Benjamin M. Greenberg, MD


Medscape General Medicine. 2003;5(2) 

In This Article

Final Diagnosis

In humans, the first confirmed death caused by tick poisoning was reported by Cleland in 1912, when a large, engorged tick caused flaccid paralysis progressing to asphyxiation in a child. By 1921, Dodd had established a definitive link between an engorged tick and clinical disease in 3 dogs, and showed that it took 5-6 days after attachment for clinical signs to develop, with motor paralysis being the major neurologic deficit.

Tick-borne diseases include Lyme disease, Rocky Mountain spotted fever, ehrlichiosis, babesiosis, relapsing fever, Q fever, and Colorado tick fever, among many others. Indeed, the number of illnesses transmitted by ticks is increasing, possibly because of reforestation, movement of people to rural areas, and outdoor recreational activity.

Tick paralysis is a well-known ailment in Australia, where it primarily affects livestock and domesticated animals. In the United States, it is found primarily in the Pacific Northwest and Southeast. Tick paralysis is not reported nationally, although Washington State used passive surveillance of the condition until 1998.

In all, 33 cases were reported in Washington State between 1946 and 1996.[1] Most cases occurred between April and June and involved girls younger than 10 years of age (long hair has been implicated as a "risk factor," but more likely represents a complicating factor to identifying a tick on a patient's scalp). The disorder is probably more common in children because their relatively small size makes them susceptible to even modest amounts of toxin. In the distant past, the fatality rate was as high as 10%[2]; currently, it is likely to be much lower because of heightened awareness and improved supportive care.

Tick paralysis can be caused by several species of tick; the Dermacentor species (wood and dog ticks) is the primary culprit in the United States and the Ixodes species predominates in Australian cases. Figure 2 provides a comparison of the illness in the 2 countries. Engorged, gravid female ticks are responsible for the condition. They tend to attach to the hairline, scalp, or pubic hair, and secrete a toxin through their saliva while feeding, before laying their eggs. Generally, the tick must be attached to the host for several days to produce the illness.

A comparison of tick paralysis in the United States with that in Australia.

Tick paralysis presents similarly to AIDP and botulism, with only subtle differences, particularly early in the disease course. The CSF is usually normal (as in early AIDP and botulism). Ataxia and areflexia can precede paralysis by several days. Unlike Guillain-Barré, sensory symptoms tend to be minimal with tick paralysis. EMG/NCS reveal reduced CMAP amplitudes, but no signs of diminished conduction velocity (which would normally be seen in a demyelinating process such as AIDP).[3]

Fever and rash have not been associated with tick paralysis. Cranial nerves are typically not affected.

Removal of the entire tick usually produces a rapid resolution of symptoms.