The number of nosocomial infections caused by Acinetobacter baumannii has increased in recent years. During a 12-month study, there were 1.8 episodes of A. Baumannii bacteremia per 1,000 adults admitted to a hospital in Seville, Spain. Seventy-nine patients were included in the study. A. baumannii bacteremia occurred after a mean (+/- SD) hospitalization of 18 +/- 20 days. In all cases the infections were acquired nosocomially; 71% wee acquired in intensive care units. Ampicillin/ sulbactam was found to be the most active agent against A. baumannii. The common source of the bacteremia was the respiratory tract (32 cases [71%]). Twenty patients (25%) had septic shock, and 24 (30%) had disseminated intravascular coagulation (DIC). Treatment with imipenem or ampicillin/sulbactam was most effective (cure rates, 87.5% and 83%, respectively). The deaths of 27 patients (34%) were related to A baumannii bacteremia. The presence of DIC (odds ratio [OR] = 116.4; P < .0001) and inappropriate antimicrobial treatment (OR = 15.2; P < .01) were independently associated with mortality. We conclude that most A. baumannii isolates are multiresistant and that nosocomial A. baumannii bacteremia may cause severe clinical disease that is associated with a high mortality.

The mortality rate of patients with cases of enterococcal bacteremia is high, although it has often been related to the patients' underlying conditions rather than to the infection itself. To analyze the attributable prognosis of enterococcal bacteremia (assessed by its attributable mortality rate and duration of hospital stay), a prospective, matched case-control study was done. All adults with an episode of enterococcal bacteremia without endocarditis were included. A control patient was randomly selected for every case patient and matched by sex, age and hospital ward. Univariate and multivariate analyses were performed. A total of 122 pairs were included, and incidence of enterococcal bacteremia was 2.3 episodes/1000 discharges. Crude 30-day mortality rates for case patients and control patients were 23% and 17%, respectively (P=.29); thus, the estimated attributable mortality rate was 6% (95% confidence interval, -4% to 16%). The mean duration of hospital stay of case patients and control patients were 38 and 17 days, respectively (P<.001); thus, the estimated attributable duration of hospital stay was 21 days (95% CI, 7-32 days). Enterococcal bacteremia without endocarditis does not increase risk of death by itself but extends the duration of hospital stay of patients who develop it.

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Using a repetitive extragenic palindromic PCR (REP-PCR), we genotypically characterized strains causing nosocomial Acinetobacter baumannii infections and analyzed the source of bacteremia in 67 patients from an institution in which infections by this bacterium were endemic. Six different genotypes were found, including 21, 27, 3, 9, 3, and 4 strains. The probable source of bacteremia, according to clinical and/or microbiological criteria, was known in 42 patients (63%): respiratory tract (n ‫؍‬ 19), surgical sites (n ‫؍‬ 12), intravascular catheters (n ‫؍‬ 5), burns (n ‫؍‬ 3), and urinary tract (n ‫؍‬ 3). The definite source of bacteremia, according to REP-PCR, could be established in 30 (71%) out of the 42 patients with strains from blood and other sites; in these cases clinical and microbiological criteria for the source of bacteremia were thus confirmed. In the remaining 12 patients (29%) the probable source was refuted by the REP-PCR method. The definite sources of bacteremia according to genotype were as follows: respiratory tract in 13 patients (31%), surgical sites in 8 (19%), intravascular catheters in 4 (9%), burns in 3 (7%), and urinary tract in 2 (5%). A comparison of strains from blood cultures and other sites with regard to their REP-PCR and antimicrobial resistance profiles was also made. Taking the REP-PCR as the "gold standard," the positive predictive value of antibiotype was 77% and the negative predictive value was 42%. In summary, the utility of the diagnosis of the source of nosocomial A. baumannii bacteremia using clinical and/or microbiological criteria, including antibiotyping, is limited, as demonstrated by REP-PCR.

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Sixteen amikacin-resistant clinical Acinetobacter baumannii isolates from nine different hospitals in Spain were investigated to determine whether the high incidence of amikacin-resistant A. baumannii was due to the dissemination of an amikacin-resistant strain or to the spread of an amikacin resistance gene. The epidemiological relationship studied by repetitive extragenic palindromic PCR and low-frequency restriction analysis of chromosomal DNA showed that the same clone was isolated in eight of nine hospitals, although other clones were also found. The strains were studied for the presence of the aph(3′)-VIaand aac(6′)-I genes, which encode enzymes which inactivate amikacin, by PCR. All 16 clinical isolates had positive PCRs with primers specific for the amplification of the aph(3′)-VIagene, whereas none had a positive reaction for the amplification of theaac(6′)-I gene. Therefore, the high incidence of amikacin resistance among clinical A. baumannii isolates in Spain was mainly due to an epidemic strain, although the spread of theaph(3′)-VI gene cannot be ruled out.

A case of Leuconostoc cremoris bacteremia in a patient with burn wounds over 45% of the body surface is presented. Leuconostoc bacteremia has not previously been reported in burn patients. The predisposing factors in this case were severe burn wounds resulting in immunocompromise, presence of both intravenous and enteral feeding catheters, several surgical interventions and previous treatment with imipenem plus amikacin. The patient was successfully treated with ampicillin 2 g l.v. every 6 hours for 21 days. Infection with Leuconostoc should be suspected when vancomycin-resistant organisms resembling streptococci are isolated.