No abstract

The pathogenicity of Escherichia coli strains that cause cervico-vaginal infections (CVI) is due to the presence of several virulence genes. The objective of this study was to define the variability regarding the genotype of antibiotic resistance, the transcription profiles of virulence genes after in vitro infection of the vaginal cell line A431 and the phylogroup composition of a group of cervico-vaginal E. coli strains (CVEC). A total of 200 E. coli strains isolated from Mexican women with CVI from two medical units of the Mexican Institute of Social Security were analysed. E. coli strains and antibiotic resistance genes were identified using conventional polymerase chain reaction (PCR), and phylogroups were identified using multiplex PCR. Virulence gene transcription was measured through reverse-transcriptase realtime PCR after infection of the vaginal cell line A431. The most common antibiotic resistance genes among the CVEC strains were aac(3)II, TEM, dfrA1, sul1, and qnrA. The predominant phylogroup was B2. The genes most frequently transcribed in these strains were fimH, papC, irp2, iroN, kpsMTII, cnf1, and ompT, mainly in CVEC strains isolated from chronic and occasional vaginal infections. The strains showed a large diversity of transcription of the virulence genes phenotype and antibiotic resistance genotype, especially in the strains of phylogroups, B2, A, and D. The strains formed 2 large clusters, which contained several subclusters. The genetic diversity of CVEC strains was high. These strains have a large number of transcription patterns of virulence genes, and one-third of them carry three to seven antibiotic resistance genes.

Periodontal disease is caused by different gram-negative anaerobic bacteria; however, Escherichia coli has also been isolated from periodontitis and its role in periodontitis is less known. This study aimed to determine the variability in virulence genotype, antibiotic resistance phenotype, biofilm formation, phylogroups, and serotypes in different emerging periodontal strains of Escherichia coli, isolated from patients with periodontal disease and healthy controls. E. coli, virulence genes, and phylogroups, were identified by PCR, antibiotic susceptibility by the Kirby-Bauer method, biofilm formation was quantified using polystyrene microtiter plates, and serotypes were determined by serotyping. Although E. coli was not detected in the controls (n = 70), it was isolated in 14.7% (100/678) of the patients. Most of the strains (n = 81/100) were multidrug-resistance. The most frequent adhesion genes among the strains were fimH and iha, toxin genes were usp and hlyA, iron-acquisition genes were fyuA and irp2, and protectin genes were ompT, and KpsMT. Phylogroup B2 and serotype O25:H4 were the most predominant among the strains. These findings suggest that E. coli may be involved in periodontal disease due to its high virulence, multidrug-resistance, and a wide distribution of phylogroups and serotypes.