The advent of carbapenem-resistant Klebsiella pneumoniae (CRKP) poses a significant challenge to public health, as carbapenems are typically employed as a last resort to treat nosocomial infections caused by such organisms, especially in intensive care units (ICUs). This study aims to characterize the CRKP isolated from patients admitted to the Zagazig University Hospitals (ZUHs) ICU in Egypt. About 56.2%, 41.0%, and 32.4% of the isolates indicated the presence of bla_NDM, bla_OXA-48, and bla_KPC, respectively. Carbapenemase-encoding genes were found in many isolates, and bla_NDM was the most predominant gene. Nevertheless, this situation has become a heavy burden in developing countries, including Egypt, and is associated with substantial morbidity, mortality, and increased healthcare expenses.

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.