Disease isolates of Streptococcus pseudopneumoniae and non-typeable S. pneumoniae presumptively identified as atypical S. pneumoniae in Spain
We aimed to obtain insights on the nature of a collection of isolates presumptively identified as atypical Streptococcus pneumoniae recovered from invasive and non-invasive infections in Spain. One-hundred and thirty-two isolates were characterized by: optochin susceptibility in ambient and CO(2)-en...
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Published in: | PloS one Vol. 8; no. 2; p. e57047 |
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Abstract | We aimed to obtain insights on the nature of a collection of isolates presumptively identified as atypical Streptococcus pneumoniae recovered from invasive and non-invasive infections in Spain. One-hundred and thirty-two isolates were characterized by: optochin susceptibility in ambient and CO(2)-enriched atmosphere; bile solubility; PCR-based assays targeting pneumococcal genes lytA, ply, pspA, cpsA, Spn9802, aliB-like ORF2, and a specific 16S rRNA region; multilocus sequence analysis; and antimicrobial susceptibility. By multilocus sequence analysis, 61 isolates were S. pseudopneumoniae, 34 were pneumococci, 13 were S. mitis, and 24 remained unclassified as non-pneumococci. Among S. pseudopneumoniae isolates, 51 (83.6%) were collected from respiratory tract samples; eight isolates were obtained from sterile sources. High frequency of non-susceptibility to penicillin (60.7%) and erythromycin (42.6%) was found. Only 50.8% of the S. pseudopneumoniae isolates displayed the typical optochin phenotype originally described for this species. None harbored the cpsA gene or the pneumococcal typical lytA restriction fragment length polymorphism. The Spn9802 and the specific 16S rRNA regions were detected among the majority of the S. pseudopneumoniae isolates (n = 59 and n = 49, respectively). The ply and pspA genes were rarely found. A high genetic diversity was found and 59 profiles were identified. Among the S. pneumoniae, 23 were capsulated and 11 were non-typeable. Three non-typeable isolates, associated to international non-capsulated lineages, were recovered from invasive disease sources. In conclusion, half of the atypical pneumococcal clinical isolates were, in fact, S. pseudopneumoniae and one-fourth were other streptococci. We identified S. pseudopneumoniae and non-typeable pneumococci as cause of disease in Spain including invasive disease. |
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AbstractList | We aimed to obtain insights on the nature of a collection of isolates presumptively identified as atypical Streptococcus pneumoniae recovered from invasive and non-invasive infections in Spain. One-hundred and thirty-two isolates were characterized by: optochin susceptibility in ambient and CO.sub.2 -enriched atmosphere; bile solubility; PCR-based assays targeting pneumococcal genes lytA, ply, pspA, cpsA, Spn9802, aliB-like ORF2, and a specific 16S rRNA region; multilocus sequence analysis; and antimicrobial susceptibility. By multilocus sequence analysis, 61 isolates were S. pseudopneumoniae, 34 were pneumococci, 13 were S. mitis, and 24 remained unclassified as non-pneumococci. Among S. pseudopneumoniae isolates, 51 (83.6%) were collected from respiratory tract samples; eight isolates were obtained from sterile sources. High frequency of non-susceptibility to penicillin (60.7%) and erythromycin (42.6%) was found. Only 50.8% of the S. pseudopneumoniae isolates displayed the typical optochin phenotype originally described for this species. None harbored the cpsA gene or the pneumococcal typical lytA restriction fragment length polymorphism. The Spn9802 and the specific 16S rRNA regions were detected among the majority of the S. pseudopneumoniae isolates (n = 59 and n = 49, respectively). The ply and pspA genes were rarely found. A high genetic diversity was found and 59 profiles were identified. Among the S. pneumoniae, 23 were capsulated and 11 were non-typeable. Three non-typeable isolates, associated to international non-capsulated lineages, were recovered from invasive disease sources. In conclusion, half of the atypical pneumococcal clinical isolates were, in fact, S. pseudopneumoniae and one-fourth were other streptococci. We identified S. pseudopneumoniae and non-typeable pneumococci as cause of disease in Spain including invasive disease. We aimed to obtain insights on the nature of a collection of isolates presumptively identified as atypical Streptococcus pneumoniae recovered from invasive and non-invasive infections in Spain. One-hundred and thirty-two isolates were characterized by: optochin susceptibility in ambient and CO(2)-enriched atmosphere; bile solubility; PCR-based assays targeting pneumococcal genes lytA, ply, pspA, cpsA, Spn9802, aliB-like ORF2, and a specific 16S rRNA region; multilocus sequence analysis; and antimicrobial susceptibility. By multilocus sequence analysis, 61 isolates were S. pseudopneumoniae, 34 were pneumococci, 13 were S. mitis, and 24 remained unclassified as non-pneumococci. Among S. pseudopneumoniae isolates, 51 (83.6%) were collected from respiratory tract samples; eight isolates were obtained from sterile sources. High frequency of non-susceptibility to penicillin (60.7%) and erythromycin (42.6%) was found. Only 50.8% of the S. pseudopneumoniae isolates displayed the typical optochin phenotype originally described for this species. None harbored the cpsA gene or the pneumococcal typical lytA restriction fragment length polymorphism. The Spn9802 and the specific 16S rRNA regions were detected among the majority of the S. pseudopneumoniae isolates (n = 59 and n = 49, respectively). The ply and pspA genes were rarely found. A high genetic diversity was found and 59 profiles were identified. Among the S. pneumoniae, 23 were capsulated and 11 were non-typeable. Three non-typeable isolates, associated to international non-capsulated lineages, were recovered from invasive disease sources. In conclusion, half of the atypical pneumococcal clinical isolates were, in fact, S. pseudopneumoniae and one-fourth were other streptococci. We identified S. pseudopneumoniae and non-typeable pneumococci as cause of disease in Spain including invasive disease. We aimed to obtain insights on the nature of a collection of isolates presumptively identified as atypical Streptococcus pneumoniae recovered from invasive and non-invasive infections in Spain. One-hundred and thirty-two isolates were characterized by: optochin susceptibility in ambient and CO2-enriched atmosphere; bile solubility; PCR-based assays targeting pneumococcal genes lytA, ply, pspA, cpsA, Spn9802, aliB-like ORF2, and a specific 16S rRNA region; multilocus sequence analysis; and antimicrobial susceptibility. By multilocus sequence analysis, 61 isolates were S. pseudopneumoniae, 34 were pneumococci, 13 were S. mitis, and 24 remained unclassified as non-pneumococci. Among S. pseudopneumoniae isolates, 51 (83.6%) were collected from respiratory tract samples; eight isolates were obtained from sterile sources. High frequency of non-susceptibility to penicillin (60.7%) and erythromycin (42.6%) was found. Only 50.8% of the S. pseudopneumoniae isolates displayed the typical optochin phenotype originally described for this species. None harbored the cpsA gene or the pneumococcal typical lytA restriction fragment length polymorphism. The Spn9802 and the specific 16S rRNA regions were detected among the majority of the S. pseudopneumoniae isolates (n = 59 and n = 49, respectively). The ply and pspA genes were rarely found. A high genetic diversity was found and 59 profiles were identified. Among the S. pneumoniae, 23 were capsulated and 11 were non-typeable. Three non-typeable isolates, associated to international non-capsulated lineages, were recovered from invasive disease sources. In conclusion, half of the atypical pneumococcal clinical isolates were, in fact, S. pseudopneumoniae and one-fourth were other streptococci. We identified S. pseudopneumoniae and non-typeable pneumococci as cause of disease in Spain including invasive disease. We aimed to obtain insights on the nature of a collection of isolates presumptively identified as atypical Streptococcus pneumoniae recovered from invasive and non-invasive infections in Spain. One-hundred and thirty-two isolates were characterized by: optochin susceptibility in ambient and CO 2 -enriched atmosphere; bile solubility; PCR-based assays targeting pneumococcal genes lyt A, ply , psp A, cps A, Spn 9802, ali B-like ORF2, and a specific 16S rRNA region; multilocus sequence analysis; and antimicrobial susceptibility. By multilocus sequence analysis, 61 isolates were S. pseudopneumoniae , 34 were pneumococci, 13 were S. mitis , and 24 remained unclassified as non-pneumococci. Among S. pseudopneumoniae isolates, 51 (83.6%) were collected from respiratory tract samples; eight isolates were obtained from sterile sources. High frequency of non-susceptibility to penicillin (60.7%) and erythromycin (42.6%) was found. Only 50.8% of the S. pseudopneumoniae isolates displayed the typical optochin phenotype originally described for this species. None harbored the cps A gene or the pneumococcal typical lyt A restriction fragment length polymorphism. The Spn 9802 and the specific 16S rRNA regions were detected among the majority of the S. pseudopneumoniae isolates (n = 59 and n = 49, respectively). The ply and psp A genes were rarely found. A high genetic diversity was found and 59 profiles were identified. Among the S. pneumoniae , 23 were capsulated and 11 were non-typeable. Three non-typeable isolates, associated to international non-capsulated lineages, were recovered from invasive disease sources. In conclusion, half of the atypical pneumococcal clinical isolates were, in fact, S. pseudopneumoniae and one-fourth were other streptococci. We identified S. pseudopneumoniae and non-typeable pneumococci as cause of disease in Spain including invasive disease. |
Audience | Academic |
Author | Rolo, Dora Sá-Leão, Raquel S Simões, Alexandra Domenech, Arnau Fenoll, Asunción Ardanuy, Carmen de Lencastre, Hermínia Liñares, Josefina |
AuthorAffiliation | 6 Laboratory of Microbiology, The Rockefeller University, New York, New York, United States of America 4 Laboratory of Molecular Microbiology of Human Pathogens, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa, Oeiras, Portugal 1 Institut d'Investigació Biomèdica de Bellvitge, Hospital Universitari de Bellvitge, Microbiology Department, Universistat de Barcelona, Barcelona, Spain 2 Centro de investigación en red de enfermedades respiratorias, Instituto de Salud Carlos III, Madrid, Spain 3 Laboratory of Molecular Genetics, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa, Oeiras, Portugal 5 National Center for Microbiology, Instituto de Salud Carlos III, Madrid, Spain Instituto Butantan, Brazil |
AuthorAffiliation_xml | – name: 1 Institut d'Investigació Biomèdica de Bellvitge, Hospital Universitari de Bellvitge, Microbiology Department, Universistat de Barcelona, Barcelona, Spain – name: 4 Laboratory of Molecular Microbiology of Human Pathogens, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa, Oeiras, Portugal – name: 6 Laboratory of Microbiology, The Rockefeller University, New York, New York, United States of America – name: 2 Centro de investigación en red de enfermedades respiratorias, Instituto de Salud Carlos III, Madrid, Spain – name: Instituto Butantan, Brazil – name: 5 National Center for Microbiology, Instituto de Salud Carlos III, Madrid, Spain – name: 3 Laboratory of Molecular Genetics, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa, Oeiras, Portugal |
Author_xml | – sequence: 1 givenname: Dora surname: Rolo fullname: Rolo, Dora organization: Institut d'Investigació Biomèdica de Bellvitge, Hospital Universitari de Bellvitge, Microbiology Department, Universistat de Barcelona, Barcelona, Spain – sequence: 2 givenname: Alexandra surname: S Simões fullname: S Simões, Alexandra – sequence: 3 givenname: Arnau surname: Domenech fullname: Domenech, Arnau – sequence: 4 givenname: Asunción surname: Fenoll fullname: Fenoll, Asunción – sequence: 5 givenname: Josefina surname: Liñares fullname: Liñares, Josefina – sequence: 6 givenname: Hermínia surname: de Lencastre fullname: de Lencastre, Hermínia – sequence: 7 givenname: Carmen surname: Ardanuy fullname: Ardanuy, Carmen – sequence: 8 givenname: Raquel surname: Sá-Leão fullname: Sá-Leão, Raquel |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23437306$$D View this record in MEDLINE/PubMed |
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ContentType | Journal Article |
Contributor | Universitat de Barcelona |
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Copyright | COPYRIGHT 2013 Public Library of Science 2013 Rolo et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. cc-by (c) Rolo, D. et al., 2013 info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/3.0/es 2013 Rolo et al 2013 Rolo et al |
Copyright_xml | – notice: COPYRIGHT 2013 Public Library of Science – notice: 2013 Rolo et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: cc-by (c) Rolo, D. et al., 2013 info:eu-repo/semantics/openAccess <a href="http://creativecommons.org/licenses/by/3.0/es">http://creativecommons.org/licenses/by/3.0/es</a> – notice: 2013 Rolo et al 2013 Rolo et al |
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DocumentTitleAlternate | S. pseudopneumoniae and Non-Typeable Pneumococci |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Competing Interests: HL is an editor for this journal. This does not alter the authors’ adherence to all the PLOS ONE policies on sharing data and materials. Revised the manuscript and approved the final version: RSL DR ASS AD AF JL HL CA. Conceived and designed the experiments: DR ASS JL CA RSL. Performed the experiments: DR ASS AD. Analyzed the data: DR ASS AD CA RSL. Contributed reagents/materials/analysis tools: AF JL HL CA RSL. Wrote the paper: DR ASS RSL. |
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Title | Disease isolates of Streptococcus pseudopneumoniae and non-typeable S. pneumoniae presumptively identified as atypical S. pneumoniae in Spain |
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