Tick paralysis in animals is caused by a salivary neurotoxin produced by certain species of ticks. Usually this is caused by the adult female tick during the period of rapid engorgement (days 5-7), although large numbers of larval or nymphal ticks may also cause paralysis.

Epidemiology

A total of more than 60 species of ticks have been implicated so far to induce tick paralysis. Clinically overt disease has been described in humans, cattle, sheep, goats, dogs, and rarely in cats. The most noted and dangerous tick in this respect is the Paralysis tick, Ixodes holocyclus, of the Eastern coast of Australia, which attacks humans, dogs, cats, foxes and many livestock animals. In the USA, mostly dogs suffer from paralysis due to the the bite of the American Dog tick (Dermacentor variabilis) and the Rocky Mountain wood tick (D. andersoni).

Tick paralysis can occur worldwide. However, the disease is endemic in Australia and in regions of Northwestern USA and Southwestern Canada where a large number of known cases occur. In other parts of the world cases of tick paralysis are observed sporadically.

Pathogenesis

Tick paralysis affects mainly motor pathways, and to less extent also autonomic and sensory pathways of the nervous system. A neurotoxin in the saliva of certain tick species interferes with acetylcholine release at the neuromuscular junction, producing a neuromuscular blockade. In most dogs paralysis of esophageal muscles develops, with or without esophageal dilatation (megaesophagus). Saliva and ingested food or fluid pool into the esophagus, and are regurgitated into the pharynx and mouth.

I. holocyclus causes reversible myocardial depression and diastolic failure, leading to cardiogenic pulmonary edema. In severe cases, increased PCV (packed cell volume) reflects a fluid shift from the circulation to the lungs. Progressive pulmonary dysfunction appears to be primarily due to edema, leading to hypoxia, hypercarbia, respiratory acidosis, and eventually death.

Removal of ticks does not immediately halt the progression of the disease, once clinical signs are apparent. The fatality rate may increase dramatically when the tick has fully engorged and depleted. Appropriate and prompt action saves ~95% of affected animals.

Death from respiratory failure is likely to occur within 1-2 days of onset of clinical signs.

Diagnosis

The presence of a tick in combination with a sudden (12-24 hours) appearance of leg weakness and/or respiratory impairment is crucial and diagnostic. The tick may no longer be attached, but a tick “crater” (a small hole surrounded by a slightly raised and inflamed area) might still be detectable in the skin and can confirm the diagnosis. Specific laboratory diagnostic techniques are not available. Procedures that may be helpful include the determination of the PCV and a lateral thoracic radiograph to assess presence and degree of pulmonary edema, megaesophagus, and potential pneumonia due to aspiration.

Differential diagnosis include botulism, Guillain-Barré syndrome, spinal cord compression, transverse myelitis, encephalomyelitis heavy metal poisoning and some other more rare causes.

Clinical signs

Tick paralysis is an acute, progressive, ascending motor paralysis. Clinical signs in dogs appear usually 5 to 7 days after the attachment and progress rapidly over the following 24 to 48 hours. Early signs may include change or loss of voice, hind limb incoordination, change in breathing rate and effort, gagging or coughing, regurgitation or vomiting, and pupillary dilation. Hind limb paralysis begins as slight to pronounced incoordination and weakness. As the fore limbs get affected, the animal becomes unable to move hind and fore limbs, stand, sit, or lift its head. Sensation usually is preserved.

Breathing abnormality is the main prognostic factor. Respiratory rate may initially increase but, as the disease progresses, becomes slower and obviously labored, especially on expiration. Regurgitation of esophageal contents, saliva pooling, depression of the pharyngeal reflex and attempts to clear the throat may produce a characteristic harsh, groaning respiratory sound.

Treatment

The treatment in tick paralysis is basically to remove the ticks thoroughly. Frequently, multiple ticks are attached to an animal. For the above mentioned North American tick species, removal of all ticks usually results in improvement within 24 hours and complete recovery within 72 hours. If an animal is severely affected, supportive care and artificial respiration may be needed.

In Australia, the disease commonly continues to progress after removal of ticks, and treatment is indicated for animals with motor or respiratory impairment. In cases in which an adult female Paralysis tick, Ixodes holocyclus, has been removed, but nevertheless clinical symptoms develop within the next 24 hours, a canine tick hyperimmune serum, also called tick antiserum (TAS), is the specific treatment against the tick paralysis. TAS should be given as early in the disease as possible; subsequent “top up” doses are not very effective. For dogs, a minimal dosage of 0.5-1.0 ml/kg, warmed up to room temperature, is given slowly intravenously.

About 5% of animals are likely to die despite all treatment efforts, especially those with advanced paralysis and dyspnea. Older animals or those with pre-existing cardiopulmonary disease are at greatest risk. For animals that recover, owners should be advised to continue searching for ticks, use appropriate preventative methods to repel and kill ticks, and avoid stressing or strenuously exercising the animal over the next two months.

Human tick paralysis

In humans, tick paralysis is most likely to be seen in children. The symptoms in humans are similar to the clinical signs in dogs. About two thirds of human cases are seen in young females. The tick bites are most often found at the head and there at the transition of hair and neck. The clinical presentation appaers as typical ascending flaccid paralysis. After aprodromal phase (paraesthesias, restlessness, irritaility, fatigue, and myalgias) neurological symptoms will start with paralysis of the lower extremities. The deep tendon reflexes are weak or absent. Duirng the next 12 to 24 hours the musclied innervated by facial nerves become weak. Without removal of the tick, finally the respiratory muscles will fail  and the patient will die of respiratory failure. Rare forms of illness include focal muscles paralysis (facial muscles, arm muscles, pupillary dilation, and acute cerebellar syndrome). Sensory findings are generally absent and therefore form an important differential diagnostic symptom to the Guillain-Barré syndrome where sensory findings are frquently found during the prodromal stage of disease.