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→Treatment: Existing text is false at least for I holocyclus, as per the wp entry for I holocyclus. See U tube /8inseERKz78&t=3424 - Doggett is the pre-eminently cited scientist for this topic. No this is not correct citing, but it is correct, and better than the uncited incorrect assertion.
 
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{{Infobox medical condition (new)
{{Infobox medical condition (new)
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'''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 [[tick]]'s [[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]]).
'''Tick paralysis''' is a type of [[paralysis]] caused by specific types of attached ticks. Unlike [[tick-borne disease]]s caused by infectious organisms, the illness is caused by a [[neurotoxin]] produced in the [[tick]]'s [[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==
==Signs and symptoms==


Tick paralysis results from injection of a toxin from tick salivary glands during a blood meal. The toxin causes [[symptom]]s within 2–7 days, beginning with weakness in both legs that progresses to [[paralysis]]. The [[Ascending paralysis|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.
Tick paralysis results from injection of a toxin from tick salivary glands during a blood meal. The toxin causes [[symptom]]s within 2–7 days, beginning with weakness in both legs that progresses to [[paralysis]]. The [[Ascending paralysis|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.{{cn|date=January 2023}}


Patients may report minor sensory symptoms, such as local numbness, but constitutional signs are usually absent. [[Deep tendon reflexes]] are usually [[Hyporeflexia|decreased]] or absent, and [[ophthalmoplegia]] and [[bulbar palsy]] can occur.
Patients may report minor sensory symptoms, such as local numbness, but constitutional signs are usually absent. [[Deep tendon reflexes]] are usually [[Hyporeflexia|decreased]] or absent, and [[ophthalmoplegia]] and [[bulbar palsy]] can occur.{{cn|date=January 2023}}


[[Electromyography|Electromyographic]] (EMG) studies usually show a variable reduction in the amplitude of compound muscle [[action potential]]s, 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.
[[Electromyography|Electromyographic]] (EMG) studies usually show a variable reduction in the amplitude of compound muscle [[action potential]]s, 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.{{cn|date=January 2023}}


==Pathogenesis==
==Pathogenesis==
Tick paralysis is believed to be due to toxins found in the tick's saliva that enter the bloodstream while the tick is feeding. The two ticks most commonly associated with North American tick paralysis are the Rocky Mountain wood tick (''[[Dermacentor andersoni]]'') and the American dog tick (''[[Dermacentor variabilis]]''); however, 43 tick species have been implicated in human disease around the world.<ref>{{cite journal |vauthors=Gothe R, Kunze K, Hoogstraal H | title=The mechanisms of pathogenicity in the tick paralyses | journal=J Med Entomol | year=1979 | volume=16 | pages=357&ndash;69 | pmid=232161 | issue=5 | doi=10.1093/jmedent/16.5.357}}</ref> Most North American cases of tick paralysis occur from April to June, when adult ''Dermacentor'' ticks emerge from hibernation and actively seek hosts.<ref>{{cite journal |vauthors=Dworkin MS, Shoemaker PC, Anderson D | title=Tick paralysis: 33 human cases in Washington state, 1946&ndash;1996 | journal=Clin Infect Dis | year=1999 | volume=29 | pages=1435&ndash;9 | doi=10.1086/313502 | pmid=10585792 | issue=6 }}</ref> In Australia, tick paralysis is caused by the tick ''[[Ixodes holocyclus]]''. Prior to 1989, 20 fatal cases were reported in Australia.<ref>{{cite journal|author1=Masina S |author2=Broady K. W. | title = Tick paralysis: development of a vaccine| journal = International Journal for Parasitology| volume = 29| issue = 4| pages = 535–541| year = 1999| doi = 10.1016/S0020-7519(99)00006-5| pmid = 10428629}}
Tick paralysis is believed to be due to toxins found in the tick's saliva that enter the bloodstream while the tick is feeding. The two ticks most commonly associated with North American tick paralysis are the Rocky Mountain wood tick (''[[Dermacentor andersoni]]'') and the American dog tick (''[[Dermacentor variabilis]]''); however, 43 tick species have been implicated in human disease around the world.<ref>{{cite journal |vauthors=Gothe R, Kunze K, Hoogstraal H | title=The mechanisms of pathogenicity in the tick paralyses | journal=J Med Entomol | year=1979 | volume=16 | pages=357–69 | pmid=232161 | issue=5 | doi=10.1093/jmedent/16.5.357}}</ref> Most North American cases of tick paralysis occur from April to June, when adult ''Dermacentor'' ticks emerge from hibernation and actively seek hosts.<ref>{{cite journal |vauthors=Dworkin MS, Shoemaker PC, Anderson D | title=Tick paralysis: 33 human cases in Washington state, 1946–1996 | journal=Clin Infect Dis | year=1999 | volume=29 | pages=1435–9 | doi=10.1086/313502 | pmid=10585792 | issue=6 | doi-access=free }}</ref> In Australia, tick paralysis is caused by the tick ''[[Ixodes holocyclus]]''. Prior to 1989, 20 fatal cases were reported in Australia.<ref>{{cite journal|author1=Masina S |author2=Broady K. W. | title = Tick paralysis: development of a vaccine| journal = International Journal for Parasitology| volume = 29| issue = 4| pages = 535–541| year = 1999| doi = 10.1016/S0020-7519(99)00006-5| pmid = 10428629}}
</ref>
</ref>


Although tick paralysis is of concern in domestic animals and livestock in the United States as well, human cases are rare and usually occur in children under the age of 10.
Although tick paralysis is of concern in domestic animals and livestock in the United States as well, human cases are rare and usually occur in children under the age of 10.{{cn|date=January 2023}}


Tick paralysis occurs when an engorged and gravid (egg-laden) female tick produces a [[neurotoxin]] in its salivary glands and transmits it to its host during feeding. Experiments have indicated that the greatest amount of toxin is produced between the fifth and seventh day of attachment (often initiating or increasing the severity of symptoms), although the timing may vary depending on the species of tick.
Tick paralysis occurs when an engorged and gravid (egg-laden) female tick produces a [[neurotoxin]] in its salivary glands and transmits it to its host during feeding. Experiments have indicated that the greatest amount of toxin is produced between the fifth and seventh day of attachment (often initiating or increasing the severity of symptoms), although the timing may vary depending on the species of tick.{{cn|date=January 2023}}


Unlike [[Lyme disease]], [[ehrlichiosis]], and [[babesiosis]], which are caused by the systemic proliferation and expansion of parasites in their hosts long after the offending tick is gone, tick paralysis is chemically induced by the tick and therefore usually only continues in its presence. Once the tick is removed, symptoms usually diminish rapidly. However, in some cases, profound paralysis can develop and even become fatal before anyone becomes aware of a tick's presence.
Unlike [[Lyme disease]], [[ehrlichiosis]], and [[babesiosis]], which are caused by the systemic proliferation and expansion of microbes after the offending tick is gone, tick paralysis is chemically induced by the tick and therefore usually only continues in its presence. Once the tick is removed, symptoms usually diminish rapidly. However, in some cases, profound paralysis can develop and even become fatal before anyone becomes aware of a tick's presence.{{cn|date=October 2023}}


==Diagnosis==
==Diagnosis==
Diagnosis is based on symptoms and upon finding an embedded tick, usually on the scalp.
Diagnosis is based on symptoms and upon finding an embedded tick, usually on the scalp{{cn|date=January 2023}}.

⚫
In the absence of a tick, the differential diagnosis includes [[Guillain–Barré syndrome]]. Early signs of tick poisoning could be a change of an animals' ‘voice’, weakness in the back legs or vomiting.{{citation needed|date=July 2018}}


⚫
In the absence of a tick, the differential diagnosis includes [[Guillain–Barré syndrome]]. Early signs of tick poisoning could be a change of an animals' ‘voice’, weakness in the back legs or vomiting.{{cn|date=July 2018}}
==Prevention==
==Prevention==


Line 53: Line 54:
==Treatment==
==Treatment==


Removal of the offending tick usually results in resolution of symptoms within several hours to days. If the tick is not removed, the toxin can be fatal, with reported mortality rates of 10&ndash;12 percent,<ref>{{cite journal |vauthors=Schmitt N, Bowmer EJ, Gregson JD | title=Tick paralysis in British Columbia | journal=Can Med Assoc J | year=1969 | volume=100 | issue=9 | pages=417&ndash;21 | pmid=5767835 | pmc=1945728 }}</ref> usually due to respiratory paralysis. The tick is best removed by grasping it as close to the skin as possible and pulling in a firm steady manner.<ref>{{cite journal | author=Needham GR | title=Evaluation of five popular methods for tick removal | journal=Pediatrics | year=1985 | volume=75 | pages=997&ndash;1002 | pmid=4000801 | issue=6}}</ref> Because the toxin lies in the tick's salivary glands, care must be taken to remove the entire tick (including the head), or symptoms may persist.
Removal of the offending tick usually results in resolution of symptoms within several hours to days. If the tick is not removed, the toxin can be fatal. A 1969 study of children reported mortality rates of 10 – 12 percent,<ref>{{cite journal |vauthors=Schmitt N, Bowmer EJ, Gregson JD | title=Tick paralysis in British Columbia | journal=Can Med Assoc J | year=1969 | volume=100 | issue=9 | pages=417–21 | pmid=5767835 | pmc=1945728 }}</ref> mostly due to respiratory paralysis. The tick is best removed by grasping it as close to the skin as possible and pulling in a firm steady manner.<ref>{{cite journal | author=Needham GR | title=Evaluation of five popular methods for tick removal | journal=Pediatrics | year=1985 | volume=75 | pages=997–1002 | pmid=4000801 | issue=6| doi=10.1542/peds.75.6.997 | s2cid=23208238 }}</ref> Because the toxin lies in the tick's salivary glands, care must be taken to remove the entire tick (including the head), or symptoms may persist, although this is not true at least of ''[[Ixodes holocyclus]]'' (Australian paralysis tick).


It is important to note that, unlike the toxin of other tick species, the toxin of Ixodes holocyclus (Australian Paralysis Tick) may still be fatal even if the tick is removed.
It is important to note that, unlike the toxin of other tick species, the toxin of ''[[Ixodes holocyclus]]'' (Australian paralysis tick) may still be fatal even if the tick is removed.


Food and water can worsen the animal's outcome, as the toxin can prevent the animal from swallowing properly. If you find a tick on your animal, remove it immediately and seek veterinary assistance if the animal shows any signs of illness. The tick can be placed in a tightly sealed plastic bag and taken to a veterinarian for identification.<ref>{{cite web | url=http://www.ava.com.au/sites/default/files/Envenomation_Tick%20Paralysis_MCannon.pdf | title=Envenomation: Tick Paralysis | last=Cannon | first=Michael | access-date=June 11, 2018}}</ref><ref>{{cite web | url=http://www.greenhounds.com.au/Uploads/File/Paralysis%20Tick.pdf | title=Australian Paralysis Tick | last=O’Keefe | first=Dr Janette | access-date=June 9, 2018}}</ref>
For affected animals, food and water intake can worsen the outcome, as the toxin can prevent the animal from swallowing properly. People who find a tick on their animal, are advised to remove it immediately and seek veterinary assistance if the animal shows any signs of illness. The tick can be placed in a tightly sealed plastic bag and taken to a veterinarian for identification.<ref>{{cite web | url=http://www.ava.com.au/sites/default/files/Envenomation_Tick%20Paralysis_MCannon.pdf | title=Envenomation: Tick Paralysis | last=Cannon | first=Michael | access-date=June 11, 2018}}</ref><ref>{{cite web | url=http://www.greenhounds.com.au/Uploads/File/Paralysis%20Tick.pdf | title=Australian Paralysis Tick | last=O’Keefe | first=Dr Janette | access-date=June 9, 2018}}</ref>


==Research==
==Research==


Although several attempts have been made to isolate and identify the neurotoxin since the first isolation in 1966, the exact structure of the toxin has still not been published.<ref>{{cite journal| author = Doube B. M.| title = Cattle and Paralysis Tick Ixodes-Holocyclus| journal = Australian Veterinary Journal| volume = 51| issue = 11| pages = 511–515| year = 1975| doi = 10.1111/j.1751-0813.1975.tb06901.x| pmid = 1220655}}</ref> The 40-80&nbsp;kDa [[protein]] fraction contains the toxin.<ref>{{cite journal|author1=B. F. Stone |author2=K. C. Binnington |author3=M. Gauci |author4=J. H. Aylward | title = Tick/host interactions forIxodes holocyclus: Role, effects, biosynthesis and nature of its toxic and allergenic oral secretions| journal = Experimental and Applied Acarology| volume = 7| issue = 1| pages = 59–69| year = 1989| doi = 10.1007/BF01200453}}
Although several attempts have been made to isolate and identify the neurotoxin since the first isolation in 1966, the exact structure of the toxin has still not been published.<ref>{{cite journal| author = Doube B. M.| title = Cattle and Paralysis Tick Ixodes-Holocyclus| journal = Australian Veterinary Journal| volume = 51| issue = 11| pages = 511–515| year = 1975| doi = 10.1111/j.1751-0813.1975.tb06901.x| pmid = 1220655}}</ref> The 40-80&nbsp;kDa [[protein]] fraction contains the toxin.<ref>{{cite journal|author1=B. F. Stone |author2=K. C. Binnington |author3=M. Gauci |author4=J. H. Aylward | title = Tick/host interactions forIxodes holocyclus: Role, effects, biosynthesis and nature of its toxic and allergenic oral secretions| journal = Experimental and Applied Acarology| volume = 7| issue = 1| pages = 59–69| year = 1989| doi = 10.1007/BF01200453 | pmid = 2667920|s2cid=23861588 }}
</ref>
</ref>


The neurotoxin structure and gene, at least for the tick species [[Ixodes holocyclus]] have since been identified and are called holocyclotoxins after the species. At least three members (HT-1<ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/nuccore/AY766147|title=Ixodes holocyclus holocyclotoxin-1 (HT1) mRNA, complete cds - Nucleotide - NCBI|website=www.ncbi.nlm.nih.gov|access-date=2018-07-29}}</ref>, HT-3<ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/nuccore/KP096303|title=Ixodes holocyclus holocyclotoxin 3 (HT3) mRNA, complete cds - Nucleotide - NCBI|website=www.ncbi.nlm.nih.gov|access-date=2018-07-29}}</ref>, and HT-12<ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/nuccore/KP963967|title=Ixodes holocyclus holocyclotoxin 12 (HT12) mRNA, complete cds - Nucleotide - NCBI|website=www.ncbi.nlm.nih.gov|access-date=2018-07-29}}</ref>) trigger paralysis by presynaptic inhibition of neurotransmitter release via a calcium dependent mechanism resulting in a reduction of quantal content, and loss of effective neuromuscular synaptic transmission.<ref>{{Cite journal|last=Chand|first=Kirat K.|last2=Lee|first2=Kah Meng|last3=Lavidis|first3=Nickolas A.|last4=Rodriguez-Valle|first4=Manuel|last5=Ijaz|first5=Hina|last6=Koehbach|first6=Johannes|last7=Clark|first7=Richard J.|last8=Lew-Tabor|first8=Ala|last9=Noakes|first9=Peter G.|date=2016-07-08|title=Tick holocyclotoxins trigger host paralysis by presynaptic inhibition|journal=Scientific Reports|language=En|volume=6|issue=1|pages=29446|doi=10.1038/srep29446|pmid=27389875|pmc=4937380|issn=2045-2322|bibcode=2016NatSR...629446C}}</ref>
The neurotoxin structure and gene, at least for the tick species [[Ixodes holocyclus]] have since been identified and are called holocyclotoxins after the species. At least three members (HT-1,<ref>{{Cite journal|url=https://www.ncbi.nlm.nih.gov/nuccore/AY766147|title=Ixodes holocyclus holocyclotoxin-1 (HT1) mRNA, complete cds - Nucleotide - NCBI|website=www.ncbi.nlm.nih.gov|date=27 October 2004|access-date=2018-07-29}}</ref> HT-3,<ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/nuccore/KP096303|title=Ixodes holocyclus holocyclotoxin 3 (HT3) mRNA, complete cds - Nucleotide - NCBI|website=www.ncbi.nlm.nih.gov|access-date=2018-07-29}}</ref> and HT-12<ref>{{Cite web|url=https://www.ncbi.nlm.nih.gov/nuccore/KP963967|title=Ixodes holocyclus holocyclotoxin 12 (HT12) mRNA, complete cds - Nucleotide - NCBI|website=www.ncbi.nlm.nih.gov|access-date=2018-07-29}}</ref>) trigger paralysis by presynaptic inhibition of neurotransmitter release via a calcium dependent mechanism resulting in a reduction of quantal content, and loss of effective neuromuscular synaptic transmission.<ref>{{Cite journal|last1=Chand|first1=Kirat K.|last2=Lee|first2=Kah Meng|last3=Lavidis|first3=Nickolas A.|last4=Rodriguez-Valle|first4=Manuel|last5=Ijaz|first5=Hina|last6=Koehbach|first6=Johannes|last7=Clark|first7=Richard J.|last8=Lew-Tabor|first8=Ala|last9=Noakes|first9=Peter G.|date=2016-07-08|title=Tick holocyclotoxins trigger host paralysis by presynaptic inhibition|journal=Scientific Reports|language=En|volume=6|issue=1|pages=29446|doi=10.1038/srep29446|pmid=27389875|pmc=4937380|issn=2045-2322|bibcode=2016NatSR...629446C}}</ref>


==Culture==
==Culture==
Line 70: Line 71:
In the TV show, ''[[Hart of Dixie]]'', Season 1, Episode 2, a patient is diagnosed with tick paralysis who has been deer hunting.
In the TV show, ''[[Hart of Dixie]]'', Season 1, Episode 2, a patient is diagnosed with tick paralysis who has been deer hunting.


In the TV show, ''[[Emergency!]]'', Season 5, Episode 4, "[[List of Emergency! episodes|Equipment]]" (first aired Oct. 4, 1975), Dr. Joe Early diagnoses a young boy who has fallen from a tree with tick paralysis, after eliminating [[Poliomyelitis|polio]] as a cause.<ref>{{cite web|title=IMDB|url=https://www.imdb.com/title/tt0570629/}}</ref>
In the TV show, ''[[Emergency!]]'', Season 5, Episode 4, "[[List of Emergency! episodes|Equipment]]" (first aired Oct. 4, 1975), Dr. Joe Early diagnoses a young boy who has fallen from a tree with tick paralysis, after eliminating [[Poliomyelitis|polio]] as a cause.<ref>{{cite web|title=IMDB|website=[[IMDb]]|url=https://www.imdb.com/title/tt0570629/}}</ref>


In the TV show, ''[[House (TV series)|House]]'', Season 2, Episode 16, "[[House (season 2)|Safe]]", Dr House diagnoses a patient (played by [[Michelle Trachtenberg]]) with tick paralysis.<ref name="House MD">{{cite web|url=http://www.housemd-guide.com/season2/216safe.php|title=House MD Episode Guide: Season Two #216 'Safe'|work=housemd-guide.com|accessdate=August 11, 2012}}</ref>
In the TV show, ''[[House (TV series)|House]]'', Season 2, Episode 16, "[[House (season 2)|Safe]]", Dr House diagnoses a patient (played by [[Michelle Trachtenberg]]) with tick paralysis.<ref name="House MD">{{cite web|url=http://www.housemd-guide.com/season2/216safe.php|title=House MD Episode Guide: Season Two #216 'Safe'|work=housemd-guide.com|access-date=August 11, 2012}}</ref>


In the TV show, ''[[Remedy (TV series)|Remedy]]'', Season 1 Episode 7, "[[Remedy (TV series)#Series overview|Tomorrow, the Green Grass]]", Rebecca is diagnosed with tick paralysis.
In the TV show, ''[[Remedy (TV series)|Remedy]]'', Season 1 Episode 7, "[[Remedy (TV series)#Series overview|Tomorrow, the Green Grass]]", Rebecca is diagnosed with tick paralysis.
Line 81: Line 82:


==See also==
==See also==
*[[Polyneuropathy in dogs and cats]] for tick paralysis in dogs
* [[Polyneuropathy in dogs and cats]] for tick paralysis in dogs
*[[Tick-borne disease]]
* [[Tick-borne disease]]


==References==
==References==
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| ICD10 = {{ICD10|T|63|4|t|51}}
| ICD10 = {{ICD10|T|63|4|t|51}}
| ICD9 = {{ICD9|989.5}}
| ICD9 = {{ICD9|989.5}}
| ICDO =
| ICDO =
| OMIM =
| OMIM =
| MedlinePlus = 001359
| MedlinePlus = 001359
| eMedicineSubj =
| eMedicineSubj =
| eMedicineTopic =
| eMedicineTopic =
| MeshID = D013985
| MeshID = D013985
| SNOMED CT = 74225001
| SNOMED CT = 74225001
}}
}}



{{Poisoning and toxicity}}
{{Poisoning and toxicity}}

Latest revision as of 00:58, 14 August 2024

Tick paralysis
SpecialtyEmergency medicine, neurology Edit this on Wikidata

Tick paralysis is a type of paralysis caused by specific types of attached ticks. Unlike tick-borne diseases caused by infectious organisms, the illness is caused by a neurotoxin produced in the tick's 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

[edit]

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.[citation needed]

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.[citation needed]

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.[citation needed]

Pathogenesis

[edit]

Tick paralysis is believed to be due to toxins found in the tick's saliva that enter the bloodstream while the tick is feeding. The two ticks most commonly associated with North American tick paralysis are the Rocky Mountain wood tick (Dermacentor andersoni) and the American dog tick (Dermacentor variabilis); however, 43 tick species have been implicated in human disease around the world.[1] Most North American cases of tick paralysis occur from April to June, when adult Dermacentor ticks emerge from hibernation and actively seek hosts.[2] In Australia, tick paralysis is caused by the tick Ixodes holocyclus. Prior to 1989, 20 fatal cases were reported in Australia.[3]

Although tick paralysis is of concern in domestic animals and livestock in the United States as well, human cases are rare and usually occur in children under the age of 10.[citation needed]

Tick paralysis occurs when an engorged and gravid (egg-laden) female tick produces a neurotoxin in its salivary glands and transmits it to its host during feeding. Experiments have indicated that the greatest amount of toxin is produced between the fifth and seventh day of attachment (often initiating or increasing the severity of symptoms), although the timing may vary depending on the species of tick.[citation needed]

Unlike Lyme disease, ehrlichiosis, and babesiosis, which are caused by the systemic proliferation and expansion of microbes after the offending tick is gone, tick paralysis is chemically induced by the tick and therefore usually only continues in its presence. Once the tick is removed, symptoms usually diminish rapidly. However, in some cases, profound paralysis can develop and even become fatal before anyone becomes aware of a tick's presence.[citation needed]

Diagnosis

[edit]

Diagnosis is based on symptoms and upon finding an embedded tick, usually on the scalp[citation needed].

In the absence of a tick, the differential diagnosis includes Guillain–Barré syndrome. Early signs of tick poisoning could be a change of an animals' ‘voice’, weakness in the back legs or vomiting.[citation needed]

Prevention

[edit]

No human vaccine is currently available for any tick-borne disease, except for tick-borne encephalitis. Individuals should therefore take precautions when entering tick-infested areas, particularly in the spring and summer months. Preventive measures include avoiding trails that are overgrown with bushy vegetation, wearing light-coloured clothes that allow one to see the ticks more easily, and wearing long pants and closed-toe shoes. Tick repellents containing DEET (N,N, diethyl-m-toluamide) are only marginally effective and can be applied to skin or clothing. Rarely, severe reactions can occur in some people who use DEET-containing products. Young children may be especially vulnerable to these adverse effects. Permethrin, which can only be applied to clothing, is much more effective in preventing tick bites. Permethrin is not a repellent but rather an insecticide; it causes ticks to curl up and fall off the protected clothing.[weasel words]

Treatment

[edit]

Removal of the offending tick usually results in resolution of symptoms within several hours to days. If the tick is not removed, the toxin can be fatal. A 1969 study of children reported mortality rates of 10 – 12 percent,[4] mostly due to respiratory paralysis. The tick is best removed by grasping it as close to the skin as possible and pulling in a firm steady manner.[5] Because the toxin lies in the tick's salivary glands, care must be taken to remove the entire tick (including the head), or symptoms may persist, although this is not true at least of Ixodes holocyclus (Australian paralysis tick).

It is important to note that, unlike the toxin of other tick species, the toxin of Ixodes holocyclus (Australian paralysis tick) may still be fatal even if the tick is removed.

For affected animals, food and water intake can worsen the outcome, as the toxin can prevent the animal from swallowing properly. People who find a tick on their animal, are advised to remove it immediately and seek veterinary assistance if the animal shows any signs of illness. The tick can be placed in a tightly sealed plastic bag and taken to a veterinarian for identification.[6][7]

Research

[edit]

Although several attempts have been made to isolate and identify the neurotoxin since the first isolation in 1966, the exact structure of the toxin has still not been published.[8] The 40-80 kDa protein fraction contains the toxin.[9]

The neurotoxin structure and gene, at least for the tick species Ixodes holocyclus have since been identified and are called holocyclotoxins after the species. At least three members (HT-1,[10] HT-3,[11] and HT-12[12]) trigger paralysis by presynaptic inhibition of neurotransmitter release via a calcium dependent mechanism resulting in a reduction of quantal content, and loss of effective neuromuscular synaptic transmission.[13]

Culture

[edit]

In the TV show, Hart of Dixie, Season 1, Episode 2, a patient is diagnosed with tick paralysis who has been deer hunting.

In the TV show, Emergency!, Season 5, Episode 4, "Equipment" (first aired Oct. 4, 1975), Dr. Joe Early diagnoses a young boy who has fallen from a tree with tick paralysis, after eliminating polio as a cause.[14]

In the TV show, House, Season 2, Episode 16, "Safe", Dr House diagnoses a patient (played by Michelle Trachtenberg) with tick paralysis.[15]

In the TV show, Remedy, Season 1 Episode 7, "Tomorrow, the Green Grass", Rebecca is diagnosed with tick paralysis.

In the TV show, Royal Pains, Season 1 Episode 3, "Strategic Planning", a US Senator's teenage son is diagnosed with and overcomes tick paralysis.

In the TV show, Chicago Med, Season 3, Episode 5, "Mountains and Molehills", a young girl returning from Australia with increasing paralysis is diagnosed with tick paralysis.

See also

[edit]

References

[edit]
  1. ^ Gothe R, Kunze K, Hoogstraal H (1979). "The mechanisms of pathogenicity in the tick paralyses". J Med Entomol. 16 (5): 357–69. doi:10.1093/jmedent/16.5.357. PMID 232161.
  2. ^ Dworkin MS, Shoemaker PC, Anderson D (1999). "Tick paralysis: 33 human cases in Washington state, 1946–1996". Clin Infect Dis. 29 (6): 1435–9. doi:10.1086/313502. PMID 10585792.
  3. ^ Masina S; Broady K. W. (1999). "Tick paralysis: development of a vaccine". International Journal for Parasitology. 29 (4): 535–541. doi:10.1016/S0020-7519(99)00006-5. PMID 10428629.
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  12. ^ "Ixodes holocyclus holocyclotoxin 12 (HT12) mRNA, complete cds - Nucleotide - NCBI". www.ncbi.nlm.nih.gov. Retrieved 2018-07-29.
  13. ^ Chand, Kirat K.; Lee, Kah Meng; Lavidis, Nickolas A.; Rodriguez-Valle, Manuel; Ijaz, Hina; Koehbach, Johannes; Clark, Richard J.; Lew-Tabor, Ala; Noakes, Peter G. (2016-07-08). "Tick holocyclotoxins trigger host paralysis by presynaptic inhibition". Scientific Reports. 6 (1): 29446. Bibcode:2016NatSR...629446C. doi:10.1038/srep29446. ISSN 2045-2322. PMC 4937380. PMID 27389875.
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