Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004610 (bacteremia)
 13,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous work suggested that C-reactive protein (CRP) may be a useful test in the diagnosis of melioidosis, the infection caused by Burkholderia pseudomallei. We reviewed patients with culture-confirmed melioidosis to define the role of this inflammatory marker in the diagnosis of melioidosis. In 175 patients, we found that the admission CRP level may be normal or only mildly elevated, including patients with severe sepsis, fatal cases, and in relapsed melioidosis. In a multivariate analysis, sepsis and bacteremia were more strongly associated with mortality than CRP. Admission levels of CRP are not a sensitive marker for the presence of melioidosis and a normal level cannot be used to exclude acute, chronic, or relapsed melioidosis in febrile patients in or from endemic regions.
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PMID:C-reactive protein in the diagnosis of melioidosis. 1515 96

Since neutropenic patients with hematological malignancies are at high risk of contracting life-threatening infections, specific markers of infection are needed in cases of febrile neutropenia. The study presented here assessed serum concentrations of C-reactive protein (CRP), procalcitonin (PCT) and interleukin-6 (IL-6) in samples obtained from 31 febrile neutropenic patients. A total of 53 episodes were evaluated, and 18 of these were associated with positive blood culture results. Procalcitonin and IL-6 concentrations differed significantly between bacteremic and non-bacteremic episodes. Procalcitonin values were 0.22 ng/ml [interquartile range (IR), 0.15-1.9] for patients with pneumonia without bacteremia, 0.22 ng/ml (IR, 0.16-0.55) for patients with fever of unknown origin, 0.2 ng/ml (IR, 0.13-0.57) for patients with non-microbial fever and 1.8 ng/ml (IR, 0.35-5.3) for patients with bacteremia. The differences between bacteremic and non-bacteremic episodes had a P-value of 0.003 using the Mann-Whitney test. For IL-6 the median values were 301 pg/ml (IR, 152-1,879) for patients with pneumonia without bacteremia, 207 pg/ml (IR, 94-445) for patients with fever of unknown origin, 177 pg/ml (IR, 142-208) for patients with non-microbial fever and 942 pg/ml (IR, 181-2,807) for patients with bacteremia. Using the Mann-Whitney test, the differences between bacteremic and non-bacteremic episodes were P=0.006. No differences were found in CRP concentrations. Cutoff levels to distinguish between bacteremic and non-bacteremic episodes were chosen using receiver operating characteristic curves: 0.62 ng/ml for PCT and 297 pg/ml for IL-6. Negative predictive values were 84% for PCT and 70% for IL-6. The results indicate that PCT and IL-6 are more reliable markers than CRP for predicting bacteremia in patients with febrile neutropenia.
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PMID:Markers of bacteremia in febrile neutropenic patients with hematological malignancies: procalcitonin and IL-6 are more reliable than C-reactive protein. 1522 17

To assess the effect of liver dysfunction on the production of C-reactive protein (CRP), CRP levels were evaluated in patients with Escherichia coli bacteremia with or without liver cirrhosis (LC). Thirty patients of each kind were selected as case and control groups, respectively. A matched control of 30 LC patients without acute infection was also included. In the patients with E. coli bacteremia, median CRP was 6.2 mg/dL (range 0.2-22.1) in the LC patients and 14.6 mg/dL (range 5.8-39.6) in the patients without liver dysfunction (P < 0.001). In the advanced LC patients in Child-Pugh class C, median CRP was 5.0 mg/dL (range 0.2-12.1) in patients with E. coli bacteremia and 0.5 mg/dL (range 0.1-1.2) in patients without acute infection (P < 0.001). Our data suggest that, although CRP levels are reduced in response to acute infection, production is nevertheless maintained even in patients with advanced liver dysfunction.
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PMID:Production of C-reactive protein in Escherichia coli-infected patients with liver dysfunction due to liver cirrhosis. 1580 12

The clinical significance of serum procalcitonin (PCT) for discriminating between bacterial infectious disease and nonbacterial infectious disease (such as systemic inflammatory response syndrome (SIRS)), was compared with the significance of endotoxin, beta-D: -glucan, interleukin (IL)-6, and C-reactive protein (CRP) in a multicenter prospective study. The concentrations of PCT in patients with systemic bacterial infection and those with localized bacterial infection were significantly higher than the concentrations in patients with nonbacterial infection or noninfectious diseases. In addition, PCT, endotoxin, IL-6, and CRP concentrations were significantly higher in patients with bacterial infectious disease than in those with nonbacterial infectious disease (P<0.001, P<0.005, P<0.001, and P<0.001, respectively). The cutoff value of PCT for the discrimination of bacterial and nonbacterial infectious diseases was determined to be 0.5 ng/ml, which was associated with a sensitivity of 64.4% and specificity of 86.0%. Areas under the receiver operating characteristic curves (POCs) were 0.84 for PCT, 0.60 for endotoxin, 0.77 for IL-6, and 0.78 for CRP in the combined group of patients with bacterial infectious disease and those with nonbacterial infectious disease, and the area under the ROC for PCT was significantly higher than that for endotoxin (P<0.001). In patients diagnosed with bacteremia based on clinical findings, the positive rate of diagnosis with PCT was 70.2%, while that of blood culture was 42.6%. PCT is thus essential for discriminating bacterial infection from SIRS, and is superior in this respect to conventional serum markers and blood culture.
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PMID:Multicenter prospective study of procalcitonin as an indicator of sepsis. 1599 Sep 80

A 36-year-old, 7-week-gravida patient with catheter-related nosocomial infective endocarditis due to methicillin-resistant Staphylococcus aureus (MRSA) is presented in this paper. The patient was admitted to our hospital because of carbon monoxide intoxication. After 14 days, MRSA catheter-related bacteremia developed. The central venous catheter was immediately removed, and teicoplanin therapy was started. Because of persistent fever, leukocytosis, and high C-reactive protein values, endocarditis was suspected. A transesophageal echocardiogram revealed 19-mm vegetation on her mitral valve, confirming the diagnosis of endocarditis. Gentamicin and rifampicin were added to the therapy regimen, and the dose of teicoplanin was increased to 12 mg/kg-day. After 8 days, a splenic abscess was detected by ultrasonography. Vegetation excision, mitral valve replacement by open-heart surgery and splenectomy were performed in the same operation. Antibiotherapy was continued for 6 weeks after surgery, and the patient's condition improved. The development of endocarditis could be prevented by proper clinical practices.
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PMID:Nosocomial methicillin-resistant Staphylococcus aureus endocarditis with splenic abscess in a pregnant woman. 1624 31

This literature review summarizes current knowledge on the systemic levels of selected markers of inflammation in periodontitis. From samples of peripheral blood the following cellular factors are discussed: total number of white blood cells, red blood cells, and thrombocytes. Further, plasma levels of acute-phase proteins, cytokines, and coagulation factors are reviewed. From the available literature it appears that the total numbers of leukocytes and plasma levels of C-reactive protein are consistently higher in periodontitis patients compared to healthy controls. Numbers of red blood cells and levels of hemoglobin are lower in periodontitis and there is a trend towards anemia of chronic disease. Most systemic markers of inflammation discussed in this review are also regarded as predictive markers for cardiovascular diseases. Therefore, changes in these markers in periodontitis may be part of the explanation why periodontitis is associated with cardiovascular diseases and/or cerebrovascular events in epidemiological studies. It is hypothesized that possibly daily episodes of a bacteremia originating from periodontal lesions are the cause for the changes in systemic markers in periodontitis; the cumulative size of all periodontal lesions in the untreated severe patient may amount to 15 to 20 cm2.
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PMID:Systemic markers of inflammation in periodontitis. 1627 83

C-reactive protein (CRP) is not an acute-phase protein in mice, and therefore, mice are widely used to investigate the functions of human CRP. It has been shown that CRP protects mice from pneumococcal infection, and an active complement system is required for full protection. In this study, we assessed the contribution of CRP's ability of activating the classical pathway of complement in the protection of mice from lethal infection with virulent Streptococcus pneumoniae type 3. We used two CRP mutants, Y175A and K114A. The Y175A CRP does not bind C1q and does not activate complement in human serum. The K114A CRP binds C1q and activates complement more efficiently than wild-type CRP. Passively administered, both CRP mutants and the wild-type CRP protected mice from infection equally. Infected mice injected with wild-type or mutant CRP had reduced bacteremia, resulting in lower mortality and increased longevity compared with mice that did not receive CRP. Thus, the protection of mice was independent of CRP-mediated activation of the classical pathway of complement. To confirm that human CRP does not differentiate between human and mouse complement, we analyzed the binding of human CRP to mouse C1q. Surprisingly, CRP did not react with mouse C1q, although both mutant and wild-type CRP activated mouse C3, indicating species specificity of CRP-C1q interaction. We conclude that the mouse is an unfit animal for exploring CRP-mediated activation of the classical complement pathway, and that the characteristic of CRP to activate the classical complement pathway has no role in protecting mice from infection.
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PMID:Role of the property of C-reactive protein to activate the classical pathway of complement in protecting mice from pneumococcal infection. 1654 75

Streptococcus pneumoniae is the most common organism responsible for community acquired pneumonia and meningitis. In pneumococcal pneumonia, a strong local inflammatory cytokine response reduces the frequency of bacteremia and increases survival. The initiation of this cytokine response by innate recognition of bacterial cell wall components through TLR has been described, but the role of soluble innate mediators has received limited attention. C-reactive protein (CRP) is an acute phase protein that binds phosphocholine residues on S. pneumoniae cell walls. CRP interacts with phagocytic cells through FcgammaRI and FcgammaRII and activates the classical complement pathway. CRP is protective in mouse pneumococcal bacteremia by increasing complement-dependent clearance and killing of bacteria. We studied the cytokine response of PBMC stimulated with CRP-opsonized S. pneumoniae to determine the effect of CRP interaction with FcgammaR. CRP dramatically increased the production of TNF-alpha and IL-1beta in response to S. pneumoniae. These increases were blocked by phosphocholine, which inhibits CRP binding to S. pneumoniae, by inhibitors of FcgammaR signaling, and by mAb to FcgammaRI and FcgammaRII. A mutated rCRP with decreased FcgammaR binding had a decreased ability to stimulate TNF-alpha release, compared with wild-type CRP. Individuals who were homozygous for the R-131 allele of FcgammaRIIA, which has a higher affinity for CRP, showed higher responses to CRP-opsonized bacteria than did individuals homozygous for the H-131 allele, further implicating this receptor. The results indicate that CRP recognition of S. pneumoniae and binding to FcgammaR may enhance the early protective cytokine response to infection.
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PMID:C-reactive protein increases cytokine responses to Streptococcus pneumoniae through interactions with Fc gamma receptors. 1675 6

Human C-reactive protein (CRP) protects mice from lethality after infection with virulent Streptococcus pneumoniae type 3. For CRP-mediated protection, the complement system is required; however, the role of complement activation by CRP in the protection is not defined. Based on the in vitro properties of CRP, it has been assumed that protection of mice begins with the binding of CRP to pneumococcal C-polysaccharide on S. pneumoniae and subsequent activation of the mouse complement system. In this study, we explored the mechanism of CRP-mediated protection by utilizing two CRP mutants, F66A and F66A/E81A. Both mutants, unlike wild-type CRP, do not bind live virulent S. pneumoniae. We found that passively administered mutant CRP protected mice from infection as effectively as the wild-type CRP did. Infected mice injected with wild-type CRP or with mutant CRP lived longer and had lower mortality than mice that did not receive CRP. Extended survival was caused by the persistence of reduced bacteremia in mice treated with any CRP. We conclude that the CRP-mediated decrease in bacteremia and the resulting protection of mice are independent of an interaction between CRP and the pathogen and therefore are independent of the ability of CRP to activate mouse complement. It has been shown previously that the Fcgamma receptors also do not contribute to such CRP-mediated protection. Combined data lead to the speculation that CRP acts on the effector cells of the immune system to enhance cell-mediated cytotoxicity and suggest investigation into the possibility of using CRP-loaded APC-based strategy to treat microbial infections.
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PMID:Human C-reactive protein protects mice from Streptococcus pneumoniae infection without binding to pneumococcal C-polysaccharide. 1720 80

This literature review summarizes current knowledge on the systemic levels of selected markers of inflammation in periodontitis. From the available literature it appears that the total numbers of leukocytes and plasma levels of C-reactive protein (CRP) are consistently higher in periodontitis patients compared with healthy controls. Some systemic markers of inflammation discussed in this review are also regarded as predictive markers for cardiovascular diseases. Therefore changes in these markers in periodontitis may be part of the explanation why periodontitis is associated with cardiovascular diseases and/or cerebrovascular events in epidemiological studies. It is hypothesized that possibly daily episodes of a bacteremia originating from the periodontal lesion are the cause of the changes in systemic markers in periodontitis; the overall size of periodontal lesions in the untreated severe patient may amount to 1500-2000 mm2.
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PMID:Systemic effects of periodontitis. 1766 87


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