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

The clinical courses of 13 consecutive intravenous drug users with Staphylococcus aureus endocarditis treated principally with vancomycin were reviewed. Two patients, one with only right-sided endocarditis and the other with tricuspid and mitral valve endocarditis, had recurrences of positive blood cultures 2 days after completing a 4-week course of vancomycin. Two patients, both of whom eventually were cured, had modifications of therapy because of bacteremia persisting 7 and 16 days into therapy. One patient required an operation for recurrent fevers, and the resected vegetation showed evidence of active infection. Time-kill studies performed with nafcillin and vancomycin for 10 isolates of S. aureus showed that vancomycin was less rapidly bactericidal than nafcillin. Although vancomycin is used as an alternative to penicillinase-resistant penicillins for treatment of staphylococcal endocarditis, these findings raise the question of whether it is equivalent to these drugs in efficacy.
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PMID:Vancomycin for Staphylococcus aureus endocarditis in intravenous drug users. 239 84

Enterococci are important human pathogens that are increasingly resistant to antimicrobial agents. These organisms were previously considered part of the genus Streptococcus but have recently been reclassified into their own genus, called Enterococcus. To date, 12 species pathogenic for humans have been described, including the most common human isolates, Enterococcus faecalis and E. faecium. Enterococci cause between 5 and 15% of cases of endocarditis, which is best treated by the combination of a cell wall-active agent (such as penicillin or vancomycin, neither of which alone is usually bactericidal) and an aminoglycoside to which the organism is not highly resistant; this characteristically results in a synergistic bactericidal effect. High-level resistance (MIC, greater than or equal to 2,000 micrograms/ml) to the aminoglycoside eliminates the expected bactericidal effect, and such resistance has now been described for all aminoglycosides. Enterococci can also cause urinary tract infections; intraabdominal, pelvic, and wound infections; superinfections (particularly in patients receiving expanded-spectrum cephalosporins); and bacteremias (often together with other organisms). They are now the third most common organism seen in nosocomial infections. For most of these infections, single-drug therapy, most often with penicillin, ampicillin, or vancomycin, is adequate. Enterococci have a large number of both inherent and acquired resistance traits, including resistance to cephalosporins, clindamycin, tetracycline, and penicillinase-resistant penicillins such as oxacillin, among others. The most recent resistance traits reported are penicillinase resistance (apparently acquired from staphylococci) and vancomycin resistance, both of which can be transferred to other enterococci. It appears likely that we will soon be faced with increasing numbers of enterococci for which there is no adequate therapy.
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PMID:The life and times of the Enterococcus. 240 68

Several antimicrobial regimens were evaluated in the treatment of experimental enterococcal endocarditis due to a beta-lactamase-producing, highly gentamicin-resistant strain of Enterococcus faecalis. Ampicillin alone cleared bacteremia in the majority of rats and reduced titers of bacteria within vegetations (6.84 versus 8.80 log10 CFU/g in controls) but did not sterilize valves. Ampicillin-sulbactam combinations, vancomycin, daptomycin, and imipenem each reduced residual bacterial titers within vegetations to 4.01 log10 CFU/g or less; in 26 to 43% of animals receiving 5 days of therapy, titers of bacteria were reduced to undetectable levels. In a separate experiment, rats received ampicillin-sulbactam, daptomycin, or vancomycin for 10 days and were then observed for 10 days after termination of therapy for evidence of relapse. In surviving rats, valves remained sterile in four of five rats treated with ampicillin-sulbactam, in five of seven treated with daptomycin, but in only one of eight receiving vancomycin.
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PMID:Treatment of experimental endocarditis caused by a beta-lactamase-producing strain of Enterococcus faecalis with high-level resistance to gentamicin. 250 3

The authors studied the activity of fosfomycin (FOS) and/or gentamicin (GEN) against a Klebsiella pneumoniae strain resistant to all beta-lactams--except cephamycins and imipenem--by production of a plasmid mediated extended broad-spectrum beta-lactamase-TEM-3, to all aminoglycosides--except gentamicin--by production of a plasmid mediated 6' aminoglycoside acetyltransferase IV, to sulfonamides and to tetracyclines. In vitro, the combination FOS (MIC = MBC = 32 mg/l) + GEN (MIC = MBC = 2) appeared indifferent (FIC = 0.75; FBC = 1). In vivo, on experimental endocarditis in rabbits, FOS alone was ineffective, GEN alone was active but only at high dose regimen, FOS - GEN combination was active as compared with controls. Fosfomycin - gentamicin combination may be an alternative in the therapy of severe infections due to multiresistant Enterobacteriacae.
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PMID:[A fosfomycin-gentamicin combination in the treatment of experimental endocarditis caused by Klebsiella pneumoniae producing type TEM-3 beta-lactamase]. 269 65

Clinical blood isolates from sequential episodes of endocarditis occurring over a six-month period of time in an addict were investigated. The pathogens were Streptococcus sanguis II, Streptococcus mitis, and a nutritionally deficient (variant) streptococcus. The authors determined the DNA relatedness of these isolates by antibiograms, plasmid profiles, chromosomal endonuclease restriction digestions, and dot blot DNA-DNA hybridization analyses. The S. sanguis II and nutritionally deficient streptococcal strain had similar antibiograms being resistant to penicillin; neither produced beta-lactamase. No plasmids were found. The restriction endonuclease chromosomal digestion patterns of these isolates were unique and epidemiologically unrelated to each other. Dot blot DNA-DNA hybridizations, using the nutritionally deficient streptococcal DNA as the probe, showed homology to the preceding clinical isolates, S. sanguis II and S. mitis, at 15.4% and 45.1% hybridization levels, respectively. The nutritionally deficient streptococcus was only 4.2% homologous to a S. mitis ATCC strain and another nutritionally deficient streptococci isolate. Therefore, this patient had endocarditis with three distinct streptococcal strains.
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PMID:Molecular analysis of viridans and nutritionally deficient (variant) streptococci causing sequential episodes of endocarditis in a patient. 271 64

Cefotetan is a new cephamycin antibiotic characterised by excellent B-lactamase stability and anti-anaerobe activity, coupled with a long half life of 3-4 h which permits twice daily dosage. A clinical trial of cefotetan in the treatment of severe oro-facial infections is presented, together with a detailed analysis of the causative organisms and their sensitivities to eight antibiotics. 50/50 patients achieved clinical cure with a treatment regime comprising cefotetan therapy and incision and drainage, with patients being transferred to oral cephradine for the final phase of therapy. Side effects were minimal and there were no instances of relapse. Significant resistance among alpha-haemolytic streptococci and bacteroides organisms to penicillin was observed. The streptococci were resistant due to mechanisms other than beta-lactamase production. In the light of these findings and the reports of other workers it is suggested that penicillin V may no longer be the most appropriate drug for endocarditis prophylaxis, despite the most recent recommendations of the American Heart Association. Furthermore, if penicillin V is used for this purpose, a penicillin free interval of 6-8 weeks may be inadequate before this drug is used. Cefotetan is not suitable for prophylaxis against endocarditis.
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PMID:Organisms isolated from severe odontogenic soft tissue infections: their sensitivities to cefotetan and seven other antibiotics, and implications for therapy and prophylaxis. 294 42

Sixty-six cases of Gram positive infections were treated with teicoplanin in an open multicenter study, comprising 7 centers in Eastern France. There were 38 male patients and 28 females. Teicoplanin was given at a dose of 400 mg daily for a mean duration of 18.4 days. The most common infections were due to Staphylococcus aureus, found in 43 out of 56 documented cases. 69 (89.9%) of the 78 Gram + strains isolated had an MIC for teicoplanin of less than or equal to 2 mg/l. There were 44 serious infections (30 septicemia, 10 endocarditis, 1 joint and bone infection, 2 mediastinitis, 1 toxic shock syndrome) and 22 less serious infections (4 urinary infections, 14 skin and soft tissue infections, 3 lower respiratory infections, 1 hepatic abscess). In 42 cases concurrent medication was given: beta-lactamase in 11 cases, rifampicin in 10 cases, aminoglycosides in 22, phosphomycin in 3, pefloxacin in 5. The clinical cure and improvement rate was 90.10%. Adverse events were reported in 11 patients, and in only 3 cases was the therapy stopped. All were reversible on stopping therapy. Teicoplanin was found to be well tolerated and effective in the treatment of Gram positive infections in this study.
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PMID:[Teicoplanin and Gram-positive coccus infections. Results of a multicenter study on 66 cases]. 295 64

Two ceftazidime-resistant variants of Pseudomonas aeruginosa (PA-48, PA-60), obtained from cardiac vegetations of rabbits with endocarditis receiving ceftazidime therapy, were studied for mechanisms of resistance. Both resistant variants were stably derepressed for the type Id beta-lactamase, which was ceftazidime inducible in the parental strain (PA-96) used to initially infect the rabbits. There was no evidence of ceftazidime bioinactivation by the resistant strains, and their outer membrane permeabilities were comparable to those of the parental strain. No alterations were observed in patterns of outer membrane proteins or membrane lipopolysaccharides in the resistant variants as compared with the parental strain. Penicillin-binding protein patterns of the resistant variants revealed the absence of penicillin-binding protein 4 in both, with acquisition of a new protein of higher apparent molecular weight in PA-60. Calculation of the rate of appearance of ceftazidime in the periplasm at sub-MICs suggested that slow enzymatic hydrolysis of the beta-lactam, rather than nonhydrolytic trapping, was the major explanation for the induced resistance in vivo in strains PA-48 and PA-60.
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PMID:Role of beta-lactamase in in vivo development of ceftazidime resistance in experimental Pseudomonas aeruginosa endocarditis. 310 50

We used a beta-lactamase-producing (beta L+) strain of Streptococcus faecalis that also had high levels of resistance to all aminoglycosides to induce experimental endocarditis in rats. The rats were treated for five or 10 days with procaine penicillin, vancomycin, gentamicin, rifampin, or ciprofloxacin (alone or in various combinations), or with penicillin plus clavulanic acid. The levels of penicillin in serum and vegetations declined rapidly in the beta L+-infected rats treated with procaine penicillin alone, unlike the sustained levels of penicillin in either beta L- -infected rats treated with procaine penicillin or beta L+-infected rats treated with penicillin plus clavulanic acid. For the beta L+-infected rats, the enterococcal counts in vegetations were significantly reduced (greater than 3 log10 cfu/g) only by vancomycin and by penicillin plus clavulanic acid. The efficacy of the latter regimen probably resulted from the inhibition of penicillin inactivation by clavulanic acid in vegetations infected with the beta L+ strain. Our in vivo findings document the biologic significance of beta-lactamase production.
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PMID:beta-Lactamase production in experimental endocarditis due to aminoglycoside-resistant Streptococcus faecalis. 310 10

We investigated the in vitro and in vivo effects of a combination of a beta-lactam (ceftazidime) and a beta-lactamase inhibitor (dicloxacillin) to synergistically kill a ceftazidime-resistant variant, Pseudomonas aeruginosa PA-48, which overproduces type Id cephalosporinase constitutively. In vitro, dicloxacillin plus ceftazidime exerted bactericidal synergy at approximately 10(5) CFU/ml of inoculum (but not at approximately 10(7)-CFU inoculum), whereas other beta-lactamase inhibitors (sulbactam, clavulanic acid) showed no enhanced killing of PA-48 when combined with ceftazidime at clinically achievable levels for each agent. Dicloxacillin was a potent competitive inhibitor of the extracted Id cephalosporinase from strain PA-48 in short-term comixture studies (less than 10 min [Ki = 2 nM]); in contrast, longer-term comixture studies (90 min) indicated that dicloxacillin functions as a competitive substrate for the enzyme. Growth of PA-48 cells in the presence of dicloxacillin (12.5 to 100 micrograms/ml) had no significant effect on the production rates or functional activity of the Id enzyme. In experimental aortic valve endocarditis due to the ceftazidime-resistant variant (PA-48), rabbits received either no therapy, ceftazidime (25 mg/kg intramuscularly, every 4 h), or ceftazidime plus dicloxacillin (200 mg/kg intramuscularly, every 4 h). The combination regimen reduced mean bacterial densities of PA-48 within cardiac vegetations significantly below those in the other groups at both days 3 and 6 of treatment (P less than 0.005). However, mean vegetation bacterial densities remained greater than 6 log10 CFU/g in the combined treatment group. This modest in vivo synergistic effect (as compared to striking in vitro synergy at approximately 10(5)-CFU inoculum) most likely reflects the high densities of PA-48 achieved in vivo within cardiac vegetations (greater than 8 log10 CFU/g).
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PMID:Bactericidal interactions of a beta-lactam and beta-lactamase inhibitors in experimental Pseudomonas aeruginosa endocarditis caused by a constitutive overproducer of type Id beta-lactamase. 312 38


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