Bacterial Pleural Effusion Research Articles

Aetiology of pleural effusions in children living in a high TB endemic setting.

<sec id="st1"><title>BACKGROUND</title>Confirming the aetiology of pleural effusion in children may be difficult in TB-endemic settings. We investigated the role of polymerase chain reaction (PCR) and routine biochemical tests in discriminating pleural effusion caused by bacteria from other aetiologies.</sec><sec id="st2"><title>METHODS</title>This is a cross-sectional post-hoc analysis among children with pleural effusion in a tertiary hospital in South Africa, incorporating new data from PCR testing of stored pleural fluid. Aetiological classification was defined by microbiological confirmation.</sec><sec id="st3"><title>RESULTS</title>Ninety-one children were enrolled; the median age 31 months (IQR 12-102). The aetiology of pleural effusion was 40% (36/91) bacteria, 11% (10/91) TB, 3% (3/91) viruses, 11% (10/91) polymicrobial and 35% (32/91) had no pathogen identified. The most common pathogen was Staphylococcus aureus (27/91, 30%) with similar yields on culture and PCR, followed by Streptococcus pneumoniae (12/91, 13%), detected more commonly by PCR. PCR reduced the number of children with unconfirmed aetiologies from 48 to 32. Characteristics of children with no pathogen most resembled those with TB. Pleural fluid lactate dehydrogenase ≥1,716 U/L best discriminated bacterial pleural effusion from other aetiologies (sensitivity of 86%; specificity 95%).</sec><sec id="st4"><title>CONCLUSION</title>PCR improved detection of pathogens and reduced number of children with unconfirmed aetiologies in presumed exudative pleural effusion.</sec>.

Handheld ultrasound as an adjunct to physical examination in the diagnosis of cardiopulmonary disease.

Handheld 2D ultrasound devices (HUDs) have become available as an adjunct to physical examinations, visualizing the heart and lungs in real time and facilitating prompt patient diagnosis and treatment of cardiopulmonar.y disorders. These devices provide simple and rapid bedside alternatives to repetitive chest x-rays, standard ultrasound examinations and thoracic CT scans. Two currently available HUDs are described. This paper discusses the use of HUDs in the diagnosis of patients with pericardial effusion and tamponade, ventricular dilation, aortic and mitral regurgitation, cardiogenic pulmonary edema, viral and bacterial pneumonia, pleural effusion and pneumothorax. The use of a HUD by physicians increases clinical diagnostic accuracy, adds quantitative information about cardiopulmonary disease severity and guides the use of medications and interventions.

Aetiology and presentation of childhood pleural infections in the post-pneumococcal conjugate vaccine era in South Africa.

Background Complications of respiratory infections including pleural effusion (PE) are associated with a high morbidity. Differentiating between PE caused by Mycobacterium tuberculosis (Mtb) infection and other bacterial infections in endemic areas is difficult in children, thus, impacting treatment. Objectives To investigate the aetiology of PE and features distinguishing tuberculosis (TB) from bacterial PE in children. Methods We conducted a prospective study in children with PE admitted to a tertiary hospital in Cape Town from December 2017 to December 2019. Clinical information and routine laboratory investigations were compared between children with bacterial, Mtb or unclassified PE, categorised according to study definitions. Results A total of 91 patients were included in the present study and their median age was 31 months (interquartile range (IQR) 11.8 - 102.1). The aetiology was bacterial in 40% (n=37), Mtb in 39% (n=36) and unclassified in 20% (n=18) of patients. Staphylococcus aureus was the most common bacterial isolate, confirmed in 65% (n=24/37) patients, and Streptococcus pneumoniae was confirmed in only 8% of patients. TB was microbiologically confirmed in 33% (n=12/36) of patients. Patients with TB were older (91.6 v. 11.8 months; p<0.001), with more weight loss (28 v. 12 patients; p<0.001), and longer cough duration (10 v. 4 days; p<0.001) than those with other bacterial PE. In contrast, the latter had significantly higher serum C-reactive protein (median 250 v. 122 mg/L; p<0.001), procalcitonin (11 v. 0.5 mg/L; p<0.001), pleural fluid lactate dehydrogenase (7 280 v. 544 U/L; p<0.001), and adenosine deaminase levels (162 v. 48 U/L; p<0.001) and lower glucose levels (1.3 v. 4 mmol/L; p<0.001). Conclusion Post 13-valent pneumococcal conjugate vaccine, S. aureus is the dominant cause of PE in children using traditional culture methods, while Mtb remains a common cause of PE in our setting. Useful clinical and laboratory differences between Mtb and other bacterial PE were identified, but the cause of PE in 20% of children was underdetermined. Molecular testing of pleural fluid for respiratory pathogens may be useful in such children.

Interleukin-20 and interleukin-22 in pleural effusion

To investigate the concentrations and clinical significance of interleukin (IL)-20 and IL-22 in pleural effusion with various etiologies. Pleural effusion (PE) and corresponding serum samples were obtained from 88 patients from Wuhan Tuberculosis Prevention and Control Institute from June 2011 to June 2013. There were 27 cases with malignant pleural effusion, 24 with tuberculous pleural effusion, 17 with bacterial pleural effusion and 20 with transudativeeffusion. The pleural and serum levels of IL-20 and IL-22 were determined by sandwich enzyme-linked immunosorbent assays (ELISA). (1) Except for transudativeeffusion, the concentration of IL-20 in malignant pleural effusion (36.8±5.1) ng/L, tuberculous pleural effusion (34.8±6) ng/L, bacterial pleural effusion (41.7±20.2) ng/L, were significantly higher than that of the corresponding serum concentration (29.7±5.97) ng/L, (27.3 ±6.7) ng/L, (25.6±4.7) ng/L (t=5.044, 3.804, 3.452, P<0.05). However, the concentration of IL-20 in pleural effusions of different causes showed no significant difference; malignant (36.8±5.1) ng/L, tuberculous(34.8±6.0) ng/L, bacterial (41.7±20.2) ng/L, transudate (34.1±7.3) ng/L (P>0.05). The concentration of IL-22 (median, quartiles) in tuberculouseffusion was 146.1 (39.8) ng/L and bacterial effusion 59.6 (484.3) ng/L was significantly higher than those in the corresponding serum concentrations 18.7 (9.8) ng/L, 15.7 (17.2) ng/L (Z value respectively -3.971, -3.290, P<0.05). The concentration of IL-22 in tuberculous pleural effusion, bacterial pleural effusion, transudative pleural effusion was significant higher than those in malignant pleural effusion respectively (all P<0.001). (2)The concentrations of IL-22 in malignant pleural effusion was correlated positively with those in serum (r=0.729, P<0.001). (3) With a cut-off value of 19.7 ng/L, pleural IL-22 exhibited a high sensitivity and specificity of 95.1% (39/41) and 88.9%(24/27) respectively, when used for distinguishing infectious pleural effusion (including tuberculous and bacterial effusion) from malignant pleural effusion (P<0.001). Higher levels of IL-22 in tuberculous and bacterial pleural effusion were found when compared with corresponding serum levels and might be involved in the pathogenesis of infectious pleural effusion. Pleural IL-22 measurement provided reliable diagnostic efficiency for distinguishing infectious from malignant pleural effusion.

Systematic Use of Universal 16S rRNA Gene Polymerase Chain Reaction (PCR) and Sequencing for Processing Pleural Effusions Improves Conventional Culture Techniques

Conventional culture of pleural fluid samples frequently provides false-negative results. Universal polymerase chain reaction (PCR) of the 16S ribosomal ribonucleic acid (rRNA) gene (16S PCR) has proven useful in the diagnosis of various bacterial infections. We conducted a prospective study to assess the value of 16S PCR in the etiologic diagnosis of pleural effusion. All pleural fluid samples received for culture were also studied using 16S PCR. Positive samples were sequenced for identification. Clinical records and conventional culture results were analyzed to classify pleural fluid samples as infected or not infected. We studied 723 samples. We excluded 188 samples because they were obtained from a long-term chest tube, there was a diagnosis of mycobacterial infection, or there were insufficient data to classify the episode. Finally, 535 pleural fluid samples were analyzed. According to our criteria, 82 (15.3%) were infected and 453 (84.7%) were not infected. In the infected samples, 16S PCR was positive in 67 samples (81.7%) while conventional culture was positive in 45 (54.9%). There were 4 false positives with 16S PCR (0.9%) and 12 with culture (2.6%). The values for the etiologic diagnosis of bacterial pleural effusion of conventional culture compared with 16S PCR were as follows: sensitivity, 54.9%/81.7%; specificity, 97.4%/99.1%; positive predictive value, 76.3%/94.4%; negative predictive value, 92.6%/96.8%; and accuracy, 90.8%/96.5%.When compared with conventional culture, 16S PCR plus sequencing substantially improves the etiologic diagnosis of infectious pleural effusion. In our opinion, this technique should be added to the routine diagnostic armamentarium of clinical microbiology laboratories.

Pleural fluid soluble triggering receptor expressed on myeloid cells-1 as a marker of bacterial infection: a meta-analysis

BackgroundPleural infection is a common clinical problem. Its successful treatment depends on rapid diagnosis and early initiation of antibiotics. The measurement of soluble triggering receptor expressed in myeloid cells-1 (sTREM-1) level in pleural effusions has proven to be a valuable diagnostic tool for differentiating bacterial effusions from effusions of other etiologies. Herein, we performed a meta-analysis to assess the accuracy of pleural fluid sTREM-1 in the diagnosis of bacterial infection.MethodsWe searched Web of Knowledge and Medline from 1990 through March 2011 for studies reporting diagnostic accuracy data regarding the use of sTREM-1 in the diagnosis of bacterial pleural effusions. Pooled sensitivity and specificity and summary measures of accuracy and Q* were calculated.ResultsOverall, the sensitivity of sTREM-1was 78% (95% CI: 72%-83%); the specificity was 84% (95% CI: 80%-87%); the positive likelihood ratio was 6.0 (95% CI: 3.3-10.7); and the negative likelihood ratio was 0.22 (95% CI: 0.12-0.40). The area under the SROC curve for sTREM-1 was 0.92. Statistical heterogeneity and inconsistency were found for sensitivity (p = 0.015, χ2 = 15.73, I2 = 61.9%), specificity (p = 0.000, χ2 = 29.90, I2 = 79.9%), positive likelihood ratio (p = 0.000, χ2 = 33.09, I2 = 81.9%), negative likelihood ratio (p = 0.008, χ2 = 17.25, I2 = 65.2%), and diagnostic odds ratio (p = 0.000, χ2 = 28.49, I2 = 78.9%). A meta-regression analysis performed showed that the Quality Assessment of Diagnostic Accuracy Studies score (p = 0.3245; RDOR, 4.34; 95% CI, 0.11 to 164.01), the Standards for Reporting of Diagnostic Accuracy score (p = 0.3331; RDOR, 1.70; 95% CI, 0.44 to 6.52), lack of blinding (p = 0.7439; RDOR, 0.60; 95% CI, 0.01 to 33.80), and whether the studies were prospective or retrospective studies (p = 0.2068; RDOR, 7.44; 95% CI, 0.18 to 301.17) did not affect the test accuracy. A funnel plot for publication bias suggested a remarkable trend of publication bias.ConclusionsOur findings suggest that sTREM-1 has a good diagnostic accuracy and may provide a useful adjunctive tool for the diagnosis of bacterial pleural effusions. However, further studies are needed in order to identify any differences in the diagnostic performance of sTREM-1 of parapneumonic effusions and empyemas.

CCL22 is involved in the recruitment of CD4+CD25high T cells into tuberculous pleural effusions

CD4(+)CD25(high) regulatory T cells are increased in tuberculous pleural effusions (TPE). However, the mechanism by which CD4(+)CD25(high) T cells infiltrate into the pleural cavity is unknown. The aim of this study was to investigate whether the chemokines CCL22 and CCL17 are present in TPE, and the chemoattractant activity of these chemokines for infiltration of CD4(+)CD25(high) T cells into the pleural space. The concentrations of CCL22 and CCL17 were measured in pleural effusions from 33 patients with tuberculous pleurisy, 21 patients with pleural bacterial infections and 18 patients with transudative pleural effusions. T lymphocyte subsets in pleural effusions were assessed by flow cytometry. Pleural effusion cells were analysed for the expression of CCL22. The chemoattractant activity of CCL22 for CD4(+)CD25(high) T cells was assessed in vitro. The frequency of CD4(+)CD25(high) T cells was significantly higher in TPE than in blood. High concentrations of CCL22 were detected in tuberculous effusions, but not in bacterial effusions or transudates. Macrophages and T cells in TPE expressed CCL22. Tuberculous pleural fluid was chemotactic for CD4(+)CD25(high) T cells in vitro, and anti-CCL22 antibody partly inhibited this chemotactic activity. CCL22 appeared to be increased in TPE compared with bacterial pleural effusions or transudates. CCL22 may be responsible for the infiltration of CD4(+)CD25(high) T cells into the pleural space of patients with tuberculous pleurisy.

Expression of soluble triggering receptor expression on myeloid cells-1 in pleural effusion

Triggering receptors expressed on myeloid cells (TREM) proteins are a family of cell surface receptors expressed broadly by cells of the myeloid lineage. The aim of this study was to investigate the clinical significance of soluble TREM-1 (sTREM-1) in pleural effusions, and to determine the effects of pneumonia on pleural sTREM-1 concentrations. Pleural fluid was collected from 109 patients who presented to the respiratory institute (35 with malignant pleural effusion, 31 with tuberculous pleural effusion, 21 with bacterial pleural effusion, and 22 with transudate). The concentrations of sTREM-1, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) were determined in effusion and serum samples by enzyme linked immunosorbent assay (ELISA). The concentrations of sTREM-1 in bacterial pleural effusion were significantly higher than those in malignant, tuberculous, and transudative groups (all P < 0.001). An sTREM-1 cutoff value of 768.1 ng/L had a sensitivity of 86% and a specificity of 93%. Pleural sTREM-1 levels were positively correlated with levels of TNF-alpha and IL-1beta. Patients with complicating bacterial pneumonia did not have elevated concentration of sTREM-1 in pleural effusion when compared with patients without pneumonia. Determination of pleural sTREM-1 may improve the ability of clinicians to differentiate pleural effusion patients of bacterial origin from those with other etiologies. The occurrence of bacterial pneumonia did not affect pleural sTREM-1 concentrations.

Expression of soluble triggering receptor expression on myeloid cells-1 in pleural effusion

Background Triggering receptors expressed on myeloid cells (TREM) proteins are a family of cell surface receptors expressed broadly by cells of the myeloid lineage. The aim of this study was to investigate the clinical significance of soluble TREM-1 (sTREM-1) in pleural effusions, and to determine the effects of pneumonia on pleural sTREM-1 concentrations. Methods Pleural fluid was collected from 109 patients who presented to the respiratory institute (35 with malignant pleural effusion, 31 with tuberculous pleural effusion, 21 with bacterial pleural effusion, and 22 with transudate). The concentrations of sTREM-1, tumor necrosis factor-α (TNF-α) and interleukin-1 β (IL-1β) were determined in effusion and serum samples by enzyme linked immunosorbent assay (ELISA). Results The concentrations of sTREM-1 in bacterial pleural effusion were significantly higher than those in malignant, tuberculous, and transudative groups (all P <0.001). An sTREM-1 cutoff value of 768.1 ng/L had a sensitivity of 86% and a specificity of 93%. Pleural sTREM-1 levels were positively correlated with levels of TNF-α and IL-1β. Patients with complicating bacterial pneumonia did not have elevated concentration of sTREM-1 in pleural effusion when compared with patients without pneumonia. Conclusions Determination of pleural sTREM-1 may improve the ability of clinicians to differentiate pleural effusion patients of bacterial origin from those with other etiologies. The occurrence of bacterial pneumonia did not affect pleural sTREM-1 concentrations.

Evaluation of a new inflammatory molecule (triggering receptor expressed on myeloid cells‐1) in the diagnosis of pleural effusion

The triggering receptor expressed on myeloid cell-1 (TREM-1) is a newly discovered molecule that is associated with the inflammatory response to microorganisms. We investigated the role of surface and soluble TREM-1 in differentiating different disease entities in pleural effusion formation. Sixty-seven patients with pleural effusion due to transudate (14), malignancy (15), tuberculous pleuritis (16), para-pneumonic effusion (10) and empyaema (12) were included in this study. Surface TREM-1 was measured by flow cytometry and was expressed as mean fluorescence intensity and soluble TREM-1 was measured by ELISA and expressed as pg/mL. Results are given as mean levels +/- SEM. Surface TREM-1 was measured in 24 patients and the levels were highest in para-pneumonic effusion (30.0 +/- 8.4) and lowest in malignant pleural effusion (5.2 +/- 1.1) and tuberculous pleuritis (5.2 +/- 2.4). Soluble TREM-1 was highest in effusions of infectious aetiology (para-pneumonic effusion (979.4 +/- 229.6) and empyaema (1712.6 +/- 299.5)) and lowest in non-infectious effusions (transudate (81.2 +/- 4.5 pg/mL) and malignancy (111.3 +/- 20.7). At a cut-off value of 114 pg/mL, soluble TREM-1 yielded a sensitivity of 87.5% and a specificity of 89.7% in differentiating non-infectious effusion from tuberculous pleuritis. At a cut-off value of 374 pg/mL, sTREM-1 yielded a sensitivity of 93.8% and a specificity of 90.9 in differentiating tuberculous pleuritis from bacterial pleural effusion. Soluble and surface TREM-1 are valuable markers in establishing the aetiology of pleural effusions.

Factors Influencing Length of Hospital Stay in Patients with Bacterial Pleural Effusion

Background: Factors influencing length of hospital stay have been poorly analyzed in parapneumonic pleural effusions (PPE). Objectives: The aim of this work is to identify the variables that determine increased hospital stay in patients with infectious pleural effusion (PE). Patients and Methods: We analyzed 112 patients with PE: empyema, complicated parapneumonic and non-complicated parapneumonic. Epidemiologic, biochemical, therapeutic and radiological variables were analyzed. Correlations with hospital stay were studied using the Student’s t test, analysis of variance, Mann-Whitney U-test and linear regression model. Results: Among the 112 patients studied, there were 32 empyema, 50 complicated and 30 non-complicated parapneumonic cases. The median of length stay for all patients was 17 days. Longer hospitalization was required in patients with empyemic PE (p = 0.015), patients with underlying diseases (p = 0.003), those needing pleural drainage (p = 0.005) or decortication (p = 0.043) and those presenting unfavorable radiological outcome after treatment (p = 0.02). Biochemical parameters associated with longer hospital stay were elevated pleural fluid polymorphonuclear elastase (p = 0.001, r = 0.307) and lactate dehydrogenase (p = 0.001, r = 0.312). After linear regression analysis, only underlying disease, pleural drainage and pleural fluid polymorphonuclear elastase values remained in the model, explaining 23.1% of the variability of days of hospitalization. Conclusions: The patients with PPE and empyema who required longer hospitalization were those with purulent fluid, underlying disease, surgical drainage and/or decortication, with unfavorable radiological outcome and higher pleural fluid levels of lactate dehydrogenase and polymorphonuclear elastase.

Accuracy of chest sonography and polymorphonuclear elastase in the assessment of bacterial pleural effusion

Background: The relationship between chest sonography findings and inflammatory markers for assessing bacterial pleural effusion is not well established. We decided to study the accuracy of chest sonography in determining the nature of bacterial pleural effusion and its relationship with polymorphonuclear elastase (PMN-E) results. Methods: Pleural sonography and PMN-E were evaluated in a prospective study of 144 consecutive patients with pleural effusion of various etiologies: 25 complicated parapneumonic, 18 uncomplicated parapneumonic, 33 tuberculous, 17 malignant, 12 transudates, and 39 of unknown etiology. The sonographer distinguished between anechoic and septated pattern. The relationship between sonographic appearance and inflammatory markers was evaluated. Results: All of the complicated parapneumonic, 11 uncomplicated parapneumonic, and 28 tuberculous effusions were septated. Septated pattern and PMN-E value were independent predictors of infectious pleural disease ( p <0.05). The simultaneous presence of a septated pattern and a PMN-E higher than 100 μg/l had a sensitivity of 79.1% and a specificity of 91.1% for the diagnosis of bacterial effusions. Conclusions: PMN-E level and the sonographic pattern of pleural fluid may be useful in the diagnosis of bacterial pleural effusions.

Measurement of vitamin D-binding protein in pleural fluids and sera by means of a turbidimetric immunoassay measuring system

Background: Vitamin D-binding protein (DBP) has been recognized as a multifunctional plasma protein that can modulate certain immune and inflammatory responses. There may be differences between the DBP concentrations in pleural fluids from various diseases involving a variety of possible responses in the pleural cavity. Methods: An anti-DBP polyclonal antibody was prepared using commercially available DBP to establish a quantitative measuring system for DBP. With a rabbit antibody, a turbidimetric immunoassay (TIA) was developed for DBP with an automatic analyzer. Using this measuring system, the concentrations of DBP were compared with the protein concentration in pleural fluid and serum specimens from patients with various diseases. Results: The fluid DBP concentrations in transudative ( n=11) and exudative ( n=41) effusions were 71.9±21.2 and 180.7±43.7 mg/l, respectively. Among the exudative effusions, the fluid DBP concentrations in the bacterial ( n=10), tuberculous ( n=13), and malignant ( n=18) effusions were 218.8±37.3, 186.7±26.2, and 155.1±41.3 mg/l, respectively. The DBP fluid/serum ratio and the fluid DBP/protein ratio in bacterial effusions were significantly higher than those in tuberculous ( p<0.005, p<0.05, respectively) and malignant effusions ( p<0.0005, p<0.005, respectively), although no statistically significant differences in the serum DBP/protein ratio between those effusions were found. Conclusions: Using the TIA assay, the DBP concentrations in bacterial pleural effusions were significantly higher than in tuberculous and malignant effusions.

Soluble Interleukin-2 Receptor(sIL-2R) Levels in Patients Tuberculous Pleurisy VS Nontuberculous Pleurisy

Background The cell mediated immunity has an important role in the pathogenesis of tuberculosis. sIL-2R has been known as a sensitive marker of T lymphocyte activation. Elevated serum levels of sIL-2R have been found in patients with lymphoproliferative disorders, organ transplantation, autoimmune diseases, and various granulomatous diseases. Elevated levels of sIL-2R have been also found in the seam and pleural fluid of the patients with tuberculosis. To evaluate the diagnostic value of sIL-2R in the differentiation of tuberculous pleurisy and. nontuberculous pleurisy. We measured the level of sIL-2R in the sera and pleural fluids of 12 patients with tuberculous pleurisy and 32 patients with nontuberculous pleurisy. Method Samples of pleural fluid and serum were centrifuged at 2500 rpm for 10 min to remove cell pellets. Soluble R-2R was measured with a sandwitch enzyme immunoassay using the Cellfree r Interleukin-2 Receptor Test kit( T-cell science, Inc. Cambridge, MA). Results The results obtained were as follows: 1) The sIL-2R level in pleural fluid of the patients with tuberculous pleurisy was higher than that of patients with nontuberculous pleurisy(P<0.005). 2) When the sIL-2R level above 5,000 u/ml in pleural fluid was used as the cut-off value to diagnose tuberculous pleurisy, it had a sensitivity of 84.6% and a specificity of 90.9%. 3) The sIL-2R level in the sera of the patients with tuberculous pleurisy was higher than that of patients with bacterial pleural effusions and normal control group(P<0.05) and there was no difference of levels compared with malignant pleural effusions and transudative pleural effusions(P>0.05). 4) In patients with tuberculous pleurisy, the mean concentration of sIL-2R in pleural fluid was higher than that in serum(P<0.005). Conclusion These findings suggest that the measurement of elevated levels of pleural fluid sIL-2R in tuberculous pleurisy may be useful in the differential diagnosis between patients with tuberculous pleurisy and nontuberculous pleurisy.

Measurement of lactic acid in pleural fluid.

Lactic acid (LA) concentrations in the pleural fluid of 75 patients were determined by the Monotest Lactate Kit (MLK). Lactic acid values in 18 cases of bacterial or tuberculous pleural infection were strikingly higher (mean 81 mg%, range 45-200 mg%), than in 42 cases with pleural effusion due to congestive heart failure, hepatic cirrhosis, nephrosis, trauma, and systemic lupus erythematosus (SLE; mean 19 mg%, range 6-47 mg/). High levels of LA were also found in the pleural fluid of 15 patients with malignancy of pleural cavity. Determination of LA can be an additional rapid tool in the differentiation between bacterial pleural inflammation and pleural effusion of various forms except in cases with malignancy of the pleural cavity.