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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe the first known Japanese patient with chronic eosinophilic pneumonia caused by Schizophyllum commune. The patient presented to Social Insurance Tagawa Hospital, Fukuoka, Japan with cough, wheezing, dyspnoea, and fever. Computed tomograms of the chest showed bilateral areas of consolidation with air bronchograms as well as interstitial infiltrates in the upper lobe, without ectasia of proximal bronchi. Fibreoptic bronchoscopy revealed no impacted mucus in the bronchi. BAL fluid from the right upper lobe yielded an increased total cell count with a high percentage of eosinophils. A transbronchial lung biopsy specimen showed a bronchoalveolar chronic inflammatory infiltrate composed of eosinophils, lymphocytes and plasma cells, associated with fibrosis of the alveolar walls. S. commune was identified in lavage fluid. Antibodies to this organism were present in the serum, confirming that S. commune was the cause of chronic eosinophilic pneumonia. Inhaled corticosteroids without accompanying oral corticosteroids or antifungal agents decreased the respiratory symptoms, and the infiltrates disappeared from the chest radiograph within a few days
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PMID:Chronic eosinophilic pneumonia associated with Schizophyllum commune. 1470 55

Postmortem human and animal studies provided important insights into the relationship between histology and bacteriology in VAP. According to the results of these studies, VAP is a multifocal and polymicrobial infectious process. The lesions are predominately located in dependent segments of lower lobes. There is no straightforward relationship between the intensity of lung damage and the local microbial burden. Histobacteriologic discrepancy may explain why even such techniques as PSB and BAL can be unreliable for the diagnosis of VAP. The histopathologic examination of the lung tissue has been traditionally regarded as the gold standard for diagnosis of VAP. Even with histology, however, pneumonia is frequently difficult to define. For daily practice, antimicrobial decisions and the guidance of antimicrobial regimens should not rely exclusively on the results of quantitative cultures in the individual patient. Instead, finding a balance between clinical judgment and microbiologic results is crucial to manage patients with VAP appropriately.
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PMID:Diagnosis of hospital-acquired pneumonia: postmortem studies. 1500 93

Pneumonia is common in those patients placed in intensive care units, especially in mechanically ventilated patients. The high mortality rate of ventilator-associated pneumonia requires a rapid initiation of the appropriate antibiotic treatment. Patients who do not respond to initial antibiotic regimens could have the additional benefit of the use of invasive techniques such as bronchoalveolar lavage. Moreover, BAL is of clinical use to identify several non-infectious pulmonary conditions that may mimic pneumonia in these patients. Such conditions include pulmonary haemorrhages, acute eosinophilic pneumonia, malignancy, drug-induced toxicity, adult respiratory distress syndrome and cardiogenic pulmonary oedema. It is important to distinguish these conditions from pneumonia because the management and prognosis of these entities is quite different.
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PMID:Bronchoalveolar lavage in intensive care units. 1536 35

In order to characterize BAL (bronchoalveolar lavage) in CEP (chronic eosinophilic pneumonia) and to investigate the possible role of mast cells and tryptase in the pathogenesis of this interstitial disease, cells and tryptase levels were determined in BAL of patients with CEP and in a group of healthy controls. The results show that a statistically significant increase in tryptase concentration was found in patients with CEP compared with the healthy controls. This is the first report that shows an increase in tryptase levels in CEP and could reflect higher mast cell activation as well as larger mast cell populations in the lungs of these patients. These results strongly support the involvement of mast cells and eosinophils in the immunopathogenesis of CEP.
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PMID:Tryptase concentrations in bronchoalveolar lavage from patients with chronic eosinophilic pneumonia. 1553 94

Dynamic precautions in the early diagnosis and treatment of hospital acquired pneumonias are necessary because of their high mortality. In these patients, invasive diagnostic approaches may be needed since clinical and radiological findings and other non-invasive approaches frequently fail to establish the diagnosis. Thirty eight patients were prospectively included in the study. Average age of patients was 45.5 +/- 16.4 years; 31 were males (81.6%) and 7 (18.4%) were females. Pneumonia was detected in 9 (23.7%) cases during the first five days and in 29 (76.3%) cases after the fifth day of admission to the hospital. Bronchoscopic interventions diagnostic purpose were carried out in 25 (65.8%) patients. The culture results were negative in 7 (18.4%) cases. While more than one pathogen was determined on the cultures of 16 (42.1%) patients only one pathogen was isolated in the cultures of 15 (39.4%) cases. The frequently isolated pathogen on cultures was Staphylococci (45.4%). Other pathogens were Enterobacter spp., Pseudomonas spp., Escherichia coli, Serratia and Streptococcus pneumoniae according to their frequency on cultures. High resistance rates to the third generation cephalosporins were determined. Eleven of 17 deaths in 38 pneumonia cases were attributable to pneumonia. As a conclusion, isolation of pathogen and antibiotic resistance should be determined in the cases with hospital acquired pneumonia. Invasive diagnostic interventions were not avoided when necessary. Although pro-BAL and PSB methods were expensive, their use in selected cases may prevent unnecessary antibiotic use and contribute to a decrease in mortality rate.
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PMID:[The pathogens and their antibiotic sensitivities in hospital-acquired pneumonia cases]. 1555 55

A rat model was used to study the effects of cirrhosis on antibiotic therapy of pneumococcal pneumonia. Cirrhotic and control male Sprague-Dawley rats were infected transtracheally with type 3 Streptococcus pneumoniae. Treatment began 18 h later with phosphate-buffered saline (PBS), azithromycin (50 mg/kg), trovafloxacin (50 mg/kg), or ceftriaxone (100 mg/kg) injected subcutaneously twice daily for 5 days. Antibiotic concentrations were measured by high-performance liquid chromatography. Azithromycin, trovafloxacin, and ceftriaxone were all equally effective at preventing mortality in both cirrhotic and normal rats. Free fraction area under the curve to minimum inhibitory concentration ratio (AUC/MIC) and maximum calculated serum concentration to MIC ratio (C(max)/MIC) and percent time that the serum concentration exceeded the MIC (%T > MIC) were greater for ceftriaxone compared with azithromycin or trovafloxacin. Azithromycin achieved higher concentrations in bronchoalveolar lavage fluid (BALF), epithelial lining fluid (ELF), and BAL white blood cells than ceftriaxone or trovafloxacin in cirrhotic rats. Macrolide, beta-lactam, or fluoroquinolone antibiotic efficacy in a pneumococcal pneumonia model does not appear to be affected by hepatic cirrhosis.
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PMID:Effect of cirrhosis on antibiotic efficacy in a rat model of pneumococcal pneumonia. 1569 15

Pneumocystis carinii f. sp. hominis is an important cause morbidity and morality, causing P. carinii pneumonia (PCP) in AIDS and other immunocompromised patients. Long thought of as protozoan, molecular analysis of the ribosomal gene locus first demonstrated that P. carinii is a member of the fungal kingdom. Currently P. carinii is considered to be fungus likely to Ascomycetes, based on its ultrastructure, certain elements of its cellular biology, and nucleotide sequences of main genetic loci. The standard method for diagnosis P. carinii is microscopic examination of stained (immunofluorescent or conventional tinctorial) invasive specimens: BAL (bronchoalveolar lavage), lung biopsy or induced sputum with sensitivity varying range from <50% to >90%. Molecular detection system have the potential to provide a higher degree of sensitivity than microscopic method. PCR technique have been applied to lower respiratory tract clinical specimens and recently to non-invasive oral washes as well. Because P. carinii infection can be rapidly progressive and success of therapy dependent to the time of the initial therapy, early diagnosis and treatment is essential.
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PMID:[Pneumocystis carinii--diagnosis based on DNA amplification technique]. 1575 51

The aim of the study was to assess the diagnostic yield of transbronchial lung biopsy (TBLB) in some of diffuse pulmonary diseases, like: sarcoidosis, organizing pneumonia--(OP), tuberculosis and neoplasmatic infiltrates of the lung. Transbronchial lung biopsy was performed in 123 patients, preceded by high resolution computed tomography (HRCT). The HRCT guidance helped to select the area of lung to be biopsied. In 80 patients (65%) TBLB enabled to diagnose 40 cases of sarcoidosis, 15 cases of OP, 13 cases of neoplasmatic infiltrates of the lung and 5 cases of tuberculosis. There were 43 cases undiagnosed by means of TBLB. In 19 patients the diagnosis was established by means of other methods like videothoracoscopy (8 cases), bronchoscopy with bronchial mucose biopsy (7 cases of sarcoidosis), mediastinoscopy (2 cases of Hodgkin's disease), transthoracic needle biopsy (2 cases of adenocarcinoma). Moreover sarcoidosis was diagnosed in 15 cases by means of clinical, radiological examination and BAL. 9 patients didn't agree for further invasive diagnostics. Transbronchial lung biopsy was shown to be efficient diagnostic method especially in sarcoidosis, OP and neoplasmatic infiltrates of the lung. However, in approximately 35% of cases of diffuse pulmonary diseases this technique doesn't allow to establish a diagnosis. This in turn implicates the necessity for further diagnostic procedures including videothoracoscopic or open lung biopsy.
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PMID:[Transbronchial lung biopsy as a diagnostic method of diffuse pulmonary diseases]. 1575 52

Respiratory Mycoplasma pneumoniae (Mp) infection is involved in several acute and chronic lung diseases including community-acquired pneumonia, asthma and chronic obstructive pulmonary disease. In the chronic disease process, recurrent respiratory bacterial infections could occur, which may result in varying degrees of symptoms and lung inflammation among patients. However, the lung immunologic differences of host responses to repeated bacterial (i.e., Mp) infections remain to be determined. In the present study, we examined cellular and humoral responses to multiple (up to 3) Mp infections in two genetically different strains of mice (BALB/c and C57BL/6). Mice were intranasally inoculated with one Mp infection, two or three Mp infections (4 weeks apart), and sacrificed on days 3, 7 and 14 after the last Mp infection. Overall, compared to C57BL/6 mice, BALB/c mice demonstrated a significantly higher degree of lung tissue inflammatory cell infiltrate, BAL cellularity, and release of pro-inflammatory cytokines (TNF-alpha, keratinocyte-derived chemokine (KC, a mouse homolog of human chemokine Gro-alpha [CXCL1], and IFN-gamma). In addition, BALB/c mice presented higher levels of serum Mp-specific IgG and IgM, but not IgA. Consistently with lung and serum data, Mp load in BAL and lung specimens was significantly higher in BALB/c mice than C57BL/6 mice. Moreover, repeated Mp infections in BALB/c, but not C57BL/6 mice, produced a greater inflammatory response than did a single Mp infection. Our results suggest that hosts with different genetic background may have different susceptibility to repeated respiratory Mp infections along with inflammatory responses.
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PMID:Repeated respiratory Mycoplasma pneumoniae infections in mice: effect of host genetic background. 1671 27

Ceftobiprole medocaril [BAL 5788, RO 65-5788, JNJ 30982081] is a prodrug in phase III clinical development with Basilea Pharmaceutica and Cilag AG (Johnson & Johnson) for the potential treatment of serious bacterial infections, including methicillin-resistant Staphylococcus aureus (MRSA). Ceftobiprole medocaril is the water-soluble prodrug of the pyrrolidinone cephalosporin, ceftobiprole [BAL 9141, RO 63-9141]. Because of the low water solubility of ceftobiprole, its clinical application was limited and Basilea began its investigations into ceftobiprole medocaril for further development. Ceftobiprole medocaril is being developed for IV administration and is currently undergoing phase III trials for complicated skin and skin structure infections (including MRSA) and hospital-acquired (nosocomial) pneumonia. Ceftobiprole medocaril has a broad spectrum of activity against Gram-positive bacteria (including methicillin-resistant staphylococci, penicillin-resistant pneumococci and Enterococcus faecalis) and Gram-negative bacteria. Ceftobiprole medocaril inhibits all transpeptidases, including the penicillin-binding protein (PBP) 2a, by a unique combination of features. PBP 2a is the primary enzyme responsible for beta-lactam drug resistance in MRSA; PBP 2a also acts as a key defense mechanism by interacting with the bacterial cell wall to form a chemical barricade that is impervious to antibiotics. Ceftobiprole medocaril has been designed specifically to bind to this penicillin-resistant target. Ceftobiprole medocaril is bactericidal and has not shown resistance development in vitro or in stringent animal models. Studies conducted by Basilea have demonstrated that ceftobiprole medocaril is readily converted to ceftobiprole, and shows markedly improved water solubility. In February 2005, Basilea Pharmaceutica AG entered into an exclusive worldwide agreement with Cilag AG International (Johnson & Johnson) to develop, manufacture and market ceftobiprole medocaril. Ortho-McNeil Pharmaceutical (Johnson & Johnson) will market ceftobiprole medocaril in the US, and its affiliate companies, known as Janssen-Cilag, will market the product outside the US (entered as World in the Licensee table). Basilea has retained an option to co-promote ceftobiprole medocaril in the US, major European countries, Japan and China. Johnson & Johnson Pharmaceutical Research and Development LLC will develop ceftobiprole medocaril in collaboration with Basilea. Roche previously retained an opt-in right on ceftobiprole medocaril. However, following Roche's decision not to exercise this right in May 2004, Basilea gained full global commercialisation rights for ceftobiprole medocaril. Roche retains its major shareholding in Basilea. Ceftobiprole medocaril is currently in phase III trials for complicated skin and skin structure infections due to MRSA, and nosocomial pneumonia (including ventilator-associated pneumonia) due to suspected or proven MRSA, and community-acquired pneumonia. The US FDA has granted fast-track status to the compound for these two indications. Phase III results are expected in 2006 and an NDA is expected to be submitted to the FDA in 2007. An additional pivotal phase III trial (STRAUSS 2, STudy of Resistant Staphyloccocus aureus in Skin and Skin structure infections) of ceftobiprole medocaril was initiated in October 2005 for complicated skin infections, including diabetic foot infections. This trial will be conducted in conjunction with Johnson & Johnson Pharmaceutical Research and Development.
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PMID:Ceftobiprole Medocaril: BAL5788, JNJ 30982081, JNJ30982081, RO 65-5788, RO 655788. 1692 91


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