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Background. Anaemia is common in sub-Saharan Africa, and parasitic infections could worsen its burden during pregnancy. Moreover, women become susceptible to malaria during pregnancy. We investigated Plasmodium falciparum (P. falciparum) and Schistosoma haematobium (S. haematobium) infections and determined their association with anaemia during pregnancy. Methods. A cross-sectional study involving 707 pregnant women attending antenatal care visits (ANC) and 446 at delivery was conducted in Battor and Adidome hospitals. Pregnant women were screened by microscopy and qPCR for P. falciparum and S. haematobium infections. Haemoglobin (Hb) levels were determined, and most participants received intermittent preventive treatment during pregnancy (IPTp) during ANC till delivery. Regression analyses were performed for associations between parasite infection and anaemia. Results. P. falciparum microscopy prevalence at ANC and delivery was 8% and 2%, respectively, and by PCR 24% at ANC and 12% at delivery. Anaemia prevalence at ANC was 52% and 49% at delivery. There was an increased risk of anaemia with P. falciparum infection (aOR = 1.92 ; p = 0.04). IPTp (p = 0.003) and age (p = 0.004) were associated with increased Hb levels at delivery. S. haematobium prevalence by microscopy was 4% at ANC and 2% at delivery. No significant correlation between S. haematobium and Hb levels was observed (coef. = − 0.62 g/dl; p = 0.07). Conclusion. High anaemia prevalence was observed during pregnancy, and P. falciparum infection was associated with anaemia at ANC. Low S. haematobium prevalence could be attributed to previous praziquantel treatment during mass drug administration. Routine diagnosis and treatment of S. haematobium infections in endemic areas could be initiated to reduce schistosomiasis during pregnancy. [ABSTRACT FROM AUTHOR]

Sepsis defined as a dysregulated immune response is a major cause of morbidity in children. In sub-Saharan Africa, the clinical features of sepsis overlap with other frequent infections such as malaria, thus sepsis is usually misdiagnosed in the absence of confirmatory tests. Therefore, it becomes necessary to identify biomarkers that can be used to distinguish sepsis from other infectious diseases. We measured and compared the plasma levels of 18 cytokines (Th1 [GM-CSF, IFN-γ, TNF-α, IL-1β, 1L-2, IL-6, IL-8, IL-12/IL-23p40, IL-15], Th2[IL-4, IL-5, IL-13), Th17 [IL17A], Regulatory cytokine (IL-10) and 7 chemokines (MCP-1/CCL2, MIP-1α/CCL3, MIP-1β/CCL4, RANTES/CCL5, Eotaxin/CCL11, MIG/CXCL9 and IP-10/CXCL10 using the Human Cytokine Magnetic 25-Plex Panel in plasma samples obtained from children with sepsis, clinical malaria and other febrile conditions. Children with sepsis had significantly higher levels of IL-1β, IL-12 and IL-17A compared to febrile controls but lower levels of MIP1-β/CCL4, RANTES/CCL5 and IP10/CXCL10 when compared to children with malaria and febrile controls. Even though levels of most inflammatory responses were higher in malaria compared to sepsis, children with sepsis had a higher pro-inflammatory to anti-inflammatory ratio which seemed to be mediated by mostly monocytes. A principal component analysis and a receiver operator characteristic curve analysis, identified seven potential biomarkers; IL-1β, IL-7, IL-12, IL-1RA, RANTES/CCL5, MIP1β/CCL4 and IP10/CXCL10 that could discriminate children with sepsis from clinical malaria and other febrile conditions. The data suggests that sepsis is associated with a higher pro-inflammatory environment. These pro-inflammatory cytokines/chemokines could further be evaluated for their diagnostic potential to differentiate sepsis from malaria and other febrile conditions in areas burdened with infectious diseases. [ABSTRACT FROM AUTHOR]

Background: Schistosomiasis remains a major public health issue with over 90% of the prevalence rates recorded in Sub-Saharan Africa. In this study, the relationships between different interleukin gene polymorphisms (IL-13-591A/G, IL-13-1055C/T, IL-13-1258A/G) and Schistosoma haematobium infection levels were evaluated; as well as the host plasma antibodies and cytokine profiles associated with schistosomiasis infection. Methodology: A total of 469 school children aged 6 to 19 years from four schistosomiasis-endemic communities in Ghana were involved. Single urine and stool samples were obtained from each pupil, processed via sedimentation and Kato-Katz, and examined via microscopy for Schistosoma and soil-transmitted helminth (STH) eggs. Next, venous blood samples were drawn from 350 healthy pupils, and used to measure antibody and plasma cytokine levels by ELISA. Single nucleotide polymorphisms in the IL-13 gene were genotyped on 71 selected blood samples using the Mass Array technique. Principal findings and conclusion: The overall prevalence of urinary schistosomiasis was 21.11%. Community-level prevalences were 17.12%, 32.11%, 20.80%, and 15.32% for Asempaneye, Barikumah, Eyan Akotoguah, and Apewosika respectively. Generally, higher S. haematobium infection prevalence and intensity were recorded for participants with genotypes bearing the IL13-1055C allele, the IL13-591A, and the IL13-1258A alleles. Also, higher S. haematobium infection prevalence was observed among participants in the 12-14-year age group with the IL13-1055C, IL13-591A, and IL13-1258A alleles. Interestingly, higher STH prevalence was also observed among participants with the IL13-1055C, IL13-591A, and IL13-1258A alleles. Furthermore, the age-associated trends of measured antibodies and cytokines of S. haematobium-infected school-children depicted a more pro-inflammatory immune profile for pupils aged up to 1l years, and an increasingly anti-inflammatory profile for pupils aged 12 years and above. This work provides insight into the influence of IL-13 gene polymorphisms on S. haematobium, and STH infections, in school-aged children (SAC). Author summary: Schistosomiasis is a neglected tropical disease with an estimated morbidity of 2.54 million disability-adjusted life years (DALYS), ranking it third among the parasitic diseases after Malaria and Dengue fever (WHO, 2018). About a decade ago, the World Health Organization (WHO) and its partners committed to intensifying efforts at increasing coverage during annual mass chemotherapy programmes in affected countries. This has influenced the reduction of the estimated disease-associated morbidity from 4.5 million DALYs in 2002 (WHO, 2002) to the current rate. Despite these gains, there is still growing concern that the persistent and extensive use of Praziquantel (PZQ) (the only approved chemotherapeutic agent) in these campaigns may lead to the development of poorly-responding phenotypes of Schistosoma sp. Strategies therefore to mitigate such possibilities may prove very advantageous, while research efforts towards the development of an effective vaccine continues. There has been growing evidence in recent years that infection of inhabitants in endemic areas may be influenced not only by environmental, but also by genetic factors as well. Of particular interest in this regard, is the region in the human genome, 5q31-q33, which bears several genes associated with immune function. One such group within this region is the T-helper 2 (Th2) cluster of genes, which are responsible for the production interleukin-4 (IL-4), IL-5, and IL-13 during immune response. We focused on single-nucleotide polymorphisms (SNPs) occurring in the IL-13 promoter region, particularly IL13-1055C/T, IL13-591A/G, and IL13-1258A/G, where we observed interesting trends with regard to participants' infection status in association with the polymorphisms they presented with. Also, we assessed their immune profiles after stratifying by age, and herein indicate trends which reflect observed age-associated trends between S. haematobium infection and the IL-13 polymorphisms. The outcomes presented indicate a need for further work which challenges the current 'one size fits all' strategy in mass chemotherapy programmes and advocates for participant-specific/sub-group tailored programmes. This is more likely to minimize the likelihood for the development of resistant Schistosoma strains to PZQ. [ABSTRACT FROM AUTHOR]

Background: Cerebral malaria (CM) is responsible for most of the malaria-related deaths in children in sub-Saharan Africa. Although, not well understood, the pathogenesis of CM involves parasite and host factors which contribute to parasite sequestration through cytoadherence to the vascular endothelium. Cytoadherence to brain microvasculature is believed to involve host endothelial receptor, CD54 or intercellular adhesion molecule (ICAM)-1, while other receptors such as CD36 are generally involved in cytoadherence of parasites in other organs. We therefore investigated the contributions of host ICAM-1 expression and levels of antibodies against ICAM-1 binding variant surface antigen (VSA) on parasites to the development of CM. Methodology/Principal Findings: Paediatric malaria patients, 0.5 to 13 years were recruited and grouped into CM and uncomplicated malaria (UM) patients, based on well defined criteria. Standardized ELISA protocol was used to measure soluble ICAM-1 (sICAM-1) levels from acute plasma samples. Levels of IgG to CD36- or ICAM-1-binding VSA were measured by flow cytometry during acute and convalescent states. Wilcoxon sign rank-test analysis to compare groups revealed association between sICAM-1 levels and CM (p<0.0037). Median levels of antibodies to CD36-binding VSA were comparable in the two groups at the time of admission and 7 days after treatment was initiated (p>0.05). Median levels of antibodies to CD36-binding VSAs were also comparable between acute and convalescent samples within any patient group. Median levels of antibodies to ICAM-1-binding VSAs were however significantly lower at admission time than during recovery in both groups. Conclusions/Significance: High levels of sICAM-1 were associated with CM, and the sICAM-1 levels may reflect expression levels of the membrane bound form. Anti-VSA antibody levels to ICAM-binding parasites was more strongly associated with both UM and CM than antibodies to CD36 binding parasites. Thus, increasing host sICAM-1 levels were associated with CM whilst antibodies to parasite expressing non-ICAM-1-binding VSAs were not. [ABSTRACT FROM AUTHOR]