Coagulase-negative staphylococci are mostly regarded as nonpathogenic commensal organisms of skin that most frequently represent contaminants when encountered in blood cultures.1 Coagulase-negative staphylococci account for less than 5% of all cases of native valve endocarditis, of which, most are due to Staphylococcus epidermidis.2 There has been an increased recognition of endocarditis due to other coagulase-negative staphylococci, such as Staphylococcus capitis, Staphylococcus lugdunensis, and Staphylococcus saprophyticus.3-5 Nine cases of Staphylococcus haemolyticus endocarditis have been previously reported, including 4 cases of prosthetic valve disease.6-10 All had aortic valve endocarditis; information was not available on 2 patients. We report the first case of mitral native valve endocarditis due to S. haemolyticus.
A 52-year-old man with a medical history of end-stage renal disease, hypertension, stroke with left-sided hemiparesis, and epilepsy presented to the hospital with a 7-day history of fatigue, nonproductive cough, difficulty in breathing, and increased lower extremity weakness. The patient also had a seizure 2 weeks before admission. The patient was on hemodialysis 3 times per week but missed the last 2 sessions of dialysis because of his symptoms. He denied any drug or alcohol use. On physical examination, the patient had a maximum temperature of 101.5°F and was tachycardic, tachypneic, and hypoxic (oxygen saturation of 88% on room air). He had an apical systolic murmur and a right arm arteriovenous graft for hemodialysis that did not seem infected. Respiratory examination showed decreased breath sounds in both the lung bases with isolated expiratory wheezes. The abdomen was soft, with no hepatosplenomegaly, mass, or free fluid. There was weakness of the left lower extremity and absent deep tendon reflexes of the right lower extremity. There were no splinter hemorrhages; Osler nodes or Janeway lesions were noted.
Chest radiograph showed cardiomegaly and bibasilar infiltrates. Two sets of blood cultures were obtained, and the patient was initiated on empirical ceftriaxone and azithromycin for suspected pneumonia. Both blood cultures grew S. haemolyticus, and therapy was changed to intravenous vancomycin after repeat blood cultures. The clinical microbiology laboratory identified the organism using VITEK 2. The isolate was susceptible to vancomycin with a minimum inhibitory concentration of 2 μg/mL but resistant to oxacillin, cefazolin, clindamycin, and norfloxacin. Repeat blood cultures obtained 4 days after admission were also positive for S. haemolyticus. Transthoracic echocardiogram performed at the time of admission demonstrated mitral valve thickening and no mitral regurgitation. Magnetic resonance imaging of the brain was obtained and showed enhancing lesion in the left parietal and occipital regions and an old area of ischemic infarction in the right parietal area with encephalomalacia and dilation of the right occipital horn (Fig. 1). Follow-up blood cultures done 2 days after initiation of vancomycin were negative. The patient had progressive difficulty in breathing. A transesophageal echocardiogram revealed severe mitral valve insufficiency and anterior mitral leaflet perforation with multiple adjacent vegetations. His right arm arteriovenous graft was removed, and a tunneled central venous dialysis catheter was placed. Operative cultures from the graft site were negative. Vancomycin levels were monitored every 3 to 5 days, and the range was 13.1 to 19.9 μg/mL. Despite therapy, the patient developed respiratory distress and became hemodynamically unstable, requiring intubation. He had urgent bioprosthetic mitral valve replacement and completed 6 weeks of intravenous vancomycin therapy. Follow-up admissions showed no evidence of relapse of infection. A follow-up brain magnetic resonance imaging demonstrated regression of enhancing lesions.
Endocarditis due to coagulase-negative staphylococci is typically subacute and frequently associated with local complications including valve perforation, ring abscess, and conduction abnormalities.6 In the prior 9 reported cases of S. haemolyticus endocarditis, 4 had prosthetic valve endocarditis, and 4 had native valve endocarditis; information was not available in 1 case.6-11 Among the 7 cases with clinical information available, all involved the aortic valve. Clinical information was available in 8 cases including our case.8-11 Most cases (87.5%) were men, and 3 patients (37.5%) including our patient were on dialysis. The onset of symptoms ranged between 10 days and 1 month. Fever was present in all cases. Prosthetic valve endocarditis occurred from 19 days to 5 years after aortic valve replacement.8,11 Cerebral angiography demonstrated mycotic aneurysm in 1 case of prosthetic valve endocarditis.11 Valve replacement was performed in 4 cases of native valve endocarditis including our case, whereas none of the cases of prosthetic valve endocarditis underwent valve replacement. Combination therapy with vancomycin, rifampin, and gentamicin was used in 4 cases, whereas vancomycin and rifampin was used in 3 cases. Mortality was reported in a case of prosthetic valve endocarditis that was complicated by mycotic aneurysm.11
The present case demonstrates that this organism may cause severe native valve infection including mitral valve with metastatic complications. There are limited additional case reports of S. haemolyticus infections.12,13 The infrequency of observed clinical infections with this organism may be explained by its poor ability to produce biofilm compared with Staphylococcus aureus and S. epidermidis.14 The source of S. haemolyticus infections, as with most coagulase-negative staphylococci, is the skin. The most likely source of initial seeding of the bloodstream in our patient was either an infection of the arteriovenous graft or a transient bacteremia during hemodialysis. The significance of negative cultures from the site of the arteriovenous graft at the time of removal is unclear because vancomycin was initiated 2 weeks before its removal.
As in our case, most S. haemolyticus isolates are resistant to a wide range of antibiotics including oxacillin and were noted to have higher mean vancomycin minimum inhibitory concentrations than S. epidermidis isolates.15 Although limited data have suggested improved outcomes with combination therapy for native valve coagulase-negative staphylococcal endocarditis, there is increased risk for nephrotoxicity with the use of combination aminoglycosides.6 Present guidelines recommend 6 weeks of vancomycin for oxacillin-resistant strains of staphylococci.16 In addition, optimal therapy should include removal of any persistent sources of bacteremia and valve repair or replacement in patients with clinical progression, despite appropriate antimicrobial therapy.17-19
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