Benoit VM, Petrich A, Alugupalli KR, Marty-Roix R, Moter A, Leong JM, Boyartchuk VL.

Department of Molecular Genetics and Microbiology, and Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, MA 01605; Institut für Mikrobiologie und Hygiene, Charité – Universitätsmedizin Berlin, Campus Charité Mitte, 10117 Berlin, Germany; Department of Microbiology and Immunology, Thomas Jefferson University, Philadelphia, PA 19107.

Host susceptibility to infection is controlled in large measure by the genetic makeup of the host. Spirochetes of the genus Borrelia include nearly 40 species of vector-borne spirochetes that are capable of infecting a wide range of mammalian hosts, causing Lyme disease and relapsing fever. Relapsing fever is associated with high-level bacteremia, as well as hematologic manifestations such as thrombocytopenia (i.e. low platelet numbers) and anemia. To facilitate studies of genetic control of susceptibility to Borrelia hermsii infection we performed a systematic analysis of the course of infection using immunocompetent and immunocompromised inbred strains of mice. Our analysis revealed that sensitivity to B. hermsii infections is genetically controlled. In addition, whereas the role of adaptive immunity to relapsing fever spirochetes is well documented, we found that innate immunity contributes significantly to reduction of bacterial burden. Similar to human infection, progression of the disease in mice was associated with thrombocytopenia and anemia. Histological and fluorescence in situ hybridization (FISH) analysis of infected tissues indicated that red blood cells were removed by tissue resident macrophages, a process that could lead to anemia. Spirochetes in the spleen and liver were often visualized associated with RBCs, lending support to the hypothesis that direct interaction of B. hermsii spirochetes with RBCs leads to clearance of bacteria from the bloodstream by tissue phagocytes.

PMID: 19995898 [PubMed – as supplied by publisher]

Background: Most cases of human babesiosis in North America are caused
by Babesia microti, which is endemic in the northeastern and upper
midwestern United States. Although the disease is usually transmitted by
a tick bite, there has been an increase in the number of
transfusion-transmitted cases reported. We describe a fatal case of
transfusion-transmitted babesiosis in a nonendemic state, Delaware.

Case Report: The patient was a 43-year-old Caucasian woman with history
of transfusion-dependent Diamond-Blackfan syndrome, hepatitis C, and
splenectomy. She was admitted initially for presumptive pneumonia. The
next day, a routine examination of the peripheral blood smears revealed
numerous intraerythrocytic ring forms, consistent with Babesia. The
parasitemia was approximately 5% to 6%. The diagnosis was confirmed by
positive polymerase chain reaction (PCR) for B. microti DNA and high
titer of antibody to B. microti (1:2048). Despite aggressive therapy
including clindamycin and quinine antibiotics, the patient expired 3
days after admission. Subsequently, 13 blood donors were tested for B.
microti. All tested donors were negative by PCR. However, one donor
living in New Jersey had a significant elevated B. microti antibody
titer (1:1024).

Conclusions: We believe that this is the first reported case of
transfusion-transmitted babesiosis in Delaware, a nonendemic state. Our
case illustrates that clinicians should consider babesiosis in the
differential diagnosis of immunocompromised patients who have fever and
recent transfusion history, even in areas where babesiosis is not
endemic. It also demonstrates the need for better preventive strategies
including more sensitive, specific, and rapid blood donor screening
tests to prevent transfusion-transmitted babesiosis.

http://dx.doi.org/10.1111/j.1537-2995.2009.02454.x