Contributors: Laurent Garosi

 Species: Feline   |   Classification: Diseases

Introduction Pathogenesis Diagnosis Treatment Outcomes Further Reading

Introduction

  • Cause: paralysis in cats in Australia, produced by a neurotoxin mostly generated by the hard-bodied tick, Ixodes holocyclus.
  • 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).
  • Prognosis: usually favorable.

Presenting Signs

  • Clinical signs observed 5-7 days (and rarely up to 2 weeks) after attachment.
  • Flaccid (lower motor neuron = LMN type), afebrile ascending motor paralysis.
  • Retching, regurgitation Regurgitation or vomiting Vomiting is commonly associated with early tick intoxication.
  • Bladder voiding dysfunction.
  • Reflexes lost but sensation preserved.
  • Pupil dilation is a common finding.
  • Facial paralysis Facial nerve neuropathy.
  • Dysphonia or aphonia.
  • Unkempt appearance.
  • Respiration signs ranging from coughing, expiratory dyspnea to cyanosis.
  • Cats often appear distressed or agitated because of physical or functional upper respiratory tract obstruction.
  • Death is uncommon but may occur within several days from respiratory failure.
  • Stress-induced hyperexcitability can immediately precede respiratory failure and death.

Geographic Incidence

  • Australia: majority of cases reported on the eastern coast of Australia with New South Wales and Queensland accounting for most of them. Majority of cases seen during spring.

Age Predisposition

  • Any age.

Breed Predisposition

  • Long-haired cats with an outdoor range seem most at risk.

Public Health Considerations

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

Cost Considerations

  • 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.

Special Risks

  • No significant risk factors in cats.

Pathogenesis

Etiology

  • Tick neurotoxin (holocyclotoxins).
  • Ixodes holocyclus is the most important species of ticks.
  • Other species that occasionally cause paralysis are:
    • Ixodes cornuatus.
    • Ixodes hirsti.
  • Several toxins have been isolated from the salivary glands of ixodes holocyclus. 
  • Attachment sites of the ticks are mostly inaccessible to scratching and grooming with the most commonly reported anatomical locations including the head, under the chin, the neck, between the shoulder blades, and caudal to the elbow.

Pathophysiology

  • Adult ticks, especially females, produce a salivary neurotoxin that circulates in the host animal and interferes with acetylcholine presynaptic release at the neuromuscular junction and/or impulse propagation along motor axon terminals. The toxin may also interfere with acetylcholine release from parasympathetic nerves, which may account for autonomic signs.
  • 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.  
  • Respiratory depression due to diaphragmatic and intercostal paralysis.
  • Pulmonary edema rather than inhalation pneumonia is more common in cats that died from tick toxicity.

Timecourse

  • 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 is uncommon but can occur rapidly 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.

Diagnosis

Presenting Problems

  • Ascending lower motor neuron (LMN) paralysis.
  • Respiratory depression.

Client History

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

Clinical Signs

  • Early signs include:
    • Dysphonia.
    • Aphonia.
    • Unkempt appearance.
  • Hind-limb weakness and/or ataxia are the most common presenting signs.
  • Withdrawal reflexes weaken as the syndrome advances until the cat is unable to rise from lateral recumbency.
  • Reflexes are lost but sensation is preserved.
  • The tail may remain unaffected by the ascending paralysis in some cases.
  • Cats are recumbent in 24-72 hours.
  • Respiration signs ranging from coughing, expiratory dyspnea to cyanosis.
  • Cats often appear distressed or agitated because of physical or functional upper respiratory tract obstruction.
  • Death is uncommon but may occur within several days from respiratory failure.
  • Stress-induced hyperexcitability can immediately precede respiratory failure and death.
  • Cranial nerve paralysis Cranial nerve neuropathy (facial paralysis and Horner syndrome Horner's syndrome) may occur and may be unilateral with ticks found ipsilaterally on the head and neck.
  • Pupillary dilation is a common finding.
  • A clinical classification for severity of gait and respiratory compromise is used to standardize the assessment of tick toxicity cases and to aid in monitoring treatment and estimating prognosis:
    • 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 animals with ticks found ispilaterally on the head or neck.
  • Others may only present with vomiting and loss of voice.

Diagnostic Investigation

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.

Gross Autopsy Findings

  • Pulmonary changes.
  • Pulmonary edema rather than inhalation pneumonia is more common in cats that died from tick toxicity.
  • Cyanosis of the tongue.
  • Local subcutaneous edema and blood staining at the site of tick attachment.
  • Endocardial and epicardial hemorrhage.

Histopathology Findings

  • Subcutaneous tissues at the site of tick attachment characterized by hemorrhage and edema, with extensive local infiltration by polymorphonuclear leukocytes, lymphocytes and plasma cells.

Differential Diagnosis

Treatment

Initial Symptomatic Treatment

  • Mulitple thorough searches of the entire body are indicated and are facilitated by clipping in longhaired cats to optimise the chances of retrieving the entire tick burden.
  • Entire tick removal, including mouth parts.
  • Canine-derived tick antiserum (recommended doses range from 1 ml/kg to 3-10 ml/cat IV) neutralizes free toxin in circulation. 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. Because the antitoxin serum is produced from the serum of hyperimmune dogs, there is potential risk of anphylaxis or anaphylactoid reactions. The number of reactions to tick antitoxin serum can be reduced by the routine use of atropine Atropine prior to administration 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 canine prospective survey, this appeared to have no effect on the clinical outcome.
  • The intraperitoneal route has also been suggested to slow the rate of tick antiserum delivery, thereby reducing the risk of subsequent reactions to the canine-derived product.

Monitoring

  • Animals should be placed in a quiet, cool, air-conditioned environment to minimize stress.
  • Adverse reactions to tick antiserum occur in approximately 6.2% cases.
  • It is recommended that adrenalin and/or soluble corticosteroids are readily available to treat a possible systemic reaction when tick antiserum is administered.
  • Adverse reactions to tick antitoxin serum are of 2 types:
    • 63% characterized by bradycardia Heart: dysrhythmia, pallor hypotension, weakness and depression associated with the Bezold-Jarisch reflex.
    • Fewer (37%) associated with anaphylaxis.

Subsequent Management

Treatment

  • Food and water withheld until the cat 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.

Outcomes

Prognosis

  • Usually favorable.
  • Respiratory and gait scores reflect disease severity and are good prognostic indicators.
  • Mortality rate reported to be very low (0.6%) in treated cases.
  • Period of hospitalization reported ranges from 0 to 7 days and reflect the clinical status of the cat on presentation and probably the treatment and management regimen used.
  • Some cats can harbor ticks without showing any clinical evidence of disease leading to suggestions that some immunity may develop from natural infestations.

Expected Response to Treatment

  • Presence of undetected ticks.

Reasons for Treatment Failure

Further Reading

Publications

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.
  • 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.
  • Schull D N, Litster A L, Atwell R B (2007) Tick toxicity in cats caused by Ixodes species in Australia: a review of published literature. J Feline Med Surg (6), 487-493 PubMed.
  • Schull D (2004) Tick paralysis in a cat with subclinical hypertrophic cardiomyopathy. Australian Veterinary Practitioner 34 (1), 32-36 ResearchGate.
  • Atwell R B & Campbell F E (2001) Reactions to tick antitoxin serum and the role of atropine in treatment of dogs and cats with tick paralysis caused byIxodes holocyclus: a pilot study. Aust Vet J  79 (6), 394-397 PubMed.
  • Collins G H & Ingwerson K (2000) Paralysis tick research. Aust Vet J 78 (5), 311 PubMed.

Other Sources of Information