Rothia dentocariosa endocarditis

Rothia dentocariosa endocarditis

BRIEF CLINICAL OBSERVATIONS Figure 1. Computed tomographic scan with contrast medium showing the hemorrhage in the left fronto-parietal region with e...

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BRIEF CLINICAL OBSERVATIONS

Figure 1. Computed tomographic scan with contrast medium showing the hemorrhage in the left fronto-parietal region with extensive edema compressing the lateral ventricle and shifting the midline.

ROTHIA DENTOCARIOSA ENDOCARDITIS

Rothia dentocariosa is a rare cause of infective endocarditis. Prior to 1988, only three cases were reported in the medical literature [1-3]. A fourth case complicated by brain abscess was reported in the February 1988 issue of the Journal [4]. I report the fifth case, which was complicated by multiple cerebral mycotic aneurysms and a cerebral hemorrhage. The patient was a 41-year-old man with known mitral valve prolapse, myxomatous degeneration, and regurgitant flow. In January 1987, the patient experienced lowgrade fevers that persisted despite oral antibiotics. In March 1987, four blood culture specimens grew a g r a m - p o s i t i v e b r a n c h i n g rod identified as a diphtheroid by two laboratories. He was admitted to a local hospital where examination revealed mitral insufficiency but none of the peripheral stigmata of infective endocarditis. Echocardiography demonstrated a vegetation. He was treated, initially with high-dose penicillin, but therapy was switched to vancomycin and 280

gentamicin after five days of fever. He became afebrile with this therapy, which was continued for five weeks. In April 1987, the patient reported a low-grade fever and was instructed to return for additional cultures. However, the following morning he was mute. Upon admissibn to the hospital, he had a temperature of 100.6°F and a tachycardia of 130/minute. He was mute, unable to follow commands, and had a right hemiparesis. The hematocrit was 35 percent, the white blood cell count 30,700/mm 3 with a left shift, and the sedimentation rate 60 ram/hour. Microscopic hematuria was present. Findings on blood cultures were negative. A computed tomographic scan of the head revealed a hemorrhage in the left frontal area with a mass effect (Figure 1). A vegetation was still present on the anterior leaflet of the m i t r a l valve by u l t r a s o n o graphy. Administration of vancomycin was resumed but treatment was then switched to penicillin G and gentamicin upon a report from the Communicable Disease Center, Atlanta, Georgia, that the original isolate was not a diphtheroid but was R. dentocariosa. After 10 days

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of therapy, the patient was transferred to Shands Hospital for further management. Carotid angiograms revealed bilateral mycotic aneurysms (Figure 2). Because of the stability of the patient's condition and the elapsed time since his stroke, no surgical intervention was undertaken. The patient received a total of four weeks of penicillin therapy during which his condition slowly improved. His hemiparesis resolved completely, and upon discharge from the hospital he had a moderate expressive aphasia and a focal seizure disorder that was controlled by phenytoin. Prior to discharge, a repeat angiogram showed resolution of the mycotic aneurysms. R. dentocariosa has a microscopic appearance similar to that of diphtheroids, and in this case the initial isolate was thought to be a diphtheroid. Since diphtheroids are often responsive only to vancomycin, it is understandable that this antibiotic would be selected for therapy. The definitive identification of the bacterium required more than six weeks. By that time, antibiotic therapy had been completed and the patient rehospital-

BRIEF CLINICAL OBSERVATIONS

Figure 2. Angiograms of the right and the left carotid systems showing the mycotic aneurysms (arrows).

ized for the treatment of his complication and probable relapse of endocarditis. Although there are therapeutic failures even with optimal therapy for endocarditis, the course of events in this patient raises doubts of the efficacy of vancomycin for this infection. Within a week of discharge from the hospital, the patient had a resumption of fever, elevated white blood cell count, elevated erythrocyte sedimentation rate, microscopic hematuria, and mycotic a n e u r y s m s . These observations suggest active endocarditis despite the negative results of blood cultures. To date, most of the patients with endocarditis caused by R. dentocariosa

have been treated successfully with penicillin with or without surgery. There are no data on the efficacy of alternative antibiotics, although the bacterium is reported to be quite sensitive to the cephalosporins in vitro [2]. The occurrence of the cerebral hemorrhage in this patient led to discussions of its appropriate management. There was an expressed opinion that the clot should be evacuated and that the aneurysm should be ligated. The observation that there were at least two aneurysms and that they occurred in both the right and the left carotid systems dampened the enthusiasm for such an approach, and surgery

August 1988

was deferred. It was gratifying to see that all the aneurysms resolved with antibiotic therapy alone. JOSEPH W. SHANDS, Jr. University of Florida College o[ Medicine GainesviUe, Florida 32610 1. PapeJ, Singer C, Kiehn T, et al: Infective endocarditis caused by Rothia dentocariosa. Ann Intern Med 1979; 91: 746-747. 2. 8chafer FJ, Wing F_J,Norden CW: Infectious endocarditis caused by Rothia dentocariosa. Ann Intern Med 1979; 91: 747-748. 3.8roeren SA, Peel MA: Endocarditis caused by Rothia dentocariosa. J Clin Pathol 1984; 37: 12981300. 4. Iseacson JH, Grenko RT: Rothia dentocariosa endocarditis complicated by brain abscess. Am J Med ]988; 84: 352-354. Submitted May 3, 1988, and accepted in revised form June 13, 1988

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