Aims: A nested case-control study of 75 patients with cardiac device infections (CDI) and 75 matched controls was conducted to evaluate time course, risk factors, culture results and frequency of CDI. Methods and results: CDI occurred in 75/3410 (2.2%) device implantation and revision procedures, performed between 2000 and 2007. The time delay between device procedure and infection ranged from 0 to 64 months (mean 14 (SD 16)), 21 patients (28%) had an early infection (,1 month), 26 (35%) a late infection (1-12 months) and 28 (37%) a delayed infection (.12 months). Of interest, 18 (24%) patients presented with an infection .24 months after the device-related procedure. Time delay until infection was significantly shorter when cultures were positive for micro-organisms compared to negative cultures (8 (12) vs 18 (18) months, p = 0.03). Pocket cultures in delayed infections remained more often negative (61% vs 23%, p = 0.01). Independent CDI risk factors were: device revision (odds ratio (OR) 3.67; 95% confidence interval (CI), 1.51 to 8.96), renal dysfunction defined as glomerular filtration rate ,60 ml/min (OR 4.64; CI, 1.48 to 14.62) and oral anticoagulation use (OR 2.83; CI 1.20 to 6.68). Conclusion: CDI occurred in 2.2% of device procedures, with 24% occurring more than two years after the devicerelated procedure. Renal dysfunction, device revisions and oral anticoagulation are potent risk factors for CDI.With expanding evidence-based indications for the implantation of permanent pacemakers, implantable cardioverter defibrillators (ICDs) and cardiac resynchronisation therapy devices (CRTs) the number of device-related procedures have increased rapidly over the past decade. 1 There are indications that the rate of cardiac device infections (CDI) has increased and that this outpaced the increase in implantation rate. 1 Reported CDI rates vary between 0.5% and 5.1%. 2-5 CDI is a serious and potentially life-threatening complication of cardiac device therapy, associated with significant morbidity and mortality usually requiring explantation of the device and lead system. Furthermore device infection results in prolonged hospital stay which is associated with significant costs. The average economic cost of CDI treatment has been estimated at $50 000 (£34 000; J39 400) per patient. 6 7 Although cardiac device therapy improves the outcome in different patient groups, CDI may negatively influence the risk-benefit ratio, especially in primary prevention patients. 1 Risk factors, although under debate, associated with CDI include sex, advanced age, diabetes mellitus, depressed immunity, number of operators, total number and duration of device-related procedures and oral anticoagulation therapy. 8 9 Moreover, CDI can occur shortly after a devicerelated procedure, but may also occur after several months and even after years. 2 Until now little is known about the occurrence and risk factors of CDI late after a device-related procedure. 10 In addition, exact data of infection rates and risk factors in acute and delayed inf...

When an optimal waste fraction sample volume of 20 ml was cultured, the contamination rate of CB was found to be approximately 13%, with low levels of < 1 colony-forming unit (CFU)/ml. Such levels of bacteria of low pathogenicity are expected to be of clinical importance only when CB is expanded in vitro for a prolonged period of time.

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, ...

Identification of Acinetobacter spp. to the DNA group level by phenotypic techniques is problematic, and there is a need for an alternative identification method for routine use. The present study validated the suitability of a rapid identification technique based on tRNA spacer (tDNA) fingerprinting in comparison with that of a commercially available assay involving carbon source utilization tests (Biolog MicroStation System) for identifying the 21 DNA-DNA hybridization groups belonging to the genus. For this purpose, 128 strains identified previously by DNA-DNA hybridization were analyzed by both techniques. tDNA fingerprinting was highly reproducible and classified all strains into 17 groups. Six DNA groups belonging to the A. calcoaceticus-A. baumannii complex were grouped into two distinct clusters, indicating the high degree of genetic similarity within this complex. Strains of the more recently described DNA groups BJ13 to BJ16 were ambiguously grouped and displayed three pattern types. The software used with the commercial carbon source utilization method grouped the 128 strains into 12 clusters, explaining the less discriminatory power of this system. We conclude that tDNA fingerprinting offers a quick and reliable method for the routine differentiation of most Acinetobacter spp. at the subgenus level.

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