Viral Tonsillitis

The most common causes of upper respiratory tract infections and pharyngo-tonsillitis in the general population, including infants and young children, are viruses such as influenza virus, Coxsackie's virus (group A), adenovirus, and the ubiquitous herpes virus Ep-stein-Barr virus [205]. EBV infects epithelial cells and B-lymphocytes of Waldeyer's ring, which represent the reservoir for life-long viral persistence [104, 186]. Primary infections with EBV occur early in infancy and childhood in developing countries and are generally asymptomatic. In contrast, in developed countries, primary infection occurs in adolescents and young adults. EBV infections may cause the mostly self-limiting acute disease infectious mononucleosis, affecting adolescents and young adults in the western world. In Japan, however, an endemic area for EBV, acute cases of infectious mononucleosis are commonly diagnosed in children less than 4 years of age [100]. The symptoms include enlarged swollen palatine tonsils, occasionally with peritonsillar abscesses, sore throat, fever, malaise, cervical lymphadenopathy, lymphocytosis and occasional hepato-splenomegaly [133]. The diagnosis in typical cases is made clinically and/or serologically [69]. Histologically, the changes of a primary EBV infection can be dramatic [30]. The surface epithelium of the palatine tonsils is often necrotic. Follicular hy-perplasia with fused or bizarre-shaped follicles and numerous tangible body macrophages and distended interfollicular areas with atypical immunoblasts, plasma cells, plasmacytoid lymphocytes and histiocytes, occasionally grouped around necrotic foci, are typical. Mitoses are numerous. Rare Reed-Sternberg-like cells with single or multiple nuclei without nucleoli may be present beneath the crypt epithelium. The often atypical immunoblasts may simulate lymphoma, but in infectious mononucleosis, they often merge with cells in the reactive follicles and paracortex (Fig. 6.6). The proliferating lymphoid cells are predominantly activated T lymphocytes with CD8-positive T-cells dominating over CD4-positive T-cells. The immunoblasts can be of B-cell or T-cell type, and are occasionally CD30-posi-tive, but CD15-negative [1]. Infected cells are reactive for EBV nuclear antigen (EBNA) [2] and latent membrane protein (LMP) [182, 186].

The most important differential diagnosis of infectious mononucleosis, especially in older patients, is the extranodal manifestation of Hodgkin's lymphoma and non-Hodgkin's lymphoma (large cell and immunoblas-tic types). Immunoglobulin rearrangements and T-cell receptor gene rearrangements are lacking in infectious mononucleosis. The differential diagnosis of ulcerating tonsillitis includes infections with herpes virus hom-inis (usually Herpes simplex virus type 1). Herpes simplex virus can produce a vesiculo-bullous pharyngitis and may involve the palatine tonsils [106, 195]. Rupture of the vesicles results in sharply circumscribed shallow ulcers infiltrated by neutrophilic granulocytes. Infected epithelial cells show the characteristic multinucleat-ed giant cells with nuclear viral inclusion. The lymphoid infiltrate and hyperplasia of a Herpes simplex virus infection may mimic a NK/T-cell lymphoma [184]. Group A Coxsackie's virus also produces punched-out vesicles and is often associated with a concomitant Herpes simplex virus infection. Rare systemic autoimmune diseases, like the anti-phospholipid antibody syndrome, may cause tonsillar ulcers [79].

Chronic and recurrent tonsillitis are typically associated with respiratory syncytial virus, reactivation of latent Epstein-Barr virus, H. influenza and Staphylococcus aureus [44, 117, 204]. After episodes of recurrent tonsillitis, the palatine tonsils show extensive fibrosis at the site of the former capsule and scarring with entrapped, "pulled up" skeletal muscle fibres at the base of the tonsil and atrophic lymphoid tissue with small lymphoid follicles with atrophic germinal centres. Granulomas may be present. The crypts are distended and filled with ke-ratinous debris, inflammatory cells and occasional aggregates of actinomyces. Retention cysts can be formed within the deep crypts of chronically irritated palatine tonsils after occlusion of the orifice. The crypt epithelium becomes keratinised. Calcification of the desquamated debris following deposition of inorganic salts may result in tonsillar calculi, so-called tonsilloliths. The presence of actinomyces is not associated causally with recurrent tonsillitis [57, 120].

Human immunodeficiency virus 1 (HIV-1) infects lymphocytes of lymph nodes and extranodal lymphoid tissue. Hypertrophy of the nasopharyngeal and palatine tonsils is among the earliest clinical manifestations of HIV-1 infections. Enlargement of the palatine tonsils is usually bilateral and large ulcers may lead to complete destruction of the tonsils [28]. The histological changes in HIV-induced tonsillar hypertrophy vary with stage and progression of the infection. The earliest changes include florid reactive follicular hyperplasia with irregularly shaped germinal centres with an attenuated or absent mantle cell zone. Another early change suggesting HIV infection is "follicle lysis", with permeation and disruption of germinal centres by "infiltrating" small lymphocytes creating a "moth eaten" appearance. Follicle lysis/ follicular involution involves loss of tangible body macrophages as well as the mantle zone of lymph follicles. In-terfollicular haemorrhage is another feature of follicular involution. Multinucleated giant cells are a typical and specific feature of HIV tonsillitis. The multinucleated gi-

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