The study identified and characterized mef(A) and mef(E) as distinct macrolide efflux genes in Streptococcus pneumoniae, highlighting their different genetic elements and insertion sites.

The study identified mef (A) and mef (E) genes as major contributors to erythromycin resistance in Streptococcus pneumoniae, along with the erm (AM) gene for methylase-mediated resistance.

The study identified tet(M), erm(B), mef(A), and mef(E) as the primary genes responsible for tetracycline and erythromycin resistance in Streptococcus pneumoniae strains.

The study identifies Tn2009, a composite transposon containing the macrolide efflux gene mef(E) and the tetracycline resistance gene tet(M) in Streptococcus pneumoniae.

The study characterizes the MefA, MefE, and msr(D) genes in Streptococcus pneumoniae clinical isolates, demonstrating that these genes confer resistance to macrolides and ketolides. The msr(D) gene was shown to function independently as an efflux pump.

The study identifies several AMR genes and mutations in Streptococcus pneumoniae, including erm(B) and mef(E) for macrolide resistance, and gyrA and parC mutations for fluoroquinolone resistance. It also reports 23S rRNA mutations linked to resistance against macrolides, telithromycin, and streptogramins.

The study characterizes the mefE gene, which encodes an efflux pump responsible for macrolide resistance in Streptococcus pneumoniae. Telithromycin was effective against mefE-producing strains with MICs up to 0.25 μg/ml in serum and 1 μg/ml in epithelial lining fluid.

The study identified mef(E), mef(A), and erm(B) as the primary macrolide resistance mechanisms in Streptococcus pneumoniae isolates from Finland in 2002, with mef(E) being the most prevalent subtype.

The study shows that increased expression of the mef(E) gene is associated with higher levels of macrolide resistance in Streptococcus pneumoniae.

The study identified a novel mef gene subclass, mef(I), in pneumococci with efflux-mediated erythromycin resistance. It also characterized the presence of tet(M) and tet(O) genes contributing to tetracycline resistance in certain isolates.

The study identified mef (E) and mef (A) genes as the primary mechanisms of erythromycin resistance in Streptococcus agalactiae, associated with the mega and Tn 1207.3 genetic elements.

The study characterizes the mef(E) gene, which encodes an efflux transporter involved in macrolide resistance in Streptococcus pneumoniae. It identifies various insertion sites of the mega element and describes a new composite transposon, Tn 2010, which carries mef(E), tet(M), and erm(B).

The study identifies the presence of mef(E) and erm(B) genes in Streptococcus pneumoniae isolates in Spain, contributing to macrolide resistance. The combination of these genes leads to a constitutive MLS(B) phenotype.

The study identifies mefE as a macrolide resistance gene in nonserotypeable pneumococci, highlighting its role in erythromycin resistance.

The study identified erm(B), mef(E), mef(A), mel, and msr(D) as key genes responsible for macrolide resistance in Streptococcus pneumoniae isolates, highlighting the role of Tn 916 family transposons in the dissemination of these resistance determinants.

The study identified the mefE gene as a determinant of erythromycin resistance in Streptococcus pneumoniae, demonstrating its acquisition via transformation with genomic DNA carrying a Tn916-like element.

The study identifies various mef subclasses (mef(E), mef(I), mef(A/E), and a novel mef) associated with resistance genes (tet(M), tet(O), and catQ) in Streptococcus pyogenes, highlighting the diversity of genetic elements involved in macrolide and tetracycline resistance.

The study identifies mef(E) as a gene encoding an efflux pump that mediates macrolide resistance in Streptococcus pneumoniae. The expression of mef(E) is induced by macrolides with a monosaccharide at the C-5 position of the lactone ring, leading to increased resistance.

The study identifies multiple AMR genes and mutations in the multidrug-resistant S. suis R61 strain, including pbp2x, pbp2b, gyrA, parC, tet(W), and mef(E), contributing to resistance against β-lactams, quinolones, tetracyclines, and macrolides.

The study identifies mef (E) and erm (B) genes as the primary drivers of macrolide resistance in Streptococcus pneumoniae isolates in Arizona, with dual-positive isolates being multidrug-resistant and predominantly belonging to clonal complex CC271.

The study identified erm(B), mef(E), and mef(A) as the primary macrolide resistance determinants in Streptococcus pneumoniae isolates from Central Greece. erm(B) conferred high-level resistance to macrolides, lincosamides, and streptogramin B, while mef(E) and mef(A) were associated with efflux-mediated resistance.

The study identified macrolide resistance genes erm(B) and mef(E) in Streptococcus pneumoniae and amino acid substitutions in the ftsI gene of Haemophilus influenzae contributing to ampicillin resistance.

The study identified the presence of mef E and erm B genes in serotype 19A Streptococcus pneumoniae isolates, which contribute to macrolide resistance. The mef E gene was detected in 62% of erythromycin-resistant isolates, while the erm B gene was found in all CC320 isolates.

The study identifies tetM, ermB, and mefE as genes responsible for tetracycline and macrolide resistance in nonencapsulated Streptococcus pneumoniae isolates, highlighting the antibiotic resistance profile of the classic lineage ST344 and ST448.

The study identifies the transcriptional start site and promoter of the mef(E)/mel operon, characterizes regulatory elements including stem-loop structures and a leader peptide, and demonstrates that transcriptional attenuation controls macrolide inducible efflux and resistance in Streptococcus pneumoniae.

The study identifies ICE Spy 009, a conjugative genetic element carrying mef(E), which confers macrolide resistance in Streptococcus pyogenes and can transfer resistance to Streptococcus pneumoniae.

The paper discusses various mechanisms of antibiotic resistance, including beta-lactamases like blaKPC, blaNDM, blaIMP, and blaVIM, which confer resistance to carbapenems. It also covers aminoglycoside modifying enzymes such as aac(6')-Ib and aac(6')-I, quinolone resistance proteins like qnr, tetracycline resistance genes such as tet(M) and tet(O), macrolide resistance genes like erm, mefA, and mefE, and efflux pump systems like mexAB-oprM and acrAB-tolC.

The study identified multiple AMR genes in Streptococcus pneumoniae isolates from children with recurrent upper respiratory tract infections, including erm(B), mef(E), tet(M), and cat pC194, which confer resistance to macrolides, tetracyclines, and chloramphenicol.

The study identifies erm(B), mef(E), and mel as key genes involved in macrolide resistance in Streptococcus pneumoniae, highlighting their roles in ribosomal modification and efflux mechanisms.

The paper discusses the prevalence and mechanisms of antimicrobial resistance in Streptococcus species, particularly focusing on macrolide, lincosamide, and tetracycline resistance. Key genes identified include erm(B), erm(A), lnuB, lnuD, mefA, mefE, msr, tet(B), tet(K), tet(L), tet(M), tet(O), and tet(S).

The study identifies a significant increase in macrolide resistance among Streptococcus agalactiae isolates causing invasive disease in non-pregnant adults in Portugal, primarily linked to the expansion of a specific capsular-transformed lineage (CC1) harboring resistance genes such as erm(B), erm(TR), erm(T), mef(E), tet(M), tet(O), and tet(L).

The study identified several AMR genes in GBS isolates from urine in Suzhou, including tetM, ermB, mefE, lnuB, and others, associated with resistance to tetracycline, erythromycin, clindamycin, and fluoroquinolones.

The study identifies novel AMR genes and mutations in XDR H. parainfluenzae isolates, including catS, mef(E), tet(M), and tet(B) for resistance to chloramphenicol, macrolides, tetracycline, and co-trimoxazole, respectively. Mutations in PBP3, GyrA, ParC, ParE, rplD, and DHFR were also found to confer resistance to β-lactams, fluoroquinolones, and co-trimoxazole.

The study identifies the Mega element [mef(E)/mel] as a cause of high-level macrolide resistance in Streptococcus pneumoniae. Deletion of mef(E)/mel eliminated macrolide resistance, demonstrating its role in resistance.

The study identified the presence of ermB, mefE, and tetM genes in meropenem-resistant Streptococcus pneumoniae serotype 19A-CC3111 strains in Japan, contributing to erythromycin and tetracycline resistance.

The study identifies multiple antimicrobial resistance genes in multidrug-resistant Bacteroides fragilis isolates, including cfiA, nim, erm, tet, and others, using hybrid genome assembly and ABRicate screening.

This review discusses the mechanisms used by Gram-positive bacteria to resist antimicrobial peptides, focusing on modifications in membrane/cell wall structure, transport systems, efflux pumps, and AMP sequestration/inactivation.

The study identifies two new metallo-beta-lactamase genes, cfiA14b and cfiA28, in Bacteroides fragilis strains resistant to meropenem-EDTA. Additionally, various other AMR genes such as aadS, aac(3'), ermF, lnu(AN2), vatA, mef(En2), tetX, tetQ, cat, bexA, bexB, qacE, cusR, mexAB-oprM, mexJK-oprM, mexXY-oprM, acrEF-tolC, and mdtEF-tolC were characterized.

The paper discusses various mechanisms of macrolide resistance, including mutations in 23S rRNA, ribosomal proteins L4 and L22, and the presence of genes such as ermB, mphA, mef(E), and efflux pumps like lpeAB and CmeABC. These mechanisms contribute to high-level macrolide resistance in several bacterial species.

The study identified ermG as a gene that increased in abundance in the feces of treated pigs compared to those that did not receive post-PRRS antimicrobials, indicating its role in macrolide, lincosamide, and streptogramin B resistance.

The study identifies Tn7100, a novel integrative and conjugative element carrying six resistance genes: blaTEM-1B, catA2, aac(6')-Im, aph(2'')-Ib, mef(E), and mel, which confer resistance to multiple antibiotics in Haemophilus influenzae.

The study characterizes various AMR genes and mutations in Streptococcus suis, highlighting resistance to beta-lactams, macrolides, lincosamides, streptogramins, amphenicols, pleuromutilins, tetracyclines, sulfonamides, trimethoprim, and fluoroquinolones.

The study found that prolonged amoxicillin treatment leads to an increase in the abundance and diversity of antimicrobial resistance genes (ARGs) in the gut microbiome, particularly beta-lactamase genes such as cfxA and its variants, as well as tetracycline and macrolide resistance genes.

The study identified several AMR genes in GBS isolates from pregnant women with PROM in Fuzhou, China, including mreA, ermB, mefA, mefE, ermA, ermTR, tetM, and tetK, which are associated with resistance to erythromycin and tetracycline.

The study identifies mef(E) and mel genes as responsible for macrolide resistance in Streptococcus pneumoniae, showing that their expression levels correlate with erythromycin MIC values and that heteroresistance is linked to the inducibility of these genes.

The study identified various AMR genes associated with resistance to macrolides, lincosamides, and streptogramins in Enterococci, including ermB, ermA, ermC, ereA, lnuA, mphC, mefA, and mefE. These genes were found to be highly prevalent and contribute to the resistance mechanisms observed in the isolates.

The study identifies mefE, an AMR gene located on a plasmid and encoding an antibiotic efflux pump, in the plaque of volunteer A using metagenomic analysis and confirms its presence using MGE-FISH.

The study identified ermB, mefE, and tetM as the primary genes responsible for macrolide, tetracycline, and quinolone resistance in Gemella sp. Additionally, specific mutations in gyrA were linked to levofloxacin resistance.

The study found that Neolamarckia cadamba leaves extract (NCLE) reduced the abundance of antibiotic resistance genes (ARGs) in cecal contents of lipopolysaccharide (LPS)-induced broilers by maintaining microbial balance.

The study identifies mefE and ermB as key genes responsible for macrolide resistance in Streptococcus pneumoniae, highlighting their role in the acquisition of resistance through transformation and recombination events in Tn916-related elements.

The study identified several AMR genes associated with macrolide, lincosamide, and tetracycline resistance in Streptococcus agalactiae isolates from Bulgaria. These include ermB, ermA/TR, ermC, mefA, mefE, msrD, lnuB, lsaC, lsaE, tetM, and tetO. High resistance rates to macrolides (60.3%) and tetracyclines (89.1%) were observed.

The study identifies ermB, ereA, msrA, mefA, and mefE as key genes associated with MLS resistance in Streptococci, highlighting the role of efflux mechanisms and ribosomal methylation in conferring resistance to macrolides, lincosamides, and streptogramins.

The study identifies the emergence of a multidrug-resistant Streptococcus pneumoniae serotype 35B-ST156 clone in Japan, characterized by resistance to beta-lactams, macrolides, and co-trimoxazole due to specific genetic mutations and gene acquisitions.

The study identifies the expansion of multidrug-resistant Haemophilus influenzae clones with cefotaxime resistance, primarily due to mutations in the ftsI gene encoding penicillin-binding protein 3 (PBP3). These mutations lead to cross-resistance to multiple beta-lactam antibiotics.

The study identified high resistance rates to erythromycin, penicillin, cefotaxime, and meropenem among Streptococcus pneumoniae isolates from pediatric patients in Japan. Key resistance genes included ermB, mefE, and tetM.

The study identifies mefE as a gene necessary for erythromycin resistance in Streptococcus pneumoniae, demonstrating its role in an efflux pump mechanism that confers resistance to macrolides.

The study identified ermB and mefE genes as mechanisms of azithromycin resistance in Streptococcus pneumoniae, with ermB encoding a macrolide ribosome methyltransferase and mefE encoding an efflux pump.

The study identified multiple penicillin-resistant Streptococcus pneumoniae isolates from Bulgaria, characterizing their resistance mechanisms through molecular techniques. Key findings include the identification of specific penicillin-binding protein genes (pbp1a, pbp2b, pbp2x) and resistance genes (ermB, mefE, tetM, cat) associated with resistance to penicillin, erythromycin, tetracycline, and chloramphenicol.