Tick paralysis

Tick paralysis is the only tick-borne disease that is not caused by an infectious organism. The illness is caused by a neurotoxin produced in the tick's salivary gland. After prolonged attachment, the engorged tick transmits the toxin to its host. The incidence of tick paralysis is unknown.

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Signs and symptoms

Tick paralysis results from inoculation of a toxin from tick salivary glands during a blood meal. The toxin causes symptoms within 2-7 days, beginning with weakness in both legs that progresses to paralysis. The paralysis ascends upward to trunk, arms, and head within hours and may lead to respiratory failure and death. The disease can present as acute ataxia without muscle weakness.

Patients may report minor sensory symptoms but constitutional signs are usually absent. Deep tendon reflexes are usually hypoactive or absent and ophthalmoplegia and bulbar palsy can occur.

Electromyographic (EMG) studies usually show a variable reduction in the amplitude of compound muscle action potentials but no abnormalities of repetitive nerve stimulation studies. These appear to result from a failure of acetylcholine release at the motor nerve terminal level. There may be subtle abnormalities of motor nerve conduction velocity and sensory action potentials.

Pathogenesis

Tick paralysis is believed to be due to toxins found in the tick's saliva that enter the bloodstream while the tick is feeding. The two ticks most commonly associated with North American tick paralysis are the Rocky Mountain wood tick (Dermacentor andersoni) and the American dog tick (Dermacentor variabilis); however, 43 tick species have been implicated in human disease around the world.^[1] Most North American cases of tick paralysis occur from April to June, when adult Dermacentor ticks emerge from hibernation and actively seek hosts.^[2]. In Australia, tick paralysis is caused by the tick Ixodes holocyclus. Up to 1989 20 fatal cases have been reported in Australia.^[3]

Tick paralysis has killed thousands of animals, mainly cows and sheep, in other parts of the world. Although tick paralysis is of concern in domestic animals and livestock in the United States as well, human cases are rare and usually occur in children under the age of 10.

Tick paralysis occurs when an engorged and gravid (egg-laden) female tick produces a neurotoxin in its salivary glands and transmits it to its host during feeding. Experiments have indicated that the greatest amount of toxin is produced between the fifth and seventh day of attachment (often initiating or increasing the severity of symptoms), although the timing may vary depending on the species of tick.

Unlike Lyme disease, ehrlichiosis, and babesiosis, which are caused by the systemic proliferation and expansion of parasites in their hosts long after the offending tick is gone, tick paralysis is chemically induced by the tick and can therefore usually only continues in its presence. Once the tick is removed, symptoms usually diminish rapidly. However, in some cases, profound paralysis can develop and even become fatal before anyone becomes aware of a tick's presence.

Diagnostic tests

Diagnosis is based on symptoms and upon finding an embedded tick, usually on the scalp.

In the absence of a tick, the differential diagnosis includes Guillain-Barre syndrome and botulism.

Treatment

Removal of the embedded tick usually results in resolution of symptoms within several hours to days. If the tick is not removed, the toxin can be fatal, with reported mortality rates of 10–12 percent,^[4] usually due to respiratory paralysis. The tick is best removed by grasping the tick as close to the skin as possible and applying firm steady pressure.^[5]

Prevention

No vaccine is currently available for any tick-borne disease, except for TBE. Individuals should therefore take precautions when entering tick-infested areas, particularly in the spring and summer months. Preventive measures include avoiding trails that are overgrown with bushy vegetation, wearing light-colored clothes that allow one to see the ticks more easily, and wearing long pants and closed-toe shoes. Tick repellents containing DEET (N,N, diethyl-m-toluamide) are only marginally effective and can be applied to skin or clothing. Rarely, severe reactions can occur in some people who use DEET-containing products. Young children may be especially vulnerable to these adverse effects. Permethrin, which can only be applied to clothing, is much more effective in preventing tick bites. Permethrin is not a repellent but rather an insecticide; it causes ticks to curl up and fall off of the protected clothing.

Toxin

Although several attempts have been made to isolate and identify the neurotoxin since the first isolation in 1966 the exact structure of the toxin is still unknown.^[6] The 40-80 kDa protein fraction contains the toxine.^[7]

See also

• Polyneuropathy in dogs and cats for tick paralysis in dogs

References

1. ^ Gothe R, Kunze K, Hoogstraal H (1979). "The mechanisms of pathogenicity in the tick paralyses". J Med Entomol 16: 357–69.
2. ^ Dworkin MS, Shoemaker PC, Anderson D (1999). "Tick paralysis: 33 human cases in Washington state, 1946–1996". Clin Infect Dis 29: 1435–9.
3. ^ Masina S, Broady K. W. (1999). "Tick paralysis: development of a vaccine". International Journal for Parasitology 29 (4): 535-541. doi:10.1016/S0020-7519(99)00006-5.
4. ^ Schmitt N, Bowmer EJ, Gregson JD (1969). "Tick paralysis in British Columbia". Can Med Assoc J 100: 417–21.
5. ^ Needham GR (1985). "Evaluation of five popular methods for tick removal". Pediatrics 75: 997–1002.
6. ^ Doube B. M. (1975). "Cattle and Paralysis Tick Ixodes-Holocyclus". Australian Veterinary Journal 51 (11): 511-515.
7. ^ B. F. Stone, K. C. Binnington, M. Gauci, J. H. Aylward (1989). "Tick/host interactions forIxodes holocyclus: Role, effects, biosynthesis and nature of its toxic and allergenic oral secretions". Experimental and Applied Acarology 7 (1): 59-69. doi:10.1007/BF01200453.