{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T17:30:09Z","timestamp":1790616609200,"version":"4.1.0"},"reference-count":45,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2009,7,1]],"date-time":"2009-07-01T00:00:00Z","timestamp":1246406400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Clin Microbiol"],"published-print":{"date-parts":[[2009,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Serotypes of group B streptococcus (GBS) that cause urinary tract infection (UTI) are poorly characterized. We conducted a prospective study of GBS UTI in adults to define the clinical and microbiological characteristics of these infections, including which serotypes cause disease. Patients who had GBS cultured from urine over a 1-year period were grouped according to symptoms, bacteriuria, and urinalysis. Demographic data were obtained by reviewing medical records. Isolates were serotyped by latex agglutination and multiplex PCR-reverse line blotting (mPCR\/RLB). Antibiotic susceptibilities were determined by disc diffusion. GBS was cultured from 387\/34,367 consecutive urine samples (1.1%): 62 patients had bacteriuria of &gt;10\n            <jats:sup>7<\/jats:sup>\n            CFU\/liter and at least one UTI symptom; of these patients, 31 had urinary leukocyte esterase and pyuria (others not tested), 50 (81%) had symptoms consistent with cystitis, and 12 (19%) had symptoms of pyelonephritis. Compared with controls (who had GBS isolated without symptoms), a prior history of UTI was an independent risk factor for disease. Increased age was also significantly associated with acute infection. Serotyping results were consistent between latex agglutination and mPCR\/RLB for 331\/387 (85.5%) isolates; 22 (5.7%) and 7 (1.8%) isolates were nontypeable with antisera and by mPCR\/RLB, respectively; and 45\/56 (80.4%) isolates with discrepant results were typed by mPCR\/RLB as belonging to serotype V. Serotypes V, Ia, and III caused the most UTIs; serotypes II, Ib, and IV were less common. Nontypeable GBS was not associated with UTI. Erythromycin (39.5%) and clindamycin (26.4%) resistance was common. We conclude that a more diverse spectrum of GBS serotypes causes UTI than previously recognized, with the exception of nontypeable GBS.\n          <\/jats:p>","DOI":"10.1128\/jcm.00154-09","type":"journal-article","created":{"date-parts":[[2009,5,14]],"date-time":"2009-05-14T00:45:14Z","timestamp":1242261914000},"page":"2055-2060","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":74,"title":["Diversity of Group B Streptococcus Serotypes Causing Urinary Tract Infection in Adults"],"prefix":"10.1128","volume":"47","author":[{"given":"Kimberly B.","family":"Ulett","sequence":"first","affiliation":[{"name":"Departments of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr.","given":"William H.","family":"Benjamin","sequence":"additional","affiliation":[{"name":"Microbiology"},{"name":"Pathology, University of Alabama at Birmingham, Birmingham, Alabama 35294"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fenglin","family":"Zhuo","sequence":"additional","affiliation":[{"name":"Centre for Infectious Diseases and Microbiology, Institute of Clinical Pathology and Medical Research, Westmead, 2145 New South Wales, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meng","family":"Xiao","sequence":"additional","affiliation":[{"name":"Centre for Infectious Diseases and Microbiology, Institute of Clinical Pathology and Medical Research, Westmead, 2145 New South Wales, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fanrong","family":"Kong","sequence":"additional","affiliation":[{"name":"Centre for Infectious Diseases and Microbiology, Institute of Clinical Pathology and Medical Research, Westmead, 2145 New South Wales, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gwendolyn L.","family":"Gilbert","sequence":"additional","affiliation":[{"name":"Centre for Infectious Diseases and Microbiology, Institute of Clinical Pathology and Medical Research, Westmead, 2145 New South Wales, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark A.","family":"Schembri","sequence":"additional","affiliation":[{"name":"School of Chemistry and Molecular Biosciences, University of Queensland, Brisbane, 4072 Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Glen C.","family":"Ulett","sequence":"additional","affiliation":[{"name":"Microbiology"},{"name":"School of Medical Sciences, Centre for Medicine and Oral Health, Griffith University Gold Coast Campus, 4222 Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajog.2007.01.006"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1055\/s-2004-835310"},{"key":"e_1_3_2_4_2","first-page":"222","year":"2000","unstructured":"Baker, C. 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