Whole-genome sequence analysis of multidrug-resistant uropathogenic strains of Escherichia coli from Mexico.

Background : Escherichia coli is the main bacterium associated with urinary tract infections (UTIs), including cystitis and pyelonephritis. Uropathogenic E. coli (UPEC) harbors numerous genes that encode diverse virulence factors contributing to its pathogenicity. The treatment of UTIs has become complicated due to the natural selection of E. coli strains that are multiresistant to several groups of antibiotics regularly used in clinical settings such as hospitals. Genomic reports of the global composition and distribution of the antibiotic resistance and virulence genes of these pathogenic strains are lacking in the Mexican population. Purpose and methods : The aim of this study was to globally characterize the genomes of a group of UPEC strains by massive parallel sequencing to determine the prevalence and distribution of virulence and antibiotic resistance genes associated with different serotypes and phylogenetic groups. Results: The strains exhibited 138-197 virulence genes and 29 antibiotic resistance genes related to antibiotics that are commonly used in clinical practice.  Conclusions: These findings are relevant to the definition of new strategies for treating urinary tract infections in public hospitals and private practice. To further define the epidemiological distribution and composition of these virulence and antibiotic resistance genes, larger studies are needed.

The clinically isolated FIZ15 bacteriophage causes lysogenic conversion in Pseudomonas aeruginosa PAO1.

FIZ15 bacteriophage, from a human clinical isolate of Pseudomonas aeruginosa, causes lysogenic conversion in the P. aeruginosa strain PAO1. The prophage-conferred phenotypes are: (1) increased resistance to phagocytosis by mouse peritoneal macrophages; (2) increased resistance to killing by normal human serum, and (3) increased adhesion to human buccal epithelial cells. These phenotypes are related to the prophage-induced change at the level of its own bacterial receptor, which appears to be the O-antigen.

The lom gene of bacteriophage lambda is involved in Escherichia coli K12 adhesion to human buccal epithelial cells.

The role of the lom gene of bacteriophage lambda in adhesion of Escherichia coli to human buccal epithelial cells (HBC) was studied testing the adherence of lamda lom+ and lambda lom::TnphoA E. coli lysogens. lambda lom+ prophage increased 50% E. coli adhesion. This effect was not observed with lambda lom::TnphoA. These results suggest that the normal Lom protein participates directly in adhesion or regulates the synthesis of other protein(s), which may be involved in adhesion.

Lambda prophage decreases Escherichia coli sensitivity to human serum bactericidal effect.

Escherichia coli C600 and C600(lambda) strains were tested for their susceptibility to the bactericidal action of 4% normal human serum. C600 survival was reduced to 30%, 23% and 16% after 60, 150 and 180 min of exposure to serum, respectively, whereas the percentage of survival of C600(lambda) was 199, 109 and 65% at the same times. The estimated exposition times for 50% killing showed an eight-fold difference, they were 23 and 202 min for C600 and C600(lambda), respectively. None of the two strains tested was killed when incubated with serum whose alternative complement pathway was inactivated by heating at 50 degrees C for 20 min, showing that this pathway, and not the classical one, was responsible of the bactericidal action, a conclusion further supported by the finding that both strains were differentially killed by the alternative complement pathway, C600 showing a 14X, 10X and 4X greater susceptibility than C600(lambda) at 60, 120 and 180 min of exposure to serum whose classical pathway was selectively inhibited by chelation with 10 mM EGTA plus 2 mM MgCl2. We feel that lambda phage may lower the serum sensitivity of its lysogen by altering the bacterial external surface, perhaps by the inclusion of some protein encoded by an accessory gene of the lambda genome, and thus interfering with either the formation, deposition or activity of the membrane attack complex.