Induction of prophages by fluoroquinolones in Streptococcus pneumoniae: implications for emergence of resistance in genetically-related clones

Antibiotic resistance in Streptococcus pneumoniae has increased worldwide by the spread of a few clones. Fluoroquinolone resistance occurs mainly by alteration of their intracellular targets, the type II DNA topoisomerases, which is acquired either by point mutation or by recombination. Increase in...

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Autores: López, Elena, Domenech, Arnau, Ferrandiz-Avellano, Maria-Jose, Frias, Maria João, Ardanuy, Carmen, Ramirez, Mario, García, Ernesto, Liñares, Josefina, de la Campa, Adela G
Tipo de recurso: artículo
Fecha de publicación:2014
País:España
Institución:Instituto de Salud Carlos III (ISCIII)
Repositorio:Repisalud
Idioma:inglés
OAI Identifier:oai:repisalud.isciii.es:20.500.12105/6914
Acceso en línea:http://hdl.handle.net/20.500.12105/6914
Access Level:acceso abierto
Palabra clave:Blotting, Southern
Chronic Disease
Ciprofloxacin
Disease Progression
Drug Resistance, Bacterial
Fluoroquinolones
Humans
Lysogeny
Mitomycin
Pneumococcal Infections
Polymerase Chain Reaction
Prophages
Streptococcus pneumoniae
Virus Activation
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spelling Induction of prophages by fluoroquinolones in Streptococcus pneumoniae: implications for emergence of resistance in genetically-related clonesLópez, ElenaDomenech, ArnauFerrandiz-Avellano, Maria-JoseFrias, Maria JoãoArdanuy, CarmenRamirez, MarioGarcía, ErnestoLiñares, Josefinade la Campa, Adela GBlotting, SouthernChronic DiseaseCiprofloxacinDisease ProgressionDrug Resistance, BacterialFluoroquinolonesHumansLysogenyMitomycinPneumococcal InfectionsPolymerase Chain ReactionProphagesStreptococcus pneumoniaeVirus ActivationAntibiotic resistance in Streptococcus pneumoniae has increased worldwide by the spread of a few clones. Fluoroquinolone resistance occurs mainly by alteration of their intracellular targets, the type II DNA topoisomerases, which is acquired either by point mutation or by recombination. Increase in fluoroquinolone-resistance may depend on the balance between antibiotic consumption and the cost that resistance imposes to bacterial fitness. In addition, pneumococcal prophages could play an important role. Prophage induction by fluoroquinolones was confirmed in 4 clinical isolates by using Southern blot hybridization. Clinical isolates (105 fluoroquinolone-resistant and 160 fluoroquinolone-susceptible) were tested for lysogeny by using a PCR assay and functional prophage carriage was studied by mitomycin C induction. Fluoroquinolone-resistant strains harbored fewer inducible prophages (17/43) than fluoroquinolone-susceptible strains (49/70) (P = 0.0018). In addition, isolates of clones associated with fluoroquinolone resistance [CC156 (3/25); CC63 (2/20), and CC81 (1/19)], had lower frequency of functional prophages than isolates of clones with low incidence of fluoroquinolone resistance [CC30 (4/21), CC230 (5/20), CC62 (9/21), and CC180 (21/30)]. Likewise, persistent strains from patients with chronic respiratory diseases subjected to fluoroquinolone treatment had a low frequency of inducible prophages (1/11). Development of ciprofloxacin resistance was tested with two isogenic strains, one lysogenic and the other non-lysogenic: emergence of resistance was only observed in the non-lysogenic strain. These results are compatible with the lysis of lysogenic isolates receiving fluoroquinolones before the development of resistance and explain the inverse relation between presence of inducible prophages and fluoroquinolone-resistance.Public Library of Science (PLOS)Instituto de Salud Carlos III20182018-12-1920142014-04-0920142014-04-09journal articlehttp://purl.org/coar/resource_type/c_6501VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/20.500.12105/6914reponame:Repisaludinstname:Instituto de Salud Carlos III (ISCIII)InglésengES SAF2009-10824 Not availableES PI 0901904 Not availableopen accesshttp://purl.org/coar/access_right/c_abf2Atribución 4.0 Internacionalhttp://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:repisalud.isciii.es:20.500.12105/69142026-06-12T12:43:37Z
dc.title.none.fl_str_mv Induction of prophages by fluoroquinolones in Streptococcus pneumoniae: implications for emergence of resistance in genetically-related clones
title Induction of prophages by fluoroquinolones in Streptococcus pneumoniae: implications for emergence of resistance in genetically-related clones
spellingShingle Induction of prophages by fluoroquinolones in Streptococcus pneumoniae: implications for emergence of resistance in genetically-related clones
López, Elena
Blotting, Southern
Chronic Disease
Ciprofloxacin
Disease Progression
Drug Resistance, Bacterial
Fluoroquinolones
Humans
Lysogeny
Mitomycin
Pneumococcal Infections
Polymerase Chain Reaction
Prophages
Streptococcus pneumoniae
Virus Activation
title_short Induction of prophages by fluoroquinolones in Streptococcus pneumoniae: implications for emergence of resistance in genetically-related clones
title_full Induction of prophages by fluoroquinolones in Streptococcus pneumoniae: implications for emergence of resistance in genetically-related clones
title_fullStr Induction of prophages by fluoroquinolones in Streptococcus pneumoniae: implications for emergence of resistance in genetically-related clones
title_full_unstemmed Induction of prophages by fluoroquinolones in Streptococcus pneumoniae: implications for emergence of resistance in genetically-related clones
title_sort Induction of prophages by fluoroquinolones in Streptococcus pneumoniae: implications for emergence of resistance in genetically-related clones
dc.creator.none.fl_str_mv López, Elena
Domenech, Arnau
Ferrandiz-Avellano, Maria-Jose
Frias, Maria João
Ardanuy, Carmen
Ramirez, Mario
García, Ernesto
Liñares, Josefina
de la Campa, Adela G
author López, Elena
author_facet López, Elena
Domenech, Arnau
Ferrandiz-Avellano, Maria-Jose
Frias, Maria João
Ardanuy, Carmen
Ramirez, Mario
García, Ernesto
Liñares, Josefina
de la Campa, Adela G
author_role author
author2 Domenech, Arnau
Ferrandiz-Avellano, Maria-Jose
Frias, Maria João
Ardanuy, Carmen
Ramirez, Mario
García, Ernesto
Liñares, Josefina
de la Campa, Adela G
author2_role author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Instituto de Salud Carlos III
dc.subject.none.fl_str_mv Blotting, Southern
Chronic Disease
Ciprofloxacin
Disease Progression
Drug Resistance, Bacterial
Fluoroquinolones
Humans
Lysogeny
Mitomycin
Pneumococcal Infections
Polymerase Chain Reaction
Prophages
Streptococcus pneumoniae
Virus Activation
topic Blotting, Southern
Chronic Disease
Ciprofloxacin
Disease Progression
Drug Resistance, Bacterial
Fluoroquinolones
Humans
Lysogeny
Mitomycin
Pneumococcal Infections
Polymerase Chain Reaction
Prophages
Streptococcus pneumoniae
Virus Activation
description Antibiotic resistance in Streptococcus pneumoniae has increased worldwide by the spread of a few clones. Fluoroquinolone resistance occurs mainly by alteration of their intracellular targets, the type II DNA topoisomerases, which is acquired either by point mutation or by recombination. Increase in fluoroquinolone-resistance may depend on the balance between antibiotic consumption and the cost that resistance imposes to bacterial fitness. In addition, pneumococcal prophages could play an important role. Prophage induction by fluoroquinolones was confirmed in 4 clinical isolates by using Southern blot hybridization. Clinical isolates (105 fluoroquinolone-resistant and 160 fluoroquinolone-susceptible) were tested for lysogeny by using a PCR assay and functional prophage carriage was studied by mitomycin C induction. Fluoroquinolone-resistant strains harbored fewer inducible prophages (17/43) than fluoroquinolone-susceptible strains (49/70) (P = 0.0018). In addition, isolates of clones associated with fluoroquinolone resistance [CC156 (3/25); CC63 (2/20), and CC81 (1/19)], had lower frequency of functional prophages than isolates of clones with low incidence of fluoroquinolone resistance [CC30 (4/21), CC230 (5/20), CC62 (9/21), and CC180 (21/30)]. Likewise, persistent strains from patients with chronic respiratory diseases subjected to fluoroquinolone treatment had a low frequency of inducible prophages (1/11). Development of ciprofloxacin resistance was tested with two isogenic strains, one lysogenic and the other non-lysogenic: emergence of resistance was only observed in the non-lysogenic strain. These results are compatible with the lysis of lysogenic isolates receiving fluoroquinolones before the development of resistance and explain the inverse relation between presence of inducible prophages and fluoroquinolone-resistance.
publishDate 2014
dc.date.none.fl_str_mv 2014
2014-04-09
2014
2014-04-09
2018
2018-12-19
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/20.500.12105/6914
url http://hdl.handle.net/20.500.12105/6914
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.relation.none.fl_str_mv ES SAF2009-10824 Not available
ES PI 0901904 Not available
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
Atribución 4.0 Internacional
http://creativecommons.org/licenses/by/4.0/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
Atribución 4.0 Internacional
http://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Public Library of Science (PLOS)
publisher.none.fl_str_mv Public Library of Science (PLOS)
dc.source.none.fl_str_mv reponame:Repisalud
instname:Instituto de Salud Carlos III (ISCIII)
instname_str Instituto de Salud Carlos III (ISCIII)
reponame_str Repisalud
collection Repisalud
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,812455

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