No abstract

Epidemiological, microbiological and clinical characteristics of 14 episodes of Xanthomonas maltophilia bacteremia in 12 seriously immunocompromised hematological patients, admitted to Rigshospitalet in Copenhagen over the 3-year period 1989-91, were evaluated. The results were compared with a randomly selected control group of 25 patients with Escherichia coli bacteremia. Hospital acquired bacteremia was more common among the patients with X. maltophilia bacteremia (p < 0.01). Treatment with broad-spectrum antibiotics before the bacteremic episode was markedly more common among the patients with X. maltophilia bacteremia (p < 0.001). The presence of a central venous catheter and previous treatment with corticosteroids were more frequent in patients with X. maltophilia bacteremia (p < 0.05). The X. maltophilia blood culture isolates were generally resistant to aminoglycosides and most beta-lactams. The mortality rates related to bacteremia caused by X. maltophilia and E. coli were 14% and 20%, respectively.

Chronic lymphocytic leukemia (CLL) and other B-cell lymphoproliferative disorders (LPDs) show clear evidence of familial aggregation, but the inherited basis is largely unknown. To identify a susceptibility gene for CLL, we conducted a genomewide linkage analysis of 115 pedigrees, using a high-density single-nucleotide polymorphism (SNP) array containing 11,560 markers. Multipoint linkage analyses were undertaken using both nonparametric (model-free) and parametric (model-based) methods. Our results confirm that the presence of high linkage disequilibrium (LD) between SNP markers can lead to inflated nonparametric linkage (NPL) and LOD scores. After the removal of high-LD SNPs, we obtained a maximum NPL of 3.14 (P=.0008) on chromosome 11p11. The same genomic position also yielded the highest multipoint heterogeneity LOD (HLOD) score under both dominant (HLOD 1.95) and recessive (HLOD 2.78) models. In addition, four other chromosomal positions (5q22-23, 6p22, 10q25, and 14q32) displayed HLOD scores >1.15 (which corresponds to a nominal P value <.01). None of the regions coincided with areas of common chromosomal abnormalities frequently observed for CLL. These findings strengthen the argument for an inherited predisposition to CLL and related B-cell LPDs.