La interacción parásito-pesticida (imidacloprid) tiene efecto sinérgico en la mortalidad de abejas meliferas
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2016
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es
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Universidad Andrés Bello
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Licencia CC
Licencia CC
Resumen
La disminución de la población de la abeja europea, Apis melífera, es un problema global. Numerosos factores aparecen como potenciales causas y se cree que una combinación de estos agentes contribuye con la pérdida de las abejas. Dentro de esos factores se encuentran la exposición no intencional de pesticidas contra plagas de la agricultura, siendo imidacloprid, un pesticida de la familia de los neonicotinoides, uno de los más tóxicos que se aplican en los cultivos agrícolas. Por otro lado, uno de los patógenos más importantes asociado a la desaparición de las abejas y presente en Chile es Nosema ceranae, un patógeno intracelular obligado formador de esporas que disminuye la vida media de las abejas. El objetivo del estudio fue evaluar in vitro, si existe un efecto sinérgico entre la exposición oral a imidacloprid y la infección con N. ceranae en A. mellifera, a través del registro de la sobrevida, el grado de infección y la expresión de genes relacionados con inmunidad individual humoral en abejas adultas. Se evaluó, a los 4 y 7 días post infección (dpi), el grado de infección de N. ceranae y los niveles de expresión de genes involucrados en la respuesta inmune (abaecina, defensina-2 e himenoptaecina), estos fueron medidos por análisis de qPCR, mientras que la sobrevida fue analizada diariamente. Para esto, abejas adultas fueron expuestas el tercer día de vida a una dosis subletal de 150 y 300 ppb de imidacloprid y a los dos días post exposición, se infectaron con 120.000 esporas de N. ceranae. Los resultados muestran que la sobrevida de las abejas expuestas a 150 ppb de imidacloprid e infectadas con N. ceranae, disminuyó en un 18% y 37% a los 4 y 7 dpi, mientras que, en abejas expuestas a 300 ppb e infectadas, la sobrevida disminuyó en un 60% y 85% a los 4 y 7 dpi. Junto con ello, se registró un aumento significativo en el grado de infección por N. ceranae en abejas expuestas a 150 ppb de imidacloprid, alcanzando las 180.000 y 300.000 esporas/abeja a los 4 y 7 dpi. Los niveles de expresión para los genes abaecina, defensina-2 e himenoptaecina, disminuyeron significativamente a los 4 dpi en abejas expuestas previamente al pesticida (150 ppb) e infectadas, esta inhibición se mantienes a los 7 dpi, al compararlo con el control de infección. Los resultados muestran que entre la exposición a dosis subletales de imidacloprid y la infección por N. ceranae, se genera un efecto sinérgico en la mortalidad de A. melífera. Lo anterior podría ser explicado porque tras la exposición al pesticida se produce una inhibición en la expresión de genes que codifican para síntesis de péptidos antimicrobianos, lo que favorecería el aumento en los niveles de infección por N. ceranae. Esto
7
puede ayudar a entender de mejor forma la potencial contribución de estos factores en el despoblamiento de las abejas.
The decline of the European honey bee, Apis mellifera, is a global concern. Several factors appear as potential causes and it is believe that a combination of these factors contribute to honey bee loss. One of these factors is the unintentional exposure to pesticides, being imidacloprid one of the most toxic neonicotinoid pesticides, applied in agricultural crops. On the other hand, one of the most important pathogens associated with honey bee loss described in Chile is Nosema ceranae, an intracellular obligate spore-forming pathogen, which decrease the half-live of bees. The aim of this thesis was to evaluate in vitro the synergistic effect between sub-lethal oral exposition to imidacloprid and Nosema ceranae infections in A. mellifera, through the recording of survival, grade of infection and expression of genes related to individual humoral immunity in adult bees. At 4 and 7 days post infection the genes expression level related to immune response (abaecin, defensin-2 and hymenoptaecin) were quantified by q-PCR analysis, the level of N. ceranae infection was also assessed and survivorship was observed daily. For this, adults honey bees at 3 days post emergence (dpe) were exposed to imidacloprid 150 and 300 ppb and at 5 dpe were infected with 120,000 N. ceranae spores. The results show that the honey bees exposed to imidacloprid (150 ppb) and infected with N. ceranae, decreased in a 18% and 37% their survival at 4 and 7 dpi, while honey bees survival exposed to imidacloprid (300 ppb) and infected, decreased in a 60% and 85% at 4 and 7 dpi respectively. Along with it, a significant increase in the infection level was observed, reaching 180,000 and 300,000 spores/bee in honey bee exposed to imidacloprid 150 ppb at 4 and 7 dpi. The gene expression levels showed, a significant decrease for abaecin, defensin-2 and hymenoptaecin when honey bees were previously exposed to imidacloprid 150 ppb and inoculated, this inhibition is maintained at 7 dpi when compared to infection control. These findings demonstrate a synergistic effect between sub-lethal imidacloprid exposition and N. ceranae infection. This could be explained because after exposure to the pesticide there is an inhibition in the expression of genes coding for antimicrobial peptide synthesis, which would advantage the increase in N. ceranae infection levels. This could help better to understand the potential contribution of these factors to honey bee depopulation.
The decline of the European honey bee, Apis mellifera, is a global concern. Several factors appear as potential causes and it is believe that a combination of these factors contribute to honey bee loss. One of these factors is the unintentional exposure to pesticides, being imidacloprid one of the most toxic neonicotinoid pesticides, applied in agricultural crops. On the other hand, one of the most important pathogens associated with honey bee loss described in Chile is Nosema ceranae, an intracellular obligate spore-forming pathogen, which decrease the half-live of bees. The aim of this thesis was to evaluate in vitro the synergistic effect between sub-lethal oral exposition to imidacloprid and Nosema ceranae infections in A. mellifera, through the recording of survival, grade of infection and expression of genes related to individual humoral immunity in adult bees. At 4 and 7 days post infection the genes expression level related to immune response (abaecin, defensin-2 and hymenoptaecin) were quantified by q-PCR analysis, the level of N. ceranae infection was also assessed and survivorship was observed daily. For this, adults honey bees at 3 days post emergence (dpe) were exposed to imidacloprid 150 and 300 ppb and at 5 dpe were infected with 120,000 N. ceranae spores. The results show that the honey bees exposed to imidacloprid (150 ppb) and infected with N. ceranae, decreased in a 18% and 37% their survival at 4 and 7 dpi, while honey bees survival exposed to imidacloprid (300 ppb) and infected, decreased in a 60% and 85% at 4 and 7 dpi respectively. Along with it, a significant increase in the infection level was observed, reaching 180,000 and 300,000 spores/bee in honey bee exposed to imidacloprid 150 ppb at 4 and 7 dpi. The gene expression levels showed, a significant decrease for abaecin, defensin-2 and hymenoptaecin when honey bees were previously exposed to imidacloprid 150 ppb and inoculated, this inhibition is maintained at 7 dpi when compared to infection control. These findings demonstrate a synergistic effect between sub-lethal imidacloprid exposition and N. ceranae infection. This could be explained because after exposure to the pesticide there is an inhibition in the expression of genes coding for antimicrobial peptide synthesis, which would advantage the increase in N. ceranae infection levels. This could help better to understand the potential contribution of these factors to honey bee depopulation.
Notas
Tesis (Magíster en Biotecnología)
Palabras clave
Abejas, Efecto de los Insecticidas, Chile, Enfermedades, Plaguicidas, Toxicidad