Survey of Handlers of 158 Police Dogs in New Zealand: Functional Assessment and Canine Orthopedic Index.

Objectives: To determine the functional assessment (FA) of fitness and Canine Orthopedic Index (COI) scores of 158 police dogs. The hypothesis was the dogs would have excellent fitness and no evidence of orthopedic disease regardless of age as reported by the handlers. Study Design: Observational, prospective study. Sample Population: Handlers of dogs >1 year of age in active duty or breeding/active duty. Methods: COI and FA questionnaires were completed via e-mail. Fisher's Exact test for count data assessed scores by age group (5 years); Wilcoxon Signed-rank test correlated COI parameters (stiffness, function, gait, quality of life) to FA. Results: The dogs were 3.2 ± 2.4 (mean ± standard deviation) years-old, 96% were German Shepherds and 111 were male. 32% of dogs could hold the “Hup” position for no longer than 4 s and 8% frequently had difficulty with this task. Difficulty jumping into vehicles occurred in 1/3 of the dogs. Overall FA was impaired in 20% (score >8), abnormal in 15% (score = 5–7), and reduced (score = 1–4) in 36% of dogs. Only 29% had normal function (FA score = 0) and these were significantly younger (2.8 ± 1.7 years, p 5 year-old group was 3.2 ± 2.4. Gait score for the 5 year group was 6.0 ± 4.3. Quality of life was close to excellent for the 5 year-olds scored higher (3.0 ± 2.5). Only the COI gait score correlated with the FA score (p = 0.30). Conclusions and Clinical Relevance: Police dogs were reported by handlers to have good to excellent QOL, however, increasing age was associated with declining FA and COI scores.fals

Clinical and genetic characterisation of dystrophin-deficient muscular dystrophy in a family of Miniature Poodle dogs

Four full-sibling intact male Miniature Poodles were evaluated at 4–19 months of age. One was clinically normal and three were affected. All affected dogs were reluctant to exercise and had generalised muscle atrophy, a stiff gait and a markedly elevated serum creatine kinase activity. Two affected dogs also showed poor development, learning difficulties and episodes of abnormal behaviour. In these two dogs, investigations into forebrain structural and metabolic diseases were unremarkable; electromyography demonstrated fibrillation potentials and complex repetitive discharges in the infraspinatus, supraspinatus and epaxial muscles. Histopathological, immunohistochemical and immunoblotting analyses of muscle biopsies were consistent with dystrophin-deficient muscular dystrophy. DNA samples were obtained from all four full-sibling male Poodles, a healthy female littermate and the dam, which was clinically normal. Whole genome sequencing of one affected dog revealed a >5 Mb deletion on the X chromosome, encompassing the entire DMD gene. The exact deletion breakpoints could not be experimentally ascertained, but we confirmed that this region was deleted in all affected males, but not in the unaffected dogs. Quantitative polymerase chain reaction confirmed all three affected males were hemizygous for the mutant X chromosome, while the wildtype chromosome was observed in the unaffected male littermate. The female littermate and the dam were both heterozygous for the mutant chromosome. Forty-four Miniature Poodles from the general population were screened for the mutation and were homozygous for the wildtype chromosome. The finding represents a naturally-occurring mutation causing dystrophin-deficient muscular dystrophy in the dog

Whole genome sequencing reveals a 7 base-pair deletion in DMD exon 42 in a dog with muscular dystrophy

Dystrophin is a key cytoskeletal protein coded by the Duchenne muscular dystrophy (DMD) gene located on the X-chromosome. Truncating mutations in the DMD gene cause loss of dystrophin and the classical DMD clinical syndrome. Spontaneous DMD gene mutations and associated phenotypes occur in several other species. The mdx mouse model and the golden retriever muscular dystrophy (GRMD) canine model have been used extensively to study DMD disease pathogenesis and show efficacy and side effects of putative treatments. Certain DMD gene mutations in high-risk, the so-called hot spot areas can be particularly helpful in modeling molecular therapies. Identification of specific mutations has been greatly enhanced by new genomic methods. Whole genome, next generation sequencing (WGS) has been recently used to define DMD patient mutations, but has not been used in dystrophic dogs. A dystrophin-deficient Cavalier King Charles Spaniel (CKCS) dog was evaluated at the functional, histopathological, biochemical, and molecular level. The affected dog’s phenotype was compared to the previously reported canine dystrophinopathies. WGS was then used to detect a 7 base pair deletion in DMD exon 42 (c.6051-6057delTCTCAAT mRNA), predicting a frameshift in gene transcription and truncation of dystrophin protein translation. The deletion was confirmed with conventional PCR and Sanger sequencing. This mutation is in a secondary DMD gene hotspot area distinct from the one identified earlier at the 5′ donor splice site of intron 50 in the CKCS breed. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00335-016-9675-2) contains supplementary material, which is available to authorized users

Arachidonic acid pathway alterations in cerebrospinal fluid of dogs with naturally occurring spinal cord injury

BACKGROUND: Canine intervertebral disc πherniation causes a naturally-occurring spinal cord injury (SCI) that bears critical similarities to human SCI with respect to both injury pathomechanisms and treatment. As such, it has tremendous potential to enhance our understanding of injury biology and the preclinical evaluation of novel therapies. Currently, there is limited understanding of the role of arachidonic acid metabolites in canine SCI. RESULTS: The CSF concentrations of PLA2 and PGE2 were higher in SCI dogs compared to control dogs (p = 0.0370 and 0.0273, respectively), but CSF LCT4 concentration in SCI dogs was significantly lower than that in control dogs (p < 0.0001). Prostaglandin E2 concentration in the CSF was significantly and positively associated with increased severity of SCI at the time of sampling (p = 0.041) and recovery 42 days post-injury (p = 0.006), as measured by ordinal behavioral scores. CONCLUSION: Arachidonic acid metabolism is altered in dogs with SCI, and these data suggest that these AA metabolites reflect injury severity and recovery, paralleling data from other model systems

Rehabilitation of companion animals following orthopaedic surgery

Physical therapy and rehabilitation following orthopaedic surgery in companion animals have become more common and new advancements in this field have been made in recent years. Surgery alone may not return the animal to its previous physical activity or work-related tasks, whether due to concurrent soft tissue trauma, arthrogenic muscle inhibition or osteoarthritis. Rehabilitation therapies following surgery can restore function as well as strength, coordination and balance. Many simple techniques such as cryotherapy and passive range of motion exercises have been shown to improve outcomes following musculoskeletal procedures and may help restore function as well as reduce pain and facilitate healing. Some techniques are more useful during different stages in order to achieve optimum tissue healing and recovery of function. During the first 72 hours, rehabilitation should focus on reduction of inflammation and pain, maintaining joint nutrition and range of motion, and stimulating vascularisation and healing; and may include cryotherapy, passive range of motion exercises, massage and therapeutic exercises. Following the initial recovery period, the goals of rehabilitation also include restoring strength, balance and normal gait patterns, as well as recovery of function. During this period the focus of therapy may shift toward therapeutic exercises, aquatic therapy and increasing activity in the animal. Therapeutic modalities such as neuromuscular electrical stimulation, photobiomodulation (laser therapy), therapeutic ultrasound and extracorporeal shock wave therapy have been reported to reduce pain and inflammation, enhance healing and reduce recovery time in the early and late stages following orthopaedic surgery.</p

IKVAV-Containing Cell Membrane Penetrating Peptide Treatment Induces Changes in Cellular Morphology after Spinal Cord Injury

A cell membrane spanning peptide was used to increase the concentration of the IKVAV motif within damaged mouse spinal cord tissue. This peptide was injected directly to the lesion 24 hours after spinal cord compression injury. Because the membrane-spanning portion of the peptide adheres to tissue upon injection with a long half-life we hypothesized that the bioactive IKVAV sequence will provide a sustained regenerative signal at the sight of injury. Five different groups of mice were used and cellular morphology observations were undertaken using light and electron microscopy. Three surgical control groups: IKVAV, peptide and mannitol; one surgical treatment group: IKVAV-peptide; and one non-surgical control group: normal, were used in this experiment. In this study, treatment with IKVAV-peptide after SCI resulted in an increased number of protoplasmic astrocytes, large active motor neurons, and regeneration of muscle bundles followed by behavioral improvement. In this paper, we describe the cellular differences between all groups.fals

IKVAV-linked cell membrane-spanning peptide treatment induces neuronal reactivation following spinal cord injury

Spinal cord regeneration following treatment with a novel membrane-spanning peptide (MSP) expressing the isoleucine-lysine-valine-alanine-valine (IKVAV) epitope was assessed in Balb-c mice. After hemilaminectomy and compression injury, mice were treated with IKVAV, IKVAV-MSP, peptide or vehicle control. Functional improvement was assessed using modified Basso, Beattie, and Bresnahan Scale (mBBB) and spinal cord segments were studied histologically 28 days after injury. IKVAV-MSP group scores increased significantly compared with control groups after 4 weeks of observation (p < 0.05). The number of protoplasmic astrocytes, neurons and muscle bundle size in the IKVAV-MSP mice were significantly increased (p < 0.001; p < 0.05 and p < 0.007; respectively). This study demonstrates that it is possible to promote functional recovery after SCI using bioactive IKVAV presenting cell membrane-spanning peptides. Lay abstract: A new potential treatment for spinal cord injury was tested in mice. Mice were treated with our membrane-spanning peptide with the IKVAV motif (IKVAV-MSP) or various control treatments. Functional improvement was assessed daily and spinal cord segments were evaluated after 4 weeks. IKVAV-MSP treatment significantly restored function compared with control groups, numbers of health nerve cells within the spinal cord were increased and muscles appeared healthier. This study demonstrates that it is possible to promote functional recovery after SCI using bioactive IKVAV presenting cell membrane-spanning peptides.fals