Tonsillitis - Causes of Penicillin Failure in The Treatment of GABHS Tonsillitis

Causes of Penicillin Failure in The Treatment of GABHS Tonsillitis

Despite its excellence in vitro efficacy, the frequently reported inability of penicillin to eradicate GABHS from patients with acute and relapsing tonsillitis is a cause for concern. Over the past 50 years, the rate of penicillin failure has consistently increased from about 7% in 1950 to almost 40% in 2000.

There are several explanations for the failure of penicillin to eradicate GABHS tonsillitis (Table 1). One explanation is the poor penetration of penicillin into the tonsillar tissues as well as into the epithelial cells. Other explanations relate to the bacterial interactions between GABHS and the other members of the pharyngo-tonsillar bacterial flora. It is hypothesized that the enzyme beta-lactamase which is secreted by beta-lactamase-producing aerobic and anaerobic bacteria, that colonize the pharynx and tonsils, may "shield" GABHS from penicillins. These organisms include S. aureus, Haemophillus influenzae, and Prevotella, Porphyromonas and Fusobacterium spp., A recent increase was noted in the recovery of MRSA which was isolated from 16% of tonsils, making it more difficult to eradicate this and other beta-lactamase producing organisms. Another possibility is the coaggregation between Moraxella catarrhalis and GABHS, which can facilitate colonization by GABHS. Normal bacterial flora can interfere with the growth of GABHS, and the absence of such competitive bacteria makes it easier for GABHS to colonize and invade the pharyngo-tonsillar area. GABHS can also be reacquired from a contact or an object (i.e., toothbrush or dental braces)

Table 1. Causes of Antibiotics Failure in Therapy of GABHS Tonsillitis

• The presence of beta-lactamase–producing organisms that "protect" GABHS from penicillins
• Coaggregation between GABHS and M. catarrhalis
• Absence of members of the oral bacterial flora capable of interfering with the growth of GABHS (through production of bacteriocins and/or competition on nutrients)
• Poor penetration of penicillin into the tonsillar cells and tonsillar surface fluid ( allowing intracellular survival of GABHS)
• Resistance (i.e., erythromycin) or tolerance (i.e., penicillin) to the antibiotic used
• Inappropriate dose, duration of therapy, or choice of antibiotic
• Poor compliance
• Reacquisition of GABHS from a contact or an object (i.e., toothbrush or dental braces)
• Carrier state, not disease