Infections caused by Nocardia species have been infrequently described in bone marrow transplant (BMT) recipients. We reviewed six cases of nocardiosis occurring in our population of BMT recipients and the four cases previously reported in the literature. The rate of nocardial infection at our institution was 0.2% (1 of 554) among autologous BMT recipients and 1.7% (5 of 302) among allogeneic BMT recipients (odds ratio, 9.3 [95% confidence interval, 1.1-80.1]; P = .046). All 10 patients had received immunosuppressive medications, and all but one allogeneic BMT recipient had acute or chronic graft-vs.-host disease (GVHD). Four patients had extensive exposure to soil or dust before nocardiosis developed. Seventy percent of the patients died, but death was less often due to progressive nocardial infection than to complications of GVHD and associated invasive infection with Aspergillus species. Three patients had nocardiosis despite receiving prophylaxis with trimethoprim-sulfamethoxazole (TMP-SMZ) on an intermittent basis two or three times a week. These data show that nocardial infection is an important if infrequent complication of bone marrow transplantation and is associated with a high rate of invasive fungal infection. TMP-SMZ prophylaxis given intermittently does not reliably protect against infection.
We performed a retrospective serologic survey of 583 organ donors and 1043 transplant recipients for antibodies to human immunodeficiency virus type 1 (HIV-1). Two (0.34%) of the 583 donors and 18 (1.7%) of the 1043 recipients had HIV-1 antibodies by enzyme immunoassay and by Western blot. Two of 5 seropositive recipients tested also had blood cultures positive for HIV-1. Seven (0.7%) of the 1043 transplant recipients had antibodies to HIV-1 before transplantation; 2 of these had hemophilia A, and 5 had previous transfusions. Eleven (1.3%) of 860 recipients followed for 45 days or more seroconverted to HIV-1 a mean of 96 days after transplantation. Likely sources of HIV-1 infection for 3 of these 11 recipients included a seropositive organ donor in 1 patient and high-risk blood donors in 2 patients. A definite source of HIV-1 infection was not found for the other 8 recipients, 3 of whom seroconverted to HIV-1 after institution of blood donor screening for HIV-1 antibodies. Seroconversion to HIV-1 was less common in kidney recipients than in liver, heart, or multiple-organ recipients (P less than 0.02). Nine (50%) of the 18 HIV-1 seropositive transplant recipients died a mean of 6 months after transplant surgery, and 9 (50%) are still alive a mean of 43 months after transplantation. AIDS-like illnesses occurred in 3 of the dead and 1 of the living patients and included pneumocystis pneumonia (3 cases), miliary tuberculosis (1 case), and recurrent cytomegalovirus infection (1 case). These data suggest that the course of HIV-1 infection is not more severe in transplant recipients receiving cyclosporine than in other hosts and that, despite screening of blood and organ donors, a small number of transplant recipients will become infected with HIV-1.
Disseminated infection with herpes simplex virus type 2 was identified in two patients 20 days after they had received kidney transplants from the same organ donor. Neither patient had neutralizing antibody to herpes simplex virus before transplantation, and both had herpes simplex virus isolated from surveillance cultures of urine before the onset of clinical symptoms. A clear focus of primary infection was not found in either patient. Analysis of the patients' isolates by DNA restriction endonuclease analysis strongly suggested that the strains were identical. These data implicate the allografts as the source of the viral infection.
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