Sepsis associated with transfusion of red cells contaminated with Yersinia enterocolitica.

Between April 1987 and May 1989, the Centers for Disease Control investigated seven cases of transfusion-associated Yersinia enterocolitica sepsis; four were caused by organisms of serotype O:3, and one each was caused by organisms of serotype O:1,2,3; O:5,27; and O:20. All seven recipients developed septic shock after receiving units of red cells (RBCs) contaminated with Y. enterocolitica; five recipients died. The cases occurred in seven states and were unrelated. There was no evidence for contamination of the RBC units during processing. Six of the seven donors had serologic evidence of recent Y. enterocolitica infection, and it is hypothesized that these donors had asymptomatic bacteremia when they donated the implicated blood. Four of the seven donors reported gastrointestinal illness in the 4 weeks before blood donation, and one donor became ill on the day he donated blood. Y. enterocolitica grows well at 4 degrees C and in the presence of dextrose and iron. If blood is contaminated at the time of collection, storage of the RBCs at 4 degrees C provides an ideal environment for bacterial growth and endotoxin production. These cases demonstrate the need for careful evaluation of patients with transfusion reactions for possible sepsis and suggest a need to screen prospective blood donors for mild gastrointestinal illness, including those illnesses not requiring physician evaluation or medication.

The clinical significance of anti-H in an individual with the Oh (Bombay) phenotype.

To evaluate the clinical significance of anti-H present in individuals with the Oh (Bombay) phenotype, red blood cell 51chromium survival studies and related serological tests were undertaken in an Oh (Bombay) individual. A small sample of group O donor red blood cells was labeled with 51chromium and infused into the patient. The T 1/2 of the infused cells was six minutes, with two percent of the cells surviving at 24 hours. A similar study using the patient's own labeled red blood cells demonstrated 100 per cent survival at 24 hours. Initial laboratory studies indicated that the anti-H was active in saline at 4, 22 and 37 C and by the indirect antiglobulin test. Analysis of the antibody in both preand posttransfusion specimens showed it to have both IgM and IgG components. The anti-H titer at 37 C rose from 1:4 prior to the infusion of the O cells to 1:32 one week postinfusion, and a partial hemolysin appeared. Saliva inhibition studies demonstrated that the antibody was neutralizable prior to the group O exposure but was not neutralizable one week post exposure. We conclude that the anti-H present in this individual rapidly destroyed infused group O red blood cells. Individuals with the Oh (Bombay) phenotype should be transfused only with Oh (Bombay) blood.