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Tick paralysis is a preventable cause of morbidity and death that, when diagnosed promptly, requires a simple low-cost intervention. The key to success is to consider tick paralysis in the differential diagnosis of ascending weakness, particularly in children, in geographic areas where this disease predominates.
Tick paralysis results from inoculation of a toxin from tick salivary glands during a blood meal. It is a relatively uncommon neuromuscular disease with a higher prevalence among young girls, although older men who get exposed to ticks may also be affected. It typically presents as an acute ascending paralysis occurring a few days after tick attachment and may result in respiratory failure and death. Patients may report minor sensory symptoms but constitutional signs are usually absent. Deep tendon reflexes are usually hypoactive or absent and ophthalmoplegia and bulbar palsy can occur. Children may be ataxic. Electromyographic studies usually show a variable reduction in the amplitude of compound muscle action potentials but no abnormalities of repetitive nerve stimulation studies. These appear to result from a failure of acetylcholine release at the motor nerve terminal level. There may be subtle abnormalities of motor nerve conduction velocity and sensory action potentials. Removal of the tick results in the very rapid reversal of clinical and physiologic deficits, quicker with North American ticks than with the Ixodes species seen in Australia.
To assess respiratory function in dogs with tick paralysis, respiratory measurements were recorded on 14 dogs experimentally infested with Ixodes holocyclus. There was a progressive fall in respiratory rate with no change in tidal volume, which resulted in a significant fall in minute respiratory volume in the latter stages of the disease. The fall in respiratory rate was possibly central in origin and was accompanied by an increased alveolar-arterial oxygen tension difference, probably caused by pulmonary congestion and oedema. The "grunting" respiration seen in tick paralysis was due to closure of the vocal cords during expiration and could represent an attempt to re-expand collapsed parts of the lung.
Glutaraldehyde treatment of the toxin of the Australian paralysis tick Ixodes holocyclus produced a potent, immunogenic toxoid. Three subcutaneous injections (2 to 4 weeks apart) into rabbits produced very high antitoxin titres in their serum, although circulating antitoxin titres declined in the absence of stimulation. Twenty weeks later, immunized rabbits were unaffected by lethal doses of toxin injected subcutaneously.
The paralysis tick of Australia, Ixodes holocyclus, causes a severe toxicosis in domestic animals such as dogs and cats, livestock, and in some cases, humans. It is characterised by a rapidly ascending flaccid paralysis. The causative agent of the toxicosis is a neurotoxin(s) produced in the tick salivary glands. The current treatment for tick paralysis is in the form of a polyclonal dog antiserum. This antiserum treatment is expensive and effective only in the early stages of paralysis. 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.
In this study the value of drugs administered with hyperimmune serum in the treatment of advanced disease produced by Ixodes holocyclus was compared under controlled conditions. All control dogs died rapidly whereas one dog survived and 3 dogs died after receiving hyperimmune serum alone. When promethazine hydrochloride was administered with hyperimmune serum 2 dogs recovered rapidly while the remaining 2 died. Administration of dexamethasone and hyperimmune serum allowed 3 dogs to survive while administration of phenoxybenzamine hydrochloride in conjunction with hyperimmune serum allowed rapid recovery of all 4 dogs. Phenoxybenzamine hydrochloride, an alpha-adrenergic blocking drug, was chosen because of its potential to attenuate the arterial hypertension previously reported (Ilkiw et al 1988). The survival of all dogs together with the rapid return to normality indicated that this drug was beneficial in the treatment of dogs with advanced signs of tick paralysis.
Tick paralysis (tick toxicosis)--one of the eight most common tickborne diseases in the United States (1)--is an acute, ascending, flaccid motor paralysis that can be confused with Guillain-Barre syndrome, botulism, and myasthenia gravis. This report summarizes the results of the investigation of a case of tick paralysis in Washington.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Tick paralysis is a rare disease characterized by acute, ascending, flaccid paralysis that is often confused with other acute neurologic disorders or diseases (e.g., Guillain-Barré syndrome or botulism). Tick paralysis is thought to be caused by a toxin in tick saliva; the paralysis usually resolves within 24 hours after tick removal. During May 26-31, 2006, the Colorado Department of Public Health and Environment received reports of four recent cases of tick paralysis. The four patients lived (or had visited someone) within 20 miles of each other in the mountains of north central Colorado. This report summarizes the four cases and emphasizes the need to increase awareness of tick paralysis among health-care providers and persons in tick-infested areas.
Paralysis of domestic stock by the paralysis tick Ixodes holocyclus is chiefly a disease of young animals (especially calves) and of non-habituated stock introduced into tick-infested country in spring. The tick has a wide host range, but its principal hosts are bandicoots. The tick has one generation per year and the adult female, which causes almost all paralysis, is abundant in spring and early summer and occurs most commonly in overgrown or regrowth country where bandicoots are abundant. The distribution and behavior of the long and the short-nosed bandicoots are reviewed. The number of ticks required to induce paralysis in cattle and the protection from paralysis afforded by prior experience of the tick are discussed.
The aim of this study was to quantify the infestation densities of Karoo and brown paralysis ticks on sheep and goats and explain it in terms of the etho-ecology of these ticks and their domestic hosts. The Karoo paralysis tick usually quests from a vantage point on the vegetation whereas the brown paralysis tick displays an appetence response from the ground and mainly engages hosts that are prostrate. Both tick species are confined chiefly to hilly areas. Temporal differences in the infestation densities of the hosts within and between tick species were evident. These differences were related to disparities in the spatial distribution of the hosts, their activity patterns and the specific appetence responses of the two tick species. Differential climatological conditions affected the quality of forage in areas with a varied topography and the feeding preferences of hosts influenced tick-host sympatry and hence infestation densities.