Babesiosis

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Basics

Description

  • 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

Etiology

  • Babesia:
    • 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

Pediatric Considerations
Transmission can occur in utero and during delivery; youngest reported case was a 4-wk-old infant.

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Basics

Description

  • 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

Etiology

  • Babesia:
    • 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

Pediatric Considerations
Transmission can occur in utero and during delivery; youngest reported case was a 4-wk-old infant.

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