Neurology: tick paralysis

• Cause: paralysis in dogs (and cats in Australia) produced by a neurotoxin generated by some strains of certain species of ticks.
• Signs: flaccid, afebrile ascending motor paralysis, progressive respiratory failure.
• Diagnosis: clinical signs, presence of ticks.
• Treatment: tick removal, topical/systemic insecticides, (neutralization of circulating toxins and supportive therapy in Australia).
• Prognosis: usually favorable; guarded in Australia.

• Clinical signs observed 5-7 days (and rarely up to 2 weeks) after attachment.
• Flaccid (lower motor neuron = LMN type), afebrile ascending motor paralysis.
• Regurgitation Regurgitation or vomiting Vomiting is commonly associated with early tick intoxication in Australia.
• Reflexes lost but sensation preserved.
• Pupil dilation.
• Facial paralysis Facial nerve neuropathies.
• Salivation and retching due to pharyngeal and esophageal dysfunction.
• Pupillary light response (PLR) progressively lost.
• Change in quality of dog's bark (dysphonia) and voice change common early sign in cats.
• Respiration slow and labored with prolonged expiratory phase and typical "grunting" noise.
• Death may occur within several days from respiratory failure (NB tick paralysis far more serious and life-threatening condition in Australia).
• As dyspnea worsens, cyanosis develops.

• Australia: Eastern seabord, from Lakes district in Victoria to far North Queensland. Majority of cases seen during spring.
• North America: Throughout range of ticks: the Rocky Mountain wood tick (Dermacentor andersoni Dermacentor andersoni ), the American dog tick (Dermacentor variabilis Dermacentor variabilis ), the Lone Star tick (Amblyomma americanum Amblyomma americanum ) and the Gulf coast tick (Amblyomma maculatum Amblyomma maculatum ).
• Australian tick paralysis was reported in a dog imported into the UK.

• Significantly greater morbidity in Australia compared with North America.

• Any age.

• Any breed.
• Cats appear to be resistant to disease in North America but are affected in Australia - though less frequently than dogs.

• Humans, principally infants and children may be affected by tick paralysis.

• Causes serious losses to livestock, horses and companion animals in Australia.
• Estimated to affect 10-20,000 domestic animals/year in Australia.
• Significant costs associated with intensive nature of supportive care and prolonged recovery times.

• Most dogs (80%) die from progressive respiratory distress (pulmonary edema Lung: pulmonary edema ), not from respiratory paralysis as originally thought.
• Australian dogs with tick paralysis were found to be at significantly higher risk of death if less than 6 months of age or if a toy breed.

• Tick neurotoxin.
• In North America, most common species are the Rocky Mountain wood tick (Dermacentor variabilis,the American dog tick (Dermacentor variabilis), the Lone Star tick(Amblyomma americanum) and the Gulf coast tick (Amblyomma maculatum).
• In Australia (especially along the East coast) Ixodes holocyclus is the most important species.
• Other species that occasionally cause paralysis are:
  • Ixodes cornuatus.
  • Ixodes hirsti.
  • Ixodes scapularis.
• Several toxins have been isolated from the salivary glands of Ixodes holocyclus.

• Adult ticks, especially females, produce a salivary neurotoxin that circulates in the host animal and interferes with acetylcholine liberation at the neuromuscular junction and/or impulse propagation along motor axon terminals.
• Effects on neuromuscular transmission shown to be temperature dependent in vitro. The clinical value of this is currently unclear but a cool environment may benefit the outcome.
• In Australia, heavy infestations with nymphs or larvae may result in paralysis.
• Respiratory depression due to diaphragmatic and intercostal paralysis.
• Cardiovascular depression in paralyzed dogs associated with primary diastolic dysfunction Murmur: overview and reduced LV fractional shortening (impaired myocardial relaxation).
• Pulmonary edema Lung: pulmonary edema of cardiogenic origin occurs and is a major cause of death.

• Onset of clinical signs gradual with dogs becoming recumbent in 24-72 hours, 5-14 days after attachment of the tick(s).
• Death from respiratory failure occurs 18-32 hours later if the ticks remain attached and no treatment is provided.
• Clinical signs can continue to progress for up to 48 hours after tick removal if tick antitoxin serum is not administered.

• Ascending lower motor neuron (LMN) paralysis.
• Respiratory depression.
• Occasionally presented with vomiting or regurgitation as the only clinical sign.

• Onset of clinical signs gradual, paralysis first evident as an inco-ordination in the pelvic limbs, resulting in an unsteady gait.

• Early signs include:
  • Altered voice.
  • Cough.
  • Dysphagia.
  • Regurgitation Regurgitation.
• Dogs recumbent in 24-72 hours.
• Reflexes are lost but sensation is preserved.
• Death may occur within several days from respiratory paralysis.

• In Australia: clinical signs usually begin with pelvic limb weakness that progresses to paralysis within a few hours.
• Ascending LMN paralysis soon involves the forelimbs.
• Cranial nerve paralysis may occur.
• Pupils widely dilated and eventually fail to respond to light.
• Respiration becomes slow and labored.
• Prolonged expiratory phase.
• A grunting noise is characteristically described.
• A clinical classification for severity of gait and respiratory compromise is used in Australia:
  • Gait score:
    • Can walk - able to stand from recumbency and ambulate.
    • Can't walk - required aid to a standing position but can then maintain stance.
    • Can't stand - unable to maintain standing position.
    • Can't right - unable to maintain sternal recumbency.
  • Respiratory score:
    • Normal character and weight (<30 breaths/min).
    • Mild compromise - normal character and increased rate (=/>30 breaths/min), normal respiratory pattern or mild expiratory effort.
    • Moderate compromise - restrictive breathing, gagging and retching. Gasping and cyanosis may be present. Respiratory rate may be decreased (<12/minute).
    • Severe compromise - expiratory grunt due to vocal cord closure during expiration, cyanosis and severe dyspnea.

• Focal forms of tick paralysis, eg asymmetrical facial paralysis, unilateral loss of cutaneous trunci reflex and anisocoria in some dogs with ticks found ispilaterally on the head or neck.
• Others may only present with vomiting and loss of voice.

Electromyography 

• Absence of spontaneous potentials and lack of motor unit action potentials Electromyography. No muscle response follows direct nerve stimulation.
• Motor and sensory nerve conduction velocity may be slower that normal.

• No significant findings aside for pulmonary changes in a significant proportion of cases.

• No significant findings aside for bronchopneumonia may be present in a significant proportion of cases and may reflect aspiration.

• Coonhound paralysis Polyradiculoneuropathies.
• Idiopathic polyradiculoneuritis Acute idiopathic polyradiculoneuritis.
• Botulism Botulism.
• Acquired myasthenia gravis Myasthenia gravis.
• Necrotizing myopathy Myopathies.

• Snake envenomation in Australia Venomous animals of Australia.

USA

• Tick removal usually results in improvement within 24 hours and recovery within 72 hours.
  A diligent search of the entire animal is necessary.
• Sponging with an insecticidal solution effective against ticks Tick control may be necessary or administering a systemic insecticide (eg cythioate Cythioate at 3-6 mg/kg, orally) to kill any undiscovered ticks.

Australia

• Entire tick removal, including mouth parts by pulling out.
• Tick antiserum (average dose 1 ml/kg IV) neutralizes free toxin in circulation with a minimum of 5-8 ml and a maximum dose of 25 ml (higher end of the dosage rate is recommended for cases with severe clinical signs or multiple ticks present). Tick antitoxin serum should be warmed, diluted in saline and administered slowly IV over 1 hour while the animal is monitored closely for anaphylaxis Anaphylaxis, urticaria and angioedema. Because the antitoxin serum is produced from the serum of hyperimmune dogs, there is potential risk of anaphylaxis or anaphylactoid reactions. The number of reactions to tick antitoxin serum can be reduced by the routine use of atropine Atropine prior to admininstration of tick antitoxin serum. Although it has previously been recommended that a small amount (0.5 ml) of tick antiserum should be injected underneath the site(s) of tick engorgement, in a recent prospective survey, this appeared to have no effect on the clinical outcome.
• Other supportive measures:
  • Acetylpromazine (0.1mg/kg)
  • Phenoxybenzamine Phenoxybenzamine (1mg/kg as 0.1% solution).
  • Other vasodilators.
• Promote afterload reduction.
  • Atropine reduces saliva pooling and if used prior to antiserum administration will prevent or reduce reactions induced via the Bezold-Jarisch reflex.
  • Dexamethazone Dexamethasone is not of proven value.
  • Regular suction  of pharynx and larynx will minimize upper respiratory distress.
  • Oxygen therapy and IPPV may be needed.
  • Frusemide Furosemide reduces pulmonary edema.

• Animals should be placed in a quiet, cool, air-conditioned environment.
• Oxygenation should be monitored and oxygen administered if hypoxia develops, commonly by the intranasal route Nasal oxygen administration or oxygen cage.
• Mechanical ventilation Anesthetic ventilators: overview will be required if respiratory paralysis and hypoventilation occur.
• Adverse reactions to tick antiserum occur in approximately 3.5% cases.
• Adverse reactions to tick antitoxin serum are of 2 types:
  • 80% characterized by bradycardia Heart: dysrhythmia , pallor hypotension, weakness and depression associated with the Bezold-Jarisch reflex.
  • Fewer (20%) associated with anaphylaxis Anaphylaxis, urticaria and angioedema.

Treatment

• Food and water withheld until the dog is mobile and has not vomited or regurgitated for at least.
• Hydration should be maintained with intravenous fluids, but fluid overload must be avoided as there may be an increased risk of development of pulmonary edema.
• Normothermia must be maintained.
• Bladder size should be monitored and the bladder should be expressed manually or catheterized to prevent overdistension and subsequent bladder atony.
• Metoclopramide Metoclopramide CRI (1-2 mg/kg/day) can be administered as a prokinetic to try to minimize vomiting and aspiration.

• Usually favorable but guarded in Australian dogs.
• Respiratory and gait scores reflect disease severity and are good prognostic indicators.
• Dogs with tick paralysis requiring mechanical ventilation to manage respiratory failure have reasonable survival probability. Dogs requiring mechanical ventilation because of hypoventilation have a higher survival probability than those with oxygenation failure.
• Mortality rates of 5% following treatment with tick antitoxin in Australia has been reported.

• Presence of undetected ticks.
• Some affected dogs in Australia may not respond to any treatment.

Refereed papers

• Recent references from PubMed and VetMedResource.
• Eppleston K R, Kelman M, Ward M P (2013) Distribution, seasonality and risk factors for tick paralysis in Australian dogs and cats. Vet Parasitol 196 (3-4), 460-468 PubMed.
• Webster R A, Mills P C, Morton J M (2013) Indications, durations and outcomes of mechanical ventilation in dogs and cats with tick paralysis caused by Ixodes holocyclus: 61 cases (2008-2011). Aust Vet J 91 (6), 233-239 PubMed.
• Webster R A, Mackie J T, Haskins S C (2013) Histopathological changes in the lungs from dogs with tick paralysis: 25 cases (2010-2012). Aust Vet J 91 (8), 306-311 PubMed.
• Holland C T (2008) Asymmetrical focal neurological deficits in dogs and cats with naturally occurring tick paralysis (ixodes holocyclus): 27 cases (1999-2006). Aust Vet J 86 (10), 377-384 PubMed.
• Adamantos S, Boag A, Church D (2005) Australian tick paralysis in a dog imported into the UK. Aust Vet J 83 (6), 352 PubMed.
• Atwell R B and Campbell F E (2001) Reactions to tick antitoxin serum and the role of atropine in treatment of dogs and cats with tick paralysis caused by Ixodes holocyclus: a pilot study. Aust Vet J 79 (6), 394-397 PubMed.
• Collins G H & Ingwersen K (2000) Paralysis tick research. Aust Vet J 78 (5), 311 PubMed.
• Atwell R B and Fitgerald M (1994) Unsolved issues in tick paralysis. Aust Vet Practit 24 (3), 156-161 VetMedResource.
• Malik R & Farrow B R (1991) Tick paralysis in North America and Australia. Vet Clin North Am Small Anim Pract 21 (1), 157-171 PubMed.
• Malik R et al (1988) Megaoesophagus associated with tick paralysis in three dogs. Aus Vet Pract 18 (4), 156-159 VetMedResource.
• Ilkiw J E et al (1987) Infestation in the dog by the paralysis tick, Ixodes holocyclus. 1. Clinical and histological findings. Aust Vet J 64 (5), 137-139 PubMed.

Other sources of information

• Braund K G (2002) Neurotoxic Disorders. In: Clinical Neurology in Small Animals - Localization, Diagnosis and Treatment. Ed K G Braund. Ithaca: International Veterinary Information Service (www.ivis.org), 2002; document no. B0223.0901.
• Merial, National Tick Paralysis Forum.Tick poisoning in dogs and cats. Bulletin 1.
• Merial, National Tick Paralysis Forum.Tick poisoning in dogs. Bulletin 2 (July 2000).