Browsing by Author "Magambo, Phillip K."

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    Genome Sequences of Bacteriophages UPEC01, UPEC03, UPEC06, and UPEC07 Infecting Avian Pathogenic Escherichia coli
    (Microbiology Resource Announcements, 2022) Kazibwe, George; Ndekezi, Christian; Alinaitwe, Ruth; Alafi, Stephen; Nanteza, Ann; Magambo, Phillip K.; Nakavuma, Jesca L.
    Here, we present the genome sequences of four bacteriophages that infect avian pathogenic Escherichia coli. The phages were isolated from raw sewage in Kampala, Uganda. The genome sizes of the phages ranged between 143,140 bp and 178,307 bp, with an average G1C content of 41.25%. Phages infecting avian pathogenic Escherichia coli (APEC) have the potential to be applied as phage therapy in the management of avian colibacillosis, a devastating disease that is responsible for significant economic losses in the poultry industry (1). The emergence of multidrug-resistant pathogenic E. coli strains has sparked interest in the search for alternative control measures for bacterial pathogens, including, among others, the use of phages (2). In this study, whole-genome sequencing of bacteriophages was carried out to determine the genetic characteristics and the taxonomic identification or classification of these phages as part of a larger study aimed at identifying and establishing phage stocks that can be used to supplement the use of antibiotics in managing avian colibacillosis in Uganda. The bacteriophages in this study were isolated from sewage at the National Water and Sewerage Corporation treatment plant (Kampala, Uganda). Several E. coli field isolates (Table 1) obtained from chicken droppings were used as isolation hosts for the phages following previously described methods (3). Briefly, 10 mL of raw sewage was centrifuged (10,000 g for 10 min) to obtain a supernatant, which was added to 10 mL of 2 tryptic soy broth (TSB) containing 100 mL of overnight E. coli broth culture. The mixture was incubated (30°C for 48 h at 120 rpm) and centrifuged (7,000 rpm for 5 min at 4°C), and the supernatant was filtered (0.45mm). The phage lysate obtained was plaque purified three times to produce a uniform phage stock. The isolated phages that could infect the APEC isolates from chickens that had died from colibacillosis were selected (4). Genomic DNA was extracted from the phages using 2% SDS and purified using a Qiagen Genomic-tip 100/G kit according to the manufacturer’s instructions.
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    No evidence for association between APOL1 kidney disease risk alleles and Human African Trypanosomiasis in two Ugandan populations
    (PLoS neglected tropical diseases, 2018) Magambo, Phillip K.; Noyes, Harry; Mulindwa, Julius; Enyaru, John; Alibu, Vincent P.; Sidibe, Issa; Mumba Ngoyi, Dieuodonne; Hertz-Fowler, Christiane; MacLeod, Annette; Tastan Bishop, Ozlem; Matovu, Enock
    Human African trypanosomiasis (HAT) manifests as an acute form caused by Trypanosoma brucei rhodesiense (Tbr) and a chronic form caused by Trypanosoma brucei gambiense (Tbg). Previous studies have suggested a host genetic role in infection outcomes, particularly for APOL1. We have undertaken candidate gene association studies (CGAS) in a Ugandan Tbr and a Tbg HAT endemic area, to determine whether polymorphisms in IL10, IL8, IL4, HLAG, TNFA, TNX4LB, IL6, IFNG, MIF, APOL1, HLAA, IL1B, IL4R, IL12B, IL12R, HP, HPR, and CFH have a role in HAT. Methodology and results We included 238 and 202 participants from the Busoga Tbr and Northwest Uganda Tbg endemic areas respectively. Single Nucleotide Polymorphism (SNP) genotype data were analysed in the CGAS. The study was powered to find odds ratios > 2 but association testing of the SNPs with HAT yielded no positive associations i.e. none significant after correction for multiple testing. However there was strong evidence for no association with Tbr HAT and APOL1 G2 of the size previously reported in the Kabermaido district of Uganda. Conclusions/Significance A recent study in the Soroti and Kaberamaido focus in Central Uganda found that the APOL1 G2 allele was strongly associated with protection against Tbr HAT (odds ratio = 0.2, 95% CI: 0.07 to 0.48, p = 0.0001). However, in our study no effect of G2 on Tbr HAT was