X-AMR, a pop-up journal

Purpose. To assess the antibiotic resistance, transposon profiles, serotype distribution and vaccine coverage rates in 110 erythromycin-resistant S. pneumoniae clinical isolates.

Methodology. Erythromycin, clindamycin, tetracycline, chloramphenicol and kanamycin susceptibilities were assessed using the E-test/disc diffusion method. Inducible macrolide resistance was tested using the erythromycin-clindamycin double disc diffusion test. Serogrouping and serotyping were performed using latex particle agglutination and the Quellung reaction, respectively. Drug resistance genes and transposon-specific genes were investigated by PCR.

Results. Of the isolates, 93  % were resistant to clindamycin; 81  % were resistant to tetracycline; 76  % were multi-drug-resistant, having resistance to both clindamycin and tetracycline; and 12  % had extended-drug resistance, being resistant to clindamycin, tetracycline, chloramphenicol and kanamycin. The majority of isolates (88.2 %) exhibited the cMLS_B phenotype. The association between the cMLS_B phenotype and tetracycline resistance was related to transposons Tn2010 (38.2 %), Tn6002 (21.8 %) and Tn3872 (18.2 %). M and iMLS_B phenotypes were observed in 7 and 5  % of the isolates, respectively. The most frequent serotype was 19 F (40 %). Among the erythromycin-resistant pneumococci, vaccine coverage rates for the 13-valent pneumococcal conjugate vaccine (PCV-13) and the 23-valent pneumococcal polysaccharide vaccine (PPSV-23) were 76.4 and 79.1  %, respectively, compared to 82.2 and 85.1 % transposon-carrying isolates.

Conclusions. Multi-drug resistance among erythromycin-resistant S. pneumoniae isolates mainly occurs due to the horizontal spread of the Tn916 family of transposons. The majority of the transposon-carrying isolates are covered by 13- and 23-valent pneumococcal vaccines. Since serotype distribution and transposons in S. pneumoniae isolates may change over time, close monitoring is essential.

Resistance to carbapenem and aminoglycoside antibiotics is a critical problem in Acinetobacter baumannii , particularly when genes conferring resistance are acquired by multiply or extensively resistant members of successful globally distributed clonal complexes, such as global clone 1 (GC1) . Here, we investigate the evolution of an expanding clade of lineage 1 of the GC1 complex via repeated acquisition of carbapenem- and aminoglycoside-resistance genes. Lineage 1 arose in the late 1970s and the Tn6168/OCL3 clade arose in the late 1990s from an ancestor that had already acquired resistance to third-generation cephalosporins and fluoroquinolones. Between 2000 and 2002, two distinct subclades have emerged, and they are distinguishable via the presence of an integrated phage genome in subclade 1 and AbaR4 (carrying the oxa23 carbapenem-resistance gene in Tn2006) at a specific chromosomal location in subclade 2. Part or all of the original resistance gene cluster in the chromosomally located AbaR3 has been lost from some isolates, but plasmids carrying alternate resistance genes have been gained. In one group in subclade 2, the chromosomally located AbGRI3, carrying the armA aminoglycoside-resistance gene, has been acquired from a GC2 isolate and incorporated via homologous recombination. ISAba1 entered the common ancestor of this clade as part of the cephalosporin-resistance transposon Tn6168 and has dispersed differently in each subclade. Members of subclade 1 share an ISAba1 in one specific position in the chromosome and in subclade 2 two different ISAba1 locations are shared. Further shared ISAba1 locations distinguish further divisions, potentially providing simple markers for epidemiological studies.

Purpose. Antimicrobial-resistant bacterial infections in low- and middle-income countries (LMICs) are a well-established global health issue. We aimed to assess the prevalence of and epidemiological factors associated with the carriage of ciprofloxacin- and ceftriaxone-resistant Escherichia coli and associated resistance genes in a cohort of 498 healthy children residing in urban Vietnam.

Methodology. We cultured rectal swabs onto MacConkey agar supplemented with resistant concentrations of ciprofloxacin and ceftriaxone. Additionally, we screened meta-E. coli populations by conventional PCR to detect plasmid-mediated quinolone resistance (PMQR)- and extended-spectrum β-lactamase (ESBL)-encoding genes. We measured the associations between phenotypic/genotypic resistance and demographic characteristics using logistic regression.

Results/Key findings. Ciprofloxacin- and ceftriaxone-resistant E. coli were cultured from the faecal samples of 67.7 % (337/498) and 80.3 % (400/498) of children, respectively. The prevalence of any associated resistance marker in the individual samples was 86.7 % (432/498) for PMQR genes and 90.6 % (451/498) for β-lactamase genes. Overweight children were significantly more likely to carry qnr genes than children with lower weight-for-height z-scores [odds ratios (OR): 1.24; 95 % confidence interval (CI): 10.5–1.48 for each unit increase in weight for height; P=0.01]. Additionally, younger children were significantly more likely to carry ESBL CTX-M genes than older children (OR: 0.97, 95 % CI: 0.94–0.99 for each additional year, P=0.01).

Conclusion. The carriage of genotypic and phenotypic antimicrobial resistance is highly prevalent among E. coli in healthy children in the community in Vietnam. Future investigations on the carriage of antimicrobial resistant organisms in LMICs should focus on the progression of carriage from birth and structure of the microbiome in obesity.

Purpose. The antimicrobial activity of N-chlorotaurine (NCT), an endogenous long-lived oxidant applied topically, was tested against Chlamydiae in vitro.

Methodology. Elementary bodies of Chlamydia pneumoniae strain CV-6 and Chlamydia trachomatis serovars A and D were incubated in 0.01, 0.1 and 1 % (w/v) NCT solution at pH 7.1 and 37 °C. After different incubation times, aliquots were removed and grown in cell culture. The number of inclusion forming units was quantified by immunofluorescence and real-time qPCR.

Results/Key findings. Chlamydia pneumoniae and Chlamydia trachomatis were inactivated by 1 and 0.1 % NCT within 1 min. Moreover, 0.025–0.1 % NCT significantly reduced the number of intracellularly growing C. pneumoniae within 30 min.

Conclusions. This is the first study demonstrating the antimicrobial activity of NCT against Chlamydiae. Clinical implications of these findings have to be investigated in further trials.

Antimicrobial resistance (AMR) is a global public-health emergency, which threatens the advances made by modern medical care over the past century. The World Health Organization has recently published a global priority list of antibiotic-resistant bacteria, which includes extended-spectrum β-lactamase-producing Enterobacteriaceae and carbapenemase-producing Enterobacteriaceae. In this review, we highlight the mechanisms of resistance and the genomic epidemiology of these organisms, and the impact of AMR.

Acinetobacter baumannii is a common causative agent of hospital-acquired infections and a leading cause of infection in burns patients. Carbapenem-resistant A. baumannii is considered a major public-health threat and has been identified by the World Health Organization as the top priority organism requiring new antimicrobials. The most common mechanism for carbapenem resistance in A. baumannii is via horizontal acquisition of carbapenemase genes. In this study, we sampled 20 A. baumannii isolates from a patient with extensive burns, and characterized the evolution of carbapenem resistance over a 45 day period via Illumina and Oxford Nanopore sequencing. All isolates were multidrug resistant, carrying two genomic islands that harboured several antibiotic-resistance genes. Most isolates were genetically identical and represented a single founder genotype. We identified three novel non-synonymous substitutions associated with meropenem resistance: F136L and G288S in AdeB (part of the AdeABC efflux pump) associated with an increase in meropenem MIC to ≥8 µg ml−1; and A515V in FtsI (PBP3, a penicillin-binding protein) associated with a further increase in MIC to 32 µg ml−1. Structural modelling of AdeB and FtsI showed that these mutations affected their drug-binding sites and revealed mechanisms for meropenem resistance. Notably, one of the adeB mutations arose prior to meropenem therapy but following ciprofloxacin therapy, suggesting exposure to one drug whose resistance is mediated by the efflux pump can induce collateral resistance to other drugs to which the bacterium has not yet been exposed.