Hong DJ, et al. Infect Chemother. 2015 Jun;47(2):81-97. https://doi.org/10.3947/ic.2015.47.2.81

Carbapenem-resistantPseudomonas aeruginosais one of the major concerns in clinical settings impelling a great challenge to antimicrobial therapy for patients with infections caused by the pathogen. While membrane permeability, together with derepression of the intrinsic beta-lactamase gene, is the global prevailing mechanism of carbapenem resistance inP. aeruginosa, the acquired genes for carbapenemases need special attention because horizontal gene transfer through mobile genetic elements, such as integrons, transposons, plasmids, and integrative and conjugative elements, could accelerate the dissemination of the carbapenem-resistantP. aeruginosa. This review aimed to illustrate epidemiologically the carbapenem resistance inP. aeruginosa, including the resistance rates worldwide and the carbapenemase-encoding genes along with the mobile genetic elements responsible for the horizontal dissemination of the drug resistance determinants. Moreover, the modular mobile elements including the carbapenemase-encoding gene, also known as theP. aeruginosaresistance islands, are scrutinized mostly for their structures.

To investigate the prevalence of plasmid-mediated fosfomycin resistance determinants among extended-spectrum β-lactamase (ESBL)-producing Escherichia coli and Klebsiella pneumoniae and their genetic environments. A total of 347 non-duplicate ESBL-producing E. coli (165) and K. pneumoniae (182) were collected. The fosfomycin MICs were determined by the agar dilution method according to CLSI guidelines. PCR was used to detect the plasmid-encoded fosfomycin resistance genes (fosA, fosA3, fosB and fosC2). For isolates harbouring plasmid-encoded fosfomycin resistance genes, sequence types (STs) were determined. The transformation experiment was performed using E. coli TOPO10 (Invitrogen, USA) as a recipient strain. With the plasmids from the transformants, plasmid replicon typing was performed and the nucleotide sequences adjacent to fosA3 were determined. The susceptibility to fosfomycin was 92.9% in E. coli and 95.2% in K. pneumoniae. Of the 21 isolates non-susceptible to fosfomycin (8 E. coli and 13 K. pneumoniae), 7 (5 E. coli and 2 K. pneumoniae) isolates harboured fosA3 and all of them co-harboured bla_CTX-M-1group or bla_CTX-M-9group. The STs of the isolates harbouring fosA3 were diverse (E. coli: ST1, ST1, ST533, ST2 and ST86; K. pneumoniae: ST11 and ST101). The plasmid replicon types of transformants co-harbouring bla_CTX-M-1group and bla_CTX-M-9group were IncF and IncN, respectively. By sequence analysis, we found the common feature that the fosA3 gene, connected to bla_CTX-M via insertion sequences, was located between two IS26 elements oriented in the opposite direction, composing an IS26-composite transposon. An IS26-composite transposon appears to be the main vehicle for dissemination of fosA3 in E. coli and K. pneumoniae of diverse clones.

Some of the previously reported clinical isolates of Elizabethkingia meningoseptica may be later named species of Elizabethkingia . We determined the accuracy of species identification (with two matrix-assisted laser desorption ionization–time of flight mass spectrometry [MALDI-TOF MS] systems and the Vitek 2 GN card), relative prevalence of three Elizabethkingia spp. in clinical specimens, and antimicrobial susceptibility of the species identified by 16S rRNA gene sequencing. Specimens for culture were collected from patients in a university hospital in Seoul, South Korea, between 2009 and 2015. All 3 Elizabethkingia spp. were detected in patients; among the 86 isolates identified by 16S rRNA gene sequencing, 17 (19.8%) were E. meningoseptica , 18 (20.9%) were Elizabethkingia miricola , and 51 (59.3%) were Elizabethkingia anophelis . Only the MALDI-TOF Vitek MS system with an amended database correctly identified all of the isolates. The majority (76.7%) of the isolates were from the lower respiratory tract, and 8 (9.3%) were from blood. Over 90% of E. meningoseptica and E. anophelis isolates were susceptible to piperacillin-tazobactam and rifampin. In contrast, all E. miricola isolates were susceptible to fluoroquinolones except ciprofloxacin. Further studies are urgently needed to determine the optimal antimicrobial agents for the treatment of infections due to each individual Elizabethkingia species.

Lee K, et al. Yonsei Med J. 2011 Nov;52(6):879-891. http://dx.doi.org/10.3349/ymj.2011.52.6.879

Ultraviolet (UV)B irradiation induces the production of matrix metalloproteinases (MMPs) by activating cellular signaling transduction pathways, which are responsible for the degradation or synthesis inhibition of collagenous extracellular matrix in connective tissues, causing skin photoaging. Using the human skin fibroblast (HS68) cell line in the present study, we investigated the inhibitory effects of fucoidan on MMP-1 expression by various in vitro experiments and elucidated the pathways of inhibition. Pretreatment with fucoidan inhibited UVB-induced MMP-1 expression in a dose-dependent manner. Extracellular signal regulated kinase (ERK) activation was markedly inhibited by treatment with fucoidan, though JNK activation was very slightly affected by fucoidan. We also found that fucoidan pretreatment significantly reduced MMP-1 mRNA expression in comparison with UVB irradiation only. In conclusion, our results demonstrate that fucoidan can mainly inhibit UVB-induced MMP-1 expression by inhibiting the ERK pathways. Therefore, fucoidan might be used as a potential agent for the prevention and treatment of skin photoaging.