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Employing a series of monoclonal antibodies directed against T cell subsets using the avidin-biotin complex method as the immunoperoxidase technique and using fluorescein-conjugated antisera directed against the major immunoglobulins, we have studied the distribution of immunocompetent cells in sections of tonsils from 21 patients with various inflammatory diseases of the tonsils, including Streptococcal tonsillitis, recurrent tonsillitis and tonsillitis associated with infectious mononucleosis. The following conclusions can be made in regard to our study. The percentage of T cells decreases in all compartments of the tonsils with increasing episodes of tonsillitis as well as with infectious mononucleosis and Streptococcal tonsillitis. Similarly, the percentage of HLA-DR positive cells decreases with increasing episodes of tonsillitis and is statistically significant in the mantle zone. The percentage of IgM B cells and IgD B cells tends to increase in the extrafollicular zone and decrease in the mantle zone with increasing episodes of tonsillitis as well as with increasing age. The percentage of IgG and IgA plasma cells is highest in children who have had 3-5 episodes of tonsillitis, but markedly decreases in the follicle and extrafollicular compartments in patients who have had more than 5 episodes of tonsillitis. FACS analysis of B cells in the tonsils and peripheral blood show a marked decrease in IgD in both the tonsil and the peripheral blood and a significant increase of IgG in the peripheral blood. These findings may suggest late clonal expansion of B cells in recurrent tonsillitis and Streptococcal tonsillitis. Finally, the distribution of immunocompetent cells in recurrent tonsillitis, Streptococcal tonsillitis and tonsillitis associated with infectious mononucleosis appears to be independent of age.
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.
BACKGROUND: Acute suppurative tonsillitis is one of the most common pediatric infectious diseases, and has Group A beta-hemolytic streptococci (GABHS) as its most frequent bacterial cause. Prevention of acute rheumatic fever is the principal goal of treatment. Antimicrobial agents, in contrast, is not needed. Therefore, the cause of acute suppurative tonsillitis in children must be determined. METHODS: Fifty-nine children were diagnosed as having acute febrile suppurative tonsillitis with the etiologies of Gr. A streptococci, adenovirus and Epstein-Barr (EB) virus. There were 25 cases of adenoviral tonsillitis, 20 cases of Epstein-Barr viral tonsillitis, and 14 cases of Gr. A streptococcal tonsillitis. This study aimed to find out whether the serum CRP, ESR or peripheral WBC counts could differentiate the etiological agents of acute tonsillitis from group A streptococcal to EB-viral or adenoviral infection. We also evaluated the effectiveness of epidemiological and clinical factors in predicting the etiology of acute suppurative tonsillitis in childhood. RESULTS: There was no difference between adenoviral and streptococcal groups in the measurement of serum CRP, neither in WBC count or the level of ESR. Patients with Gr. A streptococcal tonsillitis were significantly older than those with EB-viral or adenoviral tonsillitis (p < 0.05). Seventy-two percent of patients with adenoviral tonsillitis were under 4 years of age, 70% of the patients with EB-viral tonsillitis were under 6 years of age, whereas 71% of the patients with streptococcal tonsillitis were over 6 years of age. CONCLUSIONS: It is impossible to differentiate the etiology of acute suppurative tonsillitis by laboratory examinations (including serum CRP, peripheral WBC counts and ESR), based on its limited clinical pictures and epidemiological factors. Age was clearly the most important factor in distinguishing between viral and bacterial tonsillitis in children.
Upper respiratory tract infection including chronic tonsillitis is considered to be involved in the onset and/or the progression of IgA nephropathy. It is well known that deterioration of urinary findings occurs after episodes of upper respiratory tract infection in patients with IgA nephropathy. We previously showed that the expression of macrophage-colony-stimulating factor (M-CSF) is increased in the glomeruli of patients with IgA nephropathy and correlated with glomerular mesangial proliferation, suggesting that M-CSF plays an important role in the progression of IgA nephropathy. In the present study, we measured the serum and urinary concentrations of M-CSF in patients with IgA nephropathy associated with chronic tonsillitis. Furthermore, we evaluated the effects of the local provocation test of tonsils (mechanical tonsil stimulation) on the serum and urinary concentrations of M-CSF in the following three groups: (1) IgA nephropathy with severe mesangial proliferation, (2) IgA nephropathy with mild mesangial proliferation, and (3) patients with chronic tonsillitis without renal disease. The serum and urinary levels of M-CSF in the groups with severe and mild IgA nephropathy were significantly higher than those in the chronic tonsillitis group. The urinary M-CSF level but not the serum M-CSF level was positively correlated with the degrees of mesangial proliferation and glomerular M-CSF expression in the renal biopsy specimens. The urinary M-CSF concentration was significantly increased after tonsillitis stimulation in both mild and severe IgA nephropathy groups. Enhanced urinary excretion of M-CSF prolonged for 7 days after tonsil stimulation in the severe IgA nephropathy group; in contrast, the urinay M-CSF level was increased for only 2 days after tonsil stimulation in the mild IgA nephropathy group. The urinary M-CSF level was not changed in the chronic tonsillitis group after tonsil stimulation. The serum concentrations of M-CSF were not changed after tonsil stimulation in these three groups. Our present results suggest that tonsil stimulation contributes to the progression of IgA nephropathy via enhancement of glomerular production of M-CSF. The urinary excretion of M-CSF may be a useful predictor to evaluate the relevance of chronic tonsillitis to the disease and the indication of tonsillectomy in patients with IgA nephropathy.