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Bloodstream infections in patients with chronic lymphocytic leukemia: a longitudinal single-center study.

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Authors
Kjellander, Christian
Björkholm, Magnus
Källman, Owe
Giske, Christian G
Weibull, Caroline E
Löve, Thorvardur J
Landgren, Ola
Kristinsson, Sigurdur Y
Issue Date
2016-05

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Citation
Bloodstream infections in patients with chronic lymphocytic leukemia: a longitudinal single-center study. 2016, 95 (6):871-9 Ann. Hematol.
Abstract
Infectious complications in chronic lymphocytic leukemia (CLL) represent a major cause of morbidity and mortality. The aim of the study was to investigate temporal trends in bloodstream infections (BSIs) among patients with CLL. Individuals with blood cultures were linked to Swedish Cancer Registry and divided into three time periods (1988-1993, 1994-1999, and 2000-2006) according to year of CLL diagnosis. CLL patients (n = 275) with 1092 blood culture episodes were identified and linked to the nationwide Cause of Death Registry and Swedish Patient Registry (to retrieve information on splenectomies). The most common causes of BSI among CLL patients were Escherichia coli (11/43, 15/78, and 9/33), Streptococcus pneumoniae (7/43, 13/78, and 6/33), Pseudomonas aeruginosa (2/43, 8/78, and 3/33), Staphylococcus aureus (1/43, 6/78, and 6/33), and Viridans streptococci (5/43, 6/78, and 2/33). Coagulase-negative staphylococci was the most frequent microorganism found in blood cultures (22/70, 23/106, and 5/41, respectively) but is a frequent contaminant. Based on the largest study to date on BSI in CLL patients, we found a stable proportion of Gram-positive to Gram-negative bacteria and no temporal change of distribution was observed for BSIs 1988-2006.
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http://dx.doi.org/ 10.1007/s00277-016-2643-9
http://download.springer.com/static/pdf/72/art%253A10.1007%252Fs00277-016-2643-9.pdf?originUrl=http%3A%2F%2Flink.springer.com%2Farticle%2F10.1007%2Fs00277-016-2643-9&token2=exp=1465833314~acl=%2Fstatic%2Fpdf%2F72%2Fart%25253A10.1007%25252Fs00277-016-2643-9.pdf%3ForiginUrl%3Dhttp%253A%252F%252Flink.springer.com%252Farticle%252F10.1007%252Fs00277-016-2643-9*~hmac=41477ad39ffee9cae643b3506b0782478072593d871ce22b22f898921a03fa1b
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Archived with thanks to Annals of hematology
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10.1007/s00277-016-2643-9
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