Publications by authors named "N Pasteur"

This protocol describes approaches to qualify Wolbachia-induced cytoplasmic incompatibility (CI) patterns (compatible, uni or bidirectional) in crosses between two or more Culex pipiens isofemale lines, hosting different Wolbachia (wPip) strains. Here, we describe how to (1) collect the larvae in the field and grow them to the adult stage in the insectary, (2) set up isofemale lines in the insectary, (3) genetically characterize the wPip group of these lines, and (4) perform reciprocal crosses to qualify CI.

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Background: Insecticide resistance is a growing concern for malaria control and vector control effectiveness relies on assessing it distribution and understanding its evolution.

Methods: We assessed resistance levels and the frequencies of two major target-site mutations, L1014F-VGSC and G119S-ace-1, conferring resistance to pyrethroids (PYRs) and carbamates/organophosphates (CXs/OPs) insecticides. These data were compared to those acquired between 2006 and 2010 to follow resistance evolutionary trends over ten years.

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The Culex pipiens mosquito complex is a group of evolutionarily closely related species including C. pipiens and Culex quinquefasciatus, both infected by the cytoplasmically inherited Wolbachia symbiont. A Wolbachia-uninfected population of C.

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Special Operations Forces (SOF) medical personnel function worldwide in environments where endemic anthrax (caused by Bacillus anthracis infection) may present in one of three forms: cutaneous, pulmonary, or gastrointestinal. This report presents a rare periocular anthrax case from Haiti to emphasize the need for heightened diagnostic suspicion of unusual lesions likely to be encountered in SOF theaters.

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We investigated the genetic determinism of high chlorpyrifos resistance (HCR), a phenotype first described in 1999 in Culex pipiens mosquitoes surviving chlorpyrifos doses ⩾1 mg l(-1) and more recently found in field samples from Tunisia, Israel or Indian Ocean islands. Through chlorpyrifos selection, we selected several HCR strains that displayed over 10 000-fold resistance. All strains were homozygous for resistant alleles at two main loci: the ace-1 gene, with the resistant ace-1(R) allele expressing the insensitive G119S acetylcholinesterase, and a resistant allele of an unknown gene (named T) linked to the sex and ace-2 genes.

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