All reported cases of WA1 babesiosis have occurred in the Pacific coast region of the United States, suggesting that WA1 is limited to this geographic area. However, we detected WA1 IgG in 27% of clinical sera sent to our laboratory for WA1 IgG testing from across the United States over a 2-year period, suggesting that exposure to WA1 or a closely related organism occurs outside Pacific coast states. We sought to determine if this high WA1 IgG detection rate among clinical specimens merely reflects WA1 seroprevalence outside the Pacific region. WA1 IgG, as well as Babesia microti IgG, was measured in 900 blood donor specimens from 9 states. Overall seroprevalence was 2.0% for WA1 and 0.4% for B. microti; regional seroprevalences ranged from 0 to 4% and 0 to 2%, respectively. Additional studies were performed to determine if WA1 IgG reactivity was attributable to polyclonal B-cell activation associated with acute Epstein-Barr virus (EBV) infection; 40 WA1 IgG-positive clinical sera and the 18 WA1 IgG-positive blood donor specimens were all negative for EBV capsid antigen (EBVCA) IgM (a marker of acute EBV infection), and 40 EBVCA IgM-positive sera were all negative for WA1 IgG. These findings indicate that the high WA1 IgG detection rate among clinical specimens does not simply reflect the national WA1 seroprevalence among blood donors or nonspecific reactivity due to acute EBV infection. Rather, the findings suggest that infection with WA1 or a related organism is more common than indicated by the literature and is not limited to Pacific coast states.The babesial piroplasm WA1 was first described in 1991 following its isolation from a Washington state resident with fever, chills, and myalgia (15). Morphological and ultrastructural studies revealed that WA1 is very similar to the wellcharacterized piroplasm Babesia microti; phylogenetic analysis, however, placed WA1 in a clade separate from B. microti and other Babesia species. Based on these findings, the recommended taxonomic designation for WA1 is Babesia duncani (1). Like other piroplasms, WA1 is transmitted to humans via a tick bite, but the animal reservoir has not been identified (8).An additional 8 cases of WA1 infection have been described in the medical literature (4, 9, 13), all in males residing in Washington or California; two of these cases reflected transmission by transfusion of infected blood products from an asymptomatic donor. In serologic investigations, titers of WA1 IgG were markedly elevated (Ն1:5,120) in convalescent-phase sera from all patients and in sera from the asymptomatic blood donors implicated in transfusion-transmitted cases (4, 9, 13). Consistent with the phylogenetic data, antibodies induced by WA1 infection did not cross-react with B. microti. Small seroprevalence studies conducted in California and Washington yielded wide variation in WA1 IgG detection rates, ranging from 1% to 20% (2,4,13,15).In response to the documented emergence of WA1 as a disease-causing agent, in 1997 our laboratory (Focus Diagnostics, Inc., Cypress, C...