Staphylococcus aureus-contaminated apheresis platelets traced to donors' nasal carriage We report... more Staphylococcus aureus-contaminated apheresis platelets traced to donors' nasal carriage We report two cases of Staphylococcus aureus-contaminated apheresis platelets (PLTs) for which we used microbiologic and molecular methods to trace the source of contamination to the PLT donors' nasal carriage. In Case 1, the recipient developed chills 5 minutes and 20 mL after the transfusion had been initiated. The transfusion was discontinued, but within 2 hours, the patient developed septic shock and a temperature of 40.0°C. The patient responded to ciprofloxacin and amikacin, and 12 hours later, the temperature was 37.1°C. In Case 2, bacterial contamination of the unit of apheresis PLTs was detected during the transfusion service's routine prerelease visual swirl test. This unit of PLTs had been released for transfusion on the previous day, when no bacterial growth had been detected by the swirl method, but the transfusion was postponed. When the swirl test was repeated on the following day, contamination was detected. Both PLT donors were contacted to investigate possible sources of bacterial contamination. Neither donor had signs or symptoms of a bacterial infection. Within 10 days of the apheresis procedures, venous blood, as well as nasal and antecubital fossa swabs, were obtained and cultured. Samples were also collected from the two nurses who collected the apheresis units. We recovered S. aureus from nasal swabs from both donors and from one of the nurses. We genotyped the isolates using pulsed-field gel electrophoresis (PFGE; CHEF DRIII, Bio-Rad, Ivry sur Seine, France) with SmaI as a restriction enzyme. S. aureus isolated from Donor 1's nose, from the PLT concentrate, and from the recipient's blood had a similar PFGE pattern (Fig. 1). S. aureus isolated from Donor 2's nose and the PLT concentrate were identical and were different from the isolate from the nurse's nose (Fig. 1). Both strains were susceptible to methicillin, fluoroquinolones, and aminoglycosides, but were penicillin resistant. Molecular characterization of both strains by polymerase chain reaction 1 revealed that Strain 1 contained genes encoding toxic shock syndrome toxin (TSST-1; tst) and enterotoxins M (sem) and O (seo). Strain 2 was positive for the presence of enterotoxin genes C (s) and L (sel). Both strains did not produce Penton-Valentine leukocidin. Perpoint and coworkers 2 reported two fatalities attributed to transfusion of PLT concentrates contaminated by S. aureus-producing superantigen toxins. In one of these cases, the donor was an asymptomatic S. aureus nasal carrier. The authors also showed that the bacteria isolated from the patient's blood and the residual PLT concentrate were identical to the donor's nasal isolate. It is not
Staphylococcus aureus-contaminated apheresis platelets traced to donors' nasal carriage We report... more Staphylococcus aureus-contaminated apheresis platelets traced to donors' nasal carriage We report two cases of Staphylococcus aureus-contaminated apheresis platelets (PLTs) for which we used microbiologic and molecular methods to trace the source of contamination to the PLT donors' nasal carriage. In Case 1, the recipient developed chills 5 minutes and 20 mL after the transfusion had been initiated. The transfusion was discontinued, but within 2 hours, the patient developed septic shock and a temperature of 40.0°C. The patient responded to ciprofloxacin and amikacin, and 12 hours later, the temperature was 37.1°C. In Case 2, bacterial contamination of the unit of apheresis PLTs was detected during the transfusion service's routine prerelease visual swirl test. This unit of PLTs had been released for transfusion on the previous day, when no bacterial growth had been detected by the swirl method, but the transfusion was postponed. When the swirl test was repeated on the following day, contamination was detected. Both PLT donors were contacted to investigate possible sources of bacterial contamination. Neither donor had signs or symptoms of a bacterial infection. Within 10 days of the apheresis procedures, venous blood, as well as nasal and antecubital fossa swabs, were obtained and cultured. Samples were also collected from the two nurses who collected the apheresis units. We recovered S. aureus from nasal swabs from both donors and from one of the nurses. We genotyped the isolates using pulsed-field gel electrophoresis (PFGE; CHEF DRIII, Bio-Rad, Ivry sur Seine, France) with SmaI as a restriction enzyme. S. aureus isolated from Donor 1's nose, from the PLT concentrate, and from the recipient's blood had a similar PFGE pattern (Fig. 1). S. aureus isolated from Donor 2's nose and the PLT concentrate were identical and were different from the isolate from the nurse's nose (Fig. 1). Both strains were susceptible to methicillin, fluoroquinolones, and aminoglycosides, but were penicillin resistant. Molecular characterization of both strains by polymerase chain reaction 1 revealed that Strain 1 contained genes encoding toxic shock syndrome toxin (TSST-1; tst) and enterotoxins M (sem) and O (seo). Strain 2 was positive for the presence of enterotoxin genes C (s) and L (sel). Both strains did not produce Penton-Valentine leukocidin. Perpoint and coworkers 2 reported two fatalities attributed to transfusion of PLT concentrates contaminated by S. aureus-producing superantigen toxins. In one of these cases, the donor was an asymptomatic S. aureus nasal carrier. The authors also showed that the bacteria isolated from the patient's blood and the residual PLT concentrate were identical to the donor's nasal isolate. It is not
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