Proteus mirabilis, a common cause of urinary tract infection in hospitalized and catheterized patients, produces mannose-resistant/klebsiella-like (MR/K) and mannose-resistant/proteus-like (MR/P) hemagglutinins. The gene encoding the major structural subunit of a fimbria, possibly MR/K, was identified in two strains. A degenerate oligonucleotide probe based on the N terminus of the Proteus uroepithelial cell adhesin and antiserum raised against the denatured polypeptide were used to screen a cosmid gene bank of strain HU1069. A cosmid clone that reacted with the probe and antiserum was identified, and a fimbria-like open reading frame was determined by nucleotide sequencing. The predicted N-terminal amino acid sequence of the processed polypeptide, ENETPAPKVSSTKGEIQLKG (residues 23 to 42), did not match the uroepithelial cell adhesin N terminus but, rather, matched exactly the N-terminal amino acid sequence of a polypeptide with an apparent
Proteus mirabilis bacteria are a common cause of hospital-acquired urinary tract infection. In a previous study, we described a P. mirabilis fimbrial protein, UCA, that adhered to human uroepithelial cells. Genes sufficient for expression of UCA adherence were cloned into Escherichia coli K-12. E. coli bacteria that contained the uca recombinant plasmid adhered to human uroepithelial cells. In addition, the ucaA gene encoding the structural component of UCA pili was subcloned, and its DNA sequence was determined. Amino acid sequence homology (30 to 50%) was found between mature UcaA protein and pilins from pathogenic bacteria representing several genera, including E. coli F17, G, and type 1C pilins, Haemophilus M43 pilin, and a Bordetella pilin.
Objective: The presence of enterobacteria such as Escherichia coli in the vagina of normal women is not synonymous
with infection. However, vaginal E. coli may also cause symptomatic infections. We examined bacterial
virulenceproperties that may promote symptomatic female reproductive tract infections (RTI) and neonatal sepsis.
Methods: E. coli isolated as the causative agent from cases of vaginitis (n = 50), tubo-ovarian abscess (n = 45) and
neonatal sepsis (n = 45) was examined for selected phenotypic and genetic virulence properties. Results were
compared with the frequency of the same properties among fecal E. coli not associated with disease.
Results: A significantly greater proportion of infection E. coli exhibited D-mannose resistant hemagglutination
compared with fecal E. coli (p < 0.01). This adherence phenotype was associated with the presence of P fimbriae
(pap) genes which were also significantly more prevalent among isolates from all three infection sites (p < 0.01).
The majority of pap+ isolates contained the papG3 allele (Class II) regardless of infection type. Increased frequency
of Type 1C genes among vaginitis and abscess isolates was also noted. No significant differences in frequency of
other bacterial adherence genes, fim, sfa, uca (gaf) or dra were observed.
E. coli associated with vaginitis was significantly more likely to be hemolytic ( HIy+)
than were fecal isolates
(p < 0.05). The HIy+ phenotype was also more prevalent among tubo-ovarian abscess and neonatal sepsis isolates
(p < 0.08).
Conclusions: E. coli isolated from female RTI and neonatal sepses possess unique properties that may enhance
their virulence. These properties are similar to those associated with other E. coli extra-intestinal infections,
indicating that strategies such as vaccination or bacterial interference that may be developed against urinary tract
infections (UTI) and other E. coli extra-intestinal infections may also prevent selected female RTI.
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