71 Infectious Mononucleosis
Infectious mononucleosis is an acute infectious disease of children, adolescents, and young adults. It is caused by the Epstein-Barr virus (EB virus) and is followed by lifelong immunity.
Distribution and Incidence
On the basis of the populations investigated, it would seem that infectious mononucleosis occurs worldwide but attacks only those persons who have had no EBV antibodies. The virus replicates in the salivary glands, is present in the oropharyngeal secretions of patients ill with the disease, and continues to be shed for months following convalescence. As a lifelong inhabitant of the lymphoid tissues, it is excreted intermittently into the oropharynx.
In the underdeveloped countries it is a disease of childhood, and, since it spreads by contact with oral secretions, crowding and unhygienic Siuroundings favor its ready transmission. In more developed countries, it strikes especially those of the 15- to 25-year age group and is recognized clinically as infectious mononucleosis. In the United States, on college campuses, the disease is commonly known as the “kissing disease.”
Children of low socioeconomic state almost universally show antibodies to the virus. (In Ghana, 84 percent of infants have acquired antibodies by age 21 months.) In a worldwide prospective study of 5,000 children and young adults without EB virus antibodies, 29 percent developed antibodies within a period of 4 to 8 years. Among susceptible college students the annual incidence of the disease is about 15 percent.
Immunology
Specific antibodies to EB virus are demonstrable early after the onset of the disease. Although the higher titers may decrease in subsequent months, they remain at detectable levels throughout life, along with immunity to the disease.
Pathology and Clinical Manifestations
Although the pathological findings may be multivis- ceral, the predominant finding is follicular hyperplasia of the lymph nodes.
The lymphoid tissues show diffuse proliferation of the atypical lymphocyte that is present in the spleen and the walls of blood vessels, is periportal in the liver, and appears in the peripheral bloodstream. These monocytoid lymphocytes (Downey cells) may make up 10 percent or more of the white cells and Eire of diagnostic significance.In childhood the disease is Subclinical or masquerades as one of many episodes of upper respiratory infection. In the typical youthful adult, after an incubation period of about 5 or 6 weeks, clinical disease shows itself with prodromes of malaise, fatigue, headache, and chilliness followed by high fever, sore throat, and tender swollen cervical lymph nodes. Examination shows, in addition to the lymphadenopathy, paryngitis often with scattered petechiae and swelling of the pharyngeal lymphoid structures, Iiepatosplenomegaly, and, not infrequently, a transient maculopapular rash. Palpebral and periorbital edema may develop. Mild jaundice appears in some 10 percent of patients. Rarely are symptoms related to the central nervous system. Following an initial leukopenia, a Ieucocytosis of 15,000 to 20,000 or higher appears with an absolute lymphocytosis and with atypical lymphocytes prominent as noted above.
In most patients the disease is mild, and recovery occurs within several weeks. College students are generally up and about within a week or so. Complications in the nervous system may occasionally occur in adults, but death from the disease is extremely rare, splenic rupture being the most serious complication.
History and Geography
This disease was described first by a Russian pediatrician, Nil F. Filatov, in 1885, as idiopathic adenitis. Four years later, a German physician, Emil Pfeiffer, also described a disease that was epidemic in children and characterized by glandular enlargement. He gave it the name Drusenfieber (glandular fever). In 1896, J. P. West wrote of a similar epidemic in the United States, but it was only in 1920 that Thomas Sprunt, of Baltimore, gave it the name infectious mononucleosis.
H. Downey and C. A. McKinly described the characteristic mononuclear leucocytes in 1923. The Epstein - Barr virus was identified by W. Henle and associates in 1968.R. H. Kampmeier
Bibliography
Epstein, M.A., and B. G. Achong. 1977. Pathogenesis of infectious mononucleosis. Lancet 2: 1270—2.
Davidsohn, I., and P. H. Walker. 1935. Nature of hetero- phile antibodies in infectious mononucleosis. American Journal of Clinical Pathology 5: 455—65.
Downey, H., and C. A. McKinly. 1923. Acute lymphadenosis compared with acute lymphatic leukemia. Archives oflnternal Medicine 2: 82—112.
Henle, W., and G. Henle. 1979. The virus as the etiologic agent of infectious mononucleosis. In Epstein-Barr virus, ed. B. G. Epstein and B. G. Achong1 New York. 1981. Clinical spectrum of Epstein-Barr virus infection. In The human herpesviruses: An interdisciplinary perspective, ed. Andre J. Nahmias, Walter R. Dowdle, and Raymond F. Schinazi. New York.
Niederman, James C. 1982. Infectious mononucleosis. In Cecil’s textbook of medicine, ed. James B. Wyngaarden and Lloys H. Smith, Jr. Philadelphia.
Paul, John R., and Walls W Bunnell. 1932. Presence of heterophile antibodies in infectious mononucleosis. American Journal of Medical Science 183: 90—104.
Pfeifer, Emil. 1889. Drtisenfieber. Jahrbuch Kinderheil- kunde 29:257—64.
Sprunt, Thomas, and Frank A. Evans. 1920. Mononucleosis Ieucocytosis in reaction to acute infections (“infectious mononucleosis”). Bulletin of Johns Hopkins Hospital 31: 410—17.
Strauss, Stephen E. 1987. Editorial - EB or not EB - that is the question. Journal OfAmerican Medical Association 257: 2335—6.