Schistosoma haematobium in Guinea-Bissau: unacknowledged morbidity due to a particularly neglected parasite in a particularly neglected country

Schistosomiasis is the major neglected tropical helminthic disease worldwide. Current knowledge on the epidemiology of schistosomiasis in Guinea-Bissau is scarce and regarding to the absence of Schistosoma haematobium (S.h.). Therefore, a pilot study was undertaken to assess the prevalence and morbidity due to S.h. infection in randomly selected 90 children and adolescents aged 6 to 15 years. Prevalence of S.h. infection was 20.00 % (18/90). Microhematuria was observed in 61.11 % (11/18) of S.h.-egg-excreting vs. 37.50 % (27/72) of non-S.h.-egg-excreting children p ≤ 0.01. Body mass index (BMI) was less than 15 kg/m(2) in 52/90 (57.78 %) of all children and adolescents, but this proportion increased to 66.67 % (12/18) in S.h.-infected children who were more frequently stunted and wasted than in non-infected children. The mean weight-for-age Z score (WAZ) was reduced in S.h. infected as compared to non-infected children (-1.48 ± 1.08 SD vs. -0.80 ± 1.11 SD; p ≤ 0.01). To our knowledge, this is the first epidemiologic report on S. haematobium infection in Guinea-Bissau since 22 years. Even in this relatively small study sample, it appears that S. haematobium, besides the well-known symptoms such as hematuria, leads to significant, albeit commonly unacknowledged morbidity such as stunting and wasting. These observations underscore the notion that this vulnerable but neglected population urgently needs to be targeted for implementation of measures for treatment and control.

DNA Damage and Oxidative DNA Damage in Inflammatory Bowel Disease

Background and aims: Inflammation has long been regarded as a major contributor to cellular oxidative damage and to be involved in the promotion of carcinogenesis. Methods: We aimed to investigate the oxidative damage in inflammatory bowel disease [IBD] patients through a case–control and prospective study involving 344 IBD patients and 294 healthy controls. DNA damage and oxidative DNA damage were measured by comet assay techniques, and oxidative stress by plasmatic lipid peroxidation, protein carbonyls, and total antioxidant capacity. Results: Higher DNA damage [p < 0.001] was found both in Crohn’s disease [CD] (9.7 arbitrary units [AU]; interquartile range [IQR]: 6.2–14.0) and ulcerative colitis [UC] [7.1 AU; IQR: 4.4–11.7], when compared with controls [5.4 AU; IQR: 3.8–6.8], and this was also the case with oxidative DNA damage [p < 0.001] [CD: 3.6 AU; IQR: 1.8–6.8; UC: 4.6 AU; IQR: 2.4–8.1], when compared with controls: 2.3 AU; IQR: 1.2–4.2]. Stratifying patients into groups according to therapy (5-aminosalicylic acid [5-ASA], azathioprine, anti-TNF, and combined therapy [azathioprine and anti-TNF]) revealed significant between-group differences in the level of DNA damage, both in CD and UC, with the combined therapy exhibiting the highest DNA damage levels [11.6 AU; IQR: 9.5–14.3, and 12.4 AU; IQR: 10.6–15.0, respectively]. Among CD patients, disease behaviour [B1 and B2], and age at diagnosis over 40 years [A3] stand as risk factors for DNA damage. For UC patients, the risk factors found for DNA damage were disease activity, treatment, age at diagnosis under 40 years [A1 + A2] and disease locations [E2 and E3]. Conclusions: In IBD there is an increase in DNA damage, and treatment, age at diagnosis and inflammatory burden seem to be risk factors.