Search

International audience; Apple orchards are heavily treated crops and some sprayed insecticides are recognized to have toxic effects on non-target arthropods. Earwigs are important natural enemies in pip-fruit orchards and contribute to the biological control of aphids. In addition, due to their ease of capture and identification, they are an interesting potential bioindicator of the possible detrimental effects of different orchard management strategies. In this study, we measured the energy reserves and some morphological traits of Forficula auricularia L. sampled in apple orchards under management strategies (organic versus integrated pest management (IPM)). We observed a significant decrease in mass (22 to 27%), inter-eye width (3%), and prothorax width (2 to 5%) in earwigs from IPM compared to organic orchards. Energy body reserves also confirmed these results with a significant decrease of 48% in glycogen and 25 to 42% in lipid content in earwigs from IPM compared to organic orchards. However, the protein content was approximately 70% higher in earwigs from IPM than in organic orchards. Earwigs sampled in IPM orchards may adapt to minimize the adverse toxic effects of pesticide treatments using a large number of strategies, which are reflected in changes to their energy reserves. These strategies could, in turn, influence the population dynamics of natural enemies and impair their role in the biological control of pests in apple orchards.

International audience; In vivo distribution of the neonicotinoid insecticide, imidacloprid, was followed during 72 h in six biological compartments of Apis mellifera L: head, thorax, abdomen, haemolymph, midgut and rectum. Honeybees were treated orally with 100 µg of 14 C-imidacloprid per kg of bee, a dose close to the median lethal dose. Elimination half-life of total radioactivity in honeybee was 25 h. Haemolymph was the compartment with the lowest and rectum that with the highest level of total radioactivity during the whole study, with a maximum 24 h after treatment. Elimination half-life of imidacloprid in whole honeybee was 5 h. Imidacloprid was readily distributed and metabolised only by Phase I enzymes into five metabolites: 4/5-hydroxy-imidacloprid, 4,5-dihydroxy-imidacloprid, 6-chloronicotinic acid, and olefin and urea derivatives. The guanidine derivative was not detected. The urea derivative and 6-chloronicotinic acid were the main metabolites and appeared particularly in midgut and rectum. The olefin derivative and 4/5-hydroxy-imidacloprid preferentially occurred in head, thorax and abdomen, which are nicotinic acetylcholine receptor-rich tissues. Moreover, they presented a peak value around 4 h after imidacloprid ingestion. These results explain the prolongation of imidacloprid action in bees, and particularly the differences between rapid intoxication symptoms and late mortality.

National audience

International audience; Many laboratory studies have demonstrated that parasitoids of various species depend on sugar sources such as nectar or honeydew. However, studies about nectar acquisition by parasitoids foraging in the field are scarce. Tersilochus heterocerus Thomson is one of the more abundant and widespread parasitoids of the pollen beetle (Meligethes aeneus F.) but nothing is known about the nutritional ecology of this species. In this study we examined the nutritional state of T. heterocerus at the time of emergence and at various time periods throughout the season while foraging in the field using high-performance anion-exchange chromatography. We found that: (i) T. heterocerus emerge with relatively small amounts of sugar, composed mainly of trehalose, glucose and fructose; (ii) the first parasitoids caught just after they appeared in the field at the beginning of oilseed rape flowering had already consumed significant amounts of sugar reserves; and (iii) the total amount of sugar at the end of flowering was always significantly higher than the total amount of sugar at the beginning of flowering. This study provides valuable insights into the acquisition of sugar in the field by the parasitoid T. heterocerus and suggests that nectar acquisition takes place in the oilseed rape field or in the surrounding landscape.

Biotransformation of imidacloprid and the appearance of olefin and 5-hydroxyimidacloprid metabolites in the honeybee were studied by HPLC-MS/MS analysis. Honeybees were treated orally with imidacloprid at 20 and 50 µgkg −1 bee. Imidacloprid was metabolised relatively quickly and thoroughly. Twenty minutes after the beginning of imidacloprid ingestion, the sum of the residues from the three compounds amounted to only 70% of the actual given dose. Imidacloprid, 5-hydroxyimidacloprid and olefin represented, respectively, 50%, 9% and 8% of the actual ingested dose. Six and 24h, respectively, after ingestion of imidacloprid at 20 and 50 µgkg −1 bee, imidacloprid could no longer be detected in the honeybee. Imidacloprid had a half-life ranging between 4.5 and 5h and was rapidly metabolised into 5-hydroxyimidacloprid and olefin. Except 5-hydroxyimidacloprid in the 20 µgkg −1 treatment, these two metabolites presented a peak value 4h after ingestion of the 20 and 50 µgkg −1 doses. This time fully coincided with the appearance of mortality induced by imidacloprid after acute oral intoxication. These results suggested that the immediate neurotoxicity symptoms are due to the action of imidacloprid, whereas 5-hydroxyimidacloprid and/or olefin are involved in honeybee mortality. In addition, it was likely that the 30% of residues undetected 20min after intoxication were imidacloprid metabolites, although not 5-hydroxyimidacloprid or olefin. Thus, 5-hydroxyimidacloprid and olefin could not be the major metabolites in the worker bees.  2003 Society of Chemical Industry

Imidacloprid is a systemic nitroguanidine insecticide that belongs to the neonicotinoid family. As an agonist of the acetylcholine receptor, it attacks the insect nervous system and is extremely effective against various sucking and mining pests. Oral acute and chronic toxicity of imidacloprid and its main metabolites (5-hydroxyimidacloprid, 4,5-dihydroxyimidacloprid, desnitroimidacloprid, 6-chloronicotinic acid, olefin, and urea derivative) were investigated in Apis mellifera. Acute intoxication by imidacloprid or its metabolites resulted in the rapid appearance of neurotoxicity symptoms, such as hyperresponsiveness, hyperactivity, and trembling and led to hyporesponsiveness and hypoactivity. For acute toxicity tests, bees were treated with doses of toxic compounds ranging from 1 to 1,000 ng/bee (10-10,000 microg/kg). Acute toxicity (LD50) values of imidacloprid were about 60 ng/bee (600 microg/kg) at 48 h and about 40 ng/bee (400 microg/kg) at 72 and 96 h. Out of the six imidacloprid metabolites tested, only two (5-hydroxyimidacloprid and olefin) exhibited a toxicity close to that of imidacloprid. Olefin LD50 values were lower than those of imidacloprid. The 5-hydroxyimidacloprid showed a lower toxicity than imidacloprid with a LD50 four to six times higher than that of imidacloprid. Urea also appeared as a compound of nonnegligible toxicity by eliciting close to 40% mortality at 1,000 ng/bee (10,000 microg/kg). However, no significant toxicity was observed with 4,5-dihydroxyimidacloprid, 6-chloronicotinic acid, and desnitroimidacloprid in the range of doses tested. To test chronic toxicity, worker bees were fed sucrose solutions containing 0.1, 1, and 10 microg/L of imidacloprid and its metabolites for 10 d. Fifty percent mortality was reached at approximately 8 d. Hence, considering that sucrose syrup was consumed at the mean rate of 12 microl/d and per bee, after an 8-d period the cumulated doses were approximately 0.01, 0.1, and 1 ng/bee (0.1, 1, and 10 microg/kg). Thus, all tested compounds were toxic at doses 30 to 3,000 (olefin), 60 to 6,000 (imidacloprid), 200 to 20,000 (5-OH-imidacloprid), and1,000 to 100,000 (remaining metabolites) times lower than those required to produce the same effect in acute intoxication studies. For all products tested, bee mortality was induced only 72 h after the onset of intoxication.

International audience