CME information and disclosures![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
To see contributor disclosures related to this article, hover over this reference: [1]
Physicians may earn CME/MOC credit by searching for an answer to a clinical question on our platform, reading content in this article that addresses that question, and completing an evaluation in which they report the question and the impact of what has been learned on clinical practice.
AMBOSS designates this Internet point-of-care activity for a maximum of 0.5 AMA PRA Category 1 Credit(s)™. Physicians should claim only credit commensurate with the extent of their participation in the activity.
For answers to questions about AMBOSS CME, including how to redeem CME/MOC credit, see "Tips and Links" at the bottom of this article.
Summary![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
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,tick paralysis, and the more recently recognized alpha-gal syndrome. 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![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
Overview of tick-borne diseases [2] | |||||
---|---|---|---|---|---|
Pathogen/cause | US distribution | Clinical features | Diagnostics | Treatment | |
Lyme disease |
|
|
|
| |
Rocky Mountain spotted fever (RMSF) |
|
|
|
| |
Babesiosis |
|
|
|
|
|
Ehrlichiosis |
|
|
|
| |
|
| ||||
Tularemia [3] |
|
|
| ||
Colorado tick fever (CTF) [4] |
|
|
| ||
Tick-borne relapsing fever [5] |
|
|
|
|
|
Southern tick‑associated rash illness (STARI) |
|
|
|
| |
Tick paralysis |
|
|
|
| |
Alpha-gal syndrome [6] |
|
|
|
|
|
Rocky Mountain spotted fever (RMSF)![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
Background
- Epidemiology: ∼ 5500 cases were reported in 2018 [7]
- Pathogen: : Rickettsia rickettsii
-
Vector
- American dog tick (Dermacentor variabilis)
- Rocky Mountain wood tick (Dermacentor andersoni)
- Brown dog tick (Rhipicephalus sanguineus)
-
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 [8]
- 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. [9]
Diagnostics [9][10][11]
RMSF is a clinical diagnosis.
- Laboratory studies [10]
- Other supportive studies: ECG , CXR [9]
-
Confirmatory studies: should be performed in all patients [11]
- 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
-
Lumbar puncture: to rule out meningitis in patients with neurological features [10]
- 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. [11]
RMSF is a nationally notifiable disease in the United States. Contact the state or local health department if a potential case is suspected. [9]
Differential diagnosis [11]
- 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. [11]
- Doxycycline [11][12]
- Supportive care in severe disease: e.g., broad-spectrum antibiotics for febrile patients in septic shock
-
Options during pregnancy [11][13]
- Doxycycline [13]
- Chloramphenicol during the first and second trimester [11]
Treatment should be initiated as soon as RMSF is suspected, as it can be fatal if not treated early.
Disposition [11]
- 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 [14]
- 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![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
- 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. [15]
- Distribution: Midwestern (especially Minnesota and Wisconsin) and northeastern US
-
Clinical features
- Incubation period: 1–4 weeks [16]
- 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. [17]
-
Diagnostics
- CBC: ↓ hematocrit, thrombocytopenia, ↑ reticulocyte count
- Azotemia
- Hemoglobinuria with/without hemosiderinuria
- ↓ Serum haptoglobin
- Mildly ↑ hepatic transaminases
-
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![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
-
Pathogens
- Ehrlichia chaffeensis
- Ehrlichia ewingii
- Ehrlichia muris eauclairensis
-
Vectors
- Lone star tick (Amblyomma americanum): E. chaffeensis and E. ewingii
- Deer tick (Ixodes scapularis): E. muris eauclairensis
-
Distribution
- Mainly east of the Rocky Mountains
- Also some cases in the Southwest
-
Clinical features
- Incubation period: 1–2 weeks [18]
- 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 [19]
- Adults: ∼ 30% of cases
- Children: ∼ 60% of cases
-
Diagnostics [11]
- 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) ; [11][20]
- 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 [11][12]
- Disposition: In selected cases, consider discharge with oral antibiotics. [11]
Ehrlichiosis is a nationally notifiable disease in the United States. Contact the state or local health department if a potential case is suspected. [9]
Anaplasmosis![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
- Pathogen: Anaplasma phagocytophilum
-
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
-
Distribution
- Upper midwestern and northeastern US
- Growing number of cases on the West Coast
-
Clinical features
- Incubation period: 1–2 weeks [21]
- Fever and other flu-like symptoms (headache, chills, muscle aches)
- Gastrointestinal symptoms (e.g., nausea, vomiting, abdominal pain)
- Cough
- Typically no rash
-
Diagnostics [11]
- Anaplasmosis is a clinical diagnosis.
-
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 [11]
- Disposition: In selected cases, consider discharge with oral antibiotics. [11]
Anaplasmosis is a nationally notifiable disease in the United States. Contact the state or local health department if a potential case is suspected. [9]
Tularemia![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
- Pathogen: Francisella tularensis (facultative intracellular bacterium)
-
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
-
Clinical features [3]
- Incubation period: typically 3–5 days (range 1–21 days) [22]
- Flu-like symptoms
- High fever
- Tender regional lymphadenopathy
-
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
-
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
-
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)![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
- Pathogen: Colorado tick fever virus (CTFV), an RNA virus
- Vector: Rocky Mountain wood tick (Dermacentor andersoni)
- Distribution: western US
-
Clinical features
- Incubation period: 1–14 days [23]
- Flu-like symptoms: often biphasic (fever remits after 2–4 days and returns 1–3 days later) [24]
- Possibly conjunctival injection, pharyngeal erythema, and cervical lymphadenopathy
- Petechial or maculopapular rash
-
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 [24]
- Treatment: only supportive management
Tick-borne relapsing fever![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
- Pathogen: Borrelia hermsii
- Vector: Vector: Ornithodoros soft ticks (including O. hermsi, O. parkeri, O. turicata)
- Distribution: western US and Texas
-
Clinical features
- Incubation period: 4–18 days [25]
- Recurring episodes of high fever for 3 days and an afebrile period of 7 days [5]
- 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.
-
Diagnostics
- CBC: normal or ↑ leukocyte count, thrombocytopenia
- Mild ↑ in serum bilirubin level
- Slightly prolonged PT and aPTT
- ↑ ESR
-
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
-
Treatment
- No CNS involvement:
- First line: tetracycline
- Second line: erythromycin
- CNS involvement: ceftriaxone
- No CNS involvement:
Southern tick‑associated rash illness (STARI)![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
- Pathogen: unknown
- Vector: Lone star tick (Amblyomma americanum)
- Distribution: southeastern and eastern US
-
Clinical features
- Incubation period: ∼ 7 days [26]
- Resembles early localized Lyme disease with erythema migrans-like lesion and possibly flu-like symptoms [26]
- 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 axetil (See “Treatment of Lyme disease” for details.) [27]
Tick paralysis![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
- 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
-
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
-
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).
- CSF examination is usually normal in tick-borne paralysis.
- Differential diagnosis
-
Treatment
- Locate and remove the tick.
- Supportive therapy (e.g., ventilatory support for patients with respiratory failure)
References: [28]
Alpha-gal syndrome![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
- Definition: an allergic reaction to the oligosaccharide galactose-alpha-1,3-galactose (alpha-gal) found on the cells of nonprimate mammals (e.g., cows, pigs, lambs) that is thought to occur after a parasitic infection or the bite of a tick [6]
-
Etiology [6]
- Lone star tick (Amblyomma americanum)
- Parasitic infections (e.g., ascariasis) have also been implicated.
- Reservoir: deer (principal host)
-
Distribution [6]
- US: Midwest, southeastern and eastern US
- Worldwide: Western Europe, South Africa, Japan, Australia
-
Pathophysiology
- Sensitization: Lone star tick bite or parasitic infection → production of IgE antibodies against alpha-gal
- Type I hypersensitivity: consumption of mammalian-derived products in a sensitized individual → alpha-gal absorbed in GI tract enters the circulation → IgE against alpha-gal → mast-cell degranulation
-
Clinical features [6]
- Typically present 2–6 hours after ingestion
- May be asymptomatic [6]
- GI features
- Mucocutaneous features: urticaria, angioedema
- Anaphylaxis (most severe presentation)
- Diagnosis: primarily a clinical diagnosis, but may be supported by the following [6]
-
Management: should be specialist-guided (e.g., gastroenterology, immunology) [6]
- Alpha-gal avoidance
- Diet: Avoid mammalian-derived meats and products.
- Medical products: e.g., cetuximab, pancreatic enzymes [6]
- Pharmacotherapy: Consider immediately after exposure.
- Oral antihistamines (e.g., diphenhydramine ) [6]
- AND/OR epinephrine autoinjector
- Referral: Consider consulting immunology and/or allergy specialists for patients with cutaneous or systemic symptoms (e.g., hypotension, urticaria).
- Alpha-gal avoidance
- Prognosis: Sensitization to alpha-gal may fade or resolve over time. [6]
- Prevention: tick bite prevention (further tick bites may worsen the allergy)
Alpha-gal does not cause anemia, GI bleeding, or weight loss. If these features are present consider alternative diagnoses. [6]