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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-three patients with viridans streptococcal infective endocarditis were treated for two weeks with intramuscular procaine pencillin, 1.2 million units every 6 hours, plus streptomycin, 500 mg intramuscularly every 12 hours. Nine patients (27%) had infections with relatively penicillin-resistant microorganisms (MIC greater than 0.1 microgram/ml or MBC greater than or equal 3.12 microgram/ml). Follow-up ranged from 2 months to 3.5 years. There were no relapses; Mild vestibular toxicity developed in one patient. One patient died two months after completion of antimicrobial therapy from sudden onset of severe congestive heart failure; Seven patients required cardiac valve replacement after completion of antimicrobial therapy. None died. We believe that this therapeutic regimen is effective antimicrobial therapy for infective endocarditis caused by viridans streptococci, irrespective of in vitro microbiologic data.
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PMID:Short-term intramuscular therapy with procaine penicillin plus streptomycin for infective endocarditis due to viridans streptococci. 63 38

Serious infections due to lactobacilli have been rarely cited. We report our findings in nine recent patients with lactobacillemia. In the combined literature and current experience, endocarditis and sepsis from localized suppuration were the most common clinical syndromes, most frequently arising from prior oropharyngeal infections. Lactobacillus endocarditis showed a predilection for left-sided cardiac involvement (100 per cent) and systemic arterial embolization (55 per cent). The nine clinical isolates were tested for minimal inhibitory and bactericidal concentrations (MICs and MBCs) against five drugs with broad gram-positive spectrums; of note, these organisms demonstrated a high incidence of both unachievable MBCs (64 per cent) and widely disparate (greater than 100 fold) MIC:MBC ratios (38 per cent). This is in accord with observations in Lactobacillus endocarditis of poor in vivo clinical response despite "appropriate" regimens and achievable MICs of the organisms. Bactericidal synergistic studies on two endocarditis isolates indicated that the penicillins plus aminoglycosides may be potentially useful in the treatment of deep-seated Lactobacillus infections when single antimicrobials fail to achieve a cure.
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PMID:Lactobacillemia--report of nine cases. Important clinical and therapeutic considerations. 64 45

Infections with enterococci that are resistant to multiple antibiotics are an emerging clinical problem. We evaluated the antibiotic treatment of experimental enterococcal endocarditis caused by two strains with different mechanisms of penicillin resistance. Enterococcus faecalis HH-22 is resistant to aminoglycosides and penicillin on the basis of plasmid-mediated modifying enzymes; Enterococcus raffinosus SF-195 is susceptible to aminoglycosides but is resistant to penicillin on the basis of low-affinity penicillin-binding proteins. Animals infected with strain HH-22 received 5 days of treatment with the following: no treatment; daptomycin (20 mg/kg of body weight twice daily [b.i.d.], intramuscularly [i.m.]), vancomycin (20 mg/kg b.i.d., intravenously), or ampicillin (100 mg/kg three times daily, i.m.) plus gentamicin (2.5 mg/kg b.i.d. i.m.). Although vancomycin was superior to ampicillin-gentamicin (P less than 0.01), daptomycin was significantly better than all other treatment regimens (P less than 0.01) in reducing intravegetation enterococcal densities, although no vegetations were rendered culture negative by this agent. Animals infected with strain SF-195 received 5 days of no therapy, ampicillin, ampicillin-gentamicin, vancomycin, or daptomycin (all at the dosage regimens described above). Daptomycin, vancomycin, and ampicillin-gentamicin each lowered intravegetation enterococcal densities significantly better than did ampicillin monotherapy or no treatment (P less than 0.01); moreover, these three treatment regimens rendered significantly more vegetations culture negative than did ampicillin monotherapy or no treatment (P less than 0.05). Serum daptomycin levels remained above the MICs and MBCs for both enterococcal strains throughout the 12-h dosing interval used in the study. Daptomycin and vancomycin were both active in vivo in these models of experimental enterococcal endocarditis caused by penicillin-resistant strains, irrespective of the mechanism of resistance. This activity correlated with the unique cell wall sites of action of these agents (binding to lipoteichoic acid and pentapeptide precursor, respectively) compared with the sites of action of beta-lactams (penicillin-binding proteins). Beta-Lactamase production by strain HH-22 precluded in vivo efficacy with ampicillin-gentamicin combinations. In contrast, this combination was active in vivo against strain SF-195, which exhibited intermediate-level penicillin resistance (MIC, 32 micrograms/ml), likely reflecting the ability of high-dose ampicillin to achieve enough binding to low-affinity penicillin-binding proteins to cause augmented aminoglycoside uptake.
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PMID:Comparison of daptomycin, vancomycin, and ampicillin-gentamicin for treatment of experimental endocarditis caused by penicillin-resistant enterococci. 132 32

The efficacy of tazobactam, a beta-lactamase inhibitor, in combination with piperacillin, was studied in vitro and in rabbit experimental endocarditis due to a Klebsiella pneumoniae strain (KpR) producing an extended-spectrum beta-lactamase, TEM-3, or its nonproducing variant (KpS). In vitro, piperacillin was active against KpS (MIC = 4 micrograms/ml, MBC = 8 micrograms/ml with 10(7)-CFU/ml inoculum) but not against KpR (MIC = MBC = 256 micrograms/ml). Tazobactam (1 microgram/ml) restored the activity of piperacillin against KpR (MIC = 2 micrograms/ml, MBC = 4 micrograms/ml). Gentamicin was active against both strains (MIC = 0.25 and 0.5 micrograms/ml for KpS and KpR, respectively). The piperacillin-tazobactam-gentamicin combination was synergistic in vitro. The piperacillin/tazobactam ratio in plasma and in vegetations was always lower than the 4/1 injected dose ratio. In vivo, piperacillin (300 mg/kg of body weight four times a day [QID]) was active against KpS but not against KpR. Tazobactam (75 mg/kg QID) was able to restore the in vivo effect of piperacillin (300 mg/kg QID) against KpR (-3.0 log10 CFU/g of vegetation versus that of controls). Gentamicin (4 mg/kg twice a day [BID]) was active against both strains. Compared with controls, the combination of gentamicin plus piperacillin against KpS (-5.6 log10 CFU/g of vegetation), and the gentamicin-piperacillin-tazobactam combination against KpR (-4.4 log10 CFU/g of vegetation) achieved the greatest decrease in bacterial counts in vegetations and were the only regimens that significantly increased the proportion of sterile vegetations. It is concluded that (i) tazobactam was able to restore the effect of piperacillin against a TEM-3 extended-spectrum Beta-lactamase-producing strain of K. pneumoniae, both in vitro and in a severe experimental infection with high inoculum, when used in a 4/1 piperacillin/tazobactam dose ratio; (ii) gentamicin alone was effective because of the high peak/MBC ratio in plasma; (iii) piperacillin-tazobactam-gentamicin, probably because of the effect of gentamicin in reducing bacterial inoculum in vivo, as stressed by the results obtained by piperacillin-gentamicin against KpS, may be the most effective regimen against KpR.
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PMID:Piperacillin, tazobactam, and gentamicin alone or combined in an endocarditis model of infection by a TEM-3-producing strain of Klebsiella pneumoniae or its susceptible variant. 132 34

Using an experimental endocarditis model, we studied the activity of daptomycin used alone or in combination with gentamicin against an Enterococcus faecium strain that was highly resistant to glycopeptides and susceptible to gentamicin. In vitro, the MIC of daptomycin was 1 micrograms/ml. In vivo, daptomycin appeared to be effective only when it was used in a high-dose regimen, i.e., 12 mg/kg of body weight every 8 h (-2.5 log10 CFU/g versus controls; P < 0.05), particularly when it was combined with gentamicin (-5.0 log10 CFU/g versus controls; P < 0.01). Since the distribution of daptomycin into cardiac vegetations, as evaluated by autoradiography, appeared to be homogeneous, the poor in vivo activity of daptomycin was considered to be related to its high degree of protein binding, as suggested by killing curves studies. Since the MIC of teicoplanin for the vancomycin-resistant E. faecium strain used in the study was only 64 micrograms/ml and since an in vitro synergy between teicoplanin at high dose and gentamicin was observed, a high-dose regimen of teicoplanin, i.e., 40 mg/kg every 12 h, was also assessed in vivo. This treatment provided marginal activity only when it was combined with gentamicin (-2.3 log10 CFU/g versus controls; P < 0.05). These results suggest that the levels of daptomycin or teicoplanin in serum required to cure experimental endocarditis caused by a highly glycopeptide-resistant strain of E. faecium would not be achievable in humans.
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PMID:Daptomycin or teicoplanin in combination with gentamicin for treatment of experimental endocarditis due to a highly glycopeptide-resistant isolate of Enterococcus faecium. 133 39

Enterococci isolated from different body sites were tested for high-level gentamicin resistance. A total of 139 enterococcal isolates were screened for resistance (minimum inhibitory concentration [MIC] greater than 2000 mg l-1) by a broth-tube method. Twenty-five (18%) were found to exhibit resistance and this was confirmed by agar screening (1000 mg l-1) and agar dilution MIC determinations. The majority of isolates also showed high-level resistance to kanamycin and streptomycin. The remaining isolates showed high-level resistance to gentamicin and kanamycin but not streptomycin. A retrospective clinical review was performed. Most patients had a source of definite or likely infection (78%). Serious infections such as endocarditis or meningitis were not observed during the course of this study. Retrospective clinical data suggest that in cases not involving endocarditis or meningitis, neither infection refractory to therapy nor relapse of infection is a common sequel to infection with gentamicin-resistant enterococci in hospitalized patients.
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PMID:Clinical isolates of enterococci with high-level resistance to currently available aminoglycosides. 1935 53

Sixty-three cases of monomicrobial enterococcal infections treated with teicoplanin in two open clinical studies in Europe from 1982 to 1989 are presented. Infections were documented as endocarditis (n = 18); septicemia (n = 8); and urinary tract (n = 29), skin/soft-tissue (n = 6), or bone/joint (n = 2) infections. A total of 63 enterococcal strains were isolated; all of 29 strains tested were susceptible to teicoplanin (geometric mean MIC, 0.16 micrograms/mL; range, 0.06-0.5 micrograms/mL). Forty-eight patients were treated with teicoplanin alone and 15 were treated with teicoplanin in combination with an aminoglycoside. The rate of clinical cure was 84.1%; 4.8% of patients clinically improved, 7.9% had clinical recurrence, and 3.2% did not respond to therapy. Bacteriologic eradication was observed in 87.2% of patients; persistence, in 3.2%; recurrence, in 3.2%; and reinfection, in 4.8%. One case was not evaluable bacteriologically. Of 18 patients with endocarditis, 15 were cured with a mean daily dose of 5.4 mg/kg--six with monotherapy and nine with combination therapy. All patients with urinary tract infections were treated with monotherapy, and 89.7% were cured (mean daily dose, 4.6 mg/kg). Lower rates of clinical cure and bacteriologic eradication were observed in septicemic patients without endocarditis (62.5%). This study demonstrated a good efficacy of teicoplanin for the treatment of enterococcal infections due to susceptible strains, but further clinical studies would be useful for establishing optimal dosage and the indications for combination therapy, especially for severe infections.
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PMID:Efficacy of teicoplanin for enterococcal infections: 63 cases and review. 138 8

We studied the efficacy of continuous intravenous infusion of ampicillin compared with that of intermittent administration of ampicillin alone or in combination with gentamicin for the therapy of highly aminoglycoside-resistant enterococcal experimental endocarditis. Rabbits were infected with a gentamicin-susceptible (MIC, 256 micrograms/ml) strain of Enterococcus faecalis or a strain of E. faecalis which was highly resistant to gentamicin in vitro (MIC, greater than 2,000 micrograms/ml). Administration of ampicillin by continuous intravenous infusion did not significantly enhance the killing of enterococci in vivo compared with that by intermittent administration of ampicillin for either the aminoglycoside-susceptible or the aminoglycoside-resistant strain. In combination with gentamicin, there were no significant differences in efficacies obtained with intermittent versus continuous intravenous infusion of ampicillin therapy for experimental endocarditis caused by either strain of E. faecalis.
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PMID:Continuous intravenous versus intermittent ampicillin therapy of experimental endocarditis caused by aminoglycoside-resistant enterococci. 141 26

The interaction of bacteria with platelets at the cardiac valve surface represents a critical event in the induction of infective endocarditis. Platelets are thought to modulate induction or propagation of endocarditis via secretion of alpha-granule-derived platelet microbicidal protein (PMP) (a low-molecular-mass, cationic, heat-stable protein distinct from lysozyme). We studied representative PMP-susceptible and PMP-resistant Staphylococcus aureus isolates to determine their in vitro bacteriostatic and bactericidal susceptibilities to combinations of PMP plus antistaphylococcal antibiotics. PMP plus oxacillin exerted a synergistic bactericidal effect, in contrast to either agent alone, regardless of the intrinsic PMP susceptibility of the isolate tested. Exposure of S. aureus to PMP alone resulted in residual postexposure growth-inhibitory effects lasting from 0.9 to 1.8 h. Sequential exposure of S. aureus isolates to PMP for 30 min followed by exposure to either oxacillin or vancomycin (each at 10x the MIC for 120 min) resulted in a significant extension of the postantibiotic-effect duration compared with antibiotic exposure alone (P less than or equal to 0.05). Collectively, these findings indicate that PMP both enhances antibiotic-induced killing of S. aureus and increases the postantibiotic-effect duration in S. aureus.
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PMID:Platelet microbicidal protein enhances antibiotic-induced killing of and postantibiotic effect in Staphylococcus aureus. 141 49

The ability of three amoxycillin-resistant strains of Streptococcus sanguis 254, 24 and 297 (MIC 40 mg/L) to cause infective endocarditis (IE) in the rabbit was investigated. These strains all produced infection in the rabbit, as did an antibiotic sensitive control strain NCTC 7864. Prophylactic amoxycillin (400 mg/kg body weight) administered one hour before bacterial challenge prevented 80% of the animals developing IE irrespective of the challenging strain. It is concluded that amoxycillin-resistant strains of S. sanguis can cause IE and that amoxycillin prophylaxis can still be effective against these bacteria.
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PMID:Amoxycillin-resistant oral streptococci and experimental infective endocarditis in the rabbit. 145


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