Transfusion-transmitted and community-acquired babesiosis in New York, 2004 to 2015.

BACKGROUND: Babesiosis is a potentially life-threatening zoonotic infection most frequently caused by the intraerythrocytic parasite Babesia microti. The pathogen is usually tickborne, but may also be transfusion or vertically transmitted. Healthy persons, including blood donors, may be asymptomatic and unaware they are infected. Immunocompromised patients are at increased risk for symptomatic disease. STUDY DESIGN AND METHODS: All reported community-acquired babesiosis cases in New York from 2004 to 2015 were evaluated, enumerated, and characterized. All potential transfusion-transmitted babesiosis (TTB) cases reported through one or more of three public health surveillance systems were investigated to determine the likelihood of transfusion transmission. In addition, host-seeking ticks were actively collected in public parks and other likely sites of human exposure to B. microti. RESULTS: From 2004 to 2015, a total of 3799 cases of babesiosis were found; 55 (1.4%) of these were linked to transfusion. The incidence of both community-acquired babesiosis and TTB increased significantly during the 12-year study period. The geographic range of both ticks and tickborne infections also expanded. Among TTB cases, 95% of recipients had at least one risk factor for symptomatic disease. Implicated donors resided in five states, including in 10 New York counties. More than half of implicated donors resided in counties known to be B. microti endemic. CONCLUSION: The increasing incidence of TTB correlated with increases in community-acquired babesiosis and infection of ticks with B. microti. Surveillance of ticks and community-acquired cases may aid identification of emerging areas at risk for Babesia transfusion transmission.

Transfusion-associated babesiosis in the United States: a description of cases.

BACKGROUND: Babesiosis is a potentially life-threatening disease caused by intraerythrocytic parasites, which usually are tickborne but also are transmissible by transfusion. Tickborne transmission of Babesia microti mainly occurs in 7 states in the Northeast and the upper Midwest of the United States. No Babesia test for screening blood donors has been licensed. OBJECTIVE: To ascertain and summarize data on U.S. transfusion-associated Babesia cases identified since the first described case in 1979. DESIGN: Case series. SETTING: United States. PATIENTS: Case patients were transfused during 1979-2009 and had posttransfusion Babesia infection diagnosed by 2010, without reported evidence that another transmission route was more likely than transfusion. Implicated donors had laboratory evidence of infection. Potential cases were excluded if all pertinent donors tested negative. MEASUREMENTS: Distributions of ascertained cases according to Babesia species and period and state of transfusion. RESULTS: 159 transfusion-associated B. microti cases were included; donors were implicated for 136 (86%). The case patients' median age was 65 years (range, <1 to 94 years). Most cases were associated with red blood cell components; 4 were linked to whole blood-derived platelets. Cases occurred in all 4 seasons and in 22 (of 31) years, but 77% (122 cases) occurred during 2000-2009. Cases occurred in 19 states, but 87% (138 cases) were in the 7 main B. microti-endemic states. In addition, 3 B. duncani cases were documented in western states. LIMITATION: The extent to which cases were not diagnosed, investigated, reported, or ascertained is unknown. CONCLUSION: Donor-screening strategies that mitigate the risk for transfusion transmission are needed. Babesiosis should be included in the differential diagnosis of unexplained posttransfusion hemolytic anemia or fever, regardless of the season or U.S. region. PRIMARY FUNDING SOURCE: None.

Autoimmunity in transfusion babesiosis: a spectrum of clinical presentations.

Transfusion-acquired babesiosis can be an asymptomatic or self-limited febrile hemolytic illness in a healthy host. A persistent, relapsing, and/or fulminant course with the development of life-threatening complications may be seen in immunocompromised or splenectomized patients. As in malaria, erythrocyte parasitemia is often associated with nonimmune hemolysis, and can be treated with erythrocytapheresis. Just as warm autoantibodies have been reported in malaria infection, the development of autoantibody-mediated immune hemolysis has been reported in babesiosis. We treated a previously healthy male with multiple injuries from a motor vehicle accident necessitating massive transfusion. Late in the hospitalization, his blood smear revealed Babesia microti, confirmed by PCR study and serology. This was eventually traced to a unit of blood from an asymptomatic blood donor that was transfused during his initial trauma care. Specific antibiotic therapy was begun, and severe hemolysis from a high parasite burden required red blood cell exchange which led to rapid abatement of the hemolysis. He had a positive DAT (IgG with a pan-reactive eluate) but no serum autoantibody. This persisted for 10 days following cessation of hemolysis, and became negative while still on antibiotics while his parasite burden became undetectable. Reports of autoimmunity associated with community acquired babesiosis often have severe hemolysis from their autoantibodies, but our case shows that autoantibodies may also follow transfusion-acquired babesiosis. The nature of the autoantigen is unknown.