Tick paralysis

From Dog
Female Ixodes holocyclus, cause of tick paralysis
Female Ixodes holocyclus unfed.

In North America, the parasitic wood ticks Dermacentor variabilis and D. andersoni are incriminated most commonly as causing tick paralysis.

In Australia, Ixodes holocyclus in the most common cause. The engorging adult female tick injects a holocyclotoxin (and possibly other toxins) into the host animal. This injection commences on about the third day of attachment and peaks on the 5th and 6th days. The onset of clinical signs usually occurs 5.5 to 7 days after attachment, although death in dogs has been recorded to occur within 24 hrs of attachment.

In Australia, tick paralysis affects approximately 10,000 domestic animals annually. Tick transmitted pathogens currently identified in dogs in Australia include Babesia canis vogeli[1], Anaplasma platys[2] and Babesia gibsoni[3].

Clinical signs

A flaccid, ascending neuromuscular disorder may be caused by a neurotoxin that is introduced into the bloodstream by certain parasitic species of ticks. Ticks must be attached for 24-48 hours for a sufficient amount of neurotoxin to enter the bloodstream. The tick neurotoxin prevents pre-synaptic release of acetylcholine into the neuromuscular junction, resulting in diffuse neuromuscular paresis. Compared with dogs, cats appear to be relatively resistant to tick paralysis.

In cats, skin lesions can also occur, ranging from mild pruritic lesions to 'lumps' or papules[4]. When sufficient toxin is introduced, cats manifest neuromuscular paresis within 3-7 days of tick attachment.

Peripheral Nerve Dysfunction

Interference with pre-synaptic nerve terminal depolarisaion and acetyl choline release produces a neuro-muscular blockade. This manifests primarily as an ascending flaccid paralysis varying from Paraparesis (hind leg weakness) to Quadriplegia (paralysis of all 4 limbs and neck). There also may be progressive involvement of Cranial Nerves with effects including pupillary dilation (part due to depressed function of CN III and part due to increased sympathetic activity), prolapse of the nictitating membrane, depressed gag and swallowing reflex (allows pooling of saliva around the mouth), and a change or loss of voice (dysphonia). Localized laryngeal paresis or paresis of cranial musculature (unilateral) may occur at the site of the tick bite. Urinary incontinence develops due to loss of control of the bladder. Sensory nerve dysfunction has also been reported but not consistently, and only in severely affected dogs.Interestingly this appeared to be a descending dysfunction, beginning in the neck, with the tail distally the last area to be affected[5].

Oesophageal Dysfunction

Paralysis or weakness of the oesophageal muscle produces megaoesophagus in many tick affected cats. Dilation of the oesophagus and its filling with saliva and ingested food/fluid, negative thoracic pressure, and positive abdominal pressure produces regurgitation. Regurgitation is a passive retrograde passage of food/fluid from the oesophagus into the oral and/or nasal cavities, whereas vomiting is an active process requiring abdominal effort. Whether true vomiting occurs in tick affected dogs is doubtful. The severity of oesophageal dysfunction and its consequences in tick paralysis is not closely related to the degree of skeletal muscle paralysis present. In some cases regurgitation is the only presenting sign present in the animal. The combination of a poor gag reflex, saliva pooling, and oesophageal dilation contributes to the patient's respiratory distress. Aspiration of regurgitated material into the lungs, may produce inhalation pneumonia[6].

Treatment

Once the tick is removed, neuromuscular weakness begins to resolve within 1-3 days.

Tick antiserum is effective as an adjunct to supportinve therapy. Route is usually intraperitoneal in cats. A small amount (0.5 to 2 ml) SQ under the site of attachment (given before physical removal of the tick) may help to combat local effects of the toxin and its spread throughout the body.

Dose - Standard dose is 5 ml for cats. Higher doses are advised in severe cases, in animals with multiple ticks. Antiserum is most effective if given early. Reducing the dose as a cost cutting measure is likely to be counter productive, as treatment in such a case may turn out to be prolonged and therefore expensive, or at worst ineffective. If in doubt increase the initial dose. In cats a dose of at least 1 ml per kg is recommended, with a minimum total dose of 5 ml.

References

  1. Irwin, PJ & Hutchinson, GW (1991) Clinical and pathological findings of Babesia infection in dogs. AVJ 68:204-209
  2. Brown, GK et al (2001) Detection of Ehrlichia platys in dogs in Australia. AVJ 79:554-558
  3. Muhlnickel, CJ et al (2002) Babesia gibsoni infection in three dogs in Victoria. AVJ 80:606-610
  4. Baxter Cg et al (2009) Dermatoses caused by infestations of immature Ixodes spp on dogs and cats in Sydney, Australia. AVJ 187(5):182-187
  5. [1]
  6. Schull, DN et al (2007) Tick toxicity in cats caused by Ixodes species in Australia: a review of published literature. JFMS 9(6):487-493