Tick Paralysis

Ticks in North America may cause an acute flaccid paralysis. Engorged female ticks are believed to secrete a neurotoxin that prevents the release of acetylcholine and thereby causes a paralysis of skeletal muscles. Acetylcholine is a necessary neurotransmitter for skeletal muscle contraction. When acetylchole is absent, the result is loss of motor control. This paralysis begins in the hind legs and will progress to the front end of the patient within 24 - 48 hours and is therefore termed an ascending paralysis. Spinal reflexes are absent with tick paralysis but pain perception and anal tone are normal. Dogs are the most commonly affected species but the condition may also be seen in ruminants and man, primarily children. Cats appear more resistant to the effect of the neurotoxin and are rarely, if ever, affected in North America. Loss of sensation (sensory abnormalities) has not been reported in the dog, which contrasts human cases which document numbness and tingling in the limbs.

Clinical signs develop five to nine days after tick attachment. The presence of only one tick is sufficient to produce paralysis. Tick paralysis will progress to quadriplegia within 24 - 72 hours after the onset of clinical signs. If the tick is not removed, respiratory arrest may occur in one to five days. Removal of all ticks usually results in improvement within hours, with complete recovery seen in 24 - 72 hours. In suspected cases of tick paralysis showing no improvement, look for hard to reach sites for the presence of tick attachment, such as the ear canal, between the toes, on the prepuce, etc. Nothing should be given by mouth until the paralysis has been resolved. In advanced cases manual or mechanical ventilation may be required.

In the United States, the Rocky Mountain Wood Tick and American Dog Tick are the most common ticks implemented in causing tick paralysis. In eastern Australia, near the coast in a narrow swath, is a tick by the name of Ixodid holocyclus. The I. holocyclus tick causes a paralysis that will continue to progress even after all the ticks have been removed. The natural hosts of this tick, marsupials, are rarely affected and appear to be immune to the effects of the tick’s neurotoxin. I. holocyclus may affect dogs, cats, man, ruminants, poultry, etc. The I. holocyclus tick causes reversible myocardial depression and diastolic failure. Canine tick hyperimmune serum, also called TAS, is the specific treatment for I. holocyclus-induced tick paralysis. The earlier TAS is administered, the better the efficacy. Atropine should be used to premedicate the patient to reduce the incidence of side effects. Temporary collapse with profound hypotension and bradycardia (slow heart rate) lasting several minutes may occur following the administration of TAS.

Tick paralysis may be confused with Polyradiculoneuritis or Coonhound Paralysis, coral snake envenomation (bite), Botulism, and Myasthenia gravis. Coonhound paralysis is a rapidly ascending flaccid paralysis that generally occurs in hunting dogs with the history of being bitten by a raccoon. Myasthenia gravis is an autoimmune disease in which the host produces antibodies against its own acetylcholine receptors. In Myasthenia, you get generalized muscle weakness often accentuated by mild exercise. The course of disease tends to be progressive but is not typically acute. Botulism is an acute flaccid paralysis induced by a bacterial exotoxin.

References:

Kahn, Cynthia: The Merck Veterinary Manual 1998. Merck and Co. pp.1073-1076.

Handbook of Small Animal Practice. Third edition. W.B. Saunders, Philadelphia pp284-285.

Malik, Richard PhD, and Brian Farrow PhD. "Tick Paralysis in North America and Australia." Veterinary Clinics of North America: Small Animal Practice. Vol. 21, No. 1, Jan. 1991. pp. 157-169.