Abstract
BACKGROUND: Streptococcus anginosus group (SAG) consists of oral facultative anaerobic bacteria that are increasingly identified as causative organisms of empyema, yet they are not often considered to be a cause of community-acquired pneumonia. The objective of this study was to determine the pathogenesis of empyema caused by SAG bacteria in pure culture (ie, no other organisms grown in culture or seen on Gram stain of the exudate) and in mixed cultures. METHODS: This retrospective cohort study was conducted in 3 hospitals in an urban region of Southern California. The sample included adult patients with empyema and pleural fluid cultures positive for 1 or more SAG microorganisms. We excluded patients with bronchopleural fistulas or lung abscess because SAG bacteria are known to be a cause of those infections and can breach the physical barrier of the visceral pleura. RESULTS: Thirty-seven patients with SAG empyema were identified: 14 had had polymicrobial cultures including 1 or more species of SAG bacteria (pSAG) and 23 had pure cultures of SAG bacteria. The patients were mostly middle-aged men with comorbidities, some of which predispose to aspiration or the inability to clear aspirated secretions. The patients with pSAG empyema were more likely to have cancer and/or prior surgical disruption of the esophagus with resulting mediastinitis. Patients with SAG empyema were more likely to use substances such as alcohol, sedatives, and narcotics. All computed tomography (CT) scans were initially interpreted as atelectasis abutting the empyema, but 13 patients with SAG empyema had contrast-enhanced CT scans that were suitable for measuring Hounsfield units (HUs) in the areas of consolidation adjacent to the SAG empyema; these scans revealed that they all had pneumonia as the source of their empyema. The most common species isolated from the SAG cases was Streptococcus intermedius. CONCLUSIONS: Community-acquired SAG empyema is a complication of unrecognized SAG pneumonia. S intermedius was the most common species to cause SAG empyema and pneumonia in this small series. The pneumonias were subacute and misdiagnosed as "adjacent atelectasis." Some cases of pSAG empyema were a complication of mediastinitis in patients with malignancies. Measurement of HUs in consolidations adjacent to empyema is useful for establishing the diagnosis of pneumonia in patients who present with what appears to be primary SAG empyema. In terms of limitations, this is a retrospective analysis, and not all patients with SAG empyema had contrast-enhanced CT scans. Furthermore, none of the pSAG cases were reanalyzed to measure HUs in the consolidated lungs. We also did not use molecular methods to speciate SAG isolates or detect fastidious anaerobes in the empyema fluids, although all the exudates were cultured anaerobically on multiple media for at least 5 days.