180. Klebsiella pneumoniae and K. oxytoca Bacteremia: Differences in Host, Source, and Antibiotic Susceptibility.

Background Klebsiella species (KS) bloodstream infection (BSI) is often caused by K. pneumoniae (KP). K. oxytoca (KO) is emerging and implicated in antibiotic-associated right-sided colitis. We compared the clinical and microbiological characteristics of KP and KO. Methods We reviewed blood culture (BC) results (January 1, 2010–December 31, 2017), selected patients with KS in ≥1 BC, reviewed their medical records, abstracted patient demographics, source of bacteremia, antibiotics susceptibility, and outcome. Each patient was counted once. We compared KP and KO cases. All differences were assessed by the chi-square test and regression analysis, using SPSS. Results We encountered KS in 975/14,256 (6.8%) positive BC, representing 611 BSI including 537 KP-BSI (484 patients) and 55 KO-BSI cases (54 patients); each patient was counted once. Mean age and prevalence of diabetes and most comorbidities were similar but KO was less frequent in African Americans (40.7% vs. KP [61.3%]; P = 0.005) and in patients with neurological debility (Stroke, paraplegia, multiple sclerosis; 11.1% vs. KP [24.8%]; P = 0.03). KO BSI was more frequent in IVC BSI and was absent in pneumonia-associated BSI (table). Antibiotic resistance was rare among KO isolates except for cefazolin-intermediate susceptibility (42.6% vs. 1.7%; P < 0.001). CREs were limited to KP. Logistic regression analysis confirmed KO link to IVC (OR = 3.57; 95% CI: 1.89, 6.76; P < 0.001) and Caucasian race (OR = 2.46; CI: 1.37, 4.42; P = 0.003). Mortality rate was comparable (28.1% [KP] vs. 35.2% [KO]; P = 0.3). Source and antibiotic susceptibility (%) in K. pneumoniae and K. oxytoca bacteremia   K. pneumoniae   K. oxytoca   P   Source        IVC  12.8  33.3  <0.001  UTI  34.9  24.1  0.1  Soft/tissue bone  8.7  11.1  0.6  Abdomen  21.3  14.8  0.4  Pneumonia  8.3  0  0.03  Antibiotics resistance  Cefazolin  28.6  20.4  0.1  Ceftriaxone  25.2  5.6  0.001  Ciprofloxacin  25.6  1.9  <0.001  Gentamicin  18.2  1.9  0.001  TMP/SMX  25.4  1.9  <0.001  ESBL 25.6  3.7  <0.001    CRE  4.7  0  0.1    K. pneumoniae   K. oxytoca   P   Source        IVC  12.8  33.3  <0.001  UTI  34.9  24.1  0.1  Soft/tissue bone  8.7  11.1  0.6  Abdomen  21.3  14.8  0.4  Pneumonia  8.3  0  0.03  Antibiotics resistance  Cefazolin  28.6  20.4  0.1  Ceftriaxone  25.2  5.6  0.001  Ciprofloxacin  25.6  1.9  <0.001  Gentamicin  18.2  1.9  0.001  TMP/SMX  25.4  1.9  <0.001  ESBL 25.6  3.7  <0.001    CRE  4.7  0  0.1    K. pneumoniae   K. oxytoca   P   Source        IVC  12.8  33.3  <0.001  UTI  34.9  24.1  0.1  Soft/tissue bone  8.7  11.1  0.6  Abdomen  21.3  14.8  0.4  Pneumonia  8.3  0  0.03  Antibiotics resistance  Cefazolin  28.6  20.4  0.1  Ceftriaxone  25.2  5.6  0.001  Ciprofloxacin  25.6  1.9  <0.001  Gentamicin  18.2  1.9  0.001  TMP/SMX  25.4  1.9  <0.001  ESBL 25.6  3.7  <0.001    CRE  4.7  0  0.1    K. pneumoniae   K. oxytoca   P   Source        IVC  12.8  33.3  <0.001  UTI  34.9  24.1  0.1  Soft/tissue bone  8.7  11.1  0.6  Abdomen  21.3  14.8  0.4  Pneumonia  8.3  0  0.03  Antibiotics resistance  Cefazolin  28.6  20.4  0.1  Ceftriaxone  25.2  5.6  0.001  Ciprofloxacin  25.6  1.9  <0.001  Gentamicin  18.2  1.9  0.001  TMP/SMX  25.4  1.9  <0.001  ESBL 25.6  3.7  <0.001    CRE  4.7  0  0.1  Conclusion KO and KP BSI differ in the type of host and source, suggesting different colonization dynamics. KO remains antibiotic-susceptible but might be cefazolin less susceptible. Prospective studies are needed to confirm differential cephalosporin susceptibility and delineate host–pathogen interactions. Disclosures All authors: No reported disclosures. [ABSTRACT FROM AUTHOR]