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Tick Paralysis

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Pathogenesis

Tick paralysis affects mainly motor pathways, and to less extent also autonomic and sensory pathways of the nervous system. A neurotoxin in the saliva of certain tick species interferes with acetylcholine release at the neuromuscular junction, producing a neuromuscular blockade. In most dogs paralysis of esophageal muscles develops, with or without esophageal dilatation (megaesophagus). Saliva and ingested food or fluid pool into the esophagus, and are regurgitated into the pharynx and mouth.

Ixodes holocyclus causes reversible myocardial depression and diastolic failure, leading to cardiogenic pulmonary oedema. In severe cases, increased PCV (packed cell volume) reflects a fluid shift from the circulation to the lungs. Progressive pulmonary dysfunction appears to be primarily due to oedema, leading to hypoxia, hypercarbia, respiratory acidosis, and eventually death.

Removal of ticks does not immediately halt the progression of the disease, once clinical signs are apparent. The fatality rate may increase dramatically when the tick has fully engorged and depleted. Appropriate and prompt action saves ~95% of affected animals.

Death from respiratory failure is likely to occur within 1-2 days of onset of clinical signs.

Further information

  • Edlow JA, McGillicuddy DC: Tick paralysis. Inf Dis Clin North Am. 2008, 22, 397-414
  • Gordon BM, Giza CC: Tick paralysis presenting in an urban environment. Pediatr Neurol. 2004, 30, 122-4
  • Malik R, Farrow BR: Tick paralysis in North America and Australia. Vet Clin North Am Small Anim Pract. 1991, 21, 157-71
  • Wright IG, Stone BF, Neish AL: Tick (Ixodes holocyclus) paralysis in the dog – induction of immunity by injection of toxin. Aust Vet J. 1983, 60, 69-70

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