Rhode Island Blood Center

Across Canada, Indigenous identity data is not routinely collected in healthcare settings. This paper focuses on [province] and whether the largest and only province-wide healthcare services organization in Canada, [healthcare organization name] should implement an Indigenous identifier in their new electronic medical record system. Due to the current absence of an Indigenous identifier, it is difficult to identify Indigenous peoples in administrative healthcare data to guide healthcare decision-making specifically for Indigenous peoples and to assist with population-specific disease surveillance and prevention programs. Moreover, it is often challenging for Indigenous nations, communities, and organizations to access this data. The data that does exist in [province] frequently excludes large segments of the Indigenous population. Indigenous researchers globally have called for improved health data in alignment with Indigenous research principles, data governance and sovereignty. This paper reports on an exploratory study of potential avenues to enhance availability of Indigenous specific health data in [province]. Of interest are possible supports, concerns, and potential barriers for the introduction of a policy to collect self-disclosed Indigenous identity data in the [org] new electronic medical record system. This research included interviews and focus group sessions with diverse subject matter experts including academics, Indigenous health practitioners and healthcare administrators. The project was embedded in the [removed] which is an [province] based research network for improving primary health with and for Indigenous peoples

Human granulocytic anaplasmosis (HGA) is a tick-borne rickettsial infectious disease. To date four cases of transfusion-transmitted anaplasmosis (TTA) have been described in the literature, and only one from leukoreduced red blood cells (RBCs). A 64-year-old patient with acute gastrointestinal blood loss was admitted to the hospital and received 5 units of prestorage leukoreduced RBCs. He was stabilized and discharged. He developed headache, fever, and chills 2 days after discharge and was readmitted. On Day 5 of his second admission polymorphonuclear leukocytes containing morulae consistent with HGA were reported in the peripheral smear. Samples from the recipient tested positive by polymerase chain reaction (PCR) for Anaplasma phagocytophilum, the causative agent of HGA and a segment from one of the five donors tested positive by both serology and PCR. Leukoreduction theoretically reduces the risk of TTA but does not interdict all infections. TTA requires consideration in recipients of RBC transfusion with unexplained fever.

Babesiosis is the most common transfusion-transmitted infection reported to the Food and Drug Administration (FDA). We developed and implemented the first laboratory-based blood donor screening program for Babesia microti to help reduce and prevent transfusion-transmitted babesiosis (TTB) and report results for the initial year. Selective B. microti donor screening was performed using real-time polymerase chain reaction (PCR) and indirect immunofluorescence assay (IFA) to reduce the incidence of TTB in neonates and pediatric sickle cell and thalassemia patients under an FDA-approved investigational new drug application. We compared the reports of TTB in these patients in the first 12 months of the study with those of patients who received unscreened blood from 2005 to 2010. There were 2113 units tested with 2086 negative results, 26 positive IFA results (1.23%), and one indeterminate PCR result (0.05%). No reported case of TTB occurred with any B. microti-screened unit transfused to the targeted patients (0/787 units) or to any patient who received the screened units (0/2086 units). Before screening, there were seven cases of TTB in neonates, sickle cell, and thalassemia patients from 6500 unscreened units (one case/929 units) and 24 cases in the total transfused population from 496,545 units distributed (one case/20,686 units). Implementation of B. microti IFA and PCR screening is compatible with blood center operations to provide tested units. While the results after 1 year are not powered to demonstrate a change in the rate of TTB after testing, they are encouraging.

The detection of anti-D in a D-positive renal transplant recipient is unusual and may arise by several potential mechanisms. These include passive transfer of alloantibody and the presence of autoanti-D or alloanti-D that is due to microchimerism when the allograft is from a D-negative donor. In the latter case, overt hemolysis has been seen or suspected. The occurrence of anti-D in a D-positive renal transplant recipient without hemolysis, which is most likely attributable to microchimerism, is reported. A 51-year-old group O, D-positive woman, who was serologically HLA type A1, A2; B8, B44; DR3, DR6, DR52; DQ1, DQ2, underwent the transplantation of a kidney from a cadaveric donor who was serologically HLA type A1, A2; B8, B44; DR13, DR17, DR52; DQ1, DQ2. The donor was known to be D-negative and immunized to D. No blood components or derivatives were administered at the time of organ graft. Ten weeks after the transplant, the direct antiglobulin test was positive in the recipient, and anti-D was eluted. Polymerase chain reaction amplification using primers to distinguish DR13 (donor) from DR14 alleles (recipient split of DR6) in the peripheral blood showed the recipient to be DR14. No DR13 could be detected, and thus microchimerism could not be confirmed. However, in the peripheral blood, GM and KM allotyping of the serum (GM A,F,X B,G and KM 1,3) and eluate (G1M F, KM 3) showed a pattern of allotypes most consistent with an alloantibody. Eleven months after transplantation, the graft continued to function; the direct antiglobulin test was still positive, and elution of anti-D persisted. This case of anti-D in a D-positive renal transplant recipient is attributed to microchimerism, despite the lack of confirmation by genotypic analysis of the peripheral blood. It raises the possibility that microchimerism may be a more common phenomenon in solid allograft recipients than is realized.