Ex vivo cadaveric study of a laterally placed Leipzig stifle distractor for arthroscopic evaluation of the lateral meniscus in dogs.

OBJECTIVE: To evaluate safety and accuracy of lateral pin placement for the use of a Leipzig stifle distractor (LSD) and to assess improvements in visualization and treatment of the lateral meniscus in the canine stifle. STUDY DESIGN: Ex vivo cadaveric study. SAMPLE POPULATION: Paired canine cadaveric hind limbs (n = 10). METHODS: Pins for the LSD were placed from lateral to medial in the distal femur and proximal tibia. Safety and accuracy of lateral pin placement were evaluated via anatomical dissection, computed tomography (CT), and arthroscopy. In every case, distraction of the lateral compartment of the femorotibial joint space was evaluated arthroscopically, and the meniscus was probed. Afterward, the limbs were assigned to 1 of 2 groups, and a partial meniscectomy was attempted with or without distraction. Stifles were disarticulated to evaluate the meniscectomy and iatrogenic cartilage damage. RESULTS: Computed tomography revealed some variation in pin placement, although sufficient distraction was achieved for all stifle joints. No damage to the surrounding structures was observed during anatomical dissection, CT, or arthroscopy. Disarticulation provided evidence that using an LSD allowed for complete caudal horn meniscectomies and less articular cartilage damage than when meniscectomy was attempted with manual distraction. CONCLUSION: Lateral placement of an LSD proved to be safe and effective for the distraction of the lateral femorotibial joint space and the examination and treatment of the lateral meniscus in dogs weighing 18-42 kg. CLINICAL SIGNIFICANCE: Canine lateral meniscus pathology, although rare, leads to severe pain. A laterally placed LSD improves arthroscopic evaluation and treatment of this pathology.

Individualized mini-hemilaminectomy-corpectomy (iMHC) for treatment of thoracolumbar intervertebral disc herniation in large breed dogs.

OBJECTIVE: To assess the short-term, mid-term, and long-term results after an individualized mini-hemilaminectomy-corpectomy (iMHC) procedure for treatment of acute and chronic thoracolumbar intervertebral disc disease in non-chondrodystrophic dogs. STUDY DESIGN: Prospective study. ANIMALS: Client-owned non-chondrodystrophic large breed dogs (n = 57). METHODS: The iMHC procedure, combining mini-hemilaminectomy (MH) and partial lateral corpectomy, was performed on non-chondrodystrophic dogs with thoracolumbar disc disease. Neurological status was evaluated before surgery, for short-term outcome on days 1 and 7 after surgery, for mid-term outcome at 6 months after surgery, and for long-term outcome at the conclusion of the study. Prognostic factors were statistically evaluated. P < .05 was considered significant. RESULTS: iMHC was performed on 57 dogs, with minimal intraoperative and postoperative complications. Short-term neurological improvement was observed in 85.7% of dogs. Median hospitalization time after surgery was 2 days (range 0-14) and was significantly shorter for dogs with a chronic history of clinical signs (1 day, range 0-5) compared to acute onset (3 days, range 0-14) and for those that were ambulatory at initial presentation (1 day, range 0-5) compared to those that were not (3 days, range 0-14). Long-term evaluation included 53 surgeries with a mean follow-up time of 29.4 months. Outcome was excellent in 19 dogs and good in 29 dogs (90.6% success rate). Excellent mid-term and long-term results were significantly more common in the dogs with only 1 affected disc space. CONCLUSION: The iMHC procedure resulted in a short hospitalization time, minimal postoperative deterioration, and a high success rate.

Dorsal displacement of the rectum after proximal tail amputation and subsequent surgical repair by bilateral semitendinosus muscle transposition in a cat.

CASE DESCRIPTION: A 6-year-old cat underwent tail amputation at the sacrococcygeal joint and was evaluated 5 days later because of necrosis of the skin at the surgery site and tenesmus. Tail amputation had been necessary as a result of vehicular trauma. CLINICAL FINDINGS: Neurologic examination of the cat revealed no abnormalities. Clinical evaluation and radiography confirmed dorsal displacement of the rectum as a result of removal of the tail and transected sacrocaudal and rectococcygeal musculature as well as muscles of the pelvic diaphragm. The rectum was dilated and filled with hard feces. TREATMENT AND OUTCOME: To correct the dorsal displacement of the rectum, bilateral semitendinosus muscle transposition was performed to restore tissue to the void created by removal of the tail, sacrocaudal muscles, muscles of the pelvic diaphragm, and rectococcygeus muscle. The cat recovered uneventfully from surgery. No further displacement of the rectum occurred and no lameness attributable to bilateral transection of the semitendinosus muscles was noted during a 2-year follow-up period. CLINICAL RELEVANCE: To the authors' knowledge, dorsal displacement of the rectum after proximal tail amputation and its surgical correction in a cat have not been described previously. The favorable outcome in this case suggested that bilateral semitendinosus muscle transposition can safely be used to address large muscular defects at the level of the caudal aspect of the sacrum and the perineum in cats.

SLC19A3 Loss-of-Function Variant in Yorkshire Terriers with Leigh-Like Subacute Necrotizing Encephalopathy.

Sporadic occurrence of juvenile-onset necrotizing encephalopathy (SNE) has been previously reported in Yorkshire terriers. However, so far, no causative genetic variant has been found for this breed-specific form of suspected mitochondrial encephalomyopathy. Affected dogs showed gait abnormalities, central visual defects, and/or seizures. Histopathological analysis revealed the presence of major characteristics of human Leigh syndrome and SNE in Alaskan huskies. The aim of this study was to characterize the genetic etiology of SNE-affected purebred Yorkshire terriers. After SNP genotyping and subsequent homozygosity mapping, we identified a single loss-of-function variant by whole-genome sequencing in the canine SLC19A3 gene situated in a 1.7 Mb region of homozygosity on chromosome 25. All ten cases were homozygous carriers of a mutant allele, an indel variant in exon 2, that is predicted to lead to a frameshift and to truncate about 86% of the wild type coding sequence. This study reports a most likely pathogenic variant in SLC19A3 causing a form of SNE in Yorkshire terriers and enables selection against this fatal neurodegenerative recessive disorder. This is the second report of a pathogenic alteration of the SLC19A3 gene in dogs with SNE.

Leigh-like subacute necrotising encephalopathy in Yorkshire Terriers: neuropathological characterisation, respiratory chain activities and mitochondrial DNA.

Our knowledge of molecular mechanisms underlying mitochondrial disorders in humans has increased considerably during the past two decades. Mitochondrial encephalomyopathies have sporadically been reported in dogs. However, molecular and biochemical data that would lend credence to the suspected mitochondrial origin are largely missing. This study was aimed to characterise a Leigh-like subacute necrotising encephalopathy (SNE) in Yorkshire Terriers and to shed light on its enzymatic and genetic background. The possible resemblance to SNE in Alaskan Huskies and to human Leigh syndrome (LS) was another focus of interest. Eleven terriers with imaging and/or gross evidence of V-shaped, non-contiguous, cyst-like cavitations in the striatum, thalamus and brain stem were included. Neuropathological examinations focussed on muscle, brain pathology and mitochondrial ultrastructure. Further investigations encompassed respiratory-chain activities and the mitochondrial DNA. In contrast to mild non-specific muscle findings, brain pathology featured the stereotypic triad of necrotising grey matter lesions with relative preservation of neurons in the aforementioned regions, multiple cerebral infarcts, and severe patchy Purkinje-cell degeneration in the cerebellar vermis. Two dogs revealed a reduced activity of respiratory-chain-complexes I and IV. Genetic analyses obtained a neutral tRNA-Leu(UUR) A-G-transition only. Neuropathologically, SNE in Yorkshire Terriers is nearly identical to the Alaskan Husky form and very similar to human LS. This study, for the first time, demonstrated that canine SNE can be associated with a combined respiratory chain defect. Mitochondrial tRNA mutations and large genetic rearrangements were excluded as underlying aetiology. Further studies, amongst relevant candidates, should focus on nuclear encoded transcription and translation factors.