Quinolone antimicrobials are synthetic and widely used in clinical medicine Resistance emerged with clinical use and became common in some bacterial pathogens Mechanisms of resistance include two categories of mutation and acquisition of resistance-conferring genes Resistance mutations in one or both of the two drug target enzymes, DNA gyrase and DNA topoisomerase IV, are commonly in a localized domain of the GyrA and ParE subunits of the respective enzymes and reduce drug binding to the enzyme-DNA complex Other resistance mutations occur in regulatory genes that control the expression of native efflux pumps localized in the bacterial membrane(s) These pumps have broad substrate profiles that include quinolones as well as other antimicrobials, disinfectants, and dyes Mutations of both types can accumulate with selection pressure and produce highly resistant strains Resistance genes acquired on plasmids can confer low-level resistance that promotes the selection of mutational high-level resistance Plasmid-encoded resistance is due to Qnr proteins that protect the target enzymes from quinolone action, one mutant aminoglycoside-modifying enzyme that also modifies certain quinolones, and mobile efflux pumps Plasmids with these mechanisms often encode additional antimicrobial resistances and can transfer multidrug resistance that includes quinolones Thus, the bacterial quinolone resistance armamentarium is large

/pdf/mechanisms-of-drug-resistance-quinolone-resistance-eervm3jsw6.pdf

Mechanisms of drug resistance: quinolone resistance.

Three mechanisms for plasmid-mediated quinolone resistance (PMQR) have been discovered since 1998. Plasmid genes qnrA, qnrB, qnrC, qnrD, qnrS, and qnrVC code for proteins of the pentapeptide repeat family that protects DNA gyrase and topoisomerase IV from quinolone inhibition. The qnr genes appear to have been acquired from chromosomal genes in aquatic bacteria, are usually associated with mobilizing or transposable elements on plasmids, and are often incorporated into sul1-type integrons. The second plasmid-mediated mechanism involves acetylation of quinolones with an appropriate amino nitrogen target by a variant of the common aminoglycoside acetyltransferase AAC(6′)-Ib. The third mechanism is enhanced efflux produced by plasmid genes for pumps QepAB and OqxAB. PMQR has been found in clinical and environmental isolates around the world and appears to be spreading. The plasmid-mediated mechanisms provide only low-level resistance that by itself does not exceed the clinical breakpoint for susceptibility but nonetheless facilitates selection of higher-level resistance and makes infection by pathogens containing PMQR harder to treat.

/pdf/plasmid-mediated-quinolone-resistance-2mfyabvsek.pdf

Plasmid-Mediated Quinolone Resistance

Stenotrophomonas maltophilia is a commensal and an emerging pathogen earlier noted in broad-spectrum life threatening infections among the vulnerable, but more recently as a pathogen in immunocompetent individuals. The bacteria are consistently being implicated in necrotizing otitis, cutaneous infections including soft tissue infection and keratitis, endocarditis, meningitis, acute respiratory tract infection (RTI), bacteraemia (with/without hematological malignancies), tropical pyomyositis, cystic fibrosis, septic arthritis, among others. S. maltophilia is also an environmental bacteria occurring in water, rhizospheres, as part of the animals' microflora, in foods, and several other microbiota. This review highlights clinical reports on S. maltophilia both as an opportunistic and as true pathogen. Also, biofilm formation as well as quorum sensing, extracellular enzymes, flagella, pili/fimbriae, small colony variant, other virulence or virulence-associated factors, the antibiotic resistance factors, and their implications are considered. Low outer membrane permeability, natural MDR efflux systems, and/or resistance genes, resistance mechanisms like the production of two inducible chromosomally encoded β-lactamases, and lack of carefully compiled patient history are factors that pose great challenges to the S. maltophilia control arsenals. The fluoroquinolone, some tetracycline derivatives and trimethoprim-sulphamethaxole (TMP-SMX) were reported as effective antibiotics with good therapeutic outcome. However, TMP-SMX resistance and allergies to sulfa together with high toxicity of fluoroquinolone are notable setbacks. S. maltophilia's production and sustenance of biofilm by quorum sensing enhance their virulence, resistance to antibiotics and gene transfer, making quorum quenching an imperative step in Stenotrophomonas control. Incorporating several other proven approaches like bioengineered bacteriophage therapy, Epigallocatechin-3-gallate (EGCG), essential oil, nanoemulsions, and use of cationic compounds are promising alternatives which can be incorporated in Stenotrophomonas control arsenal.

/pdf/stenotrophomonas-maltophilia-as-an-emerging-ubiquitous-3z3vw9opty.pdf

Stenotrophomonas maltophilia as an emerging ubiquitous pathogen: Looking beyond contemporary antibiotic therapy

Tigecycline is unique glycylcycline class of semisynthetic antimicrobial agents developed for the treatment of polymicrobial infections caused by multidrug-resistant Gram-positive and Gram-negative pathogens. Tigecycline evades the main tetracycline resistance genetic mechanisms, such as tetracycline-specific efflux pump acquisition and ribosomal protection, via the addition of a glycyclamide moiety to the 9-position of minocycline. The use of the parenteral form of tigecycline is approved for complicated skin and skin structure infections (excluding diabetes foot infection), complicated intra-abdominal infections, and community-acquired bacterial pneumonia in adults. New evidence also suggests the effectiveness of tigecycline for the treatment of severe Clostridioides difficile infections. Tigecycline showed in vitro susceptibility to Coxiella spp., Rickettsia spp., and multidrug-resistant Neisseria gonnorrhoeae strains which indicate the possible use of tigecycline in the treatment of infections caused by these pathogens. Except for intrinsic, or often reported resistance in some Gram-negatives, tigecycline is effective against a wide range of multidrug-resistant nosocomial pathogens. Herein, we summarize the currently available data on tigecycline pharmacokinetics and pharmacodynamics, its mechanism of action, the epidemiology of tigecycline resistance, and its clinical effectiveness.

/pdf/tigecycline-antibacterial-activity-clinical-effectiveness-45rouh0tmz.pdf

Tigecycline antibacterial activity, clinical effectiveness, and mechanisms and epidemiology of resistance: narrative review.

The aim of this study was to detect novel variants of the Stenotrophomonas maltophilia
Smqnr gene family and analyse the prevalence of Smqnr genes in clinical isolates of S. maltophilia in China. In total, 442 clinical isolates of S. maltophilia were collected from nine hospitals in four provinces in China. Antimicrobial susceptibility testing against six commonly used antibiotics was performed on these isolates. The sequences of the Smqnr genes amplified by PCR were aligned with those of known Smqnr genes in GenBank and an Smqnr database. The resistance rate against co-trimoxazole was highest at 48.6 %, followed by resistance rates against ceftazidime, chloramphenicol, ticarcillin/clavulanate and tigecycline at 28.7, 21.3, 19.0 and 16.1 %, respectively. The highest susceptibility was shown to levofloxacin, with a resistance rate of just 6.1 %. Smqnr genes were detected in 114 isolates, and comprised 11 previously identified genes and 20 new variants, bringing the total number of known Smqnr genes to 47. The 20 novel Smqnr genes were designated Smqnr28–47 and the encoded proteins showed only 1–12 amino acid differences among each other. The most common Smqnr genes in China were Smqnr8 and its variant Smqnr35 with prevalences of 17.5 % (20/114) and 13.2 % (15/114), respectively. Both the known and the novel Smqnr genes were discovered in both quinolone non-sensitive and sensitive isolates with similar frequency, suggesting that the Smqnr gene makes little contribution to quinolone resistance in this organism.

Detection of the Smqnr quinolone protection gene and its prevalence in clinical isolates of Stenotrophomonas maltophilia in China.

Salinimicrobium sediminilitoris sp. nov., Isolated from a Tidal Flat

A novel species of the genus Gramella, designated ASW11-100T, was isolated from a tidal flat sediment in the Yellow Sea, PR China. Phylogenetic analysis based on 16S rRNA gene sequences and single-copy orthologous clusters revealed that strain ASW11-100T belonged to the genus Gramella, and exhibited 16S rRNA gene sequence similarities of 98.9, 98.8 and 98.7 % to Gramella sabulilitoris HSMS-1T, Gramella sediminilitoris GHTF-27T and Gramella forsetii KT0803T, respectively. The genome of strain ASW11-100T harbours 2950 protein-coding genes and 105 carbohydrate-active enzymes including 38 glycoside hydrolases. Seventeen of the glycoside hydrolases are organized in five distinct polysaccharide utilization loci, which are predicted to involve in the degradation of starch, glucans, arabinoxylans, arabinomannan, arabinans and arabinogalactans. The genomic DNA G+C content was 37.3 mol%. The digital DNA-DNA hybridization and average nucleotide identity values between strain ASW11-100T and its closely related relatives were in ranges of 19.8-23.9% and 76.6-80.9 %, respectively. Cells of the isolate were Gram-negative, aerobic, non-flagellated and short rod-shaped. Carotenoid pigments were produced, but flexirubin-type pigments were absent. The major fatty acids (>10 %) were iso-C15 : 0, iso-C17 : 0 3-OH and summed feature 3 (C16 : 1  ω6c and/or C16 : 1  ω7c). The sole respiratory quinone was menaquinone-6 and the major polar lipid was phosphatidylethanolamine. Based on the above polyphasic evidence, strain ASW11-100T should be considered to represent a novel Gramella species, for which the name Gramella sediminis sp. nov. is proposed. The type strain is ASW11-100T (=KCTC 82502T=MCCC 1K05580T).

Gramella sediminis sp. nov., isolated from a tidal flat of the Yellow Sea.

Alteromonas Aquimaris sp. nov., Isolated from Surface Seawater

Alteromonas salexigens sp. nov., isolated from coastal seawater

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