Tick paralysis is the only tick-borne disease that is not caused by an infectious organism. The illness is caused by a neurotoxin produced in the ticks salivary gland. After prolonged attachment, the engorged tick transmits the toxin to its host. The incidence of tick paralysis is unknown. Patients can experience severe respiratory distress (similar to anaphylaxis). Signs and symptoms
Tick paralysis results from injection of a toxin from tick salivary glands during a blood meal. The toxin causes symptoms within 2–7 days, beginning with weakness in both legs that progresses to paralysis. The paralysis ascends to the trunk, arms, and head within hours and may lead to respiratory failure and death. The disease can present as acute ataxia without muscle weakness. Patients may report minor sensory symptoms, such as local numbness, but constitutional signs are usually absent. Deep tendon reflexes are usually decreased or absent, and ophthalmoplegia and bulbar palsy can occur. Electromyographic (EMG) 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. Pathogenesis
Tick paralysis is believed to be due to toxins found in the ticks saliva that enter the bloodstream while the tick is feeding.
Patients will be monitored over time, and treatments will be provided based on the complications that arise. Surgical
Spinal Fusion for patients with severe kyphoscoliosis
Extension Osteotomy to help treat progressive joint limitation
Surgical realignment
Retinal Detachment repair
Myringotomy (surgical procedure to relieve pressure by draining fluid from the eardrum)

Non-surgical
Routine monitoring  
Oxygen support, CPAP, Bipap, Mechanical Ventilation
Physical therapy
BracingLike treatment options, the prognosis is dependent on the severity of the symptoms. Despite the various symptoms and limitations, most individuals have normal intelligence and can lead a normal life. Recent research
A recent article in 2015 reported a persistent notochord in a fetus at 23 weeks of gestation. The fetus had an abnormal spine, shortened long bones and a left clubfoot. After running postmortem tests and ultrasound, the researchers believed that the fetus suffered from hypochondrogenesis. Hypochondrogenesis is caused when type II collagen is abnormally formed due to a mutation in the COL2A1 gene. Normally, the cartilaginous notochord develops into the bony vertebrae in a human body. The COL2A1 gene results in malformed type II collagen, which is essential in the transition from collagen to bone. This is the first time that researchers found a persistent notochord in a human body due to a COL2A1 mutation. Eponym
It is named for Wilhelm Kniest. == References ==