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Biomedical subjects

A deLahunta

Publications and source records attributed to A deLahunta.

41 records · Page 3Linked to original sources

Neospora caninum infection in English Springer Spaniel littermates. Diagnostic evaluation and organism isolation.

Progressive paraparesis developed in four male English Springer Spaniel pups from a litter of five during the first 10 weeks of life. Two of the pups, which had the earliest onset of neurologic signs, were euthanatized without further workup. However, a detailed investigation was completed on the remaining two littermates at 12 weeks of age. Both pups had progressive paraparesis for 3 to 4 weeks before presentation, with one dog developing subsequent asymmetric pelvic limb extensor rigidity. Based on results from neurologic examination, cerebrospinal fluid (CSF) analysis, electrophysiology, and muscle/nerve biopsy, a presumptive diagnosis of protozoal polyradiculitis and polymyositis was made. Necropsy of the most severely affected pup confirmed the clinical diagnosis of inflammatory nerve root and muscle disease but no organisms were found. To increase the potential yield of organisms, the second pup was placed on immunosuppressive doses of corticosteroids and euthanatized 2 weeks later. Numerous organisms were found in lesions in muscle and the central nervous system. Organisms grew in tissue culture and were isolated from the peritoneal fluid of gerbils inoculated with infected tissue. Organisms were not isolated from inoculated mice, guinea pigs, rabbits, and hamsters. No parasites were seen in feces or tissues of three cats fed infected dog tissues. Serologic testing demonstrated a strong positive titer to Neospora caninum in both pups, and electron microscopy showed the characteristic morphology of this parasite.

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Clinical and clinicopathologic features in 11 cats with Cuterebra larvae myiasis of the central nervous system.

The medical records of 11 cats with histopathologic findings consistent with central nervous system (CNS) Cuterebra larvae myiasis were retrospectively examined to determine if clinical features could identify this disorder antemortem. Young to middle-aged indoor-outdoor domestic shorthaired cats presenting with acute neurologic signs from July through September predominated. Many cats recently had clinical signs consistent with upper respiratory disease. Most cats presented for depression, lethargy, or seizures. Almost all cats had abnormal rectal temperatures, either hypethermia or hypothermia. Peripheral leukocytosis and eosinophilia were not characteristic of cats with CNS cuterebriasis. Cerebrospinal fluid analysis did not consistently disclose evidence of inflammation. Common neurologic deficits included blindness, abnormal mentation, and signs of unilateral prosencephalic disease. No specific clinical or clinicopathologic test was diagnostic for CNS cuterebriasis.

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Sensory polyganglioradiculoneuritis in a dog.

Generalized reduction of nociception and conscious and unconscious proprioception were found in an approximately eight-year-old, male, Maltese mixed-breed dog presented for difficulty prehending food and experiencing ataxia of three months duration. Results of needle electromyogram, motor nerve conduction velocity, and cerebrospinal fluid analysis were normal. A diagnosis of sensory polyneuropathy was suspected. No underlying cause could be determined. Neurological signs progressed to quadriparesis over the following four months despite treatment attempts with prednisone and procarbazine. Necropsy confirmed a sensory polyganglioradiculoneuritis, but no inciting cause could be established.

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Motor neuron abiotrophy in a saluki.

A nine-week-old saluki puppy was presented to Tufts University School of Veterinary Medicine for progressive, generalized weakness and bilateral forelimb deformities. Examination suggested a diffuse neuromuscular lesion. Cerebrospinal fluid (CSF) analysis showed normal nucleated cell count and protein level; however, many macrophages had vacuolated cytoplasm. Electromyography (EMG) recordings suggested denervation in paraspinal and appendicular muscles. Tibial motor nerve conduction velocity was normal, but direct evoked muscle potential had reduced amplitude. Histopathology revealed diffuse, symmetrical, degenerative motor neuronopathy of the ventral horn of the spinal cord with associated lesions in nerves and muscles. Histopathology was consistent with an abiotrophy that was likely inherited.

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