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TICKS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Ticks are small arachnids that are found throughout the world, especially in warm, humid climates. There are approximately 900 species of ticks that are divided into 3 families: Argasidae (soft ticks), Ixodidae (hard ticks) and Nuttalliellidae (Nuttalliella namaqua; only one species identified).
    B) Please refer to the following managements for MORE DETAILED information on tickborne diseases/illnesses: EHRLICHIOSIS, LYME DISEASE, ROCKY MOUNTAIN SPOTTED FEVER, CRIMEAN-CONGO HEMORRHAGIC FEVER and TULAREMIA.
    C) This management deals specifically with ticks and diseases caused by ticks. Due to the numerous diseases associated with ticks, this management is limited to a brief discussion of other tickborne illnesses reported in the United States. These diseases/illnesses include: Anaplasmosis, Babesiosis, Colorado Tick Fever, Tickborne Relapsing Fever and Powassan Disease.

Specific Substances

    A) FAMILIES OF TICKS
    1) Amblyomma americanum
    2) Ixodidae (hard ticks)
    3) Artgasidae (soft ticks)
    4) Nuttalliellidae (one genus and one species)
    5) TICK

Available Forms Sources

    A) SOURCES
    1) Ticks are small arachnids that are found throughout the world, especially in warm, humid climates. There are approximately 900 species of ticks that are divided into 3 families: Argasidae (soft ticks; 191 species), Ixodidae (hard ticks; 701 species) and Nuttalliellidae (Nuttalliella namaqua; only one species identified). Ticks often show seasonal variation in activity, that can differ between species and developmental stages (Pfaffle et al, 2013).
    2) DISEASE ORGANISMS TRANSMITTED BY VARIOUS TICKS (Natsuaki et al, 2014; Jongejan et al, 1989; Modly & Burnett, 1988; Feldman-Muhsam, 1986; Raoult et al, 1997; Dupont et al, 1997; Pinn & Sowden, 1998; Brouqui et al, 1997; Sexton et al, 1990; Doan-Wiggins, 1991):
    ORGANISMTICK VECTOR
    Babesia microtiBabesia equiIxodes scapularis
    Borrelia burgdorferiIxodes scapularisIxodes pacificus
    Borrelia afzelii or B. garinii (Japan) Ixodes persulcatus
    Coltivirus speciesDermacentor andersoni
    Cowdria ruminantiumAmblyomma species
    Ehrlichia chaffeensisDermacentor variablilisAmblyomma americanum (Lone Star tick)
    Ehrlichia phagocytophiliaDermacentor variabilis
    Ehrlichia equiIxodes scapularis
    Borrelia spp (hermsii, turicatae, parkeri)Ornithodoros spp (hermsi, turiciata, parkeri)
    Female Tick NeurotoxinDermacentor andersoni,D.variabilis; Ixodes scapularis, Amblyomma americanum, A. maculatum
    FlaviviridaeIxodes ricinusI. persulcatus
    Francisella tularensisDermacentor andersoni,D.variabilis,Amblyomma americanum
    Rickettsia australisIxodes species
    Rickettsia burnetiiMany, non-specific
    Rickettsia conoriRhipicephalus or Hemaphysalis leachi
    Rickettsia rickettsiiDermacentor andersoni/variablilis
    Rickettsia slovaca Dermacentor marginatus
    Rickettsia africaeAmblyomma
    ORGANISMDISEASE
    Babesia microti or Babesia equiBabesios
    Borrelia burgdorferi Lyme disease
    Borrelia spp (hermsii, turicatae, parkeri, duttonii)Tick-borne relapsing fever
    Borrelia afzelii or B. garinii (Japan) Lyme disease
    Coltivirus speciesColorado Tick Fever
    Cowdria ruminantiumHeartwater disease
    Ehrlichia chaffeensisEhrlichiosis
    Ehrlichia phagocytophiliaHuman Granulocytic
    Ehrlichia equiEhrlichiosis
    Female Tick NeurotoxinTick paralysis
    Francisella tularensisTularemia
    Orientia tsutsugamushiScrub Typhus
    Rickettsia australisQueensland Tick Typhus
    Rickettsia burnettiQ Fever
    Rickettsia conoriBoutonneuse Fever Mediterranean Spotted Fever
    Rickettsia honeiFlinders Islands Spotted Fever
    Rickettsia africaeAfrican Tick-Bite Fever
    Rickettsia felisCalifornia Flea Typhus
    Rickettsia rickettsii*Rocky Mtn Spotted Fever
    Rickettsia mongolotimonaeRickettsia slovacaAstrakhan Fever
    Rickettsia akariRickettsialpox
    ORGANISMDISEASE
    Babesia microti or Babesia equiBabesios
    Borrelia burgdorferi Lyme disease
    Borrelia spp (hermsii, turicatae, parkeri, duttonii)Tick-borne relapsing fever
    Borrelia afzelii or B. garinii (Japan) Lyme disease
    Coltivirus speciesColorado Tick Fever
    Cowdria ruminantiumHeartwater disease
    Ehrlichia chaffeensisEhrlichiosis
    Ehrlichia phagocytophiliaHuman Granulocytic
    Ehrlichia equiEhrlichiosis
    Female Tick NeurotoxinTick paralysis
    Francisella tularensisTularemia
    Orientia tsutsugamushiScrub Typhus
    Rickettsia australisQueensland Tick Typhus
    Rickettsia burnettiQ Fever
    Rickettsia conoriBoutonneuse Fever Mediterranean Spotted Fever
    Rickettsia honeiFlinders Islands Spotted Fever
    Rickettsia africaeAfrican Tick-Bite Fever
    Rickettsia felisCalifornia Flea Typhus
    Rickettsia rickettsii*Rocky Mtn Spotted Fever
    Rickettsia mongolotimonaeRickettsia slovacaAstrakhan Fever
    Rickettsia akariRickettsialpox

    3) VECTOR: E. canis. Six human cases have been reported from this species which usually only infects canines (Fishbein et al, 1987).
    4) *VECTOR: Rhipicephalus sanguineus. Eleven confirmed and 5 probable Rocky Mountain spotted fever infections were identified in eastern Arizona. The implicated vector was the common brown dog tick (Rhipicephalus sanguineus) typically found in this region. Due to the hot, dry climate of this region, D. variabilis nor D. andersoni ticks are not viable in this region, while R. sanguineus is common (Demma et al, 2005).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) BACKGROUND: Ticks are small arachnids that are found throughout the world, especially in warm, humid climates. There are approximately 900 species of ticks that are divided into 3 families: Argasidae (soft ticks; 191 species), Ixodidae (hard ticks; 701 species) and Nuttalliellidae (Nuttalliella namaqua; only one species identified). Ticks often show seasonal variation in activity, that can differ between species and developmental stages. Tick bites can produce a local reaction and tick saliva can contain toxins. In addition, there are many infectious diseases that can be transmitted via tick bites. For further information on select tickborne illnesses, please SEE the following managements: Lyme Disease, Crimean-Congo Hemorrhagic Fever, Ehrlichiosis, Rocky Mountain Spotted Fever and Tularemia. This management is limited to the clinical effects and management of tick bites and a brief discussion of other tickborne illnesses including Anaplasmosis, Babesiosis, Colorado Tick Fever, Tickborne Relapsing Fever, and Powassan Disease that have been reported in the United States.
    B) TOXICOLOGY: Tick bites can often produce a dermal or inflammatory reaction at the site of injury. Ticks exert their toxic effects through several mechanisms. Some ticks have a neurotoxin in their salivary glands that can cause paralysis (tick paralysis).
    C) EPIDEMIOLOGY: Tick bites occur commonly worldwide. Tick borne disease or illness is also common (eg, Lyme disease is the most commonly reported vector borne disease in the US). Manifestations can range from mild local reactions to severe symptoms requiring hospitalization.
    D) WITH POISONING/EXPOSURE
    1) ADVERSE EFFECTS: Ticks may cause a dermal reaction or transmit other organisms and diseases in their bites. Most commonly, tick bites can produce a local reaction (ie, redness, ulcerative reaction, maculopapular or petechial rash). Hypersensitivity reactions may also occur after tick bites. TICK BORNE DISEASE: There are many tick borne diseases, which include bacterial (ie, anaplasmosis, ehrlichiosis), viral (colorado tick fever) and protozoal (babesiosis) illnesses. Many of these diseases have common symptoms including fever, chills, headache, myalgias, arthralgias, fatigue, malaise, gastrointestinal symptoms (nausea, vomiting, diarrhea, anorexia) and cough. Infrequent symptoms can include stiff neck, confusion, mild hepatomegaly or jaundice. Rarely, serious manifestations such as encephalitis, aseptic meningitis, and pericarditis can occur. TICK PARALYSIS: A rare disease that may cause ascending flaccid paralysis that may be confused with other neurologic conditions (eg, Guillain-Barre syndrome, botulism). It is caused by a toxin found in the saliva of certain ticks (ie, usually only a female tick of select genera). Patients usually recover within 24 hours of tick removal.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) Fever and chills may occur.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent. Q fever has been reported as a cause of morbidity and mortality in human pregnancies.

Laboratory Monitoring

    A) Laboratory studies may vary widely depending on the patient's symptoms. No specific studies are needed for most patients.
    B) Diagnosis of specific tick disease usually relies on various immunoassays.

Treatment Overview

    0.4.7) BITES/STINGS
    A) INFECTION OF TICK BITE
    1) There are many infectious diseases that can be transmitted via tick bites. For further information on tickborne illnesses, please SEE the following managements: Lyme Disease, Crimean-Congo Hemorrhagic Fever, Ehrlichiosis, Rocky Mountain Spotted Fever and Tularemia. This management is limited to the clinical effects and management of tick bites and a brief discussion of other tickborne illnesses including Anaplasmosis, Babesiosis, Colorado Tick Fever, Tickborne Relapsing Fever, and Powassan Disease.
    B) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) For mild to moderate toxicity, simple tick removal and supportive care for localized dermal symptoms is all that is required. Post exposure prophylaxis with a single dose of doxycycline is recommended for tick bite exposures under the following circumstances: an engorged Ixodes scapularis (blacklegged tick) tick removed after an estimated 36 hours of attachment, prophylaxis started within 72 hours of tick removal, Borrelia burgdorferi prevalence in local ticks known to be greater than 20%, and no contraindication to doxycycline. Mild to moderate symptoms from tick borne diseases again may require just supportive care for symptoms (eg, antipyretics for fever, analgesics for pain) but may require antibiotics or other treatments.
    2) TICK REMOVAL/DERMAL EXPOSURE: Remove ticks with blunt, wide blade forceps or tweezers rather than directly handling them. Grasp the tick firmly and as close to the skin as possible. Pull the tick out with a steady pull and try to avoid jerking, as that may lead to the head remaining in the skin. Be sure to remove the head of the tick, including its mouth parts, and examine the area with hand lens afterwards. Do NOT crush, puncture, burn or damage the tick as its parts or fluids may contain infective agents. In addition, do NOT apply large amounts of petroleum jelly to the tick to smother it as that may result in greater difficulty in removing it. There is also NO benefit in subcutaneous injections of local anesthesia for tick removal. After removal, clean and disinfect the bite site with soap, water, and alcohol. Place a sterile dressing or adhesive bandage over the wound, and one may apply a topical antibiotic as well. Most pain can be treated with ice applied over the injured area. Local itching or inflammation can be treated with topical corticosteroids, antihistamines and/or anesthetics. Tetanus prophylaxis should be considered.
    C) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment of severe toxicity from tick bites primarily consists of good supportive care of symptoms, which can range widely. For patients who experience severe symptoms such as meningitis, encephalitis, and pericarditis, intensive care medical management may be required as well as antibiotics depending on the disease.
    D) DECONTAMINATION
    1) PREHOSPITAL: There is no utility for prehospital activated charcoal. The focus of prehospital care should include tick removal, wound care, and supportive care (see DERMAL EXPOSURE).
    2) HOSPITAL: GI decontamination is not indicated. Treatment should include tick removal or thorough inspection of the site to be sure that all parts of the tick have been removed if performed prior to hospital care (use hand lens for examination), wound care, and supportive care (see DERMAL EXPOSURE).
    E) ANTIDOTES
    1) There is no specific antidote for tick bites.
    F) ANTIBIOTIC THERAPY
    1) TICKBORNE ILLNESS: Antibiotic therapy may be indicated in patients that develop systemic illness or disease. The following is a limited discussion of antibiotic use in some tickborne diseases.
    2) ANAPLASMOSIS: DOXYCYCLINE: Adult: 100 mg orally or IV, twice daily (max: 100 mg/dose) for 10 to 14 days; Pediatric: Children weighing less than 45.4 kg: 2.2 mg/kg per dose, orally or IV, twice daily (max: 100 mg/dose) for 10 to 14 days.
    3) BABESIOSIS: AZITHROMYCIN: Adult: Day 1: Administer 500 to 1000 mg orally and on subsequent days administer a total daily dose of 250 to 1000 mg (not to exceed 1000 mg daily) for 7 to 10 days plus atovaquone 750 mg orally every 12 hours for 7 to 10 days; 600 to 1000 mg/day of azithromycin may be used in immunocompromised patients; Pediatric: 10 mg/kg orally on day 1 (max: 500 mg/dose) followed by 5 mg/kg/day (max: 250 mg/dose) thereafter, plus atovaquone 20 mg/kg orally (max: 750 mg/dose) every 12 hours for 7 to 10 days. For severely ill patients (adults or children), clindamycin plus quinine is indicated.
    4) TICKBORNE RELAPSING FEVER: TETRACYCLINE (preferred): Adult: 500 mg orally every 6 hours for 10 days. ALTERNATIVE: Erythromycin 500 mg (12.5 mg/kg) orally every 6 hours for 10 days. If a patient exhibits signs of CNS toxicity, ceftriaxone 2 g daily for 10 to 14 days is the preferred agent.
    G) VIRAL ILLNESS
    1) COLORADO TICK FEVER virus is found in the western United States at elevations of 4,000 to 10,000 feet. There is no specific antiviral therapy; treatment is symptomatic and supportive.
    2) POWASSAN DISEASES: Powassan virus infections can be transmitted by the blacklegged tick (Ixodes scapularis) or the groundhog tick (Ixodes cookei). There is no specific antiviral treatment for this disease.
    H) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic patients or patients with minimal symptoms (eg, local skin irritation) may remain at home, but may require follow-up with their primary care physician for potential disease prophylaxis.
    2) OBSERVATION CRITERIA: Patients with worsening symptoms that do not improve with over-the-counter medications and basic home treatments should go to a healthcare facility for evaluation and further treatment. Patients who are stable with improving symptoms may be sent home.
    3) ADMISSION CRITERIA: Patients with worsening symptoms and who are unstable should be admitted to the hospital. Those with the most severe symptoms (eg, meningitis, encephalitis) may require an ICU admission. Criteria for discharge include patients that are clinically improving and physically stable.
    4) CONSULT CRITERIA: Infectious disease physicians should be involved for advice in treating patients. In addition, general practitioners and intensivists may need to be involved, depending on the severity of symptoms. Poison centers can aid treatment by serving as a public health resource for the general public seeking advice.
    I) PITFALLS
    1) The most common error in managing patients with tick bites is not considering or attributing symptoms to disease spread by tick bites. Symptoms may vary widely and may mimic symptoms of other diseases, making diagnosis difficult. Finally, the most important information regarding ticks includes prevention, avoiding direct contact with ticks (avoiding woody and bushy areas with high grass and leaf litter, walking in center of trails), repelling ticks with DEET or permethrin, and finding and removing ticks as soon as possible.
    J) PREDISPOSING CONDITIONS
    1) Patients with compromised physical conditions (eg, extremes of age, multiple comorbidities, immunocompromised) may be predisposed to toxicity. Also, people who frequent areas where ticks and tick diseases are more prevalent are more likely to suffer from tick exposure. Finally, patients who do not take precautions to protect themselves from tick bites are more likely to suffer from disease.
    K) DIFFERENTIAL DIAGNOSIS
    1) The differential diagnosis for tick disease can vary widely depending on the symptoms. Local skin irritation can mimic other arthropod bites or envenomations and more systemic diseases can mimic other viral or autoimmune diseases.

Range Of Toxicity

    A) One tick may be enough to cause an infection or tick paralysis.

Clinical Effects

Summary Of Exposure

    A) BACKGROUND: Ticks are small arachnids that are found throughout the world, especially in warm, humid climates. There are approximately 900 species of ticks that are divided into 3 families: Argasidae (soft ticks; 191 species), Ixodidae (hard ticks; 701 species) and Nuttalliellidae (Nuttalliella namaqua; only one species identified). Ticks often show seasonal variation in activity, that can differ between species and developmental stages. Tick bites can produce a local reaction and tick saliva can contain toxins. In addition, there are many infectious diseases that can be transmitted via tick bites. For further information on select tickborne illnesses, please SEE the following managements: Lyme Disease, Crimean-Congo Hemorrhagic Fever, Ehrlichiosis, Rocky Mountain Spotted Fever and Tularemia. This management is limited to the clinical effects and management of tick bites and a brief discussion of other tickborne illnesses including Anaplasmosis, Babesiosis, Colorado Tick Fever, Tickborne Relapsing Fever, and Powassan Disease that have been reported in the United States.
    B) TOXICOLOGY: Tick bites can often produce a dermal or inflammatory reaction at the site of injury. Ticks exert their toxic effects through several mechanisms. Some ticks have a neurotoxin in their salivary glands that can cause paralysis (tick paralysis).
    C) EPIDEMIOLOGY: Tick bites occur commonly worldwide. Tick borne disease or illness is also common (eg, Lyme disease is the most commonly reported vector borne disease in the US). Manifestations can range from mild local reactions to severe symptoms requiring hospitalization.
    D) WITH POISONING/EXPOSURE
    1) ADVERSE EFFECTS: Ticks may cause a dermal reaction or transmit other organisms and diseases in their bites. Most commonly, tick bites can produce a local reaction (ie, redness, ulcerative reaction, maculopapular or petechial rash). Hypersensitivity reactions may also occur after tick bites. TICK BORNE DISEASE: There are many tick borne diseases, which include bacterial (ie, anaplasmosis, ehrlichiosis), viral (colorado tick fever) and protozoal (babesiosis) illnesses. Many of these diseases have common symptoms including fever, chills, headache, myalgias, arthralgias, fatigue, malaise, gastrointestinal symptoms (nausea, vomiting, diarrhea, anorexia) and cough. Infrequent symptoms can include stiff neck, confusion, mild hepatomegaly or jaundice. Rarely, serious manifestations such as encephalitis, aseptic meningitis, and pericarditis can occur. TICK PARALYSIS: A rare disease that may cause ascending flaccid paralysis that may be confused with other neurologic conditions (eg, Guillain-Barre syndrome, botulism). It is caused by a toxin found in the saliva of certain ticks (ie, usually only a female tick of select genera). Patients usually recover within 24 hours of tick removal.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Fever and chills may occur.
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) FEVER is a common symptom reported with tickborne diseases/illnesses (Centers for Disease Control and Prevention, 2014).
    2) Fever may occur with Boutonneuse Fever (Feldman-Muhsam, 1986) or with Rickettsiosis (Parola et al, 1998). High, biphasic fever and chills may occur 4 to 5 days following a tick bite responsible for Colorado Tick Fever (Centers for Disease Control and Prevention, 2014; Cimolai et al, 1988).

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) NYSTAGMUS may occur (Fowler, 1993). Early cranial nerve involvement is a feature of tick paralysis, particularly the presence of both internal and external ophthalmoplegia (Grattan-Smith et al, 1997).
    2) CASE REPORT: Severe diplopia was reported in a 5-year-old girl who experienced bilateral cranial nerve VI weakness, bilateral facial nerve diplegia, and dysarthria. A tick was discovered in the patient's scalp and subsequently removed, resulting in rapid resolution of signs and symptoms. The patient was discharged without sequelae (Daugherty et al, 2005).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) DISORDER OF RESPIRATORY SYSTEM
    1) WITH POISONING/EXPOSURE
    a) Dyspnea may occur with Tick Paralysis, and progress to respiratory failure due to paralysis of respiratory muscles (Fowler, 1993). Babesiosis has been associated with respiratory symptoms including cough, pharyngitis and adult respiratory distress syndrome (Centers for Disease Control and Prevention, 2014; Byrd et al, 1997).
    B) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Acute respiratory distress syndrome can develop in severe cases of babesiosis (Centers for Disease Control and Prevention, 2014).
    b) Six patients developed adult respiratory distress syndrome associated with babesiosis (Byrd et al, 1997).
    C) PNEUMONIA
    1) WITH POISONING/EXPOSURE
    a) Pneumonia is encountered in 15% to 25% of tularemic patients (Byrd et al, 1997).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) PARALYSIS
    1) WITH POISONING/EXPOSURE
    a) TICK PARALYSIS
    1) A rare disease that may cause ascending flaccid paralysis that may be confused with other neurologic conditions. It is caused by a toxin found in the saliva of certain ticks. Usually only female ticks produce the toxin which enters from the salivary gland when the tick feeds (Abbott, 1944; Hamilton, 1940). Patients usually recover within 24 hours of tick removal.
    2) Signs are usually not present for 2 to 7 days after the tick has started feeding. There is a prodrome of malaise, irritability, and occasionally paresthesias, followed within 24 hours by an ascending motor neuropathy with decreased deep tendon reflexes. Paresis of legs is usually seen first. Differential diagnosis includes botulism, myasthenia gravis, and Guillain-Barre syndrome (Fowler, 1993).
    3) Weakness and ataxia may lead to an ascending paralysis with tick paralysis (Daugherty et al, 2005; Modly & Burnett, 1988). The paralysis ascends from the legs to the torso, arms, neck, throat, and face, with the patient finally becoming quadriplegic (Fowler, 1993).
    4) The progression of effects is to involve the upper extremities and respiratory muscles with bulbar involvement leading to aspiration, respiratory insufficiency, and death unless ventilatory support is instituted or the tick removed. Less commonly, ataxia may develop without muscle weakness.
    5) DISTRIBUTION: Most commonly reported in the Pacific Northwest and Rocky Mountain states but cases have been reported from southern states and in the northeastern states (Spach et al, 1993).
    6) SEASON: Occurs primarily in the Spring and summer (April through June) (Spach et al, 1993).
    b) CASE REPORT
    1) CASE REPORT: One 3-year-old had neurological symptoms 6 months after the tick was removed (Donat & Donat, 1981).
    B) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache is a common symptom reported with tickborne diseases/illnesses (Centers for Disease Control and Prevention, 2014). It has been reported with Boutonneuse fever (Feldman-Muhsam, 1986), and Colorado Tick Fever may produce severe headache (Cimolai et al, 1988).
    C) DISTURBANCE IN SPEECH
    1) WITH POISONING/EXPOSURE
    a) Slurred speech may occur with Tick Paralysis (Fowler, 1993).
    D) AMNESIA
    1) WITH POISONING/EXPOSURE
    a) Memory loss may occur if Colorado Tick Fever is left untreated (Cimolai et al, 1988).
    E) HALLUCINATIONS
    1) WITH POISONING/EXPOSURE
    a) Hallucinations may occur if Colorado Tick Fever is left untreated (Cimolai et al, 1988).
    F) MALAISE
    1) WITH POISONING/EXPOSURE
    a) Malaise may occur 4 to 5 days after a tick bite responsible for Colorado Tick Fever (Cimolai et al, 1988).
    G) NEUROPATHY
    1) WITH POISONING/EXPOSURE
    a) Facial palsy caused by neuroborreliosis is a common manifestation reported in European children (Dressler, 1994).
    b) European tick-bite meningoradiculoneuritis, a rickettsial disease transmitted by Ixodes ricinus, is characterized by distal axonal neuropathy.
    1) In reported cases, the rickettsia were not seen on ultrastructural examination (Vallat et al, 1987).
    c) CASE REPORT: A 5-year-old girl presented with diplopia and progressive weakness. A neurological examination revealed ptosis of the right eyelid with bilateral cranial nerve VI weakness, bilateral facial nerve diplegia, and dysarthria. Deep tendon reflexes of the ankles and knees were absent and her motor strength was globally diminished. A preliminary diagnosis of Guillain-Barre syndrome was made; however, a tick was discovered in the patient's scalp. Removal of the tick resulted in rapid resolution of signs and symptoms. The patient was discharged within 48 hours from symptom onset without neurologic sequelae (Daugherty et al, 2005).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) DRUG-INDUCED GASTROINTESTINAL DISTURBANCE
    1) WITH POISONING/EXPOSURE
    a) One case of an embedded tick producing appendicitis-like symptoms was reported from Nepal.
    b) CASE REPORT: An adult developed vomiting, diarrhea, fever, and right lower quadrant abdominal tenderness. A 3-mm tick was found embedded in the skin of the abdomen. Pain and other symptoms cleared after tick removal and administration of nalidixic acid (Schwartz & Shlim, 1988).
    B) DYSPHAGIA
    1) WITH POISONING/EXPOSURE
    a) There may be difficulty with chewing and swallowing in patients with Tick Paralysis (Fowler, 1993).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) ABNORMAL LIVER FUNCTION
    1) WITH POISONING/EXPOSURE
    a) Slightly elevated serum AST and ALT levels were reported, in a 50-year-old woman, one month after receiving a bite from a Rickettsia africae tick. The patient recovered slowly after treatment with doxycycline (Parola et al, 1998).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) LEUKOPENIA
    1) WITH POISONING/EXPOSURE
    a) EUROPEAN TICK-BORNE ENCEPHALITIS: During Stage 1 infection, leukopenia is the typical finding on laboratory tests; thrombocytopenia and abnormal liver function tests have also been reported. Later, during Stage 2 (encephalitis), leukocytosis is common (Lotric-Furlan & Strle, 1995).
    b) TICKBORNE DISEASES: Leukopenia can develop with Colorado Tick fever, babesiosis and anaplasmosis (Centers for Disease Control and Prevention, 2014).
    c) CASE REPORT: A 50-year-old woman was bitten on her right foot, by a tick, and, one month later, presented with leukopenia, as well as fatigue, a low- grade fever and elevated hepatic enzyme levels. Testing revealed the causative agent to be Rickettsia africae (Parola et al, 1998).
    B) THROMBOCYTOPENIC DISORDER
    1) WITH POISONING/EXPOSURE
    a) TICKBORNE DISEASES: Thrombocytopenia can develop with Colorado tick fever, babesiosis, anaplasmosis and tickborne relapsing fever (Centers for Disease Control and Prevention, 2014).
    C) ANEMIA
    1) WITH POISONING/EXPOSURE
    a) TICKBORNE DISEASES: Mild anemia can develop with anaplasmosis and hemolytic anemia has been reported with babesiosis (Centers for Disease Control and Prevention, 2014).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: Tick bites may cause irritation and may transmit diseases with dermatologic components.
    b) CASE REPORT: A 50-year-old woman was bitten on her right foot, by a tick, and subsequently noticed a 0.5-centimeter erythematous nodular lesion at the bite site and erythema at the right groin (Parola et al, 1998). The tick was later identified as Rickettsia africae.
    c) SOUTHERN TICK-ASSOCIATED RASH ILLNESS (STARI): A 51-year-old woman developed a 6.8 x 7-centimeter erythema migrans-like skin lesion on her shoulder after being bitten by an Amblyomma americanum tick, also known as the 'lone star" tick. She had no fever or systemic symptoms. Acute-phase and convalescent-phase serum samples from this patient tested negative by ELISA for antibody reactivity to B. burgdorferi. Genus-specific PCR targeting the flagellin gene found no evidence for Borrelia lonestari (or B. burgdorferi) infection in either of the A. americanum ticks removed from the patient (Haddad et al, 2005).
    B) MELANOSIS
    1) WITH POISONING/EXPOSURE
    a) A tache noir lesion is an ulcer covered with a black crust, a characteristic local reaction occurring at the presumed site of the infective bite. The patient will also probably have a severe generalized erythematous papular reaction (Modly & Burnett, 1988).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) WITH POISONING/EXPOSURE
    a) Myalgias and arthralgias are common symptoms reported with tickborne diseases/illnesses (Centers for Disease Control and Prevention, 2014). It has been reported with Boutonneuse fever (Feldman-Muhsam, 1986), and Colorado tick fever (Cimolai et al, 1988).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) ACUTE ALLERGIC REACTION
    1) WITH POISONING/EXPOSURE
    a) Hypersensitivity reactions may occur after exposure to bites, body parts, or excreta of arthropods (including ticks) (Kunkel, 1988).
    b) RHIPICEPHALUS BURSA: A 55-year-old man, with a history of allergy to be venom, developed pruritus, generalized urticaria, lip angioedema, nausea, and drowsiness after he removed a hard tick from his arm. He went to a local hospital and several more ticks were removed that were identified as Rhipicephalus Bursa found in Spain. An in-vitro study was carried out to determine if cross-reactivity exists between proteins from ticks and bee venom. It was found that bee venom extract inhibited IgE binding to some bands of tick salivary gland (proteins) extracts thus suggesting the presence of cross-reactivity between some allergenic epitopes present in ticks and others from bee venom proteins (Sanchez et al, 2014).
    B) DISORDER OF IMMUNE FUNCTION
    1) WITH POISONING/EXPOSURE
    a) A number of investigators have found that tick exposure will lead to short term immunity (Tu, 1984). Studies in cows have shown accumulations of lymphocytes and polymorphonuclear leukocytes at attachment sites (Riek, 1962). Mast cells were observed at I. ricinus attachment sites (Pavlovskii & Alfreva, 1941).
    b) Leukocyte-filled vesicles have been found beneath the attachment sites of D. variabilis in guinea pigs (Trager, 1939). Basophil accumulations at attachment sites on guinea pigs were reported by Allen (1973), and Bagnall (1975).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent. Q fever has been reported as a cause of morbidity and mortality in human pregnancies.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) OTHER
    1) Q fever has been reported as a cause of morbidity and mortality in 23 human pregnancies. Five of these occurred within a 3-year period in a small community in Southern France. Patients presented with fever associated with pneumonia, hepatitis or severe thrombocytopenia. Outcomes of the pregnancies varied from febrile abortion, premature birth, healthy full-term birth, and early neonatal death (Stein & Raoult, 1998).

Carcinogenicity

    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Laboratory studies may vary widely depending on the patient's symptoms. No specific studies are needed for most patients.
    B) Diagnosis of specific tick disease usually relies on various immunoassays.

Methods

    A) SUMMARY
    1) Below is a brief list of laboratory studies used to identify common tickborne illnesses in the US. For more detailed information SEE the individual management (ie, Ehrlichiosis, Lyme disease, Rocky Mountain Spotted Disease, and Tularemia).
    B) LABORATORY STUDIES BY TICKBORNE ILLNESS
    1) ANAPLASMOSIS: Confirmation is based on a 4-fold change in IgG-specific antibody titer by immunofluorescence assay (IFA) test in paired serum samples or detection of DNA by PCR of whole blood (most sensitive within first week of illness) (Centers for Disease Control and Prevention, 2014).
    2) BABESIOSIS: Detection of intraerythrocytic babesia parasites by light-microscopic exam of a peripheral blood smear or a positive babesia polymerase chain reaction (PCR) analysis (Centers for Disease Control and Prevention, 2014).
    3) COLORADO TICK FEVER: Neutropenia and thrombocytopenia usually occur on the 4th or 5th day of fever and can be a useful diagnostic screening test.
    a) Confirmation of infection is based on a 4-fold antibody titer rise in paired sera collected 2 to 3 weeks apart (p 17).
    4) EHRLICHIOSIS: Antibodies to Ehrlichia are detectable 7 to 10 days after the onset of illness. A 4-fold change in IgG-specific antibody titer by immunofluorescence assay (IFA) test in paired serum samples or detection of DNA by PCR on whole blood (most sensitive before antibiotics are used) (Centers for Disease Control and Prevention, 2014).
    5) LYME DISEASE: Currently, the CDC recommends a two-step process with an initial enzyme or an indirect immunofluorescence immunoassay and a confirmatory IgM or IgG Western Blot test with both tests needing to be positive for diagnosis (Centers for Disease Control and Prevention, 2014).
    6) ROCKY MOUNTAIN SPOTTED FEVER: Antibodies to R. rickettsii are detectable 7 to 10 days after the onset of illness. A 4-fold change in IgG-specific antibody titer by immunofluorescence assay (IFA) test in paired serum samples or detection of DNA in a skin biopsy or rash by polymerase chain reaction (PCR) assay (may not be accurate in acute blood samples) (Centers for Disease Control and Prevention, 2014).
    7) TULAREMIA: Isolation of organism from a specimen; or a 4-fold change in antibody titer in paired sera; or detection of organism by immunofluorescence assay (IFA) test or a single elevated serum antibody titer is supportive of the diagnosis (Centers for Disease Control and Prevention, 2014).
    8) TICKBORNE RELAPSING FEVER: Presence of Borrelia spirochetes in smears of peripheral blood, bone marrow or CSF (organisms more easily detected while the patient is febrile). Serologic testing for this condition is not standardized; results can vary (Centers for Disease Control and Prevention, 2014).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.6) DISPOSITION/BITE-STING EXPOSURE
    6.3.6.1) ADMISSION CRITERIA/BITE-STING
    A) Patients with worsening symptoms and who are unstable should be admitted to the hospital. Those with the most severe symptoms (eg, meningitis, encephalitis) may require an ICU admission. Criteria for discharge includes patients that are clinically improving and physically stable.
    6.3.6.2) HOME CRITERIA/BITE-STING
    A) Asymptomatic patients or patients with minimal symptoms (eg, local skin irritation) may remain at home, but may require follow-up with their primary care physician for potential disease prophylaxis.
    6.3.6.3) CONSULT CRITERIA/BITE-STING
    A) Infectious disease physicians should be involved for advice in treating patients. In addition, general practitioners and intensivists may need to be involved, depending on the severity of symptoms. Poison centers can aid treatment by serving as a public health resource for the general public seeking advice.
    6.3.6.5) OBSERVATION CRITERIA/BITE-STING
    A) Patients with worsening symptoms that do not improve with over-the-counter medications and basic home treatments should go to a healthcare facility for evaluation and further treatment. Patients who are stable with improving symptoms may be sent home.

Monitoring

    A) Laboratory studies may vary widely depending on the patient's symptoms. No specific studies are needed for most patients.
    B) Diagnosis of specific tick disease usually relies on various immunoassays.

Range Of Toxicity

Summary

    A) One tick may be enough to cause an infection or tick paralysis.

Minimum Lethal Exposure

    A) CASE REPORT
    1) TICK PARALYSIS: The bite of a single tick has caused paralysis in a human and a llama (Fowler, 1993).

Pharmacology Toxicology

Toxicologic Mechanism

    A) TICK PARALYSIS TOXIN - The exact structure is unknown. It is a neurotoxin that interferes with acetylcholine synthesis or liberation at neuromuscular endings. This causes a lower motor neuron paresis and paralysis (Fowler, 1993).

Animal Toxicology

Clinical Effects

    11.1.2) BOVINE/CATTLE
    A) TICK PARALYSIS -
    1) Vector: It is caused by a neurotoxin secreted by the female tick of certain species, especially Dermacentor andersoni/variabilis and Ixodes holcyclus (Australia). A single tick can cause the disease (Beasley et al, 1990). This is commonly seen in cattle and sheep in the northwestern USA.
    2) Mechanism: The toxin interferes with acetylcholine release (Nafe, 1988).
    3) Clinical Manifestations: Motor neuron ascending paralysis, apprehension, ataxia, and rarely cranial nerve deficits such as facial nerve diplegia. Without treatment, respiratory paralysis may occur as early as 5 days after onset of signs (Beasley et al, 1990).
    4) Diagnosis is based on finding a tick, removing it, and documented clinical improvement.
    5) Laboratory: Blood tests and nerve sensation are usually normal, and animals remain bright and alert.
    11.1.3) CANINE/DOG
    A) TICK PARALYSIS -
    1) Vector: Is commonly reported in dogs in the northwestern USA. Caused by a neurotoxin secreted by the female tick of certain species, especially Dermacentor andersoni/variabilis and Ixodes holocyclus (Australia). A single tick can cause the disease (Beasley et al, 1990).
    2) Mechanism: The toxin interferes with acetylcholine release (Nafe, 1988).
    3) Clinical Manifestations include motor neuron ascending paralysis, apprehension, ataxia, and rarely cranial nerve deficits such as facial nerve diplegia. Without treatment, respiratory paralysis may occur as early as 5 days after onset of signs (Beasley et al, 1990).
    4) Diagnosis is based on finding a tick, removing it, and then documented clinical improvement.
    5) Laboratory: Blood tests and nerve sensation are usually normal, and animals remain bright and alert.
    6) A canine antiserum to the toxin that causes tick paralysis is available. The antiserum prevents or reverses paralysis in domestic animals (Kincaid, 1990).
    11.1.9) OVINE/SHEEP
    A) TICK PARALYSIS -
    1) Vector: It is caused by a neurotoxin secreted by the female tick of certain species, especially Dermacentor andersoni/variabilis and Ixodes holcyclus (Australia). A single tick can cause the disease (Beasley et al, 1990). It is commonly seen in cattle and sheep in the northwestern USA.
    2) Mechanism: The toxin interferes with acetylcholine release (Nafe, 1988).
    3) Clinical manifestations include motor neuron ascending paralysis, apprehension, ataxia, and rarely cranial nerve deficits such as facial nerve diplegia. Without treatment, respiratory paralysis may occur as early as 5 days after onset of signs (Beasley et al, 1990).
    4) Diagnosis is based on finding a tick, removing it, and documented clinical improvement.
    5) Laboratory: Blood tests and nerve sensation are usually normal, and animals remain bright and alert.
    11.1.11) REPTILE
    A) REPTILE
    1) Tick paralysis does not occur in reptiles (Fowler, 1993).
    11.1.13) OTHER
    A) OTHER
    1) TICK PARALYSIS -
    a) Species in which cases have been reported include bison, llamas, dogs, grey fox, harvest mouse, ground hogs, black-tailed deer, horses, livestock, and cats. There are annual, seasonal, and species variability in outbreaks and susceptibility (Fowler, 1993).

Treatment

    11.2.1) SUMMARY
    A) GENERAL TREATMENT
    1) Remove the patient and other animals from the tick infested area.
    2) Treatment should always be done on the advice and with the consultation of a veterinarian.
    3) Additional information regarding treatment of poisoned animals may be obtained from a Board Certified (ABVT) Veterinary Toxicologist (check with nearest veterinary school or veterinary diagnostic laboratory) or the National Animal Poison Control Center.
    4) ANIMAL POISON CONTROL CENTERS
    a) ASPCA Animal Poison Control Center, An Allied Agency of the University of Illinois, 1717 S. Philo Rd, Suite 36, Urbana, IL 61802, website www.aspca.org/apcc
    b) It is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel and poison center staff for a fee. A veterinary toxicologist is available for consultation.
    c) The following 24-hour phone number is available: (888) 426-4435. A fee may apply. Please inquire with the poison center. The agency will make follow-up calls as needed in critical cases at no extra charge.
    11.2.2) LIFE SUPPORT
    A) GENERAL
    1) MAINTAIN VITAL FUNCTIONS: Secure airway, supply oxygen, and begin supportive fluid therapy if necessary.
    11.2.4) DECONTAMINATION
    A) GASTRIC DECONTAMINATION
    1) GENERAL TREATMENT
    a) Remove the offending tick if it is still on the animal. If none can be found, consider an insecticidal dip, especially with large animals, to remove ticks.
    11.2.5) TREATMENT
    A) DOGS/CATS
    1) ANAPHYLAXIS -
    a) AIRWAY - Maintain a patent airway via endotracheal tube or tracheostomy.
    b) EPINEPHRINE - For severe reactions.
    1) DOGS - 0.5 to 1 milliliter of 1:10,000 (DILUTE) solution intravenously or subcutaneously.
    2) CATS - 0.5 milliliter of 1:10,000 (DILUTE) solution intravenously or intramuscularly.
    3) DILUTION - Be sure to dilute epinephrine from the bottle (1:1000) one part to 9 parts saline to obtain the correct concentration (1:10,000).
    4) REPEAT DOSES - If indicated, doses may be repeated in 20 minutes.
    c) FLUID THERAPY -
    1) If necessary, begin fluid therapy at maintenance doses (66 milliliters solution/kilogram body weight/day) intravenously or, in hypotensive patients, at high doses (up to shock dose 60 milliliters/kilogram/hour.
    2) Monitor for urine production and pulmonary edema.
    d) ANTIHISTAMINES - Administer doxylamine succinate (1 to 2.2 milligram/kilogram subcutaneously or intramuscularly every 8 to 12 hours).
    e) STEROIDS - Administer dexamethasone sodium phosphate (1 to 5 milligrams/kilogram intravenously every 12 to 24 hours), or prednisone (1 to 5 milligram/kilogram intravenously every 1 to 6 hours).
    2) TICK PARALYSIS -
    a) Removal: Manual removal of ticks and/or insecticidal dips are necessary; closely examine ear canals, ear folds, and interdigital areas for ticks.
    b) Supportive Care: Respiration may need to be assisted for several hours until paralysis is overcome. Treat supportively; full recovery occurs within 48 hours of tick removal.
    B) RUMINANTS/HORSES/SWINE
    1) ANAPHYLAXIS -
    a) AIRWAY - Maintain a patent airway via endotracheal tube or tracheostomy.
    b) FLUIDS -
    1) HORSES - Administer electrolyte and fluid therapy as needed. Maintenance dose of intravenous isotonic fluids: 10 to 20 milliliters/kilogram per day. High dose for shock: 20 to 45 milliliters/kilogram/hour.
    a) Monitor for packed cell volume, adequate urine output and pulmonary edema. Goal is to maintain a urinary flow of 0.1 milliliters/kilogram/minute (2.4 liters/hour) for an 880 pound horse.
    2) CATTLE - Administer electrolyte and fluid therapy, orally or parenterally as needed. Maintenance dose of intravenous isotonic fluids for calves and debilitated adult cattle: 140 milliliters/kilogram/day. Dose for rehydration: 50 to 100 milliliters/kilogram given over 4 to 6 hours.
    c) EPINEPHRINE -
    1) HORSES - 3 to 5 milliliters/450 kilograms of 1:1000 epinephrine intramuscularly or subcutaneously.
    2) CATTLE & SWINE - 0.02 TO 0.03 milligrams/kilogram of 1:1000 epinephrine subcutaneously, intramuscularly, or intravenously.
    2) TICK-BORNE FEVER -
    a) Treatment of choice is oxytetracycline. Spiramycin and chloramphenicol appear to be somewhat effective (Anika et al, 1986). Aditoprim and trimethoprim have been found to be ineffective against tick-borne fever (Knoppert et al, 1988).
    b) Prophylaxis: Prophylactic use of long-acting tetracyclines in lambs (one 40 milligram/kilogram injection) provides protection from mortality for two to three weeks (Brodie et al, 1988). Improvement in bodyweights of sheep treated prophylactically with oxytetracycline was demonstrated following tick-borne fever rickettsial challenge (Cranwell, 1990).
    3) TICK PARALYSIS -
    a) Removal: Manual removal of ticks and/or insecticidal dips are necessary; closely examine ear canals, ear folds, and interdigital areas for ticks.
    b) Supportive Care: Respiration may need to be assisted for several hours until paralysis is overcome. Treat supportively; full recovery occurs within 48 hours of tick removal.

Continuing Care

    11.4.1) SUMMARY
    11.4.1.2) DECONTAMINATION/TREATMENT
    A) GENERAL TREATMENT
    1) Remove the patient and other animals from the tick infested area.
    2) Treatment should always be done on the advice and with the consultation of a veterinarian.
    3) Additional information regarding treatment of poisoned animals may be obtained from a Board Certified (ABVT) Veterinary Toxicologist (check with nearest veterinary school or veterinary diagnostic laboratory) or the National Animal Poison Control Center.
    4) ANIMAL POISON CONTROL CENTERS
    a) ASPCA Animal Poison Control Center, An Allied Agency of the University of Illinois, 1717 S. Philo Rd, Suite 36, Urbana, IL 61802, website www.aspca.org/apcc
    b) It is an emergency telephone service which provides toxicology information to veterinarians, animal owners, universities, extension personnel and poison center staff for a fee. A veterinary toxicologist is available for consultation.
    c) The following 24-hour phone number is available: (888) 426-4435. A fee may apply. Please inquire with the poison center. The agency will make follow-up calls as needed in critical cases at no extra charge.
    11.4.2) DECONTAMINATION
    11.4.2.2) GASTRIC DECONTAMINATION
    A) GASTRIC DECONTAMINATION
    1) GENERAL TREATMENT
    a) Remove the offending tick if it is still on the animal. If none can be found, consider an insecticidal dip, especially with large animals, to remove ticks.

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