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Enterococcus durans Endocarditis

Sunbul, Mustafa, MD1,*; Cerik, Hatun O., MD1; Cerik, Bugra, MD2; Gulel, Okan, MD2; Leblebicioglu, Hakan, MD1

doi: 10.1097/MJT.0000000000000519
Therapeutic Challenges

Departments of 1Infectious Diseases and

2Cardiology, Faculty of Medicine, Ondokuz Mayis, Samsun, Turkey.

Address for correspondence: Department of Infectious Diseases, Ondokuz Mayis University Medical School, Samsun 5519, Turkey. E-mail:

The authors have no conflicts of interest to declare.

Enteroccocal infective endocarditis is often seen in comorbid diseases, such as diabetes mellitus, renal failure, pulmonary insufficiency, and immunocompromised status. It is severe and usually requires long-term treatment with antibiotics, and there is increased rate of mortality in cases with underlying diseases.1 Enterococcus durans is very rare causative agent of endocarditis.2 A PubMed search from January 1, 1957, to January 28, 2016, revealed only 4 cases.2–5 This report describes a rare case of E. durans endocarditis, associated with complications and mortality.

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A 71-year-old male patient was admitted with complaints of high fever lasting for 2 weeks and shortness of breath. Physical examination findings were as follows: temperature 39°C, arterial blood pressure 110/60 mm Hg, pulse rate 96/min, respiratory rate 22/min, bilateral basal crackles on the lung, 2/6 systolic apical heart murmur, abdominal distension, splenomegaly, pretibial edema, and splinter hemorrhages in toes. His medical history was notable for chronic obstructive pulmonary disease, diabetes mellitus regulated oral antidiabetics, heart failure, and atrial fibrillation treated with warfarin. Laboratory findings were as follows: white blood cell count 17.520/µL, hemoglobin 8.5 g/dL, hematocrit 31.9% (92% neutrophils), platelet count 67.000/mm3, erythrocyte sedimentation rate 50 mm/h, C-reactive protein 13 mg/dL, alanine aminotransferase 2339 IU/L, aspartate aminotransferase 5017 IU/L, total bilirubin 1.8 mg/dL, direct bilirubin 1.1 mg/dL, sodium 128 mEq/L, and international normalization ratio 5.5.

Thoracic computed tomography showed centrilobular and paraseptal areas of emphysema in both upper lobes. In addition, there were slight irregular panlobular infiltrations, which were more prominent at bilateral peripheral zones. A transthoracic echocardiogram revealed vegetation, and a transesophageal echocardiogram confirmed the presence of a 14 × 8 mm vegetation on the atrial side of the anterior leaflet of the mitral valve (Figure 1).



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The patient was diagnosed with endocarditis, and combination of ampicillin/gentamicin was started after obtaining blood cultures. Then imipenem was added because of pneumonia. Unfortunately, respiratory arrest developed on the second day of the treatment. The patient was intubated and placed on mechanical ventilation for 1 day. Cranial diffusion magnetic resonance imaging showed diffusion restriction lesions in the deep white matter of the left precentral gyrus compatible with subacute phase infarcts (Figure 2).



On the third day of treatment, coldness and pallor of left leg was noticed; arterial doppler imaging showed an embolic filling defect in the left dorsalis pedis artery. At follow-up, ampicillin was changed to vancomycin because of a gram-positive signal on blood culture. Matrix-assisted laser desorption ionization-time of flight mass spectrometry analysis revealed E. durans in 9 blood cultures taken before the treatment. Antibiotic susceptibility testing was performed using VITEK 2 Compact (bioMérieux, Paris, France). The minimal inhibitory concentrations for ampicillin, vancomycin, teicoplanin, linezolid, gentamicin, and streptomycin were >32, 0.75, <2, 2, >256, and >1024 mg/L, respectively. Gentamicin was stopped because of a high level of aminoglycoside resistance, and therapy was continued with a combination of vancomycin and ciprofloxacin. Because of development of red man syndrome during the course of the treatment, vancomycin was replaced with daptomycin. Control blood cultures after treatment were negative. The increases in liver enzymes were considered to be associated with congestive heart failure, and after 2 weeks, enzymes and the international normalization ratio returned to normal values. Fever also subsided after 10 days of antibiotic treatment. Transthoracic echocardiography on day 22 of treatment showed that size of vegetation on the mitral valve had decreased to 6 × 4 mm. However, day 32 treatment showed no further reduction in size of vegetation, indicating an inadequate response to medical therapy. Therefore, the patient underwent surgery for mitral valve replacement on 34th day of treatment. Subsequently, the patient developed fever, tachypnea, dyspnea, and increased mucus secretion on postoperative 12th day and was intubated again. The patient was diagnosed with nosocomial pneumonia and treated with imipenem and colistin. Acinetobacter baumannii was detected in blood, catheter hubs, and sputum culture taken in febrile period. It was resistant to all antibiotics, except for colistin. Fluconazole was added to the treatment because of the growth of Candida parapsilosis in blood culture. The patient died on 69th day of treatment (on postoperative 35th day).

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Enterococci are accounted for 5% and 10% of cases of community- and hospital-acquired bacteremia, respectively. These bacteria are important because of their potential as pathogenic agents and increased antimicrobial resistance.1,6 Enterococcus durans infections are quite rare. All cases with E. durans endocarditis had comorbid diseases, were older, and were males. The characteristics of patients with E. durans endocarditis were given in Table 1. Complications, relapse, and antimicrobial treatment failure are common, and one of the cases needs surgery.

Table 1

Table 1

European Society of Cardiology recommends a combination of amoxicillin and gentamicin for 4–6 weeks as treatment regimen for beta-lactam–sensitive and gentamicin-sensitive Enterococcus spp. endocarditis. Beta-lactam resistance and vancomycin resistance have been reported for many Enterococcus faecium strains. Use of beta-lactam antibiotics against vancomycin-resistant strains and vancomycin against beta-lactam antibiotic-resistant strains is possible because dual resistance has never been reported.7

Enterococcus durans detected in our patient was resistant to ampicillin and had a high level of resistance to aminoglycoside. Thus, the patient was treated with vancomycin and ciprofloxacin combination. However, as the patient developed red man syndrome as a side effect during vancomycin treatment, vancomycin was replaced with daptomycin. After 5 weeks of medical therapy, the patient underwent valvuloplasty operation because the vegetation had not disappeared. However, multidrug-resistant A. baumannii pneumonia developed during the postoperative period. The patient in the present case had serious problems, including heart failure, chronic lung disease, and diabetes mellitus. In addition to endocarditis, the patient was diagnosed with pneumonia and then developed complications, including cerebral infarction and thromboembolism in left leg, worsening the clinical picture. Despite long-term antibiotic therapy, the vegetation did not disappear, and the patient died because of postoperative complications. Both our patient and other cases all had comorbid diseases, especially diabetes mellitus.

In conclusion, in elderly patients with known comorbidities, E. durans should be considered as a cause of endocarditis. Knowledge of antibiotic resistance profile of the agent is very important in the selection of treatment regimen.

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7. Habib G, Lancellotti P, Antunes MJ, et al. 2015 ESC guidelines for the management of infective endocarditis: the task force for the management of infective endocarditis of the European Society of Cardiology (ESC) Endorsed: European Association for Cardio-Thoracic Surgery (EACTS), the European Association of Nuclear Medicine (EANM). Eur Heart J. 2015;36:3075–3128.

Enterococcus durans; endocarditis; ampicillin; aminoglycosides; resistance

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