on behalf of the CAPNETZ Study Group ABSTRACT: The aim of the present study was to investigate the prognostic value, in patients with community-acquired pneumonia (CAP), of procalcitonin (PCT) compared with the established inflammatory markers C-reactive protein (CRP) and leukocyte (WBC) count alone or in combination with the CRB-65 (confusion, respiratory rate o30 breaths?min -1 , low blood pressure (systolic value ,90 mmHg or diastolic value f60 mmHg) and age o65 yrs) score. In total, 1,671 patients with proven CAP were enrolled in the study. PCT, CRP, WBC and CRB-65 score were all determined on admission and patients were followed-up for 28 days for survival.In contrast to CRP and WBC, PCT levels markedly increased with the severity of CAP, as measured by the CRB-65 score. In 70 patients who died during follow-up, PCT levels on admission were significantly higher compared with levels in survivors. In receiver operating characteristic analysis for survival, the area under the curve (95% confidence interval) for PCT and CRB-65 was comparable (0.80 (0.75-0.84) versus 0.79 (0.74-0.84)), but each significantly higher compared with CRP (0.62 (0.54-0.68)) and WBC (0.61 (0.54-0.68)). PCT identified low-risk patients across CRB classes 0-4.In conclusion, procalcitonin levels on admission predict the severity and outcome of community-acquired pneumonia with a similar prognostic accuracy as the CRB-65 score and a higher prognostic accuracy compared with C-reactive protein and leukocyte count. Procalcitonin levels can provide independent identification of patients at low risk of death within CRB-65 (confusion, respiratory rate o30 breaths?min -1 , low blood pressure (systolic value ,90 mmHg or diastolic value f60 mmHg) and age o65 yrs) risk classes.

Abstract. Bauer TT, Ewig S, Marre R, Suttorp N,

No abstract

Contamination of hospital water systems with legionellae is a well-known cause of nosocomial legionellosis. We describe a new real-time LightCycler PCR assay for quantitative determination of legionellae in potable water samples. Primers that amplify both a 386-bp fragment of the 16S rRNA gene from Legionella spp. and a specifically cloned fragment of the phage lambda, added to each sample as an internal inhibitor control, were used. The amplified products were detected by use of a dual-color hybridization probe assay design and quantified with external standards composed of Legionella pneumophila genomic DNA. The PCR assay had a sensitivity of 1 fg of Legionella DNA (i.e., less than one Legionella organism) per assay and detected 44 Legionella species and serogroups. Seventy-seven water samples from three hospitals were investigated by PCR and culture. The rates of detection of legionellae were 98.7% (76 of 77) by the PCR assay and 70.1% (54 of 77) by culture; PCR inhibitors were detected in one sample. The amounts of legionellae calculated from the PCR results were associated with the CFU detected by culture (r ‫؍‬ 0.57; P < 0.001), but PCR results were mostly higher than the culture results. Since L. pneumophila is the main cause of legionellosis, we further developed a quantitative L. pneumophila-specific PCR assay targeting the macrophage infectivity potentiator (mip) gene, which codes for an immunophilin of the FK506 binding protein family. All but one of the 16S rRNA gene PCR-positive water samples were also positive in the mip gene PCR, and the results of the two PCR assays were correlated. In conclusion, the newly developed Legionella genus-specific and L. pneumophila species-specific PCR assays proved to be valuable tools for investigation of Legionella contamination in potable water systems.

Staphylococcus epidermidis is a normal constituent of the healthy human microflora, but it is also the most common cause of nosocomial infections associated with the use of indwelling medical devices. Isolates from device-associated infections are known for their pronounced phenotypic and genetic variability, and in this study we searched for factors that might contribute to this flexibility. We show that mutator phenotypes, which exhibit elevated spontaneous mutation rates, are rare among both pathogenic and commensal S. epidermidis strains. However, the study revealed that, in contrast to those of commensal strains, the genomes of clinical S. epidermidis strains carry multiple copies of the insertion sequence IS256, while other typical staphylococcal insertion sequences, such as IS257 and IS1272, are distributed equally among saprophytic and clinical isolates. Moreover, detection of IS256 was found to be associated with biofilm formation and the presence of the icaADBC operon as well as with gentamicin and oxacillin resistance in the clinical strains. The data suggest that IS256 is a characteristic element in the genome of multiresistant nosocomial S. epidermidis isolates that might be involved in the flexibility and adaptation of the genome in clinical isolates.Staphylococcus epidermidis is a normal constituent of the healthy human skin and mucosal microflora. In recent decades, however, the bacterium has emerged as a nosocomial multiresistant pathogen and is now the most common cause of deviceassociated infections. Little is known of the factors that have contributed to this development, but the increasing number of immunocompromised patients, the use of indwelling medical devices, and a high selective pressure by antibiotics offer bacteria a novel ecological niche. It is unclear why just staphylococci were able to occupy this niche and by which factors pathogenic S. epidermidis differ from their commensal counterparts. In recent years, it has been shown that the ability to form biofilms on medical devices is a characteristic feature of nosocomial S. epidermidis isolates. Moreover, clinical S. epidermidis isolates exhibit an extraordinarily high phenotypic and genotypic flexibility. Thus, variants of the same parent strain can differ in terms of colony morphology, growth rate, hemolysis, biofilm formation, and antibiotic susceptibility (4, 7). The molecular mechanisms involved in this phenomenon are poorly understood, but it is assumed that the generation of phenotypic and genotypic variants is an evolutionary advantage that helps staphylococci to adapt to changing environmental conditions. The purpose of this study was therefore to search for genetic factors and mechanisms in clinical S. epidermidis that might contribute to this process. Previous studies have shown that staphylococcal biofilm formation is a highly variable factor which is influenced by both regulatory processes and genetic mechanisms such as phase variations, mutations, and chromosomal rearrangements (5,10,26,(32)(33)(34). The observation t...