The three patients who received mechanical ventilation and PEEK however, were at increased risk for the development of pneumothorax, even in the absence of PCP.’ Perhaps the presence of PCP predisposed these patients to the development of pneumothorax by the formation of cysts, blebs, cavities, or pneumatoceles. Even when these three patients are excluded from the analysis, the fact that five of the patients with PCP had pneumothorax, compared with none of the 45 patients without PCP, still achieves statistical significance (p<0.05).
In two cases (patients 1 and 2) there was autopsy evidence to prove the absence of other organisms known to be associated with the development of pneumothorax. No other pathogen known to cause pneumothorax was isolated in any of our patients before or at the time of pneumothorax, and broncho-alveolar lavage and transbronchial biopsy are very sensitive techniques for the antemortem detection of opportunistic pulmonary infections in AIDS patients. Three previous reports substantiated the association of cavity formation or pneumothorax with PCP alone, in that no other pathogen was identified at autopsy. These studies, in conjunction with a good clinical response to treatment specific for PCP, strongly suggest that P carinii was the opportunistic pathogen responsible for the pneumothoraces in our patients.
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