Detection of phylogrouping, adhesin, and extended spectrum ß-lactamases genes in hospital acquired uropathogenic Escherichia coli isolates.

BACKGROUND: It has been interesting to compare the levels of antimicrobial resistance and the virulence characteristics of uropathogenic Escherichia coli (UPEC) strains of certain phylogenetic groups. The purpose of this study was to identify the frequency of phylogenetic groups, adhesin genes, antibiotic sensitivity patterns, and extended spectrum-lactamases (ESBLs) genes in hospital-acquired UPEC. METHODS: After UPEC isolation, the disc diffusion method was used to assess its susceptibility to antibiotics. Combination disc testing confirmed the existence of ESBL producers. Polymerase chain reaction (PCR) was used to detect genes for adhesin and ESBLs. RESULTS: One hundred and twenty-eight E. coli were isolated which had the highest resistance to tetracycline (96%) followed by cefoxitin (93%), cefepime (92%), ceftazidime (79%), aztreonam (77%) and sulfamethoxazole -trimethoprim (75%). About 57% of isolates were phenotypically ESBLs positive and they were confirmed by PCR. B2 phylogroup (41%) was the most frequent in E. coli isolates then group D (30%), group A (18%), and lastly group B1 (11%). ESBLs genes were more significantly prevalent in phylogroups B2 and D than other phylogroups (P < 0.001). Regarding adhesin genes, both fim H and afa were more significantly associated with group B2 than other groups (P < 0.009, < 0.032), respectively. In ESBL-positive isolates, both genes were more significantly detected compared to negative ones (P < 0.001). CONCLUSION: Phylogroups B2 and D of UPEC are important reservoirs of antimicrobial resistance and adhesion genes. Detection of ESBL-producing E. coli is important for appropriate treatment as well as for effective infection control in hospitals.

Biofilm Formation and Aspartyl Proteinase Activity and Their Association with Azole Resistance Among Candida albicans Causing Vulvovaginal Candidiasis, Egypt.

Background: Candida albicans (C. albicans) is a major cause of vulvovaginal candidiasis (VVC), a condition that is commonly treated with azole agents. Biofilm formation and aspartyl proteinase production are important virulence factors that could be linked to azole resistance in C. albicans impeding therapy. Aim: To find out the association of both factors with azole resistance among C. albicans isolated from VVC cases in Egyptian nonpregnant women of childbearing age. Patients and Methods: In a cross-sectional study, C. albicans was isolated from nonpregnant females diagnosed clinically as having VVC during a 1-year study period. Susceptibility to azole agents was tested using the disc diffusion method. Biofilm formation and aspartyl proteinase production were assessed phenotypically. Additionally, two biofilm-related genes (ALS1 and HWP1) and three proteinase genes (SAP2, SAP4, and SAP6) were screened for using polymerase chain reaction (PCR). Results: Among 204 C. albicans isolates, azole resistance ratios were as follows: voriconazole (30.4%), itraconazole (17.6%), fluconazole (11.3%) and econazole (6.4%). Biofilm-producing capacity was detected in 63.2% of isolates, and 63.2% were proteinase producers. The frequencies of ALS1 and HWP1 were 69.6% and 74.5%, respectively, while SAP2, SAP4, and SAP6 were 69.2%, 88.7%, and 64.7%, respectively. Biofilm formation was significantly associated with azole resistance (P < 0.001 for each tested azole agent) as was proteinase production (P < 0.001 for fluconazole, voriconazole, and econazole resistance and P = 0.047 for itraconazole). Conclusion: Among nonpregnant Egyptian women of childbearing age, azole resistance in C. albicans causing VVC is significantly associated with biofilm formation and proteinase production. The development of new therapeutic agents that can target these factors is warranted.