The Experts below are selected from a list of 20679 Experts worldwide ranked by ideXlab platform
Bernard Vigues - One of the best experts on this subject based on the ideXlab platform.
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Transcriptome analyses of the Honeybee response to Nosema ceranae and insecticides.
PLoS ONE, 2014Co-Authors: Julie Aufauvre, Bernard Vigues, Catherine Texier, Frédéric Delbac, Barbara Misme-aucouturier, Nicolas BlotAbstract:Honeybees (Apis mellifera) are constantly exposed to a wide variety of environmental stressors such as parasites and pesticides. Among them, Nosema ceranae and neurotoxic insecticides might act in combination and lead to a higher Honeybee mortality. We investigated the molecular response of Honeybees exposed to N. ceranae, to insecticides (fipronil or imidacloprid), and to a combination of both stressors. Midgut transcriptional changes induced by these stressors were measured in two independent experiments combining a global RNA-Seq transcriptomic approach with the screening of the expression of selected genes by quantitative RT-PCR. Although N. ceranae-insecticide combinations induced a significant increase in Honeybee mortality, we observed that they did not lead to a synergistic effect. According to gene expression profiles, chronic exposure to insecticides had no significant impact on detoxifying genes but repressed the expression of immunity-related genes. Honeybees treated with N. ceranae, alone or in combination with an insecticide, showed a strong alteration of midgut immunity together with modifications affecting cuticle coatings and trehalose metabolism. An increasing impact of treatments on gene expression profiles with time was identified suggesting an absence of stress recovery which could be linked to the higher mortality rates observed.
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Exposure to Sublethal Doses of Fipronil and Thiacloprid Highly Increases Mortality of Honeybees Previously Infected by Nosema ceranae
2013Co-Authors: Cyril Vidau, Julie Aufauvre, Regis Fontbonne, Bernard Vigues, Marie Diogon, Catherine Texier, David G. Biron, Nicolas Blot, Hicham El Alaoui, Luc P. BelzuncesAbstract:Background: The Honeybee, Apis mellifera, is undergoing a worldwide decline whose origin is still in debate. Studies performed for twenty years suggest that this decline may involve both infectious diseases and exposure to pesticides. Joint action of pathogens and chemicals are known to threaten several organisms but the combined effects of these stressors were poorly investigated in Honeybees. Our study was designed to explore the effect of Nosema ceranae infection on Honeybee sensitivity to sublethal doses of the insecticides fipronil and thiacloprid. Methodology/Finding: Five days after their emergence, Honeybees were divided in 6 experimental groups: (i) uninfected controls, (ii) infected with N. ceranae, (iii) uninfected and exposed to fipronil, (iv) uninfected and exposed to thiacloprid, (v) infected with N. ceranae and exposed 10 days post-infection (p.i.) to fipronil, and (vi) infected with N. ceranae and exposed 10 days p.i. to thiacloprid. Honeybee mortality and insecticide consumption were analyzed daily and the intestinal spore content was evaluated 20 days after infection. A significant increase in Honeybee mortality was observed when N. ceranaeinfected Honeybees were exposed to sublethal doses of insecticides. Surprisingly, exposures to fipronil and thiacloprid had opposite effects on microsporidian spore production. Analysis of the Honeybee detoxification system 10 days p.i. showed that N. ceranae infection induced an increase in glutathione-S-transferase activity in midgut and fat body but not in 7-ethoxycoumarin-O-deethylase activity
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Parasite-insecticide interactions: a case study of Nosema ceranae and fipronil synergy on Honeybee.
Sci Rep, 2012Co-Authors: Julie Aufauvre, Regis Fontbonne, Bernard Vigues, Cyril Vidau, Marie Diogon, Luc P. Belzunces, Frédéric Delbac, David Georges Biron, Mathieu Roudel, Nicolas BlotAbstract:In ecosystems, a variety of biological, chemical and physical stressors may act in combination to induce illness in populations of living organisms. While recent surveys reported that parasite-insecticide interactions can synergistically and negatively affect Honeybee survival, the importance of sequence in exposure to stressors has hardly received any attention. In this work, Western Honeybees (Apis mellifera) were sequentially or simultaneously infected by the microsporidian parasite Nosema ceranae and chronically exposed to a sublethal dose of the insecticide fipronil, respectively chosen as biological and chemical stressors. Interestingly, every combination tested led to a synergistic effect on Honeybee survival, with the most significant impacts when stressors were applied at the emergence of Honeybees. Our study presents significant outcomes on beekeeping management but also points out the potential risks incurred by any living organism frequently exposed to both pathogens and insecticides in their habitat.
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exposure to sublethal doses of fipronil and thiacloprid highly increases mortality of Honeybees previously infected by nosema ceranae
PLOS ONE, 2011Co-Authors: Julie Aufauvre, Regis Fontbonne, Bernard Vigues, Cyril Vidau, Marie DiogonAbstract:Background The Honeybee, Apis mellifera, is undergoing a worldwide decline whose origin is still in debate. Studies performed for twenty years suggest that this decline may involve both infectious diseases and exposure to pesticides. Joint action of pathogens and chemicals are known to threaten several organisms but the combined effects of these stressors were poorly investigated in Honeybees. Our study was designed to explore the effect of Nosema ceranae infection on Honeybee sensitivity to sublethal doses of the insecticides fipronil and thiacloprid. Methodology/Finding Five days after their emergence, Honeybees were divided in 6 experimental groups: (i) uninfected controls, (ii) infected with N. ceranae, (iii) uninfected and exposed to fipronil, (iv) uninfected and exposed to thiacloprid, (v) infected with N. ceranae and exposed 10 days post-infection (p.i.) to fipronil, and (vi) infected with N. ceranae and exposed 10 days p.i. to thiacloprid. Honeybee mortality and insecticide consumption were analyzed daily and the intestinal spore content was evaluated 20 days after infection. A significant increase in Honeybee mortality was observed when N. ceranae-infected Honeybees were exposed to sublethal doses of insecticides. Surprisingly, exposures to fipronil and thiacloprid had opposite effects on microsporidian spore production. Analysis of the Honeybee detoxification system 10 days p.i. showed that N. ceranae infection induced an increase in glutathione-S-transferase activity in midgut and fat body but not in 7-ethoxycoumarin-O-deethylase activity. Conclusions/Significance After exposure to sublethal doses of fipronil or thiacloprid a higher mortality was observed in N. ceranae-infected Honeybees than in uninfected ones. The synergistic effect of N. ceranae and insecticide on Honeybee mortality, however, did not appear strongly linked to a decrease of the insect detoxification system. These data support the hypothesis that the combination of the increasing prevalence of N. ceranae with high pesticide content in beehives may contribute to colony depopulation.
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Exposure to sublethal doses of fipronil and thiacloprid highly increases mortality of Honeybees previously infected by Nosema ceranae. PLoS One 6(6):e21550
2011Co-Authors: Cyril Vidau, Julie Aufauvre, Regis Fontbonne, Bernard Vigues, Marie Diogon, Catherine Texier, David G. Biron, Nicolas Blot, Hicham El Alaoui, Luc P. BelzuncesAbstract:Background: The Honeybee, Apis mellifera, is undergoing a worldwide decline whose origin is still in debate. Studies performed for twenty years suggest that this decline may involve both infectious diseases and exposure to pesticides. Joint action of pathogens and chemicals are known to threaten several organisms but the combined effects of these stressors were poorly investigated in Honeybees. Our study was designed to explore the effect of Nosema ceranae infection on Honeybee sensitivity to sublethal doses of the insecticides fipronil and thiacloprid. Methodology/Finding: Five days after their emergence, Honeybees were divided in 6 experimental groups: (i) uninfected controls, (ii) infected with N. ceranae, (iii) uninfected and exposed to fipronil, (iv) uninfected and exposed to thiacloprid, (v) infected with N. ceranae and exposed 10 days post-infection (p.i.) to fipronil, and (vi) infected with N. ceranae and exposed 10 days p.i. to thiacloprid. Honeybee mortality and insecticide consumption were analyzed daily and the intestinal spore content was evaluated 20 days after infection. A significant increase in Honeybee mortality was observed when N. ceranaeinfected Honeybees were exposed to sublethal doses of insecticides. Surprisingly, exposures to fipronil and thiacloprid had opposite effects on microsporidian spore production. Analysis of the Honeybee detoxification system 10 days p.i. showed that N. ceranae infection induced an increase in glutathione-S-transferase activity in midgut and fat body but not in 7-ethoxycoumarin-O-deethylase activity
Cyril Vidau - One of the best experts on this subject based on the ideXlab platform.
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Differential proteomic analysis of midguts from Nosema ceranae-infected Honeybees reveals manipulation of key host functions
Journal of Invertebrate Pathology, 2014Co-Authors: Cyril Vidau, Catherine Texier, David G. Biron, Johan Panek, Luc Belzunces, Morgane Le Gall, Cédric Broussard, Frédéric Delbac, Hicham El AlaouiAbstract:Many invasive pathogens effectively bypass the insect defenses to ensure the completion of their life cycle. Among those, an invasive microsporidian species, Nosema ceranae, can cause nosemosis in Honeybees. N. ceranae was first described in the Asian Honeybee Apis cerana and is suspected to be involved in Western Honeybee (Apis mellifera) declines worldwide. The midgut of Honeybees is the first barrier against N. ceranae attacks. To bring proteomics data on Honeybee/N. ceranae crosstalk and more precisely to decipher the worker Honeybee midgut response after an oral inoculation of N. ceranae (10 days postinfection), we used 2D-DIGE (2-Dimensional Differential In-Gel Electrophoresis) combined with mass spectrometry. Forty-five protein spots produced by the infected worker Honeybee group were shown to be differentially expressed when compared to the uninfected group; 14 were subsequently identified by mass spectrometry. N. ceranae mainly caused a modulation of proteins involved in three key host biological functions: (i) energy production, (ii) innate immunity (reactive oxygen stress) and (iii) protein regulation. The modulation of these host biological functions suggests that N. ceranae creates a zone of ‘‘metabolic habitat modification’’ in the Honeybee midgut favoring its development by enhancing availability of nutrients and reducing the worker Honeybee defense.
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Exposure to Sublethal Doses of Fipronil and Thiacloprid Highly Increases Mortality of Honeybees Previously Infected by Nosema ceranae
2013Co-Authors: Cyril Vidau, Julie Aufauvre, Regis Fontbonne, Bernard Vigues, Marie Diogon, Catherine Texier, David G. Biron, Nicolas Blot, Hicham El Alaoui, Luc P. BelzuncesAbstract:Background: The Honeybee, Apis mellifera, is undergoing a worldwide decline whose origin is still in debate. Studies performed for twenty years suggest that this decline may involve both infectious diseases and exposure to pesticides. Joint action of pathogens and chemicals are known to threaten several organisms but the combined effects of these stressors were poorly investigated in Honeybees. Our study was designed to explore the effect of Nosema ceranae infection on Honeybee sensitivity to sublethal doses of the insecticides fipronil and thiacloprid. Methodology/Finding: Five days after their emergence, Honeybees were divided in 6 experimental groups: (i) uninfected controls, (ii) infected with N. ceranae, (iii) uninfected and exposed to fipronil, (iv) uninfected and exposed to thiacloprid, (v) infected with N. ceranae and exposed 10 days post-infection (p.i.) to fipronil, and (vi) infected with N. ceranae and exposed 10 days p.i. to thiacloprid. Honeybee mortality and insecticide consumption were analyzed daily and the intestinal spore content was evaluated 20 days after infection. A significant increase in Honeybee mortality was observed when N. ceranaeinfected Honeybees were exposed to sublethal doses of insecticides. Surprisingly, exposures to fipronil and thiacloprid had opposite effects on microsporidian spore production. Analysis of the Honeybee detoxification system 10 days p.i. showed that N. ceranae infection induced an increase in glutathione-S-transferase activity in midgut and fat body but not in 7-ethoxycoumarin-O-deethylase activity
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Parasite-insecticide interactions: a case study of Nosema ceranae and fipronil synergy on Honeybee.
Sci Rep, 2012Co-Authors: Julie Aufauvre, Regis Fontbonne, Bernard Vigues, Cyril Vidau, Marie Diogon, Luc P. Belzunces, Frédéric Delbac, David Georges Biron, Mathieu Roudel, Nicolas BlotAbstract:In ecosystems, a variety of biological, chemical and physical stressors may act in combination to induce illness in populations of living organisms. While recent surveys reported that parasite-insecticide interactions can synergistically and negatively affect Honeybee survival, the importance of sequence in exposure to stressors has hardly received any attention. In this work, Western Honeybees (Apis mellifera) were sequentially or simultaneously infected by the microsporidian parasite Nosema ceranae and chronically exposed to a sublethal dose of the insecticide fipronil, respectively chosen as biological and chemical stressors. Interestingly, every combination tested led to a synergistic effect on Honeybee survival, with the most significant impacts when stressors were applied at the emergence of Honeybees. Our study presents significant outcomes on beekeeping management but also points out the potential risks incurred by any living organism frequently exposed to both pathogens and insecticides in their habitat.
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exposure to sublethal doses of fipronil and thiacloprid highly increases mortality of Honeybees previously infected by nosema ceranae
PLOS ONE, 2011Co-Authors: Julie Aufauvre, Regis Fontbonne, Bernard Vigues, Cyril Vidau, Marie DiogonAbstract:Background The Honeybee, Apis mellifera, is undergoing a worldwide decline whose origin is still in debate. Studies performed for twenty years suggest that this decline may involve both infectious diseases and exposure to pesticides. Joint action of pathogens and chemicals are known to threaten several organisms but the combined effects of these stressors were poorly investigated in Honeybees. Our study was designed to explore the effect of Nosema ceranae infection on Honeybee sensitivity to sublethal doses of the insecticides fipronil and thiacloprid. Methodology/Finding Five days after their emergence, Honeybees were divided in 6 experimental groups: (i) uninfected controls, (ii) infected with N. ceranae, (iii) uninfected and exposed to fipronil, (iv) uninfected and exposed to thiacloprid, (v) infected with N. ceranae and exposed 10 days post-infection (p.i.) to fipronil, and (vi) infected with N. ceranae and exposed 10 days p.i. to thiacloprid. Honeybee mortality and insecticide consumption were analyzed daily and the intestinal spore content was evaluated 20 days after infection. A significant increase in Honeybee mortality was observed when N. ceranae-infected Honeybees were exposed to sublethal doses of insecticides. Surprisingly, exposures to fipronil and thiacloprid had opposite effects on microsporidian spore production. Analysis of the Honeybee detoxification system 10 days p.i. showed that N. ceranae infection induced an increase in glutathione-S-transferase activity in midgut and fat body but not in 7-ethoxycoumarin-O-deethylase activity. Conclusions/Significance After exposure to sublethal doses of fipronil or thiacloprid a higher mortality was observed in N. ceranae-infected Honeybees than in uninfected ones. The synergistic effect of N. ceranae and insecticide on Honeybee mortality, however, did not appear strongly linked to a decrease of the insect detoxification system. These data support the hypothesis that the combination of the increasing prevalence of N. ceranae with high pesticide content in beehives may contribute to colony depopulation.
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Exposure to sublethal doses of fipronil and thiacloprid highly increases mortality of Honeybees previously infected by Nosema ceranae. PLoS One 6(6):e21550
2011Co-Authors: Cyril Vidau, Julie Aufauvre, Regis Fontbonne, Bernard Vigues, Marie Diogon, Catherine Texier, David G. Biron, Nicolas Blot, Hicham El Alaoui, Luc P. BelzuncesAbstract:Background: The Honeybee, Apis mellifera, is undergoing a worldwide decline whose origin is still in debate. Studies performed for twenty years suggest that this decline may involve both infectious diseases and exposure to pesticides. Joint action of pathogens and chemicals are known to threaten several organisms but the combined effects of these stressors were poorly investigated in Honeybees. Our study was designed to explore the effect of Nosema ceranae infection on Honeybee sensitivity to sublethal doses of the insecticides fipronil and thiacloprid. Methodology/Finding: Five days after their emergence, Honeybees were divided in 6 experimental groups: (i) uninfected controls, (ii) infected with N. ceranae, (iii) uninfected and exposed to fipronil, (iv) uninfected and exposed to thiacloprid, (v) infected with N. ceranae and exposed 10 days post-infection (p.i.) to fipronil, and (vi) infected with N. ceranae and exposed 10 days p.i. to thiacloprid. Honeybee mortality and insecticide consumption were analyzed daily and the intestinal spore content was evaluated 20 days after infection. A significant increase in Honeybee mortality was observed when N. ceranaeinfected Honeybees were exposed to sublethal doses of insecticides. Surprisingly, exposures to fipronil and thiacloprid had opposite effects on microsporidian spore production. Analysis of the Honeybee detoxification system 10 days p.i. showed that N. ceranae infection induced an increase in glutathione-S-transferase activity in midgut and fat body but not in 7-ethoxycoumarin-O-deethylase activity
Lena Wilfert - One of the best experts on this subject based on the ideXlab platform.
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knock on community impacts of a novel vector spillover of emerging dwv b from varroa infested Honeybees to wild bumblebees
Ecology Letters, 2019Co-Authors: Robyn Manley, Lena Wilfert, Mike Boots, Ben Temperton, Toby Doyle, Daisy Gates, Sophie HedgesAbstract:Novel transmission routes can directly impact the evolutionary ecology of infectious diseases, with potentially dramatic effect on host populations and knock‐on effects on the wider host community. The invasion of Varroa destructor, an ectoparasitic viral vector in Western Honeybees, provides a unique opportunity to examine how a novel vector affects disease epidemiology in a host community. This specialist Honeybee mite vectors deformed wing virus (DWV), an important re‐emerging Honeybee pathogen that also infects wild bumblebees. Comparing island Honeybee and wild bumblebee populations with and without V. destructor, we show that V. destructor drives DWV prevalence and titre in Honeybees and sympatric bumblebees. Viral genotypes are shared across hosts, with the potentially more virulent DWV‐B overtaking DWV‐A in prevalence in a current epidemic. This demonstrates disease emergence across a host community driven by the acquisition of a specialist novel transmission route in one host, with dramatic community level knock‐on effects.
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Deformed wing virus is a recent global epidemic in Honeybees driven by Varroa mites
Science (New York N.Y.), 2016Co-Authors: Lena Wilfert, Gráinne H. Long, Helen C. Leggett, Paul Schmid-hempel, Roger K. Butlin, Stephen J. Martin, Mike BootsAbstract:Deformed wing virus (DWV) and its vector, the mite Varroa destructor, are a major threat to the world’s Honeybees. Although the impact of Varroa on colony-level DWV epidemiology is evident, we have little understanding of wider DWV epidemiology and the role that Varroa has played in its global spread. A phylogeographic analysis shows that DWV is globally distributed in Honeybees, having recently spread from a common source, the European Honeybee Apis mellifera. DWV exhibits epidemic growth and transmission that is predominantly mediated by European and North American Honeybee populations and driven by trade and movement of Honeybee colonies. DWV is now an important reemerging pathogen of Honeybees, which are undergoing a worldwide manmade epidemic fueled by the direct transmission route that the Varroa mite provides.
Marie Diogon - One of the best experts on this subject based on the ideXlab platform.
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impact of the microsporidian nosema ceranae on the gut epithelium renewal of the Honeybee apis mellifera
Journal of Invertebrate Pathology, 2018Co-Authors: Johan Panek, Marie Diogon, Frédéric Delbac, Laurianne Paris, Diane Roriz, Anne Mone, Aurore Dubuffet, Hicham El AlaouiAbstract:The invasive microsporidian species, Nosema ceranae, causes nosemosis in Honeybees and is suspected to be involved in Western Honeybee (Apis mellifera) declines worldwide. The midgut of Honeybees is the site of infection; the microsporidium can disturb the functioning of this organ and, thus, the bee physiology. Host defense against pathogens is not limited to resistance (i.e. the immune response) but also involves resilience. This process implies that the host can tolerate and repair damage inflicted by the infection- by the pathogen itself or by an excessive host immune response. Enterocyte damage caused by N. ceranae can be compensated by proliferation of intestinal stem cells (ISCs) that are under the control of multiple pathways. In the present study, we investigated the impact of N. ceranae on Honeybee epithelium renewal by following the mitotic index of midgut stem cells during a 22-day N. ceranae infection. Fluorescence in situ hybridization (FISH) and immunostaining experiments were performed to follow the parasite proliferation/progression in the intestinal tissue, especially in the ISCs as they are key cells for the midgut homeostasis. We also monitored the transcriptomic profile of 7 genes coding for key proteins involved in pathways implicated in the gut epithelium renewal and homeostasis. We have shown for the first time that N. ceranae can negatively alter the gut epithelium renewal rate and disrupt some signaling pathways involved in the gut homeostasis. This alteration is correlated to a reduced longevity of N. ceranae-infected Honeybees and we can assume that Honeybee susceptibility to N. ceranae could be due to an impaired ability to repair gut damage.
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Exposure to Sublethal Doses of Fipronil and Thiacloprid Highly Increases Mortality of Honeybees Previously Infected by Nosema ceranae
2013Co-Authors: Cyril Vidau, Julie Aufauvre, Regis Fontbonne, Bernard Vigues, Marie Diogon, Catherine Texier, David G. Biron, Nicolas Blot, Hicham El Alaoui, Luc P. BelzuncesAbstract:Background: The Honeybee, Apis mellifera, is undergoing a worldwide decline whose origin is still in debate. Studies performed for twenty years suggest that this decline may involve both infectious diseases and exposure to pesticides. Joint action of pathogens and chemicals are known to threaten several organisms but the combined effects of these stressors were poorly investigated in Honeybees. Our study was designed to explore the effect of Nosema ceranae infection on Honeybee sensitivity to sublethal doses of the insecticides fipronil and thiacloprid. Methodology/Finding: Five days after their emergence, Honeybees were divided in 6 experimental groups: (i) uninfected controls, (ii) infected with N. ceranae, (iii) uninfected and exposed to fipronil, (iv) uninfected and exposed to thiacloprid, (v) infected with N. ceranae and exposed 10 days post-infection (p.i.) to fipronil, and (vi) infected with N. ceranae and exposed 10 days p.i. to thiacloprid. Honeybee mortality and insecticide consumption were analyzed daily and the intestinal spore content was evaluated 20 days after infection. A significant increase in Honeybee mortality was observed when N. ceranaeinfected Honeybees were exposed to sublethal doses of insecticides. Surprisingly, exposures to fipronil and thiacloprid had opposite effects on microsporidian spore production. Analysis of the Honeybee detoxification system 10 days p.i. showed that N. ceranae infection induced an increase in glutathione-S-transferase activity in midgut and fat body but not in 7-ethoxycoumarin-O-deethylase activity
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Parasite-insecticide interactions: a case study of Nosema ceranae and fipronil synergy on Honeybee.
Sci Rep, 2012Co-Authors: Julie Aufauvre, Regis Fontbonne, Bernard Vigues, Cyril Vidau, Marie Diogon, Luc P. Belzunces, Frédéric Delbac, David Georges Biron, Mathieu Roudel, Nicolas BlotAbstract:In ecosystems, a variety of biological, chemical and physical stressors may act in combination to induce illness in populations of living organisms. While recent surveys reported that parasite-insecticide interactions can synergistically and negatively affect Honeybee survival, the importance of sequence in exposure to stressors has hardly received any attention. In this work, Western Honeybees (Apis mellifera) were sequentially or simultaneously infected by the microsporidian parasite Nosema ceranae and chronically exposed to a sublethal dose of the insecticide fipronil, respectively chosen as biological and chemical stressors. Interestingly, every combination tested led to a synergistic effect on Honeybee survival, with the most significant impacts when stressors were applied at the emergence of Honeybees. Our study presents significant outcomes on beekeeping management but also points out the potential risks incurred by any living organism frequently exposed to both pathogens and insecticides in their habitat.
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exposure to sublethal doses of fipronil and thiacloprid highly increases mortality of Honeybees previously infected by nosema ceranae
PLOS ONE, 2011Co-Authors: Julie Aufauvre, Regis Fontbonne, Bernard Vigues, Cyril Vidau, Marie DiogonAbstract:Background The Honeybee, Apis mellifera, is undergoing a worldwide decline whose origin is still in debate. Studies performed for twenty years suggest that this decline may involve both infectious diseases and exposure to pesticides. Joint action of pathogens and chemicals are known to threaten several organisms but the combined effects of these stressors were poorly investigated in Honeybees. Our study was designed to explore the effect of Nosema ceranae infection on Honeybee sensitivity to sublethal doses of the insecticides fipronil and thiacloprid. Methodology/Finding Five days after their emergence, Honeybees were divided in 6 experimental groups: (i) uninfected controls, (ii) infected with N. ceranae, (iii) uninfected and exposed to fipronil, (iv) uninfected and exposed to thiacloprid, (v) infected with N. ceranae and exposed 10 days post-infection (p.i.) to fipronil, and (vi) infected with N. ceranae and exposed 10 days p.i. to thiacloprid. Honeybee mortality and insecticide consumption were analyzed daily and the intestinal spore content was evaluated 20 days after infection. A significant increase in Honeybee mortality was observed when N. ceranae-infected Honeybees were exposed to sublethal doses of insecticides. Surprisingly, exposures to fipronil and thiacloprid had opposite effects on microsporidian spore production. Analysis of the Honeybee detoxification system 10 days p.i. showed that N. ceranae infection induced an increase in glutathione-S-transferase activity in midgut and fat body but not in 7-ethoxycoumarin-O-deethylase activity. Conclusions/Significance After exposure to sublethal doses of fipronil or thiacloprid a higher mortality was observed in N. ceranae-infected Honeybees than in uninfected ones. The synergistic effect of N. ceranae and insecticide on Honeybee mortality, however, did not appear strongly linked to a decrease of the insect detoxification system. These data support the hypothesis that the combination of the increasing prevalence of N. ceranae with high pesticide content in beehives may contribute to colony depopulation.
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Exposure to sublethal doses of fipronil and thiacloprid highly increases mortality of Honeybees previously infected by Nosema ceranae. PLoS One 6(6):e21550
2011Co-Authors: Cyril Vidau, Julie Aufauvre, Regis Fontbonne, Bernard Vigues, Marie Diogon, Catherine Texier, David G. Biron, Nicolas Blot, Hicham El Alaoui, Luc P. BelzuncesAbstract:Background: The Honeybee, Apis mellifera, is undergoing a worldwide decline whose origin is still in debate. Studies performed for twenty years suggest that this decline may involve both infectious diseases and exposure to pesticides. Joint action of pathogens and chemicals are known to threaten several organisms but the combined effects of these stressors were poorly investigated in Honeybees. Our study was designed to explore the effect of Nosema ceranae infection on Honeybee sensitivity to sublethal doses of the insecticides fipronil and thiacloprid. Methodology/Finding: Five days after their emergence, Honeybees were divided in 6 experimental groups: (i) uninfected controls, (ii) infected with N. ceranae, (iii) uninfected and exposed to fipronil, (iv) uninfected and exposed to thiacloprid, (v) infected with N. ceranae and exposed 10 days post-infection (p.i.) to fipronil, and (vi) infected with N. ceranae and exposed 10 days p.i. to thiacloprid. Honeybee mortality and insecticide consumption were analyzed daily and the intestinal spore content was evaluated 20 days after infection. A significant increase in Honeybee mortality was observed when N. ceranaeinfected Honeybees were exposed to sublethal doses of insecticides. Surprisingly, exposures to fipronil and thiacloprid had opposite effects on microsporidian spore production. Analysis of the Honeybee detoxification system 10 days p.i. showed that N. ceranae infection induced an increase in glutathione-S-transferase activity in midgut and fat body but not in 7-ethoxycoumarin-O-deethylase activity
Hicham El Alaoui - One of the best experts on this subject based on the ideXlab platform.
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impact of the microsporidian nosema ceranae on the gut epithelium renewal of the Honeybee apis mellifera
Journal of Invertebrate Pathology, 2018Co-Authors: Johan Panek, Marie Diogon, Frédéric Delbac, Laurianne Paris, Diane Roriz, Anne Mone, Aurore Dubuffet, Hicham El AlaouiAbstract:The invasive microsporidian species, Nosema ceranae, causes nosemosis in Honeybees and is suspected to be involved in Western Honeybee (Apis mellifera) declines worldwide. The midgut of Honeybees is the site of infection; the microsporidium can disturb the functioning of this organ and, thus, the bee physiology. Host defense against pathogens is not limited to resistance (i.e. the immune response) but also involves resilience. This process implies that the host can tolerate and repair damage inflicted by the infection- by the pathogen itself or by an excessive host immune response. Enterocyte damage caused by N. ceranae can be compensated by proliferation of intestinal stem cells (ISCs) that are under the control of multiple pathways. In the present study, we investigated the impact of N. ceranae on Honeybee epithelium renewal by following the mitotic index of midgut stem cells during a 22-day N. ceranae infection. Fluorescence in situ hybridization (FISH) and immunostaining experiments were performed to follow the parasite proliferation/progression in the intestinal tissue, especially in the ISCs as they are key cells for the midgut homeostasis. We also monitored the transcriptomic profile of 7 genes coding for key proteins involved in pathways implicated in the gut epithelium renewal and homeostasis. We have shown for the first time that N. ceranae can negatively alter the gut epithelium renewal rate and disrupt some signaling pathways involved in the gut homeostasis. This alteration is correlated to a reduced longevity of N. ceranae-infected Honeybees and we can assume that Honeybee susceptibility to N. ceranae could be due to an impaired ability to repair gut damage.
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Exposure to Sublethal Doses of Fipronil and Thiacloprid Highly Increases Mortality of Honeybees Previously Infected by Nosema ceranae
2013Co-Authors: Cyril Vidau, Julie Aufauvre, Regis Fontbonne, Bernard Vigues, Marie Diogon, Catherine Texier, David G. Biron, Nicolas Blot, Hicham El Alaoui, Luc P. BelzuncesAbstract:Background: The Honeybee, Apis mellifera, is undergoing a worldwide decline whose origin is still in debate. Studies performed for twenty years suggest that this decline may involve both infectious diseases and exposure to pesticides. Joint action of pathogens and chemicals are known to threaten several organisms but the combined effects of these stressors were poorly investigated in Honeybees. Our study was designed to explore the effect of Nosema ceranae infection on Honeybee sensitivity to sublethal doses of the insecticides fipronil and thiacloprid. Methodology/Finding: Five days after their emergence, Honeybees were divided in 6 experimental groups: (i) uninfected controls, (ii) infected with N. ceranae, (iii) uninfected and exposed to fipronil, (iv) uninfected and exposed to thiacloprid, (v) infected with N. ceranae and exposed 10 days post-infection (p.i.) to fipronil, and (vi) infected with N. ceranae and exposed 10 days p.i. to thiacloprid. Honeybee mortality and insecticide consumption were analyzed daily and the intestinal spore content was evaluated 20 days after infection. A significant increase in Honeybee mortality was observed when N. ceranaeinfected Honeybees were exposed to sublethal doses of insecticides. Surprisingly, exposures to fipronil and thiacloprid had opposite effects on microsporidian spore production. Analysis of the Honeybee detoxification system 10 days p.i. showed that N. ceranae infection induced an increase in glutathione-S-transferase activity in midgut and fat body but not in 7-ethoxycoumarin-O-deethylase activity
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Exposure to sublethal doses of fipronil and thiacloprid highly increases mortality of Honeybees previously infected by Nosema ceranae. PLoS One 6(6):e21550
2011Co-Authors: Cyril Vidau, Julie Aufauvre, Regis Fontbonne, Bernard Vigues, Marie Diogon, Catherine Texier, David G. Biron, Nicolas Blot, Hicham El Alaoui, Luc P. BelzuncesAbstract:Background: The Honeybee, Apis mellifera, is undergoing a worldwide decline whose origin is still in debate. Studies performed for twenty years suggest that this decline may involve both infectious diseases and exposure to pesticides. Joint action of pathogens and chemicals are known to threaten several organisms but the combined effects of these stressors were poorly investigated in Honeybees. Our study was designed to explore the effect of Nosema ceranae infection on Honeybee sensitivity to sublethal doses of the insecticides fipronil and thiacloprid. Methodology/Finding: Five days after their emergence, Honeybees were divided in 6 experimental groups: (i) uninfected controls, (ii) infected with N. ceranae, (iii) uninfected and exposed to fipronil, (iv) uninfected and exposed to thiacloprid, (v) infected with N. ceranae and exposed 10 days post-infection (p.i.) to fipronil, and (vi) infected with N. ceranae and exposed 10 days p.i. to thiacloprid. Honeybee mortality and insecticide consumption were analyzed daily and the intestinal spore content was evaluated 20 days after infection. A significant increase in Honeybee mortality was observed when N. ceranaeinfected Honeybees were exposed to sublethal doses of insecticides. Surprisingly, exposures to fipronil and thiacloprid had opposite effects on microsporidian spore production. Analysis of the Honeybee detoxification system 10 days p.i. showed that N. ceranae infection induced an increase in glutathione-S-transferase activity in midgut and fat body but not in 7-ethoxycoumarin-O-deethylase activity
