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Objectives: The aims of this study were to evaluate risk factors, clinical presentation, outcome and antimicrobial susceptibility in patients with Escherichia coli bacteremia occurring over seven years in a single cancer hospital., Methods: Sixty five episodes of bacteremia from E. coli appearing over seven years from 12,301 admissions in a single cancer institution were retrospectively analyzed., Results: The proportion of bacteremia caused by E. coli among Gram-negative bacteremia was 20.8% (the second most common organism after Pseudomonas aeruginosa), and infection-associated mortality was 17%. The incidence in 1989-1995 varied from 14.3 to 24.7%. The most common risk factors were: solid tumors as the underlying disease (70.7%); central venous catheter insertion (32.3%); prior surgery (46.2%), and prior chemotherapy within 48 h (44.4%). Neutropenia and urinary catheters did not place patients at high risk in any of the subgroups. When we compared the two subgroups of 61 cases of bacteremia - monomicrobial and polymicrobial (when E. coli was isolated from blood culture with another microorganism) - we found that acute leukemia and breakthrough (recurrence while receiving antibiotics) bacteremia were more frequently associated with polymicrobial E. coli bacteremia. There was also a difference in infection-associated mortality: monomicrobial bacteremia due to E. coli only had a significantly lower mortality in comparison with polymicrobial E. coli bacteremia (8.9 vs 35.0%, respectively; P<0.03)., Conclusion: The susceptibility of 115 E. coli strains isolated from 65 episodes of bacteremia was stable. Only two episodes caused by quinolone-resistant strains occurred, both in 1995, after six years of using ofloxacin for prophylaxis in neutropenic patients in our hospital. We found that 85.2-91.3% of all strains were susceptible to aminoglycosides, 97.8% to quinolones, and 90-100% to third generation cephalosporins and imipenems. The patients most commonly infected had solid tumors and the mortality was only 17%.

The aim of this study was to assess whether multiresistant gram-negative bacteremias (MRGNB) were associated with specific risk factors for higher mortality than sensitive gram-negative bacteremias. Two groups of subjects: (51 cases and 102 controls) were matched for sex, age, underlying disease, and neutropenia. There were no significant differences in the incidence of cytotoxic chemotherapy administered, vascular catheter insertion, catheter as source of bacteremia, and etiology of bacteremia. The proportion of Klebsiella-Enterobacter, Pseudomonas aeruginosa, Acinetobacter spp., and Stenotrophomonas maltophilia was similar in the two groups. Prior surgery (21.6% vs 7.9%, P < 0.05) was significantly associated with sensitive gram-negative bacteremia. Previous prophylaxis with ofloxacin (45.1% vs 24.5%; P < 0.05) and prior therapy with broad-spectrum antibiotics (41.2% vs 27.5%; P < 0.05), such as first and second generation cephalosporins (19.6% vs 7.8%; P < 0.05), third generation cephalosporins (41.2% vs 13.7%; P < 0.01), aminoglycosides (39.2% vs 9.8%; P < 0.01), ofloxacin (11.8% vs 2.0%; P < 0.005), and imipenem (19.6% vs 2.0%; P < 0.001) were significantly more frequently observed among cases than controls. Cases (patients with bacteremia due to multiresistant gram-negative bacteremias) were also significantly more frequently infected with bacteria resistant to ceftazidime (68.6% vs 17.6%; P < 0.001), amikacin (52.9% vs 7.8%; P < 0.001), imipenem (50.1% vs 23.5%; P < 0.05), ciprofloxacin (32.1% vs 5.9%; P < 0.001), and piperacillin (41.2% vs 7.8%; P < 0.01). With regard to outcome, attributable mortality was similar (15.7% vs 13.8%; not significant) in the two groups; however, cure rates were lower among cases (patients infected with MRGNB) because crude mortality was higher in cases (35.3% vs 13.8%; P < 0.01) than in controls.

Because of controversial data on virulence and mortality, six cases of fungemia caused by Candida glabrata were reviewed in a single cancer institution within 8 years. Risk factors and outcome of C. glabrata, Candida albicans, and other non-albicans Candida spp. appearing within the same period under the same antibiotic policy at the same institution were compared. Among other non-albicans Candida spp. in 1990-1997 C. glabrata fungemias showed a decreasing tendency, from 9% to 4.5% in 1997. Analyzing the proportion of C. glabrata among blood cultures, among 170 positive blood cultures 12 were caused by C. glabrata (6.2% among all pathogens and 24% among non-albicans Candida spp.). C. glabrata among all fungemias was diagnosed as the fourth most common pathogen after C. albicans, C. krusei, and C. parapsilosis. Three of six C. glabrata fungemias were breakthrough. Two appeared during prophylaxis with itraconazole and one during fluconazole prophylaxis. Five of six received broadspectrum antibiotic therapy with third-generation cephalosporines, five of six had vascular catheter insertion, four of six were neutropenic, and two of six received amphotericin B therapy. One patient died before his blood cultures were reported to be positive. Overall mortality of C. glabrata fungemia was 16.7%. One patient died of underlying disease with fungemia. There were no significant differences in risk factors between C. glabrata and C. albicans. However, overall and crude mortality was lower in C. glabrata than in C. albicans (25.5% vs. 16.7%; P = 0.03). Attributable mortality was lower in comparison to C. albicans (0 vs. 15.7% in C. albicans; P = 0.001).

The risk factors, therapy and outcome of ten cases of fungemia due to Candida krusei, appearing during the last 10 years in a single national cancer institution, are analyzed. Univariate analyses did not find any specific risk factors in comparison to 51 Candida albicans fungemias appearing at the same institution and with a similar antibiotic policy. Association with prior fluconazole prophylaxis was not confirmed because only one case appeared in a patient previously treated with fluconazole. However, attributable and crude mortality due to C. krusei fungemias was higher than for C. albicans fungemia. The authors review 172 C. krusei fungemias published within the last 10 years to compare with the incidence, therapy and outcome of C. krusei fungemia from our cancer institute.

During the last two decades, the treatment of leukaemia has changed significantly; increasing intensity of chemotherapy and bone marrow transplantation have lead to profound immunosuppression, prolonged stays in hospital, vascular catheterization, administration of broad spectrum antimicrobial agents and extensive use of prophylactic antifungal drugs. All but the last of these risk factors have increased the incidence of fungal infections in leukaemic patients and have significantly changed the spectrum of pathogens in favour of non-Candida species. In major haematological centres in Europe and the US, the proportion of non-Candida yeast isolated from patients increased from 1 to 5% in 1980 to 10 to 25% after 1990. However, there are not enough data to assess whether mortality due to these species is higher than that due to Candida spp. (30-40%) or filamentous fungi (50-70%). In this article, specific risk factors and therapeutic outcome of yeast infections other than Candida spp. in leukaemia such as Malassezia furfur, Trichosporon spp., Blastoschizomyces capitatus, Rhodotorula rubra, Saccharomyces cerevisiae, Clavispora lusitaniae, Cryptococcus laurentii and Hansenula anomala are reviewed. An analysis of risk factors from the National Cancer Institute, Bratislava has shown that non-Candida yeast infections (N = 15) in cancer patients are associated with leukaemia and neutropenia (P = < 0.002, 0.005), more often fatal than those caused by C. albicans (N = 51) (P < 0.006) but not non-albicans Candida (N = 34) and are associated with quinolone (P < 0.0001) and itraconazole prophylaxis (P < or = 0.05, 0.015) compared to both C. albicans or non-albicans Candida respectively.

Objective: The aim of the study was to assess the outcome of inappropriately treated cancer patients with documented bacteremia., Design/setting: 95 cases of inappropriately treated bacteremias in febrile cancer patients in a tertiary-care center were analyzed and compared with a group of appropriately treated bacteremias to assess risk factors for inappropriate therapy and outcome., Results: Among 285 bacteremias, 95 (33.3%) were not treated appropriately, with 42 receiving the wrong antibiotics and 17 having too short a therapeutic course of appropriate antibiotics. In 13, therapy was delayed for more than 48 hours after the onset of fever. Twenty-three patients did not receive antibiotic therapy at all despite bacteremia. A group of 95 inappropriately treated bacteremias was compared to 190 appropriately treated bacteremias occurring in the same period. Microbiological cure after the initial course of therapy was achieved more often (76.8% vs 38.9%, P < .001) in the group of appropriately treated bacteremias in all cases and also in the subgroup of leukemic patients (P < .01). Overall and attributable mortality were significantly lower in patients who were treated appropriately. There was no difference in the number of antibiotics administered in appropriately versus inappropriately treated bacteremias. Cost of therapy between both groups was similar., Conclusions: Inappropriately treated bacteremic cancer patients had outcomes that were significantly worse than patients who were treated appropriately. The reasons for inappropriate therapy were selection of the wrong antimicrobials, too short a duration of therapy, delayed onset of therapy, or absence of antimicrobial therapy.

60 patients with 60 viridans streptococcal bacteraemic episodes (42 due to penicillin-sensitive and 18 due to penicillin-resistant viridans streptococci) were analysed in a population of 12,185 admissions and 1,380 bacteraemic episodes during a 7-year period in a National Cancer Institute. The incidence of viridans streptococci among bacteraemias decreased from 11.5% in 1989 to 2.5% in 1995 after penicillin was introduced for prophylaxis of febrile neutropenia in acute leukaemia in 1993. However, the proportion of penicillin-resistant viridans streptococcal bacteraemias increased from 0 in 1989 and 1990 before any prophylaxis was given, to 12.9-16.7% after quinolones were used for prophylaxis in 1991 and 1992, and to 44.4-81.8% in 1993-1995 after penicillin was added to the quinolones. Mortality rate was higher in the subgroup of penicillin-resistant viridans streptococcal bacteraemias (p < 0.05). Statistically significant risk factors in patients with penicillin-resistant (compared with penicillin-sensitive) viridans streptococcal bacteraemia were: acute leukaemia (p < 0.03), high doses of cytarabine (p < 0.05), mucocutaneous lesions (p < 0.004), breakthrough bacteraemia during prophylaxis with ofloxacine plus penicillin (p < 0.001). Multiple logistic regression analysis showed that only acute leukaemia (OR 2.05, CI 0.85-1.85, p < 0.00452) and penicillin-resistance (OR 0.71, CI 0.103-4.887, p < 0.0209) were significant independent predictors of inferior outcome. Breakthrough bacteraemia during empiric therapy with vancomycine occurred in 5 of 116 patients treated with vancomycine, and during therapy with ampicillin plus gentamicin in 6 patients of 18 treated.

The resistance pattern of 2816 isolates from 17631 blood cultures and the etiology of isolates causing bacteremia and fungemia among 14591 admissions were investigated in an 80-bed single cancer institute during seven years (1990-1996) under the same empiric therapeutic antibiotic policy but with different prophylactic strategies. No change was found in the proportion of Gram-positive versus Gram-negative bacteria isolated from bacteremias (70% vs. 30%) during the past seven years. Furthermore, the proportion of coagulase-negative staphylococci and enterococci was about the same before and after the introduction of ofloxacin in prophylaxis. However, the proportion of Pseudomonas aeruginosa and Stenotrophomonas maltophilia causing bacteremia increased. There was no increase in Candida krusei and Candida glabrata after the introduction of fluconazole into our prophylactic regimen in 1992. Penicillin-resistance in viridans streptococci increased after penicillin was introduced into prophylaxis in acute leukemia in 1993. Until 1995 no quinolone-resistant Enterobacteriaceae were observed. Susceptibility to quinolones did not significantly change within the past seven years in Enterobacteriaceae after their introduction to prophylaxis in 1991, but Pseudomonas aeruginosa decreased from 90 to 58.2%. Glycopeptide resistance in enterococci and staphylococci was minimal in the observed period (0.9-4.3%).

The aim of this study was to retrospectively compare the incidence, risk factors, and outcome in patients seen over a 7-year period at the National Cancer Institute in the Slovak Republic, with vancomycin-sensitive or vancomycin-resistant enterococcal bacteremia. The total incidence of enterococcal bacteremia at the National Cancer Institute increased from 5.1% in 1991 to 11.1% in 1993 and then decreased to 4.3% in 1995. Analysis of the 77 episodes of enterococcal bacteremia from 66 patients showed that 69 episodes from 60 patients were due to vancomycin-sensitive Enterococcus faecalis (group 1) and 8 episodes from 8 patients were due to vancomycin-resistant Enterococcus faecium (group 2). The features most frequently associated with enterococcal bacteremia were the insertion of a central venous catheter, neutropenia lasting more than 10 days, previous therapy with cephalosporins or vancomycin, previous prophylaxis with quinolones, and the incidence of superinfections. There was no difference in the clinical course or outcome between the 2 study groups. Previous therapy with aminoglycosides, cephalosporins, vancomycin or imipenem, neutropenia less than 10 days in length, malignancies other than leukemia or solid tumors, and the incidence of breakthrough bacteremia significantly correlated with patients with vancomycin-resistant E. faecium rather than patients with vancomycin-sensitive E. faecalis. The overall mortality was similar in both groups and averaged 32.5% for all enterococcal bacteremic patients. In this study, the major risk factors associated with cancer patients for developing vancomycin-resistant enterococcal bacteremia were previous therapy with aminoglycosides, cephalosporins or vancomycin, superinfections with other organisms and the incidence of breakthrough bacteremia., (Copyright © 1996 Japanese Society of Chemotherapy and the Japanese Association for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.)

Ninety-nine patients with 101 bacteraemic episodes due to Pseudomonas aeruginosa (PA) within 6 years were divided into two groups according to their resistance to imipenem; of these 91 episodes were due to imipenem-sensitive (ISPA) and 10 due to imipenem-resistant (IRPA) strains. Risk factors, clinical course and outcome were evaluated and compared in the two groups. Acute leukaemia, long-lasting neutropenia, previous therapy with amikacin, third-generation cephalosporins, imipenem and prophylaxis with quinolones were significantly more frequently associated with IRPA than with ISPA. Imipenem-resistant PA bactereamias were associated with a higher incidence of septic shock (40% vs 19.8%) p. 161 0.02) and death 33.3%) than were ISPA bacteraemias. Since 1992, when first IRPA appeared, the incidence of imipenem-resistance increased tenfold, and in 1994, up to 10% of the PA populations causing bloodstream infections in cancer patients in our centre were imipenem-resistant.