Plasmid-mediated colistin resistance (Col-R) conferred by mcr genes endangers the last therapeutic option for multifarious β-lactamase-producing bacteria. The current study aimed to explore the mcr gene molecular epidemiology in extensively drug-resistant (XDR) bacteria. Col-R gram-negative bacterial strains were screened using a minimum inhibitory concentration (MIC) breakpoint ≥4 µg/mL. Resistant isolates were examined for mcr variants, extended-spectrum β-lactamase, AmpC, and carbapenemase genes using polymerase chain reaction (PCR). The MIC breakpoints for mcr-positive strains were determined using broth microdilution and E-test strips. Overall, 19/718 (2.6%) gram-negative rods (GNRs) harboring mcr were identified, particularly in pus (p = 0.01) and tracheal secretions (p = 0.03). Molecular epidemiology data confirmed 18/19 (95%) mcr-1 and 1/19 (5%) mcr-2 genes. Integron detection revealed 15/17 (88%) Int-1 and 2/17 (12%) Int-2. Common co-expressing drug-resistant β-lactamase genes included 8/16 (50%) bla_CTM-1, 3/16 (19%) bla_CTM-15, 3/3 (100%) bla_CMY-2, 2/8 (25%) bla_NDM-1, and 2/8 (25%) bla_NDM-5. The MIC₅₀ and MIC₉₀ values (µg/mL) were as follows: Escherichia coli, 12 and 24; Klebsiella pneumoniae, 12 and 32; Acinetobacter baumannii, 8 and 12; and Pseudomonas aeruginosa, 32 and 64, respectively. Treatment of XDR strains has become challenging owing to the co-expression of mcr-1, mcr-2, multifarious β-lactamase genes, and integrons.

The emergence of carbapenem-resistant Acinetobacter calcoaceticus-baumannii complex (CRACB) in clinical environments is a significant global concern. These critical pathogens have shown resistance to a broad spectrum of antibacterial drugs, including carbapenems, mostly due to the acquisition of various β-lactamase genes. Clinical samples (n = 1985) were collected aseptically from multiple sources and grown on blood and MacConkey agar. Isolates and antimicrobial susceptibility were confirmed with the VITEK-2 system. The modified Hodge test confirmed the CRACB phenotype, and specific PCR primers were used for the molecular identification of bla_OXA and bla_NDM genes. Of the 1985 samples, 1250 (62.9%) were culture-positive and 200 (43.9%) were CRACB isolates. Of these isolates, 35.4% were recovered from pus samples and 23.5% from tracheal secretions obtained from patients in intensive care units (49.3%) and medical wards (20.2%). An antibiogram indicated that 100% of the CRACB isolates were resistant to β-lactam antibiotics and β-lactam inhibitors, 86.5% to ciprofloxacin, and 83.5% to amikacin, while the most effective antibiotics were tigecycline and colistin. The CRACB isolates displayed resistance to eight different AWaRe classes of antibiotics. All isolates exhibited the bla_OXA-51 gene, while bla_OXA-23 was present in 94.5%, bla_VIM in 37%, and bla_NDM in 14% of the isolates. The bla_OXA-51, bla_OXA-23, and bla_OXA-24 genes co-existed in 13 (6.5%) isolates. CRACB isolates with co-existing bla_OXA-23, bla_OXA-24, bla_NDM, bla_OXA-51 and bla_VIM genes were highly prevalent in clinical samples from Pakistan. CRACB strains were highly critical pathogens and presented resistance to virtually all antibacterial drugs, except tigecycline and colistin.

Sepsis-associated acute kidney injury (S-AKI) represents a significant health problem associated with adverse outcomes. Our study aimed to assess the value of serum cystatin-C (sCysC) and TNF-α (rs361525) in combination for diagnosing S-AKI patients and predicting their adverse outcomes. The study included 100 critically ill neonates and 100 controls. Patients were categorized into an S-AKI group and a non-AKI group. TNF-α (−238, rs361525) genotyping was performed using RT-PCR, and sCysC was assessed using ELISA. Our study showed a fundamental difference in the genotype frequencies of TNF-α (−238, rs361525) and SNP between S-AKI and non-AKI patients. Furthermore, there was a significant relationship between cystatin C and TNF-α (−238, rs361525), where cystatin C was higher in patients with AA alleles than in patients with GA and GG alleles. Combining GA + AA genotypes with elevated serum cystatin-C levels can serve as a potential diagnostic and prognostic biomarker for AKI development in this population. The GA/AA genotypes independently predicted S-AKI risk (OR = 6.64, p < 0.001). At the same time, elevated sCysC (>9.4 mg/L) emerged as a sensitive biomarker (AUC = 0.848) and independent predictor of adverse outcomes. Collectively, these findings contribute to the growing field of personalized medicine and represent a strategic advantage, enabling prevention-focused care rather than the treatment of established disease.

The incidence of fungal infections, particularly those caused by Candida species, has significantly risen among immunocompromised patients in recent years. Aim: This study evaluated the species distribution, antifungal susceptibility patterns, and virulence gene profiles of Candida species isolated from critically ill ICU patients while comparing the diagnostic performance of conventional phenotypic isolation media with molecular genotypic identification methods. Materials and Methods: A total of 211 clinical specimens were obtained from 200 hospitalized patients at Menoufia University Hospitals, Egypt. Candida species were phenotypically identified using cornmeal agar supplemented with Tween 80 (CTA) and CHROMagar^TM Candida (CMA) and were molecularly confirmed at the species level by sequencing PCR-amplified ITS regions. Antifungal susceptibility profiles to fluconazole, voriconazole, and amphotericin B were evaluated using the disk diffusion method. Furthermore, real-time PCR was deployed to detect genes encoding adherence factors and Secreted Aspartyl Proteinase. Results: Candida species were recovered from 45 out of 211 clinical specimens. The most frequently isolated species was Candida albicans (15/45, 33.3%), followed by C. parapsilosis (9/45, 20.0%), C. glabrata (7/45, 15.5%), C. tropicalis (7/45, 15.5%), C. krusei (4/45, 8.8%), and C. famata (3/45, 6.7%). Among the recovered Candida isolates, the percentage rates of the ALS1, ALS3, HWP1, and SAP4 genes were 40%, 42.22%, 44.4%, and 37.78%, respectively. HWP1 was the most frequently detected pathogenicity factor, whereas SAP4 was the least prevalent. Conclusions: In the studied immunocompromised cohort, non-albicans Candida species constituted a substantial proportion of clinical isolates. Notable antifungal resistance patterns were also observed, emphasizing the value of integrated phenotypic and genotypic identification for tailored management. Furthermore, virulence-associated genes (ALS1, ALS3, HWP1, and SAP4) were detected in isolates of several Candida species, highlighting their presence in clinical strains.