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Biomedical subjects

T A Holliday

Publications and source records attributed to T A Holliday.

31 records · Page 2Linked to original sources

Rabies vaccine virus infection in three dogs.

Ascending paralysis developed in 3 dogs, 12 to 14 days following inoculation with a modified live virus, chicken embryo origin, low egg passage, Flury strain rabies vaccine. The paralysis began in the inoculated limb but rapidly involved both hindlimbs. Partial paresis of the forelimbs was seen several days following the hindlimb paralysis in all 3 dogs, and in 1 of these dogs the infection ascended rapidly to the brain as well. Two of the dogs recovered within 1 and 2 months, respectively, but the 3rd dog died within 5 days of the onset of paralytic signs. The fatal case was complicated by naturally acquired coincidental distemper. Serologic studies in 2 dogs and virus isolation from the 3rd dog indicated that rabies virus was the cause of the paralysis in 2 of the dogs and contributed to the disease syndrome in the 3rd dog. Virus could not be isolated from the saliva of CSF of the 2 surviving dogs. The virus isolated in the fatal case appeared to have some of the characteristics of the vaccine virus, as determined by its behavior in mice, cell culture, and embryonating chicken eggs and by its failure to produce Negri bodies in the brain of the infected dog.

Animals↗

Polymyositis and polyarthritis associated with systemic lupus erythematosus in a dog.

Systemic lupus erythematosus with polymyositis and polyarthritis was diagnosed in a 7-year-old female Standard Poodle. Pertinent clinical signs included extreme muscular weakness, muscle wasting, atrial fibrillation, and dysphagia due to megaesophagus. Aspiration pneumonia secondary to the megaesophagus contributed to the death of the dog. Serum muscle enzyme activities were increased. Electromyographic findings included fibrillation potentials, positive sharp waves, increased insertional activity, and bizarre high-frequency repetitive potentials. Histopathologic findings in skeletal muscle included myofiber necrosis and phagocytosis; regeneration of myofibers; perivascular and interstitial infiltrations of macrophages, lymphocytes, and plasma cells; and type I and II myofiber degeneration and vacuolation.

Animals↗

Sensory nerve conduction velocity: technical requirements and normal values for branches of the radial and ulnar nerves of the dog.

Conduction velocities of compound action potentials of sensory axons of alteral superficial radial (LSR) and dorsal ulnar nerves (DUN) of the dog were determined by averaging potentials evoked and recorded through subcutaneous needle electrodes. Suitable locations for electrodes were identified and specificities of sites for LSR and DUN were verified by recording before and after cutting the nerves. Stimulus rates of 4/second to 20/second did not markedly affect conduction velocities. Increasing stimulus intensity in steps from threshold to 8 X threshold recruited more axons into the compound action potentials but resulted in interference from movement and muscle potentials at 4 X or 8 X threshold. Mean conduction velocities at 2 X threshold were: LSR = 61.7 +/- 0.76 SEM; DUN = 68.1 +/- 2.71 SEM.

Action Potentials↗

Old dog encephalitis and demyelinating diseases in man.

Pathologic findings in mature dogs with old dog encephalitis were compared with the findings in multiple sclerosis, subacute sclerosing panencephalitis and neuromyelitis optica in man. Fluorescent antibody studies in animal and human tissues were compared. Optic neuritis in dogs with chronic distemper shows changes similar to those in the optic tract of human patients with severe demyelinating disease. The pathologic changes in multiple sclerosis, such as perivascular infiltration with lymphocytes, plasma cells and demyelination are similar to those seen in old dog encephalitis. Demyelination in old dog encephalitis is usually diffuse. The findings strongly support a possible relationship of old dog encephalitis to multiple sclerosis, subacute sclerosing panencephalitis, and neuromyelitis optica.

Animals↗

Acquired canine myasthenia gravis: immunocytochemical localization of immune complexes at neuromuscular junctions.

In the acquired form of myasthenia gravis in dogs, there are circulating antibodies to acetylcholine receptors (AChRs) and a reduction in the number of AChRs in the postsynaptic membrane. In this study, immune complexes were localized at the neuromuscular junctions in biopsy samples from 10 myasthenic dogs by immunocytochemical means employing conjugates of staphylococcal protein A and horseradish peroxidase. Immune complexes were observed in approximately 70% of the neuromuscular junctions studied in both type 1 and type 2 myofibers. Thus, acquired canine myasthenia gravis appears to involve immune-mediated mechanisms that destroy AChRs in a manner similar to myasthenia gravis in humans. Protein A was also observed to bind principally to elastic fibers in small arteries and arterioles of some myasthenic and control dogs; however, the significance of that localization is unknown.

Animals↗

Unilateral and bilateral brainstem auditory-evoked response abnormalities in 900 Dalmatian dogs.

In a survey of 900 Dalmatian dogs, brainstem auditory-evoked responses (BAER) and clinical observations were used to determine the incidence and sex distribution of bilateral and unilateral BAER abnormalities and their association with heterochromia iridis (HI). To assess the efficacy of BAER testing in guiding breeding programs, data from 749 dogs (subgroup A), considered to be a sample of the population at large, were compared with data from a subgroup (subgroup B; n = 151) in which selection of breeding stock had been based on BAER testing from the beginning of the 4-year survey. Brainstem auditory-evoked responses were elicited by applying click stimuli unilaterally, while applying a white noise masking sound to the contralateral ear. Under these conditions, BAER were either normal, unilaterally absent, or bilaterally absent. Dogs with bilaterally absent BAER were clinically deaf; dogs with unilaterally absent BAER were not clinically deaf but appeared dependent on their BAER-normal ears for their auditory-cued behavior. Dogs with unilaterally absent BAER often were misidentified as normal by uninformed observers. Among the 900 dogs, 648 (72.0%) were normal, 189 (21.0%) had unilateral absence of BAER, and 63 (7.0%) had bilateral absence of BAER or were clinically deaf and assumed to have bilaterally absent BAER (n = 4). Total incidence in the population sampled was assumed to be higher, because some bilaterally affected dogs that would have been members of subgroup A undoubtedly did not come to our attention. Among females, 24.0% were unilaterally abnormal and 8.2% were bilaterally abnormal whereas, among males, 17.8% were unilaterally abnormal and 5.7% were bilaterally abnormal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗