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Poisonous animals
 
Cnidarians (Jellyfish, Corals and Anemones)
 
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Clinic

 

Tick paralysis

Clinical studies, case reports and reviews

Dermacentor andersoni, D. variabilis

North America

Gregson 1973: 9 cases. Identification: D. andersoni removed from the patient and identified 4/9; tick removed from the patient and not identified 5/9; description of the clinical picture.

Abbott 1944: description of the clinical picture.

Donat and Donat 1981: 1 case. Identification: tick not identified.

 

Ixodes holocyclus

Australia
Hamilton 1940: 6 cases. Identification: I. holocyclus removed from the patient and identified 3/7; tick removed from the patient and not identified 4/7; description of the clinical picture.
Pearn 1977: 6 cases. Identification: I. holocyclus, identification criteria not given.

Review
Murnaghan and O'Rourke 1978

Signs & symptoms

Neurological effects

Onset of neurological symptoms after the tick had already been attached for several days (Gregson 1973, Hamilton 1940). Progressive course.

Symptoms: in some patients irritability may be apparent 12–24 h before paralysis becomes obvious. Tingling in the extremities, the face or the perioral region. Paralysis usually begins in the legs. At first the gait is affected, then there is a complete loss of strength in the legs. 1–2 days later the paralysis also affects the upper extremities and the trunk. Bulbar palsy ensues, with cranial nerve deficits. Finally paralysis of the respiratory musculature occurs. The causes of death are thus respiratory failure and aspiration pneumonia.

Findings: signs of peripheral paralysis. Deep tendon reflexes cannot be elicited.

Course of the disease after removal of the tick

There appear to be differences in the clinical course of tick paralysis in North America and Australia. In North America patients experience full recovery within 3–4 days as long as paralysis was not too far advanced at the time the tick was removed. In Australia the symptoms may only peak up to 48–72 h after removal of the tick or after the tick falls off by itself (Pearn 1977). The clinical course of Australian tick paralysis generally appears to be more acute than that of North American paralysis.

Important differential diagnoses

Lyme borreliosis, caused by B. burgdorferi and carried by Ixodes sp. Neurological symptoms occur 2–3 weeks after the tick bite, in contrast to several days with tick paralysis.

Other neurological disorders (polyradiculitis = Landry-Guillain-Barré syndrome, polyneuropathies, poliomyelitis).

There is a particular risk that tick paralysis may not be considered initially and valuable time may be lost before the tick can be located and removed so as to enable spontaneous recovery.

Laboratory and physical investigations

1. CSF
Normal.

2. Blood tests
Normal.

Treatment (symptomatic)

  1. Remove ticks as soon as possible. It is imperative to also look carefully for ticks in less obvious places, such as the scalp. 
  2. Intensive medical care if symptoms progress. Early endotracheal intubation. Artificial respiration.
  3. Neurophysiological investigations: marked reduction in the amplitude of the motor response and early appearance as well as persistence of fibrillations (Donat and Donat 1981).

Treatment (specific)

Antivenom
Australia
Tick antivenom, CSL, Parkville, Australia. See MAVIN-Antivenom index

Recommendations

Antivenom should only be administered if paralysis is present. This is a canine antivenom that cannot be processed to a high degree of purity. Thus a higher rate of adverse reactions is to be expected than with the other CSL antivenoms (Sutherland 1992).