Background Biofilms are communities of aggregated, matrix-embedded microbial cells showing a high tolerance to an in principle adequate antibiotic therapy, often resulting in treatment failure. A major challenge in the management of biofilm-associated infections is the development of adequate, standardized biofilm susceptibility testing assays that are clinically meaningful, i.e. that their results correlate with treatment outcome. Different biofilm susceptibility endpoint parameters like the minimal biofilm eradication concentration (MBEC) or the minimal biofilm inhibitory concentration (MBIC) have been suggested as a guide for treatment of biofilm-associated infections, however with inconsistent perception and use among biofilm researchers, leading to confusion and contradictions among different anti-biofilm component studies and clinical trials. Findings Evaluation of anti-biofilm effects is mostly based on the untreated reference growth control biofilm measured at the same endpoint as the treated biofilm, neglecting the possible change of the untreated reference biofilm from the time point of pre-antimicrobial exposure to the measured endpoint. In this commentary, we point out the importance of individual quantification of mature, established biofilms before antimicrobial treatment for each biofilm model in order to draw conclusions on the measured biofilm effect size, i.e. biofilm reducing (MBEC) or biofilm inhibitory (MBIC) effects. Conclusion The assessment of pre-treatment biofilms contributes to a standardized use of biofilm susceptibility endpoint parameters, which is urgently needed to improve the clinical validity of future anti-biofilm assays.

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A prospective cohort study (German Clinical Trial Registry, No. 00005273) was performed to determine pre-admission colonization rates, hospital acquisition risk factors, subsequent infection rates and colonization persistence including the respective molecular epidemiology and transmission rates of extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae (EPE). A total of 342 EPEs were isolated from rectal swabs of 1,334 patients on admission, at discharge and 6 months after hospitalization. Inclusion criteria were patients’ age > 18 years, expected length of stays > 48 hours, external referral. The EPEs were characterized by routine microbiological methods, a DNA microarray and ERIC-PCR. EPE colonization was found in 12.7 % of admitted patients, with the highest rate (23.8 %) in patients from nursing homes. During hospitalization, 8.1 % of the patients were de novo EPE colonized, and invasive procedures, antibiotic and antacid therapies were independent risk factors. Only 1/169 patients colonized on admission developed a hospital-acquired EPE infection. Escherichia coli was the predominant EPE (88.9 %), and 92.1% of the ESBL phenotypes could be related to CTX-M variants with CTX-M-1/15 group being most frequent (88.9%). A corresponding β-lactamase could not be identified in five isolates. Hospital-acquired EPE infections in patients colonized before or during hospitalization were rare. The diversity of the EPE strains was much higher than that of the underlying plasmids. In seven patients, transmission of the respective plasmid across different species could be observed indicating that the current strain-based surveillance approaches may underestimate the risk of inter-species transmission of resistance genes.

An explosive increase in carbapenemase-expressing Enterobacteriaceae contamination may have been caused by a foodborne source, and presliced vegetables should be taken into account as a putative pathogen repository. These findings underline the importance of appropriate cooling, transport, reheating, and distribution of meals and indicate that probing of nonorganic surfaces is limited by low sensitivity, which may be increased by additional overnight cultivation in appropriate media.