False-positive Mycobacterium tuberculosis culture revealed by restriction fragment length polymorphism analysis.

BACKGROUND: The microbiological analysis of respiratory specimens is the most reliable approach to diagnose active pulmonary tuberculosis. PATIENT AND METHODS: We report a 60-year-old female patient (index patient) who underwent diagnostic bronchoscopy for chronic cough. No acid-fast bacilli were detected in bronchial washings. Although cough subsided with symptomatic treatment, Mycobacterium tuberculosis grew on egg-based media after 12 weeks. A false-positive culture result was suspected. Chart review and DNA fingerprinting were carried out. RESULTS: The bronchoscope used to examine the index patient was previously used for a 30-year-old patient (source patient) with smear- and culture-positive pulmonary tuberculosis. Restriction fragment length polymorphism (RFLP) analysis based on the IS 6110 element confirmed that the two strains were identical. CONCLUSION: Cross-contamination is a reason for false-positive cultures with M. tuberculosis and should be suspected in patients with a low clinical probability for active tuberculosis.

[Dust exposure, dust-induced lung diseases and respiratory protective measures in agriculture]. / Staubbelastung, staubbedingte Lungenkrankheiten und Atemschutzmassnahmen in der Landwirtschaft.

Epidemiologic studies indicate a high prevalence of respiratory diseases among the farming population. Many of these diseases are responsible for disability and death and there is a considerable impact on the economy and health cost expenditure. Respirable organic dust plays a major pathogenetic role. Part I of this review discusses the diseases and syndromes caused by organic dust: organic dust toxic syndrome; chronic bronchitis and chronic obstructive pulmonary disease; asthma; and hypersensitivity pneumonitis. Part II describes preventive measures for dust control. Besides technical aspects in the process of agriculture production, special emphasis is placed on personal protective equipment systems (face-masks and air-purifying respirators). Applications, advantages and disadvantages of these systems are discussed and critically compared.

Endogenous production of superoxide by rabbit lungs: effects of hypoxia or metabolic inhibitors.

We find spontaneous light emission from isolated Krebs-Henseleit-perfused rabbit lungs when the light-emitting super-oxide trap lucigenin is added to the perfusate. Lucigenin light emission appears to be specific for superoxide anion, because light emission from the lung caused by a superoxide-generating system is abolished by superoxide dismutase but not by catalase or dimethylthiourea. We also studied the relative sensitivity of lucigenin photoemission to superoxide and to H2O2 in vitro. Lucigenin photoemission is three to four orders of magnitude more sensitive to superoxide than to H2O2 and probably cannot detect H2O2 in concentrations thought to occur in biological systems. Basal lucigenin photoemission by the lung is oxygen dependent, because severe hypoxia completely inhibits light emission. Superoxide dismutase reduces basal photoemission by 50%, and administration of the low-molecular-weight superoxide scavenger 4,5-dihydroxy-1,3-benzene disulfonic acid (tiron) inhibits basal photoemission by approximately 90%. These observations suggest that endogenous superoxide production is primarily intracellular and that approximately half of the superoxide reaches the extracellular space. Superoxide transport may involve anion channels, because the anion channel blocker 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid increases photoemission, suggesting intracellular accumulation of superoxide. A cytochrome P-450 inhibitor, SKF 525A, or the mitochondrial transport inhibitor antimycin decreased basal photoemission by approximately 50%, suggesting that cytochrome P-450-mediated reactions and perhaps mitochondrial function contribute to basal superoxide production in the isolated perfused lung. Endogenous superoxide production may be important in regulation of pulmonary vascular reactivity and may contribute to the pathogenesis of lung reperfusion injury.

[Amborum Special F and ASFO--2 glucocorticoid-containing herbal remedies]. / Amborum Special F und ASFO--zwei glucocorticoidhaltige Naturheilmittel.

Amborum Special F and ASFO are two names of a herbal remedy which is adulterated with the glucocorticoid betamethasone. Patients with asthma, rheumatic and chronic diseases import the drug direct from Burbank, California, USA. Its impressive antiasthmatic effect is reported in two patients. While under therapy the first patient developed Cushing's syndrome and the second showed suppression of adrenal cortisol production. The manufacturer, who claims that the drug contains no "western medicine" and in particular no cortisone, is unscrupulous enough to recommend it for children under two years of age. We have observed that a marked glucocorticoid effect and marked glucocorticoid side effects are achieved with small doses of betamethasone. A review of the literature and the two cases reported here suggest that the equivalence doses given in textbooks and tables of glucocorticoid equipotency are incorrect for betamethasone. Betamethasone is a more potent glucocorticoid than hitherto reported.

Hydroperoxide-induced chemiluminescence in rabbit lungs: role of arachidonic acid enzymes.

Low-level chemiluminescence (C) is thought to be an index of oxidant stress. We measured the relationship between low-level C, pulmonary arterial pressure, and perfusate concentration of thromboxane B2 (TxB2) in isolated perfused rabbit lungs during challenge with tert-butyl hydroperoxide (t-bu-OOH). We also measured glutathione release as another index of oxidant stress. We found that C was correlated with each variable, suggesting that oxidant stress measured by C and by glutathione release stimulated TxB2 production and pulmonary vasoconstriction. We also investigated the contribution of active O2 metabolites produced by prostaglandin (PG) peroxidase to oxidant stress by studying the effects of t-bu-OOH before and after the use of cyclooxygenase and lipoxygenase inhibitors. We found that C was augmented after inhibition, perhaps due to metabolism of t-bu-OOH by peroxidases of both arachidonic acid (AA) metabolic pathways in the absence of their normal substrates. We studied phenylbutazone, thought to inhibit peroxidases, and AA. C during t-bu-OOH administration was not augmented after phenylbutazone and was markedly inhibited after AA administration perhaps because AA competes with t-bu-OOH. To further study the role of peroxidases we pretreated the lungs with the antioxidant dithiothreitol, which inhibits peroxidases involved in both the cyclooxygenase and lipoxygenase pathways. Dithiothreitol nearly abolished C produced by t-bu-OOH and also prevented the increased light caused by eicosatetrynoic acid. We directly tested the hypothesis that C occurred as a result of the interaction of t-bu-OOH and the cyclooxygenase and lipoxygenase enzymes; we measured C when t-bu-OOH was added to purified PGH2 synthase or soybean lipoxygenase. The combination of t-bu-OOH with PGH2 synthase or lipoxygenase led to C that was inhibited by dithiothreitol and by the antioxidant phenol. These results suggest that enzymes involved in AA metabolism can interact with t-bu-OOH and that the action of these enzymes on t-bu-OOH leads to C. The results may mean that lipid peroxides can indirectly contribute to tissue oxidant stress due to production of active O2 metabolites as by-products of their metabolism by AA peroxidases.

Amiodarone causes acute oxidant lung injury in ventilated and perfused rabbit lungs.

Amiodarone (ADR), a new antiarrhythmic drug for life-threatening cardiac arrhythmias, causes pneumonitis or lung fibrosis in a sizeable minority of patients. The cause of lung damage is not known. We have shown that infusion of 10 mg amiodarone into the inflow circuit of ventilated and perfused rabbit lungs causes immediate increase in pulmonary artery pressure (mean +/- SEM) (from 13.6 +/- 1.2 to 40.6 +/- 9.5 mm Hg, p less than 0.01) and pulmonary edema with marked increase in the pulmonary generation of thromboxane and leukotrienes C4 and/or D4. Albumin (2 g%) in the perfusate prevents any increase in lung perfusion pressure or edema formation. When lung perfusion pressure increase is blocked with the combined cyclooxygenase and lipoxygenase inhibitor enolicam sodium (CG5391B, 35 microM in perfusate), significant lung edema still occurs after amiodarone, indicating that amiodarone causes increased alveolar-capillary membrane permeability. Addition of catalase (100 U/ml) or superoxide dismutase and catalase (100 U/ml each) to perfusate fails to protect from amiodarone lung injury. Immediate infusion of amiodarone (10 mg) into lungs ventilated with room air (ADR + RA) causes an increase in lung weight gain from baseline (delta W) of 5.7 +/- 1.5 g/min. Compared with ADR + RA, ventilation of lungs with 4% O2 (delta W = 0.7 +/- 0.3 g/min, p less than 0.05), pretreatment of rabbits for 3 days with butylated hydroxyanisole (BHA, 100 mg/kg/day i.p., delta W = 0.05 +/- 0.02 g/min, p less than 0.01), pretreatment of rabbits for 3 days with vitamin E (Vit E, 300 U/day orally, delta W = 0.6 +/- 0.2 g/min, p less than 0.05), or addition of N-acetylcysteine to the lung perfusate (NAC, 5 mM, delta W = 0.1 +/- 0.08 g/min, p less than 0.01) all protect from lung edema formation after amiodarone. Amiodarone (100 mg) also caused a marked increase in luminol-enhanced lung chemiluminescence, lung production of superoxide anion (O2-), and tissue levels of lung glutathione disulfide. These results suggest that amiodarone causes lung injury by an oxidant mechanism.

The role of cyclooxygenase and lipoxygenase mediators in oxidant-induced lung injury.

Infusion of the oxidant lipid peroxide tert-butyl hydroperoxide (t-bu-OOH) causes pulmonary vasoconstriction and increases vascular permeability in isolated perfused rabbit lungs. We have previously shown that t-bu-OOH stimulates arachidonic acid metabolism, increasing the synthesis of the cyclooxygenase products. The current experiments were designed to determine the role that cyclooxygenase- and lipoxygenase-derived mediators play in the lung injury caused by t-bu-OOH. In the present experiments, we found that t-bu-OOH not only increased the synthesis of the cyclooxygenase-derived products thromboxane and prostacyclin but also increased the synthesis of the lipoxygenase-derived products leukotrienes B4, C4, D4, and E4. To determine the role that these arachidonic acid metabolites play in the increase in pressure and vascular permeability caused by t-bu-OOH, we studied the effect that inhibitors of arachidonic acid metabolism or a leukotriene receptor blocker had on the pulmonary edema. We compared an uninjured control group with 4 groups of lungs given t-bu-OOH: a t-bu-OOH control group; a group pretreated with the cyclooxygenase inhibitor indomethacin (14 microM); a group pretreated with an analogue of arachidonic acid, 5-, 8-, 11-, 14-eicosatetraynoic acid (ETYA) (100 microM), that inhibits both the cyclooxygenase and lipoxygenase pathways; and a group pretreated with the leukotriene receptor antagonist FPL 55712 (38 microM). To produce lung injury, t-bu-OOH (300 microM) was infused throughout the first minute of 4 successive 10-min periods.(ABSTRACT TRUNCATED AT 250 WORDS)

[Self-monitoring of airway obstruction using the peak flowmeter]. / Die Selbstüberwachung der Atemwegobstruktion mit dem Peak-Flow-Meter.

Daily peak flow measurements provide an accurate and objective assessment of airway obstruction. The peak flow profile offers a rational basis for antiobstructive treatment. Success and failure of treatment are visualized, as are the asymptomatic beginning of an asthmatic attack, an allergen exposure or an exercise-induced obstruction. Compliance improves, and self-monitoring seems to increase patient comfort. A considerable amount of knowledge about the dynamics of airway obstruction is conveyed to the physician, and this works very much to the benefit of his patient.