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Delayed Onset of Infectious Mononucleosis Associated with Acquired Agammaglobulinemia and Red Cell Aplasia

DAVID T. PURTILO, M.D.; LEO ZELKOWITZ, M.D.; SHINJI HARADA, M.D.; CARTER D. BROOKS, M.D.; THOMAS BECHTOLD, B.A.; HELEN LIPSCOMB, Ph.D.; JOANNE YETZ, B.A.; and GERALDINE ROGERS, B.A.
[+] Article and Author Information

Grant support: in part by PHHS grant number CA30196, awarded by the National Cancer Institute; the Lymphoproliferative Research Fund; and Grant LB506 from the State of Nebraska Department of Health.

▸Requests for reprints should be addressed to David T. Purtilo, M.D.; Department of Pathology and Laboratory Medicine, University of Nebraska Medical Center, 42nd & Dewey Avenue; Omaha, NE 68105.


Omaha, Nebraska; and Kalamazoo, Michigan


©1984 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1984;101(2):180-186. doi:10.7326/0003-4819-101-2-180
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In 1974, an 11-year-old white boy with the X-linked lymphoproliferative syndrome developed hyper-IgM after becoming infected with Epstein-Barr virus. However, he failed to develop normal immune responses against the virus. In December 1981, when red cell aplasia occurred, he was given packed erythrocytes and gammaglobulin. Nine weeks later, acute infectious mononucleosis developed. Concurrently, his T4/T8 helper/suppressor ratio decreased from 2.7 to 0.2, and IgM antibodies to Epstein-Barr virus appeared. Subsequently, circulating B cells became undetectable in his blood, and agammaglobulinemia appeared. Red cell aplasia abated transiently. This patient's course was complicated by Haemophilus influenzae and Mycobacterium tuberculosis pneumonias, and red cell aplasia and agammaglobulinemia have persisted. Epstein-Barr virus acting as a slow virus probably induced the red cell aplasia and agammaglobulinemia because of the aberrant immune responses to Epstein-Barr virus. Immunodeficient responses to Epstein-Barr virus should be sought in other patients with the diseases documented in our patient.

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