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

The in vivo efficacies of pefloxacin, a new fluoroquinolone, and amikacin-ceftazidime were compared in 50 rabbits with experimental aortic endocarditis caused by Pseudomonas aeruginosa. Animals were randomly chosen to receive 4 or 10 days of no therapy (controls), pefloxacin (40 mg/kg [body weight] per day, intramuscularly [i.m.]), or amikacin (30 or 80 mg/kg per day, i.m.)-ceftazidime (150 mg/kg per day, i.m.). Pefloxacin and both amikacin regimens significantly reduced vegetation bacterial densities compared with controls at days 4 and 10 of treatment (P less than 0.0005). By day 10 of therapy, between 33 and 40% of vegetations from amikacin-ceftazidime recipients contained ceftazidime-resistant bacteria (MICs, greater than 25 micrograms/ml); nitrocefin agar overlay confirmed that these ceftazidime-resistant variants were constitutive overproducers of beta-lactamase. At therapy days 4 and 10, approximately 30% of vegetations sampled from pefloxacin recipients contained bacteria for which pefloxacin MICs were four- to eightfold higher than the MIC for the parental strain used to initially induce endocarditis (MIC, 0.19 microgram/ml). These variants also exhibited increases in ciprofloxacin and ticarcillin MICs, as well as pleotropic resistance to chloramphenicol (but not to amikacin, ceftazidime, or tetracycline). Amikacin-ceftazidime, as well as pefloxacin, was effective in this model of aortic pseudomonal endocarditis. However, in vivo development of ceftazidime resistance and step-ups in pefloxacin MICs among intravegetation isolates were associated with inability to completely eradicate P. aeruginosa from aortic vegetations.
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PMID:Development of beta-lactam resistance and increased quinolone MICs during therapy of experimental Pseudomonas aeruginosa endocarditis. 312 85

The enterococci, members of the group D streptococci and the predominant aerobic streptococci of the gastrointestinal and female genital tracts, have long been recognized as significant pathogens in infective endocarditis. Over the past 2 decades, enterococci have become increasingly important nosocomial pathogens, related to their intrinsic resistance to many antibiotics, especially the cephalosporins, and the greatly increased use of antimicrobial therapy in hospitals. Recent reports have documented an alarming increase in the frequency of high-level resistance to aminoglyclosides, and strains resistant to ampicillin by production of a beta-lactamase and to vancomycin have now been encountered. We have reviewed the clinical features and course of 153 cases of enterococcal bacteremia occurring in a university hospital over the 14-year period, 1970 to 1983, 1) to understand better the importance of enterococci as human pathogens, 2) to identify the clinical features of enterococcal bacteremia, 3) to isolate those findings that help to identify associated endocarditis, and 4) to develop guidelines for more effective antimicrobial therapy of bacteremic enterococcal infections. The annual incidence of enterococcal bacteremia in our center rose three-fold over the period reviewed. In 65 cases (42%), bacteremia was polymicrobial, caused by Enterococcus and at least 1 other microorganism, usually an aerobic gram-negative bacillus. Most bacteremias were nosocomial and derived from infections of the urinary tract (29 cases), intravenous catheters (24 cases), intra-abdominal infections or surgical wounds (46 cases), burn wounds (25 cases), or cholangitis (21 cases); only 1 case originated from a pneumonia. Endocarditis was identified in association with 12 of 35 community-acquired bacteremias, but only 1 of 118 bacteremias acquired in the hospital (P less than .001). Endocarditis was also significantly associated with pre-existent valvular heart disease and cryptogenic bacteremia, and was negatively associated with polymicrobial enterococcal bacteremia (no endocarditis in 65 cases, P less than .001). Isolated enterococcal bacteremia produced an indolent infection rarely associated with shock (3 of 64 cases evaluated, all cases due to valve destruction by endocarditis); conversely, with polymicrobial enterococcal bacteremia, primarily with gram-negative bacilli, shock or disseminated intravascular coagulation developed in 50% of cases (P less than .001).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Enterococcal bacteremia: clinical features, the risk of endocarditis, and management. 313 90

We studied a ceftazidime-resistant strain of Pseudomonas aeruginosa (PA-48) stably-derepressed for constitutive beta-lactamase overproduction, and its ceftazidime-susceptible parent (PA-96) in order to characterize the ability of clindamycin to: (1) enhance the in-vitro and in-vivo bactericidal activities of ceftazidime for PA-48; and (2) prevent beta-lactamase induction and spontaneous mutation to the derepressed state by the parental strain (PA-96). In vitro, clindamycin synergistically enhanced the bactericidal activity of ceftazidime vs PA-48. In the experimental aortic endocarditis model, the combination of clindamycin with ceftazidime significantly reduced mean intravegetation bacterial densities of PA-48 versus ceftazidime monotherapy and untreated controls at therapy days 6 and 11 (P less than 0.05). Exposure of growing PA-48 cells to clindamycin did not interfere with the hydrolytic function of extracted periplasmic beta-lactamase. Moreover, clindamycin did not suppress cefoxitin-mediated beta-lactamase induction in the parental strain (PA-96). In vitro, clindamycin prevented spontaneous mutation of PA-96 to the stably-derepressed state for beta-lactamase overproduction and also enhanced reversion of derepressed cells of PA-48 to the ceftazidime-susceptible parental phenotype by approximately 2 log10 cfu/ml. This latter effect was mirrored in vivo during clindamycin+ ceftazidime therapy of experimental endocarditis due to strain PA-48, as the proportion of ceftazidime-susceptible cells with vegetations increased by approximately 1-1.5 log10 cfu/g, versus untreated controls or ceftazidime monotherapy recipients. After clindamycin treatment ceased, vegetations contained predominantly ceftazidime-resistant variants. Clindamycin appeared to enhance bactericidal effects of ceftazidime vs PA-48 through non-beta-lactamase mechanisms probably involving promotion and maintenance of spontaneous reversion to the fully-repressed state. However, the concentrations of clindamycin required to achieve these effects are unlikely to be sustained at normal therapeutic dosage.
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PMID:In-vitro and in-vivo bacterocodal interactions of clindamycin and ceftazidime, by non-beta-lactamase mechanisms, in experimental Pseudomonas aeruginosa endocarditis caused by a constitutive beta-lactamase overproducing strain. 314 25

The mechanisms responsible for emergence of resistance during antimicrobial therapy were investigated in isolates obtained from a patient suffering from Pseudomonas aeruginosa endocarditis. The strain was first isolated from blood cultures obtained upon admission of the patient. It was sensitive to piperacillin, ticarcillin and tobramycin. Piperacillin-tobramycin therapy was therefore instituted and led to a rapid improvement of the patient's condition. Unfortunately, the patient subsequently became febrile again and blood cultures continued to yield P. aeruginosa. However, the organism isolated was now resistant to piperacillin and other penicillins tested. Cell-free extracts of the pre- and post-therapy isolates were analyzed for their beta-lactamase activity. The susceptible pre-therapy strain did not produce significant levels of beta-lactamase. In contrast, the post-therapy strain produced high levels of the enzyme. Induction experiments indicated that the production of beta-lactamase was constitutive in the post-therapy isolate. Thus, piperacillin therapy has led to the selection of resistant mutants which produced high levels of beta-lactamase constitutively. This was associated with relapse of the infection and therapeutic failure.
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PMID:Selection of resistance by piperacillin during Pseudomonas aeruginosa endocarditis. 314 26

Microbiological features, diagnostic investigations, treatment, and complication rate in 53 cases of infective endocarditis were reviewed in this study. Infection occurred both on prosthetic (47%) and native valves (38%), while in 15% of the cases no prior valvular disease was known. Streptococcal (38%) and staphylococcal (30%) infections were predominant. In 17% of the cases apparent negative blood cultures were obtained. The most frequent portal of entry was dental infection or manipulation (45%), however in 28% of the patients etiology remained obscure. Major clinical signs and symptoms included heart murmurs (96%), fever (91%), dyspnoea (32%), and splenomegaly (30%). Echocardiography revealed vegetations in 78%, aortic and mitral valve being nearly equally affected. All patients were medically treated and 53% received antibiotics prior to blood cultures. Associations of ampicillin or penicillin with an aminoglycoside (43%) and penicillinase-resistant antibiotics (30%) were most frequently administered. In 28% of the patients, it was necessary to insert a prosthetic (aortic or mitral) valve. During follow-up, heart failure (28%), embolization (11%), and infections (11%) were the major complications.
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PMID:A six years review on 53 cases of infective endocarditis: clinical, microbiological and therapeutical features. 325 78

Regimens for endocarditis caused by these bacteria are generally based on high dosage of a beta-lactam antibiotic, penicillin in the case of streptococci and a penicillinase-resistant penicillin for Staphylococcus aureus, with vancomycin substituted for beta-lactam resistant staphylococci, including coagulase-negative staphylococci. The addition of other antimicrobial agents, such as aminoglycosides (or, in the case of staphylococci, sodium fusidate or rifampicin) may increase bactericidal efficiency, or allow shorter courses, but problems of toxicity or emergence of resistance may occur. Optimal regimens are discussed, and newer agents of possible usefulness are reviewed.
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PMID:Antibiotic therapy of nonenterococcal streptococcal and staphylococcal endocarditis: current regimens and some future considerations. 329 Jan 87

Ceforanide is a 'second generation' cephalosporin administered intravenously or intramuscularly. It is similar to cefamandole and cefonicid in its in vitro superiority to 'first generation' cephalosporins against several species of Enterobacteriaceae as well as its activity against Haemophilus influenzae, including beta-lactamase-producing strains. Its activity against Staphylococcus aureus is less than that of cefamandole, cefuroxime and first generation cephalosporins. The in vitro activity against Neisseria gonorrhoeae is excellent. Pseudomonas, Acinetobacter and Serratia species, and Bacteroides fragilis are resistant, as are many strains of Proteus and Providencia species. The elimination half-life is relatively long, although shorter than that of cefonicid, and in most clinical trials ceforanide has been administered twice daily. It appeared to be comparable in therapeutic efficacy to procaine penicillin and cephazolin in the treatment of patients with community-acquired pneumonia, to cephazolin in the treatment of skin and soft tissue infections due to S. aureus or beta-haemolytic streptococci and to cefapirin in S. aureus endocarditis in parenteral drug abusers. Also, it was comparable in efficacy to cephalothin in the prophylaxis of infection in patients undergoing open heart surgery or vaginal hysterectomy, and to cephazolin in patients undergoing cholecystectomy. Thus, ceforanide is an alternative to first and certain other second generation cephalosporins in several important therapeutic and prophylactic situations. It has no advantage over other cephalosporins with regard to spectrum of antibacterial activity, but has a longer half-life than other second generation cephalosporins, except cefonicid, and can be administered according to a twice daily dosage schedule.
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PMID:Ceforanide. A review of its antibacterial activity, pharmacokinetic properties and clinical efficacy. 331 24

Variables affecting the isolation of microorganisms causing endocarditis include the volume of blood cultured, the number of blood cultures obtained, prior antimicrobial therapy, the type of microorganism involved, and blood culture technique. Culture-negative infective endocarditis is most frequently associated with prior antimicrobial therapy and nonbacterial agents, such as fungi, chlamydiae, and rickettsiae. For the diagnosis of bacterial endocarditis, culture of two to three separately collected blood samples of at least 10 ml, and preferably 20 ml, each generally suffices; however, in cases who have recently received antibiotics it may be necessary to culture an additional two to three blood samples or to consider use of beta-lactamase, antimicrobial adsorbent resins, or lysis-concentration, the last of which is also the most effective method for recovering mycobacteria and fungi from blood.
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PMID:The microbiological diagnosis of infective endocarditis. 331 62

The bacteriology, epidemiology, pathogenesis, clinical features, antimicrobial susceptibility, and therapy of Staphylococcus epidermidis infections are reviewed. Staph. epidermidis is often regarded as a culture contaminant, but its importance as a pathogen has been recognized in recent years. Except for native-valve endocarditis, most Staph. epidermidis infections are hospital-acquired. Staph. epidermidis is a common cause of infections involving indwelling foreign devices, surgical wound infections, and bacteremia in immunocompromised patients. The occult nature of these infections and low virulence of the organism make diagnosis and treatment difficult. Staph. epidermidis isolates from nosocomial infections frequently are resistant to methicillin; however, resistant isolates often appear to be susceptible to methicillin unless reliable methods of susceptibility testing are used. Cross-resistance between methicillin and cephalosporins occurs in vitro. Virtually all Staph. epidermidis isolates are susceptible in vitro to vancomycin and rifampin. Penicillin G, semisynthetic penicillinase-resistant penicillins, and cephalosporins are effective for the treatment of methicillin-sensitive Staph. epidermidis infections. Vancomycin is the drug of choice for infections caused by methicillin-resistant organisms. Vancomycin, combined with rifampin or gentamicin, or both, is recommended for therapy of serious infections caused by methicillin-resistant strains. Staph. epidermidis is an important pathogen in immunocompromised patients and patients who develop nosocomial bacteremia; treatment usually consists of antimicrobial therapy and removal of indwelling catheters or devices.
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PMID:Recognition and importance of Staphylococcus epidermidis infections. 331 61

In rats with catheter-induced sterile aortic valve vegetations we studied the efficacy of single-dose amoxicillin and single-dose erythromycin prophylaxis for the prevention of bacterial endocarditis after extractions of periodontally diseased teeth. Endocarditis after extractions occurred in 89% of control animals and was due to group G streptococci, to Staphylococcus aureus, or to both organisms. A single-dose of amoxicillin or erythromycin successfully prevented endocarditis due to these bacterial species. The analysis of the bacteremia (by culturing blood drawn 1 min after extraction on penicillinase-containing blood agar plates) indicated that amoxicillin did not influence the incidence or the magnitude of circulating group G streptococci and S. aureus, while erythromycin apparently suppressed them. However, when care was taken to eliminate blood erythromycin by a lysis-centrifugation process, the incidence and magnitude of bacteremia after erythromycin prophylaxis was similar to that in control rats. We conclude that single doses of amoxicillin and erythromycin successfully prevent experimental endocarditis after dental extractions. Since this prophylaxis was operative by mechanisms other than the prevention of the circulation of bacteria before seeding the valvular vegetations, it suggests that recommendations for prevention of bacterial endocarditis should not be aimed only at providing adequate antibiotic blood levels to suppress the bacteremia produced by the invasive procedure.
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PMID:Antibiotic prophylaxis of experimental endocarditis after dental extractions. 333 66


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