Abstract

Despite the fact that group A beta-hemolytic streptococci (GABHS) is always susceptible to penicillin, bacteriologic failure occurs in up to 20% of the patients treated with penicillin, and half of these cases are also a clinical failure. Various theories have been offered to explain this phenomenon. One explanation is that beta-lactamase-producing bacteria (BLPB) "shield" GABHS by inactivating penicillin. Beta-lactamase-producing bacteria were recovered from over 75% of the tonsils of patients who had tonsillectomy for recurrent infection. The absence of interfering aerobic and anaerobic organisms in many patients may also lead to failure of penicillin therapy in these individuals. Other explanations include noncompliance with a 10-day course of therapy, carrier state, re-infection, bacterial interference, GABHS intracellular internalization, and penicillin tolerance. Penicillin is still considered the antibiotic of choice for the therapy of GABHS tonsillitis. However, antibiotics other than penicillin were found to be more effective in eradicating the infection. These included cephalosporins (of all generations), clindamycin, macrolides, and amoxicillin-clavulanate. These agents were more effective than penicillin, especially in treating patients who failed previous penicillin therapy. Treatment of tonsillitis in patients who failed penicillin therapy is aimed at the eradication of the the BLPB that protect GABHS from penicillin, while preserving the oropharyngeal "protective" organisms. This review will describe the scientific and clinical data that demonstrate and explain the phenomena of beta-lactamase production and bacterial interference.

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