BackgroundAfter a long period of neglect, initiatives are being implemented in Sudan to control tsetse and trypanosomosis. Their planning, execution and monitoring require reliable information on the geographic distribution of the disease and its vectors. However, geo-referenced and harmonized data at the national level are lacking, despite the fact that a number of epidemiological studies were conducted over the years. The Atlas of tsetse and bovine trypanosomosis in Sudan tries to fill this gap.MethodsThe present study includes both a review of historical datasets on tsetse flies and bovine trypanosomosis, as well as the results of recent, targeted field investigations. The review includes both published and unpublished datasets collected in Sudan from 1960 onwards. Targeted field investigations were conducted for trypanosomosis in Blue Nile (2011) and Gezeira States (2012), for tsetse flies in South Darfur (2012) and Blue Nile States (2009 and 2011), and for other trypanosomosis vectors in seven States (Khartoum, Gezeira, White Nile, Blue Nile, North Kordofan, Kassala and Gadarif). The latter surveys, conducted from 2010 to 2012, also enabled us to confirm the absence of tsetse flies in a number of locations.ResultsTsetse fly infestation in Sudan appears to be limited to two relatively small areas at the south-western and south-eastern tips of the Country (South Darfur and Blue Nile State respectively). Glossina morsitans submorsitans is present in both areas, whilst G. fuscipes fuscipes is found only in the latter. In contrast, bovine trypanosomosis is widespread, its presence having being confirmed in eleven States and suspected in all the others. Both mechanical transmission by non-cyclical vectors and animal movement contribute to this broad distribution of trypanosomosis. This is especially the case for Trypanosoma vivax, which was found even in sedentary cattle at hundreds of kilometres of the tsetse belt.ConclusionsThe Atlas provides a spatially-explicit synthesis of the current knowledge of tsetse and bovine trypanosomosis in Sudan. Its various epidemiological outputs are being used to target both trypanosomosis control activities and further data collection exercises. Activities are ongoing to expand the Atlas to non-cyclical vectors and hosts other than cattle.Electronic supplementary materialThe online version of this article (doi:10.1186/s13071-016-1485-6) contains supplementary material, which is available to authorized users.

Paraoxonase-1 (PON1) is a HDL-bound antioxidant enzyme that protects LDL from oxidative modification. Discovery of the antioxidant properties of PON1 led to extensive research on its role in the initiation and progression of atherosclerosis. The Q192R (rs662; A/G) polymorphism, which results in the glutamine to arginine substitution at position 192, of the PON1 gene has been linked to increased atherosclerosis risk in several but not all population studies. Besides genetic factors, environmental variables and ethnicity have been implicated as factors responsible for the ambiguity in relating the PON1 gene with atherosclerotic risk. Here, we tested the association of the Q192R polymorphism with coronary artery disease (CAD) in Saudi ethnic subjects taking environmental factors into consideration. The genomic DNA samples from 121 angiographically confirmed CAD cases and 108 normal healthy control subjects were genotyped by PCR-RFLP analysis. The distribution of QQ, QR, and RR genotypes was significantly different between cases and controls (p < 0.005). The RR genotype was associated with CAD risk independently of several established risk factors including age, gender, smoking, obesity, and diabetes (OR 2.2, 1.4-7.4, p < 0.01). Genotype-based stratification of demographic and biochemical data revealed that the RR genotype has proatherogenic properties. This study, thus, identifies the Q192R polymorphism as an additional risk factor for CAD in the Saudi population and suggests that it may have prognostic value. The negative effect of this genetic variant is presumably due to the diminished ability of the RR variant genotype of PON1 to blunt LDL oxidation.

BackgroundThis study was conducted in response to recurring reports from eastern Sudan of camel trypanosomosis that can no longer be treated by currently available trypanocidal drugs. One hundred and eighty-nine blood samples were obtained from camels in different herds and local markets in the western part of Sudan, and a cross-sectional study was carried out between December 2015 and February 2016 to identify the causative agents and possible circulating genotypes.ResultsThe prevalence of trypanosomes detected using the conventional parasitological techniques of Giemsa-stained blood smears, wet blood smears and the microhematocrit centrifugation technique (MHCT) was 7% (13/189), 11% (21/189) and 19% (36/189), respectively. However, a multi-species KIN-PCR targeting the ITS region revealed that the prevalence of Trypanosoma evansi was 37% (70/189), while that of T. vivax was 25% (47/189). Consequently, we used a T. evansi-specific PCR (RoTat1.2 VSG gene) to analyse the KIN-PCR-positive samples and a T. vivax-specific PCR (Cathepsin L-like gene) to analyse all of the samples. The prevalence of T. evansi was 59% (41/70), while the prevalence of T. vivax was 31% (59/189). Mixed infections were detected in 18% (34/189) of the samples. These results were further confirmed by sequencing and a phylogenetic analysis of the complete internal transcribed spacer (ITS) region of T. evansi and the TviCatL gene of T. vivax.ConclusionWe conclude that T. vivax was newly introduced to the camel population and that T. evansi is no longer the single cause of camel trypanosomosis in Sudan. The presence of T. vivax in camels detected in this study is a challenge in the choice of diagnostic approaches, particularly serology, and PCRs. However, an analysis of drug resistance should be performed, and the genotypic variation should be verified. To our knowledge, this is the first molecular study on T. vivax and mixed-infection with T. vivax and T. evansi in Sudanese camels.Electronic supplementary materialThe online version of this article (doi:10.1186/s13071-017-2117-5) contains supplementary material, which is available to authorized users.

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BackgroundAltered regulation of the complement system is associated with multiple kidney diseases. CD35, CD55 and CD59 regulate the complement system, and changes in their expression have previously been linked with kidney disease. This study assessed whether changes in the expression levels of these proteins are associated specifically with chronic kidney disease (CKD) to understand its pathogenesis.Materials and methodsSixty CKD patients and 60 age-matched controls were enrolled and divided into two groups: Group I (n=30 pediatric patients and n=30 controls) and Group II (n=30 adult patients and n=30 controls). The expression of CD35, CD55 and CD59 on peripheral blood cells was evaluated by flow cytometry as the proportion of positive cells expressing the marker and mean fluorescence intensity (MFI), also the relation of these markers to the stage of CKD was also evaluated.ResultsPediatric and adult CKD patients had significantly lower proportion of erythrocytes expressing CD35, CD55 and CD59 than healthy controls (P<0.001). In pediatric CKD patients, there was no significant difference in the three studied markers on neutrophils, lymphocytes and monocytes. The changes in expression of CD35, CD55 and CD59 on leukocytes were more pronounced in adult patients, who had lower proportion of CD59-positive neutrophils, CD35- and CD59-positive lymphocytes, and CD59-positive monocytes, as well as lower expression of CD59 on neutrophils and monocytes than adult controls (P<0.001, P=0.019, P<0.001, P=0.026, P<0.001 and P=0.003, respectively). The eGFR directly correlated with the proportion of positivity of some of those markers on peripheral leukocytes while there was inverse correlation between the disease stage and the same markers.ConclusionThere are alterations in the patterns of expression of complement regulatory proteins CD35, CD55 and CD59 on peripheral blood cells of patients with CKD compared with healthy controls.