Summary
Tick-borne diseases are predominantly caused by pathogens that are transmitted by ticks (and sometimes other vectors), except tick paralysis, which is caused by a neurotoxin produced by the tick itself. Tick-borne diseases are typically associated with specific geographical regions. The most clinically significant tick-borne diseases in the US include Lyme disease, Rocky Mountain spotted fever (RMSF), babesiosis, ehrlichiosis, anaplasmosis, tularemia, Colorado tick fever, tick-borne relapsing fever, southern tick‑associated rash illness, and tick paralysis. While manifestations of these conditions vary, common symptoms include fever, flu-like symptoms, and skin rashes. Most tick-borne diseases are treated with antibiotics and patients usually respond well to treatment.
Lyme disease is covered in more detail in its own article.
Overview
Overview of tick-borne diseases [1] | |||||
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Pathogen/cause | US distribution | Clinical features | Diagnostics | Treatment | |
Lyme disease |
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Rocky Mountain spotted fever (RMSF) |
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Babesiosis |
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Ehrlichiosis |
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Tularemia [2] |
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Colorado tick fever (CTF) [3] |
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Tick-borne relapsing fever [4] |
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Southern tick‑associated rash illness (STARI) |
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Tick paralysis |
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Rocky Mountain spotted fever (RMSF)
Background
- Epidemiology: ∼ 5500 cases were reported in 2018 [5]
- Pathogen: : Rickettsia rickettsii
-
Vector
- American dog tick (Dermacentor variabilis)
- Rocky Mountain wood tick (Dermacentor andersoni)
- Brown dog tick (Rhipicephalus sanguineus)
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Distribution
- Cases reported across the contiguous US
- Higher density especially in the midwestern, northeastern, and southern US
- Pathophysiology: Rickettsia species invade capillary endothelium → inflammation → small vessel vasculitis
Clinical features [6]
- Incubation period: 4–10 days
- Flu-like symptoms (e.g., fever, headache)
-
Blanching maculopapular rash: begins on the wrists and ankles
- Spreads to the trunk, palms, and soles
- May become petechial and/or hemorrhagic
- Ankle and/or wrist swelling
- Gastrointestinal symptoms (e.g., nausea, vomiting, abdominal pain)
- Meningitis, focal neurological deficits
- Rapid clinical deterioration with shock and multiorgan dysfunction (e.g., DIC)
The rash may be less obvious in dark-skinned individuals; therefore, close inspection and a high degree of clinical suspicion are required. [7]
Diagnostics [7][8][9]
RMSF is a clinical diagnosis.
- Laboratory studies [8]
- Other supportive studies: ECG , CXR [7]
-
Confirmatory studies: should be performed in all patients [9]
- Indirect fluorescent antibody (IFA) test (gold standard): four-fold increase in IgG-specific antibodies
- PCR: detection of R. rickettsii DNA in a skin biopsy specimen or acute phase whole blood specimen
- Immunohistochemical staining of R. rickettsii in a skin biopsy specimen
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Lumbar puncture: to rule out meningitis in patients with neurological features [8]
- Pleocytosis with lymphocytic or monocytic predominance
- ↑ Protein
- Normal glucose
Do not delay treatment while waiting for confirmatory studies and do not discontinue treatment based solely on the results. [9]
RMSF is a nationally notifiable disease in the United States. Contact the state or local health department if a potential case is suspected. [7]
Differential diagnosis [9]
- Meningococcemia
- Lyme disease
- Endocarditis
- Hemorrhagic fever (e.g., Ebola fever, Hanta fever)
- Vasculitis
Treatment
Initiate empiric antibiotic treatment immediately and consider consulting local infectious disease specialists. [9]
- Doxycycline [9][10]
- Supportive care in severe disease: e.g., broad-spectrum antibiotics for febrile patients in septic shock
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Options during pregnancy [9][11]
- Doxycycline [11]
- Chloramphenicol; during the first and second trimester [9]
Treatment should be initiated as soon as RMSF is suspected, as it can be fatal if not treated early.
Disposition [9]
- Consider hospitalization for patients who:
- Require supportive care
- Have altered mental status
- Are unable to adhere to follow-up
- Escalate to critical care unit based on clinical condition.
- In selected cases, consider discharge with oral antibiotics.
Prognosis [12]
- If treated within the first 5 days, patients typically fully recover without hospitalization.
- If treated after the first 5 days, symptoms are more severe and often require hospitalization. There is also a greater risk of long-term consequences of ischemia (e.g., amputations, paralysis, hearing loss, intellectual disability).
- If not treated early enough, the disease can be fatal.
Babesiosis
- Pathogen: Babesia species (e.g., Babesia microti)
-
Vector: deer tick (Ixodes scapularis)
- Ixodes is also the vector for Borrelia burgdorferi and Anaplasma species.
- Ticks are often coinfected; therefore, patients with babesiosis often also have Lyme disease. [13]
- Distribution: Midwestern (especially Minnesota and Wisconsin) and northeastern US
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Clinical features
- Incubation period: 1–4 weeks [14]
- Fever and other flu-like symptoms
- Hemolytic anemia (e.g., dark urine, jaundice)
- Mild splenomegaly and/or hepatomegaly
- Gastrointestinal symptoms (e.g., nausea, vomiting, abdominal pain)
- Possibly petechiae, ecchymoses
- Typically no rash
- Asplenia increases the risk of severe disease. [15]
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Diagnostics
- CBC: ↓ hematocrit, thrombocytopenia, ↑ reticulocyte count
- Azotemia
- Hemoglobinuria with/without hemosiderinuria
- ↓ Serum haptoglobin
- Mildly ↑ hepatic transaminases
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Confirmatory tests
- Peripheral blood smear showing Babesia as intraerythrocytic rings and/or Maltese cross
- OR Babesia DNA detection by PCR of blood sample
- OR Isolation of Babesia after animal inoculation
- Differential diagnosis
-
Treatment
- Mild disease: atovaquone PLUS azithromycin
- Severe disease: quinine PLUS clindamycin
Ehrlichiosis
-
Pathogens
- Ehrlichia chaffeensis
- Ehrlichia ewingii
- Ehrlichia muris eauclairensis
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Vectors
- Lone star tick (Amblyomma americanum): E. chaffeensis and E. ewingii
- Deer tick (Ixodes scapularis): E. muris eauclairensis
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Distribution
- Mainly east of the Rocky Mountains
- Also some cases in the Southwest
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Clinical features
- Incubation period: 1–2 weeks [16]
- Flu-like symptoms (e.g., fever, myalgia)
- Gastrointestinal symptoms (e.g., nausea, vomiting, abdominal pain)
- Hepatomegaly
- Rarely, symptoms of meningitis and/or encephalitis (e.g., headache, altered mental status, stiff neck, neurological deficits)
-
Sometimes an erythematous maculopapular or petechial rash [17]
- Adults: ∼ 30% of cases
- Children: ∼ 60% of cases
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Diagnostics [9]
- Ehrlichiosis is a clinical diagnosis.
-
Laboratory studies
- CBC: anemia, thrombocytopenia, leukopenia
- Mild to moderate ↑ AST and/or ALT
- BMP: mild to moderate ↓ Na
-
Peripheral blood smear (with Wright stain or Giemsa stain): leukocytes with morulae (clustered inclusion bodies that resemble a mulberry) ; [9][18]
- E. chaffeensis infection: morulae within monocytes
- E. ewingii infection: morulae within granulocytes
- Confirmatory tests: should be performed in all patients
- Differential diagnosis: RMSF
- Treatment: : doxycycline [9][10]
- Disposition: In selected cases, consider discharge with oral antibiotics. [9]
Ehrlichiosis is a nationally notifiable disease in the United States. Contact the state or local health department if a potential case is suspected. [7]
Anaplasmosis
- Pathogen: Anaplasma phagocytophilum
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Vector
- Deer tick (Ixodes scapularis)
- Western black-legged tick (Ixodes pacificus)
- Ixodes is also the vector for Borrelia burgdorferi and Babesia species, so coinfection is possible.
- Reservoir: deer and mice
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Distribution
- Upper midwestern and northeastern US
- Growing number of cases on the West Coast
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Clinical features
- Incubation period: 1–2 weeks [19]
- Fever and other flu-like symptoms (headache, chills, muscle aches)
- Gastrointestinal symptoms (e.g., nausea, vomiting, abdominal pain)
- Cough
- Typically no rash
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Diagnostics [9]
- Anaplasmosis is a clinical diagnosis.
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Laboratory studies
- CBC: mild anemia, thrombocytopenia, leukopenia
- Mild to moderate ↑ AST and/or ALT
- Peripheral blood smear may show morulae within granulocytes.
- Confirmatory tests: should be performed in all patients
- Treatment: : doxycycline [9]
- Disposition: In selected cases, consider discharge with oral antibiotics. [9]
Anaplasmosis is a nationally notifiable disease in the United States. Contact the state or local health department if a potential case is suspected. [7]
Tularemia
- Pathogen: Francisella tularensis (facultative intracellular bacterium)
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Vector
- Ticks (Amblyomma americanum, Dermacentor spp.)
- Deer flies (Chrysops species)
- Transmission without a vector is also possible via:
- Inhalation of contaminated dust or aerosols (may result in pulmonary disease)
- Ingestion of contaminated food or water
- Reservoir: rabbits, hares, and rodents (e.g., voles, muskrats)
- Distribution: all states except Hawaii
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Clinical features [2]
- Incubation period: typically 3–5 days (range 1–21 days) [20]
- Flu-like symptoms
- High fever
- Tender regional lymphadenopathy
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Localized signs depending on manifestation:
- Ulceroglandular tularemia (45–85%): skin ulcer at the entry site of F. tularensis
- Glandular tularemia (10–25%): tender regional lymphadenopathy with no skin ulcer
- Oculoglandular tularemia (<5%): unilateral conjunctival injection, pain, photophobia, tender preauricular and/or cervical lymphadenopathy
- Oropharyngeal tularemia (<5%): sore throat, mouth ulcers, tonsillitis, tender cervical lymphadenopathy
- Pneumonic tularemia (< 5%): nonproductive cough, pleuritic chest pain, dyspnea
- Typhoidal tularemia (< 5%): hepatosplenomegaly
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Diagnostics
- CBC: Normal or ↑ leukocyte count, thrombocytopenia
- Hyponatremia
- ↑ Serum transaminase levels and creatine phosphokinase
- Myoglobinuria
- Sterile pyuria
-
Confirmatory test
- Positive culture (e.g., on charcoal yeast extract agar) from swabs/scrapings of skin lesions, pharyngeal swab, sputum specimen, gastric aspirate, and/or lymph node aspirate/biopsy
- OR IFA test: four-fold increase in F. tularensis-specific antibody titers between acute and convalescent serum samples
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Imaging (e.g., CXR, CT)
- When pulmonary involvement is suspected
- May show pulmonary infiltrates, hilar lymphadenopathy, and/or pleural effusion
- Differential diagnosis
- Treatment: streptomycin, gentamicin, doxycycline, OR ciprofloxacin
- Reporting: Tularemia is a notifiable condition.
Colorado tick fever (CTF)
- Pathogen: Colorado tick fever virus (CTFV), an RNA virus
- Vector: Rocky Mountain wood tick (Dermacentor andersoni)
- Distribution: western US
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Clinical features
- Incubation period: 1–14 days [21]
- Flu-like symptoms: often biphasic (fever remits after 2–4 days and returns 1–3 days later) [22]
- Possibly conjunctival injection, pharyngeal erythema, and cervical lymphadenopathy
- Petechial or maculopapular rash
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Diagnostics
- CBC: leukopenia, thrombocytopenia
- Peripheral blood smear may show atypical lymphocytes.
-
Confirmatory test
- < 2 weeks after onset of symptoms onset: viral RNA detection by RT-PCR of blood sample
- > 2 weeks after onset of symptoms: serum assay to detect CTFV-specific IgM antibodies [22]
- Treatment: only supportive management
Tick-borne relapsing fever
- Pathogen: Borrelia hermsii
- Vector: Vector: Ornithodoros soft ticks (including O. hermsi, O. parkeri, O. turicata)
- Distribution: western US and Texas
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Clinical features
- Incubation period: 4–18 days [23]
- Recurring episodes of high fever for 3 days and an afebrile period of 7 days [4]
- Arthralgia (∼ 70%)
- Gastrointestinal symptoms (e.g., nausea, vomiting, abdominal pain, diarrhea)
- Less commonly
- Hepatic manifestations (e.g., jaundice, hepatosplenomegaly)
- Symptoms of meningitis (e.g., confusion, photophobia, neck pain, nuchal rigidity)
- Macular rash or scattered petechiae may occur.
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Diagnostics
- CBC: normal or ↑ leukocyte count, thrombocytopenia
- Mild ↑ in serum bilirubin level
- Slightly prolonged PT and aPTT
- ↑ ESR
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Confirmatory test
- Direct observation of spirochetes in peripheral blood smears, bone marrow, or CSF with Giemsa-Wright stain, acridine orange stain, or dark-field microscopy
- OR IFA test: four-fold increase in Borrelia-specific antibody titers between acute and convalescent serum samples
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Treatment
- No CNS involvement:
- First line: tetracycline
- Second line: erythromycin
- CNS involvement: ceftriaxone
- No CNS involvement:
Southern tick‑associated rash illness (STARI)
- Pathogen: unknown
- Vector: lone star tick (Amblyomma americanum)
- Distribution: southeastern and eastern US
-
Clinical features
- Incubation period: ∼ 7 days [24]
- Resembles early localized Lyme disease with erythema migrans-like lesion and possibly flu-like symptoms [24]
- Not associated with clinical features of early disseminated (e.g., arthralgia, facial nerve palsy, cardiac complications) or late Lyme disease (e.g., progressive encephalomyelitis).
- Diagnostics: Clinically determined by ruling out Lyme disease.
- Treatment: doxycycline, amoxicillin, OR cefuroxime (same as the treatment for Lyme disease) [25]
Tick paralysis
- Definition: a rare syndrome caused by the salivary neurotoxin of certain ticks, characterized by acute ataxia, that progresses to ascending paralysis
- Epidemiology: most commonly occurs in children and women
-
Etiology: > 40 tick species are associated with tick paralysis
- Most common in the US: Dermacentor species (e.g., Rocky Mountain wood tick)
- Others: lone star tick (Amblyomma americanum), deer tick (Ixodes scapularis)
- Distribution: most commonly in the Rocky Mountains and northwestern US
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Pathophysiology
- Paralysis is caused by tick neurotoxin, which is produced in the tick's salivary gland and introduced into the person's blood.
- Possible mechanisms:
- Dermacentor species: inhibition of sodium flux across axonal membranes
- Ixodes species: inhibition of acetylcholine release at the neuromuscular junction
- Tick neurotoxin → impairment of motor nerve transmission → muscle weakness → paralysis
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Clinical features
- Symptoms begin within 2–7 days of the initial tick bite.
- Typically starts with weakness in the lower extremities
- Escalates to ascending flaccid paralysis that progresses rapidly and can lead to respiratory failure due to respiratory muscle weakness
- Sensory deficits are usually absent.
- Cranial nerve palsies may occur (e.g., CN III palsy).
- No fever or rash
- Diagnostics: Clinically determined by finding a tick attached to the body and/or ruling out other tick-borne diseases associated with neurological deficits (e.g., Lyme disease, Q fever).
- Differential diagnosis
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Treatment
- Locate and remove the tick.
- Supportive therapy (e.g., ventilatory support for patients with respiratory failure)
References: [26]