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ULLADULLA VETERINARY HOSPITAL
TICK PARALYSIS IN DOMESTIC ANIMALS IN AUSTRALIA
caused by Ixodes holocyclus (the Paralysis Tick) by Robert Wylie B.V.Sc.,Q.D.A.
The advice given in this article is given in good faith based on my own experience and knowledge. However no responsibility is taken for injury or illness to any animal or person following advice given below. In every case a person seeking veterinary advice should contact their own private veterinary practitioner.
Table of Contents
2. Species Affected
3. Life Cycle of Ixodes holocyclus
4. Pathophysiology of Tick Paralysis
5. Treatment of Tick Paralysis
6. Other Diseases Transmitted by the Paralysis Tick
7. References and Links
Various stages of Ixodes holocyclus.
Picture courtesy of NSW Agriculture, Cattle Tick Program.
The Australian Paralysis Tick Ixodes holocyclus lives on native animals along the eastern Australian coastal strip. It regularly attaches to domestic animals including dogs, cats, cattle, and horses, and occasionally to humans. The tick injects a neurotoxin which causes progressive motor paralysis, respiratory depression, and death in animals which have no immunity to the toxin.
Pet owners need to be aware of the signs of tick paralysis, how to prevent it, and what to do if an animal is affected. The condition can be successfully treated provided veterinary assistance is sought early enough. At the Ulladulla Veterinary Hospital we treat approximately 200 animals, mostly cats and dogs, suffering from tick paralysis each year, in most cases successfully.
This article is based on over thirty years personal experience in treating tick paralysis, plus a review of current literature and research. It is published here as a resource for pet owners and for veterinarians. Most of the information for pet owners is in the FAQ section (This is on a separate page, so unless you want more technical information you might find it easier to go there first).
The remainder of the article is intended as a resource for veterinarians and others who seek more detailed information. Pet owners are welcome to read it.
Most cases of tick paralysis seen by veterinarians are in dogs and cats, but other species can be affected. The condition has been recorded in sheep, cattle, goats, most recently a llama, and in muscovy ducks. Fatal cases have occurred in humans. In the larger species, it is the younger and smaller animals which are likely to be affected, especially if subject to the attachment of a number of female paralysis ticks.
Tick paralysis has also been observed in native fauna, but apparently not in those in the wild state. Bandicoots from an area where I. holocyclus was rare or absent devloped paralysis when infested with six to eight female ticks. The apparent natural immunity of bandicoots in the wild may be an acquired immunity following repeated light infestations with larvae and nymphs. Pet kangaroos and wallabies have also been said to have suffered from tick paralysis.
Tick paralysis has been observed in bats on the Atherton Tableland.
The natural hosts of Ixodes holocyclus include bandicoots, wallabies, kangaroos, and other marsupials. Generally these native hosts are not affected by the tick’s toxin. It will also attach to man, cattle, sheep, horses, dogs, cats, poultry, and other animals. Ixodes is a three-host tick, meaning that each tick goes through the three stages of LARVA, NYMPH, and ADULT, attaching to and feeding on one host during each stage, then falling off and moulting before re-attaching to the same or more often a different host for the next stage.
The ADULT FEMALE tick, when fully fed, drops to the ground and lays from 2000 to 3000 EGGS before she dies. After 7 to 9 weeks (in warmer weather), the eggs hatch into larvae.
Unfed LARVAE on the ground can remain alive as long as 162 days, but are active from about a week after hatching and will attach to an available host. Once attached they feed (suck blood) for 4 to 6 days before dropping to the ground, to moult into nymphs. This period between hosts varies from 19 to 41 days. However the nymph can survive up to 275 days unfed.
A week after moulting the NYMPHS reattach to a host, feed for 4 to 7 days during which the body engorges, then fall off.
After 3 to 10 weeks on the ground, the nymph moults into an ADULT, which after another week, attaches to a passing host. If no host is available, the adult can survive up to 77 days without feeding. The FEMALE ADULT feeds and engorges for 6 to 21 days, before she drops to the ground to lay eggs, thus beginning the cycle again.
The time taken for an adult female to engorge while on the host varies from 6 to 21 days, the period being longest in cool weather. Thus a dog may carry a tick up to three weeks without the tick being significantly engorged or causing paralysis. However in warm weather the female engorges rapidly, and at the same time, injects her toxin into the host thus causing paralysis if the host is susceptible.
The adult female does not inject detectable amounts of toxin until the 3rd day of attachment to the host, with peak amounts being injected on days 5 and 6.
The ADULT MALE after crawling on to the host does not attach or suck blood, but spends its time wandering around on the host looking for a female with which it can mate. The adult male is yellowish-brown, flat, oval, and smaller than the female.
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. Experimental work by Ilkiw showed the duration of illness (time from onset of clinical signs to time of death) in untreated dogs (carrying 3-4 ticks) averaged 24 hours.
The pathophysiological changes are diverse, and can be summarised as:
- Peripheral nerve dysfunction
- Oesophageal dysfunction
- Respiratory difficulty
- Cardio-vascular effects (especially hypertension)
- Haematologic and biochemical effects
- Changes in body temperature
- Other effects
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 CNIII 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 paresis of laryngeal/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 was also reported by Ilkiw et al, 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.
Oesophageal Dysfunction – Regurgitation or Vomiting?
Paralysis or weakness of the oesophageal muscle produces megaoesophagus in many tick affected dogs. 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 (ASPIRATION PNEUMONIA).
The loss of respiratory function in tick paralysis, manifested clinically as CYANOSIS and DYSPNOEA, is probably the most serious pathophysiological effect, ultimately leading to death due to RESPIRATORY FAILURE.
(a) Central Respiratory Depression caused by the toxin early in the course of paralysis causes a drop in respiratory rate but not in respiratory volume.
(b)Closure of the vocal cords during the expiratory phase of respiration may be a compensatory mechanism to re-expand collapsed alveoli. This becomes more severe as the disease progresses, prolonging expiratory time and being clinically obvious as grunting respiration.
(c) Lowered Respiratory Volume per Minute results from the combination of (a) and (b) above.
(d) Lowered Arterial Oxygen Tension (PaO2 ) manifests as Hypoxaemia. Increased arterial carbon dioxide tension = Hypercarbia.
(e) The difference between Alveolar Oxygen Tension (PAO2) and Arterial Oxygen Tension (PaO2) = Acute Ventilatory Failure.
(f) Vascular hypertension (increased pulmonary arterial pressure) produces neurogenic pulmonary oedema and congestion, plus hepatic and renal congestion.
(g) Aspiration pneumonia occurs as a result of regurgitation and oesoohageal dysfunction.
(h) Paralysis of the diaphragm and intercostal muscles reduces further the ability to breathe.
(i) All the above factors produce CYANOSIS and DYSPNOEA.
(j) Pooling of saliva in the mouth and throat produces a gurgling respiration. A harsh groan may be heard as dogs attempt pharyngeal clearing with upper airway paresis.
(k) Finally, RESPIRATORY FAILURE causes DEATH.
(a) Pulmonary oedema occurs due to cardiotoxic effects of the tick toxin, a reversible myocardial depression. In severe cases this is associated with a rise in PCV and a fluid shift into the lung. The majority of dogs which die apparently do so with pulmonary oedema.
(b) Ilkiw in her experimental cases found severe hypertension (increased blood pressure), resulting from increased peripheral vascular resistance, caused by excess efferent vasomotor sympathetic activity.
However recent work suggests that high blood pressure is not a common finding in natural cases of tick toxicity, and some dogs may actually become hypotensive.
(c) Electrocardiograph changes are not consistent or diagnostic. There is a tendency towards sympathetic tachycardia in the early stages, and a vagally mediated bradycardia in the late to terminal stages. (This may be due to myocardial hypoxia, hypokalemia, or excess sympathetic stimulation).
Haematologic & biochemical effects
Generally these changes are difficult to interpret and not marked until the late to terminal stages of the disease.
Mild acidosis and dehydration develop. Other changes include increases in blood glucose, cholesterol, phosphate, and CPK, and a decrease in blood potassium. These are probably caused by increased sympathetic and adreno-cortical activity, and by muscle cell damage which also causes muscular pain and sometimes prolonged recumbency during recovery after treatment.
Changes in body temperature
No significant changes occur until the late stages of the disease process, when the animal may become hypothermic. This is not considered a serious problem by most clinicians, though it is likely to be a greater problem in cats and small dogs.
High ambient temperatures (over 20 degrees C.) are a greater problem due to increased demand for cooling placing more load on an inefficient respiratory system.
Other Effects not related to Paralysis
Other effects of the tick on the host may include a severe local reaction to the tick bite, and possible debilitation from loss of blood if many ticks are present.
A llama affected by tick paralysis improved initially following treatment, but died soon afterwards with hepatic lipidosis.
The important components of veterinary treatment are:
A. Kill the Tick
B. Tick Antiserum (Hyper-immune Serum)
C. Symptomatic and Supportive Treatment
D. Explanation by the veterinarian to the owner of the disease, the preferred treatment (and its cost), and the prognosis for recovery.
The actual order in which these things are done, after tick paralysis has been diagnosed, is suggested as:
- ACP (or Phenoxybenzamine) to calm the animal. Atropine may also be given at this time.
- Assess gait and respiratory scores and establish prognosis.
- Explain disease and discuss treatment with the owner.
- Tick Antiserum and other medical treatment as indicated..
- In moderate to severe cases, admit the patient to Hospital for ongoing symptomatic and supportive therapy.
A. KILL THE TICK
Killing or removal of all paralysis ticks is essential. A careful body search, minimising stress to the animal, is recommended. Do not stop searching after finding just one tick!
When treating an animal in the Vet Hospital our preferred procedure is to remove the tick as soon as we find it on your animal. We may apply to the tick by dropper or spray a suitable insecticide effective against ticks eg Frontline or Permoxin to kill it first and then remove shortly after. Especially helpful with those animals that refuse to stay still long enough to remove the tick without force!
We advise clients not to use irritant substances such as turpentine, kerosene, or petrol. These will kill the tick but may not make it any easier to remove. It is possible that stimulation by these substances may cause the tick to inject more toxin before dying. They will also cause a very nasty sore at the site of the tick bite and cause the pet unnecessary pain.
To actually remove live or dead ticks grasp it between your finger and thumb and quickly pull. Try to get your fingers/nails right down under the tick to try and get the head in the removal. If it is too small to remove you may use a pair of fine tweezers or Allis forceps or with a commercially available “tick twister”. If by any chance the head of the tick stays in the skin scratch it out with your fingernail. The head will not inject any more poison once the body is removed, but it may cause a foreign body reaction similar to a splinter. The spot where you remove a well-attached tick is likely to leave a “crater” or small hole in the skin. This will heal eventually. The local effects of a tick attachment are uncomfortable, but fairly insignificant compared with the potential fatal systemic effects caused by the tick toxin throughout the body.
Clip the animal if necessary to facilitate the search. Insecticides can be applied topically, as a spray or as a bath. However bathing may cause the animal unnecessary stress and is best avoided.
Oral insecticides (Proban) may be considered but are slow to act and of no use (and possibly harmful) in a patient with oesophageal dysfunction.
Since Frontline TopSpot Dog (Fipronil) became available we have tried routinely applying a pipette of Frontline TopSpot to each affected dog early in the course of treatment. Theoretically this should spread over the entire dog in about 24 hours and then kill any attached tick (missed during searches) with which it comes in contact. This at least seems to be stress free for the dog. It is useful especially when dogs are covered with multiple larval ticks. It is also hoped this will reduce the incidence of recently treated dogs becoming reaffected after discharge from Hospital, as manufacturers claim it should give two weeks protection after application. Clinical experience however shows that it should not be relied on, and that there is no substitute for repeated careful searches of the animal’s coat to ensure all ticks are killed and/or removed.
B. TICK ANTI-SERUM
TAS, Hyper-immune Serum.
Route – usually i/v. In cats i/p is preferred.
Dose – Standard dose is 10 ml for dogs, 5 ml for cats.
Higher doses are advised in severe cases, in animals with multiple ticks, or in large dogs (0.5 to 1.0 ml/kg or more). 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 small dogs and cats a dose of at least 1 ml per kg is recommended, with a minimum total dose of 5 ml.
Temperature – Serum is allowed to warm up to approximately room temperature before i/v administration. New research suggests that this may not be necessary.
When? – It is NOT necessary to give i/v serum immediately the animal is presented for treatment. In fact if the patient is stressed (which is usual) it is better to give ACP (or Phenoxybenzamine) first, and then allow the patient to settle down for ten or fifteen minutes before injecting the serum.
Reactions – A number of dogs go into a transient state of collapse (braycardia and hypotension) following i/v TAS injection. To help prevent this hypotension it is advised to give the injection via a slow (>20minutes) IV infusion, usually with a spring syringe infuser.
Use in non-canine species – Canine hyperimmune serum is necessary to treat paralysis in all species, but there is a risk of anaphylaxis. Premedication with Dexamethasone or sub-cutaneous Adrenaline may be helpful in these species. In our practice we routinely give the antiserum intra-peritoneally to cats and have found this safe and effective.
C. SYMPTOMATIC AND SUPPORTIVE TREATMENT
- AVOID STRESS OR EXCITEMENT.
- ACEPROMAZINE (ACP).
Alpha adrenergic blocker. Usually the first medication given. Beneficial effects are sedative, hypotensive, and anti-emetic. May exacerbate hypothermia. Avoid in severely depressed animals.
- GIVE NOTHING BY MOUTH to an affected patient until recovery has occurred to the extent that the gag reflex is normal and the animal can swallow normally.
- ENVIRONMENT – Quiet, dark if possible, comfortable bedding , stress-free. The cage or run must be large enough to allow the animal to stretch out (especially its neck) without restriction. Room temperature around 20 degrees C is recommended but not critical, but avoid extremes of heat or cold.
- ATROPINE – The use of atropine to treat tick paralysis has been controversial. It is anti-cholinergic in action, i.e. it inhibits the action of acetyl choline on post-ganglionic parasympathetic nerves, autonomic ganglia, and skeletal neuro-muscular junctions – all of which should theoretically worsen the effects of tick paralysis, especially in hypertensive dogs.
However in dogs which are persistently pooling saliva, or dogs drooling saliva and dyspnoeic on presentation, a single dose injected at 0.05 mg.kg (i.e. 1 ml Atrosine mitis per 13 kg dog) appears to be clinically helpful in drying up the oral cavity and respiratory secretions.
Atropine given prior to the dose of Tick Anti-serum will also reduce the incidence of bradycardia/hypotension reactions occasionally seen after Antiserum administration.
- ANTIBIOTICS – Used in cases of inhalation pneumonia or to prevent inhalation pneumonia.
- FLUID THERAPY – In the first 24 hours fluid therapy can be deterimental to the animal due to the high risk of pulmonary oedema. It is advised in animals which are clinically dehydrated, persistently regurgitating, that have been hospitalised more than 24-48 hours without oral fluids.
We routinely use Hartmanns Solution, given SLOWLY to avoid aggravating pulmonary oedema. Sub-maintenance requirements, 20-40 ml/kg/day are considered adequate. In cats subcutaneous fluids are better to reduce the stress caused by catheter placement.
- CORTICOSTEROIDS – usually not indicated, except in small dogs which occasionally react adversely to intravenous hyperimune serum, or in non-canine species, which might react to hyperimune serum given by any route.
- FUROSEMIDE (Frudix, Frusemide) – may help to reduce pulmonary oedema.
- MILLOPHYLLINE may be useful as a central respiratory stimulant and bronchodilator. Efficacy in tick paralysis is unproven.
- OXYGEN SUPPLEMENTATION – may be necessary and helpful in the severely dyspnoeic or cyanotic patient. Best done under a non-cardiodepressive general anaesthesia allowing intubation, oxygenation, ventilation, pulmonary drainage, and suction. Requires constant supervision. If required long term becomes extremely expensive and outside the capability of clinics which cannot provide 24 hour supervision and management. Consider referral if appropriate. Newer techniques have been described such as intra-tracheal large bore catheters supplying O2.
- PATIENT POSITION – Sternal recumbency if possible. Dogs in lateral recumbency should be turned approx. twice daily, preferably AFTER giving ACP to minimise anxiety during handling.
Ixodes holocyclus is the source of 2 human diseases: Australian Spotted Fever (caused by Rickettsia australis) and Lyme Disease (caused by the spirochaete Borrelia). These diseases are most likely to affect people working or living in bushland areas especially in coastal urban populations where housing is close to bushland. Further discussion of these human diseases is beyond the scope of this article.
It is not clear whether Lyme Disease (Borreliosis) occurs in domestic animals in Australia, but it is quite possible. Very occasionally, animals may fail to recover after tick bites and develop arthritis, heart disease, or CNS disturbances. These cases may respond to antibiotic treatment. Accurate diagnosis of Lyme Disease is dependent on the development of a satisfactory diagnostic test based on the Australian organism, which is not quite the same as the American Borrelia burgdorferi.
Ixodes species around the world are vectors for other organisms including Erhlichia spp and viruses. We do not yet know whether these occur in Australia.
This is not a full list, but the following articles are some of the more important ones used in the production of this article.
Ilkiw JE, Turner DM, Howlett CR:Infestation in the dog by the paralysis tick Ixodes holocyclus:
1. Clinical & histological findings. Aust Vet J 64:137, 1987.
2. Blood-gas and pH, haematological and biochemical findings. Aust Vet J 64:139, 1987.
3. Respiratory effects. Aust Vet J 64:142, 1987.
4. Cardio-vascular effects. Aust Vet J 65:232, 1988.
5. Treatment. Aust Vet J 65:236, 1988.
Merial Australia – National Tick Paralysis Forum – Bulletin No.2, July 2000
This paper cites a number of articles by Atwell RB, Cambbell FE, Evans EA, and Fitzgerald M which are currently in press or in preparation as at July 2000.
Malik R, Farrow B.R.H: Tick Paralysis in North America and Australia.Vet Clin N Amer 21:157,1991.
Wylie R: Tick Paralysis. Post Graduate Committee in Vet. Sc., Uni. of Sydney. Control & Therapy No. 1815, 1984.
Albiston H.E. Diseases of Domestic Animals in Australia, Part 3: Arthropod Infestations (Ticks and Mites). C’wlth of Aust., Dept. of Health 1968.
Roberts F.H.S.:Insects Affecting Livestock. Angus & Robertson. 1952.
Jonsson N N and Rozmanec M: Tick paralysis and hepatic lipidosis in a Llama. Aust Vet J 75:250, April 1997.
Collins, H:Paralysis Tick – the plot thickens. Boehringer Ingelheim Newsletter No 33, August 1997.
“Know these Ticks” – leaflet produced by Boehringer Ingelheim Pty Ltd and NSW Agriculture Cattle Tick Program.
Lyme Disease in Australia – S. Doggett, Westmead Hospital, Dept of Medical Entomology
The Paralysis Tick in Australia by Norbert Fischer – a very informative and comprehensive article
Netscape Web Search – tick paralysis Australia
So far these are the only links I can find in Australia.
An index of links about tick paralysis worldwide, but mainly relating to the condition in America, caused by Dermacentor variabilis and D. andersoni, is attached.
Netscape Net Search – tick paralysis animals
Note that the paralysis caused by Ixodes holocyclus is much more severe than that caused by the American ticks.
This page is continually being developed and was last updated on 28/10/2008, by Gary Parker, Andrew Ottley and Rebecca Hofman.. Thanks to those veterinary colleagues who have contacted us with criticisms and suggestions.
We would be happy to receive any comments or questions relating to this article or to tick paralysis. Please contact us by email.