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7 results on '"lnu(B)"'

1. New genetic context of lnu(B) composed of two multi-resistance gene clusters in clinical Streptococcus agalactiae ST-19 strains

Author

Kaixin Zhou, Dongan Zhu, Ying Tao, Lianyan Xie, Lizhong Han, Yibo Zhang, and Jingyong Sun

Subjects
S. agalactiae, lnu(B), L phenotype, Composite transposon, IS1216, Infectious and parasitic diseases, RC109-216
Abstract

Abstract Background Clindamycin is a lincosamide antibiotic used to treat staphylococcal and streptococcal infections. Reports of clinical Streptococcus agalactiae isolates with the rare lincosamide resistance/macrolide susceptibility (LR/MS) phenotype are increasing worldwide. In this study, we characterised three clinical S. agalactiae strains with the unusual L phenotype from China. Methods Three clinical S. agalactiae strains, Sag3, Sag27 and Sag4104, with the L phenotype were identified from 186 isolates collected from 2016 to 2018 in Shanghai, China. The MICs of clindamycin, erythromycin, tetracycline, levofloxacin, and penicillin were determined using Etest. PCR for the lnu(B) gene was conducted. Whole genome sequencing and sequence analysis were carried out to investigate the genetic context of lnu(B). Efforts to transfer lincomycin resistance by conjugation and to identify the circular form by inverse PCR were made. Results Sag3, Sag27, and Sag4104 were susceptible to erythromycin (MIC ≤0.25 mg/L) but resistant to clindamycin (MIC ≥1 mg/L). lnu(B) was found to be responsible for the L phenotype. lnu(B) in Sag3 and Sag27 were chromosomally located in an aadE-spw-lsa(E)-lnu(B) resistance gene cluster adjacent to an upstream 7-kb tet(L)-cat resistance gene cluster. Two resistance gene clusters were flanked by the IS6-like element, IS1216. Sag4104 only contained partial genes of aadE-spw-lsa(E)-lnu(B) resistance gene cluster and was also flanked by IS1216. Conclusion These results established the presence of the L phenotype associated with lnu(B) in clinical S. agalactiae isolates in China. The lnu(B)-containing multi-resistance gene cluster possibly acts as a composite transposon flanked by IS1216 and as a vehicle for the dissemination of multidrug resistance among S. agalactiae.

Published
2019
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2. A novel genomic island harbouring lsa(E) and lnu(B) genes and a defective prophage in a Streptococcus pyogenes isolate resistant to lincosamide, streptogramin A and pleuromutilin antibiotics.

Author

Berbel, Dàmaris, Càmara, Jordi, García, Ernesto, Tubau, Fe, Guérin, François, Giard, Jean-Christophe, Domínguez, M. Ángeles, Cattoir, Vincent, and Ardanuy, Carmen

Subjects
*STREPTOCOCCUS, *STREPTOCOCCUS pyogenes, *ANTIBIOTICS, *MICROBIAL sensitivity tests, *GENES, *GENE clusters
Abstract

A lincosamide-resistant and macrolide-susceptible phenotype has not been described to date in Streptococcus pyogenes [group A streptococcus (GAS)]. The aim of this study was to characterize a GAS isolate susceptible to macrolides but resistant to lincosamide, streptogramin A and pleuromutilin antibiotics. Antimicrobial susceptibility was tested using the microdilution broth method and the resistance phenotype was tested by D-test. The GAS2887HUB isolate was subjected to whole-genome sequencing. The isolate showed a positive Gots' test (clindamycin inactivation). Whole-genome sequencing revealed that the strain was ST10 and emm 93, and had five resistance genes [ lnu (B) , ant (6)-Ia , aph (3′)-III, tet (M) and dfrG ]. The tet (M) gene was located in a Tn 916 -like transposon. The lsa (E)− lnu (B) - containing sequence (inserted downstream of the rumA gene) was formed by a 39.6-kb prophage, followed by a gene cluster encoding aminoglycoside–streptothricin resistance [ ant (6)Ia− sat4 − aph (3′)III] and lsa (E)− lnu (B) genes. This structure was not transferred by conjugation. This study identified a new genetic element carrying a determinant of lincosamide resistance in a GAS. Further molecular epidemiological surveys are needed to determine the prevalence of this mechanism of resistance in GAS. [ABSTRACT FROM AUTHOR]

Published
2019
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3. New genetic context of lnu(B) composed of two multi-resistance gene clusters in clinical Streptococcus agalactiae ST-19 strains

Author

Dongan Zhu, Ying Tao, Jingyong Sun, Lizhong Han, Lianyan Xie, Kaixin Zhou, and Yi-Bo Zhang

Subjects
0301 basic medicine, Microbiology (medical), 030106 microbiology, Erythromycin, Context (language use), Drug resistance, medicine.disease_cause, Microbiology, lcsh:Infectious and parasitic diseases, 03 medical and health sciences, 0302 clinical medicine, S. agalactiae, Gene cluster, medicine, Composite transposon, Pharmacology (medical), lcsh:RC109-216, 030212 general & internal medicine, lnu(B), business.industry, Public Health, Environmental and Occupational Health, IS1216, Lincomycin, Multiple drug resistance, Infectious Diseases, Streptococcus agalactiae, L phenotype, business, medicine.drug
Abstract

Background Clindamycin is a lincosamide antibiotic used to treat staphylococcal and streptococcal infections. Reports of clinical Streptococcus agalactiae isolates with the rare lincosamide resistance/macrolide susceptibility (LR/MS) phenotype are increasing worldwide. In this study, we characterised three clinical S. agalactiae strains with the unusual L phenotype from China. Methods Three clinical S. agalactiae strains, Sag3, Sag27 and Sag4104, with the L phenotype were identified from 186 isolates collected from 2016 to 2018 in Shanghai, China. The MICs of clindamycin, erythromycin, tetracycline, levofloxacin, and penicillin were determined using Etest. PCR for the lnu(B) gene was conducted. Whole genome sequencing and sequence analysis were carried out to investigate the genetic context of lnu(B). Efforts to transfer lincomycin resistance by conjugation and to identify the circular form by inverse PCR were made. Results Sag3, Sag27, and Sag4104 were susceptible to erythromycin (MIC ≤0.25 mg/L) but resistant to clindamycin (MIC ≥1 mg/L). lnu(B) was found to be responsible for the L phenotype. lnu(B) in Sag3 and Sag27 were chromosomally located in an aadE-spw-lsa(E)-lnu(B) resistance gene cluster adjacent to an upstream 7-kb tet(L)-cat resistance gene cluster. Two resistance gene clusters were flanked by the IS6-like element, IS1216. Sag4104 only contained partial genes of aadE-spw-lsa(E)-lnu(B) resistance gene cluster and was also flanked by IS1216. Conclusion These results established the presence of the L phenotype associated with lnu(B) in clinical S. agalactiae isolates in China. The lnu(B)-containing multi-resistance gene cluster possibly acts as a composite transposon flanked by IS1216 and as a vehicle for the dissemination of multidrug resistance among S. agalactiae.

Published
2019

5. A novel genomic island harbouring lsa(E) and lnu(B) genes and a defective prophage in a Streptococcus pyogenes isolate resistant to lincosamide, streptogramin A and pleuromutilin antibiotics

Abstract

A lincosamide-resistant and macrolide-susceptible phenotype has not been described to date in Streptococcus pyogenes [group A streptococcus (GAS)]. The aim of this study was to characterize a GAS isolate susceptible to macrolides but resistant to lincosamide, streptogramin A and pleuromutilin antibiotics. Antimicrobial susceptibility was tested using the microdilution broth method and the resistance phenotype was tested by D-test. The GAS2887HUB isolate was subjected to whole-genome sequencing. The isolate showed a positive Gots' test (clindamycin inactivation). Whole-genome sequencing revealed that the strain was ST10 and emm93, and had five resistance genes [lnu(B), ant(6)-Ia, aph(3')-III, tet(M) and dfrG]. The tet(M) gene was located in a Tn916-like transposon. The lsa(E)-lnu(B)-containing sequence (inserted downstream of the rumA gene) was formed by a 39.6-kb prophage, followed by a gene cluster encoding aminoglycoside-streptothricin resistance [ant(6)Ia-sat4-aph(3')III] and lsa(E)-lnu(B) genes. This structure was not transferred by conjugation. This study identified a new genetic element carrying a determinant of lincosamide resistance in a GAS. Further molecular epidemiological surveys are needed to determine the prevalence of this mechanism of resistance in GAS.

Published
2019

6. A novel genomic island harbouring lsa(E), lnu(B) genes and a defective prophage in a Streptococcus pyogenes isolate resistant to lincosamide, streptogramin A and pleuromutilin antibiotics

Author

François Guérin, Vincent Cattoir, Carmen Ardanuy, Dàmaris Berbel, Ernesto García, Jordi Càmara, M. Angeles Domínguez, Jean-Christophe Giard, Fe Tubau, Jonchère, Laurent, Institut d'Investigació Biomèdica de Bellvitge [Barcelone] (IDIBELL), Centro de Investigación Biomédica en Red en Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), CHU Caen, Normandie Université (NU)-Tumorothèque de Caen Basse-Normandie (TCBN), Unité de Recherche Risques Microbiens (U2RM), Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU), ARN régulateurs bactériens et médecine (BRM), Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Fondo de Investigaciones Sanitarias de la Seguridad Social (INT 15/0186, INT16/0117 and PI18/00339), Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES CB06/06/0037), European Regional Development Fund, CERCA Programme, Instituto de Salud Carlos III, European Commission, García, Ernesto [0000-0002-1741-5486], Tubau, Fe [0000-0002-6416-6451], Giard, Jean-Christophe [0000-0001-8588-2732], Cattoir, Vincent [0000-0003-4026-9912], Ardanuy, Carmen [0000-0003-0225-607X], Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), García, Ernesto, Tubau, Fe, Giard, Jean-Christophe, Cattoir, Vincent, and Ardanuy, Carmen

Subjects
0301 basic medicine, Prophages, [SDV]Life Sciences [q-bio], medicine.disease_cause, chemistry.chemical_compound, 0302 clinical medicine, Antibiotics, Genomic island, Drug Resistance, Multiple, Bacterial, lsa(E), Pharmacology (medical), 030212 general & internal medicine, Streptogramin A, Streptococcus, Defective Viruses, General Medicine, LS(A)P phenotype, 3. Good health, Anti-Bacterial Agents, Fenotip, [SDV] Life Sciences [q-bio], Infectious Diseases, Phenotype, GAS, Diterpenes, Microbiology (medical), Transposable element, DNA, Bacterial, Genomic Islands, Streptococcus pyogenes, 030106 microbiology, Antibiòtics, Microbial Sensitivity Tests, Biology, Microbiology, 03 medical and health sciences, medicine, Humans, Polycyclic Compounds, Lincosamides, Gene, Prophage, Whole Genome Sequencing, lnu(B), Estreptococs, chemistry, L phenotype, Pleuromutilin, Genome, Bacterial
Abstract

19 p.-1 fig., A lincosamide-resistant and macrolide-susceptible phenotype has not been described to date in Streptococcus pyogenes [group A streptococcus (GAS)]. The aim of this study was to characterize a GAS isolate susceptible to macrolides but resistant to lincosamide, streptogramin A and pleuromutilin antibiotics. Antimicrobial susceptibility was tested using the microdilution broth method and the resistance phenotype was tested by D-test. The GAS2887HUB isolate was subjected to whole-genome sequencing. The isolate showed a positive Gots' test (clindamycin inactivation). Whole-genome sequencing revealed that the strain was ST10 and emm93, and had five resistance genes [lnu(B), ant(6)-Ia, aph(3')-III, tet(M) and dfrG]. The tet(M) gene was located in a Tn916-like transposon. The lsa(E)-lnu(B)-containing sequence (inserted downstream of the rumA gene) was formed by a 39.6-kb prophage, followed by a gene cluster encoding aminoglycoside-streptothricin resistance [ant(6)Ia-sat4-aph(3')III] and lsa(E)-lnu(B) genes. This structure was not transferred by conjugation. This study identified a new genetic element carrying a determinant of lincosamide resistance in a GAS. Further molecular epidemiological surveys are needed to determine the prevalence of this mechanism of resistance in GAS., This study was supported by grants from Fondo de Investigaciones Sanitarias de la Seguridad Social (INT 15/0186; INT16/0117 and PI18/00339) and Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES CB06/06/0037), an initiative of the Instituto de Salud Carlos III, Madrid, Spain. Financial support was also provided by the European Regional Development Fund and by CERCA Programme.

Published
2019

7. Genetic environment of lnuB gene in Streptococcus agalactiae

Author

Montilla Piedrahíta, A., Zavala, A., Cáceres Cáceres, R., Cittadini, Roberto, Vay, Carlos, Gutkind, Gabriel Osvaldo, Famiglietti, Ángela, Bonofiglio, Laura, and Mollerach, Marta Eugenia

Subjects
Enfermedades Infecciosas, purl.org/becyt/ford/3.3 [https], CIENCIAS MÉDICAS Y DE LA SALUD, lnu(B), Flanking regions, Ciencias de la Salud, purl.org/becyt/ford/3 [https], Streptococcus agalactiae
Abstract

Fil: Montilla Piedrahíta, A.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Microbiología, Inmunología y Biotecnología; Argentina Fil: Zavala, A.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Microbiología, Inmunología y Biotecnología; Argentina Fil: Cáceres Cáceres, R.. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina Fil: Cittadini, Roberto. Sanatorio Mater Dei; Argentina Fil: Vay, Carlos. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina. Sanatorio Mater Dei; Argentina Fil: Gutkind, Gabriel Osvaldo. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Microbiología, Inmunología y Biotecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Famiglietti, Ángela. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina Fil: Bonofiglio, Laura. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Microbiología, Inmunología y Biotecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Mollerach, Marta Eugenia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Microbiología, Inmunología y Biotecnología; Argentina

Published
2014

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