Clinical features, comparative imaging findings, treatment, and outcome in dogs with discospondylitis: A multi-institutional retrospective study.

BACKGROUND: Limited recent data exists regarding discospondylitis in dogs. HYPOTHESIS/OBJECTIVES: (i) Describe the signalment, clinical and imaging findings, etiologic agents, treatment, and outcome of dogs with discospondylitis, (ii) determine diagnostic agreement between radiographs, CT, and MRI with regard to the presence of discospondylitis and its location, and (iii) determine risk factors for relapse and progressive neurological deterioration. ANIMALS: Three hundred eighty-six dogs. METHODS: Multi-institutional retrospective study. Data extracted from medical records were: signalment, clinical and examination findings, diagnostic results, treatments, complications, and outcome. Potential risk factors were recorded. Breed distribution was compared to a control group. Agreement between imaging modalities was assessed via Cohen's kappa statistic. Other analyses were performed on categorical data, using cross tabulations with chi-squared and Fisher's exact tests. RESULTS: Male dogs were overrepresented (236/386 dogs). L7-S1 (97/386 dogs) was the most common site. Staphylococcus species (23/38 positive blood cultures) were prevalent. There was a fair agreement (κ = 0.22) between radiographs and CT, but a poor agreement (κ = 0.05) between radiographs and MRI with regard to evidence of discospondylitis. There was good agreement between imaging modalities regarding location of disease. Trauma was associated with an increased risk of relapse (P = .01, OR: 9.0, 95% CI: 2.2-37.0). Prior steroid therapy was associated with an increased risk of progressive neurological dysfunction (P = .04, OR: 4.7, 95% CI: 1.2-18.6). CONCLUSIONS AND CLINICAL IMPORTANCE: Radiograph and MRI results could be discrepant in dogs with discospondylitis. Prior trauma and corticosteroids could be associated with relapse and progressive neurological dysfunction, respectively.

Negative Antigenuria in a Dog with Suspected Central Nervous System Localized Blastomycosis.

A 7 yr old female spayed mixed-breed dog was presented for a 1 wk history of neck pain and pelvic limb weakness. Examination revealed nonambulatory paraparesis and thoracolumbar hyperesthesia. MRI revealed extensive intramedullary T2-weighted/short tau inversion recovery hyperintensity and diffuse severe T1-post contrast meningeal enhancement of the thoracolumbar spinal cord. An L5-L6 cerebrospinal fluid sample revealed a suppurative pleocytosis (81% neutrophils, total protein 4362.5 mg/dL and nucleated cell count 352,000/µL). While awaiting the results of infectious disease testing, the dog was treated for suspected meningoencephalitis of unknown etiology with corticosteroids, cyclosporine, and a cytarabine arabinoside infusion. The dog neurologically declined and was started on broad-spectrum antibiotics. The dog continued to decline despite antibiotics, and infectious disease titers subsequently revealed serum antibody positivity for blastomycosis. The dog was then referred to a multispecialty referral hospital and was treated with amphotericin B followed by fluconazole. Prednisone was continued at anti-inflammatory doses. Urine blastomycosis antigen testing was submitted for subsequent disease monitoring but was negative. Five months after presentation the dog was clinically doing well with no identifiable neurologic deficits. This case demonstrates that neurologic blastomycosis may have negative urine antigen concentrations in some dogs and that other diagnostic modalities should be pursued when central nervous system fungal disease is suspected.

A Subset of Dogs with Presumptive Idiopathic Epilepsy Show Hippocampal Asymmetry: A Volumetric Comparison with Non-Epileptic Dogs Using MRI.

MRI-acquired volumetric measurements from 100 dogs with presumptive idiopathic epilepsy (IE) and 41 non-epileptic (non-IE) dogs were used to determine if hippocampal asymmetry exists in the IE as compared to the non-IE dogs. MRI databases from three institutions were searched for dogs that underwent MRI of the brain and were determined to have IE and those that were considered non-IE dogs. Volumes of the right and left hippocampi were measured using Mimics® software. Median hippocampal volumes of IE and non-IE dogs were 0.47 and 0.53 cm3, respectively. There was no significant difference in overall hippocampal volume between IE and non-IE dogs; however, IE dogs had greater hippocampal asymmetry than non-IE dogs (P < 0.012). A threshold value of 1.16 from the hippocampal ratio had an 85% specificity for identifying IE-associated asymmetry. Thirty five percent of IE dogs had a hippocampal ratio >1.16. Asymmetry was not associated with any particular hemisphere (P = 0.67). Our study indicates that hippocampal asymmetry occurs in a subset of dogs with presumptive idiopathic/genetic epilepsy, suggesting a structural etiology to some cases of IE.