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Here, we describe a phenotype of robust growth in human urine observed in ABU-causing\n            <jats:named-content content-type=\"genus-species\">S. agalactiae<\/jats:named-content>\n            (ABSA) that was not seen among uropathogenic\n            <jats:named-content content-type=\"genus-species\">S. agalactiae<\/jats:named-content>\n            (UPSA) strains isolated from patients with acute cystitis. In direct competition assays using pooled human urine inoculated with equal numbers of a prototype ABSA strain, designated ABSA 1014, and any one of several UPSA strains, measurement of the percentage of each strain recovered over time showed a markedly superior fitness of ABSA 1014 for urine growth. Comparative phenotype profiling of ABSA 1014 and UPSA strain 807, isolated from a patient with acute cystitis, using metabolic arrays of &gt;2,500 substrates and conditions revealed unique and specific\n            <jats:sc>l<\/jats:sc>\n            -malic acid catabolism in ABSA 1014 that was absent in UPSA 807. Whole-genome sequencing also revealed divergence in malic enzyme-encoding genes between the strains predicted to impact the activity of the malate metabolic pathway. Comparative growth assays in urine comparing wild-type ABSA and gene-deficient mutants that were functionally inactivated for the malic enzyme metabolic pathway by targeted disruption of the\n            <jats:italic>maeE<\/jats:italic>\n            or\n            <jats:italic>maeK<\/jats:italic>\n            gene in ABSA demonstrated attenuated growth of the mutants in normal human urine as well as synthetic human urine containing malic acid. We conclude that some\n            <jats:named-content content-type=\"genus-species\">S. agalactiae<\/jats:named-content>\n            strains can grow in human urine, and this relates in part to malic acid metabolism, which may affect the persistence or progression of\n            <jats:named-content content-type=\"genus-species\">S. agalactiae<\/jats:named-content>\n            ABU.\n          <\/jats:p>","DOI":"10.1128\/iai.00938-15","type":"journal-article","created":{"date-parts":[[2015,11,10]],"date-time":"2015-11-10T03:58:26Z","timestamp":1447127906000},"page":"307-319","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":29,"title":["Discovery and Characterization of Human-Urine Utilization by Asymptomatic-Bacteriuria-Causing Streptococcus agalactiae"],"prefix":"10.1128","volume":"84","author":[{"given":"Deepak S.","family":"Ipe","sequence":"first","affiliation":[{"name":"School of Medical Sciences, Menzies Health 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University of Alabama at Birmingham, Birmingham, Alabama, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr.","given":"William H.","family":"Benjamin","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama, USA"},{"name":"Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark R.","family":"Davies","sequence":"additional","affiliation":[{"name":"School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia"},{"name":"Wellcome Trust Sanger Institute, Hinxton, Cambridge, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samantha J.","family":"Dando","sequence":"additional","affiliation":[{"name":"Institute for Glycomics, Griffith University, Gold Coast Campus, QLD, 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