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Tonsil core specimens of 54 children, (3 to 12 years) with clinical evidence of chronic tonsillitis and/or "idiopathic" tonsillar hypertrophy, were studied for the effect of the magnitude of aerobic bacterial load on tonsil size and the absolute numbers of B- and T-cell subsets. Tonsillar core specimens obtained from ten children with no history of ear, nose, or throat infections and normal appearing tonsils served as controls. The findings of this study indicate that tonsil size was directly proportional to the mean bacterial load in colony forming units/g tonsil (CFU/g) even in the absence of a clinical history of infection (p less than 0.01). A mean bacterial load of 2.4 +/- 2.1 X 10(5) CFU/g tonsil was seen in diseased tonsils as compared to 1.6 +/- 2.4 X 10(4) CFU/g tonsil in normal controls (p less than 0.01). Hemophilus influenzae (type B and non-B), Staphylococcus aureus, Streptococcus pneumoniae and Streptococcus pyogenes were the most common pathogens recovered in the largest numbers from diseased tonsils; control tonsils harbored few bacteria in their cores. The absolute number of immunocompetent cells/g tonsil including T-helper, T-suppressor and B-cells (S-Ig+), were significantly greater in diseased tonsils than in controls (p less than 0.001). Increasing microbial load (CFU/g tonsil) correlated with increased numbers of T-helper (p less than 0.01) and B-cells (p less than 0.01). These data strongly support a bacterial etiology for chronic tonsillitis as well as "idiopathic" tonsillar hypertrophy. Bacterial induced proliferation of immunocompetent cells may be one underlying mechanism for chronic tonsillar disease in children.
Tonsil core specimens of 54 children, (3 to 12 years) with clinical evidence of chronic tonsillitis and/or "idiopathic" tonsillar hypertrophy, were studied for the effect of the magnitude of aerobic bacterial load on tonsil size and the absolute numbers of B- and T-cell subsets. Tonsillar core specimens obtained from ten children with no history of ear, nose, or throat infections and normal appearing tonsils served as controls. The findings of this study indicate that tonsil size was directly proportional to the mean bacterial load in colony forming units/g tonsil (CFU/g) even in the absence of a clinical history of infection (p less than 0.01). A mean bacterial load of 2.4 +/- 2.1 X 10(5) CFU/g tonsil was seen in diseased tonsils as compared to 1.6 +/- 2.4 X 10(4) CFU/g tonsil in normal controls (p less than 0.01). Hemophilus influenzae (type B and non-B), Staphylococcus aureus, Streptococcus pneumoniae and Streptococcus pyogenes were the most common pathogens recovered in the largest numbers from diseased tonsils; control tonsils harbored few bacteria in their cores. The absolute number of immunocompetent cells/g tonsil including T-helper, T-suppressor and B-cells (S-Ig+), were significantly greater in diseased tonsils than in controls (p less than 0.001). Increasing microbial load (CFU/g tonsil) correlated with increased numbers of T-helper (p less than 0.01) and B-cells (p less than 0.01). These data strongly support a bacterial etiology for chronic tonsillitis as well as "idiopathic" tonsillar hypertrophy. Bacterial induced proliferation of immunocompetent cells may be one underlying mechanism for chronic tonsillar disease in children.
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