Coral bleaching: the winners and the losers

Sea surface temperatures were warmer throughout 1998 at Sesoko Island, Japan, than in the 10 preceding years. Temperatures peaked at 2.8 °C above average, resulting in extensive coral bleaching and subsequent coral mortality. Using random quadrat surveys, we quantitatively documented the coral community structure one year before and one year after the bleaching event. The 1998 bleaching event reduced coral species richness by 61% and reduced coral cover by 85%. Colony morphology affected bleaching vulnerability and subsequent coral mortality. Finely branched corals were most susceptible, while massive and encrusting colonies survived. Most heavily impacted were the branched Acropora and pocilloporid corals, some of which showed local extinction. We suggest two hypotheses whose synergistic effect may partially explain observed mortality patterns (i.e. preferential survival of thick-tissued species, and shape-dependent differences in colony mass-transfer efficiency). A community-structural shift occurred on Okinawan reefs, resulting in an increase in the relative abundance of massive and encrusting coral species.     

Sequestration: causes and consequences

Adhesion of Plasmodium falciparum-infected erythrocytes to endothelial cells and to syncytiotrophoblasts lining the placenta is a key feature of malaria pathogenesis. P. falciparum erythrocyte membrane protein 1, a family of variable proteins, mediates adhesion to CD36 and intercellular adhesion molecule 1 in the systemic vasculature, and to chondroitin sulphate A and hyaluronic acid in the placenta. Recent studies of the pathology of fatal cerebral malaria and of placental malaria that follow such sequestration suggest that coagulation disturbances may have a greater role in pathogenesis than previously realized, and that monocyte infiltrates in response to malaria may initiate some of these changes. Chemokines such as macrophage inflammatory protein 1 alpha and beta and monocyte chemoattractant protein 1 may play a key role in attracting monocytes to the placenta and other organs, but the stimulus to chemokine secretion is not presently known.     

Genotyping errors: causes, consequences and solutions

Although genotyping errors affect most data and can markedly influence the biological conclusions of a study, they are too often neglected. Errors have various causes, but their occurrence and effect can be limited by considering these causes in the production and analysis of the data. Procedures that have been developed for dealing with errors in linkage studies, forensic analyses and non-invasive genotyping should be applied more broadly to any genetic study. We propose a protocol for estimating error rates and recommend that these measures be systemically reported to attest the reliability of published genotyping studies.     

Changing distributions of ticks: causes and consequences

Today, we are witnessing changes in the spatial distribution and abundance of many species, including ticks and their associated pathogens. Evidence that these changes are primarily due to climate change, habitat modifications, and the globalisation of human activities are accumulating. Changes in the distribution of ticks and their invasion into new regions can have numerous consequences including modifications in their ecological characteristics and those of endemic species, impacts on the dynamics of local host populations and the emergence of human and livestock disease. Here, we review the principal causes for distributional shifts in tick populations and their consequences in terms of the ecological attributes of the species in question (i.e. phenotypic and genetic responses), pathogen transmission and disease epidemiology. We also describe different methodological approaches currently used to assess and predict such changes and their consequences. We finish with a discussion of new research avenues to develop in order to improve our understanding of these host–vector–pathogen interactions in the context of a changing world.