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Journal of Clinical Microbiology, October 2004, p. 4893-4896, Vol. 42, No. 10
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.10.4893-4896.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

CASE REPORT

Mitral Bioprosthetic Valve Endocarditis Caused by an Unusual Microorganism, Gemella morbillorum, in an Intravenous Drug User

Ramzan M. Zakir, Anthony Al-Dehneh, Leticia Dabu, Raj Kapila, and Muhamed Saric*

Department of Medicine, New Jersey Medical School, Newark, New Jersey

Received 29 March 2004/ Accepted 11 May 2004


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ABSTRACT
 
We report a case of Gemella morbillorum mitral bioprosthetic valve endocarditis with perivalvular extension in a 44-year-old human immunodeficiency virus-positive man who is an active intravenous drug user together with review of all published cases. This is only the second reported case of Gemella morbillorum endocarditis in a patient with a prosthetic valve.


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CASE REPORT
 
A 44-year-old human immunodeficiency virus-positive man with a history of active intravenous drug use and a mitral valve replacement only 9 months earlier for native-valve endocarditis due to Staphylococcus aureus was admitted complaining of pleuritic chest pain, shortness of breath, fever, and chills.

Physical examination revealed a temperature of 99.8°F, blood pressure of 114/70 mm Hg, a regular heat rate at 98 beats per min, and a grade III/VI holosystolic murmur radiating to the axilla. No clinical signs of congestive heart failure (such as pulmonary rales or peripheral edema) were noted.

An electrocardiogram was notable for a first-degree atrioventricular block (an increased PR interval of 0.22 s) and nonspecific T wave changes. Laboratory investigations were significant for a normocytic anemia with a hemoglobin level of 10.9 g/dl and an elevated erythrocyte sedimentation rate of 108 mm per h. However, neither the total white blood cell count nor the percentage of banded neutrophils was elevated (3.72 x 109/liter and 4% bands, respectively).

Three sets of blood cultures were obtained prior to initiating antibiotic therapy. Blood samples were incubated in a continuous-monitoring culture system (Bac T/Alert; Becton Dickinson, Organon Teknika, Durham, N.C.) at 37°C. After 24 h of incubation, growth in the anaerobic bottle was noted. The samples were then subcultured at 37°C on MacConkey's agar, sheep blood agar, anaerobic CDC blood agar, and chocolate agar incubated in CO2.

After 24 h of subculture incubation, an alpha-hemolytic organism grew on all plates except the MacConkey agar. The organism was further characterized as being a gram-positive coccus that was both catalase and bile solubility negative.

These initial findings suggested that the organism was Streptococcus viridans. However, on further evaluation with an API 20 streptococcus identification system (Bio Merieux, Vitek Inc., Hazelwood, Mo.), the organism was identified as Gemella morbillorum with 98% confidence.

Antimicrobial susceptibility by disk diffusion method showed the organism to be sensitive to ceftriaxone, clindamycin, levofloxacin, tetracycline, and vancomycin, while the Etest showed sensitivity to penicillin G.

A transthoracic echocardiogram revealed severe regurgitation through incompetent leaflets of the bioprosthetic mitral valve. On spectral Doppler recording of the prosthetic inflow, a severely elevated mean diastolic gradient of 22 mm Hg at a sinus heart rate of 75 beats per min was noted. Since there were no echocardiographic signs of prosthetic stenosis (the pressure half-time was only 77 ms), this gradient was indicative of severely elevated left atrial pressure due to severe mitral regurgitation. In addition, there was moderate central aortic insufficiency.

The left atrium was enlarged (5.3 cm in diameter), as was the left ventricle (end diastolic diameter of 5.8 cm). The left ventricular ejection fraction was high normal (65 to 70%). The imaging of the right side of the heart revealed moderate tricuspid regurgitation and elevation of right atrial (>20 mm Hg) and pulmonary artery systolic (>45 mm Hg) pressures.

On a subsequent transesophageal echocardiogram the prosthetic leaflets were thickened and studded with globular echo densities consistent with vegetations (Fig. 1). In addition, they were misshapen, leading to failure of leaflet coaptation and transvalvular regurgitation.



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  		FIG. 1. Transesophageal echocardiogram of infected mitral bioprosthesis. The leaflets of the mitral bioprosthesis (arrow) are thickened and studded with globular echo densities consistent with vegetations. On color Doppler (not shown), there was severe transvalvular mitral regurgitation. LA, left atrium; LV, left ventricle.

However, between the mitral prosthetic ring and the noncoronary cusp of the native aortic valve there was a 1-cm septated echo lucency with a fistulous tract between the left ventricular outflow tract and the left atrium, seen on color Doppler imaging. These findings were consistent with a paravalvular abscess (Fig. 2). However, there was no paravalvular mitral regurgitation.



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  		FIG. 2. Transesophageal echocardiogram of paraprosthetic abscess. Extending from the mitral bioprosthetic ring and adjacent to the native aortic valve (AV) there is a septated echo-free space (arrows), a finding indicative of abscess formation. LA, left atrium; RA, right atrium.

This patient met multiple Duke criteria for a definite diagnosis of infectious endocarditis. He met two major criteria (new valvular regurgitation and positive echocardiogram) and two minor criteria (predisposing factor of intravenous drug use and a blood culture growing an organism that does not commonly cause endocarditis).

Based on the findings of severe prosthetic mitral regurgitations and a likely paraprosthetic abscess in the setting of PR prolongation on an electrocardiogram, the patient was considered for repeat valvular surgery. However, given the patient's active drug use and a high intraoperative risk, the patient was treated instead medically with ceftriaxone for 4 weeks, with gentamicin added during the first 2 weeks of therapy. Subsequent blood cultures on therapy were all negative.

Discussion. Gemella morbillorum, formally Streptococcus morbillorum, is a catalase-negative, facultatively anaerobic gram-positive coccus that was first described in 1917 by Tunnicliff (25).

In 1988, the organism was transferred to its present genus based on DNA homology, physiologic properties, and 16S RNA cataloguing (16). It is part of the commensal flora of the oropharynx, gastrointestinal tract, and genitourinary tract and an infrequent cause of infection. Although there have been reports of Gemella morbillorum causing bacteremia and localized infections such as meningitis (9, 13), arthritis (22, 27), abscesses (6, 23), and septic shock (10), the organism is most commonly associated with infectious endocarditis.

Some 22 cases of endocarditis caused by Gemella morbillorum have been reported in English previously, with the vast majority involving native (nonprosthetic) valves. (Table 1) (1-5, 7, 8, 11, 12, 14, 15, 17-22, 24, 26, 28).


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  		TABLE 1. Summary of all reported cases of Gemella morbillorum endocarditisa

The patient ages ranged from 9 to 84 years (mean, 53 years), and most were males (Table 1). Predisposing factors included poor dental hygiene, dental procedures, and colon disease and gastrointestinal diagnostic procedures. Underlying intracardiac lesions included preexisting valvular lesions, congenitally bicuspid aortic valve (17, 20), hypertrophic cardiomyopathy (15), cardiac myxoma (27a), and tetralogy of Fallot (5). The aortic, tricuspid, and mitral valves have been affected.

To the best of our knowledge, there has been only one previous report of endocarditis due to Gemella morbillorum involving a prosthetic valve and only two cases associated with intravenous drug users.

In the majority of the reported cases of endovascular infections by Gemella morbillorum, a bacteriological cure was achieved with a combination of penicillin and an aminoglycoside. In patients that were either allergic or resistant to penicillin, vancomycin or a combination of erythromycin and rifampin has been effective (19).

In seven previously reported cases, native-valve endocarditis due to Gemella morbillorum was treated with surgical valve replacement (2, 11, 17, 18, 20, 24, 26). Two patients died shortly after aortic and mitral valve replacement (14, 26), but the remaining five cases had satisfactory outcomes.

To the best of our knowledge, our patient is only the second reported case of endocarditis due to Gemella morbillorum in a patient with a prosthetic valve and only the third in an intravenous drug abuser.

Despite severe valvular and paravalvular complications, the patient was stable 6 months after discharge although he received no surgical therapy. This unusual recovery demonstrates a dramatic response of endocarditis due to Gemella morbillorum to antimicrobial therapy.


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FOOTNOTES
 
* Corresponding author. Mailing address: Echocardiography Lab, Division of Cardiovascular Diseases, New Jersey Medical School, 185 South Orange Ave., I-538, University Heights, Newark, NJ 07103. Phone: (973) 972-6084. Fax: (973) 972-4737. E-mail: saricmu{at}umdnj.edu. Back


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Journal of Clinical Microbiology, October 2004, p. 4893-4896, Vol. 42, No. 10
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.10.4893-4896.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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  • Al-Hujailan, G., Lagace-Wiens, P. (2007). Mechanical valve endocarditis caused by Gemella morbillorum. J Med Microbiol 56: 1689-1691 [Abstract] [Full Text]  

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