During the summer of 2000, a countrywide epidemic of West Nile fever (WNF) occurred in Israel, with 417 confirmed cases and 35 deaths. Immunosuppressed patients had a 31% case-fatality rate, which was significantly higher compared to non-immunosuppressed patients (13%). We describe a 42-year-old male lung-transplant recipient with serologically confirmed West Nile virus (WNV) encephalitis and deteriorating level of consciousness. He was treated with 0.4 g/kg intravenous immunoglobulin preparation from Israeli donors that contained a high titer of anti-WNV antibodies (1 : 1600). The patient showed rapid improvement within 24 h and complete disappearance of signs and symptoms within 48 h. This is the second case of an immunosuppressed patient responding to the same preparation of intravenous immunoglobulins. Larger studies are required in order to establish the therapeutic role of immunoglobulins in patients with WNF.

Docosahexaenoic acid (DHA, 22:6 n-3) is the major polyunsaturated fatty acid (PUFA) in the adult mammalian brain. DHA is an essential fatty acid (FA) since it, or its short chain precursor, ␣-linolenic acid (LnA, 18:3 n-3), have to be obtained in the diet. Moreover, dietary n-3 FA deficiency is associated with biochemical changes in the brain and with disturbances in vision and other neurological parameters. Under normal nutritional conditions, fetal brain DHA accumulation is substantial, with a ''DHA accretion spurt'' being demonstrated in the last period of gestation. This accumulation is supported by the maternal supply of DHA or LnA, but selectivity of DHA accumulation is probably a placental function whose mechanism is lately being clarified. The fetal gastrointestinal (G-I) tract may be instrumental in supplying DHA to the fetal brain under certain conditions, such as following intra-amniotic administration of ethyldocosahexaenoate (Et-DHA). In this pathway, DHA is supplied independently of the maternal metabolism, and the fetal liver is apparently involved. The fetal G-I tract may be advantageous for DHA supply in cases of maternal-placental insufficiency resulting in intrauterine growth retardation. The fetal brain itself is capable of metabolizing LnA to DHA, without the participation of the fetal liver, thus contributing to the accumulation of its own DHA during one of the most crucial periods of its development.