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Susceptibilities of 394 Bacteroides fragilis, non-B. fragilis group Bacteroides species, and Fusobacterium species to newer antimicrobial agents.

The susceptibilities of 374 selected beta-lactamase-producing gram-negative anaerobes (including 22 cefoxitin-resistant strains and 36 strains refractory to the enhancing effect of beta-lactamase inhibitors) and 20 beta-lactamase-negative strains were tested by agar dilution against selected new agents. The organisms included 217 Bacteroides fragilis group strains, 137 non-B. fragilis group Bacteroides spp., and 40 fusobacteria. All strains were susceptible to piperacillin-tazobactam, imipenem, and meropenem. For the B. fragilis group, 96% were susceptible to ampicillin-sulbactam, 95% were susceptible to amoxicillin-clavulanate and cefoperazone-sulbactam, 94% were susceptible to tosufloxacin, 91% were susceptible to cefoxitin, 88% were susceptible to trospectomycin, and 73% were susceptible to cefotetan. For the beta-lactamase-positive non-B. fragilis group Bacteroides spp., greater than or equal to 94% were susceptible to cefoxitin, amoxicillin-clavulanate, ampicillin-sulbactam, cefoperazone-sulbactam, and trospectomycin, 90% were susceptible to cefotetan, and 85% were susceptible to tosufloxacin (the most resistant strains were B. bivius and B. disiens). For the beta-lactamase-positive fusobacteria, greater than or equal to 97% were susceptible to amoxicillin-clavulanate, ampicillin-sulbactam, cefoperazone-sulbactam, trospectomycin, and cefoxitin, 90% were susceptible to cefotetan, and 89% were susceptible to tosufloxacin. All agents showed excellent activity against beta-lactamase-negative strains (for trospectomycin, 95% were susceptible; for all other drugs, 100% were susceptible). Overall, both carbapenems and piperacillin-tazobactam were most active. Amoxicillin-clavulanate, ampicillin-sulbactam, and cefoperazone-sulbactam lacked activity against some cefoxitin-resistant B. fragilis group strains but had excellent activity against other organisms. Tosufloxacin, a new quinolone, had very good activity against B. fragilis group strains (94% susceptible), good activity against other beta-lactamase-positive strains (less than or equal 85% susceptible), and excellent activity against beta-lactamase-negative strains (100% susceptible; MIC for 90% of strains, 0.5 microgram/ml). Trospectomycin was active against >90% of all strains except for B. fragilis group strains (88% susceptible; MIC for 90% of strains, 32 microgram/ml). Clinical studies are required to delineate the role of newer agents in the therapy of anaerobic infections.

Anti-Bacterial Agents↗

Comparison of serological reactions of typed Fusobacterium nucleatum strains with those of isolates from humans, canines, and a Macaca mulatta monkey.

In the present study, we compared typed F. nucleatum strains with isolates from various human periodontal diseases, canines, and a Macaca mulatta monkey. All isolates displayed biochemical reactions similar to those of the typed strains in the API 20A system (Analytab Products, Plainville, N.Y.). The human and monkey isolates displayed both type I and type II colonial morphologies on crystal violet erythromycin agar, whereas the canine isolates displayed only type I. Antigen preparations of the human isolates, typed strains, and two of the monkey strains shared lines of identity in immunodiffusion testing. An enzyme-linked immunosorbent assay in which rabbit anti-F. nucleatum and human sera were used revealed that the human and monkey isolates, when used as antigens, allowed the detection of similar degrees of antibody activity; however, no activity was observed with the canine isolates. None of the canine isolates displayed the characteristic hemagglutination of sheep erythrocytes demonstrated by the human and monkey strains. These results suggest that F. nucleatum isolates from various human periodontal diseases share antigenic determinants. Also, differences were observed in F. nucleatum isolates from canines when compared with human and monkey strains. These findings are important when considering the immunopathological mechanisms involved in human periodontal diseases and when comparing animal model systems with naturally occurring disease in humans.

Animals↗