What Is Your Neurologic Diagnosis?

Gabriela R. Wagner Metropolitan Veterinary Hospital, Fairlawn, OH 44321.
Neurology and Neurosurgery Service, Cornell University Hospital for Animals, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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Baye G. Williamson Metropolitan Veterinary Hospital, Fairlawn, OH 44321.
Neurology and Neurosurgery Service, Cornell University Hospital for Animals, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.

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A 10-year-old 8.8-kg (19.4-lb) castrated male West Highland White Terrier (vaccination status, current) was evaluated because of acute progressive tetraparesis. The dog had been initially examined by the referring veterinarian because of intermittently frantic scratching at its face over a 2-day period. Forty-eight hours after examination by the referring veterinarian, acute paraparesis and hyperreflexive patellar reflexes were evident. Twelve hours later, spinal reflexes were absent in the pelvic limbs and decreased in the right thoracic limb. Deep pain sensation was intact in all 4 limbs, and there was full range of motion in the head and neck. At 72 hours after the initial examination, the dog was reportedly tetraparetic. The referring veterinarian administered carprofena (4.5 mg/kg [2.0 mg/lb], SC), 2 doses of buprenorphine hydrochloride (0.02 mg/kg [0.009 mg/lb], IV) 6 hours apart, and doxycycline (5.6 mg/kg [2.5 mg/lb], IV). Prior to this episode, the dog was not receiving any medications. The dog was then referred for further evaluation.

What is the problem? Where is the lesion? What are the most probable causes of this problem? What is your plan to establish a diagnosis? Please turn the page.

Assessment

Anatomic diagnosis

ProblemRule out location
Nonambulatory tetraparesis with absent spinal reflexes in all limbs; no signs of painDiffuse neuropathy, myopathy, or neuromuscular junctionopathy

Likely location of 1 lesion

Diffuse lower motor neuron disease most likely attributable to neuropathy, myopathy, or neuromuscular junctionopathy

Etiologic diagnosis—The primary differential diagnoses for diffuse lower motor neuron disease in this dog included infectious disease (tick paralysis or botulism), autoimmune or inflammatory disease (polyradiculoneuritis or acquired fulminant myasthenia gravis), metabolic disease (hypoadrenocorticism or hypothyroidism), and neoplasia (lymphoma). The diagnostic plan included a CBC and serum biochemical analysis (to evaluate for evidence of infection, inflammation, metabolic derangements, or neoplasia), thoracic radiography (to evaluate for megaesophagus), and assessment of baseline serum cortisol concentration (to screen for hypoadrenocorticism). Although tick bite paralysis was considered less likely because the dog was fitted with a veterinarian-approved flea and tick collar, and a flea and tick preventativeb containing fipronil and cyphenothrin (98 mg/mL [9.8%] and 52 mg/mL [5.2%], respectively) was applied topically. Human immunoglobulin (1 g/kg [0.45 g/lb], IV, over 8 hours) was administered as an empirical treatment for polyradiculoneuritis because of concerns for the rapid disease progression. Prior to administration of human immunoglobulin, diphenhydramine (1 mg/kg) was administered IM.

Diagnostic test findings—Diagnostic testing performed initially by the referring veterinarian included a CBC, serum biochemical analysis, and thoracic radiography. The CBC revealed slight anemia (PCV, 36.7%; reference range, 37.3% to 61.7%); results of the serum biochemical analysis panel were within reference ranges. Right lateral thoracic radiography revealed no evidence of thoracic masses, metastatic disease, or megaesophagus. At the referral evaluation, the dog was persistently panting with an increased respiratory effort, but rectal temperature (37.6°C [99.7°F]) and heart rate (102 beats/min) were within reference limits. A search of the dog's body for ticks was performed, but none were found. Point-of-care blood analyses (assessments of PCV and total solids and blood glucose concentrations; urinalysis [dipstick]; and electrolyte and blood gas measurements) revealed no abnormalities other than a mildly decreased potassium concentration (3.34 mmol/L; reference range, 3.9 to 5.1 mmol/L). On repeated physical examination approximately 6 hours after the referral evaluation, an engorged tick was discovered and removed from the dog's mandible.

Improvement in the dog's neurologic condition was noted several hours after removal. The tick was later identified as Dermacentor variabilis. On the basis of the genus and species of the tick and the dog's rapid neurologic improvement after its removal, tick paralysis was determined to be the definitive diagnosis in this case.

Comments

At least 69 tick species are known to cause paralysis in many animals by producing a neurotoxin that interferes with either the propagation of impulses along motor neuron axons or with acetylcholine release at neuromuscular junctions.1–3 The neurotoxin is thought to affect both sensory and motor nerve fibers. The exact nature of the toxic agent is unknown, but it is produced in the ticks’ salivary gland and transferred to the host after prolonged attachment and engorgement. Clinical signs develop only when an attached tick is fully engorged with blood and, in most species, resolve after its removal. Hence, it is important to ensure that not only the body but also the head of the tick is removed. Often it takes 5 to 9 days after tick attachment for the affected animal's signs to be noticeable. These signs include acute, rapidly progressive, flaccid paralysis with decreased to absent spinal reflexes. Tetraplegia can develop within 12 to 72 hours after the onset of clinical signs. Additionally, cranial nerves V, VII, IX, and X involvement may occur, resulting in a variety of deficits including dysphonia, facial paralysis, dropped jaw, and loss of facial and masticatory muscle control.2,4

The most commonly reported tick species that cause paralysis are Ixodes holocyclus in Australia; Dermacentor andersoni, D variabilis, and Argas (Persicargas) radiatus in North America; Ixodes rubicundus in South Africa; Rhipicephalus evertsi and Argas (Persicargas) walkerae in Ethiopia; and A radiatus in the Nearctic region of North America.2 Along the east coast of Australia, approximately 20,000 domestic animals are affected each year,3,5 with associated signs that are more severe than those in affected animals in North America. These severe signs include acute CNS aberrations with respiratory failure progressing to death within 1 to 2 days after onset, if no treatment is provided.6 Although an antiserum is available for treatment of extremely grave cases of I holocyclus-associated illness, anaphylactic reactions to the antiserum may develop; however, such reactions can be reduced or avoided by first administering an intradermal test dose.7,8 Thus, animals with Ixodes-related infections are considered to have a graver prognosis in Australia than similarly infected animals in North America. For cases of North American origin, the prognosis is good if pressure sores are prevented, hydration and nutritional intake are maintained, and hypostatic or aspiration pneumonia is prevented. Clinical signs often resolve rapidly (within 8 to 12 hours) after removal of attached ticks.4

Prevention of tick paralysis is best achieved through regular application of acaricidal products. Protective immunity is not observed with this disease, and an episode of tick paralysis appears to increase an animal's susceptibility to future episodes.2,5,9 Cases of tick paralysis in Australia and the Midwestern and Western United States have been extensively documented, but there is no formal report of tick paralysis in a dog in the Northeastern United States, to our knowledge. The development of tick paralysis in the dog of the present report has corroborated the increased northward movement of ticks. As such, tick paralysis should remain a differential diagnosis for dogs with acute diffuse lower motor neuron disease, regardless of geographic location in the United States.

Acknowledgments

The authors thank Dr. Araceli Lucio-Forster for confirmation of the tick species.

Footnotes

a.

Rimadyl, Zoetis, Parsippany, NJ.

b.

Parastar Plus, Elanco, Greenfield, Ind.

References

  • 1. Gothe R, Neitz AWH. Tick paralysis: pathogenesis and etiology. Adv Dis Vect Res 1991;8:177204.

  • 2. Stone BF. Toxicoses induced by ticks and reptiles in domestic animals. In: Harris JD, ed. Natural toxins animal, plant, and microbial. Oxford, England: Clarendon Press 1986;5671.

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  • 3. Stone BF, Shipstone MA, Mason KV, et al. Efficacy of permethrin in controlling the Australian paralysis tick Ixodes holocyclus and the cat flea Ctneocephalides felis on dogs. Aust Vet J 1994;71:9091.

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  • 4. Eppleston KR, Kelman M, Ward MP. Distribution, seasonality and risk factors for tick paralysis in Australian dogs and cats. Vet Parasitol 2013;196:460468.

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  • 5. Penderis J, Martin-Vaquero P. Chapter 19: junctionopathies: disorders of the neuromuscular junction. In: Dewey CW, da Costa RC, eds. Practical guide to canine and feline neurology. 3rd ed. Ames, Iowa: Wiley & Sons, Inc, 2016;607632.

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  • 6. Kocan AA. Tick paralysis. J Am Vet Med Assoc 1988; 192:14981500.

  • 7. Atwell RB, Campbell FE, Evans EA. Prospective survey of tick paralysis in dogs. Aust Vet J 2001;79:412418.

  • 8. Atwell RB, Campbell FE. Reactions to tick antitoxin serum and the role of atropine in treatment of dogs and cats with tick paralysis caused by Ixodes holocyclus: a pilot survey. Aust Vet J 2001;79:394397.

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  • 9. Webster MC, Fisara P, Sargent RM. Long-term efficacy of a deltamethrin-impregnated collar for the control of the Australian paralysis tick, Ixodes holocyclus, on dogs. Aust Vet J 2011;89:439443.

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Contributor Notes

Address correspondence to Dr. Wagner (grw55@cornell.edu).
  • 1. Gothe R, Neitz AWH. Tick paralysis: pathogenesis and etiology. Adv Dis Vect Res 1991;8:177204.

  • 2. Stone BF. Toxicoses induced by ticks and reptiles in domestic animals. In: Harris JD, ed. Natural toxins animal, plant, and microbial. Oxford, England: Clarendon Press 1986;5671.

    • Search Google Scholar
    • Export Citation
  • 3. Stone BF, Shipstone MA, Mason KV, et al. Efficacy of permethrin in controlling the Australian paralysis tick Ixodes holocyclus and the cat flea Ctneocephalides felis on dogs. Aust Vet J 1994;71:9091.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 4. Eppleston KR, Kelman M, Ward MP. Distribution, seasonality and risk factors for tick paralysis in Australian dogs and cats. Vet Parasitol 2013;196:460468.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5. Penderis J, Martin-Vaquero P. Chapter 19: junctionopathies: disorders of the neuromuscular junction. In: Dewey CW, da Costa RC, eds. Practical guide to canine and feline neurology. 3rd ed. Ames, Iowa: Wiley & Sons, Inc, 2016;607632.

    • Search Google Scholar
    • Export Citation
  • 6. Kocan AA. Tick paralysis. J Am Vet Med Assoc 1988; 192:14981500.

  • 7. Atwell RB, Campbell FE, Evans EA. Prospective survey of tick paralysis in dogs. Aust Vet J 2001;79:412418.

  • 8. Atwell RB, Campbell FE. Reactions to tick antitoxin serum and the role of atropine in treatment of dogs and cats with tick paralysis caused by Ixodes holocyclus: a pilot survey. Aust Vet J 2001;79:394397.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9. Webster MC, Fisara P, Sargent RM. Long-term efficacy of a deltamethrin-impregnated collar for the control of the Australian paralysis tick, Ixodes holocyclus, on dogs. Aust Vet J 2011;89:439443.

    • Crossref
    • Search Google Scholar
    • Export Citation

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