Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ENDOCARDITIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources
PubMed2005

Successful liver and kidney transplantation from cadaveric donors with left-sided bacterial endocarditis.

Bacterial infections are frequent in cadaveric organ donors and can be transmitted to the transplantation recipient, which could have devastating consequences for the recipients if adequate preventive measures are not adopted. From the 355 consecutive brain dead cadaveric organ donors procured at our center in the last four years, 2000-2003, four of them (1.1%) had bacterial endocarditis as cause of death. The bacteria responsible for the endocarditis were Staphylococcus epidermidis, coagulase-negative Staphylococcus, Staphylococcus hominis and Streptococcus viridans, respectively. We performed five kidney and two liver transplantations on seven recipients. All donors and recipients received antibiotic treatment against the germ causing the respective endocarditis. Infection by the bacteria responsible for the endocarditis in the respective donors was not transmitted to any of the recipients. Six of the seven recipients were alive with normal-functioning grafts after between 13 and 24 months' follow-up. Transplantectomy was performed on one kidney recipient due to thrombosis of the renal vein of the graft not related to the endocarditis. Liver and kidney transplantation from donors dying from bacterial endocarditis can be performed without causing the transmission of infection to the recipient or the dysfunction of the graft.

Adult↗
PubMed1997

[Prosthetic endocarditis caused by Kingella denitrificans in a patient with diabetes mellitus].

Infective endocarditis caused by Kingella denitrificans occurs rarely. A review of the literature reveals only 6 cases of endocarditis caused by the bacillus. K. denitrificans is normally a commensal of the upper respiratory airways, may exceptionally be responsible for endocarditis. A case of possible prosthetic endocarditis caused by K. denitrificans is presented. A 78-year-old male with Type II diabetes was admitted to the hospital complaining of fever, a sore throat and arthralgia. He underwent replacement surgery of a St. Jude medical prosthesis for aortic stenosis at the age of 75. The only physical findings at admission were a temperature of 38.2 degrees C and murmurs of mild mitral regurgitation. The liver and spleen were not palpable, and there were no skin or eye lesions. Laboratory findings were as follows: white blood cell count 9500/microliters with 77% neutrophils, erythrocyte sedimentation rate 71 mm/h (Westergren), blood urea nitrogen 50.2 mg/dl, serum creatinine 1.7 mg/dl and C-reactive protein 22.2 mg/dl. The Gram-negative bacillus isolated from the blood was identified as K. denitrificans by the identification system, namely ID test.FN-20 rapid (Nissui, Japan). Although an echocardiogram detected no vegetation, infective endocarditis was diagnosed because the same bacillus was detected by separate blood cultures and an obvious source of infection was not found other than the prosthetic valve. Initial treatment was flomoxef, which was changed to Ampicillin 2 g/day after K. denitrificans was identified. Ampicillin continued for 6 weeks. The clinical course was good and he did not require further surgery. He has been afebrile for 2 years after completing treatment. This case represents the first report of prosthetic valve endocarditis caused by K. denitrificans in Japan.

Aged↗
PubMed1992

Teicoplanin versus vancomycin for prophylaxis of experimental Enterococcus faecalis endocarditis in rats.

Teicoplanin was compared with vancomycin for the prophylaxis of experimental Enterococcus faecalis endocarditis in rats. Single intravenous doses of teicoplanin (7 mg/kg of body weight) or vancomycin (15 mg/kg) were given 30 min before bacterial challenge. Two strains of E. faecalis (309 and 1209) isolated from patients with endocarditis were tested. Bacterial inocula ranged from 10(4) (i.e., the inoculum infecting 90% of the control rats [ID90]) to 10(7) CFU/ml. The MICs and MBCs of teicoplanin and vancomycin were, respectively, 0.25 to greater than 128 mg/liter and 2 to greater than 128 mg/liter for strain 309 and 0.5 to greater than 128 mg/liter and 0.5 to greater than 128 mg/liter for strain 1209. Vancomycin prevented endocarditis only in 60% (strain 309) and in 87% (strain 1209) of rats challenged with the smallest bacterial-inoculum size (ID90), whereas teicoplanin prevented endocarditis in 100% of rats challenged with the same inoculum (strain 309; P = 0.05), in 87% of rats challenged with 10 times the ID90 (strain 309; P = 0.02), and in 95% of rats challenged with 100 times the ID90 (strain 1209; P = 0.0003). The combination of teicoplanin plus gentamicin (4 mg/kg) extended the protection to inocula 100 times the ID90 (strain 309; 96% of sterile animals) and 1,000 times the ID90 (strain 1209; 100% of sterile animals). Prevention of endocarditis was likely to be due to a prolonged inhibition of bacterial growth by sustained levels of teicoplanin in serum and not to bacterial killing. Indeed, teicoplanin did not exhibit any bactericidal activity either in vitro (time-kill curves) or in vivo (serum bactericidal activity). Teicoplanin proved to be superior to vancomycin in the prophylaxis of experimental E. faecalis endocarditis in rats.

Animals↗
PubMed1996

Ampicillin-sulbactam is effective in prevention and therapy of experimental endocarditis caused by beta-lactamase-producing coagulase-negative staphylococci.

Optimal strategies for the prophylaxis and therapy of endocarditis caused by oxacillin-resistant, coagulase-negative staphylococci in patients with native or prosthetic valvular heart disease are not well defined. We compared the in vivo efficacies of ampicillin-sulbactam-based regimens with those of vancomycin-based oxacillin-resistant, beta-lactamase-producing coagulase-negative staphylococcal isolate (Staphylococcus haemolyticus SE220). Ampicillin-sulbactam (100 and 20 mg/kg of body weight, respectively, given intramuscularly in a two-dose regimen) was equivalent to vancomycin (30 mg/kg given intravenously in a two-dose regimen) in its prophylactic efficacy against the coagulase-negative staphylococcal strain (93 and 80%, respectively). The combination of ampicillin-sulbactam plus either rifampin or vancomycin did not enhance the prophylactic efficacy compared with that of ampicillin-sulbactam or vancomycin alone. In the therapy of established aortic valve endocarditis in rabbits caused by this same coagulase-negative staphylococcal strain, animals received 7-day ampicillin-sulbactam-based or vancomycin-based regimens with or without rifampin. All treatment regimens were effective at lowering intravegetation coagulase-negative staphylococcal densities and rendering vegetations culture negative compared with the coagulase-negative staphylococcal densities and vegetations of untreated controls, with ampicillin-sulbactam in combination with rifampin or vancomycin being the most active regimen. However, only the regimen of ampicillin-sulbactam in combination with vancomycin effectively prevented relapse of endocarditis posttherapy after a 5-day antibiotic-free period. For animals receiving rifampin-containing regimens, relapses of endocarditis were associated with the in vivo development of rifampin resistance among coagulase-negative staphylococcal isolates in the vegetation. Ampicillin-sulbactam was highly effective in the prevention of experimental endocarditis caused by a beta-lactamase-producing, oxacillin-resistant coagulase-negative staphylococcal strain. Ampicillin-sulbactam was also efficacious for the therapy of coagulase-negative staphylococcal endocarditis, especially when it was combined with vancomycin to prevent posttherapeutic relapses.

Ampicillin↗
PubMed2001

Efficacy of teicoplanin-gentamicin given once a day on the basis of pharmacokinetics in humans for treatment of enterococcal experimental endocarditis.

With the aim of investigating home therapy for enterococcal endocarditis, we compared the efficacy of teicoplanin combined with gentamicin given once a day or in three daily doses (t.i.d.) with the standard treatment, ampicillin plus gentamicin administered t.i.d., for treating experimental enterococcal endocarditis. The antibiotics were administered by using "human-like pharmacokinetics" (H-L), i.e, pharmacokinetics like those in humans, that simulated the profiles of these drugs in human serum. Animals with catheter-induced endocarditis were infected intravenously with 10(8) CFU of Enterococcus faecalis EF91 (MICs and MBCs of ampicillin, gentamicin, and teicoplanin, 0.5 and 32, 16 and 32, and 0.5 and 1 microg/ml, respectively) and were treated for 3 days with ampicillin H-L at 2 g every 4 h plus gentamicin H-L at 1 mg/kg every 8 h, or teicoplanin H-L at 10 mg/kg every 24 h, alone or combined with gentamicin, administered at dose of H-L at 1 mg/kg every 8 h or H-L at 4.5 mg/kg every 24 h. The results of therapy for experimental endocarditis due to EF91 showed that teicoplanin alone was as effective as ampicillin alone in reducing the bacterial load (P > 0.05). The combination of ampicillin or teicoplanin with gentamicin was more effective than the administration of both drugs alone in reducing the log(10)CFU/gram of aortic vegetation (P < 0.01 and P < 0.05, respectively). Teicoplanin plus gentamicin H-L at 4.5 mg/kg, both administered every 24 h, showed an efficacy equal to the "gold standard," ampicillin plus gentamicin H-L at 1 mg/kg t.i.d. (P > 0.05). Increasing the interval of administration of gentamicin to a single daily dose combined with teicoplanin resulted in a reduction of bacteria in the vegetations equivalent to that achieved with the recommended regimen of ampicillin plus thrice-daily gentamicin in the treatment of experimental endocarditis due to E. faecalis. Teicoplanin plus gentamicin, both administered once a day, may be useful home therapy for selected cases of enterococcal endocarditis.

Animals↗
PubMed2006

Linezolid in prophylaxis against experimental aortic valve endocarditis due to Streptococcus oralis or Enterococcus faecalis.

There are no experimental studies regarding the prophylactic efficacy of linezolid against infective endocarditis. Nonbacterial thrombotic endocarditis of the aortic valve was induced in rabbits by the insertion of a polyethylene catheter. Twenty-four hours later, animals were randomly assigned to a control group, and groups receiving either ampicillin (two doses of 40 mg/kg of body weight each, given intravenously, 2 h apart) or linezolid (a single per os dose of 75 mg/kg). The first dose of ampicillin and the single dose of linezolid were administered 0.5 and 1 h, respectively, prior to the intravenous inoculation of approximately 10(7) CFU of Streptococcus oralis or Enterococcus faecalis. Linezolid peak levels in rabbit serum were similar to the peak serum levels in humans following a 600-mg oral dose of linezolid. Linezolid prevented endocarditis in 87% of S. oralis-challenged rabbits (P < 0.001 versus controls; P = 0.026 versus ampicillin). In rabbits challenged with E. faecalis, linezolid prevented endocarditis in 73% (P = 0.003 versus controls; P = 0.049 versus ampicillin). Ampicillin prevented endocarditis due to S. oralis or due to E. faecalis in 47% (P = 0.005 versus controls) and in 30% (P = not significant versus controls) of the challenged animals, respectively. In conclusion, linezolid was effective as prophylaxis against endocarditis caused by a strain of S. oralis and to a lesser degree against that caused by a strain of E. faecalis. Its prophylactic efficacy was superior to that of ampicillin.

Acetamides↗
PubMed1989

Role of adherence in pathogenesis of Enterococcus faecalis urinary tract infection and endocarditis.

Enterococcus faecalis strains isolated from urinary tract infections (UTIs) and endocarditis were analyzed for their ability to adhere to urinary tract epithelial cells (ECs) and Girardi heart (GH) and human embryonic kidney (HEK) cell cultures. UTI isolates adhered to urinary tract ECs more efficiently than to the cultured cells, at the same time showing the least affinity for GH cells. In contrast, endocarditis isolates adhered to GH cell cultures more readily than to urinary tract ECs. Moreover, although strains isolated from endocarditis adhered to GH cells more efficiently than those derived from UTI, the latter strains adhered to urinary tract cells better than the former. Studies of the ability of GH and HEK cells to internalize E. faecalis showed that for UTI isolates, 9 to 74% of adhered bacteria were internalized, while for endocarditis isolates, the percentage varied from 76 to 82%. All strains were able to associate with human neutrophils; endocarditis strains, however, associated less efficiently than UTI isolates. Growth in serum raised the adherence of all tested strains by at least 1.5- to 3-fold, with the greatest increase being observed in UTI strain adherence to GH cells (8-fold). In contrast, the association of serum-grown cells with polymorphonuclear leukocytes was reduced by two- to fivefold. In both cases, the observed serum-dependent alterations were cancelled by a few subcultures in brain heart infusion broth. These results indicate that adhesive properties are important virulence factors in the pathogenesis of UTI and endocarditis and also suggest that UTI strains showing the highest invasion and adhesive potential invade the kidneys, cause bacteremia, and, after having expressed the serum-dependent surface modification, colonize the heart.

Adult↗
PubMed1995

FimA, a major virulence factor associated with Streptococcus parasanguis endocarditis.

Adherence of microorganisms to damaged heart tissue is a crucial event in the pathogenesis of infective endocarditis. In the present study, we investigated the role of the FimA protein as a potential virulence factor associated with Streptococcus parasanguis endocarditis. FimA is a 36-kDa surface protein that is a recognized adhesin in the oral cavity where it mediates adherence to the salivary pellicle. An insertion mutant and a deletion mutant of S. parasanguis were employed in the rat model of endocarditis to determine the relevance of FimA in endocarditis pathogenesis. Catheterized rats were infected with either the fimA deletion mutant VT929, the fimA insertion mutant VT930, or the isogenic, wild-type S. parasanguis FW213. Rats inoculated with FW213 developed endocarditis more frequently (50.9%) than animals inoculated with either the deletion mutant (2.7%) or the insertion mutant (7.6%) (P < 0.001). A series of in vitro assays were performed to explore the mechanism(s) by which FimA enhanced the infectivity of S. parasanguis. FimA did not inhibit the uptake or the subsequent killing of S. parasanguis by phagocytic granulocytes. Similarly, FimA did not play a role in the adherence to or the aggregation of platelets. Significant differences were noted between FW213 and VT929 (P < 0.05) and FW213 and VT930 (P < 0.001) in their abilities to bind to fibrin monolayers. The mean percent adherence of FW213 to fibrin monolayers (2.1%) was greater than those of VT929 (0.5%) and VT930 (0.12%). Taken together, these results indicate that FimA is a major virulence determinant associated with S. parasanguis endocarditis and further suggest that its role is associated with initial colonization of damaged heart tissue.

Animals↗
PubMed1995

Antibodies to capsular polysaccharides are not protective against experimental Staphylococcus aureus endocarditis.

The protective efficacy of antibodies to the Staphylococcus aureus capsular polysaccharide was examined in a rat model of catheter-induced endocarditis. Capsular antibodies were induced either by active immunization with killed S. aureus or by passive immunization with hyperimmune rabbit antiserum to S. aureus. Control rats were injected with phosphate-buffered saline or passively immunized with normal rabbit serum or rabbit antiserum to a nonencapsulated strain. Animals with indwelling catheters were challenged intravenously with 5 x 10(4) to 4 x 10(6) CFU of the homologous S. aureus strain (capsular serotype 5 strain Reynolds or serotype 1 strain SA1 mucoid). Both immunized and control rats developed S. aureus endocarditis. The numbers of S. aureus cells recovered from the blood and aortic valve vegetations of immunized rats were similar to those of control rats, indicating that capsule-specific antibodies were not protective. To determine whether the presence of an indwelling catheter interfered with antibody-mediated protection against S. aureus endocarditis, catheters were removed 2 h after insertion in additional groups of rats. An inoculum of 10(8) CFU of strain Reynolds was needed to provoke endocarditis in rats catheterized for 2 h, compared with 5 x 10(4) CFU for rats with indwelling catheters. Passively transferred capsular antibodies were not protective since both immunized and nonimmunized animals developed endocarditis, and quantitative cultures of blood and valvular vegetations revealed no differences between immunized and control animals. The findings of this study indicate that antibodies to the capsular polysaccharide are not protective in the rat model of experimental S. aureus endocarditis.

Animals↗
PubMed2005

Fsr-independent production of protease(s) may explain the lack of attenuation of an Enterococcus faecalis fsr mutant versus a gelE-sprE mutant in induction of endocarditis.

An Enterococcus faecalis gelE insertion disruption mutant (TX5128), which produces neither gelatinase (GelE) nor the cotranscribed (in the wild type) serine protease (SprE), was found to be attenuated in a rat endocarditis model with a significant decrease in the endocarditis induction rate versus wild-type E. faecalis OG1RF (GelE(+), SprE(+)). TX5266, which has a nonpolar deletion in fsrB and, like TX5128, is phenotypically GelE(-) under usual conditions, was also studied; fsrB is a homologue of agrB of staphylococci and participates in regulation of gelE-sprE expression. Unexpectedly, TX5266 approximated wild-type OG1RF in the endocarditis model and was significantly less attenuated than TX5128. This is in contrast to other models which have found fsr mutants to be as or more attenuated than TX5128. Further study found that the fsrB mutant produced very low levels of gelatinase activity after prolonged incubation in vitro versus no gelatinase activity with TX5128 and did not show the extensive chaining characteristic of TX5128. Reverse transcription-PCR confirmed that gelE was expressed in TX5266 at a very low level versus wild-type OG1RF and was not expressed at all in TX5128. Possible explanations for the increased induction of endocarditis by TX5266 versus TX5128 include the production of low levels of protease(s) or some other effect(s) of the inactivation of the E. faecalis fsr regulator. The equivalent ability of OG1RF and its fsr mutant to initiate endocarditis may explain why we did not find naturally occurring fsr mutants, which account for ca. 35% of E. faecalis isolates, unrepresented in endocarditis versus fecal isolates.

Animals↗
PubMed2001

Long term results of mechanical prostheses for treatment of active infective endocarditis.

OBJECTIVE: To analyse the long term results of mechanical prostheses for treating active infective endocarditis. DESIGN: Prospective cohort study of a consecutive series of patients diagnosed with infective endocarditis and operated on in the active phase of the infection for insertion of a mechanical prosthesis. SETTING: Tertiary referral centre in a metropolitan area. RESULTS: Between 1975 and 1997, 637 cases of infective endocarditis were diagnosed in the centre. Of these, 436 were left sided (with overall mortality of 20.3%). Surgical treatment in the active phase of the infection was needed in 141 patients (72% native, 28% prosthetic infective endocarditis). Mechanical prostheses were used in 131 patients. Operative mortality was 30.5% (40 patients). Ninety one survivors were followed up prospectively for (mean (SD)) 5.4 (4.5) years. Thirteen patients developed prosthetic valve dysfunction. Nine patients suffered reinfection: four of these (4%) were early and five were late. The median time from surgery for late reinfection was 1.4 years. During follow up, 12 patients died. Excluding operative mortality, actuarial survival was 86.6% at five years and 83.7% at 10 years; actuarial survival free from death, reoperation, and reinfection was 73.1% at five years and 59.8% at 10 years. CONCLUSIONS: In patients surviving acute infective endocarditis and receiving mechanical prostheses, the rate of early reinfection compares well with reported results of homografts. In addition, prosthesis dysfunction rate is low and long term survival is good. These data should prove useful for comparison with long term studies, when available, using other types of valve surgery in active infective endocarditis.

Acute Disease↗
PubMed2003

Molecular diagnosis of culture negative infective endocarditis: clinical validation in a group of surgically treated patients.

OBJECTIVE: To assess the clinical validity of polymerase chain reaction (PCR) based molecular methods in the microbiological diagnosis of culture negative infective endocarditis in a group of surgically treated patients. DESIGN: Retrospective case-control study. SETTING: Reference cardiovascular surgical centre. PATIENTS AND SAMPLES: 15 culture negative patients with infective endocarditis classified according to Duke criteria, with 17 heart valve samples; 13 age and sex matched control patients without infective endocarditis, with 13 valve samples. INTERVENTIONS: Medical records were reviewed and clinical, demographic, and microbiological data collected, including results of molecular detection of bacteria and fungi from valve samples. The clinical validity of molecular diagnosis was assessed, along with the sensitivity and speed of the systems. RESULTS: In the study group, 14 patients were PCR positive (93%). Organisms detected were streptococci (3), staphylococci (2), enterobacter (1), Tropheryma whippelii (1), Borrelia burgdorferi (1), Candida albicans (1), and Aspergillus species (2). Three cases were positive on universal bacterial detection but the pathogen could not be identified because of contaminating background. One case was negative. All but two positive cases showed clinical correlations. These two cases had no symptoms of infective endocarditis but there was agreement with the surgical findings. All control cases were PCR negative. Results were available within eight hours, and if sequencing was necessary, within 48 hours. CONCLUSIONS: PCR based molecular detection of pathogens in valve samples from surgically treated culture negative infective endocarditis patients is fast, sensitive, and reliable. The technology, combined with thorough validation and clinical interpretation, may be a promising tool for routine testing of infective endocarditis.

Adult↗
PubMed2003

Prosthetic valve endocarditis: early and late outcome following medical or surgical treatment.

OBJECTIVE: To compare the early and late outcome of medical and surgical treatment in patients with prosthetic valve endocarditis within a single unit. DESIGN: All patients with proven prosthetic valve endocarditis treated in one institution between 1989 and 1999 were studied. RESULTS: There were 66 patients (24 female, 42 male), mean (SD) age 57 (14) years. Of these, 28 were treated with antibiotics alone and 38 with a combination of antibiotics and surgery. The in-hospital mortality for the antibiotic group was 46% and for the surgical group, 24%. However, seven patients in the antibiotic group were considered too sick for curative treatment. The mortality in the remaining 21 medically treated patients (6/21; 29%) was not significantly different from that in the surgically treated patients (p = 0.15). Six patients in the medically treated group and one in the surgically treated group required late reoperation. Endocarditis recurred in three patients in the medically treated group, two of whom were treated surgically, and in one patient in the surgically treated group. Kaplan-Meier survival at 10 years was 28% in the medically treated group v 58% in the surgically treated group (p = 0.04). Freedom from endocarditis at five years was 60% in the surgically treated group and 65% in the medically treated group. CONCLUSIONS: Prosthetic valve endocarditis is a serious condition with high early and late mortality, irrespective of the treatment employed. These data show that selected patients with prosthetic valve endocarditis can be successfully treated with antibiotics alone. If required, surgery in this difficult group of patients can provide satisfactory freedom from recurrent infection.

Anti-Bacterial Agents↗
PubMed1998

Bacterial endocarditis at a tertiary hospital--how do we improve diagnosis and delay of treatment? A retrospective study of 140 patients.

During a period of 3.5 years, endocarditis was suspected in 151 patients admitted to Rigshospitalet. 140 were available for this study. In 59 of the 140 patients, the diagnosis was confirmed, and 36 had positive blood cultures. Echocardiographic findings compatible with the diagnosis were present in 92% of the 59 cases. The most common causes of endocarditis were Staphylococcus aureus and viridans streptococci. Patients with endocarditis caused by S. aureus had significantly (p = 0.002) more embolic episodes compared to patients having endocarditis caused by the viridans streptococci. The diagnosis was established at a mean of 3-4 weeks after the onset of symptoms and 2 weeks after admission to hospital. In order to minimize diagnostic delay, the following aspects may be important: (1) earlier detection of endocarditis among physicians examining patients at risk; (2) educating patients with cardiac disease and cardiac valve prosthesis; (3) earlier antibiotic therapy, and (4) developing further diagnostics for endocarditis.

Anti-Bacterial Agents↗
PubMed1978

Treatment of infective endocarditis: a 10-year comparative analysis.

The results of surgical and non-surgical treatment of active infective endocarditis in 182 patients over a 10-year period were analyzed. Heart failure, annular and myocardial abscesses, heart block, and coronary embolism, seen most frequently with staphylococcal and fungal endocarditis, were the primary causes of death in both native valve endocarditis (NVE) and prosthetic valve endocarditis (PVE). In NVE, surgery significantly improved the survival in patients with moderate or severe heart failure (P less than 0.05) and in all patients with staphylococcal endocarditis (P less than 0.03). In PVE, surgery significantly influenced survival in patients with moderate or severe heart failure (P less than 0.05) and in the entire group with late PVE (P less than 0.01). Early surgery is recommended for patients with native valve endocarditis and moderate or severe heart failure; those patients with staphylococcal NVE, regardless of hemodynamic state, should undergo early valve replacement. Early surgery is recommended for PVE patients with moderate or severe heart failure. We also recommend early valve replacement for early and late staphylococcal PVE.

Adolescent↗
PubMed1991

Protection against endocarditis due to Staphylococcus epidermidis by immunization with capsular polysaccharide/adhesin.

BACKGROUND: Staphylococcus epidermidis is the principal pathogen in prosthetic valve endocarditis. The capsular polysaccharide adhesin (PS/A) has been shown to mediate attachment of bacteria to medical devices. In this study, we investigated the efficacy of active and passive immunization against PS/A in preventing S. epidermidis endocarditis in a rabbit model. METHODS AND RESULTS: Aortic valve vegetations were produced by inserting a Teflon catheter into the left ventricle through the right carotid artery. Bacteremia and endocarditis were then established by implanting in the left jugular vein a catheter that was attached to an osmotic pump and contaminated with S. epidermidis strain RP62A. During a 3-week study period, of 64 blood cultures taken every second or third day from six nonimmune rabbits, 54 (84%) yielded strain RP62A. In rabbits actively immunized with PS/A, eight of 60 blood cultures (13%) were positive (odds ratio 5.0, 95% CI, 2.0-12.3, p = 0.005). At death, all six nonimmune rabbits had infected vegetations that yielded 10(6)-10(11) colony-forming units (cfu)/g of vegetation, whereas only one PS/A-immunized rabbit had an infected vegetation. Immunization protocols designed to elicit antibody to teichoic acid but not to PS/A afforded no protection against bacteremia or endocarditis. Infusion of monoclonal antibody to PS/A through a catheter in the right jugular vein provided a level of protection against both bacteremia and endocarditis comparable to that produced by active immunization. In vitro, antibody against PS/A was opsonic for S. epidermidis. CONCLUSIONS: Immunoprophylaxis targeted at staphylococcal PS/A is a promising new approach to the prevention of prosthetic valve endocarditis.

Animals↗
PubMed2001

Value of echocardiographic findings in predicting cardiovascular complications in infective endocarditis.

Echocardiography allows the detection of vegetations and estimation of valvular dysfunction in patients with infective endocarditis. The value of echocardiographic findings in predicting cardiac and other vascular complications in infective endocarditis is not well understood. Identification of high-risk patients and early surgery may improve their prognosis. The authors reviewed echocardiographic findings and related them to the development of congestive heart failure, systemic embolism, and the need for surgery or the risk of death without surgery in patients with infective endocarditis. There were 125 episodes of endocarditis in 114 patients (84 episodes [67%] in men) with a mean age +/- standard deviation of 37 +/- 7 years. Vegetations were detected by echocardiography on at least 1 valve in 87 episodes (70%); on the mitral valve in 36 episodes (29%); on the aortic valve in 21 episodes (17%); and on the tricuspid valve in 45 episodes (36%). Severe aortic regurgitation was present in 9 episodes (7%) and severe mitral regurgitation in 4 instances (3%). In 12 of 21 episodes (57%) of vegetations on the aortic valve compared with 15 of 104 patients (14%) without vegetations on the aortic valve (p < 0.001), and in 8 of 9 instances (89%) of severe aortic regurgitation compared with 19 of 116 episodes (16%) without severe aortic regurgitation (p<0.00001), the patients developed congestive heart failure. In 18 of 55 episodes (33%) of vegetations on the aortic/mitral valve compared with 17 of 70 episodes (25%) without vegetations on the aortic valve/mitral valve (p = NS), the patients developed systemic embolism. In 13 of 21 episodes (62%) of vegetations on the aortic valve compared with 19 of 104 episodes (19%) without vegetations on the aortic valve (p < 0.001), and in 8 of 9 episodes (89%) of severe aortic regurgitation compared with 24 of 116 episodes (21%) without severe aortic regurgitation (p < 0.00001), the patients either had surgery or died without surgery. Echocardiographic findings do not reliably predict the risk of systemic embolism in patients with infective endocarditis. Vegetations on the aortic valve and severe aortic regurgitation detected by echocardiography predict a high risk of developing congestive heart failure, and for the combined outcome of requiring surgery, or dying without surgery in infective endocarditis. Early surgery may improve the outlook for survival of these patients.

Adult↗
PubMed2006

Clinical manifestations and outcome in Staphylococcus aureus endocarditis among injection drug users and nonaddicts: a prospective study of 74 patients.

BACKGROUND: Endocarditis is a common complication in Staphylococcus aureus bacteremia (SAB). We compared risk factors, clinical manifestations, and outcome in a large, prospective cohort of patients with S. aureus endocarditis in injection drug users (IDUs) and in nonaddicts. METHODS: Four hundred and thirty consecutive adult patients with SAB were prospectively followed up for 3 months. Definite or possible endocarditis by modified Duke criteria was found in 74 patients: 20 patients were IDUs and 54 nonaddicts. RESULTS: Endocarditis was more common in SAB among drug abusers (46%) than in nonaddicts (14%) (odds ratio [OR], 5.12; 95% confidence interval [CI], 2.65-9.91; P < 0.001). IDUs were significantly younger (27 +/- 15 vs 65 +/- 15 years, P < 0.001), had less ultimately or rapidly fatal underlying diseases (0% vs 37%, P < 0.001) or predisposing heart diseases (20% vs 50%, P = 0.03), and their SAB was more often community-acquired (95% vs 39%, P < 0.001). Right-sided endocarditis was observed in 60% of IDUs whereas 93% of nonaddicts had left-sided involvement (P < 0.001). An extracardiac deep infection was found in 85% of IDUs and in 89% of nonaddicts (P = 0.70). Arterial thromboembolic events and severe sepsis were also equally common in both groups. There was no difference in mortality between the groups at 7 days, but at 3 months it was lower among IDUs (10%) compared with nonaddicts (39%) (OR, 5.73; 95% CI, 1.20-27.25; P = 0.02). CONCLUSION: S. aureus endocarditis in IDUs was associated with as high complication rates including extracardiac deep infections, thromboembolic events, or severe sepsis as in nonaddicts. Injection drug abuse in accordance with younger age and lack of underlying diseases were associated with lower mortality, but after adjusting by age and underlying diseases injection drug abuse was not significantly associated with mortality.

Adult↗