Abstract 1298

A 28-week gestation infant was delivered by emergency caesarean section because of fetal distress. His mother had a febrile illness with a maculopapular rash at 21 weeks gestation and following this she serocoverted to parvovirus B19. At delivery the infant was anaemic, hydropic and had hepatosplenomegaly with biochemical evidence of hepatitis. Umbilical cord blood showed an increased proportion of activated CD45R0+ lymphocytes (32%, normal <5%) and 109 parvovirus B19 genomes per ml (a high viraemia). The infant developed respiratory distress and a grade 1 intraventricular haemorrhage. Supportive measures were successful; he was ventilated for 15 days, and commenced oral feeds at 6 days with expressed breast milk. His early progress was hampered by an episode of necrotising enterocolitis at 10 days which initially resolved, but recurred at four weeks. At surgery for this condition the liver was macroscopically fatty: this was biopsied and parvovirus inclusion bodies were identified. By three months the infant began to thrive and his bone marrow output recovered following the use of regular weekly infusions of intravenous gammaglobulin. No viral particles were detectable from this period onwards. He remained IgM negative and had a normal lymphocyte count. Flow cytometry of his T cells demonstrated that only 30% were CD4+, 65% were CD8 and 57% were CD8+CD45R0+, that is activated. The majority of activated CD8 cells were positive to intracellular staining for interferon gamma. An MRI at 4 months demonstrated widespread white matter damage, but no other pathology. A 21 week gestation infant was therefore capable of mounting a Th 1-type cytotoxic response with CD8 cells to parvovirus B19 while remaining antibody negative.

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