Acute gastroenteritis and enteric viruses in hospitalised children in southern Brazil: aetiology,seasonality and clinical outcomes

Viral acute gastroenteritis (AG) is a significant cause of hospitalisation in children younger than five years. Group A rotavirus (RVA) is responsible for 30% of these cases. Following the introduction of RVA immunisation in Brazil in 2006, a decreased circulation of this virus has been observed. However, AG remains an important cause of hospitalisation of paediatric patients and only limited data are available regarding the role of other enteric viruses in these cases. We conducted a prospective study of paediatric patients hospitalised for AG. Stool samples were collected to investigate human adenovirus (HAdV), RVA, norovirus (NoV) and astrovirus (AstV). NoV typing was performed by nucleotide sequencing and phylogenetic analysis. From the 225 samples tested, 60 (26%) were positive for at least one viral agent. HAdV, NoV, RVA and AstV were detected in 16%, 8%, 6% and 0% of the samples, respectively. Mixed infections were found in nine patients: HAdV/RVA (5), HAdV/NoV (3) and HAdV/NoV/RVA (1). The frequency of fever and lymphocytosis was significantly higher in virus-infected patients. Phylogenetic analysis of NoV indicated that all of these viruses belonged to genotype GII.4. The significant frequency of these pathogens in patients with AG highlights the need to routinely implement laboratory investigations.     

Interactions among vanadium,iron, and cystine in rats growth,blood parameters,and organ Wt/body Wt ratios

In three fully crossed, three-way, two-by-two-by-four experiments, male weanling Long-Evans rats were fed a basal diet supplemented with vanadium (ammonium metavanadate)-at 0 and 1 μg/g, cystine at 3.0 and 8.5 mg/g, and iron (ferric sulfate) at 0 (Expts. 1 and 2) or 5 (Expt. 3), 15, 100, and 500 μg/g. After 6 wk, a relationship between vanadium and iron that was influenced by dietary cystine was found. The interaction among vanadium, iron, and cystine was demonstrated best by the hematocrit and hemoglobin findings, which were similar. In all Expts., hematocrits were depressed in rats fed the two lower levels of iron. In Expts. 2 and 3, vanadium deprivation exacerbated the depression of hematocrits in rats fed 15 μg iron and 3.0 mg cystine/g diet. In Expt. 1, the effect was similar, but less marked. On the other hand, in Expts. 1 and 3 when supplemental cystine was 8.5 mg/g, vanadium deprivation did not exacerbate, but tended to alleviate the depression of hematocrits in rats fed 15 μg iron/g diet. When dietary iron was 15 μg/g in Expt. 2, the exacerbation of the depression of hematocrits by vanadium deprivation was much less in rats fed 8.5 rather than 3.0 mg cystine/g diet. Dietary vanadium had little effect on depressed hematopoiesis in severely iron-deficient rats. The findings indicated that vanadium neither substitutes for iron at some metabolic site, nor stimulates iron absorption; but has a positive influence on the utilization of iron after absorption.