GRANULOMATOUS MENINGOENCEPHALOMYELITIS IN A DOG

Clinical and pathological findings in a 2.5-year-old speyed female dog with granulomatous meningoencephalomyelitis are described. The clinical course was progressive with the major neurological signs being referable to the posterior brain stem and cerebellum. Histological examination of the brain revealed a multifocal granulomatous meningoencephalitis predominantly associated with the blood vessels of the white matter.     

Idiopathic granulomatous and necrotising inflammatory disorders of the canine central nervous system: a review and future perspectives

Granulomatous meningoencephalomyelitis, necrotizing meningoencephalitis, and necrotizing leukoencephalitis are common inflammatory conditions of the canine central nervous system. Although each disease has unique histopathological features, these canine disorders collectively seem to be aberrant immune responses directed against the central nervous system. A review of the neurological signs and general neurodiagnostic approach to canine meningoencephalitis is followed by an overview of the specific clinical and neuropathological features of granulomatous meningoencephalomyelitis, necrotizing meningoencephalitis, and necrotizing leukoencephalitis. The aetiopathogenesis of each disorder is explored including potential genetic, immunological, and environmental factors along with the current and prospective immunomodulatory therapies for meningoencephalitis.     

Canine distemper with spinal cord lesions.

A case of distemper in a 6-month-old dog is described. The dog was presented with a history of tetraparesis suggestive of trauma. Neurological examination and clinical pathology findings of lymphopenia and pleocytosis suggested a viral cause. Microscopic findings of a nonsuppurative meningoencephalomyelitis with numerous intranuclear inclusions in the cerebellum, brain stem, and all parts of the spinal cord suggested a diagnosis of distemper.     

Otitis media/interna and suppurative meningoencephalomyelitis associated with Listeria monocytogenes infection in a llama

Listeria monocytogenes was found to be the cause of fatal suppurative meningoencephalomyelitis in a 3.5-month-old cria. The cria initially had clinical signs of unilateral peripheral vestibular disease, but on the following day, the cria developed progressive signs of encephalitis. Treatment with antibiotics, flunixin meglumine, and anticonvulsant drugs failed to stop progression of the disease, and the cria was euthanatized. Post-mortem examination revealed otitis media-interna and diffuse suppurative meningoencephalomyelitis. Listeria monocytogenes was isolated from CSF and brain tissue.     

Neurological diseases of rottweilers: Neuroaxonal dystrophy and leukoenceph- alomalacia

Neuroaxonal dystrophy (NAD) and leukoencephalomalacia (LEM) are two neurological disorders of the rottweiler that initially present as ataxia of all four limbs. Disorders to be included in the differential diagnosis are caudal cervical spondylomyelopathy, canine distemper virus meningoencephalomyelitis, other nervous system infections or inflammations and spinal cord neoplasia. All diagnostic tests including myelography, cerebrospinal fluid analysis, electrodiagnos-tic testing and serum and cerebrospinal fluid titres for canine distemper virus are normal in NAD and LEM. There is no treatment for either disease and neurological signs progressively deteriorate. Eventually neurological deficits develop besides ataxia and these help differentiate NAD from LEM. Dogs with NAD develop head tremors and nystagmus while dogs with LEM develop conscious proprioceptive deficits and quadriparesis; the short term prognosis for NAD is better than LEM. Most dogs with LEM are euthanased because of non-ambulatory tetraparesis within one year. The histopathological lesions associated with NAD include axonal spheroids in many spinal cord and caudal brainstem nuclei and reduced numbers of Purkinje cells in the cerebellum, while in LEM, multifocal areas of demyelination and malacia of the spinal cord and brainstem are the primary histopathological lesions. Both NAD and LEM are suspected to have an autosomal recessive genetic transmission.     

Chronic encephalomyelitis caused by canine distemper virus in a Bengal tiger

A chronic progressive neurologic disease was observed and monitored for 18 months in a young, tamed Bengal tiger. Clinical, serologic, and neuropathologic evidence of canine distemper virus infection was seen. Clinical signs included convulsions, myoclonus, and slowly progressive ataxia. Marked increases in neutralizing antibodies against canine distemper virus were seen in the serum and cerebrospinal fluid. Neuropathologic findings were nonsuppurative meningoencephalomyelitis, with perivascular cuffing, demyelination, and inclusion bodies typical of canine distemper virus. It was concluded that, in light of this case and an earlier report of canine distemper in lion cubs, vaccination of this subgroup of carnivores with a killed vaccine may be beneficial if exposure to other animals susceptible to canine distemper is anticipated.     

Granulomatous meningoence-phalomyelitis in 21 dogs

Granulomatous meningoencephalomyelitis (GME) is a well recognised disease entity affecting dogs. It manifests in a wide variety of clinical syndromes. The lesion is characterised by focal or disseminated non-caseating granulomas in the brain and spinal cord, non-suppurative meningitis and marked perivascular lymphoid cuffing. The clinical signs can be acute and rapidly progressive or can manifest as a chronic relapsing disease. In this survey, 12 clinical cases were referred to Murdoch University Veterinary Hospital and nine cases were submitted for necropsy. While cerebrospinal fluid examination in seven of these cases suggested inflammatory disease, necropsy confirmed the presence of GME. An immunohistochemical technique for detection of distemper virus antigen failed to identify the presence of distemper virus antigen in any of the cases. It was concluded that distemper virus was not involved in the aetiology of these 21 cases all of which were confirmed by post mortem examination.     

Halicephalobus gingivalis encephalomyelitis in a horse

An 8-year-old, Arabian mare presented with acute progressive ataxia and a firm swelling over the right mandible. Radiographs revealed multiple radiolucent areas on the mandibles. The mare's neurological signs progressed, she was consequently euthanized. Postmortem examination revealed mandibular granulomatous reactions and meningoencephalitis due to the nematode Halicephalobus gingivalis.     

Combined cytosine arabinoside and prednisone therapy for meningoencephalitis of unknown aetiology in 10 dogs

OBJECTIVES: The differential diagnosis for young to middle-aged dogs with progressive neurological signs, focal or multifocal computed tomography/magnetic resonance imaging lesions, mononuclear cerebrospinal fluid pleocytosis and negative infectious titres includes granulomatous meningoencephalomyelitis, breed-specific meningoencephalitis, infectious meningoencephalitis of unknown origin and central nervous system neoplasia. The terminology meningoencephalitis of unknown aetiology may be preferable for cases that lack histopathological diagnoses. The safety and efficacy of a combination of cytosine arabinoside and prednisone protocol is evaluated, in this study, for the treatment of meningoencephalitis of unknown aetiology in 10 dogs. METHODS: Cases were selected based on neuroanatomical localisation, negative regional infectious disease titres, cerebrospinal fluid pleocytosis and brain imaging. Clinical response was gauged through follow-up examinations, owner and referring veterinarian surveys and review of medical records. RESULTS: Partial or complete remission was achieved in all dogs; the median survival time for the 10 dogs was 531 days (range 46 to 1025 days), with five of the 10 dogs alive at the time of writing. CLINICAL SIGNIFICANCE: Prednisone/cytosine arabinoside is a safe empirical therapy for dogs with meningoencephalitis of unknown aetiology; this drug combination may prolong survival time.     

Cerebrospinal Fluid Analysis and Clinical Outcome of Eight Dogs With Eosinophilic Meningoencephalomyelitis

Eight dogs, 14 weeks to 5.5 years of age, had signs of diffuse or multifocal meningoencephalomyelitis. The total white cell counts of the cerebrospinal fluid (CSF) ranged from 11 to 5,550 cells/microliters; the percentage of eosinophils ranged from 21% to 98%. The total CSF protein content range was 19 to 1,430 mg/dl. On necropsy, two dogs had granulomatous encephalomyelitis due to protozoan infection. The other six dogs, of which three were Golden Retriever dogs, appeared to have an idiopathic eosinophilic meningoencephalitis; four of these dogs recovered. The significance of eosinophils in CSF and the possible emergence of a new encephalitic syndrome of dogs involving a hypersensitivity to an unknown agent is also discussed.     

Neuroinflammatory diseases of the central nervous system of dogs: A retrospective study of 207 cases (2008–2019)

In this study we describe 207 cases of neuroinflammatory diseases of the central nervous system (CNS) in dogs autopsied at the Athens Veterinary Diagnostic Laboratory (University of Georgia, United States) from 2008 to 2019. Idiopathic and infectious diseases were diagnosed in 111 cases (53.6%) and 96 cases (46.4%), respectively. Idiopathic diseases consisted of granulomatous meningoencephalomyelitis (n = 42; 37.8% of idiopathic cases), nonspecific lymphoplasmacytic meningoencephalomyelitis (n = 39; 35.1%), necrotizing meningoencephalomyelitis (n = 22; 19.8%), presumed steroid-responsive meningitis-arteritis (n = 6; 5.4%), and necrotizing leukoencephalitis (n = 2; 1.8%). Infectious diseases consisted of bacterial infections (n = 49; 51% of infectious cases), viral infections (n = 39; 40.6%), fungal infections (n = 5; 5.2%), and parasitic infections (n = 3; 3.1%). Our study provides an overview of the most frequent neuroinflammatory diseases of the CNS of dogs in our diagnostic routine; indicates that a comprehensive diagnostic approach, including a thorough evaluation of the pathology findings and ancillary laboratory testing results, is important for an adequate diagnosis of neurologic diseases in dogs; and underscores the problems associated with the variability in tissue sample collection methods among cases. The great number of nonspecific lymphoplasmacytic meningoencephalitis also highlights the need for development of molecular laboratory tests to identify potential infectious agents in these cases.     

MAGNETIC RESONANCE IMAGING IN THE DIAGNOSIS OF FOCAL GRANULOMATOUS MENINGOENCEPHALITIS IN TWO DOGS

Two dogs with neurologic signs were evaluated by magnetic resonance imaging of the brain. Focal space-occupying lesions were present in both dogs. In the first, the lesion was in the brain stem and in the second, in the cerebellum. In one dog the lesion was only evident after administration of gadolinium-DTPA-dimeglumine. Based on the magnetic resonance images, neoplasia was suspected in both dogs but histopathologically, granulomatous meningoencephalomyelitis was diagnosed.     

Signs of neurologic dysfunction in dogs with central versus peripheral vestibular disease

OBJECTIVE: To determine the frequency of specific signs of neurologic dysfunction in dogs with central vestibular disease (CVD) or peripheral vestibular disease (PVD) and whether the degree of head tilt, rate of nystagmus, and number of beats of postrotatory nystagmus can be used to help distinguish CVD from PVD. DESIGN: Prospective clinical study. ANIMALS: 40 client-owned dogs with vestibular system dysfunction. PROCEDURE: A standard neurologic examination was performed, along with an expanded vestibular system examination that assessed the degree of head tilt, rate of nystagmus, and number of beats of postrotatory nystagmus. RESULTS: Dogs with CVD were significantly more likely to be nonambulatory than were dogs with PVD. Dogs with PVD were significantly more likely to veer or lean in 1 direction and to have resting nystagmus than were dogs with CVD. Median rate of resting nystagmus was significantly higher for dogs with PVD, but no significant differences between groups were detected in regard to presence or degree of head tilt, presence of positional ventral strabismus, and number of beats of postrotatory nystagmus. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that nonambulatory tetraparesis is significantly more common in dogs with CVD and veering and leaning are significantly more common in dogs with PVD. Although neither the degree of head tilt nor the number of beats of postrotatory nystagmus could be used to distinguish CVD from PVD, rate of resting nystagmus may be useful in distinguishing the 2 conditions.     

Canine distemper virus-associated hypocalcemia.

A retrospective study was done to correlate serum calcium concentrations and parathyroid gland ultrastructure to clinical, immunologic, and pathologic changes experimentally induced in gnotobiotic dogs by canine distemper virus (CDV). Dogs infected with CDV had significantly reduced serum calcium concentrations associated with ultrastructural evidence of parathyroid gland inactivity, degeneration, and viral inclusions. Although CDV-infected dogs exhibited neurologic signs, minimal lesions were present in the central nervous system. It is suggested that viral-induced parathyroid dysfunction may contribute to neutrologic disturbance of CDV infection.     

Surgical technique, postoperative complications and outcome in 14 dogs treated for hydrocephalus by ventriculoperitoneal shunting

Objective: To report frequency and type of complications, and outcome in dogs with severe neurologic signs secondary to internal, suspected obstructive hydrocephalus treated by ventriculoperitoneal (VP) shunting. Study Design: Case series. Animals: Dogs (n=14). Methods: Medical records (2001–2006) was reviewed for dogs that had VP shunting. Inclusion criteria were complete medical record, progressive forebrain signs unresponsive to medical treatment, normal metabolic profile, negative antibody titers and/or cerebrospinal PCR for Toxoplasma gondii, Neospora caninum, and canine distemper virus, magnetic resonance images of the brain, confirmed diagnosis of VP shunting, and follow‐up information. Results: Hydrocephalus was idiopathic in 5 dogs and acquired (interventricular tumors, intraventricular hemorrhage, inflammatory disease) in 9 dogs. Four dogs developed complications 1 week to 18 months postoperatively, including ventricular catheter migration, infection, shunt under‐drainage, kinking of the peritoneal catheter, valve fracture, and abdominal skin necrosis. Three of these dogs had 1 or more successful revision surgeries and 1 dog was successfully treated with antibiotics. All, but 1 dog, were discharged within 1 week of surgery, and had substantial neurologic improvement. Median survival time for all dogs was 320 days (1–2340 days), for dogs with idiopathic hydrocephalus, 274 (60–420) days and for dogs with secondary hydrocephalus, 365 (1–2340) days. Conclusions: VP shunting was successful in relieving neurologic signs in most dogs and postoperative complications occurred in 29%, but were resolved medically or surgically.     

Cerebrospinal Fluid PCR and Antibody Concentrations against Anaplasma phagocytophilum and Borrelia burgdorferi sensu lato in Dogs with Neurological Signs

Background: The tick-borne bacteria Borrelia burgdorferi sensu lato (sl) and Anaplasma phagocytophilum have been suspected to cause neurological signs in dogs. Diagnosis often has been made based on positive antibody titers in serum of dogs with neurological signs, but a high seroprevalence in dogs in at-risk populations makes diagnosis difficult.
Objective: To determine if the neurological signs in dogs examined were caused by any of these bacteria.
Animals: Fifty-four dogs presented to a board-certified neurologist.
Methods: Prospective study. We divided dogs into 2 groups: those with inflammatory diseases of the central nervous system (CNS) and those with neurological signs from other diseases. Blood and cerebrospinal fluid (CSF) from all dogs were analyzed.
Results: Dogs with inflammatory CNS diseases showed no serum antibodies against any of the agents. Among dogs with neurological signs from other diseases, 10.3% had serum antibodies for B. burgdorferi sl and 20.5% for A. phagocytophilum . All blood samples analyzed for bacterial deoxyribonucleic acid (DNA) and all CSF analyzed for antibodies and bacterial DNA for the 2 agents were negative.
Conclusions and Clinical Importance: Based on this study, these bacteria are unlikely causes of neurologic disease in dogs and the presence of serum antibodies alone does not document or establish a definitive diagnosis of CNS disease caused by these organisms. Dogs that have neurologic disease and corresponding serum antibodies against these agents should have additional tests performed to assess for other potential etiologies of the signs.     

Neurologic, endocrinologic, and pathologic findings associated with large pituitary tumors in dogs: eight cases (1976-1984)

Invasive tumors of the pituitary gland were diagnosed in 8 dogs. Seven of the dogs had been treated for pituitary-dependent hyperadrenocorticism before the onset of neurologic signs. All 8 dogs had behavior abnormalities and similar neurologic signs: 6 dogs had rotary nystagmus and 7 dogs had symmetric tetraparesis. Once neurologic signs developed, the clinical course in all 8 dogs had a mean duration of 4.7 +/- 2.0 months before death or euthanasia; 5 dogs had a clinical course of less than or equal to 2 months. Necropsy was performed in 7 dogs. The histologic diagnosis was malignant pituitary adenocarcinoma in 2 dogs and pituitary adenoma in 5 dogs.     

Ischaemic encephalopathy and focal granulomatous meningoencephalitis in the cat

Three cats were presented with neurological deficits compatible with cerebral disease. Two of the cats had temporal lobe infarction diagnosed as ischaemic encephalopathy; one cat had granulomatous inflammation, diagnosed as focal granulomatous meningoencephalitis. In all three cases the lesions were characterized by necrotic, cavitated areas. Vascular insult was the cause of the ischaemic encephalopathy and the focal granulomatous meningoencephalitis may have been caused by feline infectious peritonitis (FIP) virus. An infectious aetiology, possibly FIP virus, is proposed for the ischaemic encephalopathy. A relationship between these two neurological diseases may exist.