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- Tick-borne, infectious disease caused by intraerythrocytic protozoa of the genus Babesia, infects wide array of vertebrate animals, causes lysis of host RBCs
- Asymptomatic to severe, life-threatening infection depending on the species of Babesia and the immune status of the patient
- Asymptomatic infection:
- 50% of children and 25% of adults with infection have no symptoms
- Mild–moderate disease:
- Usually immune competent patients
- Infections typically self-limited or resolve with antibiotic therapy
- Mortality usually <5%
- Severe disease:
- Defined as hospitalization >2 wk, ICU stay >2 days, or ending in death
- Typically associated with immune compromise: Splenectomy; cancer; HIV; hemoglobinopathy; chronic heart, lung, or liver disease
- Other groups at higher risk for severe disease: Neonates, >50 yr old, on immune-suppressive drugs (e.g., rituximab or anticytokine therapy [e.g., etanercept, infliximab])
- Mortality can be as high as 21% among immune-suppressed patients
- Complications develop in approximately one-half of the hospitalized patients:
- ARDS, DIC most common
- Can also see CHF, coma, liver failure, renal failure, splenic rupture
- Co-occurrence with other tick-borne diseases should be considered in endemic regions under the following conditions:
- Lyme disease (Borrelia burgdorferi) – associated rash
- Human granulocytic anaplasmosis (Anaplasma phagocytophilum) – protracted symptoms with leukopenia
- Species causing human disease:
- Babesia microti – Northern and Midwestern US (most common cause of disease in US)
- Babesia divergens – Europe
- Babesia duncani – Northern US Pacific coast
- Case reports of Babesiosis in Asia, Africa, Australia, and South America
- Animal reservoirs:
- B. microti – white-footed mouse, white-tailed deer
- B. divergens – cattle, rats
- Transmission via Ixodes tick vector:
- Most common vector for transmission of babesiosis to humans
- Ixodes requires blood meal from a vertebrate host to pass through each stage of life cycle (larva, nymph, adult)
- Most cases result from nymphal tick bites in late spring through summer, adult ticks can also transmit disease
- Pathogen life cycle, pathogenesis:
- Protozoa pass from tick salivary glands to mammalian bloodstream where they penetrate erythrocytes, mature and divide.
- Mature protozoa exit from RBC resulting in membrane damage, lysis, hemolytic anemia, and hemoglobinuria.
- Damaged RBCs become less deformable, enhancing removal by spleen; however, asplenic patients less able to clear infected RBCs, leading to more severe disease.
- Damaged RBCs may result in microvascular stasis with secondary ischemic organ injury to liver, spleen, heart, kidney, or brain.
- Transmission via transfusion of RBCs, platelets:
- >150 cases since 1979, 75% of these since 2000
- B. microti is the most common pathogen
- Low-level parasitemia may not be visible on donor blood smears, yet can still transmit disease
- Often results in severe cases as recipients of blood products often immune compromised or have significant comorbidities
Transmission can occur in utero and during delivery; youngest reported case was a 4-wk-old infant.
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