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Tick Paralysis
This is a flaccid, afebrile ascending motor paralysis in animals and people, produced by a neurotoxin generated by some but not all strains of certain species of ticks. Not all infested animals become paralyzed. Cats in the U.S. appear to be relatively resistant to tick paralysis, although signs of paralysis have been reported [179]. In North America, the common wood tick, Dermacentor variabilis, and Dermacentor andersoni (the Rocky Mountain wood tick) are incriminated most often. In Australia, especially along the east coast, Ixodes holocyclus is the most important species. Other species that occasionally cause paralysis are Ixodes cornuatus and Ixodes hirsti. Ixodes scapularis, the principal vector of the agent of Lyme disease (Borrelia burgdorferi) in the Northeast, Midwest, and Southeast of the United States, can also cause tick paralysis in dogs [180]. This tick is also a primary vector of the agent of human and rodent babesiosis. Ixodes pacificus has also been incriminated in dogs in the Grass Valley area (Nevada Co.) of northern California [181,182]. In Australia, Ixodes holocyclus is the vector for Lyme disease and spotted fever, caused by Rickettsia australis [183]. There is circumstantial evidence that some dogs bitten by Ixodes holocyclus develop signs of chronic illness similar to Lyme disease [183]. With tick paralysis, 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. In Australia, heavy infestations with nymphs or larvae may result in paralysis [184].
Onset of clinical signs is gradual, paralysis first becoming evident as an incoordination in the pelvic limbs, resulting in an unsteady gait. Altered voice, cough, and dysphagia can be early signs. Dogs become recumbent in 24 to 72 hours. Reflexes are lost but sensation is preserved. Jaw muscle weakness and facial paresis may be present. Death may occur within several days from respiratory paralysis. Electromyographic studies reveal absence of spontaneous potentials and lack of motor unit action potentials. No muscle response follows direct nerve stimulation. Motor and sensory nerve conduction velocity may be slower that normal. Prognosis is usually good with recovery occurring in 1 to 3 days following tick removal or dipping the animal in an insecticide solution. Administration of a systemic insecticide (e.g., cythioate, 3 - 6 mg/kg, PO) can be used to kill any hidden ticks on dogs. Assisted ventilation is necessary in cases with respiratory failure.
In Australia, tick paralysis is a far more serious and life-threatening condition [185-188]. Central effects include sympathetic stimulation that can produce peripheral vasoconstriction, arterial hypertension, increased pulmonary capillary hydrostatic pressure, pulmonary congestion and edema, tachyarrhythmias, and pupillary dilation. Respiratory embarrassment, in addition to diaphragmatic and intercostal paralysis, may stem from intoxication of medullary respiratory centers. Furthermore, hypoxia, hypercarbia, and respiratory acidosis may accompany respiratory failure. Clinical signs usually begin with pelvic limb weakness that progresses to paralysis within a few hours. Ascending paralysis soon involves the forelimbs. Mydriatic pupils are poorly or unresponsive to light. Other signs may include voice change, depressed gag reflex, megaesophagus, salivation, regurgitation and/or vomition, labored breathing, dyspnea, and cyanosis. Death occurs within 1 to 2 days if dogs are untreated. Similar signs are seen in cats with tick paralysis due to Ixodes sp. Focal forms of tick paralysis, such as asymmetrical facial paralysis and anisocoria, have been seen in some dogs, while others may only present with vomiting and loss of voice [184,189]. Short-term, acquired humoral immunity develops in animals following exposure to the toxin. Treatment involves removal of ticks, neutralization of circulating toxins, and supportive therapy. Painting ticks with pyrethroids and leaving the tick to die in situ may reduce mortality and analphylactoid reactions in sensitized patients [190]. Intravenous polyclonal hyperimmune serum (e.g., 0.5 - 1.0 ml/kg, IV) is suggested for dogs. For affected cats, administration of hydrocortisone (30 mg/kg, IV) followed by slow intravenous injection of serum (5 - 10 ml) is recommended [184]. This antiserum treatment is expensive and effective only in the early stages of paralysis [191]. In a recent survey from Australia, adverse reactions following tick antitoxin serum were reported in 3% of dogs and 6% of cats, with only a small percentage of these reactions associated with anaphylaxis [192]. The majority of adverse reaction were attributed to the Bezold-Jarisch reflex, a vagally mediated reflex initiated by chemical stimulation of cardiac receptors in the posterior wall of the left ventricle. Bradycardia, hypotension, reduction in total peripheral resistance and a slight reduction in myocardial contractility occurs with activation of these receptors [192]. A 1:1,000 solution of epinephrine should be available if animals show signs of anaphylaxis. Recommended dosage is 0.01 ml/kg IV or IM up to a maximum of 0.2 - 0.5 ml; repeat every 15 to 20 minutes if needed [192]. Due to the cholinergic nature of the Bezold-Jarisch reflex, atropine (at 0.1 - 0.2 mg/kg IV) will attenuate or abolish its clinical manifestations. A combination of phenoxybenzamine hydrochloride (e.g., 1 mg/kg as a 0.1% solution, given IV, over 15 minutes, every 12 to 24 hours) and acepromazine (0.05 - 0.10 mg/kg, IV, every 6 to 12 hours) produces sedation, helps relieve the respiratory distress, and resolves any cardiac arrhythmias [184,193]. Phenoxybenzamine hydrochloride, an alpha-adrenergic blocking drug, is thought to attenuate the arterial hypertension [188,193]. Some severely affected animals may require supplemental oxygen or intermittent positive pressure ventilation. Affected animals should be kept in a quiet, air-conditioned environment [184]. Food and water should be withheld until animals are walking and have not vomited for 24 hours. Weekly dips, use of collars impregnated with insecticide (e.g. permethrin) [190], or regular use of the organophosphate agent cythioate (3 mg/kg, PO, every 3 days) will help prevent tick paralysis in Australia. In a recent report from Australia, a correlation was noted between use of Lufenuron (a member of the benzoylphenylurea group of compounds used in dogs and cats for flea control) and lack of envenomation/paralysis caused by Ixodes holocyclus [194]. Despite treatment, prognosis can be guarded with this form of tick paralysis. In a recent survey of 577 dogs affected by tick paralysis, younger dogs were more likely to survive, and respiratory and gait scores reflected disease severity and were good prognostic indicators, in that dogs with mild disease recovered more quickly, whereas those with severe disease that received an additional dose of tick antitoxin serum were significantly less likely to survive [195].
Sensitive biological assays of toxin/antitoxin potency have been developed to assist in research on characterization of salivary toxins of the Australian paralysis tick Ixodes holocyclus and on immunity to tick paralysis [196]. The aim of current research is to develop a recombinant veterinary vaccine based on the tick neurotoxin peptide sequence. A successful vaccine would provide cost-effective, long-term protective immunity against tick-induced paralysis [191].

Toad Toxicity
This condition occurs in animals that bite or mouth various species of toads that contain bufotoxins within their parotid glands. Toxic species include the Colorado River toad (Bufo alvarius) and the marine toad (Bufo marinus). Toxicity is common in dogs in Florida and in Australia, especially in Queensland, where there is a seasonal incidence, primarily from September/October through April [197]. In one report from Florida, most dogs were treated during the spring and summer [198]. Toads tend to breed during the warmer and wetter months and hibernate during the colder and dryer months. Terrier breeds are commonly affected associated with their inquisitive nature and their tendencies to pursue hopping toads [197]. Cats are infrequently reported. Clinical signs develop within minutes of mouthing the toad and include profuse salivation, head shaking, ataxia, vomiting, polypnea, hemorrhagic diarrhea, and seizures in severe cases. Some dogs are presented in status epilepticus. Other neurological signs may include stupor, nystagmus, extensor rigidity, and opisthotonus [198]. Common EKG findings with Bufo Marinus include sinus arrhythmia, tachycardia, and occasionally ventricular fibrillation [198,199]. Abnormal cardiac depolarization and arrhythmias have been experimentally shown using resibufogenin and bufalin from toad venom [200]. Bufalin, from the Bufo marinus toad, is structurally and functionally similar to digitalis glycosides [201]. Death may occur within 30 minutes. Treatment involves washing the buccal mucosa with a swab or hose to dilute the toxin, intravenous diazepam (e.g., 0.25 to 1 mg/kg, IV), intravenous atropine (e.g., 0.04 mg/kg) and, if required, intravenous pentobarbital (e.g., 2.5 to 7.5 mg/kg, IV). Propranolol (e.g., 1.5 to 5.0 mg/kg, IV, rapidly, followed by a repeat dose in 20 minutes, for dogs and cats) is recommended, especially if ventricular fibrillation develops [199]. Prognosis will depend on the potency of the toxin, quantity absorbed, and size of the patient. It is usually favorable when animals are treated promptly [198], but may be guarded once seizures are seen [197].