Concurrent surveillance of blood culture isolates in a 1000-bed tertia
ry care hospital over a 7-year period from 1986 to 1993 identified 102
episodes of nosocomial fungaemia, representing 6.6% of all episodes o
f nosocomial bloodstream infections and 0.49/1000 admissions. No signi
ficant change in the frequency, rate, source or microbial aetiology of
nosocomial fungaemia occurred over the 7-year period. Candida albican
s accounted for 74%, followed by Candida (Torulopsis) glabrata (8%), C
. parapsilosis (7%), C. tropicalis (3%), C. lusitaniae (2%), C. krusei
, Malassezia furfur Saccharomyces cerevisiae, Hansenula anomala and Cr
yptococcus albidus (one each). 'Primary' fungaemia, usually attributed
to intravascular catheters, was considered to be the source in 65% of
cases, with 64% of these patients receiving total parenteral nutritio
n (TPN). Other important sources of infection included the urinary tra
ct (11%), the gastrointestinal tract (8%) and the respiratory tract (7
%). Sixty-four % of patients were in one of the hospital's seven inten
sive care units (ICUs) when their infection developed, the neonatal IC
U and adult medical/surgical ICU each accounting for 21%. Only 7% of c
ases were associated with neutropenia and another 14% with malignancy
or immunosuppression. Death occurred within 7 days of diagnosis of fun
gaemia in 23 cases. In eight instances, fungaemia was considered the m
ain cause of death. We conclude that in our hospital nosocomial fungae
mia is largely caused by C. albicans, occurring in association with in
travascular catheter use and TPN in ICU patients. Most cases are not a
ssociated with recognized immune defence defects. Fungaemia is associa
ted with a high short-term mortality rate.