The in vitro susceptibilities of 10 isolates of Erysipelothrix rhusiopathiae to 16 antimicrobial agents were determined. Penicillin and imipenem were the most active agents, foilowed by piperacillin, cefotaxime, ciprofloxacin, pefloxacin, and clindamycin. Some resistance was observed with erythromycin, tetracycline, and chloramphenicol. Activity was poor or absent with vancomycin, teicoplanin, daptomycin, trimethoprimsulfamethoxazole, gentamicin, and netilmicin.Erysipelothrix rhusiopathiae is a gram-positive bacillus that has long been recognized as pathogenic for animals and humans (2,9,15). The clinical spectrum of human infection with this organism varies from a mild, localized, self-limiting cutaneous disease often involving the fingers (erysipeloid) to a systemic infection frequently associated with endocardial infection (1,2,14). In a recent review of the literature, Gorby and Peacock (2) (2,3,12,14). Our study seems to confirm a poor activity of vancomycin against E. rhusiopathiae. Six isolates, including the human strain, were inhibited by concentrations of .32 ,ug/ml, three
Sixty-three consecutive streptococcal blood isolates from neutropenic patients, represented mainly by viridans group streptococci, were evaluated in vitro for antibiotic susceptibility. Of these isolates, 79.3% were highly susceptible to penicillin (MIC, .0.12 ,ig/mI). Overall, imipenem was the most active agent, followed by teicoplanin and vancomycin. All other agents showed decreased activity against streptococcal isolates that were not highly susceptible to penicillin.
Intravenous teicoplanin has been used to treat 23 cases of gram-positive-bacterial endocarditis, usually with 3 to 7 mg/kg every 12 h on the first day, followed by 3 to 7 mg/kg every 24 h. For some cases (staphylococcal and enterococcal endocarditis), the dosage was 8 to 14.4 mg/kg per day and/or other antibiotics were given. The mean duration was 48.2 days (range, 23 to 130 days). Of 23 patients, 21 (91.3%) had negative cultures or were cured. A total of 18 patients were treated with teicoplanin alone; of these, 4 had surgery, and all (except 2 who relapsed) were cured. Teicoplanin was combined with one or more antibiotics in five cases; in all cases appropriate cultures were negative, but three patients died during therapy or follow-up. Mild renal impairment was seen in two patients; both were receiving teicoplanin in combination with an aminoglycoside. We conclude that intravenous teicoplanin administered once a day at doses of 7 to 14 mg/kg per day is well tolerated, easy to administer, and may represent an efficacious therapy for gram-positive-bacterial endocarditis.Gram-positive microorganisms still are the most frequent cause of infective endocarditis (6, 24). Moreover, new species which are resistant to several antibiotics (i.e., JK corynebacteria) are emerging (10,16,19). Teicoplanin is a glycopeptide antibiotic with an antibacterial spectrum similar to that of vancomycin which is active against multipleantibiotic-resistant, gram-positive bacteria (4, 9, 13, 22). However, it has a longer elimination half-life, which allows once-a-day administration, and appears to be well tolerated (8,14,23). Although studies with animal models suggested good results with teicoplanin, alone or in combination with other antibiotics, for the treatment of infective endocarditis and other life-threatening infections (3,5,20), the results of recent clinical trials are somewhat conflicting (1,8,11,14,25). Moreover, only a few gram-positive-bacterial endocarditis cases were included in the above studies. The majority of these cases were caused by Staphylococcus species and were treated with a standard dose of 400 mg on the first day followed by 200 mg/day afterwards. Such a schedule of teicoplanin administration proved to be inadequate for the therapy of severe staphylococcal infections in a recent clinical trial (1). We report here our 3 years of experience with 23 cases of gram-positive-bacterial endocarditis, most of which were treated with doses of teicoplanin higher than those previously used. MATERIALS AND METHODSPatients. All subjects were inpatients in various divisions of the Policlinico Umberto I, University of Rome. They were initially considered eligible for the study if they had clinical syndromes consistent with gram-positive-bacterial endocarditis. Only those cases fitting recently recommended strict case definitions were included in the analysis of the results (15, 24). For almost all patients two-dimensional echocardiography was performed, and specific attention was paid not only to the valvular structures but...
Hospitalization for heart failure is a major health problem with high in-hospital and postdischarge mortality and morbidity. Non-potassium-sparing diuretics (NPSDs) still remain the cornerstone of therapy for fluid management in heart failure despite the lack of large randomized trials evaluating their safety and optimal dosing regimens in both the acute and chronic setting. Recent retrospective data suggest increased mortality and re-hospitalization rates in a wide spectrum of heart failure patients receiving NPSDs, particularly at high doses. Electrolyte abnormalities, hypotension, activation of neurohormones, and worsening renal function may all be responsible for the observed poor outcomes. Although NPSD will continue to be important agents to promptly resolve signs and symptoms of heart failure, alternative therapies such as vasopressine antagonists and adenosine blocking agents or techniques like veno-venous ultrafiltration have been developed in an effort to reduce NPSD exposure and minimize their side effects. Until other new agents become available, it is probably prudent to combine NPSD with aldosterone blocking agents that are known to improve outcomes.
A case of Erysipelothrix rhusiopathiae endocarditis involving the aortic and mitral valves in a 70-year-old male farmer is reported. The onset of infection was insidious, with a five-month history of low grade fever, malaise and a 20 kg weight loss. The patient eventually developed severe heart failure requiring surgery and died postoperatively of Pseudomonas aeruginosa pneumonia. In vitro studies showed the isolate to be highly susceptible to penicillin, ciprofloxacin and ofloxacin, and resistant to vancomycin.
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