Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Penicillin G alone is generally recommended for the treatment of infective endocarditis caused by Streptococcus bovis because clinical isolates of S bovis are represented as being uniformly and markedly susceptible to penicillin G. However, two strains of S bovis recovered from two patients with bacterial endocarditis were resistant to the lethal effect of penicillin G. Combination therapy, cefazolin sodium and gentamicin sulfate in patient 1 and penicillin G and gentamicin in patient 2, was necessary; synergy, as manifested by lethal activity against the infecting strains, was demonstrated in the laboratory. We stress the need to determine the minimal lethal concentration of penicillin G for clinical isolates of S bovis. Until such information is available, particularly in life-threatening infections, combination drug therapy, consisting of an aminocyclitol added to a beta-lactam antimicrobic, should be used.
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PMID:Infective endocarditis caused by Streptococcus bovis resistant to the lethal effect of penicillin G. 24 29

Haemophilus parainfluenzae endocarditis is characterized by great variation in the acuteness of presentation, difficulty in isolation of the pathogen, a 50% to 60% incidence of major arterial emboli, and variability of response to therapy. Prosthetic valve endocarditis (PVE) due to H parainfluenzae biotype II occurred in a 14-year-old girl with congenital heart disease and a Starr-Edwards mitral valve prosthesis. Management was complicated by a prolonged culture-negative period (eight days), intermittent bacteremia (only five of 15 positive blood cultures), an embolus to the right femoral artery, progressive congestive heart failure, and urgent prosthestic valve replacement. Cure was achieved with 44 days of ampicillin sodium-gentamicin sulfate therapy monitored by serum bactericidal titers.
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PMID:Prosthetic valve endocarditis due to Haemophilus parainfluenzae biotype II. 44 17

Rifampin was added to existing antibiotic regimens in two patients with Staphylococcus epidermidis infections; one patient had prosthetic valve endocarditis and the other had an infection of a CSF shunt. The addition of rifampin increased serum or CSF bactericidal titers 16-fold or greater and was correlated with a favorable clinical response. The results of tests for tube-dilution antibiotic susceptibility showed rifampin to be the most active of all antibiotics tested against the patients' organisms. The combinations of gentamicin sulfate, nafcillin sodium, or vancomycin hydrochloride with rifampin prevented the emergence of rifampin resistance in vitro and promoted enhanced killing when compared with either antibiotic alone.
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PMID:Rifampin therapy of Staphylococcus epidermidis. Use in infections from indwelling artificial devices. 67 4

The association of Pseudomonas maltophilia endocarditis in three patients with recent history of intravenous drug abuse is reported. All three patients had abnormal heart valves (two prosthetic and one rheumatic). A prominent characteristic of this uncommon pathogen is its in vitro resistance to the commonly used antimicrobials. Cure was achieved in all three cases. In two cases, synergistic antibiotic combinations were used. In one case, plasmid-mediated resistance to amikacin sulfate (Amikan, British; no comparable US product) emerged during therapy. The two patients with prosthetic valves received combined surgical and antibiotic therapy.
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PMID:Pseudomonas maltophilia causing heroin-associated infective endocarditis. 71 16

Combinations of penicillin G sodium or ampicillin plus streptomycin sulfate do not produce synergism against all strains of enterococci. This lack of synergism was considered the cause of the failure in the treatment of enterococcal endocarditis. The effect of various combinations of antibiotics on 15 enterococcus strains, which had been isolated from patients with enterococcal endocarditis, was examined. The antibiotics included those that interfere with cell-wall synthesis and those that act on cell metabolism. The in vitro results have shown that while penicillin- or ampicillin-streptomycin combination was not synergistic in eight of 15 strains, penicillin- or ampicillin-gentamicin sulfate combination was synergistic in 100% of the cases. We report seven cases of enterococcal endocarditis that were successfully treated with penicillin- or ampicillin-gentamicin combination, thus confirming the effectiveness of this therapeutic regimen.
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PMID:Synergistic treatment of enterococcal endocarditis: in vitro and in vivo studies. 92 43

In a case of staphylococcal endocarditis, we failed to eradicate Staphylococcus aureus from the blood stream with vancomycin hydrochloride therapy. The strain involved was sensitive to vancomycin by disk diffusion studies but showed a wide disparity between minimal inhibitory and minimal bactericidal concentrations. The lack of a bactericidal effect was probably responsible for the failure of treatment. A synergistic effect was demonstrated for the combination of gentamicin sulfate and methicillin sodium, and the patient was ultimately cured with this combination plus vancomycin. Bactericidal tests are important in choosing an antimicrobial agent for treatment of endocarditis.
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PMID:Failure of vancomycin treatment in Staphylococcus aureus endocarditis. In vivo and in vitro observations. 98 35

Thrombin-induced platelet microbicidal protein (PMP) is considered to play an important role in preventing an important role in preventing streptococcal endocarditis. However, the structural features and functions of PMPs have not been well characterized, and their antibacterial spectra against other common endocarditis pathogens, such as the staphylococci, are not known. Thrombin stimulation of washed rabbit platelets (10(8)/ml) yielded a PMP-rich preparation with a specific activity of approximately 25 U/mg of protein as determined by Bacillus subtilis bioassay. Twenty-eight clinical and laboratory Staphylococcus aureus isolates, exposed to a standardized PMP preparation (100 U/ml for 2 h at 37 degrees C), exhibited a Poisson-distributed heterogeneity to the bactericidal action of PMP, with approximately one-third designated as PMP resistant. Gel filtration chromatography (Sephadex G-50) identified the bioactive moiety within PMP preparations to be in the major protein elution peak; sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) presumptively identified PMP as a low-molecular-weight (MW) (8,500) protein present only in such bioactive protein peaks. Both the bioactivity of PMP preparations and the low-MW protein band were removable by specific anionic membranes (e.g., cellulose-acetate/nitrate), as well as by a variety of anionic resins, further corroborating the suspected cationic charge of PMP. In addition, both PMP bioactivity and the low-MW protein band were recoverable by 1.5 M NaCl elution of the anionic membrane filters post-PMP adsorptive removal. Adsorption of bioactive PMP preparations by highly PMP-susceptible B. subtilis (10(8) CFU/ml, 30 min) resulted in a near-complete loss of residual bioactivity; in contrast, adsorption of bioactive PMP preparations with less PMP-susceptible S. aureus strains failed to reduce bioactivity. Significant lysozyme contamination of PMP-rich preparations was ruled out by determination of differences between bioactive PMP preparations and exogenous lysozyme as regards (i) relative heat stabilities; (ii) differential bactericidal activity versus B. subtilis and Micrococcus luteus; and (iii) SDS-PAGE protein profiles. These data show that the bioactive PMP protein moiety is of low MW, is heat stable, is probably cationic (similar to leukocyte-derived defensins), and possesses potent bactericidal activity against a significant percentage of S. aureus isolates.
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PMID:Partial characterization and staphylocidal activity of thrombin-induced platelet microbicidal protein. 154 35

An 18-year-old woman who underwent an elective second-trimester abortion developed Streptococcus agalactiae (group B streptococcus) endocarditis characterized by a large, pedunculated vegetation involving a previously normal tricuspid valve. Polyarthritic symptoms, as well as multiple pulmonary emboli, were experienced, and cure followed a course of treatment using intravenous penicillin G potassium combined with gentamicin sulfate. Endocarditis caused by this pathogen usually occurs among individuals compromised by underlying chronic disorders and, today, is a rare sequela of pregnancy and abortion. When planning therapy, consideration should be given to the possibility of tolerance among clinical isolates and the need for operative intervention in selected patients.
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PMID:Group B streptococcus endocarditis following second-trimester abortion. 224 76

Infective endocarditis caused by Staphylococcus aureus may be initiated by bacterial binding to cardiac valve cells. We investigated binding of whole S. aureus organisms to preparations of isolated porcine cardiac valve proteins. Cultured endothelial and subendothelial cells were surface labeled with iodine 125. After preabsorption with Escherichia coli, an organism that only rarely causes infective endocarditis, binding of surface proteins to S. aureus was assessed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and subsequent autoradiography. The results showed that cardiac valve endothelial cells expressed a major S. aureus-binding protein with an approximate apparent molecular weight of 120,000. In contrast, cardiac valve subendothelial cells expressed on their surface a single species of binding protein with an approximate apparent molecular weight of 220,000; immunoblot analysis suggested that this protein was fibronectin. We also used radiolabeled S. aureus to probe cellular proteins transferred to nitrocellulose membranes. This technique identified a 125,000 molecular weight protein that bound S. aureus in endothelial cell extracts. We conclude that specific S. aureus binding to cardiac valve cells is mediated by different receptors for endothelial and subendothelial cells.
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PMID:Identification of Staphylococcus aureus binding proteins on isolated porcine cardiac valve cells. 229 65

A case of community-acquired endocarditis caused by Enterococcus (Streptococcus) faecalis with high-level resistance to gentamicin sulfate but not to streptomycin sulfate is described. Killing curves performed using achievable serum levels showed synergistic killing when streptomycin but not gentamicin, tobramycin, or amikacin was combined with penicillin G sodium or vancomycin hydrochloride. Combination therapy with vancomycin and streptomycin resulted in cure. Serum bactericidal levels indicated activity of the synergistic, as well as a nonsynergistic (vancomycin plus gentamicin), combination. Routine screening of blood isolates for high-level resistance to streptomycin and gentamicin can provide guidance for selection of therapeutic combinations in serious enterococcal infections, including endocarditis.
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PMID:Endocarditis due to streptomycin-susceptible Enterococcus faecalis with high-level gentamicin resistance. 250 23


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