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Logan, Latania K. MD*†; Zheng, Xiaotian MD, PhD‡§; Shulman, Stanford T. MD*†

The Pediatric Infectious Disease Journal: February 2008 - Volume 27 - Issue 2 - p 184-186
doi: 10.1097/INF.0b013e31815b1af0
Brief Reports

We describe the first pediatric case of Gemella bergeriae endocarditis in a 15-year-old boy with tetralogy of Fallot and pulmonary atresia who presented with weight loss, chills, and cold intolerance. Blood cultures revealed Gram-positive cocci that failed to type with Lancefield group antiserum. The identification of the organism was confirmed by 16S rRNA gene sequencing.

From the *Division of Infectious Diseases, Children's Memorial Hospital; †Department of Pediatrics, Northwestern University Feinberg School of Medicine; ‡Department of Microbiology, Children's Memorial Hospital, and §Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL.

Accepted for publication September 13, 2007.

Address for correspondence: Latania K. Logan, MD, Children's Memorial Hospital, 2300 Childrens Plaza, Box 20, Chicago, IL 60614. E-mail:

The genus Gemella includes catalase-negative, facultatively anaerobic, Gram-positive cocci that occur in short chains, tetrads, pairs, and occasionally, clusters.1,2 The organisms are normal flora of humans and other mammals; however, they are opportunistic pathogens and uncommonly cause a variety of severe invasive infections.3

Until 1998, there were only 2 known species of Gemella. Since that time, 4 additional species have been identified. Gemella bergeriae was identified in 1998 by comparative 16S rRNA gene sequencing studies and biochemical analysis.4

Here we describe a case of Gemella bergeriae subacute bacterial endocarditis in a 15-year-old boy and review the literature on Gemella bergeriae infections.

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A 15-year-old white boy with a history of tetralogy of Fallot and pulmonary atresia presented to our hospital on November 10, 2006, with a 3-month history of weight loss and fatigue. He had several cardiac surgeries, the majority between the ages of 5 months and 4 years, most recently on August 1, 2006, with resection of a left pulmonary artery (PA) aneurysm, placement of a small proximal left PA Gortex graft, and replacement of a conduit between his right ventricle (RV) and PA secondary to growth velocity.

A few days after surgery he began to complain of decreased appetite and early satiety. He had a documented 16-pound weight loss from August to November. Additional signs and symptoms included 1 month of nonproductive cough, chills, fatigue, and cold intolerance, a 3- to 4-week history of abdominal pain and bloating associated with dairy products, and a 2- to 3-day history of low-grade fevers, watery stools, and upper back pain relieved by acetaminophen. He denied palpitations, chest pain, joint pain, rash, dyspnea, or upper respiratory symptoms.

Other significant medical history included placement of a right PA stent in May 2006, an extrahepatic portal vein thrombosis in 2002 requiring placement of a Rex shunt, and chronic splenomegaly and thrombocytopenia. Social history was negative for sexual activity, smoking, or drug use. He had no recent travel or dental procedures. He was allergic to penicillin.

At the time of admission, he was a very thin, alert, and oriented, nontoxic appearing male with a temperature of 37.0°C, a heart rate of 107 per minute, respiratory rate of 20 per minute, oxygen saturation of 100% on room air. There was a coloboma in his left eye, and he had normal dentition. His chest was clear to auscultation, and on cardiac examination a III/VI holosystolic murmur was heard throughout a hyperdynamic precordium. Abdominal examination revealed a nontender spleen with a span of 11–12 cm palpable 6 cm below the left costal margin, and a liver palpable 2 cm below the right costal margin. There were no stigmata associated with infective endocarditis and no abnormal neurologic signs.

The leukocyte count was 4500/mm3 with 80% neutrophils, hemoglobin 12.1 g/dL, hematocrit 34.5%, platelet count 56,000/mL, total bilirubin 1.1 mg/dL, erythrocyte sedimentation rate 28 mm/h (normal 0–20 mm/h), C-reactive protein 5.67 mg/dL (normal range, 0.00–0.8 mg/dL), prothrombin time 16.5 seconds, partial thromboplastin time 30.9 seconds, and urinalysis showed trace protein, no white blood cells, and 6–10 red blood cells per high power field. All chemistries, liver and thyroid function tests, celiac disease antibodies, stool pathogen studies, and stool malabsorptive studies were negative or within normal limits.

Abdominal ultrasound revealed a patent Rex shunt. Transthoracic and transesophageal echocardiograms demonstrated no obvious vegetations; however, the proximal portion of the right ventricle to pulmonary artery conduit contained a soft echodensity, the remainder of the conduit lumen was difficult to visualize, with 35–49 mm gradient from RV to PA, and there was mild tricuspid regurgitation. The conduit was clearly patent on previous echocardiograms.

Three blood samples obtained in the 24 hours before institution of antimicrobial therapy were incubated in the BACTEC system (Becton-Dickinson, Sparks, MD). The first positive culture grew in a standard anaerobic bottle after overnight incubation, and Gram stain of the fluid demonstrated Gram-positive cocci in chains. The aerobic BACTEC PEDS PLUS/F medium bottle from the same set was positive on the following day. Blood cultures collected the following 2 days also were positive for what appeared to be the same organism. Colonies initially appeared β-hemolytic on 5% sheep blood agar and became α-hemolytic on subculture plates. The organism was catalase negative, leucine aminopeptidase positive, and pyrrolidonlyarylamidase positive. It did not group with any of the Lancefield groups including A, B, C, F, and G by agglutination (PathoDx Strep Grouping kit, by Remel Inc., Lenexa, KS). To identify the organism further, the first 500 base pairs of the 16S rRNA gene were amplified and sequenced with the MicroSeq 500 kit (Applied Biosystems, Foster City, CA). The resulting 472 base pair sequence matched completely to the sequence of Gemella bergeriae in the GenBank data base. Sensitivity testing by broth dilution method revealed minimum inhibitory concentrations (MICs) for erythromycin >1 μg/mL, gentamicin 16 μg/mL, and vancomycin, penicillin G, ceftriaxone, and rifampin <1, 0.06, 0.03, and 0.008 μg/mL, respectively.

Six blood cultures were sterile within 24 hours after administration of intravenous vancomycin and gentamicin, chosen because of the history of allergy to penicillin and the American Heart Association guidelines for treatment of infective endocarditis as a result of Gemella species.5 Within 3 days, the patient's appetite and cold intolerance improved, and he was discharged home after 10 days to receive vancomycin and gentamicin for an intended 6-week course of therapy. At 1 month follow-up, his course was complicated by pancytopenia, increased creatinine, and worsening anorexia. Antibiotics were switched to ceftriaxone and rifampin. He was readmitted briefly for hydration and nasogastric feeds for continued poor weight gain.

He ultimately did very well after 8 weeks of total therapy, demonstrating sterile blood cultures, weight gain, and normal renal function.

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The genus Gemella until 1998 comprised only 2 members, G. hemolysans and G. morbillorum, which were assigned to this genus in 1960 and 1988, respectively.6 Since 1998, 4 additional species have been identified, 2 from other warm-blooded animals, G. palaticanis and G. cuniculi, and 2 additional human clinical species, G. sanguinis and G. bergeriae. 4,7

Members of the genus typically contain DNA with a low G + C content, are catalase negative, facultatively anaerobic, leucine aminopeptidase positive, 6.5% NaCl intolerant, esculin negative, with variability among species in production of pyrrolidonlyarylamidase, Voges-Proskauer, alkaline phosphatase, and α- and β-hemolysis.1,3,4,6,8 These organisms are susceptible to vancomycin and were described in the 1990s to manifest reduced susceptibilities to penicillins and macrolides.3,6

Gemella is a normal inhabitant of the oropharynx, gastrointestinal, and genitourinary tracts and is an opportunistic pathogen that infrequently causes severe and local infections in humans, similar to those of viridans group streptococci and other microaerophilic streptococci.3,6 Most commonly, Gemella species have been associated with endovascular infections of native and prosthetic valves, but other invasive infections also are described, including meningitis, septic shock, osteomyelitis, septic arthritis, spondylodiscitis, empyema, lung abscesses, and pericarditis.9–15

The current method of choice for identification of Gemella and Gemella-like organisms is 16S rRNA gene sequence analysis.3 Standard phenotypic identification may be difficult, often yielding variable results including Gram variable appearance related to easy decolorization.

Infections with Gemella are rarely reported in children. Case reports have described infection in both immunocompromised and healthy children, and they have most commonly been associated with G. morbillorum. 2 To our knowledge, our patient with endocarditis is the first described case of pediatric infection caused by G. bergeriae.

There are only 5 cases in the literature of endocarditis caused by G. bergeriae including the one reported here (Table 1). All patients survived their infections. Clinical and treatment information is available for only 2 of the 4 other cases. These 2 patients were adults who presented with significant constitutional symptoms and were found to have a heart abnormality (mitral valve prolapse, bicuspid aortic valve) with vegetations on those valves, respectively.4,8 One patient also had significant periodontitis.4 Susceptibility of the G. bergeriae isolate to penicillin, gentamicin, and rifampin was implied in case 2 as this patient's treatment regimen involved these antimicrobials. Our isolate was also susceptible to these agents. No other information regarding antimicrobial susceptibility in endocarditis isolates is available.



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1. Murray PR, Baron EJ, Jorgenson JA, et al. Manual of Clinical Microbiology. 9th ed. Washington, DC: American Society of Microbiology; 2007.
2. Farmaki E, Roilides E, Darilis E, Tsivitanidou M, Panteliadis C, Sofianou D. Gemella morbillorum endocarditis in a child. Pediatr Infect Dis J. 2000;19:751–753.
3. La Scola B, Raoult D. Molecular identification of Gemella species from three patients with endocarditis. J Clin Microbiol. 1998;36:866–887.
4. Collins MD, Hutson RA, Falsen E, Sjöden B, Facklam RR. Gemella bergeriae sp. nov., isolated from human clinical specimens. J Clin Microbiol. 1998;36:1290–1293.
5. Baddour LM, Wilson WR, Bayer AS, et al. Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications. Circulation. 2005;111:e394–e433.
6. Woo PC, Lau SK, Fung AM, Chiu SK, Yung RW, Yuen KY. Gemella bacteraemia characterised by 16S ribosomal RNA gene sequencing. J Clin Pathol. 2003;56:690–693.
7. Collins MD, Hutson RA, Falsen E, Sjöden B, Facklam RR. Description of Gemella sanguinis sp. nov., Isolated from Human Clinical Specimens. J Clin Microbiol. 1998;36:3090–3093.
8. Elsayed S, Zhang K. Gemella bergeriae endocarditis diagnosed by sequencing of rRNA genes in heart valve tissue. J Clin Microbiol. 2004;42:4897–4900.
9. Vasishtha S, Isenberg HD, Sood SK. Gemella morbillorum as a cause of septic shock. Clin Infect Dis. 1996;22:1084–1086.
10. Condoluci C, Chessa M, Butera G, Cipriani A, Pelargonio S. Pericarditis caused by Gemella morbillorum. Minerva Pediatr. 1995;47:545–547.
11. da Costa CTKA, Porter C, Parry K, Morris A, Quoraishi AH. Empyema thoracis and lung abscess due to Gemella morbillorum. Eur J Clin Microbiol Infect Dis. 1996;15:75–77.
12. Martha B, Duong M, Buisson M, et al. Acute Gemella haemolysans spondylodiscitis in an immunocompetent patient. Presse Med. 2003;32:1273–1275.
13. Roche M, Smyth E. A case of septic arthritis due to infection with Gemella morbillorum. J Infect. 2005;51:e187–e189.
14. Van Dijk MB, Van Royen BJ, Wuisman PI, Hekker TA, van Guldener C. Trochanter osteomyelitis and ipsilateral arthritis due to Gemella morbillorum. Eur J Clin Microbiol Infect Dis. 1999;18:600–602.
15. Garavelli PL. Meningitis from Streptococcus morbillorum. Minerva Med. 1990;81:69.

Gemella; Gemella bergeriae; endocarditis; child; pediatrics

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