Browsing by Author "Paasi, George"

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    Capacity building in field epidemiology in Sub Saharan Africa : findings from Infectious Disease Field Epidemiology and Biostatistics in Africa (IDEA) Fellowship Program
    (Taylor & Francis Group, 2025) Alunyo, Patrick Jimmy; Paasi, George; Ario, Riolexus Alex; Olupot-Olupot, Peter
    Background: Emerging and re-emerging infectious diseases (EREIDs) remain a major public health threat globally, particularly in sub-Saharan Africa (SSA), where fragile health systems, inadequate infrastructure, and limited workforce training exacerbate vulnerabilities. Uganda, a recognised hotspot for outbreaks, faces increasing risk due to anthropogenic and environmental drivers. To address critical capacity gaps, the Infectious Disease Epidemiology and Biostatistics in Africa (IDEA) Fellowship was launched as Uganda’s first master’s-level programme in infectious disease field epidemiology. Led by Busitema University, in collaboration with national and international partners, the programme was funded through EDCTP-II (CSA2020E). Methods: The IDEA Fellowship combined theoretical instruction with fieldwork and research tailored to national health priorities. Activities included outbreak investigations, disease modelling, and surveillance, supported by Africa CDC, Uganda’s Ministry of Health, and UK institutions. A REDCap-based survey was administered to 202 public health professionals across SSA to assess training needs, skill gaps, and barriers. Data were analysed using descriptive statistics and thematic analysis. Results: The programme trained 15 master‘s-level fellows, strengthening Uganda’s capacity in surveillance, early detection, and outbreak response. Survey results showed that 55.4% of professionals required further training, with skill gaps in zoonotic disease management (64.4%), outbreak preparedness (64.9%), and data management (59.4%). Key barriers included limited diagnostic capacity (73.8%) and weak collaboration (49.5%). Qualitative findings highlighted inconsistent mentorship, restricted data access, and limited funding for fieldwork. Respondents advocated for structured mentorship, longer training durations (≥3–6 months), and hybrid delivery models (42.3%). Conclusion: The IDEA Fellowship demonstrates a scalable model for infectious disease capacity building in SSA. Training African scientists in local contexts promotes relevance, retention, and cost-effectiveness. Regional expansion, cross-sector collaboration, and systemic investment are essential for sustainable epidemic preparedness and global health security. Keywords: field epidemiology, capacity building, infectious disease training, Sub-Saharan Africa
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    Comprehensive analysis of molecular markers linked to antimalarial drug resistance in Plasmodium falciparum in Northern, Northeastern and Eastern Uganda
    (Springer Nature, 2025) Olupot‑Olupot, Peter; Paasi, George; Katairo, Thomas; Alunyo, Patrick Jimmy; Nakiyemba, Alice; Ocen, Gilibrays Gilbert; Pande, Stephen; Alaroker, Florance; Okiror, William; Ocen, Emmaluel; Oula, Alex; Okalebo, Benard Charles; Ongodia, Paul; Amorut, Denis; Tukwasibwe, Stephen; Ndidde, Nabadda Susan; Sewanyana, Isaac; Nsobya, L. Samuel
    Background in Uganda, antimalarial resistance in Plasmodium falciparum poses serious public health and treatment challenges. Globally, recent data have highlighted the roles of following genes in malaria resistance: Plasmodium falciparum dihydrofolate reductase (Pfdhfr), Plasmodium falciparum dihydropteroate synthetase (Pfdhps), Plasmodium falciparum chloroquine resistance transporter (Pfcrt), Plasmodium falciparum multidrug resistance gene 1 (Pfmdr1), and Plasmodium falciparum K13 propeller domain (Pfk13). This study investigated the prevalence and characteristics of P. falciparum molecular markers linked to antimalarial resistance in Northern, Northeastern, and Eastern Uganda. Methods This cross-sectional study collected 200 dried blood samples from children (2 months to 12 years) in Northern, Eastern, and Northeastern Uganda. Samples were from malaria-positive cases confirmed by rapid diagnostic tests and microscopy. Genomic DNA was extracted from these samples and analysed using Molecular Inversion Probes to detect Plasmodium falciparum genetic mutations. The sequencing was performed on the Illumina MiSeq platform, and raw data was organized and analysed with MIPTools software. Results: The study sequenced over 50% of the samples at each site as follows: Apac 87.7% (43/49), Moroto 68.0% (34/50), Soroti 65.0% (13/20) and Mbale 53.1% (43/81). The Pfk13 A675V and C469Y mutations varied from 0 to 23.3% and 8.3–14.3%, in four sites, with consistently low prevalence in Apac. The Pfdhfr N51I and S108N mutations were fixed in all districts, while C59R was fixed in Moroto and nearing fixation (92–97%) in other regions. The emerging I164L mutation ranged from 1 to 10% in all sites. The Pfdhps A437G and K540E mutations were fixed in Soroti, with 3–5% wild-type prevalence in other sites. The A581G mutation showed 2.3% mixed genotypes in Mbale only. The Pfcrt K76T was predominantly wild type, except for 5% mutants in Mbale and Moroto. The pfmdr1 N86Y were wild type across all districts, except for 15% mixed genotypes in Soroti. Conclusion: This study reveal rising partial artemisinin resistance and widespread antifolate resistance surpassing WHO thresholds in Northern, Northeastern, and Eastern Uganda. Emerging super-resistant parasites pose a serious threat to malaria control, necessitating urgent enhanced surveillance and alternative treatment strategies. Keywords Antimalarial resistance, Uganda, Pfk13, Pfdhfr, Pfdhps Pfmdr1, Pfcrt
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    Hydroxyurea pharmacokinetics in children with sickle cell anemia across different global populations
    (PubMed Central, 2025) Power-Hays, Alexandra; McElhinney, E. Kathryn; Williams, N. Thomas; Mochamah, George; Olupot-Olupot, Peter; Paasi, George; Reid, E. Marvin; Rankine-Mullings, E. Angela; Opoka, O. Robert; John, C. Chandy; McGann, T. Patrick; Quinn, T. Charles; Punt, C. Nieko; Smart, R. Luke; Latham, S. Teresa; Vinks, A. Alexander; Ware, E. Russell
    Hydroxyurea provides effective disease-modifying treatment for people with sickle cell anemia (SCA), especially when escalated to maximum tolerated dose (MTD), which has wide interpatient dosing variability due to pharmacokinetic (PK) differences. Whether hydroxyurea PK parameters differ among children with SCA in different global regions is unknown. We compared hydroxyurea PK parameters among children with SCA from 5 clinical trials: HUSTLE (United States), TREAT (United States), NOHARM (Uganda), REACH (Uganda and Kenya), and EXTEND (Jamaica). Key hydroxyurea PK parameters were determined using HdxSim, a validated hydroxyurea PK software program. The results were compared across regions by analysis of variance. PK profiles from 451 children with SCA (146 from the United States, 265 from Africa, and 40 from the Caribbean) were included. Children from Africa had slightly lower volumes of distribution, but absorption rate and clearance were similar across regions. The PK-recommended doses to achieve MTD were statistically different but clinically similar across the United States (26.6 ± 5.9 mg/kg per day), Africa (27.6 ± 6.5 mg/kg per day), and the Caribbean (25.2 ± 4.7 mg/kg per day) (P = .04). In multivariable regression, younger age and increased reticulocyte counts were associated with higher PK-recommended doses. Hydroxyurea PK parameters in children with SCA differ minimally across global populations, predicting clinically similar doses to achieve MTD. Individualized hydroxyurea dosing based on a PKpopulation model derived from US children with SCA can be used broadly to maximize the benefits of this critical medication in other global populations. These trials were registered at www.ClinicalTrials.gov as #NCT00305175 (HUSTLE), #NCT02286154 (TREAT), #NCT01976416 (NOHARM), #NCT01966731 (REACH), and #NCT02556099 (EXTEND).
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    The Impact of Diagnostic Delays and Timeliness of Response on Ebola Disease outbreak-level case-fatality Ratios in Uganda (2000–2023) : a Rapid Systematic Review and meta-analysis
    (Springer, 2025) Paasi, George; Okware, Sam; Olupot-Olupot, Peter
    Background: Uganda has experienced seven laboratory-confirmed Ebola virus disease (EBOD) outbreaks from 2000 to 2022, with reported case‐fatality ratios (CFRs) varying widely. The influence of diagnostic and response delays on outbreak‐level mortality has not been systematically assessed. We conducted a rapid systematic review and meta-analysis to quantify the effect of diagnostic and response delays on outbreak-level mortality. Methods: We registered the review on OSF and adhered to PRISMA-2020 guidelines. We searched PubMed, Embase, Scopus, Web of Science, WHO Global Index Medicus, and grey literature through 30 April 2025. Eligible reports described laboratory-confirmed human EBOD in Uganda (2000–2022) and reported case counts, deaths, or quantitative timeliness metrics. Outbreak-level CFRs were meta-analyzed using random-effects models with Freeman–Tukey transformation (metafor package in R). Mixed-effects meta-regression assessed the association between continuous delay metrics and transformed CFR. Results: Fifteen reports met inclusion criteria, spanning 741 confirmed cases and 358 deaths. The pooled CFR was 45.4% (95% CI: 26.2%–65.2%; I² = 87.8%) across seven outbreaks. By species, Sudan ebolavirus outbreaks (n = 5) had a CFR of 44.6% (95% CI: 33.7%–55.6%), Bundibugyo ebolavirus (n = 1) 24.8% (95% CI: 18.2%–32.1%), and Zaire ebolavirus (n = 1) 100% (95% CI: 61.2%–100.0%). In meta-regression, each additional day from first case report to specimen collection was associated with a significant increase in CFR (β = 0.142 on the transformed scale; p = 0.025; R² = 62%), translating to an approximate absolute increase of 3.8% points in CFR per day at a baseline risk of 45%. Conversely, longer delays from symptom onset in the index case to national outbreak declaration were linked to a slight decrease in CFR (β = − 0.00765; p = 0.047). Conclusions Uganda’s EBOD outbreaks exhibit high and variable mortality, with diagnostic delays substantially amplifying case-fatality. Rapid specimen collection and prompt public health responses are critical to reducing EBOD mortality. Strengthening laboratory networks and accelerating declaration protocols should be central to future outbreak preparedness in Uganda and similar contexts. Keywords: Ebola virus disease • Case-fatality ratio • Uganda • Diagnostic timeliness • Outbreak response • Sudan ebolavirus (SUDV) • Bundibugyo ebolavirus (BDBV) • Zaire ebolavirus (EBOV) • Systematic review and meta‐analysis.