Bird mortality related to collisions with ski–lift cables: do we estimate just the tip of the iceberg?

Collisions with ski–lift cables are an important cause of death for grouse species living close to alpine ski resorts. As several biases may reduce the detection probability of bird carcasses, the mortality rates related to these collisions are generally underestimated. The possibility that injured birds may continue flying for some distance after striking cables represents a major source of error, known as crippling bias. Estimating the crippling losses resulting from birds dying far from the ski–lift corridors is difficult and it is usually assessed by systematic searches of carcasses on both sides of the ski–lifts. Using molecular tracking, we were able to demonstrate that a rock ptarmigan hen flew up to 600 m after striking a ski–lift cable, a distance preventing its detection by traditional carcasses surveys. Given the difficulty in conducting systematic searches over large areas surrounding the ski–lifts, only an experiment using radio–tagged birds would allow us to estimate the real mortality rate associated with cable collision

Pyrenean ptarmigans decline under climatic and human influences through the Holocene.

International audienceIn Europe, the Quaternary is characterized by climatic fluctuations known to have led to many cycles of contraction and expansion of species geographical ranges. In addition, during the Holocene, historical changes in human occupation such as colonization or abandonment of traditional land uses can also affect habitats. These climatically or anthropically induced geographic range changes are expected to produce considerable effective population size change, measurable in terms of genetic diversity and organization. The rock ptarmigan (Lagopus muta) is a small-bodied grouse occurring throughout Northern hemispheric arctic and alpine tundra. This species is not considered threatened at a continental scale, but the populations in the Pyrenees are of concern because of their small population size, geographical isolation and low genetic diversity. Here, we used 11 microsatellites to investigate genetic variations and differentiations and infer the overall demographic history of Pyrenean rock ptarmigan populations. The low genetic variability found in these populations has been previously thought to be the result of a bottleneck that occurred following the last glacial maximum (i.e., 10 000 years ago) or more recently (i.e., during the last 200 years). Our results clearly indicate a major bottleneck affecting the populations in the last tenth of the Holocene. We discuss how this decline can be explained by a combination of unfavorable and successive events that increased the degree of habitat fragmentation.Heredity advance online publication, 10 July 2013; doi:10.1038/hdy.2013.62

Introgressive hybridizations of Schistosoma haematobium by Schistosoma bovis at the origin of the first case report of schistosomiasis in Corsica (France, Europe)

International audienceThis study concerns the first urinary schistosomiasis case observed in Corsica (France, Europe) occurring in a 12-year-old German boy. The aim was to identify the relationship between this Schistosoma haematobium infection and other schistosomes of the Schistosoma group with terminal-spined ova. Morphological and molecular analyses were conducted on the ova. The results showed that the schistosome responsible for the emergence of schistosomiasis in Corsica was due to S. haematobium introgressed by genes from S. bovis

FREPs knock-down mediated by RNA interference.

<p>A. Cumulative expression [Log2FC (fold change) from the DESeq2 analysis] of FREP transcripts showed that FREPs were over-represented after the secondary challenge (DPC; 5.096 log2 fold change enrichment of FREPs transcripts). Green points corresponded to the differentially represented FREPs transcripts in each samples. Purple bars represent the cumulated Log2FC of FREP transcripts. At 4DPPI no FREP transcripts were differentially expressed, thus no value appeared in the graph. B. siRNA injection against FREP2, FREP3 & FREP4 was carried out and mRNA abundance was monitored during 4 days by Q-RT-PCR. Snails were injected with siRNAs against FREP 2, 3, and 4 or GFP (control), the relevant mRNA levels were assessed following normalization with respect to the S19 gene in siGFP injected snails versus siFREPs injected snails. Knock-down of the three FREPs tested was confirmed at 96h. C. Naïve <i>B</i>. <i>glabrata</i> and siFREP-injected snails were subjected to a typical priming experiment: Snails were infected with 10 miracidia of <i>S</i>. <i>mansoni</i> as a primo-infection, 21 days later they were injected with siGFP, or SiFREP or not treated and 4 days later they were infected with another 10 miracidia as a secondary challenge. FREP siRNA-injected snails show a significant proportion of non-primed snails (15%; *, binomial test, P < 0.05).</p

RNAseq analysis of the innate immune memory response of <i>B</i>. <i>glabrata</i> to <i>S</i>. <i>mansoni</i>.

<p>Heatmap showing differentially represented transcripts compared to naïve snails, as identified by DESeq2 analysis (p < 0.1). Color scale indicates the Log2FC ratio from under-represented (blue) to over-represented (red) transcripts. Transcripts were grouped into six clusters based on their expression patterns during the process of innate immune memory. Samples were recovered at 1DPPI, 4DPPI, 15DPPI and 25DPPI following primo-infection. Following secondary challenge samples were recovered at 1 day, 4 days and 15 days and pooled into DPC sample. Six clusters are identified: Cluster 1: transcripts over represented more than once all along infection and challenge. Cluster 2: transcripts exclusively over represented in single one condition. Cluster 3: transcripts exclusively over represented after immune challenge (DPC). Cluster 4: transcripts exclusively under represented after immune challenge (DPC). Cluster 5: transcripts exclusively under-represented in single one condition. Cluster 6: transcripts under represented more than once all along infection and challenge. FREP: Fibrinogen-related protein, HSP: Heat-shock protein, PGRP 1-like: Pathogenesis-related protein 1-like, LBP/BPI: lipopolysaccharide-binding protein/bactericidal/permeability-increasing protein, BgLBP/BPI: <i>Biomphalaria glabrata</i> LBP/BPI, TEP: thioester-containing protein.</p

Role of <i>B</i>. <i>glabrata</i> plasmatic factors in innate immune memory response.

<p>A. 2D gel electrophoresis of plasma proteins. One gel of each plasma sample analysed was shown. Spot numbers of qualitative and quantitative differences were indicated. Four plasma samples were analysed from naïve (uninfected snails), 15DPPI and 25DPPI (recovered at 15 and 25 days after primo-infection) and 15DPC (recovered at 15 days after secondary challenge). B. Heat-Map of the qualitative and quantitative ratio versus naïve sample. Ratios were calculated using PDQuest software between all differentially regulated spots. Blue to red scale indicate ratio values from lower to higher represented spots. Four clusters are identified: Cluster 1: higher-represented proteins exclusively following secondary challenge (15 DPC). Cluster 2: sustained response: higher-represented proteins after the primo-infection and secondary infection. Cluster 3: higher-represented proteins at 15DPPI and thereafter down regulated at 25DPPI and 15DPC. Cluster 4: lower-represented proteins. C. Plasma transfer and effect on prevalence of <i>S</i>. <i>mansoni</i> infection. Four conditions were tested: untreated snails (Control group, n = 48); saline injected snails (control of injection, n = 25); naïve-plasma injected snails (n = 22); and primed-plasma injected snails (n = 25). For all the experimental groups, 15 days following injection, snails were infected with 10 miracidia of SmBRE. * indicated significant differences (P< 0.05).</p

The immune response of <i>B</i>. <i>glabrata</i> to <i>S</i>. <i>mansoni</i> infection.

<p>The Brazilian strain of albino <i>B</i>. <i>glabrata</i> (BgBRE) is 100% susceptible (for 10 miracidia and upwards) to its corresponding strain of <i>S</i>. <i>mansoni</i> (SmBRE). When a snail is infected with 10 miracidia of <i>S</i>. <i>mansoni</i> within the same individual compatible and incompatible interactions occur, 3 to 4 miracidia develop normally in the snail’s tissues while the others are recognized and encapsulated by the snail’s cellular immune response. A. Six-day-old sporocyst in a compatible interaction. B. Encapsulated sporocyst 48 h after primary infection in an incompatible interaction. C. Six-day-old sporocyst in a primed snail. Primed BgBRE are 100% protected against a secondary challenge with SmBRE. Sporocysts from secondary challenge were neutralized by immune humoral factors.</p