Streptococcus pneumoniae septicaemia associated with red cell transfusion
Abstract number: P1707
Polizzotto M., Borosak M., Neo H., Spelman D., Shortt J., Wong P., Wood E., Cole-Sinclair M.
Background: Bacterial contamination of blood components remains an important residual infective risk of transfusion. We report a case of red cell (RC) transfusion-transmitted bacterial infection (TTBI) caused by Streptococcus pneumoniae. This fragile non-commensal organism has not to our knowledge previously been implicated as a cause of RC TTBI.
Case and Investigation: The transfusion recipient was a 79 year old man with a myelodysplastic syndrome pancytopenia, with no history of splenectomy. Forty minutes after commencement of a RC transfusion he became febrile to 39.6°C, hypotensive and hypoxic. Transfusion was ceased, and empiric therapy with intravenous antibiotics instituted with good clinical effect.
Cultures performed on recipient samples and the RC each demonstrated heavy growth of Gram-positive alpha-haemolytic diplococci characteristic of S. pneumoniae, confirmed by automated identification and susceptibility testing. The organisms from unit and recipient were serotype four.
The implicated RC unit had been collected ten days before transfusion. Venesection and processing had been uncomplicated. The donor was a 53 year old man, with no history of splenectomy or respiratory tract infection, who had not been vaccinated against S. pneumoniae. He had donated on numerous occasions prior to the index donation without complication. There had been no infective symptoms near the time of donation. Cultures of blood and of swabs obtained from nose, throat and both antecubital fossae were negative, as was urinary testing for pneumococcal antigen.
The ability of S. pneumoniae to survive in the refrigerated conditions of RC storage was explored. An expired RC unit was inoculated with 1×103 organisms of S. pneumoniae derived from the original cultures. The RC unit was maintained at 4°C for ten days, following which samples were cultured and again demonstrated abundant growth of S. pneumoniae.
Conclusions: This case demonstrates that even organisms which are neither commensal nor psychrophilic may cause TTBI. The source of contamination could not be established definitively, but may have originated from transient donor bacteraemia. Even in retrospect no symptoms which might have led to donor deferral were identifiable. Prompt recognition of the source of sepsis enabled institution of appropriate therapy and liaison with the blood service to enable immediate recall of associated components.
|Session name:||18th European Congress of Clinical Microbiology and Infectious Diseases|
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