Vaginal (61) and fecal (61) Escherichia coli isolates from pregnant and nonpregnant women (18–45 years old) were surveyed for papG alleles by PCR technique. papG allele II was the most prevalent among both vaginal (32.7%) and fecal (3.2%) isolates, whereas other alleles were found only among vaginal isolates (1.6% for alleles I and III and 3.2% for alleles II + III). papG+ pregnant women's isolates did not differ significantly from those of nonpregnant in possession of papG allele II (90% versus 73.3%), whereas both (32.7%) differed significantly ( ) in comparison with fecal isolates (3.2%). The vast majority of papG allele II+ vaginal isolates were clustered in group B2 (81.8%) and much less in group D (18.1%). Also, most of them were positive for fimH (100%), papC (100%), iucC (90.9%), and hly (72.7%), and about half of them were positive for sfa/foc (45.4%). In addition, the mean of VFs' gene possession was 3.5 (range from 2 to 5). It can be concluded that vaginal colonization by papG allele II+ E. coli is possibly one of the predisposing factors of both pregnant and nonpregnant women to pyelonephritis, but its potential may be modified by other factors especially host factors. 1. Introduction Bacterial adherence is an essential step in all infections which involves surface interactions between specific receptors on the mammalian cell membrane and ligands on the bacterial surface. Tissue specificity of infection is determined significantly by the presence or absence of specific receptors on mammalian cells [1]. The ability of uropathogenic Escherichia coli (UPEC) to adhere to host uroepithelia is an important stage in the successful colonization of the urinary tract and pathogenesis of urinary tract infection (UTI). The principal adherence organelle of UPEC is P fimbriae, which mediates Gal(α1-4)Gal-specific binding via the adhesin molecule PapG [2]. The three molecular variants (I to III) of the adhesin are coded by the adhesin gene papG of which there are three known alleles [3]. These variants exhibit different receptor binding specificities [4]. Naturally, papG alleles occurin four combinations, that is, class Ι plus III, class III only, class II plus III, and class II only [2, 5]. According to the receptor specificity of the PapG adhesin, p-fimbriated uropathogenic E. coli is clinically divided into two subtypes: papG allele II+ strains associated with pyelonephritis and bacteremia, and papG allele III+ strains associated with cystitis but have been found in pyelonephritis and bacteremia [2, 5–7]. The most common extraintestinal E. coli
References
[1]
G. F. Brooks, K. C. Carroll, J. S. Butel, and S. A. Morse, Jawetz, Melnick, & Adelberg's Medical Microbiology, McGraw-Hill, New York, NY, USA, 24th edition, 2007.
[2]
M. C. Lane and H. L. T. Mobley, “Role of P-fimbrial-mediated adherence in pyelonephritis and persistence of uropathogenic Escherichia coli (UPEC) in the mammalian kidney,” Kidney International, vol. 72, no. 1, pp. 19–25, 2007.
[3]
B.-I. Marklund, J. M. Tennent, E. Garcia et al., “Horizontal gene transfer of the Escherichia coli？？pap and prs pili operons as a mechanism for the development of tissue-specific adhesive properties,” Molecular Microbiology, vol. 6, no. 16, pp. 2225–2242, 1992.
[4]
N. Stromberg, B.-I. Marklund, B. Lund et al., “Host-specificity of uropathogenic Escherichia coli depends on differences in binding specificity to Gal-1-4Gal-containing isoreceptors,” EMBO Journal, vol. 9, no. 6, pp. 2001–2010, 1990.
[5]
J. R. Johnson, T. A. Russo, J. J. Brown, and A. Stapleton, “papG alleles of Escherichia coli strains causing first-episode or recurrent acute cystitis in adult women,” Journal of Infectious Diseases, vol. 177, no. 1, pp. 97–101, 1998.
[6]
I. Johanson, R. Lindstedt, and C. Svanborg, “Roles of the pap- and prs-encoded adhesins in Escherichia coli adherence to human uroepithelial cells,” Infection and Immunity, vol. 60, no. 8, pp. 3416–3422, 1992.
[7]
J. R. Johnson, K. Owens, A. Gajewski, and M. A. Kuskowski, “Bacterial characteristics in relation to clinical source of Escherichia coli isolates from women with acute cystitis or pyelonephritis and uninfected women,” Journal of Clinical Microbiology, vol. 43, no. 12, pp. 6064–6072, 2005.
[8]
D. L. Kasper, E. Braunwald, A. S. Fauci, S. L. Hauser, D. L. Longo, and J. L. Jameson, Harrison's Principles of Internal Medicine, McGraw-Hill, New York, NY, USA, 16th edition, 2005.
[9]
S. H. Gillespie and P. M. Hawkey, Principles and Practical Clinical Bacteriology, John Wiley & Sons, London, UK, 2nd edition, 2006.
[10]
T. M. Hooton, “Pathogenesis of urinary tract infections: an update,” Journal of Antimicrobial Chemotherapy, vol. 46, supplement 1, pp. 1–7, 2000.
[11]
M. Obata-Yasuoka, W. Ba-Thein, T. Tsukamoto, H. Yoshikawa, and H. Hayashi, “Vaginal Escherichia coli share common virulence factor profiles, serotypes and phylogeny with other extraintestinal E. coli,” Microbiology, vol. 148, no. 9, pp. 2745–2752, 2002.
[12]
A. E. Stapleton, C. L. Fennell, D. M. Coder, C. L. Wobbe, P. L. Roberts, and W. E. Stamm, “Precise and rapid assessment of Escherichia coli adherence to vaginal epithelial cells by flow cytometry,” Clinical Cytometry, vol. 50, no. 1, pp. 31–37, 2002.
[13]
E. Birosoval, L. Siegfried, M. Kmet'ova et al., “Detection of virulence factors in α-haemolytic Escherichia coli strains isolated from various clinical materials,” Clinical Microbiology and Infection, vol. 10, no. 6, pp. 569–573, 2004.
[14]
T. A. Russo and J. R. Johnson, “Medical and economic impact of extraintestinal infections due to Escherichia coli: focus on an increasingly important endemic problem,” Microbes and Infection, vol. 5, no. 5, pp. 449–456, 2003.
[15]
K. Plos, H. Connell, U. Jodal et al., “Intestinal carriage of P fimbriated Escherichia coli and the susceptibility to urinary tract infection in young children,” Journal of Infectious Diseases, vol. 171, no. 3, pp. 625–631, 1995.
[16]
J. F. MacFaddin, Biochemical Tests for Identification of Medical Bacteria, Lippincott Williams and Wilkins, London, UK, 3rd edition, 2000.
[17]
B. A. Forbes, D. F. Sahm, and A. S. Weissfeld, Bailey & Scott's Diagnostic Microbiology, Mosby, St. Louis, Mo, USA, 11th edition, 2002.
[18]
S. Yamamoto, A. Terai, K. Yuri, H. Kurazono, Y. Takeda, and O. Yoshida, “Detection of urovirulence factors in Escherichia coli by multiplex polymerase chain reaction,” FEMS Immunology and Medical Microbiology, vol. 12, no. 2, pp. 85–90, 1995.
[19]
J. R. Johnson and J. J. Brown, “A novel multiply primed polymerase chain reaction assay for identification of variant papG genes encoding the Gal(α1–4)Gal-binding papG adhesins of Escherichia coli,” Journal of Infectious Diseases, vol. 173, no. 4, pp. 920–926, 1996.
[20]
S. W. Cook, H. A. Hammill, and R. A. Hull, “Virulence factors of Escherichia coli isolated from female reproductive tract infections and neonatal sepsis,” Infectious Diseases in Obstetrics and Gynecology, vol. 9, no. 4, pp. 203–207, 2001.
[21]
O. Clermont, S. Bonacorsi, and E. Bingen, “Rapid and simple determination of the Escherichia coli phylogenetic group,” Applied and Environmental Microbiology, vol. 66, no. 10, pp. 4555–4558, 2000.
[22]
C. Le Bouguenec, M. Archambaud, and A. Labigne, “Rapid and specific detection of the pap, afa, and sfa adhesin-encoding operons in uropathogenic Escherichia coli strains by polymerase chain reaction,” Journal of Clinical Microbiology, vol. 30, no. 5, pp. 1189–1193, 1992.
[23]
E. Bingen, S. Bonacorsi, N. Brahimi, E. Denamur, and J. Elion, “Virulence patterns of Escherichia coli K1 strains associated with neonatal meningitis,” Journal of Clinical Microbiology, vol. 35, no. 11, pp. 2981–2982, 1997.
[24]
J. R. Johnson and A. L. Stell, “Extended virulence genotypes of Escherichia coli strains from patients with urosepsis in relation to phylogeny and host compromise,” Journal of Infectious Diseases, vol. 181, no. 1, pp. 261–272, 2000.
[25]
S. M. Ross, Introduction to Probability and Statistics for Engineers and Scientists, Elsevier, London, UK, 4th edition, 2009.
[26]
S. Watt, P. Lanotte, L. Mereghetti, M. Moulin-Schouleur, B. Picard, and R. Quentin, “Escherichia coli strains from pregnant women and neonates: intraspecies genetic distribution and prevalence of virulence factors,” Journal of Clinical Microbiology, vol. 41, no. 5, pp. 1929–1935, 2003.
[27]
S. Yamamoto, “Molecular epidemiology of uropathogenic Escherichia coli,” Journal of Infection and Chemotherapy, vol. 13, no. 2, pp. 68–73, 2007.
[28]
M. R. Tiba, T. Yano, and D. D. S. Leite, “Genotypic characterization of virulence factors in Escherichia coli strains from patients with cystitis,” Revista do Instituto de Medicina Tropical de Sao Paulo, vol. 50, no. 5, pp. 255–260, 2008.
[29]
S.-H. Huang, C. Wass, Q. Fu, N. V. Prasadarao, M. Stins, and K. S. K. Kwang Sik Kim, “Escherichia coli invasion of brain microvascular endothelial cells in vitro and in vivo: molecular cloning and characterization of invasion gene ibe10,” Infection and Immunity, vol. 63, no. 11, pp. 4470–4475, 1995.
[30]
K. Melican, R. M. Sandoval, A. Kader et al., “Uropathogenic Escherichia coli P and type 1 fimbriae act in synergy in a living host to facilitate renal colonization leading to nephron obstruction,” PLoS Pathogens, vol. 7, no. 2, Article ID e1001298, 2011.
[31]
A. Ovalle and M. Levancini, “Urinary tract infections in pregnancy,” Current Opinion in Urology, vol. 11, no. 1, pp. 55–59, 2001.
[32]
A. Andru, “Pathogenesis of urinary tract infections,” Enfermedades Infecciosas y Microbiología Clínica, vol. 23, supplement 4, pp. 15–21, 2005.
