GPGuillermo Prats

Guillermo Prats

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

The organizations/institutes from the scholar's latest article


Guillermo Prats has a total of 13 co-authors. Here are the top co-authors by number of shared publications:

  • Beatriz Mirelis

    <!--label omitted: 1-->Departament de Microbiologia, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma 08025 Barcelona, Spain

    2 shared publications
  • Adam Stell

    <!--label omitted: 3-->Department of Medicine, University of Minnesota, Minneapolis, Minnesota3

    1 shared publication
  • Carmen Muñoz

    Servei de Microbiologia, Hospital de la Santa Creu i Sant Pau, 08025 Barcelona, Spain

    1 shared publication
  • David Dalmau

    <!--label omitted: 2-->Departament de Medicina, Unitat de Malalties Infeccioses, Hospital Mutua de Terrassa, 08221 Terrassa,2 Spain, and Minneapolis Veterans Affairs Medical Center and

    1 shared publication
  • Elisenda Miró

    Department of Genetics and Microbiology, Autonomous University of Barcelona, 08193 Bellaterra (Cerdanyola del Vallès), Spain

    1 shared publication
  • Ferran Navarro

    <!--label omitted: 1-->Departament de Microbiologia, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma, 08025 Barcelona,1 and

    1 shared publication

Latest Publications

  • Open Access

    Antibiotic Resistance Trends in Enteropathogenic Bacteria Isolated in 1985–1987 and 1995–1998 in Barcelona

    by Guillermo Prats, Beatriz Mirelis, Teresa Llovet, Carmen Muñoz, Elisenda Miró, Ferran Navarro

    Trends in resistance to antimicrobial agents used for therapy have been evaluated with 3,797 enteropathogenic bacteria, Campylobacter , Salmonella , Shigella , and Yersinia , between 1985–1987 and 1995–1998. The greater increase in the rate of resistance was observed in Campylobacter jejuni for quinolones (from 1 to 82%) and tetracycline (from 23 to 72%) and in gastroenteric salmonellae for ampicillin (from 8 to 44%), chloramphenicol (from 1.7 to 26%), and trimethoprim-sulfamethoxazole and nalidixic acid (from less than 0.5 to 11%). Multidrug resistance was detected in several Salmonella serotypes. In the 1995–1998 period, 76% of Shigella strains were resistant to trimethoprim-sulfamethoxazole, 43% were resistant to ampicillin, and 39% were resistant to chloramphenicol. Seventy-two percent of Yersinia enterocolitica O3 strains were resistant to streptomycin, 45% were resistant to sulfonamides, 28% were resistant to trimethoprim-sulfamethoxazole, and 20% were resistant to chloramphenicol.


  • Escherichia coli Serotype O15:K52:H1 as a Uropathogenic Clone

    by Guillem Prats, Ferran Navarro, Beatriz Mirelis, David Dalmau, Nuria Margall, Pere Coll, Adam Stell, James R. Johnson

    To clarify the clinical and bacteriological correlates of urinary-tract infection (UTI) due to Escherichia coli O15:K52:H1, during a 1-year surveillance period we prospectively screened all 1,871 significant E. coli urine isolates at the Hospital de la Santa Creu i Sant Pau, Barcelona, Spain, for this serotype and assessed the epidemiological features of community-acquired UTI due to E. coli O15:K52:H1 versus other E. coli serotypes. We also compared the 25 O15:K52:H1 UTI isolates from the present study with 22 O15:K52:H1 isolates from other, diverse geographic locales and with 23 standard control strains (8 strains from the ECOR reference collection and 15 strains of nonpathogenic O:K:H serotypes) with respect to multiple phenotypic and genotypic traits. Although E. coli O15:K52:H1 caused only 1.4% of community-acquired E. coli UTIs during the surveillance period, these UTIs were more likely to present as pyelonephritis and to occur in younger hosts, with similar risk factors, than were UTIs due to other E. coli serotypes. Irrespective of geographic origin, E. coli O15:K52:H1 strains exhibited a comparatively restricted repertoire of distinctive virulence factor profiles (typically, they were positive for papG allele II, papA allele F16, and aer and negative for sfa , afa , hly , and cnf1 ), biotypes, ribotypes, and amplotypes, consistent with a common clonal origin. In contrast, their antimicrobial resistance profiles were more extensive and more diverse than those of control strains. These findings indicate that E. coli O15:K52:H1 constitutes a broadly distributed and clinically significant uropathogenic clone with fluid antimicrobial resistance capabilities.


    • 10 February 1999
      • Vol. 72  (5) , 435-6

    [Diagnosis of meningococcal disease using PCR].

    by G Prats, N Margall, M Majó

    • 9 October 1998
      • Vol. 16  (6) , 280-4

    [Population structure and bacterial clonality].

    by G Prats