The rhesus incompatible pregnancy and its consequences for affected fetuses and neonates.

Rhesus incompatibility in pregnancy may result in haemolytic disease of the fetus and newborn (HDFN). This review discusses the fetal, neonatal and long-term consequences of HDFN and its management. Untreated, the fetal and neonatal prognosis of HDFN is poor. Provision of intravascular intrauterine transfusion (IUT) in a dedicated referral centre significantly reduces perinatal loss. Early-onset, severe fetal anaemia carries a greater risk of adverse fetal and neonatal outcomes and is less amenable to treatment with IUT. Interventions to prevent and treat severe, early onset disease have been investigated, however evidence from randomised controlled trials is required. Neonatal consequences of Rhesus haemolytic disease include early and late postnatal anaemia, and hyperbilirubinaemia leading to bilirubin-induced neurological dysfunction. Neurodevelopmental impairment and adult cardiovascular disease are long-term complications that have been reported in association with severe fetal anaemia. Strategies to prevent fetal hydrops, and further research into the long-term impacts of fetal anaemia may improve health outcomes for adult survivors of HDFN.

SHV-34: an extended-spectrum beta-lactamase encoded by an epidemic plasmid.

OBJECTIVES: To elucidate the causes for treatment failure in children given extended-spectrum cephalosporins. METHODS: During April 1998-March 2000, 18 isolates of members of the family Enterobacteriaceae, fulfilling microbiological criteria for carriage of extended-spectrum beta-lactamases (ESBLs) and carrying blaSHV, were isolated from paediatric inpatients. The collection was subjected to a retrospective molecular analysis. RESULTS: Three species were represented in the collection: Citrobacter koseri (one isolate), Escherichia coli (one isolate) and Klebsiella pneumoniae (16 isolates). A common plasmid was found in these bacteria, as judged by restriction endonuclease digestion. This was able to transfer an ESBL phenotype from donors to a laboratory strain of E. coli. Nucleotide sequence analysis revealed that this phenotype was associated with a new variant in blaSHV encoding SHV-34. CONCLUSIONS: Analysis reveals the presence of an epidemic plasmid in this collection of bacteria. This carries a gene encoding the SHV-34 ESBL, described for the first time in this report. Nucleotide sequence analysis shows that there is a mutation from A-->G affecting the codon at amino acid position 64 (GAA-->GGA), changing the glutamic acid typically seen in this position to glycine.