BACKGROUND: Bacterial contamination of platelet (PLT) products occurs at low concentrations requiring a period of incubation for growth to minimize sampling error. Culture‐based detection methods also need sufficient incubation time; together these periods may limit the useful life of PLTs. This study characterizes the impact of sampling and detection times with two commercially available bacteria detection products.
STUDY DESIGN AND METHODS: Apheresis PLTs inoculated with nine bacterial species at low concentrations were sampled immediately and 24 hours after inoculation. Test results were analyzed after incubation at 16, 20, and 24 hours after sampling with two bacterial detection systems.
RESULTS: When sampled immediately after inoculation, two commercially available bacterial detection systems (BacT/ALERT, bioMérieux; and eBDS, Pall Corp.) failed to detect some PLTs inoculated with Staphylococcus epidermidis, Serratia liquefaciens, or Pseudomonas aeruginosa and S. epidermidis, S. liquefaciens, Bacillus cereus, or P. aeruginosa, respectively. The BacT/ALERT was better at 20 hours (p < 0.02), but not at 16 or 24 hours for Time 0 sampling. When sampling occurred 24 hours after inoculation, there were no difference between the two systems.
CONCLUSION: Results suggest that for either bacteria detection system, holding PLTs for 24 hours before sampling improves the detection sensitivity for PLTs contaminated with low concentrations of bacteria, and longer incubation periods improve detection.
Neonatal alloimmune thrombocytopenia (NAIT) is a rare but clinically important etiology of intracranial hemorrhage. There have been no reported cases of intracranial hemorrhage caused by anti-group A or anti-group B antibodies. A Japanese boy weighing 1550 g was born at 37 weeks. He suffered from refractory thrombocytopenia and developed severe intracranial hemorrhage on his second day. Despite repeated platelet, red-cell and fresh-frozen-plasma transfusions, he died at day 10 of life. Serological studies and genotyping of the patient and his parents were performed. There were no incompatible genotypes of platelet antigens between the patient and the mother. Serological studies revealed that the mother had extremely high-titer anti-group A immunoglobulin G(2) (4096-fold) that reacted strongly with the father's platelets. The reaction against the father's platelets disappeared when her serum was adsorbed with group A red blood cells. Maternal anti-group A antibody was associated with NAIT and severe bilateral intracranial hemorrhage.
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