Dramatic increase of third-generation cephalosporin-resistant E. coli in German intensive care units: secular trends in antibiotic drug use and bacterial resistance, 2001 to 2008

Abstract

IntroductionThe objective of the present study was to analyse secular trends in antibiotic consumption and resistance data from a network of 53 intensive care units (ICUs).MethodsThe study involved prospective unit and laboratory-based surveillance in 53 German ICUs from 2001 through 2008. Data were calculated on the basis of proportions of nonduplicate resistant isolates, resistance densities (that is, the number of resistant isolates of a species per 1,000 patient-days) and an antimicrobial usage density (AD) expressed as daily defined doses (DDD) and normalised per 1,000 patient-days.ResultsTotal mean antibiotic use remained stable over time and amounted to 1,172 DDD/1,000 patient-days (range 531 to 2,471). Carbapenem use almost doubled to an AD of 151 in 2008. Significant increases were also calculated for quinolone (AD of 163 in 2008) and third-generation and fourth-generation cephalosporin use (AD of 117 in 2008). Aminoglycoside consumption decreased substantially (AD of 86 in 2001 and 24 in 2008). Resistance proportions were as follows in 2001 and 2008, respectively: methicillin-resistant Staphylococcus aureus (MRSA) 26% and 20% (P = 0.006; trend test showed a significant decrease), vancomycin-resistant enterococcus (VRE) faecium 2.3% and 8.2% (P = 0.008), third-generation cephalosporin (3GC)-resistant Escherichia. coli 1.2% and 19.7% (P < 0.001), 3GC-resistant Klebsiella pneumoniae 3.8% and 25.5% (P < 0.001), imipenem-resistant Acinetobacter baumannii 1.1% and 4.5% (P = 0.002), and imipenem-resistant K. pneumoniae 0.4% and 1.1%. The resistance densities did not change for MRSA but increased significantly for VRE faecium and 3GC-resistant E. coli and K. pneumoniae. In 2008, the resistance density for MRSA was 3.73, 0.48 for VRE, 1.39 for 3GC-resistant E. coli and 0.82 for K. pneumoniae.ConclusionsAlthough total antibiotic use did not change over time in German ICUs, carbapenem use doubled. This is probably due to the rise in 3GC-resistant E. coli and K. pneumoniae. Increased carbapenem consumption was associated with carbapenem-resistant K. pneumoniae carbapenemase-producing bacteria and imipenem-resistant A. baumannii.

Extended-spectrum β-lactamase/AmpC-producing uropathogenic Escherichia coli from HIV patients: do they have a low virulence score?

“…Previous studies have documented an undoubted link between the increased use of cephalosporins and the emergence of ESBL-producing Enterobacteriaceae (Meyer et al, 2010). As anticipated, the majority of our bla TEM (68.3 %) and bla CTX-M (83.3 %) positive isolates were from HIV patients.…”

Emergence of Imipenem-Resistant Gram-Negative Bacilli in Intestinal Flora of Intensive Care Patients

“…These GNB are increasingly resistant to antibiotics and particularly to broad-spectrum cephalosporins, because of the global spread of extendedspectrum ␤-lactamase (ESBL)-producing Enterobacteriaceae and because of the emergence of Enterobacteriaceae and P. aeruginosa producing high levels of AmpC cephalosporinase (1)(2)(3). Carbapenems are currently the only active beta-lactams effective against these bacteria; this has led to an increase in their use not only for documented infections but also for empirical treatment of acquired hospital infections such as those occurring in ICU patients (3). Thus, selective pressure for carbapenem resistance has spread progressively (4); in response, resistance to carbapenems emerged rapidly during the 1990s and continues to increase worldwide not only in nonfermenter GNB but also in Enterobacteriaceae (5).…”

Studies on avian pathogenic Escherichia coli in commercial broiler chicken in South East Queensland

“…The majority of these sequence types have been previously described and are globally distributed amongst humans as well as animals (Fernandes et al, 2016;Kim et al, 2011;Maluta et al, 2014;Sola-Gines et al, 2015). This may suggest that the resistant isolates originated from humans (Meyer et al, 2010), wild birds and/or from the farm environment such as water sources (Alves et al, 2014;Sjolund et al, 2008) and then gained access to the poultry production environment.…”

“…Identification of resistance in the absence of antimicrobial selection may indicate that these resistant isolates originated from humans (Meyer et al, 2010), wild birds and/or from the environment (Alves et al, 2014;Sjolund et al, 2008) and gained access to the poultry production environment. Further screening and characterisation of antimicrobial resistant E. coli isolates from wild bird species, wild animals and the environment as occurred in some studies already (Guenther et al, 2011;Radhouani et al, 2014) could provide evidence of a potential risk pathway for the transmission of bacteria as well as the resistance genes.…”