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

We report the case of a 48-year-old man with native valve endocarditis caused by Kingella denitrificans. He was successfully treated with a combination of beta-lactam antibiotics and aminoglycosides, after which he underwent valve replacement surgery. This case represents the first report in the literature of elective native valve replacement. Previously reported cases are discussed together with management options, including suggestions for the treatment of patients with beta-lactam allergy and those infected with beta-lactamase producing strains.
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PMID:Endocarditis caused by Kingella denitrificans. 830 23

Haemophilus parainfluenzae is a frequent cause of "culture-negative" endocarditis (i.e., endocarditis owing to a fastidious organism which may require longer incubation periods and/or enrichment media for detection compared to traditional pathogens). More cases will probably be identified with improvements in growth and isolation techniques. A case of H. parainfluenzae endocarditis is presented in a patient with mitral valve prolapse, which illustrates the difficulty in diagnosing endocarditis when initial blood cultures are negative. Particularly, it emphasizes the difficulty in selecting appropriate antibiotic therapy since beta-lactamase producing organisms are being isolated with increased frequency. This report is unique in that it documents successful treatment with a cephalosporin and what is, to our knowledge, the third reported case of a beta-lactamase producing H. parainfluenzae causing endocarditis. The authors believe that beta-lactamase stable second or third generation cephalosporins should constitute initial treatment of H. parainfluenzae endocarditis until sensitivity studies become available, since beta-lactamase production by this organism would nullify the effect of the previous agent of choice, ampicillin.
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PMID:Haemophilus parainfluenzae endocarditis in a patient with mitral valve prolapse. 832 54

The model of plastic-catheter induced left-sided enterococcal endocarditis has been used since 1970 in rabbits and since 1978 in rats in order to describe the pathophysiology of this unique infectious disease and to assess the most efficacious antibiotic regimens for treatment and prevention. A critical review of the experimental design is presented with a proposal of longer duration of therapy, recognition of relapse, and reisolation of infecting strains for susceptibility testing. The natural history of left-sided experimental enterococcal endocarditis is described and the results of classical beta-lactam-aminoglycoside combinations are reviewed. Interesting new observations on antibiotic dosing principles are discussed and new combinations of antibiotics against beta-lactamase producing enterococcal strains, strains highly resistant to gentamicin or resistant to glycopeptide antibiotics, are appraised for treatment and prophylaxis.
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PMID:The Enterococcus endocarditis model in experimental animals and its relevance to human infection. 833 27

Increasing antibiotic resistance in the enterococci, including the capacity for beta-lactamase production and the development of high-level aminoglycoside resistance, has complicated the treatment of serious enterococcal infections, which often require synergistic antibiotic combinations for cure. We utilized the rabbit model of aortic valve endocarditis to investigate the effects of various antibiotics, alone and in combination, against a multiply antibiotic-resistant isolate of Enterococcus faecalis. Female New Zealand White rabbits were infected with either a beta-lactamase-producing, gentamicin-resistant isolate of E. faecalis or a non-beta-lactamase-producing, aminoglycoside-susceptible isolate, and the mean log10 CFU per gram of vegetation were determined. The most active agents were low-dose ampicillin-sulbactam (200 mg/kg of body weight per day), high-dose ampicillin-sulbactam (400 mg/kg of body weight per day), and vancomycin (150 mg/kg of body weight per day), which reduced the titers of bacteria by 2.27, 2.76, and 2.85 log10 (CFU/g, respectively, compared with controls. While ampicillin-sulbactam and vancomycin were equally efficacious in reducing titers of bacteria in vegetations, no animals were cured (defined as < 2 log10 CFU/g of vegetation) by either agent, whether treatment was continued for 3 or 7 days. The addition of gentamicin was not associated with increased killing in rabbits infected with the aminoglycoside-resistant isolate. Both high-dose ampicillin-sulbactam and vancomycin regimens demonstrated significant, continued reduction in bacterial titers with the longer periods of treatment (P < or = 0.05); 7-day treatment with high-dose ampicillin-sulbactam produced a greater reduction in bacterial titers in vegetation than 7-day treatment with vancomycin (P < or = 0.05). We conclude that ampicillin-sulbactam and vancomycin are equally effective in the treatment of experimental endocarditis due to beta-lactamase-producing, highly gentamicin-resistant E. faecalis. The optimum therapy for such infections in humans is not known.
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PMID:Comparison of ampicillin-sulbactam with vancomycin for treatment of experimental endocarditis due to a beta-lactamase-producing, highly gentamicin-resistant isolate of Enterococcus faecalis. 836 74

Using a rat model of aortic valve infective endocarditis, we previously found that oxacillin was equally effective against an oxacillin-susceptible strain of Staphylococcus aureus and a beta-lactamase-hyperproducing borderline oxacillin-susceptible strain of S. aureus; also, ampicillin-sulbactam was less effective than oxacillin against both isolates and at low doses was less effective against the borderline-susceptible strain than against the fully oxacillin-susceptible strain (C. Thauvin-Eliopoulos, L. B. Rice, G. M. Eliopoulos, and R. C. Moellering, Jr., Antimicrob. Agents Chemother. 34:728-732, 1990). In the present study, we extended this work, using alternative treatment schedules and additional bacterial strains. Extending treatment with low doses of ampicillin-sulbactam (500 and 250 mg/kg of body weight per day, respectively) to 6.5 days resulted in equalization of effectiveness against the previously studied strains BOSSA-1 and OSSA-1 (3.75 +/- 1.61 log10 and 4.71 +/- 1.79 log10 CFU of residual viable bacteria per g, respectively). Against the borderline oxacillin-susceptible strain BOSSA-1, increasing the sulbactam dosage from 500 to 2,000 mg/kg/day while maintaining a fixed dose of ampicillin (1,000 mg/kg/day) by continuous infusion resulted in lower bacterial counts (4.93 +/- 1.84 log10 versus 3.65 +/- 1.26 log10 CFU of residual viable bacteria per g, respectively), but this difference was of only borderline significance; differences in efficacy between the low-dose and high-dose sulbactam regimens were exaggerated when intermittent intravenous administration was used (6.19 +/- 1.90 log10 versus 3.37 +/- 1.41 log10 CFU/g, respectively; P < 0.001). However, for any individual sulbactam dosage, the model of administration (continuous versus intermittent infusion) did not affect the activity of the regimen. When additional strains were used in the model, oxacillin and ampicillin-sulbactam (1,000 plus 2,000 mg/kg/day) were equally effective against both oxacillin-susceptible and borderline oxacillin-resistant strains of S. aureus. These results support the predictions that oxacillin would be clinically effective in the treatment of infections caused by borderline oxacillin-susceptible strains of S. aureus and that, except at very low doses, ampicillin-sulbactam would also be as effective against borderline-susceptible strains as against fully oxacillin-susceptible strains of S. aureus.
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PMID:Activity of ampicillin-sulbactam and oxacillin in experimental endocarditis caused by beta-lactamase-hyperproducing Staphylococcus aureus. 846 Sep 19

There are few well-documented cases of infective endocarditis due to highly aminoglycoside-resistant enterococci reported to date. Nevertheless, strains with high-level resistance to both streptomycin and gentamicin are now sufficiently common that the number of cases of endocarditis due to these organisms will undoubtedly continue to increase. Serious efforts to develop appropriate alternative treatment strategies are now clearly necessary. All high-level gentamicin-resistant bloodstream isolates from patients with suspected or proven endocarditis should be screened for high-level streptomycin resistance. Because these two resistance traits are mediated by distinct genetic elements, a significant minority of highly gentamicin-resistant enterococci will be susceptible to synergistic killing by combinations of cell wall-active antibiotics with streptomycin. For strains highly resistant to both aminoglycosides, there is no evidence of benefit from use of these toxic antimicrobials, and treatment with a cell wall-active agent alone is warranted. Based on older literature and animal models, perhaps as many as 40% to 50% of cases of enterococcal endocarditis might be curable by such regimens. Alternative combinations using a cell wall-active antibiotic together with a fluoroquinolone or rifampin cannot be specifically recommended based on any firm data from the literature, but possible merits of such combinations can be explored in vitro under appropriate circumstances. For ampicillin- and vancomycin-susceptible strains, ampicillin would seem preferable because this drug typically demonstrates greater bactericidal activity in vitro as a single agent. Consideration could be given to administration of ampicillin by continuous intravenous infusion. Several animal studies indicating effectiveness of penicillins for enterococcal endocarditis have used dosing regimens resulting in sustained serum levels. It is unknown whether these observations are relevant to human enterococcal infections. Testing for beta-lactamase production should be undertaken if penicillins are to be used. For strains that are resistant to achievable concentrations of penicillins, or when the patient is intolerant of beta-lactams, vancomycin can be used. In animal models, teicoplanin has appeared to be superior to vancomycin, but high concentrations must be attained. This drug is not yet approved for clinical use, however, and it is unclear if any advantage would exist in treatment of human infections. The recent emergence of enterococci which are resistant to glycopeptides has introduced another potential complicating factor; some of these are also substantially resistant to beta-lactams as well. In some reports, favorable interactions between vancomycin and beta-lactams have been observed against vancomycin-resistant strains.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Aminoglycoside resistant enterococcal endocarditis. 846 48

Black-pigmented Gram-negative anaerobic rods are found on mucosal surfaces as indigenous flora. With mucosal damage due to disease, trauma or surgery, these organisms may invade tissues and set up infection. Other important factors determining whether or not infection results include 'inoculum' size, synergy with other organisms and production of virulence factors that include capsules, lipopolysaccharide, attachment factors, proteases, collagenase, neuraminidase, and phospholipase A; also, they may have fibrinolytic and anti-phagocytic activity and may degrade complement and IgG and IgM. Pigmented anaerobes are found in all types of infections including such serious infections as bacteraemia, endocarditis, intracranial abscess, necrotizing pneumonia and necrotizing fasciitis, generally as part of a mixed infecting flora, and they play a key role in experimental mixed infections. They dominate or are prominent in infections involving organisms originating in the oropharynx, such as central nervous system, head and neck, dental and pleuropulmonary infections. Therapy of infections involving pigmented anaerobes includes surgery plus antimicrobial agents; a significant percentage of strains produce beta-lactamase. Much remains to be done to determine the relative importance of the various taxa of black-pigmented Gram-negative anaerobes and of the different virulence factors produced by them.
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PMID:The importance of black-pigmented gram-negative anaerobes in human infections. 851 64

Zwitterionic 7-methoxyimino cephalosporins (cefpirome, cefepime, cefclidin, DQ2556, FK037 and SCE2787) possess a variable substitution at C3 which contains a quarternary nitrogen. These cephalosporins display low affinities for Class I beta-lactamase and rapid penetration through the outer membrane of Gram-negative bacilli, so that an increased number of periplasmic beta-lactam molecules interact with PBP's per unit of time. As a consequence, the new zitterionic compounds remain active against some, but not all, ceftazidime-resistant Enterobacteriaceae producing high levels of Class I beta-lactamase or Bush type 2b beta-lactamases. Antipseudomonas activities are generally similar to that of ceftazidime except that cefclidin is more active. The new zwitterionic compounds, especially cefpirome and FK037, express greater antistaphylococcal potency than does ceftazidime. A variety of animal models including meningitis and endocarditis have confirmed the potential of these compounds in-vivo. On the basis of structural and antibacterial characteristics, the expression 'forth generation' is acceptable to describe the zwitterionic 7-methoxyimino cephalosporins.
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PMID:Laboratory assessment of antibacterial activity of zwitterionic 7-methoxyimino cephalosporins. 862 56

The activity of penicillin, alone and in combination with sulbactam, against a heterogeneously methicillin-resistant, penicillinase-producing clinical isolate of Staphylococcus aureus and its penicillinase-negative derivative was investigated in vitro and in a rabbit experimental endocarditis model. Penicillin was significantly more effective than vancomycin against the penicillinase-negative derivative in vivo (P < 0.001), and it sterilized 25% of the vegetations. The combination of penicillin and sulbactam exhibited an in vivo synergistic effect on the penicillinase-producing strain (P < 0.01) but did not produce any advantage over treatment with vancomycin, even when a high dose of sulbactam was used (100 mg/kg of body weight every 6 h). This combination was significantly less effective against the penicillinase-producing strain than was penicillin alone against the penicillinase-negative derivative (P < 0.03). In addition, the most resistant subpopulation of the surviving bacteria, which grew on agar containing 16 micrograms of methicillin per ml, was detected in 5 of 6 animals treated with penicillin and a high dose of sulbactam against the penicillinase-producing strain compared with only 1 of 12 animals treated with penicillin alone against the penicillinase-negative derivative (P < 0.01). We conclude that penicillin is highly effective against penicillinase-negative methicillin-resistant S. aureus and that penicillinase production, rather than methicillin resistance, appears to be the limiting factor for the activity of the penicillin-sulbactam combination against penicillinase-producing, methicillin-resistant S. aureus.
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PMID:Importance of penicillinase production for activity of penicillin alone or in combination with sulbactam in experimental endocarditis due to methicillin-resistant Staphylococcus aureus. 872 70

Teicoplanin is a glycopeptide antibiotic whose activity is selectively oriented against Gram-positive aerobic and anaerobic bacteria, including Staphylococcus aureus, coagulase-negative staphylococci, Clostridium difficile, Peptostreptococcus spp. and Corynebacterium jeikeium; such activity is affected by neither methicillin resistance nor beta-lactamase production. Teicoplanin is not significantly absorbed from the gastrointestinal tract; consequently, it has to be administered intravenously (either by infusion or by rapid injection) or intramuscularly. Its long half-life allows regimens based upon once daily administration. The adverse effects most frequently associated with teicoplanin treatment are local and hypersensitivity reactions, such as itching and drug fever; anaphylactoid reactions (the 'red man syndrome') are seldom observed. Teicoplanin also has less potential than vancomycin to cause nephrotoxicity, especially when administered in combination with an aminoglycoside. Teicoplanin has been proven to be effective in the treatment of microbiologically documented Gram-positive infections, including 'difficult to treat infections' such as endocarditis and prosthetic infections. Furthermore, recent trials in patients with haematological malignancies or other cancers have clearly demonstrated that teicoplanin is at least as efficacious as vancomycin in the empirical initial antibiotic regimen for febrile neutropenic patients, and is associated with fewer adverse effects. Finally, owing to its good tolerability profile and the advantage of once daily administration by both intravenous and intramuscular routes, teicoplanin has proven to be very useful for the outpatient treatment of serious Gram-positive infections. In conclusion, teicoplanin is potentially an effective alternative to vancomycin both in immunocompetent and immunocompromised patients, with the advantage over vancomycin of single daily dose administration and lower toxicity. Further comparative studies with vancomycin are, however, required to better define the therapeutic role of teicoplanin for particular infections (i.e. infective endocarditis).
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PMID:A risk-benefit assessment of teicoplanin in the treatment of infections. 878 19


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