Tick paralysis is a rare life-threatening disorder caused by envenoming from ixodid tick bites
- can cause respiratory paralysis
- less than 5 cases of severe envenoming each year in Australia
- no deaths in Australia since 1945 and the advent of improved respiratory support
Only 3 species of ixodid or ‘hard’ tick (out of over 70 species in Australia) cause tick paralysis:
- Ixodes holocyclus
- Ixodes hirsti
- Ixodes cornuatus
- Ixodid tick saliva contains neurotoxins and various agents that modulate the hemostatic and inflammatory responses of the host
- I. holocyclus neurotoxins are ~ 5 kDa proteins known as holocyclotoxins that prevent acetylcholine release from presynaptic nerve terminals
- Both male and female adult ticks attach onto humans
- Ticks find a host by ‘questing‘ — they climb up vegetation waiting for host to pass by
- Natural hosts in Australia include bandicoots, koalas, possums and kangaroos
- confined to the bush and scrub lands near the eastern coast of Australia, from North Queensland to Victoria
- also reported in Tasmania
Tick paralysis also occurs in many other parts of the world where members of the Ixodidae family are found:
- Dermacentor andersoni — Western United States and Canada (British Columbia)
- D. variabilis — Central and Eastern United States
- Ixodes holocyclusand I. hirsti — Eastern Australia
- I. cornuatus — Tasmania (Australia)
- I. tancitarius — Mexico
- I. rubicundus — Africa
- Rhipicephalus simus — South Africa, Somalia
- R. evertsi evertsi — Africa
Severe toxicity and death is usually seen in children under the age of 3 years
- onset of symptoms is usually 4-5 days after tick attachment
- there may be local itch and swelling at the tick attachment site. Local nerve palsies (e.g. CN7 palsy) may occur in proximity to the tick attachment site. Allergic reactions may occur
- systemic toxicity is heralded by a nonspecific prodrome of ataxia (unsteady gait) and drowsiness or lethargy
- a progressive ascending symmetrical flaccid paralysis occurs over a period of days
- eventually cranial nerve palsies occur — typically ptosis, extraocular palsies, CN7 palsies, dysphagia and impaired airway reflexes
- death may result following the onset of respiratory paralysis
In the Australian setting, paralysis may progress for about 2 days following the removal of the tick in the symptomatic patient.
- diagnosis is made clinically
- Life threats include loss of airway reflexes and respiratory paralysis
- Intubation and ventilation may be required, and once performed is usually continued for day to weeks
Removal of the tick as soon as possible
- use fine forceps or suture material to grasp the tick’s mouth parts close to the skin at the site of attachment
- Remove the tick, with mouth-parts intact, by carefully applying steady traction
- Don’t worry about twisting clockwise or anti-clockwise!
- ensure that there are no retained mouth-parts, which may lead to granuloma formation
- it is controversial whether the tick should be killed before removal, due to concerns about toxin release during removal
Supportive care and monitoring
- Spirometry or serial peak expiratory flow monitory may be used to monitor the progression of respiratory paralysis
- Regular neurological observations
- CSL Tick paralysis antivenom is no longer available for use in humans
- Patients with the potential for respiratory failure require HDU/ ICU level care
- Symptomatic patients should not be discharged until ongoing neurological recovery is observed
- The asymptomatic patients does not need to be admitted for observation following the removal of a tick!
References and Links
- Toxicology Conundrum 039 — Paralysis and a head lump
Journal articles and textbooks
- Brown AF, Hamilton DL. Tick bite anaphylaxis in Australia. J Accid Emerg Med. 1998 Mar;15(2):111-3. PMC1343038.
- Edlow JA, McGillicuddy DC. Tick paralysis. Infect Dis Clin North Am. 2008 Sep;22(3):397-413, vii. PMID: 18755381.
- Grattan-Smith PJ, Morris JG, Johnston HM, Yiannikas C, Malik R, Russell R, Ouvrier RA. Clinical and neurophysiological features of tick paralysis. Brain. 1997 Nov;120 ( Pt 11):1975-87. PMID: 9397015.
Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.
After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.
He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE. He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.
His one great achievement is being the father of three amazing children.
On Twitter, he is @precordialthump.
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