Viridans streptococci (VS) are a heterogeneous group of streptococci that remain when β-hemolytic streptococci, enterococci, and pneumococci are excluded¹. VS, part of the normal microbial flora of humans, are most prevalent in the oral cavity and upper respiratory tract, followed by the gastrointestinal tract and female genital tract, particularly the vagina^2,3. VS are generally considered harmless commensals but their introduction to sterile sites outside of normal habitats can cause severe infections, such as endocarditis⁴. Although VS were previously thought to rarely cause community-acquired pneumonia (CAP)⁵, they have emerged as a causative agent of lung abscess and empyema in several case series^3,6,7,8. In recent studies, VS were reported to be the main etiologic agent of empyema^9,10 and lung abscess^11,12,13.

Community-acquired respiratory tract infection caused by VS is not as rare as previously believed; VS accounted for 3%-15% of CAP in a few studies^8,13. However, data are sparse regarding the clinical and radiologic features of community-acquired VS pneumonia with or without parapneumonic effusion. The aim of the present study was to investigate the clinical characteristics of CAP by comparing the clinical and computed tomography (CT) parameters between patients with CAP caused by VS and those with pneumococcal pneumonia.

The present study showed that, although uncommon, VS may be a cause of community-acquired respiratory infection. Compared with pneumococcal pneumonia, respiratory tract infection due to VS was characterized by less frequent productive cough and more frequent bed-ridden status. One-third of patients presented with complicated parapneumonic effusion or empyema. However, treatment outcome and prognosis of VS pneumonia did not differ from those of pneumococcal pneumonia.

Similar to previous studies^8,13, we found VS to be the causative agent in 5.9% of CAP cases, suggesting that pneumonia caused by VS might not be as rare as previously reported. VS are normal microbial flora of the mouth, upper respiratory tract, gastrointestinal tract, and vagina³. VS can cause respiratory tract infection through the following routes: (1) aspiration of oral secretions; (2) direct implantation due to trauma or surgery; (3) by extension from contiguous foci of infection; and (4) via the bloodstream from distant sites⁷. In contrast to a previous study⁹, no patients in this study had a history of trauma or surgery, which excludes direct implantation as a likely pathogenic route. No contiguous foci of infection were detected on CT scans of 25 patients whose CT scans were available. Although only six patients from the VS group underwent echocardiography, multiple nodules or multifocal infiltrates suggestive of septic pulmonary embolism²² were not observed. Consequently, aspiration of oral secretions is the most plausible access route of VS into the respiratory tract. Furthermore, a previous study reported mixed infections comprising anaerobes and members of S. milleri group to be common in thoracic infections, especially lung abscess and empyema⁸. These results suggest that respiratory tract infection caused by VS may commonly present with aspiration pneumonia. However, there was no difference in aspiration risk factors between the VS and S. pneumoniae groups in the present study, which corresponds to a previous study where only a half of patients with S. milleri pulmonary infections were predisposed to aspiration⁸.

VS are one of the main etiologic agents of empyema. In the same context, we found that two-thirds of patients with VS infection had pleural effusion and one-third presented with complicated pleural effusion or empyema. This is a major feature that distinguishes VS infection from pneumococcal pneumonia. By contrast, pulmonary parenchymal lesions, such as consolidation and GGO, were less frequently observed in patients with VS infection. Similarly, productive cough occurred less commonly in the VS group than in the S. pneumoniae group. Serum procalcitonin elevation reflects severe bacterial infection, in particular pneumonia²³. Serum procalcitonin level was significantly lower in the VS group, although the p-value did not reach a statistical significance in multivariate analysis. This finding was in line with lower PSI and CURB-65 score in the VS group despite no statistical significance, suggesting that VS might cause less severe infection compared with S. pneumoniae.

Like pneumococcal pneumonia, most patients with VS pneumonia were successfully treated with antibiotics with or without pleural drainage. In addition, there were no differences in in-hospital mortality, hospital stay, and mechanical ventilation or inotropic support between the two groups. These results can be explained by the fact that all VS isolates were susceptible to commonly used antibiotics, such as cefotaxime (data not shown).

The present study has some limitations. Due to its retrospective nature, the potential for selection bias should be noted. However, to minimize this potential, all consecutive patients were enrolled in the study. Because VS pneumonia was diagnosed only on the basis of positive blood or pleural fluid cultures, the proportion of patients with VS pneumonia might be underestimated and the possibility that more severe form of VS pneumonia was chosen could not be excluded. As VS is also a common pathogen causing infective endocarditis, this diagnosis required exclusion. Of 21 patients from whom VS were cultured only using blood samples, six underwent echocardiography, which showed no evidence of endocarditis. However, the remaining patients had typical CT findings suggestive of lobar pneumonia or bronchopneumonia. Thus, the possibility of endocarditis was considered to be low.

In conclusion, CAP caused by VS commonly presents with complicated parapneumonic effusion or empyema. It is characterized by less frequent productive cough, more frequent bed-ridden status, and less common pulmonary parenchymal lesions on CT scans. However, its clinical course and treatment outcome are similar to those of pneumococcal pneumonia.