Abstract

Beta-lactamase-producing bacteria (BLPB) can play an important role in polymicrobial infections. They can have a direct pathogenic impact in causing the infection as well as an indirect effect through their ability to produce the enzyme beta-lactamase. BLPB may not only survive penicillin therapy but can also, as was demonstrated in in vitro and in vivo studies, protect other penicillin-susceptible bacteria from penicillin by releasing the free enzyme into their environment. This phenomenon occurs in upper respiratory tract, skin, soft tissue, surgical and other infections. The clinical, in vitro, and in vivo evidence supporting the role of these organisms in the increased failure rate of penicillin in eradication of these infections and the implication of that increased rate on the management of infections is discussed.

Highlights

  • Penicillins have been the agents of choice for the therapy of a variety of bacterial infections

  • Beta lactamase (BL) producing of AGNB protected a penicillin-sensitive Fusobacterium necrophorum [5] and Group A beta hemolytic streptococci (GABHS) [6] from penicillin therapy in mice

  • The total number of potential pathogens and Beta-lactamase-producing bacteria (BLPB) were lower in those treated with amoxicillin/clavulante or clindamycin [54,55] amoxicillin/clavulante was superior to amoxicillin in achieving clinical cure (92% vs 64%) and reducing the number of potential

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Summary

Conclusions

The above studies illustrate that the successful management of polymicrobial infections is enhanced by directing antimicrobial therapy at the eradication of both aerobic and anaerobic BLPB. This approach is useful in management infections such as tonsillitis where BLPB are part of the normal flora at the infection site and is often employed it the treatment of other infections at all body sites. Some of these are polymicrobial where one of the pathogens is a BLPB while in others the role of the BLPB as a primary pathogen is unclear BL: Beta lactamase; BLPB: Beta lactamase producing bacteria; GABHS: group A Beta hemolytic bacteria

Doern GV
Brook I
17. Brook I
24. Jacobs MR
34. Brook I
36. Brook I
45. Massell BF
52. Brook I
Findings
59. Brook I
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