Review Article1: The Mechanisms of Pathogenicity in the Tick Paralyses

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Abstract
Some 43 tick species in 10 genera have been more or less definitely incriminated as causing tick paralysis in humans, other mammals, or birds. The pathomechanism of the different tick paralyses has been partially studied, but exclusively in the disease syndromes caused by Dermacentor andersoni, D. variabilis, Ixodes holoryclus, and Argas (persicargas) walkerae. From results of limited research devoted to I. holocyclus-induced paralysis, it is concluded that the pathogenic principle of this paralysis differs basically from that of the others, especially in respect to the functional integrity of the peripheral nerves. Experimental studies of the pathomechanism of Dermacentor and Argas paralyses show marked reduction in maximal motor nerve conduction velocities, clear decrease in compound action potentials of nerves and their corresponding muscles, and impairment of impulse propagation of afferent fibers together with simultaneous increase of the stimulating current potentials necessary to elicit a response. The Argas paralysis also shows impairment in the distal nerve section or in the myoneural synapse. This impairment. together with the reversible functional modifications in cable properties of the whole peripheral nerve, can be influenced by acetylcholine and by blocking acetylcholinesterase. The myocardium and the stimulus-conducting system of the heart are not directly affected in the tick paralyses. Ultrastructural defects have not been observed. The Dermacentor and Argas paralyses are generally defined essentially as motor polyneuropathies with only limited participation of the afferent pathways. The postulated toxin has membranophilic properties; its primary point of attack is possibly in the region of the nodes of Ranvier and/or at the membrane in general. The somatic toxin bond, however, is very labile. The pathogenic mechanism of I. holocyclus paralysis cannot be explained on the basis of present investigations. The amplitudes of nerve compound action potentials are said to be unchanged. It is suggested from in vitro experiments that this paralysis is due to a temperature-dependent inhibition of evoked release of acetylcholine at the neuromuscular junction.

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