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Streptococcus anginosus InfectionsCrossing Tissue Planes in S anginosus Infections: Crossing Tissue Planes FREE TO VIEW

Bernie Y. Sunwoo, MBBS; Wallace T. Miller, Jr, MD
Author and Funding Information

From the Department of Medicine, Division of Pulmonary, Allergy, Critical Care Medicine, Division of Sleep Medicine (Dr Sunwoo) and Department of Radiology (Dr Miller), Perelman School of Medicine, The University of Pennsylvania, Philadelphia, PA.

CORRESPONDENCE TO: Bernie Y. Sunwoo, MBBS, Department of Medicine, Division of Pulmonary, Allergy, Critical Care Medicine, Division of Sleep Medicine, Perelman School of Medicine, Perelman Center for Advanced Medicine, University of Pennsylvania, 1st Floor, W Pavilion, 3400 Civic Center Blvd, Philadelphia, PA 19104; e-mail: bernie.sunwoo@uphs.upenn.edu


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;146(4):e121-e125. doi:10.1378/chest.13-2791
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Streptococcus anginosus has long been recognized to cause invasive pyogenic infections. This holds true for thoracic infections where S anginosus has a propensity for abscess and empyema formation. Early diagnosis is important given the significant morbidity and mortality associated with thoracic S anginosus infections. Yet, distinguishing thoracic S anginosus clinically is difficult. We present three cases of thoracic S anginosus that demonstrated radiographic extension across tissue planes, including the interlobar fissure, diaphragm, and chest wall. Few infectious etiologies are known to cross tissue planes. Accordingly, we propose S anginosus be considered among the differential diagnosis of potential infectious etiologies causing radiographic extension across tissue planes.

Figures in this Article

The Streptococcus anginosus group, consisting of three distinct species, Streptococcus intermedius, Streptococcus constellatus, and Streptococcus anginosus, has long been recognized to cause invasive pyogenic infections. This holds true for thoracic infections where thoracic S anginosus has a propensity for abscess and empyema formation. Cases of mediastinitis have been reported.1-3 Early diagnosis and a high clinical suspicion are essential given the significant morbidity and mortality associated with thoracic S anginosus infections.4

Few pulmonary infections are known to cross pleural surfaces, leading to chest wall, mediastinal, or abdominal invasion. Infections reported to cause these problems include actinomycosis, nocardiosis, blastomycosis, TB, and mucormycosis.5-11 As such, an imaging demonstration of extension of infection across pleural boundaries into the adjacent tissues is of use in suspecting these unusual infections as a cause of the patient’s clinical illness.

We present three cases of thoracic S anginosus that demonstrated radiographic extension across tissue planes. We propose S anginosus be considered among the differential diagnosis of potential infectious etiologies causing extension across tissue planes.

The study was approved by the center’s institutional review board (IRB#7, Protocol 813882), and informed consent was waived due to the retrospective nature of the project.

Case 1

A 62-year-old white man with a history of bipolar disorder was hospitalized to the psychiatric unit for mania. A chest radiograph (CXR) was performed on admission for cough and right-sided chest pain that revealed right middle lobe opacity. He was treated with levofloxacin and clindamycin for 1 week but had continued chest pain with progressive productive cough, low-grade fevers, and weight loss. He was smoking one pack of cigarettes daily but denied other illicit drug or alcohol use. He had no pets and denied recent travel or occupational exposures. On physical examination, he was afebrile, had poor oral dentition with no cervical lymphadenopathy, globally reduced breath sounds, and crackles in the right lower zone. A chest CT scan was performed for continued chest pain following a second course of levofloxacin; it showed mass-like consolidation in the peripheral right middle lobe extending across the oblique fissure into the adjacent anterior right lower lobe (Fig 1). Sputum cultures showed moderate mouth flora. Bronchoscopy was performed, revealing copious purulent secretions emanating from the right middle lobe with no endobronchial lesions seen. BAL and transbronchial biopsies showed many polymorphonuclear cells and S anginosus susceptible to penicillin (minimum inhibitory concentration [MIC], 0.094). Cultures were negative for anaerobes, mycobacteria, and fungi, and no evidence of malignancy was seen. Blood cultures remained negative. HIV testing was negative. His course was complicated by empyema requiring multiple chest tubes. He was treated with IV ampicillin/sulbactam for 2 weeks followed by oral amoxicillin/clavulanate for an additional 4 weeks with clinical and radiographic improvement.

Figure Jump LinkFigure 1 –  Invasion across fissures. Sagittal reconstruction from an unenhanced CT scan demonstrates a focal area of consolidation (black arrow) in the right middle lobe that has invaded across the major fissure (white arrows) into the right lower lobe.Grahic Jump Location
Case 2

A patient in his 20s with Crohn’s disease (status: postileostomy) on no medications presented with 3 weeks of left-sided pleuritic chest pain and dyspnea. He was smoking one pack of cigarettes per week but denied illicit drug or alcohol use. He had no pets and denied recent travel or occupational exposures. On physical examination, he was afebrile but diaphoretic, tachycardic, tachypneic, with BP 113/58 mm Hg without pulsus paradoxus. The jugular venous pressure was elevated with distant heart sounds. The chest was clear. He had diffuse abdominal tenderness maximal over the right upper quadrant with no peritonism, and his ileostomy site was intact. ECG showed diffuse ST elevation and PR depression. Laboratory data were significant for the following: WBC count 31.7 with 19% bands, hemoglobin 8.2 g/dL, platelets 734, acute renal failure, negative cardiac enzymes, total bilirubin 4.1 mg/dL, alkaline phosphastase 229 units/L, aspartate aminotransferase 59 units/L, alanine aminotransferase 84 units/L, and lactic acidosis 3.3 mg/dL. CXR revealed massive cardiomegaly but clear lung fields. A transthoracic echocardiogram was performed showing a moderate to large pericardial effusion with evidence of increased intrapericardial pressure that did not meet criteria for tamponade, ejection fraction of 50%, and no vegetations. Pericardiocentesis was attempted but was unsuccessful with an apparent loculated effusion. Right-sided heart catheterization revealed no tamponade physiology. An abdominal CT scan was obtained, showing new hypodense areas occupying the entire left lobe and portions of the right lobe of the liver and thickening of the gallbladder wall with extension of the abscess through the diaphragm into the adjacent pericardial space (Fig 2). The patient was initiated on broad-spectrum antibiotics and taken to the operating room for a pericardial window and drainage of his liver. Foul-smelling, purulent fluid (1,000 mL) was drained from his pericardium, and 700 mL of similar appearing fluid was drained from his liver where a drain was placed. An intraoperative transesophageal echocardiogram did not show vegetations. Pericardial fluid, hepatic fluid, and blood cultures all grew S anginosus susceptible to penicillin (MIC, 0.064). No anaerobes, fungi, or mycobacteria were isolated. He was treated with IV ceftriaxone with a hepatic drain in place for 6 weeks with clinical improvement.

Figure Jump LinkFigure 2 –  Invasion across the diaphragm. Coronal reconstruction of an abdominal CT scan demonstrates a large abscess (black arrows) in the left lobe of the liver. The contiguity of the abscess with the pericardial effusion suggests that the abscess has invaded across the diaphragm (white arrow) causing a large pericardial effusion (white arrowheads).Grahic Jump Location
Case 3

A 78-year-old man presented with cough, fatigue, and weight loss over several weeks. His past medical history was significant for diabetes mellitus and third-degree atrioventricular block (status: post pacemaker). He was a nonsmoker who denied illicit drug or alcohol use. He had no pets and denied recent travel or occupational exposures except possible mold in his office. On physical examination, he was afebrile and had left-sided crackles and tender left axillary lymphadenopathy. CXR revealed left upper zone opacity. He was treated with azithromycin followed by levofloxacin with no clinical improvement and developed left-sided chest pain. A repeat CXR was performed showing worsening mass-like opacity. A chest CT scan was obtained showing mass-like consolidation involving the left upper lobe. Laboratory data were significant for the following: WBC 17.7, hemoglobin 10.9 g/dL, platelets 438, mild renal insufficiency, negative quantiferon gold, and negative Histoplasma and cryptococcal antigens. Blood cultures were negative. A bronchoscopy with transbronchial biopsies was nondiagnostic with no evidence of malignancy, no granulomas seen, and negative cultures including anaerobes, fungi, and mycobacteria. Subsequently, a CT scan-guided core needle biopsy was performed showing organizing pneumonia with negative cultures. He was started on prednisone at 40 mg, tapered over 2 months, until admitted with worsening fevers, dyspnea, weight loss, and night sweats. A repeat chest CT scan showed again ill-defined mass-like consolidation involving most of the left upper lobe with a new cavitary component. Bronchoscopy was repeated showing moderate thick secretions in the trachea and left upper lobe. Gram-positive cocci were seen but cultures remained negative. A second CT scan-guided core needle biopsy was performed. The CT scan demonstrated extension of the mass into the chest wall (Fig 3). His second core needle biopsy material from the chest wall demonstrated fibrocollagenous tissue with suppurative inflammation and numerous bacteria that grew S anginosus susceptible to penicillin (MIC 0.047). A transthoracic echocardiogram revealed no vegetations. The patient had a history of penicillin and sulfa allergy and was initially treated with clindamycin, later changed to vancomycin, but had clinical and radiographic progression. He eventually had a left extrapleural lobectomy with extensive lysis of adhesions. Following penicillin skin testing, he was switched to amoxicillin/clavulanate to complete 8 weeks with clinical improvement.

Figure Jump LinkFigure 3 –  Invasion into the chest wall. Axial CT image demonstrates a large zone of consolidation (white arrows) in the left upper lobe with central cavitation (black arrows). There is extension of infection into the chest wall causing a chest wall abscess (white arrowheads). Note how the normal left pectoralis muscle tissue planes are absent as a result of the dissection of infection from the lung to the chest wall.Grahic Jump Location

The S anginosus group, often referred to as Streptococcus milleri, are commensals of the oropharyngeal, GI, and genitourinary microflora that can cause invasive pyogenic infections in various sites. While more commonly associated with CNS, abdominal, head and neck, bloodstream, and thoracic infections, the three species that make up S anginosus have been associated with differing clinical manifestations.3,12-15 Thoracic infections represented one-fifth of all S anginosus group infections in one series.1 Like other sites, thoracic S anginosus has a propensity for abscess and empyema formation with various virulence factors implicated.1,2,14,16-18

The S anginosus group of organisms is known to be highly virulent and rapidly progressive, and it is not surprising that they might cross tissue planes. However, we believe that these three cases represent the first documented cases of potential invasion across tissue planes: the major fissure in case 1, the diaphragm in case 2, and the chest wall in case 3.

Radiographic extension across thoracic tissue planes raises a unique differential diagnosis. This phenomenon is most often a manifestation of malignancies: bronchogenic carcinoma and lymphoma. Few infectious etiologies are known to cross tissue planes, including Actinomyces, Nocardia, tuberculous, Mucorales, and Blastomyces species.3,5-11,19 Empyema necessitatis refers to the extension of empyema beyond the parietal pleura to adjacent soft tissues of the chest wall and has most commonly been described with TB, actinomycosis, and methicillin-resistant Staphylococcus aureus.20-22 These were the infections that were most strongly considered in the evaluation of the three patients presented here, and we were surprised to diagnose S anginosus in each case. Our case series would suggest S anginosus be considered among this select list.

Early diagnosis of thoracic S anginosus is critical given reported mortality rates between 15% to 30%.4 Clinically, S anginosus may be suspected by predisposing factors including male sex, periodontal disease, alcoholism, cancer, HIV, and possibly cystic fibrosis.1,4,17,23 Distinguishing S anginosus clinically, however, is difficult, and unlike other sites of infections, bacteremia in thoracic S anginosus is uncommon.1 The visualization of radiographic extension across tissue planes may be an additional tool for clinicians in early consideration of S anginosus infections, thereby prompting appropriate tissue specimen collection and laboratory request. Microbiologically, the S anginosus group is recognized by its microaerophilic or anaerobic growth requirements, formation of minute colonies, and frequent presence of a characteristic caramel-like odor but identification of S anginosus can be difficult.4

Clinically, S anginosus infections have responded well to penicillin G and cephalosporins but the potential for penicillin and cephalosporin resistance exists.4,24 Additionally, as demonstrated in all three cases, surgical drainage of pyogenic collections is often required, highlighting once again the importance of early diagnosis. Given the potential utility of radiographic extension across tissue planes in raising the differential of S anginosus, further research on the radiographic presentations of thoracic S anginosus is needed.

Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Miller’s wife is an employee of Bristol-Myers Squibb Company. Dr Sunwoo has reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Other contributions: We thank Morris Swartz, MD, for his assistance in the preparation of this manuscript. CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.

CXR

chest radiograph

MIC 

minimum inhibitory concentration

Porta G, Rodríguez-Carballeira M, Gómez L, et al. Thoracic infection caused by Streptococcus milleri. Eur Respir J. 1998;12(2):357-362. [CrossRef] [PubMed]
 
Stelzmueller I, Biebl M, Berger N, et al. Relevance of group Milleri streptococci in thoracic surgery: a clinical update. Am Surg. 2007;73(5):492-497. [PubMed]
 
Molina JM, Leport C, Bure A, Wolff M, Michon C, Vilde JL. Clinical and bacterial features of infections caused by Streptococcus milleri. Scand J Infect Dis. 1991;23(6):659-666. [CrossRef] [PubMed]
 
Petti CA, Stratton IV. Streptococcus anginosusgroup.. In:Mandell GL, Bennett JE, Dolin R., eds. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases.7th ed. Philadelphia, PA: Churchill Livingstone Elsevier; 2010:2681-2685.
 
Ahmed N, Watanakunakorn C, Sarac E. Pleuro-pulmonary tuberculosis presenting as a chest wall mass in a patient undergoing long-term hemodialysis. Infect Dis Clin Pract. 2001;10(7):403-404. [CrossRef]
 
Bansal M, Martin SR, Rudnicki SA, Hiatt KM, Mireles-Cabodevila E. A rapidly progressing Pancoast syndrome due to pulmonary mucormycosis: a case report. J Med Case Reports. 2011;5:388. [CrossRef]
 
Flynn MW, Felson B. The roentgen manifestations of thoracic actinomycosis. Am J Roentgenol Radium Ther Nucl Med. 1970;110(4):707-716. [CrossRef] [PubMed]
 
Hathur B, Mahesh PA, Babu SM, Shankarappa VG, Jayaraj BS. A cavitary lesion in the lung crossing the fissure. Lung India. 2011;28(3):222-225. [CrossRef] [PubMed]
 
Kepron MW, Schoemperlen, Hershfield ES, Zylak CJ, Cherniack RM. North American blastomycosis in Central Canada. A review of 36 cases. Can Med Assoc J. 1972;106(3):243-246. [PubMed]
 
Magazine R, Mohapatra AK, Manu MK, Srivastava RK. Herniation of unruptured tuberculous lung abscess into chest wall without pleural or bronchial spillage. Lung India. 2011;28(4):297-299. [CrossRef] [PubMed]
 
Poe RH, Vassallo CL, Plessinger VA, Witt RL. Pulmonary blastomycosis versus carcinoma—a challenging differential. Am J Med Sci. 1972;263(3):145-155. [CrossRef] [PubMed]
 
Claridge JE III, Attorri S, Musher DM, Hebert J, Dunbar S. Streptococcus intermedius,Streptococcus constellatus, andStreptococcus anginosus(“Streptococcus milleri group”) are of different clinical importance and are not equally associated with abscess. Clin Infect Dis. 2001;32(10):1511-1515. [CrossRef] [PubMed]
 
Siegman-Igra Y, Azmon Y, Schwartz D. Milleri group streptococcus—a stepchild in the viridans family. Eur J Clin Microbiol Infect Dis. 2012;31(9):2453-2459. [CrossRef] [PubMed]
 
Whiley RA, Beighton D, Winstanley TG, Fraser HY, Hardie JM. Streptococcus intermedius, Streptococcus constellatus, andStreptococcus anginosus(the Streptococcus milleri group): association with different body sites and clinical infections. J Clin Microbiol. 1992;30(1):243-244. [PubMed]
 
Whiley RA, Fraser H, Hardie JM, Beighton D. Phenotypic differentiation ofStreptococcus intermedius, Streptococcus constellatus, andStreptococcus anginosusstrains within the “Streptococcus milleri group”. J Clin Microbiol. 1990;28(7):1497-1501. [PubMed]
 
Shinzato T, Saito A. The Streptococcus milleri group as a cause of pulmonary infections. Clin Infect Dis. 1995;21(suppl 3):S238-S243. [CrossRef] [PubMed]
 
Wong CA, Donald F, Macfarlane JT. Streptococcus milleri pulmonary disease: a review and clinical description of 25 patients. Thorax. 1995;50(10):1093-1096. [CrossRef] [PubMed]
 
Okada F, Ono A, Ando Y, et al. High-resolution CT findings in Streptococcus milleri pulmonary infection. Clin Radiol. 2013;68(6):e331-e337. [CrossRef] [PubMed]
 
Kwong JS, Müller NL, Godwin JD, Aberle D, Grymaloski MR. Thoracic actinomycosis: CT findings in eight patients. Radiology. 1992;183(1):189-192. [CrossRef] [PubMed]
 
Llamas-Velasco M, Domínguez I, Ovejero E, Pérez-Gala S, García-Diez A. Empyema necessitatis revisited. Eur J Dermatol. 2010;20(1):115-119. [PubMed]
 
Marks MI, Eickhoff TC. Empyema necessitatis. Am Rev Respir Dis. 1970;101(5):759-761. [PubMed]
 
Haddad CJ, Sim WK. Empyema necessitatis. Am Fam Physician. 1989;40(4):149-152. [PubMed]
 
Parkins MD, Sibley CD, Surette MG, Rabin HR. The Streptococcus milleri group—an unrecognized cause of disease in cystic fibrosis: a case series and literature review. Pediatr Pulmonol. 2008;43(5):490-497. [CrossRef] [PubMed]
 
Giuliano S, Rubini G, Conte A, et al. Streptococcus anginosusgroup disseminated infection: case report and review of literature [published correction appears inInfez Med.2012;20(4):316]. Infez Med. 2012;20(3):145-154. [PubMed]
 

Figures

Figure Jump LinkFigure 1 –  Invasion across fissures. Sagittal reconstruction from an unenhanced CT scan demonstrates a focal area of consolidation (black arrow) in the right middle lobe that has invaded across the major fissure (white arrows) into the right lower lobe.Grahic Jump Location
Figure Jump LinkFigure 2 –  Invasion across the diaphragm. Coronal reconstruction of an abdominal CT scan demonstrates a large abscess (black arrows) in the left lobe of the liver. The contiguity of the abscess with the pericardial effusion suggests that the abscess has invaded across the diaphragm (white arrow) causing a large pericardial effusion (white arrowheads).Grahic Jump Location
Figure Jump LinkFigure 3 –  Invasion into the chest wall. Axial CT image demonstrates a large zone of consolidation (white arrows) in the left upper lobe with central cavitation (black arrows). There is extension of infection into the chest wall causing a chest wall abscess (white arrowheads). Note how the normal left pectoralis muscle tissue planes are absent as a result of the dissection of infection from the lung to the chest wall.Grahic Jump Location

Tables

References

Porta G, Rodríguez-Carballeira M, Gómez L, et al. Thoracic infection caused by Streptococcus milleri. Eur Respir J. 1998;12(2):357-362. [CrossRef] [PubMed]
 
Stelzmueller I, Biebl M, Berger N, et al. Relevance of group Milleri streptococci in thoracic surgery: a clinical update. Am Surg. 2007;73(5):492-497. [PubMed]
 
Molina JM, Leport C, Bure A, Wolff M, Michon C, Vilde JL. Clinical and bacterial features of infections caused by Streptococcus milleri. Scand J Infect Dis. 1991;23(6):659-666. [CrossRef] [PubMed]
 
Petti CA, Stratton IV. Streptococcus anginosusgroup.. In:Mandell GL, Bennett JE, Dolin R., eds. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases.7th ed. Philadelphia, PA: Churchill Livingstone Elsevier; 2010:2681-2685.
 
Ahmed N, Watanakunakorn C, Sarac E. Pleuro-pulmonary tuberculosis presenting as a chest wall mass in a patient undergoing long-term hemodialysis. Infect Dis Clin Pract. 2001;10(7):403-404. [CrossRef]
 
Bansal M, Martin SR, Rudnicki SA, Hiatt KM, Mireles-Cabodevila E. A rapidly progressing Pancoast syndrome due to pulmonary mucormycosis: a case report. J Med Case Reports. 2011;5:388. [CrossRef]
 
Flynn MW, Felson B. The roentgen manifestations of thoracic actinomycosis. Am J Roentgenol Radium Ther Nucl Med. 1970;110(4):707-716. [CrossRef] [PubMed]
 
Hathur B, Mahesh PA, Babu SM, Shankarappa VG, Jayaraj BS. A cavitary lesion in the lung crossing the fissure. Lung India. 2011;28(3):222-225. [CrossRef] [PubMed]
 
Kepron MW, Schoemperlen, Hershfield ES, Zylak CJ, Cherniack RM. North American blastomycosis in Central Canada. A review of 36 cases. Can Med Assoc J. 1972;106(3):243-246. [PubMed]
 
Magazine R, Mohapatra AK, Manu MK, Srivastava RK. Herniation of unruptured tuberculous lung abscess into chest wall without pleural or bronchial spillage. Lung India. 2011;28(4):297-299. [CrossRef] [PubMed]
 
Poe RH, Vassallo CL, Plessinger VA, Witt RL. Pulmonary blastomycosis versus carcinoma—a challenging differential. Am J Med Sci. 1972;263(3):145-155. [CrossRef] [PubMed]
 
Claridge JE III, Attorri S, Musher DM, Hebert J, Dunbar S. Streptococcus intermedius,Streptococcus constellatus, andStreptococcus anginosus(“Streptococcus milleri group”) are of different clinical importance and are not equally associated with abscess. Clin Infect Dis. 2001;32(10):1511-1515. [CrossRef] [PubMed]
 
Siegman-Igra Y, Azmon Y, Schwartz D. Milleri group streptococcus—a stepchild in the viridans family. Eur J Clin Microbiol Infect Dis. 2012;31(9):2453-2459. [CrossRef] [PubMed]
 
Whiley RA, Beighton D, Winstanley TG, Fraser HY, Hardie JM. Streptococcus intermedius, Streptococcus constellatus, andStreptococcus anginosus(the Streptococcus milleri group): association with different body sites and clinical infections. J Clin Microbiol. 1992;30(1):243-244. [PubMed]
 
Whiley RA, Fraser H, Hardie JM, Beighton D. Phenotypic differentiation ofStreptococcus intermedius, Streptococcus constellatus, andStreptococcus anginosusstrains within the “Streptococcus milleri group”. J Clin Microbiol. 1990;28(7):1497-1501. [PubMed]
 
Shinzato T, Saito A. The Streptococcus milleri group as a cause of pulmonary infections. Clin Infect Dis. 1995;21(suppl 3):S238-S243. [CrossRef] [PubMed]
 
Wong CA, Donald F, Macfarlane JT. Streptococcus milleri pulmonary disease: a review and clinical description of 25 patients. Thorax. 1995;50(10):1093-1096. [CrossRef] [PubMed]
 
Okada F, Ono A, Ando Y, et al. High-resolution CT findings in Streptococcus milleri pulmonary infection. Clin Radiol. 2013;68(6):e331-e337. [CrossRef] [PubMed]
 
Kwong JS, Müller NL, Godwin JD, Aberle D, Grymaloski MR. Thoracic actinomycosis: CT findings in eight patients. Radiology. 1992;183(1):189-192. [CrossRef] [PubMed]
 
Llamas-Velasco M, Domínguez I, Ovejero E, Pérez-Gala S, García-Diez A. Empyema necessitatis revisited. Eur J Dermatol. 2010;20(1):115-119. [PubMed]
 
Marks MI, Eickhoff TC. Empyema necessitatis. Am Rev Respir Dis. 1970;101(5):759-761. [PubMed]
 
Haddad CJ, Sim WK. Empyema necessitatis. Am Fam Physician. 1989;40(4):149-152. [PubMed]
 
Parkins MD, Sibley CD, Surette MG, Rabin HR. The Streptococcus milleri group—an unrecognized cause of disease in cystic fibrosis: a case series and literature review. Pediatr Pulmonol. 2008;43(5):490-497. [CrossRef] [PubMed]
 
Giuliano S, Rubini G, Conte A, et al. Streptococcus anginosusgroup disseminated infection: case report and review of literature [published correction appears inInfez Med.2012;20(4):316]. Infez Med. 2012;20(3):145-154. [PubMed]
 
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