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• W1867417493 abstract "G LANDULAR fever, or infectious mononucleosis, is an interesting and baffling J1 disease giving rise to difficulty in diagnosis in general practice. The aetiology of the disease is obscure and there is no specific treatment. Nevertheless, the precise diagnosis is of importance because there are many other diseases which present with similar symptoms and signs including the presence of atypical mononuclear cells in the peripheral blood film, and several of these other conditions are common, require precise therapy, and have a better immediate prognosis. The clinical syndrome of glandular fever was first described by Pfeiffer in 1889, and renamed infectious mononucleosis by Sprunt and Evans in 1920. In 1923 Downey and McKinley reported the presence in the peripheral blood of atypical cells which resembled primitive monocytes. These abnormal cells had oval or horseshoe-shaped nuclei with abundant bluish-grey cytoplasm that frequently contained azurophil granules. Such cells often showed pseudopodia-like irregularities of the cell membrane and fenestration ofthe cytoplasm. Downey and McKinley divided these cells into three typesType III in which the presence of nucleoli and vacuolated dark blue cytoplasm produced an immature appearance, and Types I and II which were characteristically more mature. In 1932 Paul and Bunnell reported the occurrence in the patient's serum of heterophil antibodies to sheep red blood cells, and in 1934 Tidy wrote a detailed paper in which the classical symptoms and signs of the disease, namely fever, sore throat, enlargement of the lymph glands and malaise were described. Despite the apparent straight-forward nature of these clinical and laboratory features of the classical form of the disease, difficulty in diagnosis in general practice has arisen from the protean clinical manifestations with which patients may present (Read and Helwig 1945, Vander Meer et al. 1945). Many of the organ systems of the body may be affected; central nervous system (Bernstein and Wolff 1950), heart and lungs (Weschler et al. 1946), the haemopoietic system (Clarke and Davies 1946), liver (Rosalki et al. 1960, Kilpatrick 1966) and the renal tract (Tidy and Morley 1921). Patients presenting with atypical mononuclear cells in the peripheral blood, even when they show all the clinical features of the disease, may have repeatedly negative Paul-Bunnell tests (Shubert et al. 1954, Hobson et al. 1958). Moreover these atypical cells may occur in other virus diseases such as upper respiratory tract infections (Warren 1941), tonsillitis (Wilson and Cunningham 1929), measles (Benjamin and Ward 1932), rubella and toxoplasmosis (Whitby and Britton 1963), infectious hepatitis (Havens and Marck -1946), brucellosis (Wise 1943), cytomegalic inclusion disease (Klemola and Kaariainen 1965), and allergic conditions (Randolph and Gibson 1944). The presence of atypical mononuclear cells has even been reported in the blood, particularly after contact with anticoagulants, in normal individuals without obvious disease (Efrati and Rosenszajn 1960, Wood and Frenkel 1967). More recently Wood and Frenkel (1967), in reviewing the literature on the atypical lymphocyte or mononuclear cell, have listed 48 different conditions in which these" @default.
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• W1867417493 title "Atypical mononucleosis and glandular fever." @default.
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