Changes in the Core Tonsillar Bacteriology of Recurrent Tonsillitis: 1977-1993

Abstract

Microbiological studies of the core of tonsils removed from children with recurrent tonsillitis due to group A beta-hemolytic streptococci were conducted during three periods, with 50 patients in each period: 1977-1978 (period 1), 1984-1985 (period 2), and 1992-1993 (period 3). Mixed flora were present in all tonsils, with 8.1 organisms per tonsil (3.8 aerobes and 4.3 anaerobes). The predominant isolates in each period were Staphylococcus aureus, Moraxella catarrhalis, Peptostreptococcus species, pigmented Prevotella species, Porphyromonas species, and Fusobacterium species. The rate of recovery of Haemophilus influenzae type b increased from 24% in period 1 to 76% in period 2 (P < .001); a decline to 12% in period 3 correlated with a concomitant increase in the frequency of recovery of non-type b strains of H. influenzae from 4% and 10% in periods 1 and 2, respectively, to 64% in period 3 (P < .001). Both the rate of recovery of beta-lactamase-producing bacteria and the number of these organisms per tonsil increased over time. Specifically, beta-lactamase-producing strains were detected in 37 tonsils (74%) during period 1, in 46 tonsils (92%) during period 2, and in 47 tonsils (94%) during period 3, and the number of such strains per tonsil increased from 1.1 in period 1 to 2.9 and 3.3 in periods 2 and 3, respectively.

Comparison of the Surface and Core Bacteria in Tonsillar and Adenoid Tissue With Beta-Lactamase Production

“…This data supports the theories lately discussed in the literature as; S. aureus, H. influenzae and Bacteroides spp. inactivate the penicillin and might shield penicilin susceptible pathogens like GABHS [6,7,28]. The significant togetherness of S. aureus and other BLPB in our study also supports these theories.…”

“…Several ideas explaining this phenomenon are; inappropriate and interrupted antibiotherapy, supression of host immunity due to unnecessary antibiotherapy, penicillin resistant L-form production of beta-haemolytic streptococci, inactivation of antibiotics by BLPB found in oropharyngeal and tonsillar flora such as S. aureus, H. influenzae, Bacteroides spp. and therefore protection of GABHS [6,7].…”

“…Kundsin and Miller [24] found higher S. aureus rates in patients with penicillin treatment failure. Brook et al [7,25,26] determined that beta-lactamase producing S. aureus plays a role in transferring beta-lactamase resistance to bacteria formerly having no beta-lactamase resistance. We also found the togetherness of S. aureus with other BLPB statistically significant (P \ 0.05).…”

“…Especially in recent years the domination of the beta-lactamase producing bacteria (BLPB) such as Staphylococcus aureus and Haemophilus influenzae in microflora cause penicillin resistance [6,7]. Several researchers have claimed that the failure of antibiotherapy may be due to the underestimation of the resistant microorganisms [6][7][8].…”

Significant pathogens in peritonsillar abscesses

“…Immune responses to Fusobacterium nucleatum and Prevotella intermedia have been detected in patients with PTA [23][24], as well as in patients suffering from recurrent acute tonsillitis (RT) [25], AT [26], peritonsillar cellulitis [23][24], and mononucleosis [27]. However, Fusobacterium nucleatum and Prevotella intermedia are also commonly found in clinically non-infected tonsils [28][29][30].…”