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- W2087901220 abstract "Staphylococcus lugdunensis is a coagulase-negative species which tends to cause a substantially more virulent form of infectious endocarditis than do other coagulase-negative staphylococci.1 The first description of human infection by S. lugdunensis dates back to 1988, and only a few cases of endocarditis due to this organism have been reported since then.2 The infection is frequently complicated by embolic events and carries a high mortality rate. Contrary to other coagulase-negative staphylococci which respond to antibiotics, it has a high morbidity rate despite in vitro susceptibility to most antibiotics, including penicillins and cephalosporins. It resembles Staphylococcus aureus in pathologic spectrum and virulence. Multiple emboli are a frequent finding in the literature.1-5 We report a case of mitral prosthetic valve endocarditis (PVE) complicated by ring abscess formation and septic emboli. CASE The patient is a 50-year-old man who was brought to our Emergency Department from an outpatient dialysis unit. His presenting symptoms were fever, confusion, shortness of breath, and a nonproductive cough. He denied any chest pain, headache, neck stiffness, photophobia, urinary symptoms or diarrhea. He also denied recent dental work. His past medical history included end-stage renal disease on hemodialysis, congestive heart failure, hypertension, hepatitis C, chronic obstructive pulmonary disease, and mitral valve replacement due to a prior history of Staphylococcus endocarditis. On admission, the patient had a temperature of 102.9°F. He was hypotensive with blood pressure of 76/48 mm Hg and a pulse of 116 beats per minute. His physical examination revealed an acutely ill man, alert but disoriented. Extraocular muscles were intact. Pupils were equal and reactive to light. He had icteric sclera. His neck was supple. Neck veins were distended. The pharynx was clear without erythema or exudates. The heart examination revealed regular tachycardia with a systolic click and 2/6 murmur. Crackles were heard bilaterally halfway up the lung fields. He had 2+ edema of the lower extremities. The abdominal examination was benign. Neurologic examination was nonfocal. There was no evidence of splinter hemorrhages. Laboratory tests on admission revealed a WBC count 23,500 cells/mm3 with a differential count of 80% neutrophils, 9% bands, 2% lymphocytes, 8% monocytes and 1% eosinophils. The platelet count was 158,000 cells/mm3, hemoglobin and hematocrit levels were 10.7 and 32 g/dL, respectively. Creatinine was 7.5 mg/dL, alanine aminotransferase was 99 U/L, and AST was 433 U/L. The sedimentation rate was 105 mm/h. The urinalysis was essentially normal except for a few red blood cells. The chest radiograph showed patchy opacities in both lungs consistent with venous congestion. A computed tomography scan of the head showed a low-density lesion in the right frontal parietal region consistent with an early infarct. Vancomycin 1 g every week and gentamicin at each hemodialysis were started empirically after blood cultures were drawn. The patient was transferred to the intensive care unit for vasopressor therapy. On the second day of hospitalization, the admission blood cultures, 4/4, grew S. lugdunensis. All the isolates were sensitive to vancomycin, gentamicin, and all the cephalosporins. Subsequent blood cultures remained positive, and ceftriaxone and rifampin were added. A transesophageal echocardiogram showed a large echodense mass, 2 × 2.5 cm on the prosthetic mitral valve with ring abscess. While awaiting valve replacement, the patient defeversced and blood cultures were negative for growth on hospital day 5. His mental status, however, worsened and a brain MRI performed then showed a small frontal infarct. An indium scan revealed abnormal collection in the right lower lung consistent with probable abscess versus septic emboli. This finding was confirmed on a CT scan of the chest, abdomen, and pelvis, which showed nodular opacities in the right lung and low attenuation areas in the spleen consistent with infarct or septic emboli. The patient's condition deteriorated on appropriate therapy, and he developed progressive coagulopathy. Surgery was postponed due to worsening of his clinical status. On day 19 of admission, he became unresponsive and he expired a few hours later. DISCUSSION Coagulase-negative staphylococci (CoNS) are seen now more frequently as causing a wide range of infections in humans. Strains of S. epidermidis, S. hominis, and S. hemolyticus, earlier viewed as clinically insignificant, are now being reported more and more often as causes of nosocomial and other infections, whereas new CoNS species have been isolated and described as human pathogens. S. lugdunensis, a coagulase-negative organism, was originally described in 1988 by Freney et al6 in a study of 11 strains isolated from clinical specimens. Since then, the organism has been reported as a cause of a variety of infections, most commonly skin and soft tissue infections,8 but also peritonitis,12 toxic shock syndrome,15 vertebral osteomyelitis,13 knee arthritis,14 breast abscess,21 and multiple cases of infective endocarditis.1-4,8,9,16,17,20 In a review of S. lugdunensis isolates, Herchline and Ayers8 reported the presence of the organism over the entire surface of human skin as well as in the respiratory secretions (8.3%), urogenital specimens (9.6%, and other deep sites (12.9%). Clinical isolates were associated with skin surface-related sites in up to 80% of cases, and only 9.6% were related to vascular devices. The initial event in the development of infection was usually nonspecific, with trauma or immunosuppression seen in half the cases. Between 1988 and 1998, over 30 cases of S. lugdunensis endocarditis involving both native and prosthetic heart valves have been reported.17 In almost all cases, a fatal outcome could be attributed to the highly aggressive and destructive nature of this pathogen. This is usually not the case for other CoNS. Staphylococcus lugdunensis endocarditis occurs most frequently as a community-acquired infection in the fifth and sixth decades of life (range: 16-83 years), and shows no sex predominance. In all previously described cases where involvement of the left side of the heart had been shown, none of the patients were intravenous drug abusers, with the single exception of a patient who presented with right-sided (tricuspid valve) endocarditis who had a history of parenteral substance abuse.2 In most instances, endocarditis involves native valves, approximately half of which were known or determined to be damaged by preexisting valvular heart disease. Unfortunately, in the majority of described cases of S. lugdunensis endocarditis, the source of the organism remains unclear.8 Because S. lugdunensis endocarditis usually has an acute presentation with rapidly deteriorating course, frequently accompanied by embolic phenomena with high mortality, early replacement surgery may improve outcome of disease. The aggressive and fulminant course makes these infections similar to disease caused by more virulent organism such as S. aureus.3,17,20 Our case of prosthetic mitral valve endocarditis is caused by S. lugdunensis infection, and is similar to the majority of previously described cases: rapid progression and destructive complications with high mortality. The presentation resembles more the course of native valve endocarditis caused by the coagulase-positive human pathogen, S. aureus, than that of usual coagulase-negative staphylococcal endocarditis. In terms of treatment, in contrast to S. aureus strains, S. lugdunensis is usually susceptible to most antimicrobial agents including β-lactam antibiotics. Analysis of strains isolated in Europe showed high susceptibility of the organism to β-lactam agents (only 4% of French strains produced β-lactamase).5,20 American strains appear to be somewhat more resistant to this group of antimicrobics with β-lactamase production detected in 24% to 29% of studied strains.7,8 Because of the severity of infections caused by S. lugdunensis, isolation of CoNS from the blood of patients with invasive disease may necessitate the identification of etiologic agent to species level. However, differentiation of S. lugdunensis in the clinical laboratory may prove difficult because of the frequency of positive results for clumping factor and other rapid agglutination tests, which are usually positive for S. aureus, but not for CoNS.3 Cases of misidentification of S. lugdunensis using different commercially available identification systems have been reported.16,17 A positive ornithine decarboxylase test is considered particularly specific for this organism and is useful in the identification panel.1,7 Specific virulence factors for S. lugdunensis have not yet been defined. Production of α- and γ-hemolysins,7,10,19 esterase,10 protease,10 glycocalyx,10 and lipase,10 have been reported. Vandenesch et al18 demonstrated an arg-like gene in S. lugdunensis, which has been interpreted as a possible virulence factor. The gene regulator (arg) is an established major determinant for S. aureus virulence. A report by Leung et al11 described colonial variations in isolates of S. lugdunensis which may be helpful in earlier recognition of the pathogen. Similar colonial polymorphism was noted in the case described here. Whether this is a stable morphologic characteristic of this organism that can be employed as an aid in identification awaits further study. Clearly, S. lugdunensis is a rare but significant pathogen, causing more aggressive, destructive, and complicated infections than other CoNS.21 To the best of our knowledge, this is the first case of mitral PVE due to S. lugdunensis complicated by paravalvular abscess." @default.
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- W2087901220 title "Staphylococcus lugdunensis Prosthetic Mitral Valve Endocarditis Complicated by Paravalvular Abscess and Septic Emboli" @default.
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