• Hannah M Wexler.
• GLA VA Healthcare System and UCLA School of Medicine, Los Angeles, CA, USA. hwexler@ucla.edu
• J. Antimicrob. Chemother. 2004 Jun 1; 53 Suppl 2: ii11-21.

AbstractErtapenem is a long-acting, 1beta-methyl parenteral Group 1 carbapenem antibiotic that has a broad antibacterial spectrum and once-a-day dosing supported by clinical studies. Ertapenem is active against both Gram-positive and Gram-negative bacteria, including Enterobacteriaceae, Streptococcus pneumoniae and most species of anaerobic bacteria. Isolates from a variety of infections (intra-abdominal infections, skin/soft-tissue infections, community-acquired pneumonia, pelvic infections and urinary tract infections) are inhibited by ertapenem. It has restricted activity against nosocomial pathogens such as Pseudomonas aeruginosa, Acinetobacter species, methicillin-resistant staphylococci and enterococci. Ertapenem has potent activity against the majority of anaerobic isolates from intra-abdominal infections, and against most of the aerobes isolated from these infections, with the exceptions of the nosocomial pathogens mentioned above. MIC(90)s for most species of Enterobacteriaceae were <1 mg/L, significantly lower than those of imipenem. MIC(90)s for most Bacteroides fragilis group isolates ranged from 1 to 4 mg/L, and MIC(90)s were species specific for Clostridium, ranging from 0.06 mg/L for Clostridium perfringens to 4 mg/L for Clostridium clostridioforme. Ertapenem was equivalent to or better than piperacillin-tazobactam in activity against most anaerobic species isolated from these infections, and was more potent than piperacillin-tazobactam and ceftriaxone against the most common skin pathogens (e.g. methicillin-susceptible Staphylococcus aureus). Ertapenem was highly active against most of the pathogens isolated from patients with community-acquired pneumonia, except for isolates of methicillin-resistant S. aureus (which are infrequent causes of community-acquired infection); these isolates were also resistant to ceftriaxone. Resistance to ertapenem is most commonly attributable to a variety of mechanisms including alterations in penicillin-binding proteins in Gram-positive organisms, and combinations of potent metallo-beta-lactamase enzymes, porin protein defects and efflux pumps in Gram-negative organisms.

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