- Email: [email protected]
Enterococcus: Prevalence, resistance and susceptibility testing
50
Enterococcus: Prevalence, Resistance and Susceptibility Testing Recent experience at several institutions and evidence documented in a preliminary survey by CDC (The National Nosocomial Infectious Surveillance System--NNISS) has attested to the increasing frequency of enterococcal bacteremia in the United States. 1 Nine species make up the genus Enterococcus; E. faecalis and E. faecium are perhaps the two most important clinically. Formerly, the enterococci were assigned to the Group D family of streptococci as characterized by Lancefield. The therapeutic arsenal to treat serious enterococcal infections is limited. Therapy frequently consists of a penicillin (usually ampicillin) or a glycopeptide (vancomycin or teicoplanin) in combination with an aminoglycoside (streptomycin or gentamicin). Most cephalosporins are inactive against the enterococci. Of the two clinically predominant enterococcal species, E. faecium is usually more refractory to the synergistic combined antibiotic therapy than E. faecalis, especially when aminoglycosides other than gentamicin are incorporated in the combination. Because E. faecium comprises about 30% of the strains associated with serious disease, infectious disease experts recommend the use of gentamicin. A recent review of enterococcal bacteremia evidenced that 50% of patients were treated with two antimicrobial agents--commonly ampicillin and gentamicin; 90% of these patients demonstrated clinical improvement. 2 Surprisingly, 56% of the patients followed were receiving cephalosporin therapy, which may have contributed to the risk of disease.
THE ANTIMICROBIC NEWSLETTER, VOLUME 6, NUMBER 6, JUNE 1989
Associated with the increasing frequency of enterococcal infections is the awareness of strains resistant to high concentrations of penicillins and/or resistant to high levels of aminoglycosides-- streptomycin or, in some geographic locations, gentamicin. 3 Enterococcal resistance to penicillins has been attributed to mutations affecting PBPs (penicillin-binding proteins), the penicillin targets, or because of a penicillin destructive e n z y m e - beta-lactamase that is plasmid mediated. Another disturbing facet related to enterococcal treatment is the recent finding of strains resistant to vancomycin. 4 Conventional antimicrobic susceptibility testing methods demonstrate that most cephalosporins are relatively inactive against enterococci. Two clinical situations highlight contrasting outcomes. The poor activity of moxalactam has been associated with a serious risk of enterococcal colonization or superinfection, whereas for the similarly poor in vitro performance of cefotaxime, enterococcal superinfections in patients receiving cefotaxime therapy appears to be less common. Recent efforts by Eliopoulos and coworkers have shed some light on this. s It had been previously observed that when sheep blood was added to the test medium an augmented antimicrobial activity against group D streptococci was noted. 6 Eliopoulos' group investigated the enhancing effect of sheep blood on several cephalosporin compounds when tested against 86 clinical isolates of E. faecalis. They found that the augmented effect was demonstrable against one-half of the isolates when tested against cefotaxime. For the cephalosporins studied, the heightened potency was specific to the syn-configura-
© 1989 BY ELSEVIER SCIENCE PUBLISHING CO., INC.
tion of the oxime moiety of the beta-lactam compounds. When alpha 1-, beta-, and gamma-globulin fractions and albumin fractions of human serum were used, no augmentation was observed, and antagonistic activity was frequently demonstrated. However, the alpha 2-globulin human serum fraction was shown to be responsible for the enhanced activity. The clinical implications of these findings were examined in a rat peritoneal abscess model. Using the animal model, it was shown that cefotaxime significantly reduced bacterial titers within abscesses whereas moxalactam, whose in vitro activity proved not to be augmented by serum, was ineffective in the rat model. REFERENCES
1. Horan T, et al: Pathogens causing nosocomial infections: Preliminary data from the National Nosocomial Infections Surveillance System. The Antimicrobic Newsletter 5:65-67, 1988. 2. Gullberg RM, Homann SR, Phair JP: Enterococcal bacteremia: Analysis of 75 episodes. Revs Infect Dis 11:7485, 1989. 3. Amsterdam D: Simple detection of high level resistant of Enterococcus faecalis: An alternate to synergy testing. The Antimicrobic Newsletter 5:36-38, 1988. 4. Leclercq R, et al: Plasmid mediated resistance to vancomycin and teicoplanin in Enterococcus faecium. N Eng J Med 319:157-161, 1988. 5. Eliopoulos GM, et al: Effect of blood product medium supplements on the activity of cefotaxime and other cephalosporins against Enterococcus faecalis. Diagn Microbiol Infec Dis 12:149-156, 1989. 6. Sahm DF, Baker CN, Jones RN, Thornsberry C: Influence of growth medium on the in vitro activities of second- and third-generation cephalosporins against Streptococcus faecalis. J Clin Microbiol 20:561-567, 1984.
0738-1751/89/$0.00 + 2.20
Enterococcus: Prevalence, Resistance and Susceptibility Testing Recent experience at several institutions and evidence documented in a preliminary survey by CDC (The National Nosocomial Infectious Surveillance System--NNISS) has attested to the increasing frequency of enterococcal bacteremia in the United States. 1 Nine species make up the genus Enterococcus; E. faecalis and E. faecium are perhaps the two most important clinically. Formerly, the enterococci were assigned to the Group D family of streptococci as characterized by Lancefield. The therapeutic arsenal to treat serious enterococcal infections is limited. Therapy frequently consists of a penicillin (usually ampicillin) or a glycopeptide (vancomycin or teicoplanin) in combination with an aminoglycoside (streptomycin or gentamicin). Most cephalosporins are inactive against the enterococci. Of the two clinically predominant enterococcal species, E. faecium is usually more refractory to the synergistic combined antibiotic therapy than E. faecalis, especially when aminoglycosides other than gentamicin are incorporated in the combination. Because E. faecium comprises about 30% of the strains associated with serious disease, infectious disease experts recommend the use of gentamicin. A recent review of enterococcal bacteremia evidenced that 50% of patients were treated with two antimicrobial agents--commonly ampicillin and gentamicin; 90% of these patients demonstrated clinical improvement. 2 Surprisingly, 56% of the patients followed were receiving cephalosporin therapy, which may have contributed to the risk of disease.
THE ANTIMICROBIC NEWSLETTER, VOLUME 6, NUMBER 6, JUNE 1989
Associated with the increasing frequency of enterococcal infections is the awareness of strains resistant to high concentrations of penicillins and/or resistant to high levels of aminoglycosides-- streptomycin or, in some geographic locations, gentamicin. 3 Enterococcal resistance to penicillins has been attributed to mutations affecting PBPs (penicillin-binding proteins), the penicillin targets, or because of a penicillin destructive e n z y m e - beta-lactamase that is plasmid mediated. Another disturbing facet related to enterococcal treatment is the recent finding of strains resistant to vancomycin. 4 Conventional antimicrobic susceptibility testing methods demonstrate that most cephalosporins are relatively inactive against enterococci. Two clinical situations highlight contrasting outcomes. The poor activity of moxalactam has been associated with a serious risk of enterococcal colonization or superinfection, whereas for the similarly poor in vitro performance of cefotaxime, enterococcal superinfections in patients receiving cefotaxime therapy appears to be less common. Recent efforts by Eliopoulos and coworkers have shed some light on this. s It had been previously observed that when sheep blood was added to the test medium an augmented antimicrobial activity against group D streptococci was noted. 6 Eliopoulos' group investigated the enhancing effect of sheep blood on several cephalosporin compounds when tested against 86 clinical isolates of E. faecalis. They found that the augmented effect was demonstrable against one-half of the isolates when tested against cefotaxime. For the cephalosporins studied, the heightened potency was specific to the syn-configura-
© 1989 BY ELSEVIER SCIENCE PUBLISHING CO., INC.
tion of the oxime moiety of the beta-lactam compounds. When alpha 1-, beta-, and gamma-globulin fractions and albumin fractions of human serum were used, no augmentation was observed, and antagonistic activity was frequently demonstrated. However, the alpha 2-globulin human serum fraction was shown to be responsible for the enhanced activity. The clinical implications of these findings were examined in a rat peritoneal abscess model. Using the animal model, it was shown that cefotaxime significantly reduced bacterial titers within abscesses whereas moxalactam, whose in vitro activity proved not to be augmented by serum, was ineffective in the rat model. REFERENCES
1. Horan T, et al: Pathogens causing nosocomial infections: Preliminary data from the National Nosocomial Infections Surveillance System. The Antimicrobic Newsletter 5:65-67, 1988. 2. Gullberg RM, Homann SR, Phair JP: Enterococcal bacteremia: Analysis of 75 episodes. Revs Infect Dis 11:7485, 1989. 3. Amsterdam D: Simple detection of high level resistant of Enterococcus faecalis: An alternate to synergy testing. The Antimicrobic Newsletter 5:36-38, 1988. 4. Leclercq R, et al: Plasmid mediated resistance to vancomycin and teicoplanin in Enterococcus faecium. N Eng J Med 319:157-161, 1988. 5. Eliopoulos GM, et al: Effect of blood product medium supplements on the activity of cefotaxime and other cephalosporins against Enterococcus faecalis. Diagn Microbiol Infec Dis 12:149-156, 1989. 6. Sahm DF, Baker CN, Jones RN, Thornsberry C: Influence of growth medium on the in vitro activities of second- and third-generation cephalosporins against Streptococcus faecalis. J Clin Microbiol 20:561-567, 1984.
0738-1751/89/$0.00 + 2.20