Clinical and neuropathological findings of acute carbon monoxide toxicity in chihuahuas following smoke inhalation.

Three adult Chihuahuas were presented for evaluation after smoke inhalation during a house fire. All three dogs received supportive care and supplemental oxygen. After initial improvement, the dogs developed seizures. Despite anticonvulsant therapy and supportive care, the dogs died. The brains of two dogs were examined. Lesions were identified that were compatible with acute carbon monoxide (CO) toxicity. Lesions were confined to the caudate nucleus, the globus pallidus, and the substantia nigra bilaterally, as well as the cerebellum, cerebral cortex, and dorsal thalamus. This case report describes the clinicopathological sequelae in acute CO toxicity.

Congenital hemicerebral anomaly in a stranded Pacific harbor seal (Phoca vitulina richardsi).

A stranded 5-month-old female Pacific harbor seal (Phoca vitulina richardsi) was presented displaying tachypnea and diminished lung sounds. No neurological abnormalities were noted. The animal was treated for verminous pneumonia, but died 2 wk later. Gross necropsy examination revealed a severe obstructive verminous pneumonia associated with large numbers of Otostrongylus circumlitus. In addition, the majority of the right cerebral hemisphere was absent, with hypoplasia of the left cerebellar hemisphere, absence of the right pyramid, and malformation of the right occipital bone. Histopathologic findings included multifocal thrombosis and inflammation of pulmonary arteries, verminous pneumonia, and mild vacuolation of the subependymal white matter in the third ventricle representing swelling of myelin sheaths and edema. This is the first report of a hemicerebral anomaly in a marine mammal.

The influence of age on patellar reflex response in the dog.

The patellar tendon reflex is a clinical parameter commonly used to assess neurological status. Factors such as quadriceps muscle fiber composition, femur length, and patient age have been reported to influence total and fractionated reflex times in human beings. The purpose of this blinded, cross-sectional study was to examine the effect of age on the patellar reflex in the dog. Eighty-six dogs without evidence of neurological impairment or orthopedic disease of the stifle (eg, patellar luxation or cranial cruciate ligament rupture) were assigned to 1 of 2 groups on the basis of age: group 1, <10 years old (n = 72); or group 2, > or =10 years old (n = 14). Patellar reflexes were elicited in both pelvic limbs by a reflex hammer while the dog was in lateral recumbency. The reflex was scored as present or absent by a blinded individual. Two dogs in group I had reflexes absent in both limbs, 3 dogs in group 2 had reflexes absent in both limbs, and 1 dog in group 2 lacked a response in 1 limb. The proportion of dogs with absent patellar reflexes in group 2 (4 of 14, 95% CI, 8-58%) was significantly higher than the proportion of dogs with absent patellar reflexes in group 1 (2 of 72, 95% CI, 0-10%) (P < .006). Furthermore, dogs lacking at least 1 patellar reflex were older than those having both reflexes present (P = .04). Weight was not related to the presence of both reflexes (P = .49). These findings suggest that neurologically normal dogs may have an age-dependent decline in patellar reflex magnitude or a prolongation of total reflex time (TRT).

Meningioangiomatosis in young dogs: a case series and literature review.

Meningioangiomatosis (MA) is a proliferative disorder of the central nervous system (CNS) that has been reported rarely in humans and sporadically in dogs. Meningioangiomatosis may occur in the brainstem or cervical spinal cord of young dogs and can be identified tentatively by magnetic resonance imaging. The histopathologic hallmark of MA is a leptomeningeal plaque that extends along the CNS microvasculature and invades the adjacent neural parenchyma. This case series describes the neurologic signs, clinical progression, diagnostic imaging, and neuropathology of 4 dogs with MA. The 4 dogs with MA are compared and contrasted with 4 previously reported cases in dogs as well as with their human counterpart.

Polymerase chain reaction (PCR) amplification of parvoviral DNA from the brains of dogs and cats with cerebellar hypoplasia.

Cerebellar hypoplasia in cats is caused most commonly by an in utero or perinatal infection with feline panleukopenia virus (parvovirus). Cerebellar hypoplasia has been reported infrequently in dogs, but no viral etiology has been identified to date. DNA was extracted from archival, paraffin-embedded, cerebellar tissue from 8 cats and from 2 canine littermates with cerebellar hypoplasia, 2 canine littermates with cerebellar cortical abiotrophy, 6 dogs with congenital cerebellar vermal defects, 1 dog with congenital hydranencephaly, and 15 dogs and cats with various encephalitdes. The DNA extracted from each cerebellum was subject to polymerase chain reaction (PCR) amplification by 3 primer pairs specific for parvovirus DNA. Sequence analysis of PCR products from each of the 8 cats and 2 dogs with cerebellar hypoplasia confirmed their identity with parvoviral DNA. The 6 dogs with cerebellar vermal defects, 2 dogs with cortical abiotrophy, 1 dog with congenital hydranencephaly, and all control samples were PCR negative for parvovirus. Parvoviral structural proteins were not identified by immunohistochemistry in either dog with cerebellar hypoplasia. This study shows that parvoviral DNA can be amplified from feline and canine archival brain tissue and that cerebellar hypoplasia in dogs might be associated with in utero parvovirus infection.

Thoracolumbar spinal cord compression due to vertebral process degenerative joint disease in a family of Shiloh Shepherd dogs.

Five young Shiloh Shepherd Dogs (4 males and 1 female) related by a common sire were studied because of progressive pelvic limb weakness and incoordination. All dogs had a spastic paraparesis and pelvic limb ataxia consistent with an upper motor neuron and general proprioceptive lesion between spinal cord segments T3 and L3. Proliferative lesions involving one or more of the articular processes from the 11th thoracic vertebrae to the 2nd lumbar vertebra were observed on radiographs of the thoracolumbar vertebrae. Dorsal compression of the spinal cord was identified during imaging studies at these sites. Abnormalities of the synovial joints and bony proliferation of the involved articular processes were identified at postmortem examination in 2 dogs. The articular processes and associated vertebral arches protruded into the vertebral canal, indenting the dorsal surface of the spinalcord. Degenerative joint disease (DJD) was identified histologically. A compressive myelopathy was diagnosed in the spinal cord. These dogs were affected by a compressive myelopathy as a consequence of vertebral process DJD that likely has a geneticcomponent. The DJD could have been caused by a primary vertebral malformation or an injury to the processes at a young age causing malarticulation.

Use of a multiplex polymerase chain reaction assay in the antemortem diagnosis of toxoplasmosis and neosporosis in the central nervous system of cats and dogs.

OBJECTIVE: To develop a multiplex polymerase chain reaction (PCR) assay for the detection of Toxoplasma gondii and Neospora caninum DNA in canine and feline biological samples. SAMPLE POPULATION; Biological samples from 7 cats with systemic (n = 4) or CNS (3) toxoplasmosis, 6 dogs with neospora- or toxoplasma-associated encephalitis, and 11 animals with nonprotozoal disease. PROCEDURE: Primers for T gondii, N caninum, and the canine ferritin gene (dogs) or feline histone 3.3 gene (cats) were combined in a single PCR assay. The DNA was extracted from paraffin-embedded brain tissue, CSF, or skeletal muscle. The PCR products with positive results were cloned, and sequence identity was confirmed. RESULTS: Of 7 cats and 4 dogs with immunohistochemical or serologic evidence of toxoplasmosis, PCR results were positive for all cats and 3 dogs for T gondii, and positive for T gondii and N caninum for 1 dog. Another dog had negative PCR results for both parasites. Of 2 dogs with immunohistochemical or serologic evidence of neosporosis, PCR results were positive for 1 for N caninum and positive for the other for T gondii. All negative-control samples yielded negative results for T gondii and N caninum on the PCR assay. CONCLUSIONS AND CLINICAL RELEVANCE: Standard tests for toxoplasmosis or neosporosis associated with the CNS rely on serologic, histologic, or immunohistochemical analysis and can be difficult to interpret. The multiplex PCR assay with built-in control reactions could be a complementary clinical tool for the antemortem diagnosis of toxoplasmosis or neosporosis associated with the CNS.

Feline spinal cord gliomas: Clinicopathologic and diagnostic features of seven cases

Intraparenchymal spinal cord tumors in the cat are rarely reported and often as single case reports. In the current study, the clinical, magnetic resonance imaging (MRI), histologic, and immunohistochemical features of 7 cases of intraparenchymal spinal cord tumors in the cat are described. All cats were domestic breed, ranged from 4 to 12 years of age (median 8 years), and included spayed females (5/7) and neutered males (2/7). The duration of clinical signs ranged from 2 weeks to 3 months. MRI revealed lesions that were hyperintense on T2-weighted images with variable contrast enhancement. All 7 tumors had histologic features consistent with glial origin: 3 were astrocytic (gemistocytic or fibrous), and 2 were oligoastrocytic. Single cases of oligodendroglioma and gliomatosis cerebri were also present in the study. Glial fibrillary acidic protein immunoreactivity was robust in the tumors that were predominately astrocytic, and the gliomatosis cerebri case had extensive BLA.36 and Iba1 immunoreactivity. Ki-67 immunoreactivity was variable and most abundant in the case of malignant oligoastrocytoma. The majority of peritumoral lymphocytes were CD3 positive. The current study expands upon the known reports of spinal cord neoplasia in the cat, confirms a caudal cervical segment predilection, and includes a report of gliomatosis cerebri in the spinal cord of a cat.

Adult-onset cerebellar cortical abiotrophy and retinal degeneration in a domestic shorthair cat.

A 4-year-old, neutered male domestic shorthair cat presented for evaluation of ataxia and visual deficits. Neurological examination revealed severe cerebellar ataxia with symmetrical hypermetria and spasticity, a coarse whole-body tremor, positional vertical nystagmus, and frequent loss of balance. A menace response was absent bilaterally, and the pupils were widely dilated in room light. A funduscopic examination revealed markedly attenuated to absent retinal vessels and pronounced tapetal hyperreflectivity, findings consistent with end-stage retinal degeneration. Blood work evaluation included retroviral testing, a complete blood count, serum biochemistry analysis, taurine levels, and toxoplasma immunoglobulin G and immunoglobulin M titers. All were within reference ranges. The patient was euthanized, and a necropsy was performed. Microscopically, lesions of the nervous system were confined to the cerebellum and were consistent with cerebellar cortical abiotrophy. Selective photoreceptor degeneration was seen on histopathological examination of the retina with a reduction in the number of rods and cones. The combination of clinical findings and histopathological lesions seen here has not been previously reported in the cat.