Search

Group A rotavirus (RVA) is an important cause of diarrhea in people, especially children, and animals globally. Due to the segmented nature of the RVA genome, animal RVA strains have the potential to adapt to the human host through re‐assortment with other co‐infecting human viruses. Macaques share food and habitat with people, resulting in close interaction between these two species. This study aimed to detect and characterize RVA in rhesus macaques (Macaca mulatta) in Bangladesh. Fecal samples (N = 454) were collected from apparently healthy rhesus macaques from nine different sites in Bangladesh between February and March 2013. The samples were tested by one‐step, real‐time, reverse transcriptase polymerase chain reaction (PCR). Four percent of samples (N = 20; 95% CI 2.7%–6.7%) were positive for RVA. RVA positive samples were further characterized by nucleotide sequence analysis of two structural protein gene fragments, VP4 (P genotype), and VP7 (G genotype). G3, G10, P[3] and P[15] genotypes were identified and were associated as G3P[3], G3P[15] and G10P[15]. The phylogenetic relationship between macaque RVA strains from this study and previously reported human strains indicates possible transmission between humans and macaques in Bangladesh. To our knowledge this is the first report of detection and characterization of rotaviruses in rhesus macaques in Bangladesh. These data will not only aid in identifying viral sharing between macaques, human and other animals, but will also improve the development of mitigation measures for the prevention of future rotavirus outbreaks.

A new species, Eimeria mauritiensis (Apicomplexa: Eimeriidae) is reported from the pink pigeon, Nesoenas mayeri (Aves: Columbiformes) in Mauritius. Oocysts are sub-spherical 17.8 × 19.7 (16–19 × 18– 22) μm: Shape index (mean length / mean width) 1.1. A micropyle, oocyst residuum and polar granules are absent. Sporocysts are 6.6 × 12.0 (6–7 × 8–14) μm with Stieda and substieda bodies.Key words: Eimeria mauritiensis n.sp., pink pigeon, Nesoenas mayeri.

Biodiversity is of critical value to human societies, but recent evidence that bio-diversity may mitigate infectious-disease risk has sparked controversy among researchers. The majority of work on this topic has focused on direct assessments of the relationship between biodiversity and endemic-pathogen prevalence, without disentangling intervening mechanisms; thus study outcomes often differ, fuelling more debate. Here, we suggest two critical changes to the approach researchers take to understanding relationships between infectious disease, both endemic and emerging, and biodiversity that may help clarify sources of controversy. First, the distinct concepts of hazards versus risks need to be separated to determine how biodiversity and its drivers may act differently on each. This distinction is particularly important since it illustrates that disease emergence drivers in humans could be quite different to the general relationship between biodiversity and transmission of endemic pathogens. Second, the interactive relationship among biodiversity, anthropogenic change and zoonotic disease risk, including both direct and indirect effects, needs to be recognized and accounted for. By carefully disentangling these interactions between humans' activities and pathogen circulation in wildlife, we suggest that conservation efforts could mitigate disease risks and hazards in novel ways that complement more typical disease control efforts. This article is part of the themed issue 'Conservation, biodiversity and infectious disease: scientific evidence and policy implications'.