Inability to open his mouth & oral hemorrhage.
Tick Paralysis - Crispin
Crispin was evaluated in June 2015 for a several day history of ataxia (wobbly walking) and weakness. His signs progressed quickly to not being able to walk or move any of his limbs at all. Crispin was referred from his primary veterinarian in Yakima to Seattle Veterinary Specialists for a neurologic evaluation.
Crispin was evaluated by Dr. Sean Sanders and Dr. Dani Powers at Seattle Veterinary Specialists for his neurologic signs. Based on his exam findings the primary concern was for a lower motor neuron condition. There are three main causes most common with lower motor neuron disease, which includes tick paralysis, botulism toxicity, and polyradiculoneuritis (Coon Hound paralysis). During Crispin’s exam a large engorged tick was found and removed. Given the presence of the tick, the presumption for Crispin would be Tick Paralysis. Crispin showed improvement within 12 hours of tick removal. He was also treated with a topical tick product, just in case we did not find any lingering ticks.
By 24 hours after tick removal Crispin was up and walking again and he was discharged 2 days after he presented unable to walk.
Tick paralysis is a condition that occurs after attachment and engorgement of feeding female ticks. The tick secretes a neurotoxin that results in impaired neuromuscular transmission and clinical weakness. The neurotoxin can affect both motor and sensory nerve fibers. In most cases, pain fibers are not affect and so painful stimuli are perceived. The most common tick species that result in paralysis include Dermacentor (D. variablis and D. andersoni are common to the US) and Ixodes (I. holcyclus is common to Australia).
Clinical signs usually become apparent within 7 to 9 days after attachment of the tick. Weaknessis usually manifested with ataxia (walking like they are drunk) with rapid progression to non-ambulatory paresis to paralysis in all 4 limbs. Reflexes are reduced to absent and they have hypotonic/flaccid limbs. Rarely are cranial nerves noted to be affected in the US, but possible; this is more common in Australia. Rarely respiratory failure is possible.
The diagnosis is usually made based clinical history and finding a tick, or rapid improvement after treatment with insecticide products. An MRI and spinal fluid analysis are usually not necessary. Some cases can be distinguished from other lower motor neuron disease if necessary with electrodiagnostics, but this is a low yield test and not usually performed. Treatment revolves around tick removal and also insecticide application. You must ensure the tick head is full removed, as the neurotoxin is still present if just the body is removed.