Native Mitral Valve Endocarditis Caused by Staphylococcus lugdunensis in a 22-Year-Old Woman

Abstract

Infective native valve endocarditis caused by Staphylococcus aureus accounts for approximately 35% of cases in patients without intravenous drug abuse and for 61% of cases in intravenous drug abusers [1]. While coagulase-negative staphylococci are the most commonly isolated organisms in prosthetic valve endocarditis, only 5% of cases of native valve endocarditis are due to these pathogens [2].The species Staphylococcus lugdunensis was described for the first time in 1988 [3].This organism differs from other coagulase-negative staphylocci in that it tends to cause a more virulent form of infective endocarditis, characterized by an acute onset and destructive clinical course with a high mortality rate similar to that of S. aureus endocarditis [4].An analysis of the 22 cases reported in the English language literature until 1997 revealed severe sequelae of S. lugdunensis endocarditis: Seven of eight patients who received only antibiotic treatment died and five of 14 patients with antibiotic treatment and operative valve replacement did not survive. 15 of these 22 patients developed severe cardiac complications such as heart insufficiency, perforation or destruction of valve, rupture of chordae tendineae or myocardial abscess [5].A previously healthy 22-year-old woman became acutely ill 8 days before admission with fever and fatigue.One week prior to the onset of symptoms, she had returned from a 3-week beach holiday in Bali. Further medical history was negative except for rhinitis atopica. Physical examination revealed a patient in good general health with a core temperature of 39.3 °C, heart rate 110/min and blood pressure 140/60 mmHg. A loud pansystolic murmur was heard at the apex. Peripheral signs of bacterial endocarditis were not detected. Transthoracic and transesophageal echocardiography identified a peduncular vegetation, measuring 1.5 ϫ 0.8 cm, on the anterior leaflet of the mitral valve ( Figure 1) with mild regurgitation. Left ventricular diameters and pump function were normal and all other valves showed no evidence of vegetations. Flow in the pulmonary veins was normal. Five days later regurgitation was increased and could be traced back to the pulmonary veins. C-reactive protein was 131 mg/l, the erythrocyte sedimentation rate was 95 mm in the first hour and hemoglobin 11.8 g/dl. ␣1-, ␣2-and ␤-globulins were slightly elevated in serum protein electrophoresis (5.9, 11.2 and 12.9 rel.%, respectively). Leukocyte count and the other values of clinical chemistry were within the normal range. Figure 1. Vegetation at the anterior mitral valve leaflet.

Purulent Meningitis as an Unusual Presentation ofStaphylococcus aureusEndocarditis: A Case Report and Literature Review

“…In our case, we carried out serial echocardiographic examinations in order to monitor the clinical course of the disease; in fact S. aureus can be a cause of destructive valve endocarditis, and its pathogenic potency is explained by the expression of binding factors promoting the adherence to valves as fibrinogen binding protein [30]. Moreover, we performed both transthoracic echocardiography and transesophageal echocardiography; this is because transesophageal echocardiography is a highly valuable adjunct to other diagnostic tests and would appear to be of benefit in patients with a risk of complicated clinical course who may have additional cardiac lesions not demonstrated by transthoracic echocardiography [31, 32].…”

Epidemiology and Clinical Impact of Glycopeptide Resistance in Staphylococcus aureus

“…Infections caused by S. aureus may be relatively mild and easy to treat, or may take a dramatic, and at times life-threatening course, as is illustrated by numerous case reports and studies [8,9]. In addition to S. aureus, other staphylococcal species such as Staphylococcus lugdunensis have a high pathogenic potential due to the expression of binding factors and may cause severe infections such as rapidly destructive endocarditis [10,11].…”