Doctor of Philosophy / General Summary: 1. The mechanisms involved in the pathogenesis of tick paralysis have been investigated in vivo in paralysed dogs and in vitro using nerve-muscle preparations removed from paralysed mice. 2. Neurologic and electromyographic examination of paralysed dogs indicated that tick paralysis involved a failure of neuromuscular transmission* No abnormality of conduction in the nerve trunk could be demonstrated and it was considered that the lesion was likely to be at or near the neuromuscular junction. 3. Nerve-muscle preparations from affected mice were found to be paralysed when examined in vitro. The paralysis was found to be temperature dependent. Results of these experiments supported the contention that the lesion was near the neuromuscular junction. 4. Neuromuscular transmission was examined in preparations from paralysed mice. No abnormality of nerve conduction could be demonstrated. The release of acetylcholine in response to nerve stimulation was depressed due to a reduction in quantal content rather than quantal size. Lowering the temperature of the preparation partially reversed this effect. These results indicated that tick paralysis is due to an abnormality in the mechanism which couples nerve terminal depolarisation and acetylcholine secretion. 5. There is some indication that crude toxin extracted from partially engorged ticks could affect nerve-muscle preparations incubated in it. 6. Apart from some secondary changes no significant morphological abnormalities could be demonstrated in nerve fibres, muscle fibres or neuromuscular junctions from tick paralysed mice.

Thesis (Ph. D.)--University of Hong Kong, 1976. / Typescript.

published_or_final_version / Biochemistry / Doctoral / Doctor of Philosophy

Doctor of Philosophy / General Summary: 1. The mechanisms involved in the pathogenesis of tick paralysis have been investigated in vivo in paralysed dogs and in vitro using nerve-muscle preparations removed from paralysed mice. 2. Neurologic and electromyographic examination of paralysed dogs indicated that tick paralysis involved a failure of neuromuscular transmission* No abnormality of conduction in the nerve trunk could be demonstrated and it was considered that the lesion was likely to be at or near the neuromuscular junction. 3. Nerve-muscle preparations from affected mice were found to be paralysed when examined in vitro. The paralysis was found to be temperature dependent. Results of these experiments supported the contention that the lesion was near the neuromuscular junction. 4. Neuromuscular transmission was examined in preparations from paralysed mice. No abnormality of nerve conduction could be demonstrated. The release of acetylcholine in response to nerve stimulation was depressed due to a reduction in quantal content rather than quantal size. Lowering the temperature of the preparation partially reversed this effect. These results indicated that tick paralysis is due to an abnormality in the mechanism which couples nerve terminal depolarisation and acetylcholine secretion. 5. There is some indication that crude toxin extracted from partially engorged ticks could affect nerve-muscle preparations incubated in it. 6. Apart from some secondary changes no significant morphological abnormalities could be demonstrated in nerve fibres, muscle fibres or neuromuscular junctions from tick paralysed mice.

Thesis (Ph. D.)--University of Sydney, 1977. / Title from title screen (viewed April 1, 2008). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Department of Veterinary Pathology and Bacteriology, Faculty of Veterinary Science. Degree awarded 1997; thesis submitted 1976. Includes bibliographical references. Also available in print form.

Inaug.-Diss.--Zürich.

Submitted in fulfillment of the requirements for the Master of Technology: Biotechnology, Technikon Natal, 1999. / "Paralysis syndrome" was first described by Dr M.J Versveld in 1993. The disease appeared to be confined to the Natal area with a few sporadic outbreaks in Gauteng, but none in the Cape region, nor in non-Rainbow flocks. The syndrome tended to re-appear on affected farms but not necessarily in the same houses. There was no correlation between affected flocks and their parent flock or hatchery identity (Maharaj, pers.comms.1994). / M

Thesis (Ph.D.) - Carleton University, 2002. / Includes bibliographical references (p. 152-169). Also available in electronic format on the Internet.

Thesis (M.A. in speech and hearing sciences)--Washington State University, May 2010. / Title from PDF title page (viewed on Feb. 9, 2010). "Department of Speech and Hearing Sciences." Includes bibliographical references (p. 26-30).

No description available.