Acinetobacter junii caused sepsis in six preterm infants in our neonatal un
it within 48 h. Each infant with clinical signs of systemic infection and a
ctivation of the acute phase response had two positive blood cultures with
Acinetobacter. junii. The sudden onset, the short duration of the outbreak
and the fact that none of the infants were colonized by A. junii suggested
a common source of A. junii administered directly into the blood. The only
feature shared by all six affected newborns was an intravenous fat emulsion
(Intralipid 10%), which was shown to be an excellent growth medium for A.
junii. Sepsis did not occur in four infants with 20% fat emulsion or amino
acids only. Vaminolact(R) did not support growth of the outbreak strain. Th
e immediate source of the outbreak could not be identified: samples of the
actual feeds given were not available for investigation, but A. junii was n
ot isolated from parenteral solutions with identical batch numbers used in
the septic infants. We conclude that Acinetobacter junii can cause a life-t
hreatening infection in preterm neonates. Contaminated intravenous fat emul
sion is implicated as a possible source of the infection. As a part of rigi
d infection control, intravenous feedings should be prepared under aseptic
conditions.