MAGNETIC RESONANCE IMAGING CHARACTERISTICS IN FOUR DOGS WITH CENTRAL NERVOUS SYSTEM NEOSPOROSIS

Neosporosis is a polysystemic disease that can affect dogs of any age and can cause inflammation of the central nervous system. Antemortem diagnosis can be challenging, as clinical and conventional laboratory test findings are often nonspecific. A previous report described cerebellar lesions in brain MRI studies of seven dogs and proposed that these may be characteristic for central nervous system Neosporosis. The purpose of this retrospective study was to describe MRI characteristics in another group of dogs with confirmed central nervous system neosporosis and compare them with the previous report. The hospital's database was searched for dogs with confirmed central nervous system neosporosis and four observers recorded findings from each dog's MRI studies. A total of four dogs met inclusion criteria. Neurologic examination was indicative of a forebrain and cerebellar lesion in dog 2 and multifocal central nervous system disease in dogs 1, 3, and 4. Magnetic resonance imaging showed mild bilateral and symmetrical cerebellar atrophy in three of four dogs (dogs 2, 3, 4), intramedullary spinal cord changes in two dogs (dogs 3, 4) and a mesencephalic and metencephalic lesion in one dog (dog 2). Multifocal brain lesions were recognized in two dogs (dogs 1, 4) and were present in the thalamus, lentiform nucleus, centrum semiovale, internal capsule, brainstem and cortical gray matter of the frontal, parietal or temporal lobe. Findings indicated that central nervous system neosporosis may be characterized by multifocal MRI lesions as well as cerebellar involvement in dogs.     

The subacute neurotoxicity of excess pyridoxine HCl and clioquinol (5-chloro-7-iodo-8-hydroxyquinoline) in beagle dogs. II. Pathology

The lesions caused by excess oral pyridoxine hydrochloride (150 mg/kg body weight/day) and clioquinol (200 mg/kg body weight/day), given individually and in combination to adult Beagle dogs, were evaluated. The experimental period was 100 to 112 days, except that four dogs in each of the clioquinol and combined-treatment groups were killed early because of severe debilitation or neurologic disease, and one dog given both compounds died on the third day of compound administration. Degenerative neurologic lesions had distribution specific for the compound given. Pyridoxine-treated dogs had lesions limited to tracts and nerves with neuronal bodies of their nerve fibers in the spinal and trigeminal ganglia. Clioquinol-treated dogs had neurologic lesions limited to the central nervous system. The most lesions were in the rostral dorsal funiculus and distal aspects of the optic nerve fibers, but minimal to mild degenerative changes also occurred in distal aspects of the corticospinal and spinocerebellar tracts. Dogs given both pyridoxine hydrochloride and clioquinol had a combination of the lesions in dogs given pyridoxine or clioquinol individually. Several dogs given clioquinol or pyridoxine plus clioquinol had extraneural lesions, including myocardial degeneration and thyroidal alterations.     

Natural bovine lentiviral type 1 infection in Holstein dairy cattle. I. Clinical,serological, and pathological observations

Clinical, serological, and pathological abnormalities observed in Holstein cows naturally infected with bovine lentivirus 1 bovine immunodeficiency virus (BIV) and other infections were progressive and most commonly associated with weight loss, lymphoid system deficiency, and behavioral changes. Clinical evidence of meningoencephalitis was dullness, stupor, and occasional head or nose pressing postures. The polymerase chain reactions associated the BIV provirus with the lesions in the central nervous system and lymphoid tissues. Multiple concurrent infections developed in retrovirally infected cows undergoing normal stresses associated with parturition and lactation. A major functional correlate of the lymphoreticular alterations was the development of multiple secondary infections which failed to resolve after appropriate antibacterial therapy. The chronic disease syndrome in dairy cows associated with BIV may be useful as a model system for investigation of the pathogenesis of the nervous system lesions and lymphoid organ changes that occur in humans with lentiviral infection.     

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.     

Diarrhea associated with myenteric ganglionitis in a dog

Diarrhea in a Border Terrier was associated with inflammatory lesions of the myenteric plexus. This lesion has been documented rarely in dogs. It is speculated that the myenteric plexus lesions were responsible for an autonomic nervous system dysfunction, which resulted in extreme intestinal hypermotility and subsequent diarrhea. Suggested tests for dogs suspected to have autonomic dysfunction are given.     

NORMAL VARIATION IN SIZE OF THE LATERAL VENTRICLES OF THE LABRADOR RETRIEVER DOG AS ASSESSED BY MAGNETIC RESONANCE IMAGING

Detecting canine brain lesions on computed tomography (CT) or magnetic resonance (MR) scans can be difficult if the lesions do not enhance well following administration of intravenous contrast material. Changes in the shape and position of the ventricular system can be important in the diagnosis of such lesions. Normal variation within the canine ventricular system has not been documented. MR scans from 62 normal Labrador retriever type dogs were evaluated. Five dogs had symmetric enlargement of the ventricles, while nineteen dogs had mild to severe ventricular asymmetry. The incidence of asymmetry in normal dogs must be considered when using ventricular configuration as an indication of central nervous system abnormality.     

A comparison of clinical,magnetic resonance imaging and pathological findings in dogs with gliomatosis cerebri,focusing on cases with minimal magnetic resonance imaging changes‡

The primary study objective was to determine whether clinical examination and magnetic resonance imaging (MRI) can underestimate canine gliomatosis cerebri (GC); we also investigated immunohistochemical features. Seven dogs with GC were studied; four recruited specifically because of minimal MRI changes. Neuroanatomic localization and the distribution of MRI, gross and sub‐gross lesions were compared with the actual histological distribution of neoplastic cells. In six cases, clinical examination predicted focal disease and MRI demonstrated a single lesion or appeared normal. Neoplastic cells infiltrated many regions deemed normal by clinical examination and MRI, and were Olig2‐positive and glial fibrillary acid protein‐negative. Four dogs had concurrent gliomas. GC is a differential diagnosis for dogs with focal neurological deficits and a normal MRI or a focal MRI lesion. Canine GC is probably mainly oligodendrocytic. Type II GC, a solid glioma accompanying diffuse central nervous system neoplastic infiltration, occurs in dogs as in people.     

Primary canine and feline nervous system tumors: intraoperative diagnosis using the smear technique

The recent application of neuroimaging techniques in veterinary neurology has led to the accurate localization of many types of intracranial lesions but has also created a clinical need, particularly with brain tumors, for a specific intraoperative diagnosis. For human brain tumors, a smear technique has been used successfully for many years to provide an extremely rapid, highly accurate intraoperative diagnosis. In similar smear preparations of intracranial lesions, obtained either by computed tomography (CT)-guided stereobiopsy or from a craniotomy, we have described distinguishing cytologic features of some primary spontaneous nervous system tumors in 80 dogs and 13 cats. A final diagnosis was confirmed by evaluation of paraffin-embedded sections from the same sample and, when appropriate, by immunocytochemical staining. Preliminary findings indicate that, in dogs and cats, this procedure is useful for rapid, accurate intraoperative diagnosis of many primary nervous system tumors. The distinguishing features of the canine and feline tumors bear a remarkably close resemblance to their human counterparts.     

Intracranial Lesions in Dogs With Hemangiosarcoma

A retrospective analysis of 85 dogs with hemangiosarcoma (HSA) that underwent complete necropsy, including gross examination of the brain, was conducted. Grossly identifiable intracranial lesions were present in 17 dogs. Twelve of 85 dogs (14.2%) had brain metastases. Four of 85 dogs (4.7%) had hemorrhagic lesions and/or ischemic necrosis without identifiable tumor. One dog had a primary central nervous system tumor. Signs of intracranial disease were present in six of 85 dogs (7.1%) with HSA; four had brain metastases and two had nonneoplastic lesions. Metastases had a propensity for cerebrum and gray matter. Dogs with brain metastases had more widely disseminated disease than dogs without brain metastases (P less than 0.001). Dogs with pulmonary metastases were at greater risk for developing brain metastases than dogs without pulmonary metastases (odds ratio = 8.31). Although thoracic radiography accurately identified ten of 12 dogs (83%) with pulmonary metastases, too few cases were available to assess the applicability/accuracy of thoracic radiography in predicting the presence or absence of brain metastases in dogs with malignancy and signs of intracranial disease.     

Prevalence of behavioral changes associated with age-related cognitive impairment in dogs

OBJECTIVE: To determine the prevalence of age-related behavioral changes, namely impairment, in a randomly chosen population of dogs. DESIGN: Age-stratified cohort study. ANIMALS: 97 spayed female and 83 castrated male dogs that were 11 to 16 years old. PROCEDURE: Data on possible impairment in 4 behavioral categories (ie, orientation in the home and yard, social interaction, house training, and sleep-wake cycle) linked to cognitive dysfunction were obtained from dog owners, using a structured telephone interview. Hospital records of dogs had been screened to exclude dogs with dysfunction in organ systems that may cause behavioral changes. Dogs with behavioral impairment were those with > or = 2 signs of dysfunction within a category. Dogs with impairment in 1 category were considered mildly impaired and those with impairment in > or =2 categories were considered severely impaired. RESULTS: Age by sex interactions for dogs with impairment in any category were not significant, and, therefore, data on castrated males and spayed females were pooled for analyses across ages. The prevalence of age-related progressive impairment was significant in all categories. The percentage of 11- to 12-year-old dogs with impairment in > or = 1 category was 28% (22/80), of which 10% (8/80) had impairment in > or = 2 behavioral categories. Of 15- to 16-year-old dogs, 68% (23/34) had impairment in > or =1 category, of which 35% (12/34) had impairments in > or = 2 categories. There were no significant effects of body weight on the prevalence of signs of dysfunction in the behavioral categories. CONCLUSIONS AND CLINICAL RELEVANCE: Data collected provide estimates of the prevalence of various degrees of age-related behavioral changes associated with cognitive dysfunction in dogs. Age-related behavioral changes may be useful indicators for medical intervention for dogs with signs of cognitive impairment.     

Progressive ataxia due to central demyelination in Rottweiler dogs

A clinicopathological study of a neurologic disease in Rottweiler dogs was conducted. Clinical data were available on 16 dogs, 11 of which were examined pathologically. All dogs had a history of progressive gait abnormalities, which had commenced insidiously at an age varying from 1.5 to 3.5 years. In most dogs the fore limbs were affected prior to the hind limbs. At neurologic examination ataxia of all 4 limbs was seen, in some instances accompanied by an apparent paresis. Proprioceptive positioning was delayed whereas spinal reflexes were often hyperactive. Plain and contrast radiographs of the spine did not reveal any compressive lesions in 5 dogs examined. Cerebrospinal fluid analysis in 4 dogs was normal. Electrodiagnostic testing in 3 dogs revealed no abnormalities. At pathologic examination demyelinating lesions were found in the central nervous system. These were largely confined to the cervical spinal cord and brain stem and had a rather characteristic more or less symmetric distribution. Pedigree data suggested that the disease is transmitted genetically.     

Age-related changes in the brain of the dog.

Although many age-related changes have been described in the nervous system of different species, few authors have specifically studied the topic. Knowledge of such changes is essential to veterinary pathologists, who must distinguish the lesions of specific pathologic processes from those arising as a result of normal aging. The brains of 20 old dogs, ranging in age from 8 to 18 years, were compared with those of 10 young dogs using routine staining techniques (hematoxilin and eosin, periodic acid-Schiff), special staining techniques (periodic acid-methenamine silver stain), and immunohistochemical techniques to detect glial fibrillary acid protein, neurofilaments, ubiquitin, and beta-amyloid. Changes affected meninges and choroid plexuses, meningeal and parenchymal vessels, neurons, and glial cells. Of special interest was the presence of polyglucosan bodies, cerebrovascular amyloid deposition, senile plaques, and ubiquitinated bodies. Some of the age-related changes found, particularly lipofuscin, polyglucosan bodies, and beta-amyloid protein deposition, may play a role in the pathogenesis of the canine cognitive dysfunction syndrome. The dog could be used as a natural animal model for the study of normal aging and human neurodegenerative diseases.     

EPENDYMAL AND PERIVENTRICULAR MAGNETIC RESONANCE IMAGING CHANGES IN FOUR DOGS WITH CENTRAL NERVOUS SYSTEM BLASTOMYCOSIS

Rapid detection of central nervous system (CNS) involvement is important for dogs with blastomycosis, as this can affect antifungal drug selection and has been associated with an increased risk of death. Previous reports describing magnetic resonance imaging (MRI) characteristics of canine CNS blastomycosis primarily identified mass lesions. The purpose of this retrospective study was to determine whether other MRI characteristics of CNS blastomycosis may also occur. Medical records of the Purdue University Veterinary Teaching Hospital were searched and four dogs met inclusion criteria. Magnetic resonance imaging characteristics included periventricular edema, periventricular and meningeal contrast enhancement, and ventriculomegaly. Periventricular lesions most commonly involved the rostral horn of the lateral ventricles and the third ventricle. Increased meningeal contrast enhancement involved the cerebrum, thalamus, sella turcica, and brainstem. Findings indicated that, in addition to mass lesions, MRI characteristics of periventricular hyperintensity, contrast enhancement, and ventriculomegaly may also occur in dogs with CNS blastomycosis.     

Ochratoxin A and citrinin induced nephrosis in Beagle dogs. III. Terminal renal ultrastructural alterations

The extent and type of renal ultrastructural changes in Beagle dogs varied with the administration of ochratoxin A and citrinin alone and in the two dosage combinations. The three predominant changes were cytoplasmic vacuolation, myelin figure formation and lesions designated as cytoplasmic disarray. These changes were mainly of the endomembane system of the tubular epithelial cells. Cytoplasmic vacuoles were within proximal and distal tubules and collecting ducts and were most numerous in dogs given 10 mg/kg critrinin. Vacuolation of similar distribution, but less severe, was seen in renal tubular cells of dogs given the higher dose of the combined mycotoxins (0.2 mg/kg ochratoxin A + 10 mg/kg citrinin). This damage was limited to the proximal tubular cells in dogs given only ochratoxin A (0.1 or 0.2 mg/kg). Myelin figures were in proximal epithelial cells of dogs given ochratoxin A alone or combined with citrinin. There was cytoplasmic disarray in dogs of all groups except for dogs given 5 mg/kg citrinin. This lesions was usually limited to the proximal tubules. The lesions, however, was found in cells of the distal tubules of dogs given 10 mg/kg citrinin alone.     

Heart rate modulation by sympathetic nerves in dogs with heart failure

To clarify heart rate modulation by the sympathetic nervous system, dogs with naturally acquired and experimentally induced heart failure were examined. Heart rate and plasma catecholamine concentrations were measured in clinically healthy dogs (control dogs) and dogs with mitral regurgitation (MR) during a resting period, a standing period, a period of standing in a medical examination room (to which the dogs were unaccustomed), a running period, and a period of recovery after running. The heart rate and plasma catecholamine concentration increased in control dogs during the standing period and the medical examination room period, relative to the resting period. However, dogs with MR did not exhibit any clear increase in heart rate or catecholamine concentration under these light stress conditions. Running stress increased plasma catecholamine levels in control dogs; however, dogs with MR did not exhibit any significant changes. Thirty-two dogs with naturally acquired heart disease were classified as grades I to III on the ISACHC scale. The degree of increase in heart rate and plasma catecholamine levels in dogs with naturally acquired heart failure depended on their degree of heart failure. In conclusion, an increased heart rate and an activated sympathetic nervous system were observed, even in mild heart failure. This chronically activated sympathetic activity is expected to increase myocardial oxygen consumption, myocardial hypertrophy, and fibrosis, and to portend a poorer prognosis in heart failure.     

Sequences and polymorphisms of the canine monoamine transporter genes SLC6A2, SLC6A3, and SLC6A4 among five dog breeds

Monoamine transporters have roles to regulate the monoamine concentrations in synaptic clefts in the central nervous system and are the targets of antidepressants and psychostimulants. They include transporters for norepinephrine, dopamine and serotonin, which are encoded by the SLC6A2, SLC6A3, and SLC6A4 genes, respectivily. We sequenced the full lengths of the coding regions of these genes for dogs and identified four single nucleotide polymorphisms (SNPs) in SLC6A2 and four in SLC6A3. One SLC6A3 SNP was non-synonymous and caused an amino acid substitution from threonine to serine. The genotype frequencies of these polymorphisms differed significantly among five breeds with different behavioral traits, suggesting that novel SLC6A2 and SLC6A3 SNPs would provide additional useful information for behavioral genetic studies in dogs.     

Insulinoma and Subclinical Peripheral Neuropathy in Two Dogs

Two dogs with diffuse, subclinical polyneuropathy associated with insulinoma are reported. Seizures were the dominant sign of central nervous system disease. One dog had clinical signs of facial nerve paralysis. Lesions in selected appendicular and cranial nerves included a mixture of demyelination, remyelination, and axonal degeneration. The incidence (range: 18-47%) of these changes far exceeded that of comparable nerves from six control dogs (range 0-11%). Myopathic and electrodiagnostic findings were compatible with the nerve changes.     

SENSITIVITY OF LOW‐FIELD T2* IMAGES FOR DETECTING THE PRESENCE AND SEVERITY OF HISTOPATHOLOGIC MENISCAL LESIONS IN DOGS

The sensitivity of low‐field magnetic resonance (MR) T2^* images for predicting the presence of meniscal lesions was determined in 12 dogs with naturally‐occurring cranial cruciate ligament rupture and three control dogs, using histopathology as the reference standard. Previously published grading systems were used to grade the severity of meniscal lesions on MR images, gross inspection and histopathology. Focal areas of increased signal intensity were detected in 11/12 symptomatic dogs and 3/3 control dogs. Lesions mimicking meniscal tears (pseudotears) were identified at junctions between meniscal margins and adjacent connective tissue in control dogs and dogs with naturally occurring disease. Histopathologic lesions were present in all menisci of both symptomatic and control dogs, including the menisci from two affected dogs that appeared grossly normal but were removed and submitted based on MR imaging findings. Histopathologic lesions identified included hyaline cartilage metaplasia and changes in the amount of ground substance and cellularity. The sensitivity of MR imaging for detecting the presence of meniscal histopathologic lesions was 90% in symptomatic dogs and 91% in control dogs. However, agreement between severity scores for the different tests was poor. Low‐field MR imaging is a sensitive test for predicting the presence but not severity of meniscal histopathologic lesions in dogs with naturally‐occurring cranial cruciate ligament rupture. Findings also supported previous studies indicating that histopathologic lesions can be present in dogs with grossly normal menisci. An improved grading system for comparing MR images and histopathologic severity of meniscal lesions in dogs is needed.     

Brain and spinal cord haemorrhages associated with Angiostrongylus vasorum infection in four dogs

Multifocal haemorrhages associated with Angiostrongylus vasorum infection were observed in the central nervous system of four dogs with neurological signs including depression, seizures, spinal pain and paresis. In magnetic resonance images the majority of the lesions were isointense or slightly hyperintense in T1-weighted images, hyperintense in T2-weighted images and hypointense in T2*-weighted (gradient echo) images, compatible with haemorrhages more than seven days old. Lesions were found in the brain of three of the dogs and in the spinal cord of two. The cerebrospinal fluid contained high concentrations of protein and evidence of erythrophagia. All the dogs had coagulopathy and pulmonary haemorrhage of varying severity. A vasorum larvae were detected in the faeces of each of the dogs. Neural A vasorum was confirmed at postmortem examination in two dogs.