Evaluation of a treatment protocol in dogs with intraspinal spirocercosis.

OBJECTIVE: To evaluate the efficiency and safety of a doramectin-based treatment protocol in dogs affected by intraspinal spirocercosis (Spirocerca lupi). ANIMALS: Client-owned dogs that were admitted to a veterinary hospital during 2021 to 2022 with acute onset of neurological signs and diagnosed with intraspinal spirocercosis. All dogs underwent complete neurological evaluation, CSF analysis, PCR confirmation of CNS S lupi infection, and follow-up evaluation of at least 6 months. PROCEDURES: Upon diagnosis, dogs were treated with doramectin at a dose of 400 µg/kg, SC, q 24 h for 3 consecutive days, followed by the same dose once a week for 6 weeks. Prednisone was administered at a dose of 1 mg/kg, PO, q 24 h and tapered every 3 days. Antimicrobial clindamycin was administered at a dose of 12.5 mg/kg, PO, q 12 h for 7 days to reduce the risk of secondary spinal cord infection. Short- and long-term outcomes (1 week to 56 months) were recorded. RESULTS: 8 dogs fulfilled the inclusion criteria, 7 of which presented with neurological deficits and 1 with cervical pain. Initiation of treatment was associated with stopping the deterioration in 7 of 8 dogs. Seven dogs improved and 6 recovered ambulation. One dog was euthanized due to lack of improvement. Six of the recovered dogs were still ataxic on the last follow-up examination at 6 to 56 months. No adverse effects of the drug were noted. CLINICAL RELEVANCE: Frequent administration of doramectin was found to be safe and effective in preventing neurological deterioration in dogs with intraspinal spirocercosis.

Blood-brain barrier dysfunction in canine epileptic seizures detected by dynamic contrast-enhanced magnetic resonance imaging.

OBJECTIVE: Dogs with spontaneous or acquired epilepsy exhibit resemblance in etiology and disease course to humans, potentially offering a translational model of the human disease. Blood-brain barrier dysfunction (BBBD) has been shown to partake in epileptogenesis in experimental models of epilepsy. To test the hypothesis that BBBD can be detected in dogs with naturally occurring seizures, we developed a linear dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) analysis algorithm that was validated in clinical cases of seizing dogs and experimental epileptic rats. METHODS: Forty-six dogs with naturally occurring seizures of different etiologies and 12 induced epilepsy rats were imaged using DCE-MRI. Six healthy dogs and 12 naive rats served as control. DCE-MRI was analyzed by linear-dynamic method. BBBD scores were calculated in whole brain and in specific brain regions. Immunofluorescence analysis for transforming growth factor beta (TGF-ß) pathway proteins was performed on the piriform cortex of epileptic dogs. RESULTS: We found BBBD in 37% of dogs with seizures. A significantly higher cerebrospinal fluid to serum albumin ratio was found in dogs with BBBD relative to dogs with intact blood-brain barrier (BBB). A significant difference was found between epileptic and control rats when BBBD scores were calculated for the piriform cortex at 48 hours and 1 month after status epilepticus. Mean BBBD score of the piriform lobe in idiopathic epilepsy (IE) dogs was significantly higher compared to control. Immunohistochemistry results suggested active TGF-ß signaling and neuroinflammation in the piriform cortex of dogs with IE, showing increased levels of serum albumin colocalized with glial acidic fibrillary protein and pSMAD2 in an area where BBBD had been detected by linear DCE-MRI. SIGNIFICANCE: Detection of BBBD in dogs with naturally occurring epilepsy provides the ground for future studies for evaluation of novel treatment targeting the disrupted BBB. The involvement of the piriform lobe seen using our linear DCE-MRI protocol and algorithm emphasizes the possibility of using dogs as a translational model for the human disease.

Clinical characteristics of Spirocerca lupi migration in the spinal cord.

Spirocerca lupi is a nematode infecting dogs mostly in tropical and subtropical areas. Although its typical target is the esophageal wall, aberrant migration is not uncommon, including migration of unknown incidence into the spinal cord. While successful treatment of intraspinal S. lupi (ISSL) infection depends on early diagnosis, tools for definitive ante-mortem diagnosis are unavailable. We therefore aimed at characterizing clinical signs and clinical pathology findings of ISSL in dogs. For that, we analyzed medical records of dogs hospitalized in 2005-2016 presenting with neurological signs consistent with ISSL, which were diagnosed definitively post-mortem. Retrieved information included signalment, medical history, chief complaint, physical and neurological evaluation, neuroanatomical localization at presentation, clinical pathology, imaging findings, treatment, outcome and post-mortem findings. Ten midsize to large breed dogs were included, 7 of which had received prophylactic treatment. In all 10 dogs, onset was acute and neurological deterioration until presentation (2 h-6 d) was fast. Neurological examination localized the lesions within the spinal cord and paresis or paralysis was asymmetric in all dogs. Spinal pain was documented in 9/10 dogs. Cerebrospinal fluid (CSF) analysis was abnormal in all dogs and was characterized by pleocytosis in 8/10, whereas cytology revealed the presence of eosinophils in all dogs. Advanced imaging excluded spinal cord compression in all dogs tested. Post-mortem examination detected spinal cord migration tract in all cases. Nematodes were found in the spinal cord parenchyma (8/10) or adjacent to it (2/10) in all dogs. A larva was found in the subarachnoid space of one dog and an adult nematode in the thoracic intervertebral artery of another. Esophageal nodules were found in 5/10 dogs. These findings suggest that the combination of sudden onset of acute asymmetric paresis accompanied by pain, presence of eosinophils in the CSF and lack of compressive lesion may serve as sufficient evidence for tentative diagnosis of ISSL in endemic areas.

Retrospective evaluation of combined mycophenolate mofetil and prednisone treatment for meningoencephalomyelitis of unknown etiology in dogs: 25 cases (2005-2011).

OBJECTIVE: To evaluate the use of a combined protocol of prednisone and mycophenolate mofetil (MMF) for the treatment of meningoencephalomyelitis of unknown etiology (MUE) and to describe response, adverse effects, and outcome. DESIGN: Retrospective study (2005-2011). SETTING: University teaching hospital. ANIMALS: Twenty-five client-owned dogs with clinical signs, neuroimaging, and cerebrospinal abnormalities consistent with MUE. Five dogs whose MMF treatment was discontinued after 7-14 days due to gastrointestinal clinical signs were evaluated only for adverse effects. INTERVENTIONS: Dogs were initially treated with prednisone 2 mg/kg PO every 12 hours and with MMF 20 mg/kg PO or IV every 12 hours. Prednisone was tapered after 4 days to 1 mg/kg every 12 hours for 14 days, then to every 24 hours for 30 days, and again reduced by half every 2-4 months thereafter. When prednisone was tapered completely or to 0.5 mg/kg every 24-48 hours without clinical relapse, MMF was tapered in a similar manner. MEASUREMENTS AND MAIN RESULTS: Partial or complete clinical response was achieved in 95% (19/20) of the dogs. Median survival time by the end of the study was 250 days (range 6 to >1,679) with 40% (8/20) of the dogs still alive (336-1,679 days after diagnosis). All Pug dogs (4/20) included in the study died with a median survival time of 14 days. Adverse effects attributed to MMF, which included hemorrhagic diarrhea within the first 2 weeks of treatment, were recorded in 20% (5/25) of the dogs. CONCLUSIONS: MMF can be used as an adjunctive treatment for dogs with MUE. This protocol enables reduction of prednisone treatment or, in some cases, its complete withdrawal. The possibility of intravenous administration is advantageous in cases with severe neurological abnormalities and mentation changes, often seen in MUE. Attention is warranted for gastrointestinal adverse effects, especially in the first 2 weeks of treatment.

Spontaneous intradural disc herniation with focal distension of the subarachnoid space in a dog.

Myelo-computed tomography of a paraparetic 14-year-old dog revealed subarachnoid distension with an intradural filling defect above the T13-L1 disc space. T12-L1 hemilaminectomy followed by durotomy allowed removal of a large piece of degenerated disc material that compressed the spinal parenchyma. Full return to function was achieved 10 days post-surgery. The distension was likely secondary to the intradural herniation, and is a rare and distinct finding.

Hernie discale intra-durale spontanée avec distension focale de l'espace sous-arachnoïdien chez un chien. Une myélo-tomographie par ordinateur d'un chien paraparétique âgé de 14 ans a révélé une distension sous-arachnoïdienne avec un défaut de remplissage intradural au-dessus de l'espace du disque T13­L1. Une hémilaminectomie de T12­L1 suivie d'une durotomie ont permis l'enlèvement d'un grand morceau de matériel dégénéré du disque qui comprimait le parenchyme rachidien. Un retour complet à la fonction a été obtenu 10 jours après la chirurgie. La distension était probablement secondaire à l'hernie intradurale et représente une constatation rare et distincte.(Traduit par Isabelle Vallières).