Procalcitonin levels predict to identify bacterial strains in blood cultures of septic patients.

BACKGROUND: We examined whether the values obtained from principal component analysis (PCA) on laboratory tests can be used to predict bacterial infections and identify bacterial strains in blood culture (BC). METHOD: This study is a single-center retrospective analysis of 315 patients suspected of having sepsis. We applied PCA on procalcitonin (PCT) and laboratory test biomarkers, namely, platelet (PLT), white blood cell, and C-reactive protein (CRP) as well as BC. RESULTS: Principal component analysis showed that PCT, CRP, and PLT contributions to component 1 were associated with bacterial infection. The number of patients who had BC-negative results, gram-positive cocci (GPC), and gram-negative rods (GNRs) were 124, 28, and 19, respectively. The mean value of component 1 in GNR-positive patients was 1.58±1.41 and was significantly higher than that in GPC-positive patients (0.28±0.87; P<.0001). Furthermore, the mean values of component 1 in both GNR- and GPC-positive patients were significantly higher than that in BC-negative patients (-0.31±0.65; P<.0001 and P<.002, respectively). One certain range showing higher value more than 2.00 for component 1 and -1.00 for component 2 only included GNR-positive patients. There were no BC-positive patients who showed less than -1.00 for component 1. CONCLUSION: The present results obtained by PCA on laboratory tests involving PCT, PLT, white blood cell, and CRP suggest the potential of PCA-obtained values to not only predict bloodstream infection but also identify bacterial strains. This provides some clinical significance in the management of sepsis in acute care.

Prediction of blood culture results by measuring procalcitonin levels and other inflammatory biomarkers.

BACKGROUND: It would be helpful if we could predict positive or negative blood culture results. This study considered the usefulness of measuring procalcitonin (PCT) level and standard clinical biomarkers such as white blood cell (WBC) count, C-reactive protein (CRP) level, and platelet (PLT) count to predict blood culture results. METHOD: We retrospectively analyzed the data from 422 specimens collected at our emergency center within the preceding 36 consecutive months. Primary component analysis (PCA) was used for detecting the degree of the relational contribution of each of the 4 biomarkers to the blood culture results. RESULTS: Procalcitonin alone (cut-off value, 0.5 ng/mL) yielded a positive blood culture rate of 34.0%. Procalcitonin plus 3 biomarkers (WBC, CRP, and PLT) analyzed by PCA yielded 45.9% or 35.3% when a case was in the first or fourth quadrant, which was significantly higher than cases in the second or third quadrant. Primary component analysis also revealed that positive blood culture results were mainly affected by primary component 1, to which PCT and PLT (not WBC or CRP) predominantly contribute. CONCLUSION: Although it is difficult to predict blood culture results, even using 4 biomarkers analyzed by PCA, our new finding that blood culture results are affected not by WBC and CRP, but mainly by PCT and PLT, might help explain the mechanism of sepsis.

Antimicrobial susceptibilities and distribution of resistance genes for beta-lactams and macrolides in Streptococcus pneumoniae isolated between 2002 and 2004 in Tokyo.

Antimicrobial susceptibilities of 205 Streptococcus pneumoniae strains isolated between 2002 and 2004 in Japan were examined and the distribution of genes for resistance to penicillins and macrolides were investigated by polymerase chain reaction. The molecular epidemiology of 92 randomly selected isolates was also examined by pulsed-field gel electrophoresis (PFGE). The numbers of S. pneumoniae isolates resistant to benzylpenicillin, clarithromycin and tetracycline were, respectively, 39 (19%), 111 (54%) and 155 (76%), and the numbers increased annually. All isolates were susceptible to amoxicillin, fluoroquinolones, vancomycin and linezolid. Analysis of mutations in the genes for penicillin-binding protein showed that 92% of isolates had mutations in pbp1a, pbp2b and/or pbp2x. Susceptibility to benzylpenicillin decreased with increasing number of mutated pbp genes. The macrolide resistance genes ermB and mefA were found in 99 (48%) and 76 (37%) isolates, respectively. The presence of ermB was associated with high-level resistance to macrolides, and the percentage of isolates with ermB increased annually. The presence of mefA also increased with increasing number of mutated pbp genes. Although the 92 isolates belonged to 74 PFGE types, three groups with an 80% similarity in their PFGE patterns were found at high frequency. Two of the three groups contained no isolates susceptible to penicillin and/or tetracycline, and their percentages increased annually. Our results suggest that the number of S. pneumoniae isolates with reduced susceptibility due to accumulation of resistance genes has been increasing.

Susceptibility and resistance genes to fluoroquinolones in methicillin-resistant Staphylococcus aureus isolated in 2002.

The activity of six fluoroquinolones (FQs) was determined against 100 methicillin-resistant Staphylococcus aureus (MRSA) isolated in 2002 along with mutations in the grlA and gyrA genes and in the norA promoter of these isolates. Of the isolates tested, 97% had mutations in grlA and gyrA. A single mutation in grlA and gyrA resulted in a decrease of susceptibility to old generation FQs (norfloxacin, enoxacin, ciprofloxacin, fleroxacin, sparfloxacin and levofloxacin) but not to new generation FQs (gatifloxacin and moxifloxacin). Double mutations of both grlA and gyrA resulted in high-level resistance to all FQs tested. All norA mutants (15%) contained double mutations in grlA and gyrA and showed no decrease of MIC in the presence of reserpine, which is known to inhibit the drug-efflux pump. Our results showed that double mutations in grlA and gyrA were necessary for the expression of high-level resistance to new generation FQs. As different FQ-resistant mutants occur in the same PFGE type, FQ-resistant MRSA may well develop individually.