Transfusion Service
Timothy Pancioli, DO (he/him/his)
Versiti Blood Center Michigan
Grand Rapids, Michigan, United States
Anaplasma phagocytophilium is a gram-negative, intracellular bacterium transmitted by bite primarily from the Ixodes scapularis tick. In humans, this causes human granulocytic anaplasmosis. To date, there are no case reports of a plasma product being implicated in transmission of anaplasma. Here we present a potential case of TT-HGA where one unit of fresh frozen plasma (FFP) is implicated.
A 67 year-old woman was diagnosed with thrombotic thrombocytopenia purpura (TTP) and admitted for therapeutic plasma exchange (TPE). One month into her hospital course, unclassified neutrophil inclusions were noted on peripheral smear (Figure A). A PCR-based tick-borne DNA panel was ordered and resulted as positive for Anaplasma phagocytophilum. The patient was promptly treated with doxycycline. Peripheral blood smears from earlier in her admission were reviewed and confirmed no presence of the inclusions. The patient denied history of tick bites or lifestyle risk factors. During TPE treatment, she was transfused with 199 blood products between 7/28 and 8/30, only one of which was a red blood cell unit, with the remaining being plasma products from 198 individual donors.
Study
Design/Methods:
The donor of the red cell unit was contacted and tested negative by anti-anaplasma IgG/IgM upon follow-up. With no clear source of infection, letters were drafted and sent to the donors of the FFP units to screen for history of recent tick bites or environmental risk.
Results/Findings: 87 of the plasma donors responded to the inquiry. 8 donors reported exposure risk, with 7/8 testing negative for anti-anaplasma IgG/IgM. One donor reported having been bitten by a tick and saw his primary care physician after becoming ill. Lyme disease testing was performed on 7/14 which was negative, and no antibiotic treatment was received. The donor’s illness was self-limited and he donated approximately 3.5 weeks later on 8/8, feeling fine at time of donation. The implicated FFP unit was transfused on 8/19 with few intracellular anaplasma inclusions noted in the patient’s peripheral smear 6 days later (8/25). The following day, the inclusions were noted as numerous. Months later at time of testing, the donor’s anti-anaplasma IgG and IgM were positive with titers of 1:512 and 1:20, respectively. This result was interpreted as “recent/current infection” by the laboratory.
Conclusions: Our case appears to be the first to demonstrate potential transfusion-transmitted HGA through transfusion of FFP. Our workup is not without its shortcomings, however. No additional untransfused units from the donor were available for confirmation of anaplasma. The window for collecting a PCR positive sample from the donor had also passed by the time of follow-up. Given the timeline of events, positive donor serology, and lack of patient risk factors, transmission of anaplasma through transfusion of FFP remains the most likely scenario.