Context The risk of acquiring babesiosis by blood transfusion is largely unknown since in areas where it is endemic it is often an asymptomatic infection. Objective To investigate and treat a cluster of blood transfusion-associated babesiosis cases. Design Case series and epidemiologic investigation. Setting Urban inner-city hospital. Patients Six persons who received Babesia microti-infected blood components from a donor. Main Outcome Measure Diagnosis and successful therapy of babesiosis following transfusion. Results Six individuals (1 adult, 1 child, and 4 neonates) were exposed to products from a single blood donation by an asymptomatic Babesia-infected donor. Three of the 6 exposed patients became parasitemic. Polymerase chain reaction testing, animal inoculation studies, and indirect immunofluorescent antibody testing were used to confirm the presence of Babesia microti in the donor's blood and to establish the presence of infection in 3 of the 6 recipients. The 3 infected recipients and 1 additional recipient were treated without incident. Conclusion Physicians should consider babesiosis in the differential diagnosis of a febrile hemolytic disorder after blood transfusion. Prompt diagnosis is important since babesiosis is responsive to antibiotic therapy and, untreated, can be a fatal disease in certain risk groups.

Thiolation-mediated PEGylation of RBCs with Mal-Phe-PEG-5000 and Mal-Phe-PEG-20000 converts Group A Rh(D)+ and B Rh(D)+ RBCs into RBCs with serologic behavior comparable to Group O Rh(D)- RBCs that are considered as universal RBCs for transfusion.

Plasmapheresis (PP) and intravenous immunoglobulin (IVIg) remove donor-specific antibodies, a cause of acute humoral rejection (AHR). We describe the use of PP and IVIg as rescue therapy for AHR. The records of 143 renal transplants performed between October 1, 2000 and April 1, 2002 were reviewed. Patients who underwent PP and IVIg therapy for AHR were identified. The data reviewed included age, sex, source of transplant, number of human leukocyte antigen mismatches, transplant number, number of PP and IVIg treatments, dose of IVIg, time of AHR, serum creatinine (SCr) level at AHR, SCr level after PP and IVIg at 3 months, days to achieve 30% decline in SCr, and graft survival. Immunosuppression included basiliximab induction, tacrolimus, and prednisone (+/- sirolimus or mycophenolate mofetil [CellCept, Roche Pharmaceutical, Nutley, NJ]). PP was followed by IVIg infusion. Nine patients were treated for AHR with PP and IVIg. All nine patients demonstrated biopsy-proven AHR. One graft was lost. Mean 3-month and 1-year SCr levels were 1.9 and 1.8, respectively, in the remaining eight patients. AHR in renal transplantation can be effectively treated with PP and IVIg.

Patients with AIDS may not form alloantibodies to the D antigen. This may be attributable to their immunodepressed state, particularly to the decrease in CD4+ T lymphocytes. Therefore, during blood shortages, transfusion of D+ blood to D- AIDS patients may be without any subsequent consequence.