The medical records of 17 dogs diagnosed with spinal arachnoid cysts at North Carolina State University Veterinary Teaching Hospital were retrospectively examined to identify trends in signalment, history, neurological status, treatment, and short- and long-term prognosis. The typical case was that of a nonpainful, progressive ataxia frequently characterized by hypermetria and incontinence. Cysts typically occurred in the dorsal subarachnoid space at the first to third cervical vertebrae of young, large-breed dogs or the caudal thoracic vertebrae of older, small-breed dogs. Although 14 of 15 dogs treated surgically did well in the short term, long-term successful outcomes were achieved in only eight of the 12 dogs that were followed for >1 year. Significant predictors of good, long-term outcome were not identified; however, factors associated with a trend toward a good outcome included <3 years of age, <4 months' duration of clinical signs, and marsupialization as the surgical technique.

There are several reports of Sarcocystis sarcocysts in muscles of dogs, but these species have not been named. Additionally, there are two reports of Sarcocystis neurona in dogs. Here, we propose two new names, Sarcocystis caninum, and Sarcocystis svanai for sarcocysts associated with clinical muscular sarcocystosis in four domestic dogs (Canis familiaris), one each from Montana and Colorado in the USA, and two from British Columbia, Canada. Only the sarcocyst stage was identified. Most of the sarcocysts identified were S. caninum. Sarcocysts were studied using light microscopy, transmission electron microscopy (TEM), and polymerase chain reaction. Based on collective results two new species, S. caninum and S. svanai were designated. Sarcocystis caninum and S. svanai were structurally distinct. Sarcocystis caninum sarcocysts were up to 1.2 mm long and up to 75 μm wide. By light microscopy, the sarcocyst wall was relatively thin and smooth. By TEM, the sarcocyst wall was "type 9", 1-2 μm thick, and contained villar protrusions that lacked microtubules. Bradyzoites in sections were 7-9 μm long. Sarcocysts of S. svanai were few and were identified by TEM. Sarcocystis svanai sarcocysts were "type 1", thin walled (< 0.5 μm), and the wall lacked villar protrusions but had tiny blebs that did not invaginate. DNA was extracted either from infected frozen muscle biopsies or formalin-fixed paraffin-embedded sections. Dogs were either singly infected with S. caninum or multiply co-infected with S. caninum and S. svanai (the result of a mixed infection) based on multilocus DNA sequencing and morphology. BLASTn analysis established that the sarcocysts identified in these dogs were similar to, but not identical to Sarcocystis canis or Sarcocystis arctosi, parasites found to infect polar bears (Ursus maritimus) or brown bears (Ursus arctosi), respectively. However, the S. caninum sequence showed 100% identify over the 18S rRNA region sequenced to that of S. arctica, a parasite known to infect Arctic foxes (Vulpes lagopus).

OBJECTIVES:To assess long-term clinical and imaging outcomes in giant breed dogs with cervical stenotic myelopathy treated surgically.STUDY DESIGN:Retrospective case series.ANIMALS:Dogs (n = 7).METHODS:All dogs had lateral or dorsolateral cord compression at 1 or more sites and were treated with cervical distraction and stabilization using PMMA plugs. Four dogs had follow-up CT or CT/myelography performed at least 6 months postoperatively. Spinal canal stenosis measurements were compared between pre- and postoperative CT images. Long-term clinical neurologic re-evaluation ranged from 4 to 7 years. Outcome was considered positive, satisfactory, or negative. Recurrence was defined as signs of a cervical myelopathy in dogs that initially improved or had stable disease postoperatively.RESULTS:All dogs had immediate postoperative improvement. Recurrence (4 months to 4 years postoperatively) occurred in 3 dogs that had multiple sites of compression. Long-term outcome was positive in 4 of 7 dogs. Postoperative imaging revealed subjective regression of bony proliferation at surgical sites in 2 of 4 dogs that improved clinically but morphometric data showed no change in canal measurements. An adjacent site lesion was confirmed in 1 dog.CONCLUSIONS:Distraction and stabilization with PMMA plugs and bone grafts is a safe surgical option for giant breed dogs with CSM with a single site of lateral or dorsolateral compression. Long-term recurrence was common among dogs with multiple sites of compression. Follow-up of 4 years or more among a larger population is indicated to fully assess implications of surgical intervention and determine recurrence rates.

CASE DESCRIPTION:2 full-sibling male German Shorthaired Pointer (GSHP) puppies (dogs 1 and 2) with X-linked muscular dystrophy and deletion of the dystrophin gene (gene symbol, DMD) each had poor growth, skeletal muscle atrophy, pelvic limb weakness, episodic collapse, and episodes of coughing.CLINICAL FINDINGS:Initial examination revealed stunted growth, brachygnathism, trismus, and diffuse neuromuscular signs in each puppy; clinical signs were more severe in dog 2 than in dog 1. Immunohistochemical analysis revealed a lack of dystrophin protein in both dogs. During the next 3 years, each dog developed hyperinflation of the lungs, hypertrophy of the cervical musculature, and hypertrophy of the lateral head of the triceps brachii muscle.TREATMENT AND OUTCOME:Monitoring and supportive care were provided at follow-up visits during an approximately 7-year period. No other specific treatment was provided. Neuromuscular signs in both dogs remained stable after 3 years of age, with dog 2 consistently more severely affected than dog 1. The dogs had multiple episodes of aspiration pneumonia; dogs 1 and 2 were euthanatized at 84 and 93 months of age, respectively.CLINICAL RELEVANCE:The clinical course of disease in these dogs was monitored for a longer period than has been monitored in previous reports of dystrophin-deficient dogs. The clinical progression of muscular dystrophy in the 2 GSHPs was compared with that for other breeds and species with dystrophin-deficient conditions, and the potential basis for the phenotypic variation observed between these littermates, along with potential therapeutic ramifications for dogs and humans, was evaluated.

Equine Veterinary EducationVolume 17, Issue 3 p. 118-122 Stringhalt associated with a pasture infested with Hypochoeris radicata S. Y. Gardner, Corresponding Author S. Y. Gardner Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USADepartment of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorA. G. Cook, A. G. Cook Departments of Large Animal Clinical Sciences, Virginia Maryland Regional College of Veterinary Medicine, Virginia-Tech and University of Maryland, Blacksburg, Virginia 24061, USA Davie County Large Animal Hospital, 928 Farmington Rd, Mocksville, North Carolina 27028, USASearch for more papers by this authorB. S. Jortner, B. S. Jortner Biomedical Sciences and Pathobiology, Virginia Maryland Regional College of Veterinary Medicine, Virginia-Tech and University of Maryland, Blacksburg, Virginia 24061, USASearch for more papers by this authorB. V. Troan, B. V. Troan Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorN. J. H. Sharp, N. J. H. Sharp Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA Animal Critical Care Group, 1410 Boundary Road, Burnaby, British Columbia V5K 4V3, CanadaSearch for more papers by this authorN. B. Campbell, N. B. Campbell Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorC. F. Brownie, C. F. Brownie Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this author S. Y. Gardner, Corresponding Author S. Y. Gardner Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USADepartment of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorA. G. Cook, A. G. Cook Departments of Large Animal Clinical Sciences, Virginia Maryland Regional College of Veterinary Medicine, Virginia-Tech and University of Maryland, Blacksburg, Virginia 24061, USA Davie County Large Animal Hospital, 928 Farmington Rd, Mocksville, North Carolina 27028, USASearch for more papers by this authorB. S. Jortner, B. S. Jortner Biomedical Sciences and Pathobiology, Virginia Maryland Regional College of Veterinary Medicine, Virginia-Tech and University of Maryland, Blacksburg, Virginia 24061, USASearch for more papers by this authorB. V. Troan, B. V. Troan Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorN. J. H. Sharp, N. J. H. Sharp Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA Animal Critical Care Group, 1410 Boundary Road, Burnaby, British Columbia V5K 4V3, CanadaSearch for more papers by this authorN. B. Campbell, N. B. Campbell Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorC. F. Brownie, C. F. Brownie Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this author First published: 05 January 2010 https://doi.org/10.1111/j.2042-3292.2005.tb00349.xCitations: 9 AboutPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume17, Issue3June 2005Pages 118-122 RelatedInformation

OBJECTIVES:To describe the clinical and magnetic resonance imaging features of cervical vertebral malformation-malarticulation in Bernese mountain dogs.METHODS:Seven Bernese mountain dogs (four males and three females) were diagnosed with cervical vertebral malformation-malarticulation by magnetic resonance imaging. The following data were evaluated retrospectively: (1) abnormalities of the cervical vertebral column and spinal cord, (2) spinal cord compression, (3) intervertebral disc degeneration and herniation, (4) severity of clinical signs pretreatment and after treatment, (5) type of treatment and (6) outcome.RESULTS:Spin echo T1-weighted and T2-weighted images disclosed multi-level, extradural compressive spinal cord lesions (ventral, dorsolateral or both) spanning from intervertebral disc spaces C3-4 to C6-7. In all seven dogs, T2-weighted images disclosed one or more intramedullary hyperintensities associated with extradural spinal cord compression. Surgery was performed in five dogs. Two dogs were managed medically. The prognosis for surgical or conservative management in Bernese mountain dogs was similar to cervical vertebral malformation-malarticulation in other breeds.CLINICAL SIGNIFICANCE:Cervical vertebral malformation-malarticulation is an important differential diagnosis for young to middle-aged Bernese mountain dogs with a C1-5 or C6-T2 neuroanatomic localisation. Dorsolateral spinal cord compression associated with articular process hypertrophy was the most common feature of cervical vertebral malformation-malarticulation in the seven Bernese mountain dogs evaluated.

BACKGROUND:The magnetic resonance imaging (MRI) characteristics of necrotizing meningoencephalitis (NME) are not well documented.OBJECTIVES:To describe common MRI features of NME, to compare the MRI features to histopathologic findings, and to determine whether or not MRI lesions are predictive of survival time.ANIMALS:Eighteen Pugs with NME.METHODS:Retrospective MRI case study of Pugs identified by a search of medical records at 6 veterinary institutions. Eighteen dogs met inclusion criteria of histopathologically confirmed NME and antemortem MRI exam. MRI lesions were characterized and compared with histopathology with the kappa statistic. Survival times were compared with MRI findings by use of Mann-Whitney U-tests and Spearman's rho.RESULTS:Twelve of 18 lesions were indistinctly marginated with mild parenchymal contrast enhancement. Prosencephalic (17/18) lesion distribution included the parietal (16/18), temporal (16/18), and occipital (16/18) lobes. There were cerebellar (4/18) and brainstem (3/18) lesions. Asymmetric lesions were present in both gray and white matter in all dogs. Falx cerebri shift was common (11/18), and 6 dogs had brain herniation. Leptomeningeal enhancement was present in 9/18 dogs. A moderate positive association was found between parenchymal contrast enhancement and both necrosis (kappa= 0.45; P= .045) and monocytic inflammation (kappa= 0.48; P= .025). Higher MRI lesion burden was correlated with longer time from disease onset to MRI (P= .045). MRI lesion burden did not correlate to survival time.CONCLUSIONS AND CLINICAL IMPORTANCE:Asymmetric prosencephalic grey and white matter lesions with variable contrast enhancement were consistent MRI changes in Pugs with confirmed NME. While not pathognomonic for NME, these MRI characteristics should increase confidence in a presumptive diagnosis of NME in young Pugs with acute signs of neurologic disease.

OBJECTIVE:To describe diagnostic findings, surgical technique, and outcome in dogs with thoracic spinal canal stenosis and vertebral instability secondary to congenital vertebral anomalies.STUDY DESIGN:Retrospective clinical study.ANIMALS:Dogs (n=9) with thoracic spinal canal stenosis.METHODS:Medical records (1995-1996; 2000-2006) of 9 dogs with a myelographic diagnosis of spinal canal stenosis and/or vertebral instability secondary to congenital vertebral anomaly that were surgically managed by vertebral stabilization with or without laminectomy were reviewed. Data on pre- and postoperative neurologic status, diagnostic findings, surgical techniques, and outcomes were retrieved. Follow-up evaluations were performed at 1, 2, and 6 months. Long-term outcome was assessed by means of clinical examination or owner telephone interviews.RESULTS:Spinal cord compression was confirmed by myelography, and in 2 dogs, dynamic compression by stress myelography. Eight dogs regained the ability to ambulate postoperatively. One dog with a partial recovery regained voluntary movement but did not become ambulatory.CONCLUSIONS:Spinal cord injury secondary to congenital vertebral anomaly may have a good outcome when treated by vertebral stabilization with or without laminectomy. Adequate stabilization of the vertebrae and improved neurologic outcome were achieved in most dogs.CLINICAL RELEVANCE:Vertebral stabilization using positively threaded profile pins and polymethylmethacrylate with or without laminectomy is an effective treatment for spinal canal stenosis and vertebral instability secondary to congenital thoracic vertebral anomalies.

CASE DESCRIPTION:An 8-year-old Labrador Retriever with diabetes mellitus in which bilateral phacoemulsification had been performed 3 weeks earlier was evaluated for acute onset of blepharospasm, and a 7-year-old Miniature Schnauzer with chronic immune-mediated thrombocytopenia was reevaluated for keratoconjunctivitis sicca that had been diagnosed 4 weeks earlier.CLINICAL FINDINGS:Dendritic corneal ulcerations were detected in both dogs. Canine herpesvirus-1 (CHV-1) was isolated from corneal swab specimens obtained during the initial evaluation of each dog and during recheck examinations performed until the ulcerations were healed. Canine herpesvirus-1 serum neutralization titers were detected in both dogs. Results of virus isolation from oropharyngeal and genital swab specimens were negative for both dogs. The isolated viruses were identified as CHV-1 via immunofluorescence, transmission electron microscopy, PCR assay, and gene sequencing. Negative controls for PCR assay and virus isolation included conjunctival swab specimens from 50 dogs without extraocular disease and corneal swab specimens from 50 dogs with corneal ulcers, respectively.TREATMENT AND OUTCOME:Lesions resolved in both dogs after topical administration of idoxuridine or trifluridine and discontinuation of topically administered immunosuppressive medications.CLINICAL RELEVANCE:To the authors' knowledge, this is the first report of corneal ulcerations associated with naturally occurring CHV-1 infection and may represent local ocular recrudescence of latent CHV-1 infection. The viruses isolated were identified as CHV-1, and the morphology, antigenicity, and genotype were similar to those for CHV-1 isolates obtained from a puppy that died from systemic CHV-1 infection.

The objective of this investigation was to determine whether or not herpesvirus (herpes-), adenovirus (adeno-), or canine parvovirus DNA is present in the brains of dogs with necrotizing meningoencephalitis (NME), necrotizing leukoencephalitis (NLE), and granulomatous meningoencephalitis (GME). Paraffin-embedded brain specimens from 12 histopathologically confirmed dogs with NME, 3 with NLE, and 7 with GME were screened for viral DNA with degenerate herpes- and adenovirus polymerase chain reaction (PCR) and a canine parvovirus-specific PCR. Positive-control specimens included genomic viral DNA and paraffin-embedded tissues from dogs with confirmed herpes-, adeno-, or canine parvovirus infections. Herpes-, adeno-, or canine parvovirus DNA was amplified by PCR from the corresponding positive-control specimens. Negative controls included 7 dogs with various brain disorders and produced no viral amplicons. The 22 dogs with NME, NLE, and GME were negative for viral DNA. Additional studies testing for other viruses or inherited genetic mutations are warranted to gain insight into the etiologies of NME, NLE, and GME. We discuss potential etiologies and provide a clinical and histopathologic overview of these common canine encephalitides.

This report describes a 3-year-old male castrated Mastiff dog that died unexpectedly with locally extensive, acute, necrotizing myocarditis and myocardial infarction. Intralesional protozoal tachyzoites in the affected myocardium were confirmed to be Neospora caninum by a novel multiplex polymerase chain reaction (PCR) and immunohistochemistry. Protozoal organisms were not identified in other tissues by histology, immunohistochemistry, or PCR. The multiplex PCR assay was used to quickly provide preliminary results on fresh myocardium to differentiate N. caninum and Toxoplasma gondii. Neosporosis is an uncommon cause of myocarditis in adult dogs and differential diagnoses for myocarditis in this population of dogs are reviewed.