Tick-borne intraerythrocytic protozoal infection (Babesia microti in US); causes hemolytic anemia, fever, and severe disease in asplenic or immunocompromised hosts.
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Risk factors
- Outdoor activity in endemic areas during late spring through summer
- Asplenia or hyposplenism (much more severe disease)
- Age >50 years
- Immunocompromised state: HIV, malignancy, rituximab, post-transplant
- Receipt of red blood cell transfusion from infected donor (no FDA-licensed screen until recently in endemic states)
- Co-infection with Lyme disease or anaplasmosis
Pathophysiology
Babesia sporozoites injected by tick saliva invade erythrocytes, where they replicate and lyse cells in a manner analogous to malaria. Hemolysis, hemoglobinuria, and microvascular sludging produce anemia and end-organ ischemia. Splenic clearance is critical; asplenic patients are at greatest risk for fulminant disease.
Clinical presentation
Symptoms
- Gradual onset of fever, chills, sweats, fatigue, myalgia, headache 1-4 weeks after tick exposure
- Anorexia, nausea, abdominal pain, dark urine (hemolysis)
- Dyspnea and chest discomfort
- Asplenic or immunocompromised patients: rapidly progressive severe disease with high parasitemia and multiorgan failure
- Asymptomatic parasitemia in many immunocompetent hosts
Signs / physical exam
- Fever, tachycardia
- Mild splenomegaly or hepatomegaly
- Jaundice and scleral icterus in significant hemolysis
- Petechiae uncommon (in contrast to viral hemorrhagic fevers)
- Rash is NOT typical — distinguishing feature from erythema migrans of Lyme
Classic findings
Patient from coastal Massachusetts or eastern Long Island with summer tick exposure, fever, hemolytic anemia, and intraerythrocytic ring forms or pathognomonic Maltese cross tetrads on Giemsa-stained thin blood smear.
Differential diagnosis
- Malaria — Travel history to endemic region, fever paroxysms; Plasmodium species on blood smear; cross-reaction possible — geography and exposure key
- Lyme disease — Erythema migrans rash, arthritis, neurologic features; serology; co-infection common with babesiosis
- Anaplasmosis / ehrlichiosis — Fever, leukopenia, thrombocytopenia, elevated LFTs in same vector region; PCR or morulae in granulocytes
- Hemolytic anemia (other causes) — Autoimmune, drug-induced, hereditary; Coombs, smear without intracellular parasites
- Sepsis with DIC — Source identification, blood cultures, coagulation profile
- TTP/HUS — Microangiopathic hemolysis with schistocytes, neurologic or renal signs; ADAMTS13
Diagnostic workup
Diagnostic criteria
Definitive: visualization of Babesia parasites on blood smear or positive PCR. Serology supports diagnosis but does not establish active infection alone.
Labs
- Giemsa- or Wright-stained thin blood smear — intraerythrocytic ring forms; Maltese cross (4 merozoites in tetrad) is pathognomonic but uncommon
- Babesia microti PCR (more sensitive at low parasitemia)
- Babesia serology (IgM and IgG; supports rather than establishes diagnosis)
- CBC: hemolytic anemia, thrombocytopenia, leukopenia
- Hemolysis labs: LDH elevated, haptoglobin low, indirect bilirubin elevated, reticulocytosis
- BMP and LFTs (renal failure and transaminase elevation in severe disease)
- Parasitemia level (% parasitized RBCs) is important for severity classification and treatment monitoring
- Concurrent testing for Lyme and anaplasmosis given shared vector
Imaging
- Generally not required for diagnosis
- Chest imaging if dyspnea or hypoxia for ARDS or pulmonary edema
- Abdominal imaging if splenic infarct or rupture suspected
Treatment
First-line
- Mild to moderate disease: atovaquone 750 mg PO BID + azithromycin 500 mg PO on day 1 then 250 mg daily for 7-10 days
- Severe disease (parasitemia >=4%, hemodynamic instability, end-organ dysfunction, asplenia, immunocompromise): clindamycin 300-600 mg IV every 6 hours + quinine 650 mg PO every 6-8 hours for at least 7-10 days
- Red blood cell exchange transfusion for parasitemia >10%, severe anemia (Hb <10), hemodynamic instability, end-organ failure
- Supportive care: transfusion, hemodialysis if needed, ICU monitoring
- Concurrent treatment for Lyme disease if co-infection identified
Second-line / adjunct
- Highly immunocompromised hosts (especially post-rituximab B-cell depletion) may require prolonged combination therapy (6+ weeks) and have higher relapse rates
- Atovaquone + azithromycin can be substituted for severe disease in some patients with less toxicity than clindamycin/quinine
- Reporting to state and local health department; transfusion-transmitted cases must be reported
Complications
- Severe hemolytic anemia and DIC
- ARDS, congestive heart failure
- Acute kidney injury
- Splenic infarct or rupture
- Persistent or relapsing infection in immunocompromised hosts
- Coma and death in fulminant disease
- Transfusion-transmitted infection in blood-bank settings
PANCE pearls
- Maltese cross tetrads on a thin blood smear are pathognomonic for Babesia but seen in only a minority of cases; PCR is more sensitive.
- No rash — helps distinguish from Lyme disease (erythema migrans) and from spotted-fever rickettsioses.
- Asplenic patients tolerate babesiosis poorly and are candidates for early aggressive therapy and exchange transfusion.
- Co-infection with Lyme disease and/or anaplasmosis is common — test for all three in patients with tick-borne febrile illness in endemic regions.
- Atovaquone + azithromycin is preferred for outpatient mild disease; clindamycin + quinine is reserved for severe disease (and is poorly tolerated).
References
- IDSA 2020 — Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA), American Academy of Neurology (AAN), and American College of Rheumatology (ACR) for the prevention, diagnosis, and treatment of Lyme disease (Lantos et al., Clin Infect Dis 2021) — includes co-infection with babesiosis
- CDC — CDC — Babesiosis: epidemiology, diagnosis, and treatment
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