A marked increase in hemodialysis bacteremia occurred in 1996, associated with increased reliance on CVCs for vascular access in hemodialysis patients during a period of healthcare restructuring.

Concurrent surveillance of blood culture isolates in a 1000-bed tertiary care hospital over a 7-year period from 1986 to 1993 identified 102 episodes of nosocomial fungaemia, representing 6.6% of all episodes of nosocomial bloodstream infections and 0.49/1000 admissions. No significant change in the frequency, rate, source or microbial aetiology of nosocomial fungaemia occurred over the 7-year period. Candida albicans 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 Cryptococcus 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 nutrition (TPN). Other important sources of infection included the urinary tract (11%), the gastrointestinal tract (8%) and the respiratory tract (7%). Sixty-four % of patients were in one of the hospital's seven intensive care units (ICUs) when their infection developed, the neonatal ICU and adult medical/surgical ICU each accounting for 21%. Only 7% of cases were associated with neutropenia and another 14% with malignancy or immunosuppression. Death occurred within 7 days of diagnosis of fungaemia in 23 cases. In eight instances, fungaemia was considered the main cause of death. We conclude that in our hospital nosocomial fungaemia is largely caused by C. albicans, occurring in association with intravascular catheter use and TPN in ICU patients. Most cases are not associated with recognized immune defence defects. Fungaemia is associated with a high short-term mortality rate.

To determine treatment regimens and epidemiological patterns in the occurrence of candidemia, a review of cases occurring from 1992 to 1996 in three large Canadian hospitals, University of Alberta Hospital (UAH) and Royal Alexandra Hospital (RAH), Edmonton, and Foothills Medical Center (FMC), Calgary, was carried out. Cases were detected by reviewing microbiology laboratory records. There were 202 cases in all (UAH 104, FMC 70, RAH 28). For the five study years the candidemia rate was 4.5/10 000 discharges (UAH 7.6, FMC 4.9, and RAH 1.7; P < 0.05 for all interhospital comparisons). The rate remained stable between 1992 and 1995 but rose dramatically in 1996 to 7.6/10 000 (P < 0.01 compared to 1995) as a result of increases at UAH and RAH. Of the 208 species identified, Candida albicans accounted for 135 (65%). During hospitalization 93 (46%) patients died. Species did not influence outcome. Antifungal treatment with fluconazole alone was given to 14% of patients, and increased in frequency throughout the study. No antifungal therapy was given to 47 patients (23%). This group had a much higher mortality (68%) than those who received treatment (39% P < 0.01). Twenty of the untreated patients had already died by the time the blood culture had been reported as growing a yeast. Candidemia rates vary significantly between hospitals and increased in some but not all over the five study years. As many patients with candidemia will have died by the time laboratory diagnosis is made, presumptive antifungal therapy in high-risk patients may be necessary if outcome is to be improved.

The occurrence of cases of Stenotrophomonas maltophilia peritonitis in chronic peritoneal dialysis (PD) patients prompted a review of our experience with this condition. A search of microbiology records revealed seven episodes of S. maltophilia peritonitis in 7 patients in 1996 — 3.8% of all PD patients — compared to no cases in 1994 and 1995 ( p = 0.01). Patients ranged in age from 16 to 64 years; there were 3 males and 4 females. Six of seven episodes of peritonitis were community acquired and one was hospital acquired. No temporal clustering of cases was seen. Patients were from different urban and rural communities. Patients used the same commercially supplied dialysate fluid, different dialysis techniques, and were taught a no-touch technique for connection. Treatment of peritonitis required removal of the Tenckhoff catheter in 4 of 7 cases. Fingerprinting of six available isolates by polymerase chain reaction using primers derived from the conserved region of the 16/23Sr RNA gene sequence and pulsed field gel electrophoresis revealed all to be unique strains. A case-control study comparing 7 S. maltophilia cases to 21 PD controls showed case patients to be younger and more likely to be on immuno-suppressive therapy. We conclude that S. maltophilia has emerged as an important cause of peritonitis in our continuous ambulatory PD population. Evidence to date suggests community acquisition with no evidence of a common source.