Lymphadenitis caused by infection with measles virus.

Measles virus, a paramyxovirus, produces an acute, highly contagious, exanthematous infection in unimmunized patients. The measles virus does not have a natural reservoir other than in humans, and therefore its persistence in a community depends on the presence of unimmunized persons (1). In developed countries, measles is usually mild and causes periodic epidemics that most commonly affect children 5 to 7 years of age (1).

In primitive communities, measles affects children <2 years old, whereas in the United States, older children and teenagers may acquire the infection, which in such cases tends to be more severe (1). Multiplication of the virus in macrophages and lymphocytes facilitates its dissemination to various organs. Pharyngitis, conjunctivitis, otitis, pneumonia, and, in severe cases even encephalomyelitis, may occur. The characteristic giant cells may be found not only in the tonsils but also in lymph nodes, intestinal Peyer patches, and appendix. Immunization against measles is achieved with formalin-inactivated virus and more effectively with attenuated live virus vaccine. Measles lymphadenitis may occur in the course of measles infection or days to weeks after vaccination with live attenuated virus (1,2,3). The axillary, cervical, and inguinal lymph nodes are most commonly involved.

The lymph node architecture displays the pattern of diffuse paracortical immunoblastic hyperplasia common to most viral lymphadenitides (4). This is characterized by the diffuse proliferation of immunoblasts and the relative depletion of small lymphocytes, which results in a mottled (moth-eaten) pattern (Figs. 14.1 and 14.2). In one case of severe reaction to measles vaccination, thrombosis of blood vessels and partial hemorrhagic necrosis of the regional inguinal lymph nodes were noted (5). Multinucleated giant cells, independently described by Warthin and Finkeldey, usually appear in the prodromal phase of measles in various hyperplastic lymphoid tissues, including tonsils, adenoids, lymph nodes, spleen, appendix, and thymus (1,2,6,7). They tend to disappear with the rise in antibody titers or when the cutaneous eruption is established (1). These polykaryocytes, which are large syncytia, are round or lobulated, 25 to 150 μm in diameter, with abundant acidophilic cytoplasm and from four to 50 darkly stained nuclei distributed in grapelike clusters (mulberry cells) in the center of cells (8,9) (Figs. 14.1 and 14.2). Cellular inclusions may be infrequently observed in the cytoplasm of giant cells (1) or endothelial cells (5). Polykaryocytes resembling the Warthin-Finkeldey giant cells associated with measles have also been seen in a variety of reactive and neoplastic lesions of lymph nodes (9,10). Morphologically indistinguishable from the Warthin-Finkeldey cells, they may be present in reactive lymphoid hyperplasia and other benign lymphadenopathies, including pattern A in the acute phase of HIV lymphadenitis (11). In lymphoma, polykaryocytes are occasionally noted in the lesions of the lymphocyte-predominant type of Hodgkin lymphoma and in well-differentiated or poorly differentiated lymphocytic non-Hodgkin lymphomas (9,10). In general, these cells seem to be associated with lymphadenitides of viral origin and with lymphomas of low-grade malignancy (9,10).