The prevalence of the currently known Acinetobacter species and related trends of antimicrobial resistance in a Dutch university hospital were studied. Between 1999 and 2006, Acinetobacter isolates from clinical samples were collected prospectively. Isolates were analyzed by amplified fragment length polymorphism fingerprinting. For species identification, a profile similarity cutoff level of 50% was used, and for strain identification, a cutoff level of 90% was used. Susceptibility for antimicrobial agents was tested by disk diffusion by following the CLSI guideline.The incidences of Acinetobacter isolates ranged from 1.7 to 3.7 per 10,000 patients per year, without a trend of increase, during the study years. Twenty different species were distinguished. Acinetobacter baumannii (27%) and Acinetobacter genomic species (gen. sp.) 3 (26%) were the most prevalent. Other species seen relatively frequently were Acinetobacter lwoffii (11%), Acinetobacter ursingii (4%), Acinetobacter johnsonii (4%), and Acinetobacter junii (3%). One large cluster of A. baumannii, involving 31 patients, and 16 smaller clusters of various species, involving in total 39 patients, with at most 5 patients in 1 cluster, occurred. Overall, 37% of the A. baumannii isolates were fully susceptible to the tested antibiotics. There was a borderline significant (P ‫؍‬ 0.059) trend of decreasing susceptibility. A. baumannii was the Acinetobacter species causing the largest burden of multiple-antibiotic resistance and transmissions in the hospital.More than 30 named and unnamed species of Acinetobacter have been described (14), some of which are of clinical importance, including A. baumannii, Acinetobacter gen. sp. 3, and Acinetobacter gen. sp. 13TU, while other species, like A. junii, A. johnsonii, A. ursingii, and Acinetobacter schindleri, can also incidentally be associated with infections (8). Much attention has been paid to outbreaks caused by acinetobacters (28), which in most cases are caused by A. baumannii (15,23). Notably, in diagnostic microbiology, isolates identified as A. baumannii may also include the closely related species Acinetobacter gen. sp. 3 or Acinetobacter gen. sp. 13TU. Bacteria belonging to other Acinetobacter species are frequently not further identified as or designated Acinetobacter species, as this would require genotypic methods that are usually not available in clinical diagnostic microbiology. These difficulties in identification explain why, overall, not much is known about the occurrences of the different Acinetobacter species in the hospital.The aim of the present study was to determine the prevalences of the currently known Acinetobacter species and related trends of antimicrobial resistance in our hospital through the years. To this aim, we identified all available Acinetobacter isolates obtained from our hospital in the period between 1999 and 2006 to the species level by amplified fragment length polymorphism (AFLP) analysis, a well-validated method for Acinetobacter species identification (7,8). Furthermore, ...

To confirm the results obtained in an earlier study, the incidence of infection was evaluated in 54 patients (62 periods of admission), nursed in conventional rooms and given a regimen of antimicrobial agents intended to modulate the intestinal flora selectively as a method to prevent infection during severe granulocytopenia. In 62 patients receiving selective antimicrobial modulation (SAM), 18% acquired major infections which was similar to 19% in patients on SAM in an earlier double-blind placebo controlled study and lower than 47% in the controls. Evaluation of a large number of surveillance cultures showed that the presence of specific potentially pathogenic aerobic bacteria was associated with the occurrence of major infection. If the bacterial species in question were not found in the cultures the chance of becoming infected was less than 5%, whereas the chance ranged between 42 and 62% depending on the species involved when these microorganisms were isolated.

The results of bacteriologic cultures of blood and heparin-lock fluid, both drawn from the central venous catheters of 54 consecutive oncohematologic patients, have been used to determine their value for the diagnosis of systemic and catheter-associated infection. In 30 patients with clinical signs of infection (bacteremia or septicemia), 74 of 1000 (7.4%) heparin-lock fluid cultures, 114 of 542 (21%) catheter-drawn blood cultures, and 36 of 134 (26%) venipuncture blood cultures became positive, whereas in 24 patients without clinical signs of infection the respective values were 5 of 700 (0.7%), one of 220 (0.4%), and none of ten cultures. Comparison of the results of cultures sampled on the same day reveals that the positive and negative predictive values for catheter-drawn blood cultures, with the venipuncture blood cultures taken as the standard for bacteremia, are 82% and 95% respectively. The results of heparin-lock fluid are indicative for clinically relevant colonization of the catheter. Three or more positive heparin-lock fluid cultures, sampled on subsequent days, were correlated with the occurrence of bacteremia or septicemia with a positive predictive value of 100%. The conclusions are supported by the results of scanning electron microscopy.

In order to study the effect of modulation of the intestinal flora on granulopoiesis, conventional mice were given drinking water with or without a combination of antimicrobial drugs, i.e. neomycin, polymyxin B, amphotericin B and nalidixic acid. These antimicrobial drugs, which selectively eliminate the aerobic gram-negative rods and suppress yeasts, are currently administered to our patients to prevent infection during granulocytopenia (nalidixic acid has been replaced by pipemidinic acid). After sublethal irradiation, mice on antimicrobial drugs were granulocytopenic longer than the controls. Although these differences were rather small, i.e. two days, the impact on the course of an experimental infection at the end of the period of granulocytopenia was substantial. After injection of 1 x 10(5) live bacteria into the thigh muscle, both groups of granulocytopenic mice exhibited an initial increase in the number of bacteria in the thigh muscle. After 18 h a further increase in the number of bacteria was found for 63% of the mice receiving antimicrobial drugs, whereas the number had dropped below the baseline in 77% of the controls. These differences were reflected in the incidence of bacteremia, i.e. positive blood cultures for the bacteria injected into the thigh muscle were found for 26% of the mice on antimicrobial prophylaxis versus only 2% of the control mice. Remarkably, the number of peripheral blood granulocytes correlated with the number of CFU isolated from the thigh 18 h after injection for the animals on prophylaxis but not for the controls. This might mean that modulation of the intestinal flora affects not only the number of circulating granulocytes, but also other host defense factors.