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Thorax 2003;58:594-597
© 2003 BMJ Publishing Group & British Thoracic Society


RESPIRATORY INFECTION

Asymptomatic carriage of Pneumocystis jiroveci in subjects undergoing bronchoscopy: a prospective study

N A Maskell1, D J Waine1, A Lindley2, J C T Pepperell1, A E Wakefield2, R F Miller3, R J O Davies1

1 Oxford Centre for Respiratory Medicine, Churchill Hospital, Oxford Radcliffe NHS Trust, Oxford OX3 7LJ, UK
2 Department of Paediatrics, Weatherall Institute of Molecular Medicine, Oxford Radcliffe NHS Trust, Oxford OX3 9DU, UK
3 Windeyer Institute of Medical Sciences, Royal Free and University College Medical School, University College London, London, UK

Correspondence to:
Correspondence to:
Dr R J O Davies, Oxford Centre for Respiratory Medicine, Churchill Hospital, Oxford Radcliffe NHS Trust, Oxford OX3 7LJ, UK;
robert.davies{at}ndm.ox.ac.uk

Background: The opportunistic fungus Pneumocystis jiroveci is a common cause of respiratory infection in immunocompromised patients. By contrast, pneumocystis pneumonia (PCP) occurs only rarely in immunocompetent individuals. Asymptomatic colonisation with P jiroveci has recently been described in patients who are either minimally immunosuppressed or who have underlying lung disorders such as bronchiectasis. We sought to determine the prevalence of asymptomatic colonisation by P jiroveci in a cohort of adult patients undergoing diagnostic bronchoscopy.

Methods: A prospective observational cohort study was performed in patients who required bronchoscopy and bronchoalveolar lavage (BAL) as part of their routine clinical assessment. All the samples underwent standard microbiological analysis and a Grocott methenamine silver stain was performed where clinically indicated to detect the presence of P jiroveci. Polymerase chain reaction for detection of P jiroveci specific DNA was also performed.

Results: Ninety three consecutive BAL fluid samples were analysed, 17 (18%) of which contained P jiroveci DNA. Of the potential predictors examined, only glucocorticoid use was significantly associated with detectable P jiroveci DNA. Eighteen patients were receiving oral glucocorticoids (equivalent to >20 mg/day prednisolone) at the time of bronchoscopy, of whom eight (44%) had detectable P jiroveci DNA. In contrast, P jiroveci was detected in only nine of 75 patients (12%) who were not receiving glucocorticoids (difference between proportions 32%, 95% CI 8 to 57; p=0.004, two tailed Fisher’s exact test).

Conclusions: P jiroveci colonisation, as determined by detection of P jiroveci DNA in BAL fluid, is common in HIV negative patients with primary respiratory disorders undergoing bronchoscopy and BAL. The higher prevalence in patients receiving corticosteroids suggests that oral glucocorticoid therapy is an independent risk factor for colonisation. In contrast, underlying lung cancer or COPD did not appear to be risk factors.


Keywords: Pneumocystis jiroveci; corticosteroids; bronchoalveolar lavage; immunosuppression




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