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Transplacental Transmission of Human Babesiosis

Krause, Peter J. MD*; Vannier, Edouard PhD

Infectious Diseases in Clinical Practice: November 2012 - Volume 20 - Issue 6 - p 365–367
doi: 10.1097/IPC.0b013e3182769089
Editorial Comment

From the *Yale School of Public Health and Yale School of Medicine, New Haven, CT; and †Tufts Medical Center and Tufts University School of Medicine, Boston, MA.

Correspondence to: Peter J. Krause, MD, Yale School of Public Health, New Haven, CT.

Funding provided by the Gordon and Llura Gund Foundation (Drs Krause and Vannier) and the National Institutes of Health (R01 AG019781, to Dr Vannier; and R21 AI088079, to Dr Krause).

The authors have no conflicts of interest to disclose.

Babesiosis is an infectious disease caused by intraerythrocytic protozoan parasites of the genus Babesia.1 Approximately 100 Babesia species cause infection in a wide range of wild and domestic animals. Of the few species that cause human disease, Babesia microti is the most common. B. microti infection is endemic in the northeastern and upper midwestern United States, where this pathogen is transmitted to humans by the hard-bodied tick Ixodes scapularis. In the last decade, an increasing number of cases have been caused by transfusion of blood products. B. microti is currently the most common transfusion-transmitted pathogen reported to the US Food and Drug Administration, and transfusion is the most common mode of acquisition of neonatal babesiosis.1–5 The possibility of transplacental transmission was proposed in several reports for those neonatal cases that did not receive a blood transfusion and whose mothers denied exposure of their infants to ticks.6–10 Tick exposure could not be conclusively ruled out, however, because symptoms were not noted until 3 to 5 weeks of age and parasitemia was not demonstrated in the mothers. Stronger evidence for congenital infection was recently documented in a neonate who presented with symptoms of babesiosis at 6 weeks of age but whose heel stick blood specimen obtained at 3 days of age contained B. microti IgG antibody.11 In addition, B. microti DNA was amplified from placental tissue. In this issue of Infectious Diseases in Clinical Practice, the case of perinatal babesiosis reported by Cornett et al definitively establishes that B. microti can be transplacentally transmitted. Babesia parasites were found in maternal blood and in amniotic fluid the day before delivery and in the infant’s blood on the day of birth. B. microti DNA was amplified in the blood of the mother. Furthermore, both mother and child presented with symptoms of babesiosis.12

Neonates are at risk of severe disease and may suffer some of the complications typically seen in older patients, including respiratory distress syndrome, liver impairment, and severe anemia requiring transfusion or exchange transfusion.2,4,11–13 The clinical presentation of the case described by Cornett et al differs from those of the 5 reported cases of probable congenital babesiosis, most notably by symptomatic illness in the mother who was asplenic and the onset of illness in the infant at birth. Mothers in previous reports were asymptomatically infected, and their infants developed a febrile illness 3 to 6 weeks after birth.6–11 Parasitemia in the infants at diagnosis ranged from 2% to 15%, and all of them required at least one blood transfusion for severe anemia. Treatment also included the combination of atovaquone and azithromycin or clindamycin and quinine for 9 to 10 days. All infants improved on therapy with apparent resolution of infection, although cure was specifically mentioned in only half the cases. From the limited number of reported cases, it can be concluded that congenital babesiosis becomes apparent anytime between birth and 6 weeks after birth with an onset of fever and either lethargy, irritability, poor feeding, pallor, jaundice, and/or hepatosplenomegaly in an infant whose mother usually is asymptomatic.

Health care workers should be aware of transplacentally transmitted babesiosis, especially obstetric and pediatric health care providers. Although it is uncommon, neonatal babesiosis may cause significant morbidity and may be mistaken for other infections, especially malaria. Most antimalarial drugs are ineffective for the treatment of babesiosis. Any case of babesiosis in neonates should prompt an evaluation of the probable route of transmission, either congenital, tick-borne, or through blood transfusion. Management differs for each transmission route. For congenital infection, diagnosis and treatment of maternal infection is necessary. Congenital infection probably can be prevented if the mother’s condition is diagnosed and appropriately treated.14,15 For tick-transmitted infection, adoption of tick preventive measures should be considered. For transfusion-transmitted infection, a search for the infected blood donor is required so that transfusion transmission can be confirmed, the donor may receive antibiotic treatment (if appropriate), and be informed that they can no longer donate blood.5 Much remains unknown about the pathogenesis, clinical course, and prognosis of congenital babesiosis, but the report by Cornett et al is a useful initial step. As the incidence and recognition of babesiosis continue to increase, additional reports of congenital babesiosis are expected and should contribute to a better understanding of this rare condition.

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1. Vannier E, Krause PJ. Human babesiosis. N Engl J Med. 2012; 366: 2397–2407.
2. Fox LM, Wingerter S, Ahmed A, et al.. Neonatal babesiosis: case report and review of the literature. Pediatr Infect Dis J. 2006; 25: 169–173.
3. Herwaldt BL, Linden JV, Bosserman E, et al.. Transfusion-associated babesiosis in the United States: a description of cases. Ann Intern Med. 2011; 155: 509–519.
4. Kjemtrup AM, Lee B, Fritz CL, et al.. Investigation of transfusion transmission of a WA1-type babesial parasite to a premature infant in California. Transfusion. 2002; 42: 1482–1487.
5. Leiby DA. Transfusion-transmitted Babesia spp.: bull’s-eye on Babesia microti. Transfusion. 2011; 24: 14–28.
6. Esernio-Jenssen D, Scimeca PG, Benach JL, et al.. Transplacental/perinatal babesiosis. J Pediatr. 1987; 110: 570–572.
7. New DL, Quinn JB, Qureshi MZ, et al.. Vertically transmitted babesiosis. J Pediatr. 1997; 131; 163–164.
8. Scimeca PG, Weinblatt ME, Schonfeld G, et al.. Babesiosis in two infants from Eastern Long Island, NY. Am J Dis Child. 1986; 140: 971.
9. Sethi S, Alcid D, Kesarwala H, et al.. Probable congenital babesiosis in an infant, New Jersey, USA. Emerg Infect Dis. 2009; 15: 788–791.
10. Aderinboye O, Syed SS. Congenital babesiosis in a four-week-old female infant. Pediatr Infect Dis J. 2010; 29: 188.
11. Joseph JT, Purtill K, Wong SJ, et al.. Vertical transmission of Babesia microti, United States. Emerg Infect Dis. 2012; 18: 1318–1321.
12. Cornett JK, Malhotra A, Hart D. Vertical transmission of babesiosis from a pregnant, splenectomized mother to her neonate. Infect Dis Clin Pract. 2012; 20: 408–410.
13. Simonsen KA, Harwell JI, Lainwala S. Clinical presentation and treatment of transfusion-associated babesiosis in premature infants. Pediatrics. 2011; 128: e1019–e1024.
14. Feder HM, Lawlor M, Krause PJ. Babesiosis in pregnancy. N Engl J Med. 2003; 349: 195–196.
15. Raucher HS, Jaffin H, Glass JL. Babesiosis in pregnancy. Obstet Gynecol. 1984; 63 (suppl): 7S–9S.
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