Treatment of rabbit cheyletiellosis with selamectin or ivermectin: a retrospective case study

<p>Abstract</p> <p>Background</p> <p>A retrospective study of rabbits treated against cheyletiellosis was performed to evaluate the efficacy and safety of selamectin or ivermectin in clinical practice.</p> <p>Methods</p> <p>Medical records from 53 rabbits with microscopically confirmed <it>Cheyletiella </it>infestation were collected from two small animal clinics. The rabbits were divided into three groups, based on treatment protocols. Group 1 included 11 rabbits treated with ivermectin injections at 200–476 μg kg^-1subcutaneously 2–3 times, with a mean interval of 11 days. In Group 2, 27 rabbits were treated with a combination of subcutaneous ivermectin injections (range 618–2185 μgkg^-1) and oral ivermectin (range 616–2732 μgkg^-1) administered by the owners, 3–6 times at 10 days interval. The last group (Group 3) included 15 rabbits treated with selamectin spot-on applications of 6.2–20,0 mgkg^-1, 1–3 times with an interval of 2–4 weeks. Follow-up time was 4 months–4.5 years.</p> <p>Results</p> <p>Rabbits in remission were 9/11 (81,8%), 14/27 (51,9%) and 12/15 (80,8%) in groups 1, 2 and 3, respectively.</p> <p>Conclusion</p> <p>All treatment protocols seemed to be sufficiently effective and safe for practice use. Though very high doses were used in Group 2 (ivermectin injections followed by oral administration), the protocol seemed less efficacious compared to ivermectin injections (Group 1) and selamectin spot on (Group 3), respectively, although not statistically significant. Controlled prospective studies including larger groups are needed to further evaluate efficacy of the treatment protocols.</p

Sphingosine 1-phosphate modulates antigen capture by murine langerhans cells via the S1P2 receptor subtype

Dendritic cells (DCs) play a pivotal role in the development of cutaneous contact hypersensitivity (CHS) and atopic dermatitis as they capture and process antigen and present it to T lymphocytes in the lymphoid organs. Recently, it has been indicated that a topical application of the sphingolipid sphingosine 1-phosphate (S1P) prevents the inflammatory response in CHS, but the molecular mechanism is not fully elucidated. Here we indicate that treatment of mice with S1P is connected with an impaired antigen uptake by Langerhans cells (LCs), the initial step of CHS. Most of the known actions of S1P are mediated by a family of five specific G protein-coupled receptors. Our results indicate that S1P inhibits macropinocytosis of the murine LC line XS52 via S1P2 receptor stimulation followed by a reduced phosphatidylinositol 3-kinase (PI3K) activity. As down-regulation of S1P2 not only diminished S1P-mediated action but also enhanced the basal activity of LCs on antigen capture, an autocrine action of S1P has been assumed. Actually, S1P is continuously produced by LCs and secreted via the ATP binding cassette transporter ABCC1 to the extracellular environment. Consequently, inhibition of ABCC1, which decreased extracellular S1P levels, markedly increased the antigen uptake by LCs. Moreover, stimulation of sphingosine kinase activity, the crucial enzyme for S1P formation, is connected not only with enhanced S1P levels but also with diminished antigen capture. These results indicate that S1P is essential in LC homeostasis and influences skin immunity. This is of importance as previous reports suggested an alteration of S1P levels in atopic skin lesions

A COL7A1 Mutation Causes Dystrophic Epidermolysis Bullosa in Rotes Höhenvieh Cattle

We identified a congenital mechanobullous skin disorder in six calves on a single farm of an endangered German cattle breed in 2010. The condition presented as a large loss of skin distal to the fetlocks and at the mucosa of the muzzle. All affected calves were euthanized on humane grounds due to the severity, extent and progression of the skin and oral lesions. Examination of skin samples under light microscopy revealed detachment of the epidermis from the dermis at the level of the dermo epidermal junction, leading to the diagnosis of a subepidermal bullous dermatosis such as epidermolysis bullosa. The pedigree was consistent with monogenic autosomal recessive inheritance. We localized the causative mutation to an 18 Mb interval on chromosome 22 by homozygosity mapping. The COL7A1 gene encoding collagen type VII alpha 1 is located within this interval and COL7A1 mutations have been shown to cause inherited dystrophic epidermolysis bullosa (DEB) in humans. A SNP in the bovine COL7A1 exon 49 (c.4756C>T) was perfectly associated with the observed disease. The homozygous mutant T/T genotype was exclusively present in affected calves and their parents were heterozygous C/T confirming the assumed recessive mode of inheritance. All known cases and genotyped carriers were related to a single cow, which is supposed to be the founder animal. The mutant T allele was absent in 63 animals from 24 cattle breeds. The identified mutation causes a premature stop codon which leads to a truncated protein representing a complete loss of COL7A1 function (p.R1586*). We thus have identified a candidate causative mutation for this genetic disease using only three cases to unravel its molecular basis. Selection against this mutation can now be used to eliminate the mutant allele from the Rotes Höhenvieh breed

Intérêt du chien dans la pathologie comparée et la génétique : exemples de ressources et de programmes partagés [The importance of dogs for comparative pathology and genetics: Examples of shared resources and programmes]

International audienceThis review has been published by the Société centrale canine (SCC) and the Fédération cynologique internationale (FCI) on the occasion of the 3rd International Dog Health Workshop in Paris (April 2017), as a chapter of the book: “Standards, health and genetics in dogs” (Guintard and Leroy, 2017), as a tribute and dedicated to Raymond Triquet and Renée Sporre-Willes, who were the two last presidents of the FCI standard commission and worked for many years for recognition and health of dog breeds. Its reprint was made possible with permission of editors (SCC, FCI) and authors. The authors thought it important to demonstrate the need for collaboration between disciplines: between veterinarians, researchers, doctors, breeders and dog fanciers, in the interest of dogs to ensure better health and better genetic management of breeds in a context in which the emerging genetic tests may prove very useful, but must be used wisely. Working in close collaboration for many years between the CNRS genetic research team in Rennes and Doctors Gilles Chaudieu, Eric Guaguère, Jean-Pierre Genevois and Patrick Devauchelle permit to propose a focus on the state of knowledge and on certain projects led by the Rennes lab in ophthalmology, dermatology, orthopedics and oncology. In dogs, the quest for conformation with the breed standard has resulted in the selection of specific alleles to meet the desired criteria (different aptitudes, morphological and physiological traits). Indeed, dogs, with more than 400 breeds, represent genetic isolates within which individuals belonging to the same breed share the same phenotype and almost the same genotype in order to meet the desired criteria. Unfortunately, this selection has also resulted in the concentration of deleterious alleles, causing genetic diseases in many dog breeds. We will therefore stress the importance of exchange, collaboration, comparison and complementary expertise, in order to use the resources and the genetic methods now available to us, with mutual understanding between actors in veterinary medicine, dog breeding and research. Moreover, we will use selected examples to demonstrate the importance of comparative pathology and genetics in dogs for veterinary and human medicine in order to identify the genetic causes of homologous diseases between humans and dogs, and to eventually improve the screening and treatment of these diseases in the dogs and their owners. © 2017 AFVA

L’ichtyose du Golden retriever due à une mutation de la PNPLA1 est associée à une accumulation de lipides neutres et de phospholipides dans le Stratum Corneum (SC)

National audienceno abstrac

UN MODÈLE SPONTANÉ CANIN DE NEUROPATHIE SENSORIELLE HUMAINE : IDENTIFICATION D’UNE MUTATION EN AMONT D’UN FACTEUR NEUROTROPHIQUE

International audienceIn this study, we sought the genetic cause of self-mutilation syndrome in sporting dogs, which corresponds to human Hereditary Sensory and Autonomic Neuropathies (HSAN). We have identified a genetic mutation upstream of the gene encoding Glial cell line-Derived Neurotrophic Factor (GDNF). This mutation is responsible for insensitivity to pain in four sporting dog breeds and it perfectly segregates with the disease in 250 sporting dogs of known clinical status. Moreover, it was not found in any of the 900 unaffected dogs from 130 different breeds. Since this mutation is localized in a long non-coding RNA, we performed an in-depth analysis of the genomic region (locus) as well as gene expression analyses to understand its role in the pathophysiology of the disease. Thus, in addition to the discovery of a novel candidate gene for HSAN in humans, we propose a transcriptional regulation mechanism based on a “partnership” between GDNF and a long non-coding RNA (lncRNA).Dans cette étude, nous avons recherché la cause génétique du syndrome d’automutilation chez les chiens de chasse, qui correspond chez l’Homme à une neuropathie sensitive de type HSAN. Nous avons identifié une mutation en amont d’un gène codant un facteur neurotrophique : GDNF (« Glial cell line-Derived Neurotrophic Factor »). Cette mutation ségrége parfaitement avec la maladie chez 250 chiens de chasse de statut clinique connu et est absente chez 900 chiens indemnes de 130 autres races. Cette mutation étant située dans un ARN long non codant, une analyse fine de la région chromosomique et des études d’expression de gènes ont été réalisées pour comprendre son rôle dans la physiopathologie de la maladie. Ainsi, non seulement, nous apportons un nouveau gène candidat pour les neuropathies humaines, mais nous proposons également un mécanisme de régulation transcriptionnelle original, basé sur un « partenariat » entre le gène codant le facteur neurotrophique et l’ARN long non codant