung
Bei den wenigen bis heute berichteten Fällen intrauteriner CMV-Infektionen bei „Immunität“ der Mutter fehlten bisher schwere Verlaufsformen. Bei dem hier vorgestellten Fall zeigten sich nach 20 SSW im fetalen Ultraschall ein echogener Darm, nachfolgend Hepatomegalie, Aszites, Perikarderguss und Hydrops fetalis bei erheblich vergrößerter Plazenta. Bei pathologischem Kardiotokogramm wurde nach 28 SSW per Sectio caesarea entbunden. Das Kind war apnoeisch mit aufgetriebenem Abdomen und petechialen Hautblutungen und musste primär intubiert und beatmet werden. Im Verlauf nahmen die respiratorische und metabolische Azidose zu. Im ZNS fanden sich sonographisch viele periventrikuläre, echoreiche Areale mit Schallschatten. Das Kind verstarb nach 8 h im unbeeinflussbaren kardiorespiratorischen Versagen. Im kindlichen Blut wurde CMV-DNA gefunden, im mütterlichen Serum hochavide IgG-Antikörper gegen CMV bei negativem CMV-IgM. Dies spricht für eine Infektion mit CMV vor der jetzigen Schwangerschaft. Es fanden sich eine ausgedehnte Mikropolygyrie und ein Maturationsarrest des ZNS entsprechend der 22–23. SSW sowie bilaterale Verkalkungen in beiden Marklagern. In kindlichen Geweben wurden Viruseinschlüsse (Eulenaugenzellen) mit CMV-Protein nachgewiesen. Als Ursache eines nichtimmunologischen Hydrops fetalis sollte somit auch bei „Immunität“ gegen CMV bei der Mutter eine CMV-Infektion in Betracht gezogen werden.
Abstract
CMV infection of the fetus in CMV-seropositive pregnant women usually results in asymptomatic or mild disease. Life-threatening manifestations have not been reported up to now. In an 18-year-old Asian mother at 20 weeks of gestation, an echogenic bowel was detected by fetal ultrasound and later on fetal hepatomegaly, ascites, pericardial effusion, and hydrops fetalis with an enlarged placenta. Cesarean section was performed after 28 weeks of gestation because of a pathological cardiotocogram. After delivery, the baby was apneic with a distended abdomen and petechiae and had to be intubated and ventilated. In the clinical course increasing respiratory and metabolic acidosis occurred. Cranial ultrasound revealed periventricular signal intense areas with “shadows.” The baby died at an age of 8 h due to cardiorespiratory failure. Postmortal PCR examination of the peripheral blood of the infant led to detection of CMV DNA. In the blood of the mother high avidity IgG antibodies against CMV and no CMV IgM could be found. Pathohistological examination showed extensive micropolygyria and maturational arrest of CNS development corresponding to the 22–23 weeks of pregnancy. Owl eye cells with CMV proteins were detected in nephrotubular, alveolar, and trophoblast cells of the placenta, bile duct epithelia, and hepatocytes. A comprehensive literature search revealed that such a severe case of fetal CMV infection had not been reported in mothers with preconception immunity against CMV. In conclusion, even in pregnant mothers with preconception CMV antibodies, CMV infection should be considered as a cause of nonimmunological hydrops.
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Wintergerst, U., Hübener, C., Strauss, A. et al. Schwere kongenitale CMV-Infektion trotz maternem CMV-Durchseuchungstiter. Monatsschr Kinderheilkd 154, 558–564 (2006). https://doi.org/10.1007/s00112-004-1030-0
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DOI: https://doi.org/10.1007/s00112-004-1030-0