Human African trypanosomiasis due to Trypanosoma brucei rhodesiense is invariably fatal if untreated with up to 12.3 million people at a risk of developing the disease in Sub-Saharan Africa. The disease is characterized by a wide spectrum of clinical presentation coupled with differences in disease progression and severity. While the factors determining this varied response have not been clearly characterized, inflammatory cytokines have been partially implicated as key players. In this review, we consolidate available literature on the role of specific cytokines in the pathogenesis of T. b. rhodesiense sleeping sickness and further discuss their potential as stage biomarkers. Such information would guide upcoming research on the immunology of sleeping sickness and further assist in the selection and evaluation of cytokines as disease stage or diagnostic biomarkers.

We carried out a baseline survey of cattle in Kaberamaido district, in the context of controlling the domestic animal reservoir of Trypanosoma brucei rhodesiense human African trypanosomiasis (rHAT) towards elimination. Cattle blood was subjected to capillary tube centrifugation followed by measurement of the packed cell volume (PCV) and examination of the buffy coat area for motile trypanosomes. Trypanosomes were detected in 561 (21.4%) out of 2621 cattle screened by microscopy. These 561 in addition to 724 apparently trypanosome negative samples with low PCVs (≤25%) were transported to the laboratory and tested by PCR targeting the trypanosomal Internal Transcribed Spacer (ITS-1) as well as suspect Tick-Borne Diseases (TBDs) including Anaplasmamosis, Babesiosis, and Theileriosis. PCR for Anaplasma sp yielded the highest number of positive animals (45.2%), followed by Trypanosoma sp (44%), Theileria sp (42.4%) and Babesia (26.3%); multiple infections were a common occurrence. Interestingly, 373 (29%) of these cattle with low PCVs were negative by PCR, pointing to other possible causes of aneamia, such as helminthiasis. Among the trypanosome infections classified as T. brucei by ITS-PCR, 5.5% were positive by SRA PCR, and were, therefore, confirmed as T. b. rhodesiense. Efforts against HAT should therefore consider packages that address a range of conditions. This may enhance acceptability and participation of livestock keepers in programs to eliminate this important but neglected tropical disease. In addition, we demonstrated that cattle remain an eminent reservoir for T. b. rhodesiense in eastern Uganda, which must be addressed to sustain HAT elimination.

Pseudocercospora angolensis is the causative agent of Pseudocercospora leaf and fruit spot disease in citrus which can result in up to 100% yield loss. Early diagnosis of this disease is vital for effective control. This study aimed at developing a loop-mediated amplification (LAMP) system for detecting P. angolensis in sweet oranges in comparison with Polymerase Chain Reaction (PCR) and using microscopy as a gold standard. Twelve non-target species were used to assess the analytical specificity of LAMP and PCR whereas the analytical sensitivity was determined using serial dilutions of P. angolensis DNA. The diagnostic accuracies of the two assays were evaluated using DNA from 150 diseased and 50 non-diseased sweet orange leaf samples. The analytical sensitivity and detection time of LAMP were of 10 ⁻⁴ ng/ μl and 40 minutes, respectively. The analytical sensitivity of PCR was 10ng/μl and it was specific to P. angolensis whereas three relatives of P. angolensis were detectable by LAMP. The diagnostic sensitivities of LAMP (93%) and microscopy (100%) were significantly different ( X ² = 8.38, P = 0.0038) unlike the diagnostic specificities (90%) and (100%), respectively ( X ² = 3.37, P = 0.066). Microscopy was significantly more sensitive than PCR (32.6%) ( X ² = 149.26, P < 2.2e-16) and equally specific as PCR ( P =NA). The positive predictive values of PCR and LAMP were 100% and 96.5% respectively whereas the negative predictive values were 33.1% and 81.8% respectively. The LAMP assay developed in this study offers a great tool for routine screening sweet orange samples for P. angolensis .

Human African trypanosomiasis (HAT) due to Trypanosoma brucei rhodesiense in East and southern Africa is reported to be clinically diverse. We tested the hypothesis that this clinical diversity is associated with a variation in trypanosome genotypes. Trypanosome DNA isolated from HAT patients was genotyped using 7 microsatellite markers directly from blood spotted FTA cards following a whole genome amplification. All markers were polymorphic and identified 17 multi-locus genotypes with 56% of the isolates having replicate genotypes. We did not observe any significant clustering between isolates and bootstrap values across major tree nodes were insignificant. When genotypes were compared among patients with varying clinical presentation or outcome, replicate genotypes were observed at both extremes showing no significant association between genetic diversity and clinical outcome. Our study shows that T. b. rhodesiense isolates are homogeneous within a focus and that observed clinical diversity may not be associated with parasite genetic diversity. Other factors like host genetics and environmental factors might be involved in determining clinical diversity. Our study may be important in designing appropriate control measures that target the parasite.

This study aimed to develop a safe bio-control approach for therapy and decontamination of Aeromonas hydrophila. The study focused on determination of the drug susceptibility ofAeromonas isolates from diseased tilapia; and establishment of a stock of partially characterized Aeromonas hydrophila bacteriophages. Eighteen (18) Aeromonas spp isolates were tested for antimicrobial resistance against 10 antibiotics. The susceptibility of the isolates to various antibiotics ranged from 0 to 100%. For bacteriophages, three lytic phages that had the highest host range (78.6% to 92.8%, n=28) were selected. Further characterization revealed a burst period of 20 ± 5 to 40 ± 5 minutes, a latent period that varied from 10 ± 5 to 40 ± 5 minutes; and burst size of 98–171 virions per infected cell. There were no significant changes in phage titers on exposure at 40℃ and 50℃ for 60 minutes (P = 0.05). However, a gradual decrease in the titres was observed at 60℃ while a fast decline was noted at 70℃-90℃. All phages demonstrated at least some activity in the pH range of 1-13. In water stability testing, the phages survived up to 22 days of the experiment, with a sharp decrease of 1 log PFU/mL to have been encountered within the first day. The findings of this study suggest phages as bio-control agents against Aeromonas infection in fish. However, further genomic characterization is required.