Increased frequency of false-positive bacterial detection after implementation of new guidelines for large-volume delayed sampling of platelets.

BACKGROUND: The updated guidance for improving bacterial detection (BD) of platelets has included the implementation of large-volume delayed sampling (LVDS) with the addition of anaerobic culture bottles (BPNs) and sampling of each platelet split product. METHODS: The frequency of BD was reviewed during this LVDS time period in comparison with pre-LVDS and the Post-Approval Surveillance Study of Platelet Outcomes, Release Tested (PASSPORT) study (when BPNs were last used). RESULTS: There was more than a twofold increase in bottles inoculated per collection during LVDS, with an almost fivefold increase in sample volume collected. During LVDS, the concordance of split products within an initial reactive collection was only 8.7%. There was no difference in LVDS aerobic culture bottle (BPA) true positives (TPs), but there was a significant increase in LVDS false positives (FPs), p < .0001, compared to both PASSPORT and pre-LVDS, respectively. There was an increase in BPN TPs during LVDS (p < .05 compared to PASSPORT), with predominance of Cutibacter acnes (C. acnes), noted exclusively in BPN, and accounting for more than two-fifths of all organisms detected. Time to alarm during LVDS for TPs had two peaks with one due to C. acnes at 96 h compared to 17 h for non-C. acnes. DISCUSSION: The high FP frequency, along with low clinical significance of TPs found in BPNs, has led to the needless discard of inventory, as the utility of BPNs in BD for platelets is yet to be established and may require much larger studies.

Altered parasite life-cycle processes characterize Babesia divergens infection in human sickle cell anemia.

Babesia divergens is an intra-erythrocytic parasite that causes malaria-like symptoms in infected people. As the erythrocyte provides the parasite with the infra-structure to grow and multiply, any perturbation to the cell should impact parasite viability. Support for this comes from the multitude of studies that have shown that the sickle trait has in fact been selected because of the protection it provides against a related Apicomplexan parasite, Plasmodium, that causes malaria. In this paper, we examine the impact of both the sickle cell anemia and sickle trait red blood cell (RBC) environment on different aspects of the B. divergens life-cycle, and reveal that multiple aspects of parasite biological processes are altered in the mutant sickle anemia RBC. Such processes include parasite population progression, caused potentially by defective merozoite infectivity and/or defective egress from the sickle cell, resulting in severely lowered parasitemia in these cells with sickle cell anemia. In contrast, the sickle trait RBC provide a supportive environment permitting in vitro infection rates comparable to those of wild-type RBC. The elucidation of these naturally occurring RBC resistance mechanisms is needed to shed light on host-parasite interaction, lend evolutionary insights into these related blood-borne parasites, and to provide new insights into the development of therapies against this disease.