Oral vitamin A as an adjunct treatment for canine sebaceous adenitis.

Medical records of dogs with sebaceous adenitis diagnosed by histopathology over an 18-year period were reviewed. From a total of 40 cases, 24 were treated with oral vitamin A. Dogs ranged from 9 months to 12 years of age at the time of disease onset. Purebred as well as mixed-breed dogs were affected. Akitas represented approximately one-third of the affected population. No sex predilections were observed. Vitamin A was administered for a minimum of 1 month. Doses varied from 380 to 2667 IU/kg/day, with a mean of 1037 IU/kg/day. Two dogs received oral vitamin A exclusively. Concurrent treatments included systemic antibiotics, systemic antifungal medications, fatty acid supplementation and various topical treatments. Of 24 dogs treated with vitamin A, three were lost to follow-up. Twelve owners were satisfied with the overall appearance of their dogs, reporting ≥25% improvement in clinical signs, including level of pruritus, amount of scale, alopecia and overall coat quality, compared with pretreatment appearance. Three owners observed adequate initial improvement, with regression to pretreatment state within 6 months of starting treatment. Two owners reported 25-50% improvement in clinical signs while on oral vitamin A supplementation; however, changes were attributed to concurrent topical treatment. Six owners reported no improvement and discontinued oral administration of vitamin A within 7 months. No correlations could be made between vitamin A dosage and response to treatment; prognoses could not be made based on clinical and histopathological findings.

Morphologic, immunohistochemical, and molecular characterization of a novel Lankesterella protozoan in two White's tree frogs (Litoria caerulea).

Two White's tree frogs (Litoria caerulea) housed at a zoological park died after a short period of lethargy, weight loss, and edema. Detailed postmortem examinations were performed on both frogs, including bacterial cultures and complete histologic examinations. Intracytoplasmatic as well as free protozoan parasites were identified in multiple organs from both frogs. The parasites were identified within erythrocytes, leukocytes, endothelial cells, and hepatocytes. Immunohistochemistry demonstrated a cross-reaction with Toxoplasma gondii antisera. Parasite ultrastructural analysis was performed by transmission electron microscopy. The parasites demonstrated an apical complex containing a conoid, rhoptries, and micronemes, demonstrating it was a member of the phylum Apicomplexa. In addition, the parasites had bipolar paranuclear bodies, organelles that are typical of coccidian sporozoites. The organisms were tentatively identified as members of the genus Lankesterella on the basis of histologic and ultrastructural morphology. A portion of the 18s ribosomal RNA (rRNA) gene was amplified via a polymerase chain reaction, sequenced, and used in a Basic Local Alignment Search Tool search of the GenBank database. The 18s rRNA gene sequence was found to be most similar to gene sequences isolated from Lankesterella organisms (88%). In aggregate, these data support the classification of these protozoa as a novel species of Lankesterella. A causal relationship between frog morbidity and protozoal parasitism was not determined. This is the first report of Lankesterella sp. in White's tree frogs.

Canine epidermal neural crest stem cells: characterization and potential as therapy candidate for a large animal model of spinal cord injury.

The discovery of multipotent neural crest-derived stem cells, named epidermal neural crest stem cells (EPI-NCSC), that persist postnatally in an easy-to-access location-the bulge of hair follicles-opens a spectrum of novel opportunities for patient-specific therapies. We present a detailed characterization of canine EPI-NCSC (cEPI-NCSC) from multiple dog breeds and protocols for their isolation and ex vivo expansion. Furthermore, we provide novel tools for research in canines, which currently are still scarce. In analogy to human and mouse EPI-NCSC, the neural crest origin of cEPI-NCSC is shown by their expression of the neural crest stem cell molecular signature and other neural crest-characteristic genes. Similar to human EPI-NCSC, cEPI-NCSC also expressed pluripotency genes. We demonstrated that cEPI-NCSC can generate all major neural crest derivatives. In vitro clonal analyses established multipotency and self-renewal ability of cEPI-NCSC, establishing cEPI-NCSC as multipotent somatic stem cells. A critical analysis of the literature on canine spinal cord injury (SCI) showed the need for novel treatments and suggested that cEPI-NCSC represent viable candidates for cell-based therapies in dog SCI, particularly for chondrodystrophic dogs. This notion is supported by the close ontological relationship between neural crest stem cells and spinal cord stem cells. Thus, cEPI-NCSC promise to offer not only a potential treatment for canines but also an attractive and realistic large animal model for human SCI. Taken together, we provide the groundwork for the development of a novel cell-based therapy for a condition with extremely poor prognosis and no available effective treatment.

Evaluation of epidemiological, clinical, and pathological features of neuroaxonal dystrophy in Quarter Horses.

OBJECTIVE: To describe epidemiological, clinical, and pathological features of neuroaxonal dystrophy in Quarter Horses (QHs) on a single farm. DESIGN: Prospective case series. Animals-148 horses. PROCEDURES: Neurologic, pathological, and toxicological evaluations were completed in selected neurologically affected horses over a 2-year period. Descriptive statistical analysis was performed. RESULTS: 87 QHs and 1 QH-crossbred horse were affected. Most (50/88 [56.8%]) affected horses were 1 to 2 years old (median age, 2 years [range, 2 months to 34 years]). Neurologic deficits included obtundation (53/88 [60%] horses), decreased to absent menace response (33/88 [37.5%]), proprioceptive positioning deficits, wide-based stance, ataxia, and dysmetria (88/88 [100%]). Most (78/88 [88.6%]) horses had mild ataxia, but some (10/88 [11.4%]) had moderate to severe ataxia. Low serum concentrations of vitamin E (≤ 2 mg/L) were detected in 3 index case horses and 16 of 17 randomly selected horses (13/14 affected and 3/3 unaffected) during study year 1. Dietary vitamin E supplementation did not improve neurologic deficits in affected horses; vitamin E administration in pregnant mares appeared to decrease but not prevent disease development among offspring born the following year. Lesions detected at necropsy included bilaterally symmetric neuroaxonal degeneration with axonal spheroids in the nucleus gracilis, nucleus cuneatus medialis, nucleus cuneatus lateralis, and nucleus thoracicus (5/5 horses). CONCLUSIONS AND CLINICAL RELEVANCE: Neuroaxonal dystrophy should be considered in evaluation of young horses with ataxia and proprioceptive positioning deficits. Vitamin E deficiency may contribute to disease severity.