Management

Penicillin has been the mainstay for treatment of tonsillar infections because of its effectiveness against GABHS. However, the rate of penicillin failure in eradicating GABHS from infected tonsils has slowly increased over the past 50 years from about 7% to 38% (39,40). As a final resort, many of these patients are referred for tonsillectomy. Penicillin failure in eradicating GABHS tonsillitis has several explanations. These include noncompliance with 10-day course of therapy, carrier state, GABHS intracellular internalization, reinfection, the absence of bacterial interfering bacteria, and penicillin tolerance. One explanation is that repeated penicillin administration results in a shift in the oral microflora with selection of aerobic (S. aureus, Haemophilus spp., M. catarrhalis) and anaerobic (Fusobacterium spp. and pigmented Prevotella and Porphyromonas spp.) BLPB.

The emergence of anaerobic BLPB has important implications for chemotherapy (41). These bacteria can produce enzymes that degrade penicillins or cephalosporins in the tonsils protecting not only themselves but also GABHS. The presence of aerobic and anaerobic BLPB in recurrently inflamed tonsils has been extensively studied (1,5,6,12,13) (Table 2). Assays of the free enzyme in the tissues demonstrated its presence in 33 of 39 (85%) tonsils that harbored BLPB, while the enzyme was not detected in any of the 11 tonsils without BLPB (42).

The ability of BLPB to protect penicillin-sensitive microorganisms has been demonstrated in vitro. When mixed with cultures of B.fragilis, the resistance of GABHS to penicillin increased at least 8500-fold (43). Simon and Sakai (44) have demonstrated the ability of S. aureus, and Scheifele and Fussel (45) showed the ability of Haemophilus parainfluenzae to protect GABHS from penicillin.

These phenomena are demonstrated in Figure 1. S. aureus is resistant to penicillin (it grew close to the penicillin disk), while GABHS is very susceptible to it (i.e., growth on the plate was inhibited to a large extent, as is evident by the zone of the beta-hemolysis). When these two organisms were plated mixed together (middle plate), however, GABHS were able to grow in close proximity to the penicillin disk, thus showing resistance to the penicillin that was acquired by the beta-lactamase produced by S. aureus.

This phenomenon was demonstrated in vivo by studies of mixed infections of penicillin-resistant and penicillin-susceptible bacteria. Hackman and Wilkins (46,47) showed that penicillin-resistant strains of B. fragilis, P. melaninogenica, and Prevottela oralis protected Fusobacterium necrophorum, a penicillin-sensitive pathogen, from penicillin therapy in mice.

Brook et al. (48), utilizing subcutaneous abscess models in mice, demonstrated protection of GABHS from penicillin by B. fragilis and P. melaninogenica. However, clindamycin, or the combination of penicillin and clavulanic acid (a beta-lactamase inhibitor), active against both GABHS and AGNB, was effective in eradicating the infection.

Brook and Gober (49,51) and Tuner and Nord (50) have demonstrated the rapid emergence of BLPB following penicillin therapy. Brook and Gober followed 26 children treated with penicillin (51) and observed continued colonization with BLPB in 35% of children 40 to 45 days after completion of therapy and in 27% of children 85 to 90 days after therapy.

Beta Strep.

FIGURE 1 Effect of Staphylococcus aureus on the susceptibility of GABHS to penicillin. A10-U (6 ng) penicillin G disk is placed in the center of each blood agar plate. (Left): S. aureus is resistant to penicillin. (Right): GABHS is susceptible to penicillin. (Middle): Mixed with S. aureus, GABHS is resistant to penicillin. Abbreviation: GABHS, group A beta-hemolytic Streptococcus.

Beta Strep.

FIGURE 1 Effect of Staphylococcus aureus on the susceptibility of GABHS to penicillin. A10-U (6 ng) penicillin G disk is placed in the center of each blood agar plate. (Left): S. aureus is resistant to penicillin. (Right): GABHS is susceptible to penicillin. (Middle): Mixed with S. aureus, GABHS is resistant to penicillin. Abbreviation: GABHS, group A beta-hemolytic Streptococcus.

A direct association was demonstrated between the presence of BLPB even before therapy and the outcome of 10-day oral penicillin therapy (52). Roos et al. (53) found that patients with recurrent GABHS tonsillitis had significantly more often detectable amounts of beta-lactamase in their saliva when compared with healthy individuals or patients who did not fail penicillin treatment.

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