Background: The spread of extended-spectrum β-lactamase-producing Klebsiella is an emerging public health concern presenting severe clinical impacts. This problem is particularly severe in developing countries where irrational use of antibiotics makes the treatment of such infections more challenging. Methods: In this cross-sectional study, we investigated antibiotic resistance among clinical Klebsiella pneumoniae isolates from 256 patient specimens from Al-Diwaniyah hospitals, using standard microbiological methods followed by PCR. Antimicrobial susceptibility testing identified resistance rates and proportions of multidrug-resistant (MDR) and extensively drug-resistant (XDR) strains. Carbapenemase genes were detected by multiplex PCR and sequencing. Mutations were characterized, and their functional significance was predicted using in silico prediction tools. Results: Fifty Klebsiella pneumoniae isolates were recovered, exhibiting high resistance rates (42–100%) to penicillins, cephalosporins, fluoroquinolones and carbapenems, with 62% classified as MDR and 38% as XDR. Carbapenemase genes were highly prevalent (blaOXA-48 56%, blaIMP 44%, blaVIM 30%, blaKPC 28%, blaNDM 26%), with 60% of isolates co-harbouring ≥ two genes. Most mutations were predicted to be structurally tolerated, while active-site-proximal substitutions (H120L in NDM-52 and V120L in OXA-48) were predicted to affect enzyme activity. However, docking analysis suggested no significant alteration in carbapenem binding affinity. Conclusions: Our results highlight a very high prevalence of MDR/XDR Klebsiella pneumoniae, associated with diverse carbapenemase genes and resistance-related polymorphisms that may indicate potential functional impacts. To the best of our knowledge, this is the first study in Iraq to combine carbapenemase gene mutation analysis with structural modelling and molecular docking. This study emphasizes the urgent need for effective antimicrobial resistance surveillance in Iraq.

Background/Objectives: β-thalassemia major is a common inherited hemoglobin disorder caused by Hemoglobin Subunit Beta (HBB) mutations and often complicated by iron overload and oxidative stress. This study characterized the clinical, hematological, biochemical, and molecular profile of β-thalassemia major in Al-Diwaniyah, Iraq, focusing on HBB mutations and CAT promoter polymorphisms as oxidative modifiers. Methods: A retrospective case–control study included 100 transfusion-dependent patients and 50 healthy controls. Sociodemographic data, complete blood count, ferritin, lipid profile, catalase (CAT), and malondialdehyde (MDA) were assessed. HBB mutations, namely IVSI-1 (G>A), IVSI-6 (T>C), and CD39 (C>T), and CAT polymorphisms, namely rs1001179 (C>T) and rs7943316 (A>T), were genotyped. Results: Patients had high rates of family history (80%), consanguinity (80%), rural residence (74%), low education (60.6%), and poor socioeconomic status (71.4%). Compared with controls, they showed lower RBC, HGB, HCT, HDL, LDL, and CAT but higher ferritin, triglycerides, and MDA (all p < 0.001). Overall, 69% of patients carried at least one studied HBB mutations, while 31% remained uncharacterized. Mutant allele frequencies were 29% for IVSI-1 (A) and 25.5% each for IVSI-6 (C) and CD39 (T). The CAT polymorphism rs1001179 (C>T) was associated with disease risk (CT: 33% vs. 14%; OR = 3.25, p = 0.019), whereas rs7943316 (A>T) was not. IVS-I-1 (G>A)/CD39 (C>T) β⁰ mutations were associated with lower CAT activity (β = −0.205; p = 0.046). Conclusions: β-thalassemia in Al-Diwaniyah, Iraq, shows substantial clinical, genetic, and oxidative heterogeneity. Integrated HBB–CAT analysis may improve molecular diagnosis, risk stratification, and preventive strategies in high-consanguinity populations.