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As of March 22, 1995, an addendum has been appended to this article.

A 7-year-old girl was taken to her physician for evaluation of acute, ascending motor paralysis and speech difficulties. The girl's parents indicated that she had no history of motor difficulties and that the current symptoms developed quite rapidly. The family lived in a rural area, and the child often played in the woods accompanied by her pet dog. Results of laboratory investigations were not remarkable. A single engorged female tick was found attached to the girl's neck, and it was determined that the child had tick paralysis. Speech and motor function improved rapidly after the tick was removed, and the child recovered within hours and without complications. The parents were concerned about the child's association with her dog and the possible role that the pet might have played in the tick-associated condition. As a result, they called their veterinarian with the following questions:

Q: Is tick paralysis a disease that is transmitted from animals to man?

A: Zoonoses, as defined by the 1959 and 1967 Joint FAO/WHO Expert Committees, are "those diseases and infections, which are naturally transmitted between vertebrate animals and man." Many contend, however, that zoonoses should include not only infections that human beings acquire from animals, but also diseases induced by noninfective agents, such as toxins and poisons.¹ As such, tick paralysis is a zoonotic disease of importance to the general public as well as to veterinarians and the animals they treat.

Q: What is tick paralysis?

A: Tick paralysis is a disease caused by numerous species of ticks from several genera^2,3 and is characterized by an acute, ascending, flaccid motor paralysis. The paralysis affects the myoneural junctions, particularly the conduction rate of slower conducting terminal fibers of small diameter.⁴ The paralysis acts on motor nerves by diminishing the liberation of acetylcholine and by causing damage to receptor sites. Although detected worldwide, there are notable variations in the paralytic responses. Localized toxic reactions also have been described, often making the separation of paralytic and toxic manifestations difficult.⁵

Q: Who can get tick paralysis and what is the geographic distribution?

A: In North America, tick paralysis in human beings and animals is caused primarily by Dermacentor andersoni, with the highest prevalence being in the northwestern states and Canada. In the eastern and southern states, D variabilis, Amblyomma americanum, and A maculatum have been associated with human cases along the mid-Atlantic seaboard^5,6 as well as the Tennessee Valley and southern Midwest. Dermacentor andersoni appears to be the major cause of livestock paralysis in British Columbia, with additional cases reported in Montana and Oregon. In British Columbia, tick paralysis has been diagnosed in more than 3,800 sheep and cattle since 1900, with up to 320 animals per incident. In California, D occidentalis appears to be the major species involved, with disease developing in cattle, horses, and wildlife.^5,6 Thus far, human cases have not been attributed to D occidentalis. Infestations with D variabilis and D andersoni generally are responsible for cases in wildlife and companion animals, although a case of paralysis in a dog in California has been attributed to an infestation with Ixodes pacificus.⁵ Ixodes spp and Argas spp are reported to cause paralysis in birds.⁵ With only a few exceptions, tick paralysis is not detected in Mexico and South America.

In Australia, I holocyclus is the tick most often associated with paralysis, although several genera have been implicated. Dogs, and perhaps sheep, are the domestic animals most often involved on that continent. In Africa, the major tick associated with paralysis is I rubicundus, with cases seen mainly in sheep, goats, cattle, and rarely, in dogs. Tick paralysis in Eurasia is variable, with a wide variety of ticks affecting several domestic animal species.⁵

Q: What are the clinical signs of tick paralysis?

A: In general, the degree of paralysis appears to be related to the duration of time that tick(s) feed, as well as to the number of attached ticks.^1,2,6 In North America, female ticks are most commonly involved, although males have been reported to cause limited paralysis.⁵ The association between cases and the presence of female ticks may be related to their longer feeding period rather than to a specific difference between male and female ticks. In North America, human involvement is more prevalent in girls < 10 years old who acquired the tick 4 to 6 days before the appearance of the first symptoms. Paralysis in human beings is ascending, with motor difficulties and limb numbness being the first notable signs. Complete locomotor paralysis can develop within 24 hours of the initial signs, with concomitant speech difficulties, respiratory paralysis, and occasionally death. The location of the tick(s) (especially D andersoni) usually is along the neck and is often hidden by hair. Removal of the tick commonly results in complete recovery; however, in cases of deep paralysis, full recovery may take several weeks. In Australia, human cases of tick paralysis differ from those seen in North America. Most human cases in Australia are caused by I holocyclus and result in acute illness and vomiting. Surprisingly, peak paralytic difficulties develop 36 to 48 hours after the tick is removed, and recovery may take several weeks.

Q: What specifically causes the paralysis?

A: Most investigators believe that tick paralysis is caused by a toxin, but its nature is not well characterized. Generally, it is believed that the toxin is produced in the salivary glands of the female tick. Supporting this hypothesis is the fact that feeding larvae of I holocyclus⁷ and unmated female D andersoni have been shown to induce paralysis.⁸ Additionally, paralysis generally will not appear until 4 to 6 days after tick attachment, although ticks transferred from paralyzed to clinically normal animals induce paralysis sooner (12 to 18 hours).⁹ An alternative hypothesis is that the toxin accumulates in the tick ovaries and passes to the salivary glands during the later stages of tick engorgement. A toxin identical to that injected by engorged ticks has been recovered from the eggs of known paralysis-inducing ticks, but similar substances also have been recovered from the eggs of ticks that are not known to induce paralysis.^5,10,11 Recent investigations have focused on the structure and function of specific glandular acini present in the salivary glands of feeding female ticks that appear to have morphologic similarities to structures seen in some venomous vertebrates.¹⁰ Morphologic studies indicate that cell "b" of acinus 11 is the best candidate as the source of toxin.¹⁰ Some investigators think that paralysis is caused by a host reaction against components of tick saliva that results in a metabolic toxemia; however, others suggest that one or several of the symbiotic rickettsial organisms commonly found in tick salivary glands produce toxins during the feeding process.⁵ Recent data indicate that a proteinaceous toxin (holocyclotoxin) is secreted via the salivary glands into the host. A toxoid obtained from a holocyclotoxin preparation appears to have potential in the development of a tick paralysis vaccine.^10,11 Whatever the origin of the toxin, it appears to be metabolized rapidly or excreted after removal of the tick. Additionally, there does not appear to be evidence of a common tick toxin, because, at least under experimental conditions, only some ticks are able to induce paralysis.

Q: Can you get tick paralysis from your dog or livestock?

A: No. There are several factors, however, that can relate directly to tick infestations on these animals and to human paralysis. One is that people and their companion animals or livestock often have common exposure rates because of tick populations in the environment. People that frequent areas suitable for high tick numbers would be the group at highest risk. Additionally, pets may bring ticks into contact with their owners by having unattached ticks on their coats, which may then transfer to the owner, attach, and begin to feed.

Q: Can you prevent tick paralysis?

A: Preventing tick bites appears to be the only sure means of avoiding paralysis, because the exact nature of the toxin is not known; however, because paralysis generally does not develop until late in feeding, examination of human beings, pets, and livestock, and removal of ectoparasites greatly reduces the risk of paralysis. Management practices, including habitat modification, pasture spelling, and treatment of livestock with acaricides may reduce tick populations, and thus reduce the possibility of exposure and subsequent paralysis. Careful examination of the neck and head regions of children and adults would reduce the chances of developing paralysis.

Q: Can the paralysis be treated once signs are observed?

A: Although drugs that reduce the effects of paralysis have not been identified, Australian workers have found that serum from dogs on which I holocyclus ticks have repeatedly fed can be used to aid in the recovery of human beings suffering from paralysis.¹² Furthermore, animals that recover from paralysis resulting from infestations with this tick may be refractory to paralysis for several months.¹² Similar studies with D andersoni in North America have not indicated the same protection.^5,12

Discussion

Although cases of tick paralysis have been reported throughout the world, it appears that some localized areas have a higher prevalence. The importance of human and animal cases of tick paralysis should not be underestimated, because the onset of clinical signs can be quite rapid, and the paralysis can quickly affect heart and respiratory function. In addition to avoiding paralysis, the timely removal of ticks can reduce the chances of transmission of other tick-transmitted diseases, including Rocky Mountain spotted fever and Borrelia burgdorferi borrelioses.^13,17

Methods of tick removal are important because improper removal can contribute to transmission of some disease agents.^13,14 The safest way to remove the ticks is to grasp the tick as close as possible to the point of attachment, with forceps, tweezers, or fingers protected by gloves or facial tissue. Even pressure should be applied at the point of attachment so as not to damage the tick during removal. Hands should be washed thoroughly with soap and water after removal of ticks, to minimize the possibility of transmission of disease agents through intact mucosae or abraded skin.

References

1. Soulsby EJL. Parasitic zoonoses--clinical and experimental studies. New York: Academic Press Inc, 1974; 402.

2. Gothe R, Kunze K, Hoogstrall H. The mechanism of pathogenicity in the tick paralysis. J Med Entomol 1979; 16:357-369.

3. Gregson JD. Tick paralysis: an appraisal of natural and experimental data. Monograph No. 9, Canada Department of Agriculture; 1973; 109.

4. McLennen H, Oikawa I. Changes in function of the neuromuscular junction occurring in tick paralysis (caused by Dermacentor andersoni Stiles). Can J Physiol Pharmacol 1972; 50:53-58.

5. Harwood RF, James MT. Entomology in human and animal health. New York: Macmillan Inc, 1979; 460-463.

6. Wilkinson JD. Tick paralysis. A first report of paralysis of deer by Dermacentor andersoni (Stiles) and notes on the host potential of deer in British Columbia. Proc Entomol Soc BC 1965; 62:28-30.

7. Arthur DR. Ticks and diseases. New York: Pergamon Press Inc, 1962; 445.

8. Gregson JD. Host susceptibility to paralysis by the tick Dermacentor andersoni Stiles. Can Entomol 1958; 90:421-424.

9. Gregson JD. Tick paralysis in groundhogs, guinea pigsand hamsters. Can J Comp Med 1959; 23:266-268.

10. Stone BF, Binnington KC. The paralyzing toxin and other immunogens of the tick Ixodes holocyclus and the role of the salivary gland in their biosyntheses. In: Sauer JR, Hair JA eds. Morphology, physiology and behavioral biology of ticks. New York: Ellis Horwood, 1986; 75-99.

11. Kemp DH, Stone BF, Binnington KC. Tick attachment and feeding: role of the mouthparts, feeding apparatus, salivary gland secretions and the host response. In: Obenchai FD, Galun R, eds. Physiology of ticks, Vol 1. New York: Pergamon Press Inc 1982; 119-168.

12. Kaire GH. Isolation of tick paralysis toxin from Ixodes holocyclus. Toxicon 1966; 4:91-97.

13. Green CE. Rocky Mountain spotted fever. J Am Vet Med Assoc 1987; 191:666-671.

14. Needham GR. Evaluation of five popular methods for tick removal. Pediatrics 1985; 75:997-1002.

15. Spielman A, Etkind P, Spiesman J, et al. Reservoir hosts of human babesiosis on Nantucket Island. Am J Trop Med Hyg 1981; 30:560-565.

16. Ruebush T. Human babesiosis in North America. Trans R Soc Trop Med Hyg 1980; 74:149-152.

17. Burgdorfer W, Lane RS, Barbour AG, et al. The western black-legged tick, Ixodes pacificus: a vector of Borrelia burgdorferi. Am J Trop Med Hyg 1985; 34:925-930.

Addendum (1995)

Recent studies dealing with tick paralysis have focused principally on the identification, characterization, and localization of a paralysis toxin. Most studies have implicated the "b" cells of the salivary glands from several tick species. Indications are that the toxin is made up of 3 identical subunits, with only the trimeric form being toxic. It has further been proposed that the primary function of the toxin is a down-regulatory effect on protein synthesis and as such, the paralytic effect on a host may be secondary.

The primary concern of physicians or veterinarians remains early and proper diagnosis, followed by proper treatment. Conclusive diagnosis depends on the presence of an ascending paralysis that is cured after removal of the tick. Variations in recovery time can be influenced by individual susceptibility, concurrent disease, or duration the tick was allowed to feed.

Treatment is limited to tick removal and symptomatic and supportive therapy. Administration of hyperimmune serum has been reported to be of value, although its availability is limited in the United States. A thorough description of the effects and application of hyperimmune serum, as well as drugs that reduce peripheral vascular resistance and other more extensive therapies in dogs has been published.¹

Reference

1. Malik R, Farrow, BH. Tick paralysis in North America and Australia. Vet Clin North Am: Small Anim Pract 1991;21:157-171.