Trends in Extended Spectrum Beta-Lactamase (ESBL) Producing Enterobacteriaceae and ESBL Genes in a Dutch Teaching Hospital, Measured in 5 Yearly Point Prevalence Surveys (2010-2014)

This paper describes the trends in prevalence of ESBL producing Enterobacteriaceae (ESBL-E) and ESBL genes, measured in five consecutive yearly Point Prevalence Surveys (PPS). All patients present in the hospital and in a day-care clinic (including patients on dialysis) on the day of the survey, were screened for perianal ESBL-E carriage. Perianal swabs were taken and cultured using an enrichment broth and a selective agar plate. Both phenotypic and genotypic methods were used to detect the production of ESBL, presence of ESBL-genes and clonal relatedness. Out of 2,695 patients, 135 (5.0%) were tested ESBL-E positive. The overall ESBL-E prevalence was stable over the years. Overall 5.2% of all ESBL-E were acquired by nosocomial transmission. A relative decrease of CTX-M-1-1-like ESBL genes (from 44 to 25%, p = 0.026) was observed, possibly related to the strong (>60%) decrease in antibiotic use in livestock in our country during the same period

AFLP patterns from all ESBL-E <i>E</i>. <i>coli</i>, <i>E</i>. <i>cloacae complex</i> and <i>K</i>. <i>pneumonia</i> eligible for cluster analyses.

<p>Strains clustering with a similarity between 90 and 100% were defined as identical strains. Strains clustering with a similarity above 35% were defined as different strains of the same species and strains clustering with a similarity below 35% were defined as different species. Identical strains are indicated in color. Each strain was coded with the number of the year in combination with a letter. * three ESBL positive strains cultured in a sample from patient 2012-N showed fenotypic differences. Therefore AFLP analyses was performed from all three samples.</p

ESBL prevalence over time, including bacterial species and ESBL genes.

<p>^& = Number of ESBL positive patients divided by the number of evaluable cultures (patients)</p><p>^# = Primary = patients with a unique isolates and index patients</p><p>^$ = Secondary = patients with ESBL isolates caused by nosocomial transmission</p><p>ESBL prevalence over time, including bacterial species and ESBL genes.</p

ESBL-E prevalence within the different medical specialties.

<p>^# = percentages refer to the number of ESBL-E positive patients divided by the total within medical specialty</p><p>ESBL-E prevalence within the different medical specialties.</p

Baseline characteristics of screened patients.

<p>^# = percentages refer to the number divided by the total patients with evaluable cultures</p><p>Baseline characteristics of screened patients.</p

Proportion of CTX-M-1 like ESBL genes over time.

<p>The vertical bars represent the percentage of CTX-M-1 like ESBL genes divided by the total number of ESBL genes. The line represents the logarithmic trendline.</p

ESBL-E prevalence in relation with the duration of hospitalisation (patients in day-care were excluded).

<p>Vertical bars represent the 95% confidence intervals.</p

Decline in AmpC β-lactamase-producing Escherichia coli in a Dutch teaching hospital (2013-2016)

OBJECTIVE: The objective of this study is to determine the prevalence of rectal carriage of plasmid- and chromosome-encoded AmpC β-lactamase-producing Escherichia coli and Klebsiella spp. in patients in a Dutch teaching hospital between 2013 and 2016. METHODS: Between 2013 and 2016, hospital-wide yearly prevalence surveys were performed to determine the prevalence of AmpC β-lactamase-producing E. coli and Klebsiella spp. rectal carriage. Rectal swabs were taken and cultured using an enrichment broth and selective agar plates. All E. coli and Klebsiella spp. isolates were screened for production of AmpC β-lactamase using phenotypic confirmation tests and for the presence of plasmid-encoded AmpC (pAmpC) genes. E. coli isolates were screened for chromosome-encoded AmpC (cAmpC) promoter/attenuator alterations. RESULTS: Fifty (2.4%) of 2,126 evaluable patients were identified as rectal carrier of AmpC β-lactamase-producing E. coli. No carriage of AmpC β-lactamase producing Klebsiella spp. was found. Nineteen (0.9%) patients harboured isolates with pAmpC genes and 30 (1,4%) patients harboured isolates with cAmpC promoter/attenuator alterations associated with AmpC β-lactamase overproduction. For one isolate, no pAmpC genes or cAmpC promotor/attenuator alterations could be identified. During the study period, a statistically significant decline in the prevalence of rectal carriage with E. coli with cAmpC promotor/attenuator alterations was found (p = 0.012). The prevalence of pAmpC remained stable over the years. CONCLUSIONS: The prevalence of rectal carriage of AmpC-producing E. coli and Klebsiella spp. in patients in Dutch hospitals is low and a declining trend was observed for E. coli with cAmpC promotor/attenuator alterations