ABSTRACT 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.

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.

To determine the risk factors involved in the development of enterococcal bacteremia, a prospective, observational, case-control study was carried out over 18 months. All episodes of enterococcal bacteremia with clinical significance detected in adults were included. A control matched by sex, age and hospitalization ward (medical, surgical or intensive care unit) was selected randomly for each patient with enterococcal bacteremia. Uni- and multivariate analyses of the epidemiological characteristics of both groups were performed. Etiologic fractions of every risk factor were also determined. One hundred twenty-two pairs were included. The severity of the chronic underlying diseases was similar in both groups. Neutropenia, cirrhosis, organ transplantation, intravascular catheter, urinary catheter, nasogastric tube, parenteral nutrition and previous administration of cephalosporins and imipenem were the factors associated with enterococcal bacteremia in the univariate analysis. The factors independently associated with enterococcal bacteremia in the multivariate analysis were neutropenia (odds ratio [OR] = 8), urinary catheter (OR = 3) and previous administration of cephalosporins (OR = 4) and imipenem (OR = 10). Their respective etiologic fractions were 9%, 44%, 11% and 29%. Efforts to reduce the occurrence of enterococcal bacteremia should be focused on appropriate use of cephalosporins, imipenem and external devices.

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')-VIa and 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')-VIa gene, whereas none had a positive reaction for the amplification of the aac(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 the aph(3')-VI gene cannot be ruled out.

Pneumocystis carinii is a common opportunistic pathogen in patients infected with the human immunodeficiency virus (HIV). Pneumocystis carinii pneumonia is common, while extrapulmonary infections with Pneumocystis carinii have been reported sparingly. The clinical features are frequently nonspecific. The detection of Pneumocystis carinii in cerebrospinal fluid (CSF) has not been reported thus far. In this report, an unusual case of Pneumocystis carinii meningoradiculitis in an HIV-infected patient who had previously received primary prophylaxis with trimethoprim-sulfamethoxazole is presented.

A case ofLeuconostoc 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 enterai feeding catheters, several surgical interventions and previous treatment with imipenem plus amikacin. The patient was successfully treated with ampicillin 2 g i.v. every 6 hours for 21 days. Infection withLeuconostoc should be suspected when vancomycinresistant organisms resembling streptococci are isolated.

The clinical features and the outcomes of eight cases of nosocomial Acinetobacter baumannii meningitis treated with ampicillin/sulbactam are reported. All the patients had fever, neck stiffness or meningeal signs, and a low consciousness level, and in their cerebrospinal fluid (CSF), pleocytosis, a low glucose level, and an elevated protein level were noted. For all CSF isolates of A. baumannii, the MIC of ampicillin/sulbactam was < or = 8/4 microg/mL. The MICs of sulbactam by microdilution in two cases were 4 microg/mL. All isolates were resistant to cefotaxime, ceftriaxone, ceftazidime, ureidopenicillins, ciprofloxacin, and gentamicin. Seven isolates were resistant to imipenem. A. baumannii was isolated from other samples in seven episodes. All patients were treated with ampicillin/sulbactam (seven with 2 g/l g every 6 hours and one with 2 g/l g every 8 hours). Six patients were cured and two patients died of meningitis. There were no side effects with the ampicillin/sulbactam treatment. In conclusion, ampicillin/sulbactam may be effective as therapy for meningitis caused by A. baumanii resistant to imipenem and other beta-lactam drugs.

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.