RESUMEN
BACKGROUND: Canine flank alopecia (CFA) is characterized by seasonally recurring noninflammatory, occasionally hyperpigmented alopecia predominantly in the thoracolumbar area. Previous studies suggest that reduced production of endogenous melatonin may play a role in the pathogenesis of this condition, and placebo-controlled studies on the efficacy of preventative melatonin treatment are lacking. OBJECTIVE: To evaluate the efficacy of subcutaneous slow-release melatonin implants in the prevention of CFA recurrence. ANIMALS: Twenty-one client-owned dogs with a history of CFA were included in the study. MATERIALS AND METHODS: At time (T)0, a general physical and dermatological examination was performed on each dog, blood was collected for serum biochemistry analysis and two skin biopsies were taken from alopecic areas on the nonsedated affected dogs after subcutaneous injection with 2% lidocaine. Dogs with normal blood work and histological results compatible with CFA were included in the study. Participating dogs were randomly assigned to receive either placebo or 18 mg melatonin subcutaneously in the interscapular area, approximately 2 months before expected CFA onset (T1). CFA recurrence was scored qualitatively as complete, ≤50% recurrence, or no recurrence at 5 and 7 months after the intervention (T2 and T3, respectively). RESULTS: At T3, in dogs treated with placebo (nine of 17), the percentages for complete recurrence, ≤50% recurrence and no recurrence were 44%, 0% and 56%, respectively. In dogs treated with melatonin (eight of 17), these percentages were 25%, 50% and 25%, respectively. There were no statistically significant differences in the scores between melatonin-treated dogs and placebo-treated dogs (p = 0.40). In three of eight melatonin-treated dogs, mild transient swelling was observed at the injection site. CONCLUSIONS: This study did not provide evidence that an 18 mg melatonin implant treatment, although well-tolerated, is efficacious in preventing recurrence of CFA in affected dogs.
Asunto(s)
Enfermedades de los Perros , Melatonina , Perros , Animales , Melatonina/uso terapéutico , Enfermedades de los Perros/tratamiento farmacológico , Enfermedades de los Perros/prevención & control , Enfermedades de los Perros/patología , Alopecia/veterinaria , Método Doble Ciego , Piel/patologíaRESUMEN
The immunological mechanisms explaining development of an allergy in some individuals and not in others remain incompletely understood. Insect bite hypersensitivity (IBH) is a common, seasonal, IgE-mediated, pruritic skin disorder that affects considerable proportions of horses of different breeds, which is caused by bites of the insect Culicoides obsoletus (C. obsoletus). We investigated the allergen-specific immune status of individual horses that had either been diagnosed to be healthy or to suffer of IBH. Following intradermal allergen injection, skin biopsies were taken of IBH-affected and healthy ponies and cytokine expression was determined by RT-PCR. In addition, allergen-specific antibody titers were measured and cytokine expression of in vitro stimulated, allergen-specific CD4 T-cells was determined. 24 hrs after allergen injection, a significant increase in mRNA expression of the type-2 cytokine IL-4 was observed in the skin of IBH-affected Shetland ponies. In the skin of healthy ponies, however, an increase in IFNγ mRNA expression was found. Analysis of allergen-specific antibody titers revealed that all animals produced allergen-specific antibodies, and allergen-specific stimulation of CD4 T-cells revealed a significant higher percentage of IFNγ-expressing CD4 T-cells in healthy ponies compared to IBH-affected ponies. These data indicate that horses not affected by IBH, in contrast to the so far established dogma, are not immunologically ignorant but have a Th1-skewed allergen-specific immune response that appears to protect against IBH-associated symptoms. To our knowledge this is the first demonstration of a natural situation, in which an allergen-specific immune skewing is protective in an allergic disorder.
Asunto(s)
Alérgenos/administración & dosificación , Ceratopogonidae/clasificación , Hipersensibilidad/inmunología , Mordeduras y Picaduras de Insectos , Alérgenos/inmunología , Animales , Anticuerpos/sangre , Linfocitos T CD4-Positivos/inmunología , Ceratopogonidae/inmunología , Caballos , Humanos , Tolerancia Inmunológica , Interferón gamma/inmunologíaRESUMEN
The pathology of maldronksiekte, a sporadic neurological disorder of cattle caused by the ingestion of the plant Solanum kwebense in certain parts of South Africa, was studied in three chronic field cases. There was loss of cerebellar Purkinje cells with the remaining neurons either swollen or shrunken and showing degeneration and necrosis. Ultrastructurally, neurons with a swollen perikaryon showed depletion and empty dilated cisternae of granular endoplasmic reticulum. In a few Purkinje cells, the cytoplasm contained small numbers of lamellar and membranous bodies. In the shrunken neurons, the highly condensed cytoplasm contained distended Golgi saccules, dense clusters of granular endoplasmic reticulum and swollen mitochondria. Lectin histochemistry revealed that the cytoplasmic vacuoles in some distended Purkinje cells stained strongly with Canavalia ensiformis (ConA) agglutinin and weakly with Triticum vulgaris (WGA) and succinyl-WGA (S-WGA) agglutinin. The pattern of lectin binding only partially agreed with that reported in calves poisoned with Solanum fastigiatum, causing a presumed glycolipid storage disease. Apoptosis was not detected in neurons using a commercial deoxyuridine triphosphate nick-end labelling (TUNEL) method. The pathogenesis of the cerebellar lesions is unknown but the intoxication may have resulted from the inability of neurons, in particular Purkinje cells, to metabolise a plant toxin or cellular substrate.