An outbreak of trichomonosis in European greenfinches Chloris chloris and European goldfinches Carduelis carduelis wintering in Northern France

Avian trichomonosis is a common and widespread disease, traditionally affecting columbids and raptors, and recently emerging among finch populations mainly in Europe. Across Europe, finch trichomonosis is caused by a single clonal strain of Trichomonas gallinae and negatively impacts finch populations. Here, we report an outbreak of finch trichomonosis in the wintering populations of Chloris chloris (European greenfinch) and Carduelis carduelis (European goldfinch) from the Boulonnais, in northern France. The outbreak was detected and monitored by bird ringers during their wintering bird ringing protocols. A total of 105 records from 12 sites were collected during the first quarter of 2017, with 46 and 59 concerning dead and diseased birds, respectively. Fourteen carcasses from two locations were necropsied and screened for multiple pathogens; the only causative agent identified was T. gallinae. Genetic characterization was performed by four markers (small subunit ribosomal RNA, hydrogenosomal iron-hydrogenase, and RNA polymerase II subunit 1 genes, and the internal transcribed spacers (ITS) region) and confirmed the T. gallinae strain to be A1, which affects the finch populations of Europe. This was also confirmed by an ITS-based phylogenetic analysis which further illustrated the diversity of the Trichomonas infecting birds. Preliminary data on the survival and dispersion of infected birds were obtained from ring-returns of diseased individuals. The anthropogenic spread of diseases through bird feeding practices is highlighted and some suggestions to prevent pathogen transmission via backyard supplementary feeders for garden birds are given

An outbreak of trichomonosis in European greenfinches Chloris chloris and European goldfinches Carduelis carduelis wintering in Northern France

International audienceAvian trichomonosis is a common and widespread disease, traditionally affecting columbids and raptors, and recently emerging among finch populations mainly in Europe. Across Europe, finch trichomonosis is caused by a single clonal strain of Trichomonas gallinae and negatively impacts finch populations. Here, we report an outbreak of finch trichomonosis in the wintering populations of Chloris chloris (European greenfinch) and Carduelis carduelis (European goldfinch) from the Boulonnais, in northern France. The outbreak was detected and monitored by bird ringers during their wintering bird ringing protocols. A total of 105 records from 12 sites were collected during the first quarter of 2017, with 46 and 59 concerning dead and diseased birds, respectively. Fourteen carcasses from two locations were necropsied and screened for multiple pathogens; the only causative agent identified was T. gallinae. Genetic characterization was performed by four markers (small subunit ribosomal RNA, hydrogenosomal iron-hydrogenase, and RNA polymerase II subunit 1 genes, and the internal transcribed spacers (ITS) region) and confirmed the T. gallinae strain to be A1, which affects the finch populations of Europe. This was also confirmed by an ITS-based phylogenetic analysis which further illustrated the diversity of the Trichomonas infecting birds. Preliminary data on the survival and dispersion of infected birds were obtained from ring-returns of diseased individuals. The anthropogenic spread of diseases through bird feeding practices is highlighted and some suggestions to prevent pathogen transmission via backyard supplementary feeders for garden birds are given

Impaired Hippocampus-Dependent and Facilitated Striatum-Dependent Behaviors in Mice Lacking the Delta Opioid Receptor

International audiencePharmacological data suggest that delta opioid receptors modulate learning and memory processes. In the present study, we investigated whether inactivation of the delta opioid receptor modifies hippocampus (HPC)- and striatum-dependent behaviors. We first assessed HPC-dependent learning in mice lacking the receptor (Oprd1(-/-) mice) or wild-type (WT) mice treated with the delta opioid antagonist naltrindole using novel object recognition, and a dual-solution cross-maze task. Second, we subjected mutant animals to memory tests addressing striatum-dependent learning using a single-solution response cross-maze task and a motor skill-learning task. Genetic and pharmacological inactivation of delta opioid receptors reduced performance in HPC-dependent object place recognition. Place learning was also altered in Oprd1(-/-) animals, whereas striatum-dependent response and procedural learning were facilitated. Third, we investigated the expression levels for a large set of genes involved in neurotransmission in both HPC and striatum of Oprd1(-/-) mice. Gene expression was modified for several key genes that may contribute to alter hippocampal and striatal functions, and bias striatal output towards striatonigral activity. To test this hypothesis, we finally examined locomotor effects of dopamine receptor agonists. We found that Oprd1(-/-) and naltrindole-treated WT mice were more sensitive to the stimulant locomotor effect of SKF-81297 (D1/D5), supporting the hypothesis of facilitated striatonigral output. These data suggest, for the first time, that delta receptor activity tonically inhibits striatal function, and demonstrate that delta opioid receptors modulate learning and memory performance by regulating the HPC/striatum balance