Browsing by Author "Nakabuye, Hellen"
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Item Evaluation of three protocols for direct susceptibility testing for gram negative-Enterobacteriaceae from patient samples in Uganda...(Nature Publishing Group, 2024-02-01) Aruhomukama, Dickson; Magiidu, Walusimbi Talemwa; Katende, George; Ebwongu, Robert Innocent; Bulafu, Douglas; Kasolo, Rajab; Nakabuye, Hellen; Musoke, David; Asiimwe, BenonIn Uganda, the challenge of generating and timely reporting essential antimicrobial resistance (AMR) data has led to overreliance on empirical antibiotic therapy, exacerbating the AMR crisis. To address this issue, this study aimed to adapt a one-step AMR testing protocol alongside an SMS (Short Message Service) result relay system (SRRS), with the potential to reduce the turnaround time for AMR testing and result communication from 4 days or more to 1 day in Ugandan clinical microbiology laboratories. Out of the 377 samples examined, 54 isolates were obtained. Notably, E. coli (61%) and K. pneumoniae (33%) were the most frequently identified, majority testing positive for ESBL. Evaluation of three AMR testing protocols revealed varying sensitivity and specificity, with Protocol A (ChromID ESBL-based) demonstrating high sensitivity (100%) but no calculable specificity, Protocol B (ceftazidime-based) showing high sensitivity (100%) and relatively low specificity (7.1%), and Protocol C (cefotaxime-based) exhibiting high sensitivity (97.8%) but no calculable specificity. ESBL positivity strongly correlated with resistance to specific antibiotics, including cefotaxime, ampicillin, and aztreonam (100%), cefuroxime (96%), ceftriaxone (93%), and trimethoprim sulfamethoxazole (87%). The potential of integrating an SRRS underscored the crucial role this could have in enabling efficient healthcare communication in AMR management. This study underscores the substantial potential of the tested protocols for accurately detecting ESBL production in clinical samples, potentially, providing a critical foundation for predicting and reporting AMR patterns. Although considerations related to specificity warrant careful assessment before widespread clinical adoption.Item Genomic variations in Mycobacterium tuberculosis from the lungs and blood of HIV-infected individuals in Uganda: insights into compartmentalization.(African Health Sciences, 2024-12) Nakabuye, Hellen; Aruhomukama, Dickson; Galiwango, Ronald; Kateete, David P.Mycobacterium tuberculosis (MTB) clinical strains are relatively varied at the genome level. This in-silico study analyzed genomic differences between MTB isolates from the blood and lungs of TB-HIV positive cohorts in Uganda. The hypothesis was that isolates from the blood have distinct SNPs and INDELs that make them better survivors. Twenty-four MTB-blood and -lung sequences were aligned against the H37Rv reference genome and analyzed using BWA-MEM, IGV, SAMtools, FreeBayes, and SnpEff. Comparative analysis revealed that MTB-blood isolates had 11 virulence genes with distinctive non-synonymous SNPs involved in increasing colony-forming units, lowering host survival, enhancing tissue pathology, and allowing for human host persistence. The majority of INDELs were found in non-virulence genes, with the remainder in both MTB-blood and -lung sequences. The study suggests that MTB-blood isolates have distinctive SNPs that explain their capacity to persist outside of the lungs. However, further research is needed to understand the significance of these SNPs in the pathogenesis of MTB. Mycobacterium tuberculosis (MTB) clinical strains have high genomic variability, and there is a knowledge gap on the genomic differences between MTB isolates from the blood and lungs of TB-HIV positive patients in Uganda. This study found that MTB-blood isolates had 11 virulence genes with distinctive non-synonymous SNPs that may contribute to their capacity to persist outside of the lungs. These findings provide insight into the genomic basis of MTB adaptation in different host environments, but further research is needed to fully understand the significance of these SNPs in MTB pathogenesis.