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

Staphylococcal infective endocarditis is a severe event requiring aggressive therapy. Antibiotic regimen depends mainly on (1) the species of Staphylococcus (Staphylococcus aureus versus coagulase-negative staphylococci) and its resistance pattern (resistance to penicillin, to methicillin, to multiple classes of antibiotics); (2) the type of infected valve (native versus prosthetic); (3) the site of infection (left side versus right side endocarditis); (4) some underlying conditions of the host, in particular the presence or not of intravenous drug abuse. Based on in vitro susceptibility results, animal models and clinical trials, the following regimens are currently recommended. For native valve endocarditis, penicillin G 20 million units per day i.v. for 4-6 weeks for penicillin-susceptible strains; a penicillinase-resistant penicillin (oxacillin) 2 g i.v. q 4 h for 4-6 weeks plus an aminoglycoside (gentamicin) 1.0 mg.kg-1 i.v. q 8 h for 1 week, for penicillin-resistant, methicillin-susceptible strains; for methicillin resistant strains, vancomycin 30 mg.kg.day-1 i.v. in 2-4 doses for 4-6 weeks with the addition or not of rifampin 600-900 mg.day-1 orally. For a prosthetic valve endocarditis, a three-drug regimen (oxacillin or vancomycin, plus gentamicin and rifampin) and a longer duration (6 weeks or more) are generally recommended. Shorter (2 weeks) treatment could be delivered to uncomplicated cases of right-sided endocarditis. In view of an increased resistance to classic drugs and suboptimal efficacy of some of them, new therapeutic modalities should be looked at, in particular for endocarditis cases due to methicillin-resistant strains.
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PMID:Medical treatment of staphylococcal infective endocarditis. 767 31

Serious staphylococcal infections remain a significant clinical problem despite advances in antibacterial therapy. Resistance to penicillin is common and methicillin-resistant staphylococci have become troublesome nosocomial pathogens in many institutions. Penicillinase-resistant penicillins (e.g. flucloxacillin, cloxacillin and oxacillin) are the preferred drugs for all methicillin-susceptible staphylococcal infections, although first generation cephalosporins, beta-lactam/beta-lactamase inhibitor combinations, clindamycin, and occasionally erythromycin and cotrimoxazole (trimethoprim/sulfamethoxazole) are alternatives. Serious infections due to methicillin-resistant staphylococci should be treated with parenteral vancomycin. Teicoplanin, where available, is a suitable alternative. Rifampicin, fusidic acid and some fluoroquinolones may be useful oral alternatives, although resistance develops rapidly if they are used as single agents. Cotrimoxazole and minocycline have also proven useful when strains are susceptible. Staphylococcal toxic shock syndrome often requires aggressive resuscitation and anti-staphylococcal therapy for generally 10 to 14 days. Staphylococcus aureus bacteraemia remains a life-threatening condition which, in all but one-third of cases, is associated with an underlying septic focus such as endocarditis, osteomyelitis or occult abscess. Differentiating between complicated and uncomplicated bacteraemia is critical to define the appropriate treatment regimen. Serious staphylococcal sepsis such as endocarditis and acute osteomyelitis generally requires prolonged (4 to 6 weeks) antibiotic treatment. Coagulase-negative staphylococci are the commonest cause of prosthetic device infection, and generally require prolonged therapy with an agent to which they have proven to be sensitive, e.g. a penicillinase-resistant penicillin or vancomycin. Removal of infected foreign or prosthetic material, and drainage of deep collections remain a critical aspect of all therapy.
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PMID:Optimum treatment of staphylococcal infections. 768 6

Ampicillin or amoxicillin at 625-800 mg/kg/day, in combination with a beta-lactamase inhibitor, each is as effective as vancomycin in animal models of methicillin-resistant Staphylococcus aureus endocarditis. Studies were done to determine whether the addition of rifampin would permit lowering the dose of ampicillin into the range recommended for use in humans without loss of efficacy. The efficacy of ampicillin/sulbactam (300/150 or 150/75 mg/kg/day intramuscularly, in three divided doses) in combination with rifampin (5 mg/kg intramuscularly, three times daily) was compared with that of vancomycin (25 mg/kg intravenously, twice daily, or 30 mg/kg intramuscularly, three times daily) in the rabbit model of methicillin-resistant S. aureus aortic valve endocarditis. Neither ampicillin/sulbactam nor rifampin alone was effective. The ampicillin/sulbactam/rifampin regimen was as effective as vancomycin. This regimen may be an alternative to vancomycin in treatment of methicillin-resistant S. aureus infections.
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PMID:Ampicillin, sulbactam, and rifampin combination treatment of experimental methicillin-resistant Staphylococcus aureus endocarditis in rabbits. 770 17

An intravenous drug addict was treated with cloxacillin for septicaemia with Staphylococcus aureus because of pneumonia and suspected endocarditis. After 51 days of treatment Staphylococcus aureus was still found in blood and expectorate despite continued treatment with intravenous cloxacillin 1 g three and later four times daily and oral rifampicin. The staphylococcal isolates were all of phage type 94/96. Investigations have shown that Staphylococci aurei of phage type 94/96 produce large amounts of penicillinase, and that methicillin is the most penicillinase-resistant of the penicillinase-resistant penicillins followed by dicloxacillin and cloxacillin. The penicillinase production of the patient's Staphylococcus aureus strain was 304-362 units per mg bacteria which is high compared to typical values of 50-200. After 50 days of cloxacillin treatment, the treatment was changed to methicillin 2 g four times daily. Within a week the staphylococci had disappeared from the expectorate, and were never again recovered from the blood. It is suggested that methicillin should have superior efficiency in serious infections with Staphylococcus aureus of phage type 94/96.
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PMID:[Is methicillin better than cloxacillin in serious infections caused by strong penicillinase-producing staphylococci (phage-type 94/96)?]. 772 65

Enterococci do not possess the common virulence factors found in many other bacteria, but they have a number of other characteristics which make them particularly pathogenic. These organisms are intrinsically resistant to a number of antimicrobial agents, including beta-lactams (penicillins and cephalosporins), polymyxins and the lincosamides. They are also tolerant to the bactericidal activity of penicillins and glycopeptides, and some of the group have acquired resistance to a number of other clinically important antimicrobial agents including ampicillin, aminoglycosides, chloramphenicol and erythromycin. Numerous national and international studies have demonstrated the changes in the antibiotic resistance of enterococci. Many strains now exhibit multiple drug resistance, the most important being high-level resistance to streptomycin and gentamicin. Organisms exhibiting this high-level resistance are usually resistant to all synergistic combinations of beta-lactam antibiotics and aminoglycosides. Ampicillin-resistant strains are now emerging, some of which are beta-lactamase producers. While resistance to glycopeptides remains rare, it is increasing dramatically in many areas of the world. As nosocomial isolates of enterococci have displayed resistance to essentially every useful antimicrobial agent, it is likely to become increasingly difficult to treat and control enterococcal infections. The glycopeptide antibiotics vancomycin and, particularly, teicoplanin are the only alternatives currently available. Although a bactericidal combination of antibiotics appears necessary only in endocarditis and meningitis and although knowledge of the prevalence of resistant strains can be used to guide the selection of appropriate therapy, optimal regimens for the treatment of infections caused by multiresistant strains have yet to be determined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enterococci: susceptibility patterns and therapeutic options. 772 70

Right-sided endocarditis caused by Staphylococcus aureus is a frequent complication of injection drug use. Fortunately, the prognosis for this infection when treated with the standard regimen of 4 to 6 weeks of parenteral antistaphylococcal antibiotics is favorable. Nevertheless, in many cases, once drug users feel better, they leave the hospital against medical advice before completing the full course of antibiotic therapy. This problem has stimulated interest in shortening the duration of antibiotic to a penicillinase-resistant penicillin. Data from in vitro synergy studies and animal models of endocarditis suggest that S. aureus can be eradicated more quickly by combination therapy than by monotherapy. Reports of three prospective, nonrandomized clinical trials have been published that support the use of a 2-week course of a penicillinase-resistant penicillin and an aminoglycoside antibiotic to treat uncomplicated, exclusively right-sided endocarditis caused by methicillin-susceptible S. aureus in injection drug users.
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PMID:Short-course antibiotic therapy for right-sided endocarditis caused by Staphylococcus aureus in injection drug users. 797 1

The kinetics of tumor necrosis factor (TNF) levels in serum during therapy with cell wall-active agents (ceftriaxone, imipenem) and gentamicin were investigated in rabbits with experimental endocarditis caused by an isogenic pair of Klebsiella pneumoniae strains: a TEM-3 beta-lactamase-producing strain (KpR) or its susceptible variant (KpS). In vitro, KpR was resistant to ceftriaxone and was susceptible to gentamicin and imipenem, while KpS was susceptible to all three antibiotics. Serum TNF levels were determined in control rabbits hourly after bacterial inoculation and then daily; they were determined in treated animals hourly after the first antibiotic injection and then daily during a 4-day therapy with either imipenem (60 mg/kg of body weight four times daily), ceftriaxone (75 mg/kg once daily), or gentamicin (4 mg/kg once daily) alone or in combination with ceftriaxone. After a transient peak (10.2 +/- 3.1 ng/ml) at 90 min following bacterial challenge, serum TNF levels remained low and stable in control animals. The peak in the serum TNF levels occurred 4 h after the first antibiotic injection and with ceftriaxone was significantly higher (P < 0.05) against KpS (1.99 +/- 0.52 ng/ml) than against KpR (1.40 +/- 0.17 ng/ml). Against the KpR strain, the levels observed with ceftriaxone were significantly higher (P < 0.05) than those obtained with the other therapeutic regimens (0.70 to 0.80 ng/ml). On the day of sacrifice, effective regimens were associated with low TNF levels. We concluded that TNF production depends on (i) the antiobiotic's mechanism of action and the susceptibility of the strain at the early phase of therapy, without any effect of the rapidity of bacterial killing, and (ii) the final reduction of the bacterial count at a later stage of therapy.
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PMID:Influence of antimicrobial therapy on kinetics of tumor necrosis factor levels in experimental endocarditis caused by Klebsiella pneumoniae. 806 31

Sparfloxacin and clinafloxacin alone and in combination with gentamicin, were evaluated for the treatment of experimental endocarditis in rabbits caused by ampicillin-resistant enterococci. Clinafloxacin was tested against Enterococcus faecalis strain WH245, a beta-lactamase producer lacking high-level gentamicin resistance (MIC 12.5 mg/L). Sparfloxacin was tested against Enterococcus faecium strain SF2149 a non-producer of beta-lactamase (ampicillin MIC 400 mg/L, gentamicin MIC 12.5 mg/L). For strain WH245, clinafloxacin alone significantly reduced enterococcal counts in vegetations (7.7 log10 cfu/g) and for strain SF2149, sparfloxacin significantly reduced counts (7.0 log10 cfu/g) compared with untreated controls (WH245, 8.8 log10 cfu/g and SF2149, 9.3 log10 cfu) or treatment with ampicillin plus gentamicin (WH245, 9.7 log10 cfu/g). The addition of gentamicin resulted in no further reduction of bacterial counts in vegetations but resulted in an increase in sterilization of blood for strain SF2149. These results suggest that sparfloxacin and clinafloxacin and may prove useful in the therapy of infections due to ampicillin-resistant enterococci.
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PMID:Sparfloxacin and clinafloxacin alone or in combination with gentamicin for therapy of experimental ampicillin-resistant enterococcal endocarditis in rabbits. 812 36

The pharmacokinetics and efficacy of isepamicin were compared with those of amikacin and gentamicin in a rabbit model of endocarditis due to Klebsiella pneumoniae CF104 producing beta-lactamase TEM-3 and aminoglycoside acetyltransferase AAC(6')-IV. Only isepamicin and gentamicin, alone or combined with ceftriaxone, were effective as determined by titration of viable bacteria in vegetations. Variants highly resistant to ceftriaxone without change in MICs of aminoglycosides were isolated at the end of each therapeutic regimen except with the most effective one (ceftriaxone plus gentamicin). Examination of the bacterial outer membrane proteins as well as the 50% inhibition of the beta-lactamase activity in intact and sonified cells suggested a permeability defect as being responsible for the increased MICs of ceftriaxone. The activity of isepamicin was superior to that of amikacin against the TEM-3-AAC(6')-IV-producing strain. The combination of gentamicin plus ceftriaxone was the most effective regimen in terms of efficacy and prevention of emergence of resistant strains. Suboptimal aminoglycoside monotherapy might be responsible for selection of permeability mutants to beta-lactams.
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PMID:Activity of isepamicin and selection of permeability mutants to beta-lactams during aminoglycoside therapy of experimental endocarditis due to Klebsiella pneumoniae CF104 producing an aminoglycoside acetyltransferase 6' modifying enzyme and a TEM-3 beta-lactamase. 819 10

The activity of cefoperazone with and without sulbactam was studied in vitro and in vivo against strains of methicillin-resistant and methicillin-susceptible Staphylococcus aureus. Cefoperazone with or without sulbactam was inactive in vitro against the methicillin-resistant strain and was bound by penicillin-binding protein 2a with an IC50 of 190 mg/L (the concentration that reduced radio-labelling with 3H-penicillin by 50%). Cefoperazone was hydrolysed by beta-lactamase in vitro but sulbactam improved cefoperazone activity in a rabbit model of aortic valve endocarditis caused by a beta-lactamase producing methicillin-susceptible strain.
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PMID:Efficacy of cefoperazone in combination with sulbactam in experimental Staphylococcus aureus endocarditis in rabbits. 826 67


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