Cases reported "Endocarditis, Bacterial"

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1/40. endocarditis due to aerococcus urinae: diagnostic tests, fatty acid composition and killing kinetics.

    Two cases of aerococcus urinae endocarditis are reported. The organism is not included in any database of commercial identification systems at this time. Formation of tetrades and positive reactions for leucine arylamidase and beta-glucuronidase pointed strongly to A. urinae. The cellular fatty acid pattern was similar to that of aerococcus viridans, with predominantly C16:0, C18:1 omega 9c and C18:0; the presence of C18:1 omega 7t differentiated our isolates from A. viridans and can support the diagnosis of A. urinae. Furthermore, susceptibility to penicillin but resistance to cotrimoxazole represents a pattern opposite to that of A. viridans. Minimal inhibition concentrations of gentamicin and netilmicin were < or = 64 mg/l but those of tobramycin were > or = 256 mg/l. Penicillin combined with either gentamicin or netilmicin showed distinct synergy in killing kinetics. These combinations seem to be the appropriate regimen to treat A. urinae endocarditis.
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2/40. Infective endocarditis complicated with progressive heart failure due to beta-lactamase-producing cardiobacterium hominis.

    We describe a 66-year-old woman with infective endocarditis due to cardiobacterium hominis whose condition, complicated by severe aortic regurgitation and congestive heart failure, necessitated aortic valve replacement despite treatment with ceftriaxone followed by ciprofloxacin. The blood isolate of C. hominis produced beta-lactamase and exhibited high-level resistance to penicillin (MIC, >==256 microgram/ml) and reduced susceptibility to vancomycin (MIC, 8 microgram/ml).
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3/40. Polyclonal Staphylococcal endocarditis caused by genetic variability.

    Cultures of blood obtained from a patient with staphylococcus epidermidis prosthetic valve endocarditis yielded 15 strains of S. epidermidis. genome macrorestriction and amplified fragment-length polymorphism analyses of these strains showed that they belonged to 4 different, very closely related clones, suggesting that they were the result of genetic variability of an infecting strain during the infectious episode. In vivo experiments in a rat model for foreign body infections using 1 of the S. epidermidis strains from the patient showed genetic variability similar to that of the infecting strain. In the rat model, we also detected the simultaneous presence of different clones that were identical to those isolated from our patient, thus confirming the possibility of genetic variability. It is important to note that the 4 clones isolated from our patient presented with 2 different antibiograms. Therefore, in cases of foreign device-related infections due to coagulase-negative staphylococci, the possibility of polyclonal infection has to be taken into account, particularly as regards differences in antibiotic susceptibility.
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4/40. Prosthetic biologic valve endocarditis caused by a vancomycin-resistant (vanA) enterococcus faecalis: case report.

    We recently observed (February 1999) a 68-year old patient with endocarditis on a prosthetic biologic valve caused by a vancomycin-resistant enterococcus faecalis. Broth dilution tests showed susceptibility to ampicillin (MIC=0.5 microg/ml), no high resistance to aminoglycosides (MIC for gentamicin <500 microg/ml) and resistance to vancomycin (MIC >256 microg/ml) and teicoplanin (MIC >16 microg/ml). A PCR assay detected vanA gene in this strain. A transthoracic echocardiogram did not show valvular vegetations. A possible endocarditis was diagnosed and the patient received ampicillin for 8 weeks and gentamicin for 6 weeks. The patient remained afebrile after a 4-month follow-up when he underwent surgical replacement of the dysfunctional bioprosthetic valve. mitral valve was sterile on culture, but histology confirmed the diagnosis of previous endocarditis. This is the third case of endocarditis caused by vancomycin-resistant E. faecalis reported to date.
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5/40. listeria monocytogenes tricuspid valve endocarditis with septic pulmonary emboli in a liver transplant recipient.

    listeria monocytogenes has long been known as a pathogen of immunocompromised hosts, including solid organ and bone marrow transplant recipients. Its principal manifestations include bacteremia and meningitis. endocarditis due to Listeria is far less common and in general affects the left side of the heart. We here report an unusual case of Listeria tricuspid valve endocarditis and septic pulmonary emboli in a sulfa-intolerant liver transplant recipient with a history of relapsing cytomegalovirus (CMV) hepatitis and an indwelling Hickman catheter. The literature on Listeria endocarditis and infections in transplant recipients is reviewed. The possible relationship between susceptibility to Listeria infection and the discontinuation of trimethoprim-sulfamethoxazole prophylaxis is of interest.
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6/40. Relapsing bacteremia in patients with ventricular assist device: an emergent complication of extended circulatory support.

    BACKGROUND: Ventricular assist devices (VAD) are currently approved for use as a bridge for transplantation. Although reports have suggested acceptable rates of survival of patients with VAD, there is little information regarding the mechanism and etiology of bacteremia in these patients. methods: We prospectively followed patients who underwent VAD implantation and developed bacteremia during VAD support at the University of Pittsburgh Medical Center. Relapsing bacteremia was defined as at least two episodes of positive blood cultures with a genetically related organism on 2 different days. Species identification and susceptibility testing were performed on all isolates. pulse field gel electrophoresis was performed on selected blood and VAD isolates. RESULTS: Between January 1998 and August 1999, 3 patients with VAD developed relapsing bacteremia, which was treated with full courses of antibiotic agents, 2 of whom also developed VAD endocarditis. All 3 patients had documented driveline or device pocket infections with these isolates. Consecutive blood and VAD isolates were found to be genetically related within each patient. CONCLUSIONS: These patients with bacteremia after VAD implantation had relapse due to the same strain, which may have originated from indolent driveline infection. Endovascular infection in this setting is difficult to eradicate with antibiotic agents and carries a high mortality. These patients should be considered to have priority for orthotopic heart transplantation.
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7/40. The "surreptitious Staphylococcus": staphylococcus lugdunensis endocarditis in a child.

    A child with congenital heart disease developed infective endocarditis caused by staphylococcus lugdunensis. Despite an apparent excellent response to initial antibiotic treatment in clinical, inflammatory and echocardiographic indices, the patient's valve damage progressed silently and surgical intervention was required. This case highlights the potential for misidentification of S. lugdunensis, its usual susceptibility to penicillin and in particular the aggressive nature of endocarditis caused by this coagulase-negative staphylococcus. The epidemiology and treatment of endocarditis caused by this organism are reviewed.
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8/40. vancomycin treatment failure associated with heterogeneous vancomycin-intermediate staphylococcus aureus in a patient with endocarditis and in the rabbit model of endocarditis.

    Heterogeneous resistance to vancomycin is thought to precede emergence of intermediate susceptibility to vancomycin in staphylococcus aureus, but the clinical significance of heterogeneous resistance is unknown. Paired S. aureus isolates from a patient with endocarditis who relapsed after vancomycin treatment were tested for heterogeneous resistance to vancomycin. The pretreatment and the relapse clinical isolates (strains SF1 and SF2, respectively) were genotyped by pulsed-field gel electrophoresis. Susceptibility to vancomycin was assessed by the broth dilution method, population analysis, and time-kill studies and in the rabbit model of endocarditis. Strains SF1 and SF2 had similar genotypes, and the vancomycin MICs for the strains were vancomycin. vancomycin eradicated SF1 in the rabbit model of endocarditis, while SF2 persisted at pretreatment levels. vancomycin treatment failure in this patient with endocarditis was attributable to heterogeneous resistance to vancomycin.
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9/40. Report of a case with polymicrobial endocarditis related to multiresistant strains.

    We present a patient with polymicrobial endocarditis who had been operated on previously for a mycotic aneurysm and was seen at the cardiology clinic because of palpitations related to effort. A transesophageal echocardiogram revealed a 15-mm vegetation on his aortic valve. staphylococcus epidermidis and corynebacterium striatum were isolated from the blood cultures. Both strains were multiresistant (susceptible to 3 antibiotics at most) against chemotherapy in vitro. Microbiological eradication was not achieved from blood cultures even after applying antimicrobial therapy with effective antibiotics as determined with an antibiotic susceptibility test. For this reason, the patient underwent valve replacement. He was discharged from hospital in fairly good health.
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10/40. Fatal case of endocarditis due to weissella confusa.

    This is the first reported case of endocarditis due to the lactobacillus-like vancomycin-resistant gram-positive bacillus weissella confusa. Full identification and susceptibility testing of lactobacillus-like organisms recovered in blood culture should be performed for patients with clinical presentations that suggest endocarditis.
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