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Pseudomonas aeruginosa is a non-capsulate and non-sporing Gram-negative bacillus that most commonly affects the lower respiratory system in humans. Burkholderia (previously Pseudomonas) cepacia has emerged as an important respiratory pathogen in patients with cystic fibrosis (CF). The ability of P. aeruginosa to persist and multiply in moist environments and equipment, such as humidifiers in hospital wards, bathrooms, sinks and kitchens, maybe of importance in cross-infection. P. aeruginosa infections of the lower respiratory tract can range in severity from colonisation (without an immunological response) to a severe necrotising bronchopneumonia. Infection is seen in patients with CF and other chronic lung diseases such as non-CF bronchiectasis. In patients with CF, once P. aeruginosa is established in the airways it is almost impossible to eradicate, but prior to this, aggressive treatment can delay the development of chronic infection. 30 to 40% of the present paediatric population with CF will have chronic pseudomonal infection. B. cepacia has a particular predisposition to infect patients with CF and may be distinguished from P. aeruginosa by accelerated lung disease in about one-third of patients. Overwhelming septicaemia and necrotising pneumonia are well described (cepacia syndrome); events that are rare with P. aeruginosa. With the propensity for social cross-infection, segregation policies have been accepted as means of controlling outbreaks. A number of antipseudomonal agents are available. The most commonly used are the extended-spectrum penicillins, aminoglycosides, cephalosporins, fluoroquinolones, polymixins and the monobactams. An aminoglycoside with a β-lactam penicillin is usually considered to be the first line treatment. No trial has shown any significant clinical advantage of any particular combination regimen over another. The emergence of resistance continues to be a concern. Pipericillin, piperacillin/tazobactam and meropenem have good but equivalent antibacterial activity against P. aeruginosa. However, B. cepacia is characterised by in vitro resistance to colistin (colomycin), aminoglycosides and ciprofloxacin but better susceptibility to ceftazidime. Nebulised delivery of antipseudomonal antibiotics is thought to prevent recurrent exacerbations, reduce antibiotic usage and maintain lung function, particularly in patients with CF. Colistin, tobramycin and gentamicin are currently the most commonly prescribed nebulised antibiotics. Much effort is directed at treating chronic P. aeruginosa infection but as chronic infection is seldom if ever eradicated when first established, prevention is preferable. Early intensive treatment for P. aeruginosa infection is advocated in order to maintain pulmonary function and postpone the onset of chronic P. aeruginosa infection. [ABSTRACT FROM AUTHOR]

The article discusses the new respiratory therapies for patients with cystic fibrosis. The efficacy of several developments to respiratory therapy such as antimicrobial chemotherapy is explored. Ways to clear secretions are tackled, including physiotherapy and modification of sputum electrolyte milieu. The treatment of complications is also discussed. Other developments include lung transplantation, immunomodulation and gene therapy.

Nine of 14 asthmatic patients who presented with persistent dysphonia while taking inhaled corticosteroids had a bilateral adductor vocal cord deformity with bowing of the cords on phonation. This causes the dysphonia and usually occurs without candidiasis. It was seen with beclomethasone dipropionate (in both pressurised aerosol and dry powder preparations), betamethasone valerate, and budesonide. It was related to the dose and potency of inhaled steroid and may represent a local steroid myopathy. It was reversed when the inhaled steroid was stopped, although resolution sometimes took weeks. Laryngeal candidiasis may have contributed to the vocal cord abnormality in two of these nine patients. Of the five patients without vocal cord deformity, laryngeal candidiasis was the sole cause of dysphonia in three. In the remaining two dysphonia was thought to be psychogenic. The vocal cord deformity may exist subclinically. Of nine patients who started to take aerosol steroid and who were examined monthly for one year, three developed vocal cord deformity but only one had persistent dysphonia. Vocal abuse did not appear to contribute to dysphonia. [ABSTRACT FROM AUTHOR]

Fourteen (29%) of 48 children with cystic fibrosis had a greater than 15% improvement in forced expiratory volume in one second, or in forced vital capacity after inhalation of salbutamol. All these children were atopic (one or more positive prick tests) and had a significantly higher mean serum IgE than either non-atopic subjects or those atopic subjects without airways reversibility (p less than 0.02). Half of those with airways reversibility had or subsequently developed the clinical picture of allergic bronchopulmonary aspergillosis. Of the whole group 81% were atopic, of whom 77% had a positive reaction to A fumigatus, 64% to housedust, and 56% each to grass pollen and cat hair. Children who were not atopic had significantly better spirometry (p greater than 0.05) than those who were. Children with skin hypersensitivity to A fumigatus had identical spirometry to those who were atopic without reactivity to A fumigatus. Serum precipitins to A fumigatus were present in 48%. Serum precipitins to pancreatin were present in 71%, but the presence of these precipitins did not correlate with atopy, airways reversibility, or serum IgE. [ABSTRACT FROM AUTHOR]

Large lung bullae are a rare manifestation of pulmonary sarcoidosis. Of three patients with this complication, all had pulmonary infiltrates at presentation and two had bilateral hilar adenopathy. Hypercalcaemia developed during the course of the illness in all three patients. In each case the bullae had developed within four years of the diagnosis of sarcoidosis. In one woman a bulla resolved almost completely after it had become infected. [ABSTRACT FROM AUTHOR]

Measurement of serum theophylline concentration is usually recommended before intravenous aminophylline is given to patients taking oral theophylline. Fifty patients with worsening airflow obstruction, all of whom were taking oral theophyllines and who had no contraindication to the use of parenteral aminophylline, were randomly allocated into two groups before treatment was given. The dose of aminophylline was calculated without (group A) and with (group B) knowledge of admission serum theophylline concentration. In group A a regimen incorporating corrections to account for factors affecting theophylline clearance was used in an attempt to represent a "knowledgeable" approach; in group B a formula incorporating the known serum theophylline concentration at the time of admission was used. All loading doses were given over 30 minutes as "mini infusions." The two groups were well matched for age, blood gas tensions, and severity of airflow obstruction. The results for four patients (one from group A and three from group B) were excluded from analysis after completion of the study. In each group the mean admission serum theophylline concentration measured (group A: 8.4 (SD 6.0)mg/l; group B: 7.2 (5.7)mg/l) and the aminophylline doses used (group A: loading bolus 172 (45.5)mg, infusion 815 (198)mg; group B: loading bolus 233(189)mg, infusion 788(214)mg) were similar. Mean serum theophylline concentrations during 24 hours' aminophylline treatment, number of patients with a serum theophylline concentration greater than 20 mg/l, symptoms of toxicity, and outcome were also similar in the two groups. Although satisfactory use of parenteral aminophylline was achieved for most patients without knowledge of serum theophylline concentration at the time of admission to hospital (with the aid of a "knowledgeable" clinical approach and constant infusion pumps), prompt measurement of serum theophylline concentration at the time of admission identified patients with either suboptimal or potentially hazardous theophylline concentrations. [ABSTRACT FROM PUBLISHER]

The effect of adding slow release nifedipine to oral theophylline has been studied in eight patients with stable but symptomatic asthma, a double blind placebo controlled crossover protocol being used. No change in asthma control occurred during the nifedipine treatment period as assessed by serial peak flow measurements and symptom scores. Serum theophylline concentrations were significantly lower after nifedipine than after placebo (6.8 v 9.7 micrograms/ml) and in three patients were well below the therapeutic range (less than 4 micrograms/ml). [ABSTRACT FROM PUBLISHER]