SOD and SDD have marked effects on the bacterial ecology in an ICU, with rising ceftazidime resistance prevalence rates in the respiratory tract during intervention and a considerable rebound effect of ceftazidime resistance in the intestinal tract after discontinuation of SDD.

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Objectives: Carbapenem resistance mediated by mobile genetic elements has emerged worldwide and has become a major public health threat. To gain insight into the molecular epidemiology of carbapenem resistance in The Netherlands, Dutch medical microbiology laboratories are requested to submit suspected carbapenemase-producing Enterobacterales (CPE) to the National Institute for Public Health and the Environment as part of a national surveillance system. Methods: Meropenem MICs and species identification were confirmed by E-test and MALDI-TOF and carbapenemase production was assessed by the Carbapenem Inactivation Method. Of all submitted CPE, one species/carbapenemase gene combination per person per year was subjected to next-generation sequencing (NGS). Results: In total, 1838 unique isolates were received between 2014 and 2018, of which 892 were unique CPE isolates with NGS data available. The predominant CPE species were Klebsiella pneumoniae (n ¼ 388, 43%), Escherichia coli (n ¼ 264, 30%) and Enterobacter cloacae complex (n ¼ 116, 13%). Various carbapenemase alleles of the same carbapenemase gene resulted in different susceptibilities to meropenem and this effect varied between species. Analyses of NGS data showed variation of prevalence of carbapenemase alleles over time with bla OXA-48 being predominant (38%, 336/892), followed by bla NDM-1 (16%, 145/892). For the first time in the Netherlands, bla OXA-181 , bla OXA-232 and bla VIM-4 were detected. The genetic background of K. pneumoniae and E. coli isolates was highly diverse. Conclusions: The CPE population in the Netherlands is diverse, suggesting multiple introductions. The predominant carbapenemase alleles are bla OXA-48 and bla NDM-1. There was a clear association between species, carbapenemase allele and susceptibility to meropenem.

The occurrence of high-level aminoglycoside resistance (HLAmR) was determined for 73 enterococci and 54 group A streptococci by the high-load disc method, tube macrodilution and the polymerase chain reaction (PCR). The PCR method revealed the presence of genes coding for aminoglycoside-3'-O-phosphoryltransferase-III (APH(3')-III), aminoglycoside-6'-N-acetyltransferase/2''-O-phosphoryltransferase (AAC(6')/APH(2'')), or both, in 20.6%, 9.6% and 4.1% of the enterococci, respectively. The prevalence of HLAmR to at least one aminoglycoside among local enterococci was 37% (27/73). Only one of 54 Streptococcus pyogenes isolates produced APH(3')-III and exhibited high-level resistance to kanamycin and streptomycin. In general, the three methods yielded comparable results, with only three discrepancies among the 127 isolates examined. High-load disc screening and tube macrodilution proved to be practical, reliable and reproducible, and thus suitable for routine screening. Of 20 Enterococcus faecalis strains tested, all were penicillin-tolerant. Only one of seven penicillin-tolerant S. pyogenes strains was HLAmR. No association between the two forms of resistance was found.

Failure of treatment of group A streptococcal pharyngitis and tonsillitis is well documented. One of the possible explanations for treatment failure is penicillin tolerance in group A streptococci. Reports on the prevalence of penicillin tolerance among group A streptococci (0-100%) and the presumed relationship with therapeutic failure vary considerably. Therefore, it appears worthwhile to review pharyngotonsillitis studies, devoting special attention to the variables of MIC-MBC laboratory determinations such as inoculum preparation, composition and volume of test medium, and the criteria used to define penicillin tolerance. Alternative methods (gradient-replica plate method, beta-lactamase disk test, time-kill assay, and cell-lysis assay) are discussed. It is concluded that technical factors and the definitions used influenced the reported rates of penicillin tolerance. The epidemiological data suggest that tolerance is not limited to a single streptococcal serotype. Furthermore, there is not sufficient data to support a correlation between in vitro penicillin tolerance of group A streptococci and treatment failure, either in clinical cases or in animal studies. On the other hand, evidence to exclude penicillin tolerance as a cause of treatment failure is also not available. Therefore, at present penicillin tolerance cannot be ruled out as a cause of penicillin treatment failures.