Pleural infection: changing bacteriology and its implications

The incidence of pleural infection continues to rise worldwide. Identifying the causative organism(s) is important to guide antimicrobial therapy. The bacteriology of pleural infection is complex and has changed over time. Recent data suggest that the bacterial causes of empyema are significantly different between adult and paediatric patients, between community-acquired and nosocomial empyemas and can vary among geographical regions of the world. Since the introduction of pneumococcal vaccines, a change has been observed in the distribution of the serotypes of Streptococcus pneumoniae in empyema. These observations have implications on therapy and vaccine strategies. Clinicians need to be aware of the local bacteriology of empyema in order to guide antibiotic treatment.     

The definitions and epidemiology of pleural space infection

Infections of the pleural space are caused by a diverse group of clinical conditions that include trauma, post-operative states, and pneumonia. Although pleural effusions accompany bacterial pneumonia in up to 60% of patients, they uncommonly influence management because the effusion in most patients disappears with antibiotic administration. Unfortunately, the large number of patients with pneumonia provide an abundant supply of patients who fail to respond to antibiotic administration alone and subsequently present with pleural fluid loculation, pleural sepsis, or empyema. This article provides an overview of the classification schemes that have been used to characterize pleural space infections and highlight the epidemiology of those patients who present with complicated parapneumonic effusions and empyema.     

The spectrum and significance of pleural disease in blastomycosis

To determine the incidence and significance of pleural disease in blastomycosis, we reviewed the chest roentgenograms and medical records of 26 consecutive patients with biopsy- or culture-proved Blastomyces dermatitidis infection. Twenty-three of the 26 (88 percent) had radiographic evidence of blastomycotic pleural disease. Pleural reaction that regressed on therapy was mild (less than 1.0 cm thickening on EPA chest film) in 12. More extensive pleural thickening (1.5 to 3.0 cm) was observed in five, while four had effusions, and two had pneumothoraces. The 15 patients with mild or no visible pleural thickening were considered to have minor pleural involvement, while the 11 patients with greater than 1.5 cm pleural reaction, effusions, or pneumothoraces were considered to have major pleural disease. The ages, incidence of serious underlying disorders, and extra-thoracic dissemination were similar in both groups. Chest pain was more frequent in those with major pleural involvement (8/11 vs 4/15, p = 0.02), and their white blood cell count (14,300 +/- 1,200 c/mm3) was significantly higher than that of those with minor pleural involvement (10,600 +/- 1400, p less than 0.05). All of the patients with minor pleural disease responded to amphotericin therapy, but four of 11 (36 percent) with major pleural disease had an unfavorable outcome (relapse = two, death = two) (p = 0.02). In these patients with blastomycosis, pleural involvement was extremely common. Major pleural disease was associated with an adverse prognosis and may be an indication for prolonged therapy.     

葡萄糖转运蛋白1在恶性胸腔积液的表达及意义

目的评价葡萄糖转运蛋白l(GLUT-1)在恶性胸腔积液中的诊断价值。方法采用免疫细胞化学SP法检测肿瘤性和非肿瘤性胸腔积液中脱落细胞GLUT-1的表达以及ELISA法测定胸水中GLUT-1的水平。结果两组胸液脱落细胞GLUT-1的表达率恶性组为89.33%,良性组为3.17%,两组间具有统计学差异(P0.01);两组胸液上清中GLUT-1的表达水平恶性组为(1.18±0.35)pg/ml,良性组为(0.85±0.24)pg/ml,两组间具有统计学差异(P0.05)。结论 GLUT-1对恶性胸腔积液的诊断具有较高的敏感度,可以作为鉴别恶性胸腔积液的可靠标记之一。     

血清和胸液肿瘤坏死因子及受体检测对鉴别结核性和癌性 …

通过检测结核性及癌性胸液患者血清及胸液中肿瘤坏死因子α（ＴＮＦ－α）及可溶性受体（ｓＴＮＦＲ－Ⅰ、ｓＴＮＦＲ－Ⅱ）水平,探讨其对临别良恶性疾病的意义。方法采用双抗体夹心免疫酶标（ＥＬＩＳＡ）法检测２５例结核性胸液,２８例癌性胸液患者血清及胸液及３２例正常人血清中ＴＮＦ－α及ｓＴＮＦＲ－Ⅰ、ｓＴＮＦＲ－水平。     

Fitting the standard genetic code into its triplet table

Minimally evolved codes are constructed here; these have randomly chosen standard genetic code (SGC) triplets, completed with completely random triplet assignments. Such “genetic codes” have not evolved, but retain SGC qualities. Retained qualities are basic, part of the underpinning of coding. For example, the sensitivity of coding to arbitrary assignments, which must be < ∼10%, is intrinsic. Such sensitivity comes from the elementary combinatorial properties of coding and constrains any SGC evolution hypothesis. Similarly, assignment of last-evolved functions is difficult because of late kinetic phenomena, likely common across codes. Census of minimally evolved code assignments shows that shape and size of wobble domains controls the code’s fit into a coding table, strongly shifting accuracy of codon assignments. Access to the SGC therefore requires a plausible pathway to limited randomness, avoiding difficult completion while fitting a highly ordered, degenerate code into a preset three-dimensional space. Three-dimensional late Crick wobble in a genetic code assembled by lateral transfer between early partial codes satisfies these varied, simultaneous requirements. By allowing parallel evolution of SGC domains, this origin can yield shortened evolution to SGC-level order and allow the code to arise in smaller populations. It effectively yields full codes. Less obviously, it unifies previously studied chemical, biochemical, and wobble order in amino acid assignment, including a stereochemical minority of triplet–amino acid associations. Finally, fusion of intermediates into the final SGC is credible, mirroring broadly accepted later cellular evolution.

The form of the standard genetic code (SGC) offers authoritative information about its origin. By calculating evolved coding tables via different pathways (1), the SGC’s implications for its creation can be investigated. More frequent SGC-like results quantitatively signal superior explanations. Consequently, initial hypotheses about code descent can be improved. In fact, respecting Bayes’ theorem, multiple successful explanations rapidly strengthen an accurate hypothesis by Bayesian convergence (2).The existing result is late Crick wobble (3). “Late” implies that NNR (R = purine) and NNY (Y = pyrimidine) wobble was deferred, being preceded by unique triplet pairing assignments. Unique triplet pairing does not require support from a highly evolved allosteric ribosome (4, 5); it does not require a specific, highly optimized tRNA anticodon loop-and-stem structure (6, 7) or control of varied isomerization of wobble-paired bases (8). Accurate Crick wobble (9), with these multiple requirements, would therefore likely be a later, more modern code refinement. Late wobble also shows superior ability to fill an SGC-like coding table and offers more probable SGC access to evolving codes (1, 3). Moreover, the first wobble (the SGC necessarily uses ambiguous wobble coding) probably resembled simplified Crick wobble, defined here as translation of NNY and NNR codons, each with one adaptor RNA (9). For comparison, superwobble, translation of four NNY/R codons with one unmodified adaptor (10), is less probable because it less frequently yields the SGC (3). Other evolutionary routes to SGC-like coding can be evaluated comparably, within this simulated framework.     

Pathogenesis of pleural infection

The pleura responds to the presence of infecting organisms with a vigorous inflammatory response associated with an exudation of white blood cells and proteins. The development and outcome of pleural infections is a function of a balance between the virulence of the invading microorganism and the immune reaction involving professional immune cells as well as the pleural mesothelial cells. Most commonly, pleural infection occurs after invasion through the lung parenchyma and a breach in the viscera pleura resulting in the formation of a parapneumonic process. Upon infection, the microorganisms are recognized by the pleural mesothelial cell, which remains the first line of defence. Pleural responses to infection include those of innate immunity as well as adaptive or acquired immunity. Innate and acquired immune responses are closely linked. In this review, we discuss the different virulence factors that allow microorganisms to infect the pleura and the role of the pleural mesothelial cells in bridging the innate and acquired immune responses.     

恶性胸液中GLUT-1和iNOS的表达及临床意义

目的探讨恶性胸液中葡萄糖转运蛋白-1(GLUT-1)和诱导型一氧化氮合成酶(iNOS)的表达水平及临床意义。方法检测70例胸腔积液患者(良性积液30例、恶性积液40例)血清和胸液中GLUT-1和iNOS的表达水平,并将检测结果进行对比。结果恶性组胸液中GLUT-1和iNOS水平显著高于良性组水平(P<0.01),血清中GLUT-1和iNOS水平略高于良性组,但无统计学意义(P>0.05),两组患者胸液中的GLUT-1和iNOS水平均高于同组血清中的水平。结论 GLUT-1和iNOS在恶性胸液中高表达,临床上检测二者的水平可能有助于恶性胸腔积液的诊断。     

Diagnostic significance of pleural fluid lactate concentration in pleural and pulmonary diseases

Pleural fluid samples from 198 patients were analysed in order to evaluate the usefulness of lactate concentration as a diagnostic test for separating infectious from non-infectious processes in the pleural cavity. Pleural fluid lactate was quantified by means of a gas chromatographic method. The highest lactate levels were found in patients with septic pleuritis. Significantly lower values were observed in cases with malignancies. With a cut off value of 10 mmol/l, the predictive value of a positive test was 0.94 and of a negative test 1.0. Because of the high predictive values of the test, measurement of lactate concentration in pleural fluid offers a rapid and useful information in the differentiation between infectious and non-infectious pleural disease.     

Use of indwelling pleural catheters for chronic pleural infection

Recurrent, chronic pleural infection creates difficult management issues. Surgical drainage is currently recommended for patients who have failed initial "medical treatment" (ie, tube thoracostomy and antibiotic therapy), but the options for patients not fit for surgery are limited. Prolonged closed tube drainage may be an option in this group, although concerns exist regarding the efficacy and risk of catheter blockage. Long-term indwelling pleural catheters are increasingly used for the treatment of recurrent malignant pleural effusion. Pleural infection is recognized as a complication and is cited as a contraindication to insertion of an indwelling pleural drain within the product literature. We report two patients with empyema in a fixed pleural space in whom the insertion of an ambulatory catheter produced successful drainage. Long-term indwelling pleural catheters may have a role in maintaining the drainage of a chronically infected pleural space that is not readily treated in other ways.     

血清和胸液IFN-γ检测对鉴别结核性和癌性胸液的价值

目的探讨血清和胸液IFN-γ检测对鉴别结核性和癌性胸液的价值。方法用酶联免疫吸附试验（ELISA）法分别检测36例结核性胸液（结核组）、20例癌性胸液（肺癌组）及13例漏出液（对照组）患者血清和胸液中IFN-γ水平。结果结核组IFN-γ明显高于肺癌组、对照组（P〈0.05），肺癌组与对照组无区别；60岁以下患者血清和胸液IFN-γ浓度结核组高于肺癌组。结论IFN-γ在结核和癌性胸液的者血清和胸液中浓度不同，可作为鉴别诊断的参考依据。