| The potential for inducing paralysis has been demonstrated, described, or suspected in 64 species of ticks belonging to 7 ixodid and 3 argasid genera. On the eastern coast of Australia, the Australia paralysis tick I holocyclus (and to a lesser extent I cornuatus and I hirstii ) causes the most severe form of tick paralysis. In North America, D andersoni (the Rocky Mountain wood tick) and D variabilis (the American dog tick) are the most common causes, but D albipictus , I scapularis , Amblyomma americanum , A maculatum , R sanguineus , and O megnini may cause paralysis. In fowls, Argas radiatus and A persicus have caused paralysis. In Africa, I rubicundus (Karoo tick paralysis) and R punctatus in South Africa, R evertsi evertsi and Argas walkerae in subSaharan Africa, and R evertsimimeticus in Namibia can cause the disease. In North America, D andersoni and D variabilis affect dogs most commonly, but sheep, cattle, and humans have also been paralyzed. Cats appear to be resistant to the disease caused by these ticks. Clinical signs of ascending flaccid paralysis are seen 5-9 days after tick attachment, and progress from hindlimb weakness to quadriplegia over the next 24-72 hr. If ticks are not removed, death may occur from respiratory paralysis in 1-5 days. Removal of all ticks usually results in improvement within 24 hr and complete recovery within 72 hr. |
| I holocyclus in Australia cause a more severe disease than that seen in North America. Dogs and cats are affected, as well as sheep, calves, foals, pigs, flying foxes, poultry, and humans. The natural hosts (marsupials) are rarely affected, presumably acquiring immunity at an early age. Clinical signs in dogs and cats appear usually 5-7 days (occasionally up to 14 days or more) after attachment, and progress rapidly over the following 24-48 hr. Removal of ticks does not immediately halt progression of the disease once clinical signs are apparent. Death from respiratory failure is likely within 1-2 days of onset of signs. Appropriate and timely treatment saves ~95% of affected animals. |
| Host factors influencing epidemiology include sensitivity to toxin, age, immunity, behavior, reactivity, and population density. Antitoxic immunity, starting at least 2 wk after primary tick exposure and lasting a few weeks, can be boosted by further infestations. Tick factors include the dynamics and virulence of paralysis-inducing capability, sexual activity, rate of infestation, and the sucking phase. The maximal incidence of tick paralysis is associated with seasonal activity of female ticks, mainly in spring and early summer, but in some areas tick activity continues throughout the year. Environmental factors such as temperature and humidity also play a role. Modern rapid transport of ticks attached to people, animals, plant material, etc can give rise to isolated cases of tick paralysis far removed from the particular geographic area where the ticks are naturally found. |
| Toxicity follows secretion of toxin in tick saliva and its injection into the host animal. Usually this is caused by the adult female ixodid tick during its period of rapid engorgement (days 5-7), although large numbers of larval or nymphal ticks may also cause paralysis. Tick paralysis affects mainly motor pathways. There appears to be some effect on autonomic and possibly on sensory pathways. The neurotoxin interferes with acetylcholine release at the neuromuscular junction, producing a neuromuscular blockade. This manifests primarily as an ascending flaccid paralysis varying from paraparesis (hindleg weakness) to quadriplegia. |
| I holocyclus causes reversible myocardial depression and diastolic failure, leading to cardiogenic pulmonary edema. In severe cases, increased PCV reflects a fluid shift from the circulation to the lungs. Progressive pulmonary dysfunction appears to be primarily due to edema, leading to hypoxia, hypercarbia, respiratory acidosis, and eventually death. Other factors contributing to pulmonary failure include bronchoconstriction (especially in cats), paralysis and fatigue of respiratory muscles, and aspiration of esophageal or gastric contents. |
Paralysis of esophageal muscles develops in most dogs, with or without esophageal dilatation (megaesophagus). Saliva and ingested food or fluid pool in the esophagus, and are regurgitated into the pharynx and mouth. Loss of the gag reflex makes it difficult for the animal to clear this material from the airway, which may result in aspiration pneumonia. Vomiting may occur in I holocyclus paralysis, but is not common. A central action of toxin on the vomiting center has been suggested. Most cases of “vomiting” reported by clients are probably regurgitation, although drug-induced vomition may be a complication.
| Clinical Findings: |
| Early signs may include change or loss of voice (due to laryngeal paresis), hindlimb incoordination, change in breathing rate and effort, gagging or coughing, regurgitation or vomiting, and pupillary dilation. Hindlimb paralysis begins as slight to pronounced incoordination and weakness. As paralysis ascends, the animal becomes unable to move hindlimbs and forelimbs, stand, sit, or lift its head. Sensation usually is preserved. Breathing abnormality is of greater prognostic importance than limb paralysis. Respiratory rate may initially increase but, as the disease progresses, becomes slower and obviously labored, especially on expiration. Regurgitation of esophageal contents, saliva pooling, depression of the gag reflex, and attempts to clear the throat may produce a characteristic harsh, groaning respiratory sound. Temperature is normal in the early stages. Paralyzed animals with low body mass (especially cats) may become hypothermic. Conversely, animals kept at high ambient temperatures may need to cool themselves by panting, adding to respiratory difficulty. |
Blood and fluid values are unchanged in the early stages. Increased PCV indicates a fluid shift into the lungs and a poor prognosis. Other changes may include increased blood glucose, cholesterol, phosphate, and CK, and a decrease in blood potassium. In electrophysiologic studies, motor nerve conduction velocities, nerve compound action potentials, and compound potentials from the corresponding muscles are all decreased. The electroencephalogram is normal.
| Diagnosis: |
| The presence of a tick in conjunction with the sudden (12-24 hr) appearance of leg weakness and/or respiratory impairment is diagnostic. The offending tick may no longer be attached, but a tick “crater” (a small hole surrounded by a slightly raised and inflamed area) in the skin confirms the diagnosis. In Australia these animals require treatment. Sometimes neither tick nor crater can be found, but with the appropriate clinical signs in a known tick area, treatment is indicated. Recovery following treatment confirms the provisional diagnosis. Specific laboratory diagnostic techniques are not available. Procedures that may be helpful include a PCV and a lateral thoracic radiograph to assess presence and degree of pulmonary edema, megaesophagus, and any pneumonia due to aspiration. |
Botulism, polyradiculoneuritis, acute peripheral neuropathies, and snakebite are differential diagnoses. In regions where ticks are endemic, tick paralysis is usually high on the list of differential diagnoses for any flaccid ascending motor paralysis. It should also be considered in the differential diagnosis of megaesophagus, unexplained vomiting, acute left-sided congestive heart failure (dogs), or asthma (cats).
| Treatment: |
| Removal of the tick(s) is necessary. Frequently, multiple ticks are attached to an animal. The entire integument should be searched diligently and repeatedly, especially on long-haired animals. Most ticks are found around the head or neck, but can be anywhere on the body. Some practitioners prefer to kill the tick before removal, using a suitable acaricide. |
| In North America, removal of all ticks usually results in obvious improvement within 24 hr. Failure to recover indicates that at least one tick may be still be attached, or that the diagnosis should be reviewed. |
| In Australia, the disease commonly continues to progress after removal of ticks, and treatment is indicated for animals with motor or respiratory impairment. In cases in which an adult female I holocyclus has been removed but the animal shows no adverse clinical signs, the owner should monitor the animal for 24 hr and return for treatment if signs of tick paralysis develop. |
| Canine tick hyperimmune serum, also called tick antiserum (TAS), is the specific treatment for I holocyclus -induced tick paralysis. This should be given as early in the disease as possible; subsequent “top up” doses are not very effective. For dogs, a minimal dosage of 0.5-1.0 mL/kg, warmed to room temperature, is given slowly IV. Animals with multiple ticks or in the acute stages of paralysis should receive a higher dose. Some debate exists about the required dose of TAS. It has been suggested that a standard dose should be given, based on the amount needed to neutralize the toxin from one tick, not on the weight of the dog. On this basis, a minimal dose of 10 mL is recommended for dogs, but increased for multiple ticks or severely affected animals. Atropine (0.1-0.2 mg/kg, SC) is recommended before giving TAS; this reduces the incidence of an adverse effect that is seen in some small dogs soon after the injection is given—a temporary collapse with profound hypotension and bradycardia lasting several minutes, associated with the Bezold-Jarisch reflex. |
| TAS is given to cats at 1.0 mL/kg; 5 mL is the usual minimal dose. Giving canine serum IV to a cat involves a risk of anaphylaxis. This risk is minimized by routine SC injection of 3 mL of 1:10,000 epinephrine 3-4 min before administration of the TAS. |
| Minimization of stress and anxiety cannot be overemphasized. Acepromazine may be given SC before any other medication or handling that may upset the animal. However, acepromazine should be avoided or given at a reduced dose if the animal is depressed or hypothermic. Opiates are an alternative. Any procedure (eg, IV injection, searching for ticks) that may excite the animal should be postponed until the animal settles. |
| The animal’s condition can be expected to deteriorate for the next 24 hr after ticks are removed. Hospitalization, with monitoring and good nursing care, is advised during this period. The animal should be kept in a quiet, dark, comfortable place. Sternal recumbency should be maintained if comfortable; otherwise, the animal should be positioned in lateral recumbency with its shoulder being the highest point. Eye protectants should be used to prevent corneal ulceration or dry eyes, and the bladder expressed once or twice daily. Suction of the pharynx, larynx, and proximal esophagus minimizes respiratory distress caused by saliva pooling and esophageal dysfunction. An esophageal tube may be inserted to provide drainage. General anesthesia may be indicated in animals that are severely dyspneic to allow administration of oxygen, esophageal suction, and pulmonary drainage. Mechanical or manual ventilation may be required for 24 hr. |
| Nothing should be given PO until paralysis has resolved. IV fluid support is not routinely needed during the first 48 hr of hospitalization. IV fluids may add to pulmonary edema, so they should be used slowly and minimally. If the PCV is > 50%, colloid or heta/penta starch fluids should be considered rather than crystalloids. Furosemide can be given IV to help reduce pulmonary edema. |
| During hospitalization, regular searches for attached ticks should be done. Long or matted hair should be clipped. Application of an acaricide may kill ticks missed in searching. However, the stress of clipping or bathing can be detrimental in severely affected or nervous animals and may increase hypothermia. |
| About 5% of animals are likely to die despite all treatment efforts, especially those with advanced paralysis and dyspnea. Older animals or those with pre-existing cardiopulmonary disease are at greatest risk. |
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