Tick Paralysis

HISTORY: Tick paralysis is a well-known paralytic syndrome that occurs in many vertebrate hosts throughout the world and may be induced by at least 46 species of ticks (Stone, 1988). In North America, cats appear to be resistant to tick paralysis, and show no clinical signs other than prolonged attachment of numerous ticks (Malik and Farrow, 1991). In consultation with the Veterinary Medical Data Base, West Lafayette, Indiana, USA, no cases of tick paralysis in the feline have been documented from the reporting member institutions (colleges/schools of veterinary medicine) across North America., however a single case of tick paralysis due to an engorged female tick of the genus Dermacentor has been reported from a cat in Georgia, USA (Anderson, 1985).

However, tick paralysis due to an Australian tick Ixodesholocyclus presents as a far more harmful syndrome than that produced by its North American counterpart (Malik and Farrow, 1991). Ixodesholocyclus, which is indigenous to Australia, was first described by Captain W. H. Howell in a diary reporting his expedition from Lake George to Port Phillip in 1824-25. This tick is the most common cause of tick paralysis in eastern Australia (Prescott, 1984). A case of tick paralysis due to Ixodescornuatus in a cat from Tasmania was reported in 1974 (Mason, et al., 1974). These authors also noted an additional case of paresis in a cat from northern Tasmania; other cases of feline tick paralysis had been previously reported by Roberts (1970). Early experimental studies of tick paralysis in the canine were performed by Ross (1927). Later, Ilkiw, et al. (1987, 1988) and Ilkiw and Turner (1987, 1987a, 1988), provided an extensive treatise on the clinical, histologic, blood-gas, hematologic, biochemical findings and cardiovascular and respiratory effects and treatment of Ixodesholocyclus infestations in dogs. However, similar controlled studies have not been performed in cats.

GEOGRAPHIC DISTRIBUTION: Although several species of ticks in North America are able to produce tick paralysis, Dermacentorandersoni (the Rocky Mountain wood tick) and Dermacentorvariabilis (the American dog tick) are most often identified as causative agents of tick paralysis in cattle, sheep and humans (Malik and Farrow, 1991). The tick that produced the isolated case of feline tick paralysis in North America was a Dermacentor species (Anderson, 1985).

Three different species of ticks comprise the Ixodesholocyclus group. These are Ixodesmyrmecobii in Western Australia, Ixodescornuatus in Tasmania, Victoria and the southern coastal areas of New South Wales bordering Victoria and overlapping with this distribution, Ixodes holocyclus in the coastal area of Victoria to the Tambo River and the coastal areas of New South Wales and Queensland (Kemp, 1979). The distribution of Ixodesholocyclus is largely determined by that of its principal hosts, the shortnosed bandicoot Isoodonmacrourus and the longnosed bandicoot Peramelesnasuta. This tick commonly occurs in moist environments, in areas of dense undergrowth with abundant leaf litter (Stone and Wright, 1979). Beveridge (1991) noted the occurrence of Ixodesholocyclus in the western suburbs of Melbourne, a report which extended the known geographic range of this tick 250 km to the west. Ixodeshirsti has also been associated with tick paralysis (Malik and Farrow, 1991) and is restricted to Southern Australia, Western Australia, southern New South Wales, Victoria and Tasmania. Ixodescornuatus is restricted to southern New South Wales, Victoria and Tasmania (Stone, 1988). In Tasmania, Ixodescornuatus has been associated with tick paralysis in cats (Mason, et al., 1974).

LOCATION IN HOST: Paralysis results from the engorgement of members of the genus Ixodes, most commonly Ixodesholocyclus, although Ixodescornuatus, Ixodesmyrmecobii and Ixodeshirsti have been implicated in some cases of paralysis (Kemp, 1979). The syndrome will not develop until the ticks have been attached for at least 4 days. Attachment to the skin of the definitive host is most common in the spring and summer. Most cases of tick paralysis are seen during this period. The syndrome usually occurs after infestation with adult female ticks, however heavy infestations with nymphs or larvae may produce paralysis (Malik and Farrow, 1991). Male ticks usually do not become attached to the host, but may be found free in the coat (Prescott, 1984). The ticks from the North American case was attached over the cranial thoracic vertebrae (Anderson, 1985), an area that is difficult to impossible for a cat to reach during the grooming process.

IDENTIFICATION: Ross provided extensive gross descriptions of the larval, nymphal and adult male and female stages of Ixodesholocyclus (Ross, 1924). Ixodesholocyclus, Ixodescornuatus and Ixodeshirsti are members of the subgenus Sternalixodes. Homsher, et al. (1988) utilized scanning electron microscopy to study the structure of Haller's organ in eight of the nine members of the subgenus Sternalixodes. Among the ticks examined, these researchers found the morphology of Haller's organ to be remarkably uniform. The general shape of the organ; shape and depth of the anterior trough; type, number and arrangement of the anterior trough setae and tarsal hump setae; and location, size and shape of the capsular aperture are virtually identical in the eight species examined. Some differences are evident, especially in the prominence of the tarsal hump and the steepness of the tarsal hump walls. Ixodesholocyclus was the most variable species in this study. The differences between male and female specimens of this species are as great as those observed when separate sexes are compared. It was concluded that more specimens of Ixodesholocyclus should be examined to discern if these differences are consistent.

Members of the adult Ixodesholocyclus group demonstrate small and not always constant structural differences. These differences lie in the shape of the cornuae, palpal article I and the spur on coxa I. Ixodesholocyclus is identified by the characteristic circle around its anus. Larvae of Ixodesholocyclus and Ixodescornuatus are more easily identified than their adult counterparts. Some of the structures, particularly the pattern of hairs are distinctly different (Kemp, 1979).

LIFE CYCLE: The adult Ixodesholocyclus is a flat, oval tick with prominent mouthparts and brown legs. There are four developmental stages in its life cycle: egg, larva, nymph and adult. The female is a productive egg-layer, laying 2,000 to 3,000 eggs which hatch in 49 to 61 days. The larvae (or seed ticks) become active in about one week and attach themselves to a host where they feed for 4 to 6 days. Suitable hosts may be the bandicoot, the echidna, possum, all domesticated animals and even man. Following engorgement, the larva drops off and, during a period of 19 to 41 days, molts and develops to the nymphal stage. The engorged nymph develops to the adult stage in 3 to 10 weeks and after molting to the adult stage, attaches itself to the third host where it engorges for 6 to 21 days (Prescott, 1984). Large numbers of larvae, nymphs and adults may be found on the same animal (Ross, 1924). Although all feeding stages of the tick can cause paralysis, adult females are responsible for most of the cases.

CLINICAL PRESENTATION AND PATHOGENESIS: Most information concerning tick paralysis in small animals has been gathered from observations in dogs. Clinical signs are usually observed 5 to 7 days following attachment of the tick. The rate of engorgement of the parasites will determine the length of time prior to the onset of symptoms. This period may be prolonged up to 2 weeks in colder weather. In massive infestations, clinical signs may appear until as early as the fourth day (Malik and Farrow, 1991). Tick paralysis presents initially with loss of appetite and voice, incoordination, following by ascending flaccid paralysis, ocular irritation, excessive salivation, and asymmetric pupillary dilatation. Tetraplegia and respiratory distress occur later, and are almost inevitably followed by death if treatment is not instituted (Stone, 1988).

Affected cats typically are distressed and agitated. Initially there is a change in voice which is especially noticeable in Siamese and Burmese cats. Retching or coughing may accompany this sign. Pupillary dilation is common, however vomiting is rare in comparison to that observed in the dog (Malik and Farrow, 1991). Roberts noted two cases of tick paralysis in cats. Both cats were exhibiting signs of tick paralysis, one cat "crawling with its front legs and dragging its hind legs on the ground" and the other "walking as though it was properly drunk." The cats died 7 and 10 days respectively after the signs were observed. The causative agent was Ixodeshirsti (Roberts, 1961). A cat from Tasmania presented with a flaccid paralysis and dilated pupils. On the second day of illness, it exhibited obvious signs of respiratory distress. On the third day, the cat died and was submitted for post mortem examination. At necropsy, the cat exhibited a cyanosed tongue and nose. Behind the ear was an engorged female Ixodescornuatus. At the attachment site, the subcutaneous tissues were locally edematous and stained by blood pigments. Other gross lesions were endocardial and epicardial hemorrhages, the endocardial hemorrhage was especially severe on the papillary muscles of the left ventricle. Histologically, the subcutaneous tissue was characterized by hemorrhage and edema with extensive local infiltration by polymorphonuclear leukocytes, lymphocytes and plasma cells (Mason, et al., 1974).

In the case of tick paralysis in the North American cat, the cat presented with a history of acute listlessness and paresis, anorexia but no vomition or diarrhea. On physical examination, the cat was markedly depressed and nonresponsive. Both hindlimbs demonstrated flaccid paralysis. Respiratory distress was not evident. The cat was 7 to 8% dehydrated. Within 8 hours of tick removal, improvement was noted. The cat became more alert and responsive and made attempts to move about. Within 24 hour, all evidence of flaccid paralysis had subsided.

DIAGNOSIS: Identification of larval, nymphal, and adult male and female ticks of the genus Ixodes infesting the skin and haircoat of affected cats is the best method of definitive diagnosis of tick paralysis. Diagnosis is confirmed following rapid improvement of the affects cat following removal of the ticks. The diagnosis is certain in classical cases of rapidly ascending flaccid motor paralysis associated with identification of engorged female ticks of the genus Ixodes. The change in voice, referable to laryngeal paresis is suggestive of tick paralysis. Detailed neurologic testing reveals reduced muscle tone and diminished to absent myotactic reflexes early in the course of the disease. Although withdrawal reflexes are initially normal, they become progressively slower and weaker as the syndrome advances. Although proprioception and cutaneous sensation are thought to be preserved, diminished perception of noxious tactile stimuli occasionally has been noted. The gag reflex is constantly depressed, and the inability to swallow results in drooling of saliva. Rapid commencement of clinical signs is associated with more severe disease and an increased likelihood of death (Malik and Farrow, 1991).

TREATMENT: There are three stages in the treatment regimen for tick paralysis caused by Ixodesholocyclus: removal of offending tick(s), counteraction of circulating toxin, and commencement of symptomatic and supportive therapy.

After a diagnosis of tick paralysis is made, a thorough search of the cat's haircoat is indicated. Ticks can be found on almost any part of the body. In cats, they are usually found in areas that are inaccessible to grooming, eg., under the chin, on the neck, or between the shoulder blades. If only one tick is found, the search should be continued and be as thorough as possible. If all ticks are not removed, recovery may not occur. In long-haired cats, clipping the haircoat often expedites the detection of additional ticks.

Ticks are best removed by sliding the blades of a partially opened pair of scissors between the tick and the cat's skin. Using a levering action, the tick can be maneuvered from the attachment site with its mouthparts intact. This strategy prevents additional release of toxin into the cat. Efforts should be made to determine if the tick is one of the species that produces tick paralysis. Removal of the offending tick may prevent the development of tick paralysis, if the cat has not yet begun to demonstrate clinical signs. Nevertheless, if the cat is exhibiting signs, removal of the tick is not adequate. The syndrome is likely to advance for up to 48 hours without proper therapy.

Hence, hyperimmune serum should be administered intravenously in cats to neutralize the effects of the circulating tick toxins. Since hyperimmune serum is derived from canine sources, risk is associated with its administration to other species (anaphylaxis is rare in cats initially receiving antitick serum). Intravenous hydrocortisone (30 mg/kg) can be routinely administered just prior to the slow intravenous injection of antitick serum (5-10 ml) to seriously affected cats. Epinephrine (1.0 ml of a 1:10,000 solution) should be accessible in the event of anaphylaxis. An alternate regimen is to administer hyperimmune sera to cats either intraperitoneally or intravenously following premedication with acepromazine or an antihistamine. Canine hyperimmune serum should initially be withheld from mildly affected cats, pending their response to tick extraction.

In mildly affected cats with a definitive ascending paralysis, removal of ticks and administration of hyperimmune serum usually results in obvious clinical improvement within 24 to 48 hours, however there is little clinical change during the first 12 hours. If the cat fails to respond to hyperimmune serum after a suitable time, the cat should be reexamined for undetected ticks.

Cats with more advanced tick paralysis gain from administration of drugs that decrease peripheral vascular resistance, thereby easing respiratory distress associated with pulmonary congestion and edema. The alpha-adrenoreceptor antagonist phenoxybenzamine (1 mg/kg diluted into at least 20 ml of 0.9% NaCl and repeated every 12-24 hours if necessary) and the phenothiazine tranquilizer acepromazine (0.05-0.10 mg/kg every 6-12 hours) given slowly intravenously have been used most often in this situation. A vasodilator should be administered to cats with clinical signs related to pulmonary congestion and edema. Both phenoxybenzamine and phenothiazine produce effective sedation as well as alleviating the respiratory distress. Afterload reducers, such as hydralazine and sodium nitroprusside have not been tested clinically or experimentally in cats with tick paralysis. Furosemide may be used as an aid to remove fluid from the lungs. Cats with pulmonary edema may benefit from supplementary oxygen. This is easily provided by piping 100% oxygen into a cat induction chamber though a disposable plastic nebulizer. It is imperative to avoid hypothermia in affected animals.

Persistent nursing care is essential in animals with tick paralysis. Since any stress adversely affects the course of the disease, cats should be attended with minimal interference in the quietest part of the hospital. They should be maintained in a cool, air-conditioned environment since neuromuscular blockade is aggravated ny increased temperatures. To minimize ventilation/perfusion mismatch, animals should be placed in sternal recumbency on a well-padded surface using towels and sandbags. Following episodes of vomiting or regurgitation, the pharynx should be swabbed clean to reduce the risk of aspiration.

Submaintenance fluid requirements should be provided after the first day (0.45% NaCl containing 16 mmol KCl/L; 20-40 ml/kg/day), especially in animals in which recovery is prolonged. Fluids must be given slowly because of the predisposition of affected animals to develop pulmonary congestion and edema.

Prophylactic antibiotics are inappropriate in tick paralysis and atropine is contraindicated. Cardiac arrhythmias directly or indirectly result from sympathetic over activity and tend to resolve following the administration of phenoxybenzamine and acepromazine and require no specific treatment. Although high doses of glucocorticosteroids (0.5 mg/kg dexamethasone every 12 hours) have been shown to be advantageous in advanced cases of tick paralysis, their conventional use is unwarranted due to the threat of aspiration pneumonia. The role and efficacy of antiemetics have not been adequately described.

Food and water should be withheld from paralyzed animals because pharyngeal dysfunction, megaesophagus, laryngeal paresis and a weak cough create a tendency for aspiration pneumonia. They should be withheld until the patient is mobile and has not vomited for 24 hours. Small volumes of water can then be given; food can be offered subsequently if there is no vomiting. Following recovery, a convalescence phase should be imposed with restriction of exercise and avoidance of high temperatures. Strenuous exercise within a day of complete recovery from tick paralysis has resulted in collapse and sudden death. Extreme temperature may cause recovered animals to relapse into paralysis (Malik and Farrow, 1991).

EPIZOOTIOLOGY: Tick paralysis is seen in man and domesticated animals who either reside in or have had a history of visiting the bush and scrub country along the coastal fringe of eastern Australia. Long-haired cats are at a definite disadvantage with regard to the owner's inability to detect ticks within the haircoat. Facts on the seasonal incidence of Ixodesholocyclus are patchy, but there are indications that female ticks are most common in spring and early summer, larval ticks in summer and autumn, and nymphs in autumn and winter. Regardless, adults occur in low numbers at all times during the year. The host seeking behavior of females is said to be more aggressive during warm, moist weather which follows spring storms. Adult male and female ticks are abundant in areas of overgrowth or regrowth, especially around the base of small trees or shrubs surrounded by low vegetation (e.g. wild raspberry, crofton weed and lantana). Ticks occur on the mat of vegetation and in the lower foliage and leaf litter. These are areas frequented by bandicoots which are of most importance in the ecology of the paralysis tick (Doube, 1975).

HAZARDS TO OTHER ANIMALS: The normal hosts of Australian tick paralysis ticks include bandicoots, brush-tailed possums, macropods and koalas. These native mammals are relatively resistent to the toxins produced by the ticks, often carrying heavy burdens of ticks without showing evidence of harm (Stone and Wright, 1979, Stone, 1988).

Ixodesholocyclus has been reported to be the most consistently toxic paralyzing tick in the world. Not only does it cause serious economic loss to the Australian livestock industry, it is also of significant importance to pet owners. It has been reported that there may be at least 20,000 domestic animals in Australia affected by tick paralysis each year. Of these, at least 10,000 may have been companion animals referred to veterinarians for treatment. Livestock are also vulnerable to tick paralysis toxin; as many as 10,000 calves have died in New South Wales alone. Adult cattle, horse sheep, goats and deer are affected by heavier infestations. However, juvenile piglets, foals, kids, lambs, and fawns in deer farming programs are at greatest risk. It has been estimated that tick paralysis affects as many as 100,000 animals or more each year. Ixodescornuatus and Ixodeshirsti can produce a similar paralysis. Ixodescornuatus has been incriminated in paralysis of dogs in Victoria and Tasmania and of sheep and calves in Victoria (Stone, 1988).

In North America, dogs, sheep and cattle have fallen victim to the paralytic effects of Dermacentorandersoni (the Rocky Mountain wood tick), Dermacentorvariabilis (the American dog tick), and several other species of ticks in North America (Malik and Farrow, 1991).

HAZARDS TO HUMANS:Ixodesholocyclus has been reported to produce paralysis in humans, notably infants. Human infestations with this tick are occurring with increasing frequency, even in areas once not considered to be in its geographic distribution (Beveridge, 1991). The symptoms of tick paralysis in human beings are similar to those observed in animals. They include ascending paralysis characterized by unsteadiness in walking and/or lethargy, weakness in upper limbs, difficulty in swallowing, respiratory distress and even death in the absence of treatment. Other effects may be photophobia, double vision, pupillary dilatation and occasionally myocarditis. Localized paralysis, particularly of the face, occasionally occurs.

Ixodescornuatus infestations of humans have caused abdominal pain, vomiting, and headache as well as severe pain at the bite site. A single case of tick paralysis in a human that was attributable to Ixodescornuatus has been reported (Stone, 1988).

CONTROL/PREVENTION: Daily examination is the least expensive and most effective form of prevention. The syndrome will not develop until the ticks have been attached for at least 4 days. In the future, it may be possible to vaccinate cats using toxoids derived from the different toxins of Ixodesholocyclus (Malik and Farrow, 1991). Cats should be restricted from roaming in heavily wooded areas and areas with thick underbrush. This control technique is difficult to accomplish with outdoor cats.


Anderson WI. 1985. Tick paralysis in a cat. Mod Vet Prac 66:1006.

Beveridge I. 1991. Ixodesholocyclus in the Melbourne metropolitan area. Aust Vet J. 68:214.

Doube BM. 1975. Cattle and the paralysis tick Ixodesholocyclus. Aust Vet J. 51:511-515.

Homscher PJ, Keirans JE, Robbins RG, Irwin-Pinkley L, and Sonenshine DE. 1988. Scanning electron microscopy of ticks for systematic studies: Structure of Haller's organ in eight species of the subgenus Sternalixodes of the genus Ixodes (Acari: Ixodidae). J Med Entomol. 25:348-353.

Ilkiw JE, and Turner DM. 1987. Infestation in the dog by the paralysis tick, Ixodesholocyclus 2. Blood gas and pH, haematological and biochemical findings. Aust Vet J. 64:139-142.

Ilkiw JE, and Turner DM. 1987a. Infestation in the dog by the paralysis tick, Ixodesholocyclus 3. Respiratory effects. Aust Vet J. 64:142-144.

Ilkiw JE, Turner DM, and Howlett CR. 1987. Infestation in the dog by the paralysis tick Ixodesholocyclus 1. Clinical and histological findings. Aust Vet J. 64:137-139.

Ilkiw JE, and Turner DM. 1988. Infestation in the dog by the paralysis tick, Ixodesholocyclus 5. Treatment. Aust Vet J. 65:236-238.

Ilkiw JE, Turner DM, and Goodman AH. 1988. Infestation in the dog by the paralysis tick, Ixodesholocyclus 4. Cardiovascular effects. Aust Vet J. 65:232-235.

Kemp DH. 1979. Identity of Australian paralysis ticks. Proc 56th Annu Conf Aust Vet Assoc 1979. Pp. 73-74.

Malik R, and Farrow BRH. 1991. Tick paralysis in North America and Australia. Vet Clin N Am. 21:157-171.

Mason RW, Kemp DH, and King SJ. 1974. Ixodescornuatus and tick paralysis. Aust Vet J. 50:580.

Prescott CW. 1984. Ticks, spiders, insects, cane toads, platypus venom intoxications - II. Aust Vet Practit. 14:111-116.

Roberts FHS. 1961. Tick paralysis in South Australia. Aust Vet J. 37:440.

Roberts FHS. 1970. Australian ticks. CSIRO Melbourne, p. 59.

Ross IC. 1924. The bionomics of Ixodesholocyclus Neumann, with a redescription of the adult and nymphal stages and a description of the larvae. Parasitol. 16:365-381.

Ross IC. 1927. An experimental study of tick paralysis in Australia. Aust Vet J. 3:71-74.

Stone BF. 1988. Tick paralysis, particularly involving Ixodesholocyclus and other Ixodes species. In: Advances in Disease Vector Research, Volume 5. Edited by K.F. Harris. New York. Springer-Verlag. pp. 61-85.

Stone BF and Wright IG. 1979. Toxins of Ixodesholocyclus and immunity to paralysis. Proc 56th Annu Conf Aust Vet Assoc 1979. Pp. 75-78.