Prosthetic valve endocarditis caused by Acinetobacter calcoaceticus subsp. lwoffi

I Weinberger, E Davidson, Z Rotenberg, J Fuchs, J Agmon
1987 Journal of Clinical Microbiology  
Acinetobacter spp. are uncommon etiologic agents of prosthetic valve endocarditis. Two patients with Acinetobacter calcoaceticus subsp. lwoffi prosthetic valve endocarditis are described. The patients were successfully treated with antibiotics (cefotaxime sodium and gentamicin sulfate); thus, we suggest medical treatment rather than early valve replacement in this particular type of infection. Acinetobacter spp. are gram-negative, pleomorphic bacteria which may be found among the flora of the
more » ... the flora of the skin, oropharynx, and perineum and are divided into two subspecies, Acinetobacter calcoaceticus subsp. lwoffi (formerly Mima polymorpha) and A. calcoaceticus subsp. anitratus (formerly Herella vaginicola) (9). Nosocomial sources of infection of Acinetobacter spp. include intravenous catheters, respiratory equipment used in conjunction with endotracheal tubes or tracheotomy, and room air humidifiers (12). Previous surgery or antimicrobial therapy and residence in an intensive care unit increase susceptibility to Acinetobacter spp. infections (3). In spite of all the above, prosthetic valve endocarditis (PVE) caused by Acinetobacter spp. is very rare, and only sporadic cases have been reported (2, 14, 17) . Two patients suffering from PVE caused by A. calcoaceticus subsp. lwoffi successfully treated with antibiotics (cefotaxime sodium and gentamicin sulfate) are reported. Case reports. Patient 1. A 47-year-old man was admitted for evaluation of fever up to 38°C which developed 1 month before admission. Six weeks before admission the patient was involved in a road accident with multiple lacerations and was treated with oral ampicillin sodium. Fourteen years before he had undergone an aortic valve replacement (McGovern valve) for severe aortic stenosis (congenital bicuspid aortic valve). On physical examination his body weight was 69 kg, his temperature was 38°C, and he had a regular heart rate of 90 beats per min and blood pressure of 110/70. Few raies were heard over the lung bases. An early diastolic murmur grade 2/6 was heard at the lower left sternal border. There were no splenomegaly, purpura, petechiae, or signs of peripheral embolization. The erythrocyte sedimentation rate was 78 mm in the first hour, the hemoglobin concentration was 12.9 g/dl, and the leukocyte count was 5,800/mm3 with 70% neutrophils. Liver and renal function tests were normal. Chest roentgenogram showed diffuse interstitial congestion, left ventricular enlargement, and the prosthetic valve. An initial electrocardiogram showed sinus rhythm with prolongation of the PR interval up to 0.26 s. Left bundle branch block appeared the next day and aroused suspicion of conduction system abscesses. A two-dimensional echocardiogram showed diminished contractions of the left and right ventricle compatible with severe cardiomyopathy. Thickening at the base of the anterior aspect of the prosthetic aortic valve was interpreted as a * Corresponding author. vegetation. An M-mode echocardiogram showed fluttering of the mitral leaflets, as evidence of aortic insufficiency, and severe calcifications of the aortic valve. The distance between the mitral valve and the interventricular septum was more than 2 cm, indicating low left ventricular function. Three of three blood cultures yielded A. calcoaceticus subsp. lwoffi susceptible to cefotaxime, gentamicin, chloramphenicol, colistin, and co-trimoxazole. In light of the above-described clinical and laboratory findings, a diagnosis of PVE was made; in accord with susceptibility data, intravenous treatment with cefotaxime sodium (3 g/day) and gentamicin sulfate (240 mg/day), divided into three doses at 8-h intervals, was started. After 4 days, the patient's body temperature returned to normal, and repeated blood cultures were negative. The treatment with cefotaxime was continued for 4 weeks, and the gentamicin treatment was continued for 10 days. Two weeks after the beginning of treatment the left bundle branch block disappeared. After 12 months the patient was well without fever. Two-dimensional echocardiography showed that the left ventricular function had improved significantly, and no vegetation was seen. Patient 2. A 52-year-old patient was admitted for persistent fever up to 38°C which started 2 months after a second aortic valve replacement because of aortic insufficiency (Bjork-Shelly valve). Eight years before, he had undergone his first aortic valve replacement (Starr-Edwards valve) for severe aortic stenosis due to rheumatic fever. Two weeks before admission the patient underwent tooth extraction without antibiotic prophylaxis. On physical examination, the patient's body weight was 71 kg, he had a temperature of 38°C, his blood pressure was 130/70, and his heart rate was 90 beats per min and regular. There were no signs of heart failure. An early diastolic murmur grade 2/6 was heard along the left sternal border. The liver was not enlarged. The spleen was palpated 2 cm below the left costal margin. There were no purpura, petechiae, or signs of peripheral embolization. The erythrocyte sedimentation rate was 74 mm in the first hour, the hemoglobin concentration was 11 g/dl, and the leukocyte count was 11,500/mm3 with a normal differential count. Liver and renal function tests were all normal. Chest X ray showed interstitial pulmonary congestion and left ventricular enlargement. An electrocardiogram showed normal sinus rhythm. An M-mode echocardiogram revealed decreased opening of the mitral valve, indicating poor left ventricular function. Two-dimensional echocardiography showed flutter of the mitral leaflets and thickening of the prosthetic aortic valve, interpreted as vegetation. Three of 955
doi:10.1128/jcm.25.5.955-957.1987 fatcat:k4xke5ax2baerf2rjlta54h7ja