Early bronchopulmonary involvement in Crohn disease: a case report.
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BACKGROUND: Bronchopulmonary manifestations of Crohn disease have been rarely described in children, including both subclinical pulmonary involvement and severe lung disease. CASE PRESENTATION: A 6.5-year-old girl is described with early recurrent bronchopulmonary symptoms both at presentation and in the quiescent phase of Crohn disease. Pulmonary function tests (lung volumes and flows, bronchial reactivity and carbon monoxide diffusing capacity) were normal. Bronchoalveolar cytology showed increased (30%) lymphocyte counts and bronchial biopsy revealed thickening of basal membrane and active chronic inflammation. CONCLUSIONS: Clinical and histological findings in our young patient suggest involvement of both distal and central airways in an early phase of lung disease. The pathogenesis of Crohn disease-associated lung disorders is discussed with reference to the available literature. A low threshold for pulmonary evaluation seems to be advisable in all children with CD. (+info)
Nucleotide sequence and organization of plasmid pMVSCS1 from Mannheimia varigena: identification of a multiresistance gene cluster.
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OBJECTIVES: A small resistance plasmid of Mannheimia varigena was analysed with regard to its gene organization and the development of a multiresistance gene cluster. MATERIALS AND METHODS: The 5621 bp plasmid pMVSCS1 was transformed into Escherichia coli JM107, cloned and sequenced completely. RESULTS: Three intact resistance genes, sulII, catAIII and strA, a truncated strB gene and a novel replication gene were identified. A potential recombination site for the integration of catAIII in the spacer region between sulII and strA was identified. CONCLUSION: The physical linkage of the plasmid-borne resistance genes organized in a cluster would facilitate the spread of the different resistance genes by co-selection, even in the absence of a direct selective pressure. (+info)
Complications following peripheral angioplasty.
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BACKGROUND: Peripheral angioplasty is increasingly the first choice intervention in patients with peripheral vascular disease. The aim of the current study was to audit prospectively all major complications, especially the requirement for emergency surgical intervention. PATIENTS AND METHODS: A prospective audit of outcome after peripheral angioplasty in 988 patients undergoing 1377 interventional procedures between 1 October 1995 and 30 September 1998 at which 1619 vessel segments were angioplastied. RESULTS: Major medical morbidity (bronchopneumonia, stroke, renal failure, myocardial infarction) complicated 33/1377 procedures (2.4%). Emergency surgical intervention was required after 31/1377 procedures (2.3%) with the commonest aetiologies being acute limb ischaemia and haemorrhagic complications. The amputation rate following angioplasty was 0.6% and no patient presenting with claudication or graft complications underwent amputation. The amputation rate following angioplasty for critical limb ischaemia was 2.2%. Overall, the risk of death and/or major medical complication and/or requiring emergency surgical intervention was 3.5%. The rate of complications was no different for subintimal as opposed to transluminal angioplasties. CONCLUSIONS: Peripheral angioplasty is associated with a low risk of major medical and surgical complications. (+info)
Familial non-cystic fibrosis mucus inspissation of respiratory tract.
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Perlman, M., Williams, J., Hirsch, M., and Bar-Ziv, J. (1975). Archives of Disease in Childhood, 50, 727. Familial non-cystic fibrosis mucus inspissation of respiratory tract. Two sibs, whose parents are first cousins, have had chronic obstructive airways disease from birth with recurrent otitis media, sinusitis, and mastoiditis. The disease, associated with clinically abnormal mucus, differs from other familial obstructive airways diseases and probably constitutes a new entity. (+info)
Cytology of tracheobronchial aspirates in horses.
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Tracheobronchial aspirates were obtained from 27 normal horses and from 57 horses with respiratory disease. Aspirates from normal horses contained mainly ciliated columnar epithelial cells, mononuclear cells, a few neutrophils and mucus. Aspirates from horses with acute suppurative bronchopneumonias or chronic bronchiolitis had predominantly neutrophils and usually large amounts of mucus; in severe suppurative inflammatory diseases, many of the cells were degenerated, and there were coils of fibrinous material resembling Curschmann's spirals. Eosinophils were rarely found, even from horses with histories suggestive of allergic respiratory disease. Aspirates from horses with epistaxis frequently had macrophages with intracytoplasmic green globules (hemosiderin). Tracheobronchial aspirates occasionally revealed subclinical lung disease. Four horses with no clinical signs of lung disease and lungs that were unremarkable on percussion and normal on auscultation had adpirates suggestive of inflammation; histologic examination confirmed bronchiolitis. (+info)
Immunomodulatory and protective effects of moxifloxacin against Candida albicans-induced bronchopneumonia in mice injected with cyclophosphamide.
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In a previous study, moxifloxacin was shown to ameliorate immunosuppression and enhance cytokine production in several tissues, including the lungs of cyclophosphamide-injected mice. We examined here the effects of moxifloxacin on Candida albicans lung infection in cyclophosphamide-injected mice. Mice were injected on day 0 with 250 mg of cyclophosphamide/kg, and on days 1 to 4 they were given moxifloxacin at 22.5 mg/kg/day compared to controls given ceftazidime at 75 mg/kg/day or saline. On day 6, C. albicans (10 7 CFU/mouse) was inoculated intratracheally, and animals were observed for the development of bronchopneumonia, weight loss, mortality, the presence of C. albicans, and lung cytokine production. Histopathology on day 10 postinoculation revealed bronchopneumonia in 50, 67, and 0% of saline-, ceftazidime-, and moxifloxacin-treated mice, respectively (P < 0.05). The mortality rates were 28, 17, and 5%, respectively (P < 0.05), and weight loss occurred at 20, 32, and 0%, respectively (P < 0.05). By day 15, C. albicans was eliminated from all moxifloxacin-treated mice but was still isolated from lung homogenates of 50 to 60% of the saline- and ceftazidime-treated groups. Among the cytokines tested on days 0 to 15, we found an increased production of tumor necrosis factor alpha, KC (functional interleukin-8), and gamma interferon in the lungs of ceftazidime- and saline-treated controls compared to the moxifloxacin pretreatment that abolished their secretion. In conclusion, moxifloxacin protected cyclophosphamide-injected mice from C. albicans-induced lung infection and significantly reduced pneumonia, weight loss, and mortality despite the lack of direct antifungal activity. This is most likely due to an immunomodulating activity conferred by moxifloxacin, as shown in this model and in our previous studies. Its potential protective role should be studied in patients undergoing chemotherapy and immune suppression. (+info)
Influence of lung aeration on pulmonary concentrations of nebulized and intravenous amikacin in ventilated piglets with severe bronchopneumonia.
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BACKGROUND: Pulmonary concentrations of aminoglycosides administered intravenously are usually low in the infected lung parenchyma. Nebulization represents an alternative to increase pulmonary concentrations, although the obstruction of bronchioles by purulent plugs may impair lung deposition by decreasing lung aeration. METHODS: An experimental bronchopneumonia was induced in anesthetized piglets by inoculating lower lobes with a suspension of 10(6) cfu/ml Escherichia coli. After 24 h of mechanical ventilation, 7 animals received two intravenous injections of 15 mg/kg amikacin, and 11 animals received two nebulizations of 40 mg/kg amikacin at 24-h intervals. One hour following the second administration, animals were killed, and multiple lung specimens were sampled for assessing amikacin pulmonary concentrations and quantifying lung aeration on histologic sections. RESULTS: Thirty-eight percent of the nebulized amikacin (15 mg/kg) reached the tracheobronchial tree. Amikacin pulmonary concentrations were always higher after nebulization than after intravenous administration, decreased with the extension of parenchymal infection, and were significantly influenced by lung aeration: 197 +/- 165 versus 6 +/- 5 microg/g in lung segments with focal bronchopneumonia (P = 0.03), 40 +/- 62 versus 5 +/- 3 microg/g in lung segments with confluent bronchopneumonia (P = 0.001), 18 +/- 7 versus 7 +/- 4 microg/g in lung segments with lung aeration of 30% or less, and 65 +/- 9 versus 2 +/- 3 microg/g in lung segments with lung aeration of 50% or more. CONCLUSIONS: In a porcine model of severe bronchopneumonia, the nebulization of amikacin provided 3-30 times higher pulmonary concentrations than the intravenous administration of an equivalent dose. The greater the lung aeration, the higher were the amikacin pulmonary concentrations found in the infected lung segments. (+info)
Bronchoalveolar lavage fluids of patients with lung injury activate the transcription factor nuclear factor-kappaB in an alveolar cell line.
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In bronchoalveolar lavage (BAL) fluid from ventilated patients, cytotoxic oxidant activity is correlated with neutrophil activation. The aim of the present study was to investigate the hypothesis that BAL fluid induces activation of the transcription nuclear factor-kappaB (NF-kappaB) in human alveolar cells, in correlation with inflammatory mediators. We measured endotoxin, inflammatory cytokines [interleukin-1beta (IL-1beta), IL-8], nitrated proteins and the activity of myeloperoxidase (MPO) in BAL fluid from ventilated patients developing bronchopneumonia ( n =19 samples) or with acute respiratory distress syndrome (ARDS) ( n =14), and from ARDS/infection-free patients ( n =11). We also exposed alveolar cells to the BAL fluid or to human MPO, H(2)O(2) or HOCl, and tested nuclear extracts for the activation of NF-kappaB. IL-1beta, IL-8, nitrated protein, MPO and endotoxin levels were significantly higher in BAL fluid from patients with bronchopneumonia than in that from the ARDS and ARDS/infection-free groups. A correlation was observed between IL-8 and MPO values ( r =0.82). The level of NF-kappaB activity induced by the BAL fluid was correlated with levels of IL-1beta ( P <0.001), IL-8 ( P <0.005) and MPO ( P <0.002), and with the neutrophil count ( P <0.002), and was higher for BAL fluid from the bronchopneumonia group. NF-kappaB activation by MPO was also demonstrated. The activation of NF-kappaB by BAL fluid, especially that from bronchopneumonia patients, suggests that a similar phenomenon may occur in vivo, leading to potential amplification of the inflammatory reaction. (+info)