[Micromedex][POISINDEX][Managements] TICKS (Ixodida) bite 蜱咬傷 @ 快樂小藥師 Im pharmacist nichts glücklich

tick，蜱，另外一個比較容易聽到的名字，叫做牛蚤，Ixodida蜱科生物，一般來說，寄生在動物身上，有時候也會存在一般家庭飼養的貓狗身上。

會經由貓狗傳染到人類，屬於人畜共通傳染病。

被寄生的人類就像這樣：

如果不經過治療，很有可能會因為蜱下蛋之後繁殖而導致失明。

0.0 OVERVIEW

LIFE SUPPORT

CLINICAL EFFECTS

LABORATORY/MONITORING

TREATMENT OVERVIEW

RANGE OF TOXICITY

0.1 LIFE SUPPORT

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

0.2 CLINICAL EFFECTS

0.2.1 SUMMARY OF EXPOSURE

A) WITH POISONING/EXPOSURE

1) Ticks may cause a dermal reaction or transmit other organisms and diseases in their bites. A summary of these illnesses is listed below.
2) BOUTONNEUSE FEVER - Clinical manifestations include sudden headache, fever, and pain in the joints and muscles developing after an incubation period of 5 to 7 days. A few days after incubation a generalized maculopapular rash appears. An ulcerative lesion appears at the bite site.
3) COLORADO TICK FEVER -

a) Manifestations include high, biphasic fever, chills, myalgia, severe headache, photophobia, and malaise occurring 4 to 5 days following a tick bite. The illness is self-limited and usually resolves within 7 to 10 days. In 50 percent of untreated patients symptoms recur within 3 days and the second course of illness lasts 2 to 4 days.
b) Less common manifestations include a transient petechial or macular rash, leukopenia and thrombocytopenia. Rarely complications such as encephalitis, aseptic meningitis, pericarditis, orchitis, atypical pneumonia and hepatitis may develop. Most patients recover uneventfully.
c) DISTRIBUTION - Mountainous regions of Colorado, Utah, South Dakota, Montana, Wyoming, Idaho, Washington, Oregon, California, New Mexico and Nevada.
d) SEASON - Most patients acquire the disease between late May and early July.

4) TICK PARALYSIS -

a) 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.
b) 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.
c) 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.
d) SEASON - Occurs primarily in the Spring and summer (April through June).

5) EUROPEAN TICK-BORNE ENCEPHALITIS (TBE) -

a) CLINICAL MANIFESTATIONS - Stage 1: Fever, headache, and myalgia. One-third of patients will develop Stage 2 about one week later: meningoencephalitis. Sequelae may persist for years.
b) DISTRIBUTION - Two subtypes of the causative flavivirus exist: the western subtype occurs in western and central Europe (excepting Great Britain, Ireland, the Netherlands, Belgium, Luxembourg, Spain, and Portugal); and the eastern subtype occurs in eastern Russia.
c) SEASON - April to November, with most cases occurring July to September.

6) OTHER INFECTIONS TRANSMITTED BY TICKS -

a) BACTERIAL - tularemia (Francisella tularensis); Relapsing fever (Borrelia hermsii, Borrelia duttonii); Q fever (Coxiella burnetti); Siberian tick typhus (Rickettsia sibirica); Queensland tick typhus fever (Rickettsia australis); Japanese spotted fever (Rickettsia japonica); scrub typhus (orientia tsutsugamushi); Flinders Island Spotted Fever (Rickettsia honei); Astrakhan fever; California flea typhus (Rickettsia felis); African tick bite fever (Rickettsia africae); rickettsialpox (Rickettsia akari); and other rickettsial diseases not yet named caused by Rickettsia mongolotimonae and Rickettsia slovaca.
b) VIRAL - Arboviruses: Thogota infection; Congo-Crimean hemorrhagic fever; Quaranfil virus fever; Louping ill; Russian spring-summer encephalitis.
c) PROTOZOAL - Babesiosis (Babesia microti).

0.2.3 VITAL SIGNS

A) WITH POISONING/EXPOSURE

1) Fever and chills may occur.

0.2.4 HEENT

A) WITH POISONING/EXPOSURE

1) Nystagmus and diplopia may occur with tick paralysis.

0.2.6 RESPIRATORY

A) WITH POISONING/EXPOSURE

1) Tick paralysis may cause respiratory arrest due to paralysis of respiratory muscles. Babesiosis can have associated respiratory symptoms including cough, pharyngitis and adult respiratory distress syndrome. Tularemia can cause cough, pharyngitis, pleural inflammation, pneumonia and adult respiratory distress syndrome.

0.2.7 NEUROLOGIC

A) WITH POISONING/EXPOSURE

1) Weakness and ataxia may progress to general paralysis in tick paralysis. Headache may occur with a number of tick-borne diseases.
2) Malaise, memory loss, and hallucinations are possible if Colorado Tick Fever is untreated.

0.2.8 GASTROINTESTINAL

A) WITH POISONING/EXPOSURE

1) Tick Paralysis may produce dysphagia. One rare case of an embedded tick mimicking appendicitis was reported.

0.2.13 HEMATOLOGIC

A) WITH POISONING/EXPOSURE

1) Thrombocytopenia and neutropenia usually occur on the 4th or 5th day of Colorado Tick fever.

0.2.14 DERMATOLOGIC

A) WITH POISONING/EXPOSURE

1) Tick bites may cause irritation and may transmit diseases with dermatologic components. Characteristic lesions include tache noir lesions with Boutonneuse Fever.

0.2.15 MUSCULOSKELETAL

A) WITH POISONING/EXPOSURE

1) Myalgias and arthralgias occur with a number of tick-borne illnesses.

0.2.19 IMMUNOLOGIC

A) WITH POISONING/EXPOSURE

1) Hypersensitivity reactions may occur after exposure to bites, body parts, or excreta of arthropods (including ticks). Short term immunity may occur after an exposure.

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.

0.3 LABORATORY/MONITORING

A) COLORADO TICK FEVER - Neutropenia and thrombocytopenia usually occur on the 4th or 5th day of fever and can be a useful diagnostic screening test. Confirmation of infection is based on a 4-fold antibody titer rise in paired sera collected 2 to 3 weeks apart.
B) TICK PARALYSIS - Hematologic and serum chemistries are normal.

0.4 TREATMENT OVERVIEW

0.4.7 BITES/STINGS

A) SYMPTOMATIC/SUPPORTIVE TREATMENT

1) PAIN - Most pain can be treated with an ice cube placed over the injured area.
2) ITCHING/INFLAMMATION - A topical corticosteroid, antihistamine, local anesthetic combination may be of value.
3) TICK REMOVAL

a) Don't handle the tick, it may harbor infectious agents that could enter via broken skin or mucous membranes.
b) Use blunt, wide blade forceps or tweezers.
c) Grasp the tick firmly and as close to the skin as possible. Pull out easily with a steady pull. Jerking the tick may cause the head to be left in the skin. Be sure you remove the head, including the mouthparts. Examine wound with hand lens.
d) Do not crush, puncture, or damage the tick, since its parts and fluids may contain infective agents.
e) After removal, clean and disinfect the bite site using soap, water, and alcohol.
f) Place sterile dressing or bandaid over the wound. Some physicians apply an antibiotic cream.
g) Do NOT apply hot match head to the tick. This may burn the patient, or rupture the tick.
h) Do NOT apply large amounts of petroleum jelly to the tick in hopes of smothering it. This may make it difficult to grasp and remove.
i) Subcutaneous injection of local anesthetics (lidocaine with or without epinephrine, chloroprocaine) have NOT been found to assist with tick removal in animal models.

B) ALLERGIC REACTION: MILD/MODERATE: antihistamines with or without inhaled beta agonists, corticosteroids or epinephrine. SEVERE: oxygen, aggressive airway management, antihistamines, epinephrine (ADULT: 0.3 to 0.5 mL of a 1:1000 solution subcutaneously; CHILD: 0.01 mL/kg, 0.5 ml max; may repeat in 20 to 30 min), corticosteroids, ECG monitoring, and IV fluids.
C) SEIZURES: Administer a benzodiazepine IV; DIAZEPAM (ADULT: 5 to 10 mg, repeat every 10 to 15 min as needed. CHILD: 0.2 to 0.5 mg/kg, repeat every 5 min as needed) or LORAZEPAM (ADULT: 2 to 4 mg; CHILD: 0.05 to 0.1 mg/kg).

1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children > 5 years).
2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, hypoxia.

D) BABESIOSIS - Either atovaquone plus azithromycin or clindamycin plus quinine may be used for 7 to 10 days as the treatment for patients with babesiosis; in patients with severe babesiosis, clindamycin (intravenous) plus quinine is recommended.

1) ADULTS DOSING

a) Azithromycin 500 to 1000 mg ORALLY on day 1 followed by 250 mg/day thereafter 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.
b) Quinine 650 mg ORALLY every 6 to 8 hours plus clindamycin 600 mg ORALLY every 8 hours or 300 to 600 mg IV every 6 hours (in patients with severe babesiosis) for 7 to 10 days.

2) CHILDREN DOSING

a) Azithromycin 10 mg/kg ORALLY on day 1 (maximum 500 mg/dose) followed by 5 mg/kg/day (maximum 250 mg/dose) thereafter plus atovaquone 20 mg/kg ORALLY (maximum 750 mg/dose) every 12 hours for 7 to 10 days.
b) Quinine 8 mg/kg ORALLY every 8 hours (up to a maximum of 650 mg/dose) plus clindamycin 7 to 10 mg/kg ORALLY or IV (in patients with severe babesiosis) every 6 to 8 hours (up to a maximum of 600 mg/dose) for 7 to 10 days.

E) BOUTONNEUSE FEVER - Boutonneuse Fever is less virulent than Rocky Mountain Spotted Fever, and is easily treated with tetracycline, doxycycline, chloramphenicol, or chlortetracycline.
F) COLORADO TICK FEVER - Treatment is symptomatic and supportive.
G) TICK PARALYSIS - Tick removal will usually reverse the paralysis. In most cases (in North America), tick removal will lead to recovery within 3 to 4 days.

1) A canine antiserum to the toxin that causes tick paralysis is available. The antiserum prevents or reverses paralysis in domestic animals.
2) Anti-toxin has a role in the treatment of seriously ill children but there is a high incidence of acute allergy and serum sickness.

0.5 RANGE OF TOXICITY

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

1.0 SUBSTANCES INCLUDED/SYNONYMS

THERAPEUTIC/TOXIC CLASS

SPECIFIC SUBSTANCES

DESCRIPTION

GEOGRAPHICAL LOCATION

AVAILABLE FORMS/SOURCES

1.1 THERAPEUTIC/TOXIC CLASS

A) This management deals specifically with ticks and diseases caused by ticks.
B) PLEASE REFER TO THE FOLLOWING MANAGEMENTS FOR MORE INFORMATION: EHRLICHIOSIS, LYME DISEASE, ROCKY MOUNTAIN SPOTTED FEVER.
C) Ticks are Arachnida of the order Acarina and the superfamily Ixodiodea. There are three major families of ticks: the hard ticks (Ixodidae), the soft ticks (Artgasidae), and the Nuttalliellidae (one genus and one species) (Tu, 1984).

1.2 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

1.3 DESCRIPTION

A) DISEASES CAUSED BY TICKS

1) Below are listed summaries of several tick-caused illness. Specific symptoms are also listed under individual medical system in the clinical effects section.
2) BOUTONNEUSE FEVER

a) ORGANISM: Rickettsia conorii.
b) VECTOR: Ripicephalus or Hemaphysalis leachi
c) ONSET: An incubational period of 5 to 7 days.
d) CLINICAL MANIFESTATIONS: Sudden headache, fever, and pain in the joints and muscles. A few days after incubation a generalized maculopapular rash appears. At the bite site a "tache noir" ulcerative lesion appears (Feldman-Muhsam, 1986).
e) SEVERITY: Less virulent than Rocky Mountain Spotted Fever, but deaths have occurred.

3) COLORADO TICK FEVER

a) CLINICAL MANIFESTATIONS: High, biphasic fever, chills, myalgia, severe headache, photophobia, and malaise occurring 4 to 5 days following a tick bite. The illness is self-limited and usually resolves within 7 to 10 days. In 50 percent of untreated patients symptoms recur within 3 days and the second course of illness lasts 2 to 4 days (Spach et al, 1993). If untreated, memory loss and hallucinations may occur (Cimolai et al, 1988).

1) Less common manifestations include a transient petechial or macular rash, leukopenia and thrombocytopenia. Rarely complications such as encephalitis, aseptic meningitis, pericarditis, orchitis, atypical pneumonia and hepatitis may develop (Spach et al, 1993). Most patients recover uneventfully.

b) SEROLOGY: Confirmation of infection is based on a 4-fold antibody titer rise in paired sera collected 2 to 3 weeks apart (p 17).
c) GEOGRAPHIC RANGE: Mountainous regions of Colorado, Utah, South Dakota, Montana, Wyoming, Idaho, Washington, Oregon, California, New Mexico and Nevada.
d) SEASON: Most patients acquire the disease between late May and early July (Spach et al, 1993).

4) EUROPEAN TICK-BORNE ENCEPHALITIS (TBE)

a) DISTRIBUTION/SYNONYMS: TBE includes two viral subtypes distributed over a large area of Europe. Synonyms: Central European encephalitis (CEE); Russian spring-summer encephalitis (RSSE); diphasic meningoencephalitis; diphasic milk fever; Schneider's disease; Ryssjukan; Kumlingesjukan.
b) ORGANISM: Flavivirus (RNA virus). Two antigenic subtypes exist: CEE virus, found in central Europe; and RSSE virus, found in far eastern Russia.
c) VECTOR: CEE subtype: Ixodes ricinus. RSSE subtype: Ixodes persulcatus. Other tick species suspected as vectors: Ixodes arboricola and hexagonus; Dermacentor marginalis and reticulatus; and Haemaphysalis punctata and concinna. CEE subtype may also be transmitted by ingestion of infected unpasteurized dairy products (especially goat's milk).
d) SEASON: April to November, with most cases occurring July to September.
e) CLINICAL MANIFESTATIONS

1) ONSET of illness ranges from 2 to 28 days following a tick bite, average 7 to 14 days. The disease has a biphasic course.
2) STAGE 1: Lasts 1 to 8 days. Moderate fever, headache, and myalgia occurs. The patient is viremic. Leukopenia is the typical finding on laboratory tests; thrombocytopenia and abnormal liver function tests also have been reported. One-third of patients will proceed to second stage illness after an asymptomatic period of 1 to 20 days, usually about one week.
3) STAGE 2: Central nervous system signs: meningoencephalitis. CSF contains high levels of protein. Adults are often more seriously affected than children. About 10% of patients will develop cranial or peripheral nerve paresis. Stage 2 may last from a few days to months, and may require lengthy hospitalization. RSSE strain is often more serious, with deaths and long-term or permanent neurological sequelae (focal epilepsy, shoulder girdle flaccid paralysis) reported.

f) SEROLOGY: ELISA is commonly used to verify infection. Vaccination is available and is widely practiced in Austria; hemagglutination inhibition or the neutralization test are most commonly used to evaluate response to vaccination. IgG ELISA may give false positive results in a vaccinated person. HIV-infected persons receiving the vaccine may not develop adequate immunity.
g) PREVALENCE: TBE antibodies in unvaccinated populations living in endemic areas varies from 0 to 22%; most areas are under 5%. Forty to 80% of vaccinated populations will have antibodies.
h) (Gustafson, 1994; Lotric-Furlan & Strle, 1995; Kenyon et al, 1992) WHO, 1994a and b; (Heinz & Mandl, 1993) Wolf et al, 1992; (Sander et al, 1994; Juhasz & Szirmai, 1993; Gustafson et al, 1992) Gustafson et al, 1993a and b.)

5) SOUTHERN TICK-ASSOCIATED RASH ILLNESS (STARI)

a) ORGANISM: Possibly Borrelia lonestari, on the basis of its identification by PCR in approximately 2% of A. americanum ticks from many locations in the US (Haddad et al, 2005).
b) VECTOR: Amblyomma americanum tick; also known as the "lone star" since adult females have a distinctive white spot on the dorsal surface (Haddad et al, 2005).
c) CLINICAL MANIFESTATIONS: Skin lesions; indistinguishable from erythema migrans, a characteristic skin manifestation of Borrelia burgdorferi infection (Lyme disease) (Haddad et al, 2005).

6) TICK PARALYSIS

a) DEFINITION: An ascending paralysis caused by sustained bites of ticks. Usually only female ticks produce the toxin which enters from the salivary gland when the tick feeds (Abbott, 1944; Hamilton, 1940) Gothe et al, 1979).
b) Human poisonings have occurred from nymphs and larva of Ixodes holocyclus (Australia) and Argas persicus (Africa), and South American male ticks of Dermacentor andersoni, Hyalomma truncatum, and Rhipicephalus simus (Fowler, 1993).
c) VECTORS: Forty-three species in 10 different genera have been incriminated, including ticks of the genera Amblyomma, Dermacentor, Haemaphysalis, Hyalomma, Ixodes, Rhinicephalus, and Rhipicephalus.
d) Some representative ticks and their geographic locations are listed below (Daugherty et al, 2005; Southcott, 1986; Stone et al, 1982a; Pearn, 1977; Schmitt et al, 1969; Henderson, 1961; Rose, 1954):

TICK SPECIES (COMMON NAME)	GEOGRAPHIC LOCATION
Amblyomma americanum	Southeastern US; Georgia, Maryland, Missouri, North Carolina, South Carolina
Amblyomma maculatum (Gulf Coast Tick)	Southeastern US
Dermacentor andersoni (Wood Tick)	Pacific Northwest
Dermacentor variabilis (Dog Tick)	Southeastern and Northeastern US
Haemaphysalis puncata	Crete
Hyalomma truncata	South Australia
Ixodes cornuatus (Tasmanian Paralysis Tick)	Tasmania, Australia
Ixodes hirsti (Hirst's Marsupial Tick)	Victoria, Australia
Ixodes holocyclus (Scrub Tick)	Australia
Ixodes ricinus	Crete
Rhinicephalus simus	South Africa
Rhipicephalus evertsi (Red-legged Tick)	South Africa

e) TOXIN: A neurotoxin is in the salivary gland of the feeding tick (Stone & Neish, 1984; Stone et al, 1982a; Stone et al, 1982). Not all individual ticks of the genera listed above will produce paralysis; the cause for this variation is unknown.
f) CLINICAL MANIFESTATIONS

1) 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 (Fowler, 1993).
2) 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 (Henderson, 1961). Less commonly, ataxia may develop without muscle weakness (Spach et al, 1993).

g) GEOGRAPHIC LOCATION: Most commonly reported in the Pacific Northwest and Rocky Mountain states but cases have been reported from southern states (Spach et al, 1993).
h) SEASON: Spring and summer (Spach et al, 1993).

7) OTHER INFECTIONS TRANSMITTED BY TICKS

a) BACTERIAL

1) TULAREMIA: (Francisella tularensis); various species of ticks; signs include regional adenopathy and ulcer.
2) RELAPSING FEVER: (Borrelia hermsii); Ornithodoros species ticks; signs include chills, headache, and fever.
3) Q FEVER: (Coxiella burnetii); indirect vector; signs include pneumonitis, headache, hepatitis, endocarditis, and fever (Caron et al, 1998).
4) QUEENSLAND TICK TYPHUS: (Rickettsia australis); signs include malaise, headaches, local skin lesions, lymphadenopathy, myalgia, thrombocytopenia, and a maculopapular rash with occasional petechiae or vesicles (Pinn & Sowden, 1998; Sexton et al, 1990).
5) AFRICAN TICK-BITE FEVER: (Rickettsia africae); characterized by multiple taches noire, lymphadenopathy, lymphangitis, edema. Usually no rash or a discrete rash is noted (Brouqui et al, 1997).
6) Other rickettsial infections include Siberian tick typhus (Rickettsia sibirica); Japanese spotted fever (Rickettsia japonica); scrub typhus (Orientia tsutsugamushi); Flinders island Spotted Fever (Rickettsia honei); Astrakhan fever; California flea typhus (Rickettsia felis); and other rickettsial diseases not yet named caused by Rickettsia mongolotimonae and Rickettsia slovaca (Raoult et al, 1997).

b) VIRAL

1) ARBOVIRUSES: All cause clinical signs that include fever, rash, and hemorrhagic episodes. Thogota infection (transmitted by various ticks); Congo-Crimean hemorrhagic fever (Hyalomma marginatum); Quaranfil virus fever (Argas species ticks); Louping ill (Ixodes ricinus).

c) PROTOZOAL

1) BABESIOSIS: (Babesia microti); Ixodes scapularis ticks; signs include fever, arthralgia, chills, depression, and jaundice.

d) Reference: Middleton, 1994.

1.4 GEOGRAPHICAL LOCATION

A) Ticks are found throughout the world.
B) Some representative ticks and their geographic locations are listed below (Daugherty et al, 2005; Southcott, 1986; Stone et al, 1982a; Pearn, 1977; Schmitt et al, 1969; Henderson, 1961; Rose, 1954):

TICK SPECIES (COMMON NAME)	GEOGRAPHIC LOCATION
Amblyomma americanum	Southeastern US
Amblyomma maculatum (Gulf Coast Tick)	Southeastern US
Dermacentor albipictus	Midwestern US
Dermacentor andersoni (Wood Tick)	Pacific Northwest
Dermacentor variabilis (Dog Tick)	Southeastern, Midwestern, and Northeastern US
Haemaphysalis puncata	Crete
Hyalomma truncata	South Australia
Ixodes cornuatus (Tasmanian Paralysis Tick)	Tasmania, Australia
Ixodes hirsti (Hirst's Marsupial Tick)	Victoria, Australia
Ixodes holocyclus (Scrub Tick)	Australia
Ixodes ricinus	Crete
Ixodes scapularis (Deer tick)	Midwestern US
Rhinicephalus simus	South Africa
Rhipicephalus evertsi (Red-legged Tick)	South Africa
Rhinicephalus sanguineus (brown dog tick)	Midwestern US

1.6 AVAILABLE FORMS/SOURCES

A) SOURCES

1) DISEASE ORGANISMS TRANSMITTED BY VARIOUS TICKS (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).

ORGANISM	TICK VECTOR
Babesia microti Babesia equi	Ixodes scapularis
Borrelia burgdorferi	Ixodes scapularis Ixodes pacificus
Coltivirus species	Dermacentor andersoni
Cowdria ruminantium	Amblyomma species
Ehrlichia chaffeensis	Dermacentor variablilis Amblyomma americanum (Lone Star tick)
Ehrlichia phagocytophilia	Dermacentor variabilis
Ehrlichia equi	Ixodes scapularis
Borrelia spp (hermsii, turicatae, parkeri)	Ornithodoros spp (hermsi, turiciata, parkeri)
Female Tick Neurotoxin	Dermacentor andersoni, D.variabilis; Ixodes scapularis, Amblyomma americanum, A. maculatum
Flaviviridae	Ixodes ricinus I. persulcatus
Francisella tularensis	Dermacentor andersoni, D.variabilis, Amblyomma americanum
Rickettsia australis	Ixodes species
Rickettsia burnetii	Many, non-specific
Rickettsia conori	Rhipicephalus or Hemaphysalis leachi
Rickettsia rickettsii	Dermacentor andersoni/variablilis
Rickettsia slovaca	Dermacentor marginatus
Rickettsia africae	Amblyomma

ORGANISM	DISEASE
Babesia microti or Babesia equi	Babesios
Borrelia burgdorferi	Lyme disease
Borrelia spp (hermsii, turicatae, parkeri, duttonii)	Tick-borne relapsing fever
Coltivirus species	Colorado Tick Fever
Cowdria ruminantium	Heartwater disease
Ehrlichia chaffeensis	Ehrlichiosis
Ehrlichia phagocytophilia	Human Granulocytic
Ehrlichia equi	Ehrlichiosis
Female Tick Neurotoxin	Tick paralysis
Francisella tularensis	Tularemia
Orientia tsutsugamushi	Scrub Typhus
Rickettsia australis	Queensland Tick Typhus
Rickettsia burnetti	Q Fever
Rickettsia conori	Boutonneuse Fever Mediterranean Spotted Fever
Rickettsia honei	Flinders Islands Spotted Fever
Rickettsia africae	African Tick-Bite Fever
Rickettsia felis	California Flea Typhus
Rickettsia rickettsii*	Rocky Mtn Spotted Fever
Rickettsia mongolotimonae Rickettsia slovaca	Astrakhan Fever
Rickettsia akari	Rickettsialpox

ORGANISM	DISEASE
Babesia microti or Babesia equi	Babesios
Borrelia burgdorferi	Lyme disease
Borrelia spp (hermsii, turicatae, parkeri, duttonii)	Tick-borne relapsing fever
Coltivirus species	Colorado Tick Fever
Cowdria ruminantium	Heartwater disease
Ehrlichia chaffeensis	Ehrlichiosis
Ehrlichia phagocytophilia	Human Granulocytic
Ehrlichia equi	Ehrlichiosis
Female Tick Neurotoxin	Tick paralysis
Francisella tularensis	Tularemia
Orientia tsutsugamushi	Scrub Typhus
Rickettsia australis	Queensland Tick Typhus
Rickettsia burnetti	Q Fever
Rickettsia conori	Boutonneuse Fever Mediterranean Spotted Fever
Rickettsia honei	Flinders Islands Spotted Fever
Rickettsia africae	African Tick-Bite Fever
Rickettsia felis	California Flea Typhus
Rickettsia rickettsii*	Rocky Mtn Spotted Fever
Rickettsia mongolotimonae Rickettsia slovaca	Astrakhan Fever
Rickettsia akari	Rickettsialpox

2) VECTOR: E. canis. Six human cases have been reported from this species which usually only infects canines (Fishbein et al, 1987).
3) *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).

3.0 CLINICAL EFFECTS

SUMMARY OF EXPOSURE

VITAL SIGNS

HEENT

CARDIOVASCULAR

RESPIRATORY

NEUROLOGIC

GASTROINTESTINAL

HEPATIC

HEMATOLOGIC

DERMATOLOGIC

MUSCULOSKELETAL

IMMUNOLOGIC

REPRODUCTIVE

CARCINOGENICITY

OTHER

3.1 SUMMARY OF EXPOSURE

A) WITH POISONING/EXPOSURE

4) TICK PARALYSIS -

5) EUROPEAN TICK-BORNE ENCEPHALITIS (TBE) -

6) OTHER INFECTIONS TRANSMITTED BY TICKS -

3.3 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 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 (Cimolai et al, 1988).

3.4 HEENT

3.4.1 SUMMARY

A) WITH POISONING/EXPOSURE

1) Nystagmus and diplopia may occur with tick paralysis.

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).

3.5 CARDIOVASCULAR

3.5.2 CLINICAL EFFECTS

A) ENDOCARDITIS

1) WITH POISONING/EXPOSURE

a) Blood culture-negative endocarditis is the most prominent clinical expression of chronic Q fever; incidence has approached 68% (Brouqui et al, 1993; Stein & Raoult, 1998).

3.6 RESPIRATORY

3.6.1 SUMMARY

A) WITH POISONING/EXPOSURE

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 can have associated respiratory symptoms including cough, pharyngitis and adult respiratory distress syndrome. Tularemia can cause cough, pharyngitis, pleural inflammation, pneumonia and adult respiratory distress syndrome (Byrd et al, 1997).

B) ACUTE LUNG INJURY

1) WITH POISONING/EXPOSURE

a) Six patients have had adult respiratory distress syndrome associated with babesiosis (Byrd et al, 1997).
b) In 12% of patients, tularemia progresses to adult respiratory distress syndrome (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).

3.7 NEUROLOGIC

3.7.1 SUMMARY

A) WITH POISONING/EXPOSURE

3.7.2 CLINICAL EFFECTS

A) PARALYSIS

1) WITH POISONING/EXPOSURE

a) 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).
b) 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 may occur with Boutonneuse fever (Feldman-Muhsam, 1986). 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 (Cimoloai et al, 1988).

E) HALLUCINATIONS

1) WITH POISONING/EXPOSURE

a) Hallucinations may occur if Colorado Tick Fever is left untreated (Cimoloai 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 (Cimoloai 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).

3.8 GASTROINTESTINAL

3.8.1 SUMMARY

A) WITH POISONING/EXPOSURE

1) Tick Paralysis may produce dysphagia. One rare case of an embedded tick mimicking appendicitis was reported.

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).

3.9 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 female, one month after receiving a bite from a Rickettsia africae tick. The patient recovered slowly after treatment with doxycycline (Parola et al, 1998).

3.13 HEMATOLOGIC

3.13.1 SUMMARY

A) WITH POISONING/EXPOSURE

1) Thrombocytopenia and neutropenia usually occur on the 4th or 5th day of Colorado Tick fever.

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) CASE REPORT - A 50-year-old female 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) Thrombocytopenia and neutropenia usually occur on the 4th or 5th day of Colorado Tick fever.

3.14 DERMATOLOGIC

3.14.1 SUMMARY

A) WITH POISONING/EXPOSURE

1) Tick bites may cause irritation and may transmit diseases with dermatologic components. Characteristic lesions include tache noir lesions with Boutonneuse Fever.

3.14.2 CLINICAL EFFECTS

A) ERUPTION

1) WITH POISONING/EXPOSURE

a) CASE REPORT - A 50-year-old female 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.
b) 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).

3.15 MUSCULOSKELETAL

3.15.1 SUMMARY

A) WITH POISONING/EXPOSURE

1) Myalgias and arthralgias occur with a number of tick-borne illnesses.

3.15.2 CLINICAL EFFECTS

A) MUSCLE PAIN

1) WITH POISONING/EXPOSURE

a) Myalgias and arthralgias may occur with Boutonneuse Fever (Feldman-Muhsam, 1986), and Colorado Tick Fever (Cimolai et al, 1988).

3.19 IMMUNOLOGIC

3.19.1 SUMMARY

A) WITH POISONING/EXPOSURE

1) Hypersensitivity reactions may occur after exposure to bites, body parts, or excreta of arthropods (including ticks). Short term immunity may occur after an exposure.

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) 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).

3.20 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).

3.21 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.

3.23 OTHER

3.23.2 CLINICAL EFFECTS

A) SECONDARY INFECTION

1) WITH POISONING/EXPOSURE

a) Tularemia may be carried to humans via tick vectors.

4.0 LABORATORY/MONITORING

4.1 MONITORING PARAMETERS/LEVELS

4.1.1 SUMMARY

4.1.2 SERUM/BLOOD

A) SPECIFIC AGENT

1) 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).

2) TICK PARALYSIS - Hematologic and serum chemistries are normal (Fowler, 1993).

6.0 TREATMENT

LIFE SUPPORT

MONITORING

BITE/STING EXPOSURE

6.1 LIFE SUPPORT

A) Support respiratory and cardiovascular function.

6.4 MONITORING

6.10 BITE/STING EXPOSURE

6.10.1 FIRST AID

A) Remove tick as explained below.

6.10.2 TREATMENT

A) SUPPORT

1) PAIN - Most pain can be treated with a cube of ice placed over the injured area.
2) ITCHING/INFLAMMATION - A topical corticosteroid, antihistamine, local anesthetic combination may be of value. Itch Balm Plus (R), containing hydrocortisone acetate 0.5%, diphenhydramine 2 percent, and tetracaine 1 percent has been recommended (Russell, 1988).
3) TETANUS - Prophylaxis should be considered.
4) TICK REMOVAL - Don't handle the tick, it may harbor infectious agents that could enter via broken skin or mucous membranes.

a) Use blunt, wide blade forceps or tweezers.
b) Grasp the tick firmly and as close to the skin as possible. Pull out easily with a steady pull. Jerking the tick may cause the head to be left in the skin. Be sure you removed the head, including the mouthparts. Examine wound with hand lens.
c) Do not crush, puncture, or damage the tick, since its parts and fluids may contain infective agents.
d) After removal, clean and disinfect the bite site using soap, water, and alcohol.
e) Place sterile dressing or a bandaid over the wound. Some physicians apply an antibiotic cream.
f) Do NOT apply hot match head to the tick. This may burn the patient, or rupture the tick.
g) Do NOT apply large amounts of petroleum jelly to the tick in hopes of smothering it. This may make it difficult to grasp and remove.
h) Subcutaneous injection of local anesthetics (lidocaine with or without epinephrine, chloroprocaine) has NOT been found to assist with tick removal in animal models.
i) (REFERENCES - Anon, 1986; (Needham, 1985; Lee et al, 1995)

B) ANAPHYLAXIS

1) SUMMARY

a) Mild to moderate allergic reactions may be treated with antihistamines with or without inhaled beta adrenergic agonists, corticosteroids or epinephrine. Treatment of severe anaphylaxis also includes oxygen supplementation, aggressive airway management, epinephrine, ECG monitoring, and IV fluids.

2) BRONCHOSPASM

a) ALBUTEROL

1) ADULTS: 2.5 to 5 milligrams in 2 to 4.5 milliliters of normal saline delivered per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 2.5 to 10 mg every 1 to 4 hours as needed, or 10 to 15 mg/hr by continuous nebulization as needed (National Heart,Lung,and Blood Institute, 2007). CHILDREN: 0.15 milligram/kilogram (minimum 2.5 milligrams) per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 0.15 to 0.3 mg/kg (up to 10 mg) every 1 to 4 hours as needed, or 0.5 mg/kg/hr by continuous nebulization (National Heart,Lung,and Blood Institute, 2007).

3) CORTICOSTEROIDS

a) METHYLPREDNISOLONE - Adults: 1 to 2 milligrams/kilogram intravenously every 6 to 8 hours. Children: 1 to 2 milligrams/kilogram intravenously (maximum 125 milligrams) every 6 hours.
b) PREDNISONE - Adults: 40 to 60 milligrams/day. Children: 1 to 2 milligrams/kilogram/day divided twice daily. Prolonged therapy generally not needed.

4) MILD CASES

a) DIPHENHYDRAMINE

1) ADULTS: 50 milligrams orally, intravenously, or intramuscularly initially, then 25 to 50 milligrams orally every 4 to 6 hours for 24 to 72 hours.
2) CHILDREN: 1.25 milligrams/kilogram orally, intravenously, or intramuscularly initially, then 5 milligrams/kilogram/day orally in four divided doses for 24 to 72 hours.

5) MODERATE CASES

a) EPINEPHRINE: 0.3 to 0.5 milliliter of a 1:1000 solution subcutaneously or intramuscularly (children: 0.01 milliliter/kilogram, 0.5 milliliter maximum); may repeat in 20 to 30 minutes (American Heart Association, 2005).

6) SEVERE CASES

a) EPINEPHRINE

1) INTRAVENOUS BOLUS: 1:10,000 solution, 5 to 10 milliliters diluted in 10 milliliters 0.9% saline slow intravenous push over 5 to 10 minutes (American Heart Association, 2005) (children: 0.1 milliliter/kilogram); give if systolic blood pressure less than 70 mmHg (adults); it is safest to titrate to effect in small increments, 1 to 2 milliliters at a time.
2) INTRAVENOUS INFUSION: An alternative method of intravenous epinephrine by constant infusion has been advocated as safer: 1 milligram of a 1:1000 dilution of epinephrine added to 250 milliliters dextrose 5 percent in water. Start infusion at 1 microgram/minute and titrate to systolic blood pressure of 100 mmHg (or mean arterial pressure of 80 mmHg).

7) AIRWAY MANAGEMENT

a) OXYGEN: 5 to 10 liters/minute via high flow mask.
b) INTUBATION: Perform early if any stridor or signs of airway obstruction.
c) CRICOTHYROTOMY: Use if unable to intubate with complete airway obstruction.
d) BRONCHODILATORS are recommended for mild to severe bronchospasm.
e) ALBUTEROL: ADULTS: 5 to 10 milligrams in 2 to 4.5 milliliters of normal saline delivered per nebulizer every 20 minutes up to 3 doses. If incomplete response repeat every hour. CHILDREN: 0.15 milligram/kilogram (minimum 2.5 milligrams) per nebulizer every 20 minutes up to 3 doses. If incomplete response repeat every hour.

8) MONITORING

a) CARDIAC MONITOR: All complicated cases.
b) IV ACCESS: Routine in all complicated cases.

9) HYPOTENSION

a) IF hypotensive give 500 to 2000 milliliters crystalloid initially (20 milliliters/kilogram in children) and titrate to desired effect (stabilization of vital signs, mentation, urine output); adults may require up to 6 to 10 liters/24 hours. Central venous or pulmonary artery pressure monitoring is recommended in patients with persistent hypotension.

1) VASOPRESSORS: Should be used in refractory cases unresponsive to repeated doses of epinephrine and after vigorous intravenous crystalloid rehydration.
2) DOPAMINE: Mix 400 to 800 milligrams in 250 milliliters of dextrose 5 percent in water (1600 or 3200 micrograms/milliliter). Initial dose is 2 to 5 micrograms/kilogram/minute intravenously; titrate to desired hemodynamic response.

10) DIPHENHYDRAMINE

a) ADULTS: 50 milligrams intravenously initially, then 25 to 50 milligrams intravenously or orally every 4 to 6 hours for 24 to 72 hours.
b) CHILDREN: 2 milligrams/kilogram intravenously initially, then 5 milligrams/kilogram/day intravenously or orally in four divided doses for 24 to 72 hours.

11) METHYLPREDNISOLONE

a) Adults: 1 to 2 milligrams/kilogram intravenously every 6 to 8 hours. Children: 1 to 2 milligrams/kilogram intravenously (maximum 125 milligrams) every 6 hours.

12) DYSRHYTHMIAS

a) Dysrhythmias may occur primarily or iatrogenically as a result of pharmacologic treatment (epinephrine). Monitor and correct serum electrolytes, oxygenation and tissue perfusion. Treat with antiarrhythmic agents as indicated.

C) GENERAL TREATMENT

1) BABESIOSIS - Either atovaquone plus azithromycin or clindamycin plus quinine may be used for 7 to 10 days as treatment for adults and children with babesiosis. In patients with severe babesiosis, clindamycin plus quinine is recommended. Treatment is not recommended in symptomatic patients whose serum contains antibody to babesia but whose blood lacks identifiable babesial parasite on smear or babesial DNA by PCR. Additionally, asymptomatic patients should not receive treatment, regardless of the results of serologic examination, blood smears, or PCR. These studies should be repeated in asymptomatic patients with positive babesial smears and/or PCR, and a course of treatment should be considered if parasitemia persists for longer than 3 months. Retreatment may be considered if babesial parasites or amplifiable babesial DNA are detected in blood 3 months or longer after initial therapy, regardless of symptom status (Wormser et al, 2006):

a) ADULTS DOSING

1) Azithromycin 500 to 1000 milligrams (mg) orally on day 1 followed by 250 mg/day thereafter 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 (Wormser et al, 2006).
2) Quinine 650 milligrams (mg) orally every 6 to 8 hours plus clindamycin 600 mg orally every 8 hours or 300 to 600 mg intravenously every 6 hours (in patients with severe babesiosis) for 7 to 10 days (Wormser et al, 2006).

b) CHILDREN DOSING

1) Azithromycin 10 milligrams/kilogram (mg/kg) orally on day 1 (maximum 500 mg/dose) followed by 5 mg/kg/day (maximum 250 mg/dose) thereafter plus atovaquone 20 mg/kg orally (maximum 750 mg/dose) every 12 hours for 7 to 10 days (Wormser et al, 2006).
2) Quinine 8 milligrams/kilogram (mg/kg) orally every 8 hours (up to a maximum of 650 mg/dose) plus clindamycin 7 to 10 mg/kg orally or IV (in patients with severe babesiosis) every 6 to 8 hours (up to a maximum of 600 mg/dose) for 7 to 10 days (Wormser et al, 2006).

2) BOUTONNEUSE FEVER - Boutonneuse Fever is less virulent than Rocky Mountain Spotted Fever, and is easily treated with tetracycline, doxycycline, chloramphenicol, or chlortetracycline (Feldman-Muhsam, 1986).
3) COLORADO TICK FEVER - Treatment is symptomatic and supportive.
4) TICK PARALYSIS - REMOVAL - of the tick will usually reverse the paralysis. In most cases (in North America), tick removal will lead to recovery within 3 to 4 days. In one case, a 2-year-old went from complete paralysis to normal within 8 hours of the tick being removed (McDermott, 1957).

a) I. holocyclus removal will not necessarily lead to immediate improvement. Maximum symptoms may appear 48 hours after removal (Tu, 1984).
b) Severe cases may require several weeks before the patient is fully recovered. However, even with bulbar involvement, respiratory assistance will save most patients (Gregson, 1937).
c) A canine antiserum to the toxin that causes tick paralysis is available. The antiserum prevents or reverses paralysis in domestic animals (Kincaid, 1990).
d) Anti-toxin has a role in the treatment of seriously ill children but there is a high incidence of acute allergy and serum sickness (Grattan-Smith et al, 1997).

D) SEIZURE

1) SUMMARY

a) Attempt initial control with a benzodiazepine (diazepam or lorazepam). If seizures persist or recur administer phenobarbital or propofol.
b) Monitor for respiratory depression, hypotension and dysrhythmias. Endotracheal intubation should performed in patients with persistent seizures.
c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose ADULT: 50 milliliters IV, CHILD: 2 milliliters/kilogram 25% dextrose).

2) DIAZEPAM

a) ADULT DIAZEPAM DOSE: 5 to 10 milligrams initially, repeat every 5 to 10 minutes as needed. Monitor for hypotension, respiratory depression and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after diazepam 30 milligrams.
b) PEDIATRIC DIAZEPAM DOSE: 0.2 to 0.5 milligram per kilogram (5 milligrams maximum); repeat every 5 to 10 minutes as needed. Monitor for hypotension, respiratory depression and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after diazepam 10 milligrams in children over 5 years or 5 milligrams in children under 5 years of age.
c) MAXIMUM RATE: Administer diazepam intravenously over 2 to 3 minutes (maximum rate = 5 milligrams/minute).

3) NO INTRAVENOUS ACCESS

a) DIAZEPAM may be given per rectum or intramuscularly. Recommended rectal dose is 0.2 mg/kg in adults and 0.5 mg/kg in children. LORAZEPAM may also be given intramuscularly or rectally (Manno, 2003).
b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. PEDIATRIC MIDAZOLAM DOSE: INTRAMUSCULAR: 0.2 milligram/kilogram (maximum 7 milligrams) (Chamberlain et al, 1997); INTRANASAL: 0.2 milligram/kilogram (Lahat et al, 2000). BUCCAL midazolam, 10 milligrams, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).

4) LORAZEPAM

a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 milligrams/minute (Prod Info lorazepam injection, 2004).
b) ADULT LORAZEPAM DOSE: 2 to 4 milligrams intravenously. Initial doses may be repeated in 10 minutes if seizures persist (Manno, 2003).
c) PEDIATRIC LORAZEPAM DOSE: 0.05 to 0.1 milligram/kilogram intravenously, (maximum 4 milligrams/dose) repeated twice at intervals of 10 to 15 minutes if seizures persist (Benitz & Tatro, 1995).

5) PHENOBARBITAL

a) ADULT PHENOBARBITAL LOADING DOSE: 20 milligrams per kilogram diluted in 0.9 percent saline given at 25 to 50 milligrams per minute.
b) REPEAT ADULT DOSE: An additional 10 milligrams/kilogram may be given if seizures persist or recur (Manno, 2003).
c) MAXIMUM SAFE ADULT PHENOBARBITAL DOSE: No maximum safe dose has been established. Patients in status epilepticus have received as much as 100 milligrams/minute until seizure control was achieved. Patients receiving high doses will require endotracheal intubation and may require vasopressor support.
d) PEDIATRIC PHENOBARBITAL LOADING DOSE: 15 to 20 milligrams per kilogram of phenobarbital intravenously given at a maximum rate of 25 to 50 milligrams per minute.
e) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 10 milligrams per kilogram may be given every 20 minutes if seizures persist.
f) MAXIMUM SAFE PEDIATRIC PHENOBARBITAL DOSE: No maximum safe dose has been established. Children in status epilepticus have received doses of 30 to 120 milligrams/kilogram within 24 hours. Vasopressors and mechanical ventilation were needed in many patients receiving these doses.
g) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation.
h) NEONATAL PHENOBARBITAL LOADING DOSE: 20 to 30 milligrams/kilogram intravenously at a rate of no more than 1 milligram/kilogram per minute in patients with no preexisting phenobarbital serum concentrations.
i) NEONATAL PHENOBARBITAL MAINTENANCE DOSE: Repeat doses of 2.5 milligrams/kilogram every 12 hours may be given; adjust dosage to maintain serum concentrations of 20 to 40 micrograms/milliliter.
j) MAXIMUM SAFE NEONATAL PHENOBARBITAL DOSE: Doses of up to 20 milligrams/kilogram/minute up to a total of 30 milligrams/kilogram have been tolerated in neonates.
k) CAUTIONS: Adequacy of ventilation must be continuously monitored in children and adults. Intubation will be necessary with increased doses. Hypotension may develop with large doses and vasopressors may be required.
l) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over next 12 to 24 hours for maintenance of therapeutic concentrations (20 to 40 micrograms per milliliter).

6) PHENYTOIN/FOSPHENYTOIN

a) Benzodiazepines and/or barbiturates are generally preferred to phenytoin or fosphenytoin in the treatment of drug or withdrawal induced seizures.
b) PHENYTOIN

1) PHENYTOIN INTRAVENOUS PUSH VERSUS INTRAVENOUS INFUSION:

a) Manufacturer does not recommend intravenous infusions due to lack of solubility and resultant precipitation, however infusions are commonly used.
b) Manufacturer does not recommend intravenous infusions due to Administer phenytoin undiluted, by very slow intravenous push or dilute 50 milligrams per milliliter solution in 50 to 100 milliliters of 0.9 percent saline.
c) PHENYTOIN ADMINISTRATION RATE: Rate of administration by either method should not exceed 0.5 milligram per kilogram per minute or 50 milligrams per minute.
d) ADULT PHENYTOIN LOADING DOSE: 15 to 18 milligrams per kilogram of phenytoin initially. Rate of administration by very slow intravenous push or diluted to 50 milligrams per milliliter should not exceed 0.5 milligram per kilogram per minute or 50 milligrams per minute.
e) ADULT PHENYTOIN MAINTENANCE DOSE: Manufacturers recommend a maintenance dose of 100 milligrams orally or intravenously every 6 to 8 hours. The goal is to maintain a serum concentration between 10 to 20 micrograms/milliliter.
f) PEDIATRIC PHENYTOIN LOADING DOSE: 15 to 20 milligrams per kilogram or 250 milligrams/square meter of phenytoin. Rate of intravenous administration should not exceed 0.5 to 1.5 milligrams per kilogram per minute.
g) PEDIATRIC PHENYTOIN MAINTENANCE DOSE: Repeat doses of 1.5 milligrams per kilogram may be given every 30 minutes to a maximum daily dose of 20 milligrams per kilogram.
h) CAUTIONS: Administer phenytoin while monitoring ECG. Stop or slow infusion if arrhythmias or hypotension occur. Be careful not to extravasate. Follow each injection with injection of sterile saline through the same needle.
i) SERUM LEVEL MONITORING: Monitor serum levels over next 12 to 24 hours for maintenance of therapeutic levels (10 to 20 micrograms per milliliter).
j) FOSPHENYTOIN
k) ADULT DOSAGE AND ADMINISTRATION: The dose, concentration in dosing solutions, and infusion rate of fosphenytoin are expressed as phenytoin sodium equivalents.
l) ADULT LOADING DOSE FOSPHENYTOIN: 15 to 20 milligrams/kilogram of phenytoin sodium equivalents at a rate of 100 to 150 milligrams phenytoin equivalent/minute.
m) Fosphenytoin should not be infused at rates greater than 150 milligrams phenytoin equivalent/minute because of the risk of hypotension.
n) CAUTIONS: Perform continuous monitoring of respiratory function, cardiac rhythm, and blood pressure throughout infusion and for at least 30 minutes thereafter.
o) ADULT MAINTENANCE DOSING: 4 to 6 milligrams phenytoin equivalents/kilogram/day. Rate of administration should not exceed 150 milligrams phenytoin equivalent/minute.
p) SERUM LEVEL MONITORING: Monitor serum phenytoin levels over the next 12 to 24 hours; therapeutic levels 10 to 20 microgram/milliliter. Do not obtain serum phenytoin concentrations until at least 2 hours after infusion is complete to allow for conversion of fosphenytoin to phenytoin.

E) EXPERIMENTAL THERAPY

1) Experimentally induced immunity has been accomplished using larval extracts, salivary gland components, internal organs, and tissue cultures (Trager, 1939; Bagnall, 1975; Kohler et al, 1967; Brossard, 1976; Ackerman et al, 1980) Tu, 1984).
2) This has not been tried clinically in humans.

7.0 RANGE OF TOXICITY

SUMMARY

MINIMUM LETHAL EXPOSURE

7.1 SUMMARY

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

7.3 MINIMUM LETHAL EXPOSURE

A) CASE REPORTS

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

9.0 PHARMACOLOGY/TOXICOLOGY

9.2 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).

11.0 ANIMAL TOXICOLOGY

CLINICAL EFFECTS

TREATMENT

CONTINUING CARE

11.1 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).

11.2 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 -

11.4 CONTINUING CARE

11.4.1 SUMMARY

11.4.1.2 DECONTAMINATION/TREATMENT

A) GENERAL TREATMENT

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.

12.0 REFERENCES

12.2 GENERAL BIBLIOGRAPHY

1) Abbott KH: Tick borne diseases (with particular reference to tick paralysis). Dis Nerv Syst 1944; 5:19-21.
2) Ackerman S, Floyd M, & Sonenshine DE: Artificial immunity to Dermacentor variabilis (Acari: Ixodidae): Vaccination using tick antigens. J Med Entomol 1980; 17:391-397.
3) American Heart Association: 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2005; 112(24 Suppl):IV 1-203. Available from URL: http://circ.ahajournals.org/content/vol112/24_suppl/. As accessed 12/14/2005.
4) Anika SM, Nouws JFM, & Vree TB: The efficacy and plasma disposition of chloramphenicol and spiramycin in tick-borne fever-infected dwarf goats. J Vet Pharmacol Ther 1986; 9:433-435.
5) Anon: Tick-borne disease in Colorado. Colorado Disease Bulletin, No. 17 (May 19), 1989.
6) Bagnall BG: Cutaneous immunity to the tick Ixodes holocyclus. Ph. D thesis, University of Sydney, Sydney, Australia, 1975.
7) Beasley VR, Dorman DC, & Fikes JD: A Systems Affected Approach to Veterinary Toxicology, 2nd ed, University of Illinois, Urbana, IL, 1990.
8) Benitz WE & Tatro DS: The Pediatric Drug Handbook, 3rd ed, Mosby-Year Book Inc, Chicago, IL, 1995.
9) Brossard M: Relations immunologiques entre Bovius et Tiques, plus particulierement entre Bovius et Boophilus microplus. Acta Trop 1976; 33:15-36.
10) Brouqui P, Harle JR, & Delmont J: African tick-bite fever: an imported spotless rickettsiosis. Arch Intern Med 1997; 157:119-124.
11) Brouqui P, Tissot-Dupont H, & Drancourt M: Chronic Q-fever. Arch Intern Med 1993; 153:642-648.
12) Byrd RP, Vasquez J, & Roy TM: Respiratory manifestations of tick-borne diseases in the southeastern United States. South Med J 1997; 90:1-4.
13) Caron F, Meurice JC, & Ingrand P: Acute Q fever pneumonia: a review of 80 hospitalized patients. Chest 1998; 114:808-813.
14) Chamberlain JM, Altieri MA, & Futterman C: A prospective, randomized study comparing intramuscular midazolam with intravenous diazepam for the treatment of seizures in children. Ped Emerg Care 1997; 13:92-94.
15) Cimolai N, Anand CM, & Gish GJ: Human Colorado tick fever in southern Alberta. CMAJ 1988; 139:45-46.
16) Cranwell MP: Efficacy of long-acting oxytetracycline for the prevention of tick-borne fever in calves. Vet Rec 1990; 126:334-336.
17) Daugherty RJ, Posner JC, Henretig FM, et al: Tick paralysis: atypical presentation, unusual location. Ped Emerg Care 2005; 21:677-680.
18) Demma LJ, Traeger MS, Nicholson WL, et al: Rocky Mountain spotted fever from an unexpected tick vector in Arizona. N Engl J Med 2005; 353(6):587-594.
19) Doan-Wiggins L: Tick-borne diseases. Emerg Med Clin North America 1991; 9:303-325.
20) Donat JR & Donat JF: Tick paralysis with persistent weakness and electromyographic abnormalities. Arch Neurol 1981; 38:59-61.
21) Dupont HT, La Scola B, & Williams R: A focus of tick-borne relapsing fever in Southern Zaire. Clin Infect Dieases 1997; 25:139-144.
22) Feldman-Muhsam B: Ixodid tick attacks on man in Israel: medical implications. Israel J Med Sci 1986; 22:19-23.
23) Fowler ME: Veterinary Zootoxicology, CRC Press, Boca Raton, Florida, 1993.
24) Grattan-Smith PJ, Morris JG, & Johnston HM: Clinical and neurophysiological features of tick paralysis. Brain 1997; 120:1975-1987.
25) Gustafson R, Svenungsson B, & Forsgren M: Two-year survey of the incidence of lyme borreliosis and tick-borne encephalitis in a high-risk population in Sweden. Eur J Clin Microbiol Infect Dis 1992; 11:894-900.
26) Gustafson R: Epidemiologic studies on lyme borreliosis and tick-borne encephalitis. Scand J Infect Dis 1994; Suppl 92:8-32.
27) Haddad FA, Schwartz I, Liveris D, et al: A skin lesion in a patient from Kentucky. Clin Infect Diseases 2005; 40:429, 475-476.
28) Hamilton DG: Tick paralysis: a dangerous disease in children. Med J Aust 1940; 1:759-765.
29) Heinz FX & Mandl CW: The molecular biology of tick-borne encephalitis virus. APMIS 1993; 101:735-745.
30) Henderson FW: Tick paralysis: report of a case in Florida. JAMA 1961; 175:615-617.
31) Jongejan F, Wassink LA, & Thielemans MJC: Serotypes in Cowdria ruminantium and their relationship with Ehrlichia phagocytophila determined by immunofluorescence. Vet Microbiol 1989; 21:31-40.
32) Juhasz C & Szirmai I: Spectral EEG parameters in patients with tick-borne encephalitis: a follow-up study. Clin Electroencephalography 1993; 24:53-58.
33) Kenyon RH, Ripper MK, & McKee KT: Infection of macaca radiata with viruses of the tick borne encephalitis group. Microbial Pathogen 1992; 13:399-409.
34) Kincaid JC: Tick bite paralysis. Seminars in Neurology 1990; 10:32-34.
35) Knoppert NW, Mijmeijer SM, & Van Duin CTM: Some pharmacokinetic data of aditoprim and trimethoprim in healthy and tick-borne fever infected dwarf goats. J Vet Pharmacol Ther 1988; 11:135-144.
36) Kohler G, Hoffman G, & Horchner F: Immunobiologische undersuchugen an Kanichen mit Ixoden-Infestationen. Berl Munch Tieraerztl Wochenschr 1967; 80:396-400.
37) Kunkel DB: The sting of the arthropd. Emerg Med 1988; 20:41-48.
38) Lahat E, Goldman M, & Barr J: Comparison of intranasal midazolam with intravenous diazepam for treating febrile seizures in children: prospective randomized study. BMJ 2000; 321:83-86.
39) Lee MD, Sonenshine DE, & Counselman FL: Evaluation of subcutaneous injection of local anesthetic agents as a method of tick removal. Amer J Emerg Med 1995; 13:14-16.
40) Lotric-Furlan S & Strle F: Thrombocytopenia-a common finding in the initial phase of tick-borne encephalitis. Infection 1995; 23:203-206.
41) Manno EM: New management strategies in the treatment of status epilepticus. Mayo Clin Proc 2003; 78(4):508-518.
42) McDermott AE: Tick paralysis. Report of a case. Mo Med J 1957; 54:1054.
43) Modly CE & Burnett JW: Tick-borne dermatologic diseases. Cutis 1988; 41:244-246.
44) Nafe LA: Tick paralysis. Vet Clin North Am Small Anim Pract 1988; 18:598-604.
45) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
46) Needham GR: Evaluation of five popular methods for tick removal. Pediatrics 1985; 75:997-1002.
47) Parola P, Jourdan J, & Raoult D: Tick-borne infection caused by rickettsia africae in the West Indies (letter). N Eng J Med 1998; 338:1391.
48) Pearn J: Neuromuscular paralysis caused by tick envenomation. J Neurol Sci 1977; 34:37-42.
49) Pinn TG & Sowden D: Queensland tick typhus. Aust NJ Med 1998; 28:824-826.
50) Product Information: lorazepam injection, lorazepam injection. Bedford Laboratories, Bedford, OH, 2004.
51) Raoult D, Berbis PH, & Roux V: A new tick-transmitted disease due to Rickettsia slovaca. Lancet 1997; 350(9071):112-113.
52) Riek RF: Studies on the reactions of animals to infestation with ticks. VI. Resistance of cattle to infestation with the tick Boophilus microplus. Aust J Agric Res 1962; 13:532-550.
53) Rose I: A review of tick paralysis. Can Med Assoc J 1954; 70:175-176.
54) Sander D, Scholz CW, & Eiben P: Postvaccinal plexus neuropathy following vaccination against tick-borne encephalitis and tetanus in a competitive athlete. Clin Investig 1994; 72:399.
55) Schmitt N, Bowmer EJ, & Gregson JD: Tick paralysis in British Columbia. Can Med Assoc J 1969; 100:417-421.
56) Schwartz E & Shlim DR: Tick bite appendicitis. JAMA 1988; 259:3561.
57) Scott R, Besag FMC, & Neville BGR: Buccal midazolam and rectal diazepam for treatment of prolonged seizures in childhood and adolescence: a randomized trial. Lancet 1999; 353:623-626.
58) Sexton DJ, King G, & Dwyer B: Fatal Queensland tick typhus. J Infect Diseases 1990; 162:779-780.
59) Southcott RV: Some harmful Australian arthropods: scorpions, mites, ticks and myriapods. Med J Aust 1986; 145:590-595.
60) Stein A & Raoult D: Q fever during pregnancy: a public health problem in southern France. Clin Infect Diseases 1998; 27:592-596.
61) Stone BF & Neish AL: Tick-paralysis toxoid: an effective immunizing agent the toxin of Ixodes hyolocyclus. Aust J Exp Biol Med Sci 1984; 62:189-191.
62) Stone BF, Cowie MR, & Kerr JD: Improved toxin/antitoxin assays for studies on the Australian paralysis tick Ixodes holocyclus. Aust J Exp Biol Med Sci 1982; 60:309-318.
63) Stone BF, Neish Al, & Wright IG: Immunization of rabbits to produce high serum titres of neutralizing antibodies and immunity to the paralyzing toxin of Ixodes holocyclus. Aust J Exp Biol Med Sci 1982a; 60:351-358.
64) Trager W: Acquired immunity to ticks. J Parasitol 1939; 25:57-81.
65) Vallat JM, Hugon J, & Lubeau M: Tick-bite meningoradiculoneuritis: clinical electrophysiologic, and histologic findings in 10 cases. Neurology 1987; 37:749-753.
66) Wormser GP, Dattwyler RJ, Shapiro ED, et al: The clinical assessment, treatment, and prevention of lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis 2006; 43(9):1089-1134.

Last Modified: September 24, 2010

醫藥知識疾病介紹傳染病人畜共通傳染病 tick 蜱牛蚤 Ixodida

快樂小藥師

快樂小藥師 Im pharmacist nichts glücklich

快樂小藥師發表在痞客邦留言(1) 人氣()

E-mail轉寄

快樂小藥師 Im pharmacist nichts glücklich

快樂小藥師在此提供醫藥訊息、醫藥知識，還有很多小藥師的生活點點滴滴……

快樂小藥師