eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Mononucleosis and Epstein-Barr Virus Infection: Differential Diagnoses & Workup

Author: Nicholas John Bennett, MB, BCh, PhD, Fellow in Pediatric Infectious Disease, Department of Pediatrics, State University of New York Upstate Medical University
Coauthor(s): Joseph Domachowske, MD, Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York-Upstate Medical University
Contributor Information and Disclosures

Updated: Oct 20, 2009

Differential Diagnoses

Hepatitis A
Herpesvirus 6 Infection
Hepatitis B
Human Immunodeficiency Virus Infection
Hepatitis C
Streptococcal Infection, Group A
Herpes Simplex Virus Infection
Toxoplasmosis

Other Problems to Be Considered

Drug reaction to phenytoin or sulfa
Lymphoma
Acute Myelocytic Leukemia
Acute Lymphoblastic Leukemia
Adenovirus
Rubella

Workup

Laboratory Studies

  • Classic criteria: The 3 classic criteria for laboratory confirmation of acute infectious mononucleosis include (1) lymphocytosis, (2) the presence of at least 10% atypical lymphocytes on peripheral smear, and (3) a positive serologic test result for Epstein-Barr virus (EBV).
  • CBC count
    • Leukocytosis with a WBC count of 10,000-20,000 cells/mL (10-20 X 109/L) is found in 40-70% of patients with acute infectious mononucleosis. By the second week of illness, approximately 10% of patients have a WBC count greater than 25,000 cells/mL.
    • Approximately 80-90% of patients have lymphocytosis with more than 50% lymphocytes. Lymphocytosis is most severe during the second and third weeks of illness and lasts for 2-6 weeks. Usually, 20-40% of the lymphocytes are atypical, although not all patients have more than 10% atypical lymphocytes.
    • The atypical lymphocytes of 3 Downey types are larger, have a lower nuclear-to-cytoplasmic ratio, and have a nucleus that is less dense than that of normal lymphocytes. Most of these atypical lymphocytes are polyclonal-activated CD8 cytotoxic-suppressor T lymphocytes, although CD4 helper T cells and CD11 natural killer cells are also present.
    • Mild thrombocytopenia occurs in 25-50% of patients.
  • Liver function tests
    • Most (ie, 80-100%) patients with acute infectious mononucleosis have elevated liver function test results.
    • Alkaline phosphatase, aspartate aminotransferase (AST), and bilirubin levels peak 5-14 days after onset, and gamma-glutamyltransferase (GGT) levels peak at 1-3 weeks after onset.
    • Lactic acid dehydrogenase (LDH) levels are increased in approximately 95% of patients.
    • Occasionally, GGT levels remain mildly elevated for as long as 12 months, but most liver function test results are normal within 3 months.
  • Heterophile antibody test: Epstein-Barr virus infection stimulates polyclonal secretion of antibodies by infected B cells, including transient production of heterophile antibodies. These are antibodies that agglutinate cells from other species and are not directed against Epstein-Barr virus. The Paul-Bunnell test for heterophile antibodies is based on the fact that serum obtained from patients with acute mononucleosis contains antibodies that agglutinate sheep RBCs in a tube dilution assay, whereas such antibodies are absent or nearly absent in the serum of healthy persons.
    • Differential absorption
      • Antibodies other than those produced during acute infectious mononucleosis can agglutinate sheep RBCs. Such antibodies include those formed in serum sickness and during drug reactions and naturally occurring antibodies to the Forssman antigen.
      • Differential absorption permits identification of the antibody type. Bovine RBCs absorb infectious mononucleosis heterophile antibodies from serum but do not absorb Forssman antibodies. Guinea pig kidney cells absorb Forssman antibodies, leaving the infectious mononucleosis heterophile antibodies. Antibodies formed in serum sickness are absorbed by both guinea pig kidney cells and bovine RBCs. Thus, in terms of absorbing infectious mononucleosis heterophile antibodies, clinicians use the saying, "cow can, pig can't."
      • Serum from a patient with infectious mononucleosis agglutinates sheep RBCs after absorption with guinea pig cells, but no agglutination occurs after absorption with bovine RBCs.
    • Heterophile antibody titers
      • The titer of Paul-Bunnell—heterophile antibody is determined with tube dilution. Depending on the dilution system, a titer of 1:40 or 1:28 after absorption with guinea pig cells is considered positive for acute infectious mononucleosis.
      • Titer level does not correlate with severity of clinical illness.
      • Heterophile antibodies are measurable in approximately 50% of patients in the first week of illness, and 60-90% of patients have test results that are positive for heterophile antibodies in the second or third weeks. The titer begins to decline during the fourth or fifth week and is often less than 1:40 within 2-3 months after symptom onset.
      • As many as 20% of patients have positive titer results 1-2 years after acquisition. Also, because horse RBC agglutinins are more sensitive than sheep RBCs, 75% of patients have positive horse RBC agglutinin findings at 1 year.
      • Only 10-30% of children younger than 2 years and 50-75% of children aged 2-4 years develop heterophile antibodies with primary Epstein-Barr virus infection.
    • Monospot
      • Rapid slide agglutination tests, including Monospot assays, have been developed to measure acute infectious mononucleosis heterophile antibodies in a rapid qualitative fashion. Slide tests use either horse RBCs or bovine RBCs. Horse RBCs are more sensitive than sheep RBCs or bovine RBCs and can be treated with formalin to extend the shelf life of the test. Bovine RBCs are specific for acute infectious mononucleosis heterophile antibodies and, thus, do not require differential absorption.
      • All commercial kits for rapid diagnosis of acute infectious mononucleosis heterophile antibodies have low sensitivity (63-84%), with a negative predictive value of more than 10%.
      • Spot tests rarely yield false-positive results in patients with lymphoma or hepatitis.
  • Epstein-Barr virus serology
    • Infection with Epstein-Barr virus is characterized by development of the specific antibodies to antigenic components of the virus. These antigens appear at different stages of infection and differ in lytic versus latent infection.
    • Antibodies to Epstein-Barr virus antigens measured for clinical purposes include antibodies to viral capsid antigen (VCA), early antigens (EAs), and EBNA.
      • EAs are expressed early in the lytic cycle, whereas VCA and membrane antigens are structural viral proteins expressed late in the lytic cycle.
      • EBNA is expressed in latently infected cells.
      • Antibodies to membrane antigens are not usually measured, but their presence correlates with viral-neutralizing activity.
      • Antibodies to these proteins are measured with enzyme immunoassays, indirect immunofluorescence assays, and immunoblot assays.
      • EAs are expressed in cells early in the lytic cycle. These antigens are nonstructural Epstein-Barr virus proteins, which are classified into 2 groups based on cell distribution and stability with methanol treatment.
      • The restricted component of early antigens (EA/R) is found in the cytoplasm of infected cells and is methanol sensitive. Antibody to EA/R is usually measurable in children younger than 4 years with primary Epstein-Barr virus infection or in patients with nonsymptomatic infection.
      • Approximately 80% of patients with infectious mononucleosis have antibodies to the diffuse-staining component of EA (EA/D).
      • EA/D antibody levels are elevated in patients with nasopharyngeal carcinoma, and the levels of antibodies to EA/R are high in individuals with Epstein-Barr virus–associated Burkitt lymphoma. Patients who are immunocompromised and have persistent or reactivated Epstein-Barr virus infections often have high levels of antibodies to EA/D or EA/R.
    • In early primary Epstein-Barr virus infection, oropharyngeal epithelial cells are lytically infected, and the above antigens are expressed. Antibodies are measurable at the onset of clinical symptoms or even slightly before.
    • Although not always measurable, EA antibody levels increase upon symptom onset. EA/D is more common, although EA/R is present more often in patients with asymptomatic infection or in children younger than 4 years. The levels of antibodies to EA rise for 3-4 weeks, then usually quickly decline to undetectable levels by 3-4 months, although low levels may be intermittently detected for years. However, in patients with a more prolonged symptomatic illness, EA/D may become unmeasurable, and EA/R results may become positive.
    • VCA-IgM levels are usually measurable at symptom onset, peak at 2-3 weeks, and then decline and become unmeasurable within 3-4 months. VCA-IgG levels rise shortly after symptom onset, peak at 2-3 months, then drop slightly but persist for life. Antibodies to EBNA appear during convalescence and remain present for life.
    • Primary acute Epstein-Barr virus infection is associated with VCA-IgM, VCA-IgG, and absent EBNA antibodies.
    • The antibody pattern in recent infection (3-12 mo) includes positive findings for VCA-IgG and EBNA antibodies, negative VCA-IgM antibodies, and, usually, positive EA antibodies.
    • After 12 months, the pattern is the same as in recent infection, except EA antibodies are not present.

Imaging Studies

  • Acute infectious mononucleosis
    • No specific imaging studies are indicated in diagnosing acute infectious mononucleosis. 
    • Chest radiography reveals mediastinal adenopathy in fewer than 1% of patients. Mediastinal lymph node enlargement should prompt consideration of other diagnoses.
    • Abdominal CT scanning is the preferred imaging modality to assess for splenic rupture but can be performed only in patients who are hemodynamically stable. Ultrasonography or radionuclide scanning of the spleen may also assist in ascertaining the diagnosis.
    • Lateral neck films are occasionally helpful to document tonsillar hypertrophy and exclude epiglottis or retropharyngeal abscess in a patient with upper airway obstruction or stridor.
  • Posttransplant lymphoproliferative disorder (PTLD): In patients with PTLD, chest radiography may reveal nodular lesions. Chest CT scanning with contrast may reveal the characteristic peripheral nodules, and abdominal CT scanning with contrast can define the extent of intra-abdominal lesions.

Other Tests

  • Quantitative polymerase chain reaction (PCR) can be used to measure Epstein-Barr virus DNA in plasma during acute infectious mononucleosis. levels decline during convalescence and are rarely measurable in latently infected individuals. However, Epstein-Barr virus DNA in serum may be detectable with PCR with reactivation of infection, such as in patients with PTLD.
  • An Epstein-Barr early region (EBER) probe can be used to identify the Epstein-Barr virus messenger RNA in the nuclei of Epstein-Barr virus–infected lymphoid cells by in situ hybridization.
  • Recent work has suggested that quantitative PCR in bronchoalveolar lavage fluid (BALF) for Epstein-Barr virus may be predictive of PTLD in lung-transplant recipients and is superior to plasma levels.11

Histologic Findings

  • Acute mononucleosis
    • Serum: Epstein-Barr virus infection is characterized by the presence of atypical lymphocytes in the peripheral blood. The cells are activated CD8 T cells, which are not infected but are mobilized to destroy the infected B cells.
    • Lymph nodes: During acute mononucleosis, lymph nodes are enlarged, with enlarged germinal centers and lymphoid follicles. Perifollicular areas of the tonsils contain many infected B lymphocytes, which express Epstein-Barr virus–specific antigens, including LMP1, EBNA1, and EBNA2.
    • Spleen: The spleen is larger, with lymphocytic infiltration of the capsule and trabeculae. Pleomorphic blast cells are present in the hyperplastic red pulp. Vascular congestion is coupled with focal and subcapsular hemorrhages.
    • Liver: Histologic changes in the liver are usually minimal, with mild swelling in hepatic sites and bile ducts and lymphocytic portal infiltration.
    • CNS: In fatal infectious mononucleosis, degenerative changes are observed in the neurons of the CNS. Neuronal degeneration, perivascular cuffing, and astrocytic hyperplasia may be present.
  • PTLD: This is characterized by homogeneous lymphocytic proliferation with an immunoblastic component. Lesions may efface lymphoid organ architecture or develop ectopically in nonlymphoid organs. The Epstein-Barr virus–infected cells in patients with PTLD express EBER.

More on Mononucleosis and Epstein-Barr Virus Infection

Overview: Mononucleosis and Epstein-Barr Virus Infection
Differential Diagnoses & Workup: Mononucleosis and Epstein-Barr Virus Infection
Treatment & Medication: Mononucleosis and Epstein-Barr Virus Infection
Follow-up: Mononucleosis and Epstein-Barr Virus Infection
Multimedia: Mononucleosis and Epstein-Barr Virus Infection
References
[ CLOSE WINDOW ]

References

  1. Epstein MA. Virus particles in cultured lymphoblasts from Burkitt's lymphoma. Lancet. 1964;1:702.

  2. Henle G, Henle W, Diehl V. Relation of Burkitt's tumor-associated herpes-ytpe virus to infectious mononucleosis. Proc Natl Acad Sci U S A. Jan 1968;59(1):94-101. [Medline].

  3. Sawyer RN, Evans AS, Niederman JC, McCollum RW. Prospective studies of a group of Yale University freshmen. I. Occurrence of infectious mononucleosis. J Infect Dis. Mar 1971;123(3):263-70. [Medline].

  4. Flavell JR, Baumforth KR, Wood VH, et al. Down-regulation of the TGF-beta target gene, PTPRK, by the Epstein-Barr virus encoded EBNA1 contributes to the growth and survival of Hodgkin lymphoma cells. Blood. Jan 1 2008;111(1):292-301. [Medline]. [Full Text].

  5. Baumforth KR, Birgersdotter A, Reynolds GM, et al. Expression of the Epstein-Barr virus-encoded Epstein-Barr virus nuclear antigen 1 in Hodgkin's lymphoma cells mediates Up-regulation of CCL20 and the migration of regulatory T cells. Am J Pathol. Jul 2008;173(1):195-204. [Medline]. [Full Text].

  6. Chaganti S, Ma CS, Bell AI, et al. Epstein-Barr virus persistence in the absence of conventional memory B cells: IgM+IgD+CD27+ B cells harbor the virus in X-linked lymphoproliferative disease patients. Blood. Aug 1 2008;112(3):672-9. [Medline].

  7. Lung ML, Chang GC, Miller TR, Wara WM, Phillips TL. Genotypic analysis of Epstein-Barr virus isolates associated with nasopharyngeal carcinoma in Chinese immigrants to the United States. Int J Cancer. Dec 15 1994;59(6):743-6. [Medline].

  8. Katz BZ, Shiraishi Y, Mears CJ, Binns HJ, Taylor R. Chronic fatigue syndrome after infectious mononucleosis in adolescents. Pediatrics. Jul 2009;124(1):189-93. [Medline].

  9. Candy B, Chalder T, Cleare AJ, et al. Predictors of fatigue following the onset of infectious mononucleosis. Psychol Med. Jul 2003;33(5):847-55. [Medline].

  10. Halvorsen JA, Brevig T, Aas T, Skar AG, Slevolden EM, Moi H. Genital ulcers as initial manifestation of Epstein-Barr virus infection: two new cases and a review of the literature. Acta Derm Venereol. 2006;86(5):439-42. [Medline].

  11. Michelson P, Watkins B, Webber SA, Wadowsky R, Michaels MG. Screening for PTLD in lung and heart-lung transplant recipients by measuring EBV DNA load in bronchoalveolar lavage fluid using real time PCR. Pediatr Transplant. Jun 2008;12(4):464-8. [Medline].

  12. Candy B, Chalder T, Cleare AJ, Wessely S, Hotopf M. A randomised controlled trial of a psycho-educational intervention to aid recovery in infectious mononucleosis. J Psychosom Res. Jul 2004;57(1):89-94. [Medline].

  13. Lockey TD, Zhan X, Surman S, Sample CE, Hurwitz JL. Epstein-Barr virus vaccine development: a lytic and latent protein cocktail. Front Biosci. May 1 2008;13:5916-27. [Medline]. [Full Text].

  14. Aldrete JS. Spontaneous rupture of the spleen in patients with infectious mononucleosis. Mayo Clin Proc. Sep 1992;67(9):910-2. [Medline].

  15. Andersson J, Britton S, Ernberg I, et al. Effect of acyclovir on infectious mononucleosis: a double-blind, placebo-controlled study. J Infect Dis. Feb 1986;153(2):283-90. [Medline].

  16. Boyle GJ, Michaels MG, Webber SA, et al. Posttransplantation lymphoproliferative disorders in pediatric thoracic organ recipients. J Pediatr. Aug 1997;131(2):309-13. [Medline].

  17. Cheeseman SH, Henle W, Rubin RH, et al. Epstein-Barr virus infection in renal transplant recipients. Effects of antithymocyte globulin and interferon. Ann Intern Med. Jul 1980;93(1):39-42. [Medline].

  18. Collins M, Fleisher G, Kreisberg J, Fager S. Role of steroids in the treatment of infectious mononucleosis in the ambulatory college student. J Am Coll Health. Dec 1984;33(3):101-5. [Medline].

  19. Connelly KP, DeWitt LD. Neurologic complications of infectious mononucleosis. Pediatr Neurol. May 1994;10(3):181-4. [Medline].

  20. Copperman SM. "Alice in Wonderland" syndrome as a presenting symptom of infectious mononucleosis in children: a description of three affected young people. Clin Pediatr (Phila). Feb 1977;16(2):143-6. [Medline].

  21. Cyran EM, Rowe JM, Bloom RE. Intravenous gammaglobulin treatment for immune thrombocytopenia associated with infectious mononucleosis. Am J Hematol. Oct 1991;38(2):124-9. [Medline].

  22. Deacon EM, Pallesen G, Niedobitek G, et al. Epstein-Barr virus and Hodgkin's disease: transcriptional analysis of virus latency in the malignant cells. J Exp Med. Feb 1 1993;177(2):339-49. [Medline].

  23. Dupre L, Andolfi G, Tangye SG, et al. SAP controls the cytolytic activity of CD8+ T cells against EBV-infected cells. Blood. Jun 1 2005;105(11):4383-9. [Medline]. [Full Text].

  24. Erzurum S, Kalavsky SM, Watanakunakorn C. Acute cerebellar ataxia and hearing loss as initial symptoms of infectious mononucleosis. Arch Neurol. Nov 1983;40(12):760-2. [Medline].

  25. Evans AS, Niederman JC, Cenabre LC, West B, Richards VA. A prospective evaluation of heterophile and Epstein-Barr virus-specific IgM antibody tests in clinical and subclinical infectious mononucleosis: Specificity and sensitivity of the tests and persistence of antibody. J Infect Dis. Nov 1975;132(5):546-54. [Medline].

  26. Foerster J. Infectious mononucleosis. In: Lee. Wintrobe's Clinical Hematology. 10th ed. 1999:1926-1955.

  27. Gasser O, Bihl FK, Wolbers M, et al. HIV Patients Developing Primary CNS Lymphoma Lack EBV-Specific CD4(+) T Cell Function Irrespective of Absolute CD4(+) T Cell Counts. PLoS Med. Mar 27 2007;4(3): e96.:[Medline]. [Full Text].

  28. Green M, Bueno J, Rowe D, et al. Predictive negative value of persistent low Epstein-Barr virus viral load after intestinal transplantation in children. Transplantation. Aug 27 2000;70(4):593-6. [Medline].

  29. Greenspan JS, Greenspan D, Lennette ET, et al. Replication of Epstein-Barr virus within the epithelial cells of oral "hairy" leukoplakia, an AIDS-associated lesion. N Engl J Med. Dec 19 1985;313(25):1564-71. [Medline].

  30. Haller A, von Segesser L, Baumann PC, et al. Severe respiratory insufficiency complicating Epstein-Barr virus infection: case report and review. Clin Infect Dis. Jul 1995;21(1):206-9. [Medline].

  31. Hanto DW. Classification of Epstein-Barr virus-associated posttransplant lymphoproliferative diseases: implications for understanding their pathogenesis and developing rational treatment strategies. Annu Rev Med. 1995;46:381-94. [Medline].

  32. Heath CW Jr, Brodsky AL, Potolsky AI. Infectious mononucleosis in a general population. Am J Epidemiol. Jan 1972;95(1):46-52. [Medline].

  33. Hickey SM, Strasburger VC. What every pediatrician should know about infectious mononucleosis in adolescents. Pediatr Clin North Am. Dec 1997;44(6):1541-56. [Medline].

  34. Hsieh WC, Chang Y, Hsu MC, et al. Emergence of anti-red blood cell antibodies triggers red cell phagocytosis by activated macrophages in a rabbit model of epstein-barr virus-associated hemophagocytic syndrome. Am Jour Path. May 2007;170(5):1629-39. [Medline].

  35. Klein G. Viral latency and transformation: the strategy of Epstein-Barr virus. Cell. Jul 14 1989;58(1):5-8. [Medline].

  36. Liebowitz D. Nasopharyngeal carcinoma: the Epstein-Barr virus association. Semin Oncol. Jun 1994;21(3):376-81. [Medline].

  37. Linderholm M, Boman J, Juto P, Linde A. Comparative evaluation of nine kits for rapid diagnosis of infectious mononucleosis and Epstein-Barr virus-specific serology. J Clin Microbiol. Jan 1994;32(1):259-61. [Medline].

  38. Maddern BR, Werkhaven J, Wessel HB, Yunis E. Infectious mononucleosis with airway obstruction and multiple cranial nerve paresis. Otolaryngol Head Neck Surg. Apr 1991;104(4):529-32. [Medline].

  39. Manika K, Alexiou-Daniel S, Papakosta D, et al. Epstein-Barr virus DNA in bronchoalveolar lavage fluid from patients with idiopathic pulmonary fibrosis. Sarcoidosis Vasc Diffuse Lung Dis. Sep 2007;24(2):134-40. [Medline].

  40. Miller CS, Avdiushko SA, Kryscio RJ, Danaher RJ, Jacob RJ. Effect of prophylactic valacyclovir on the presence of human herpesvirus DNA in saliva of healthy individuals after dental treatment. J Clin Microbiol. 2005;43(5):2173-2180.

  41. Navarro WH, Kaplan LD. AIDS-related lymphoproliferativedisease. Blood. 2006;107(1):13-20.

  42. Okano M, Gross TG. Epstein-Barr virus-associated hemophagocytic syndrome and fatal infectious mononucleosis. Am J Hematol. Oct 1996;53(2):111-5. [Medline].

  43. Pereira MS, Blake JM, Macrae AD. EB virus antibody at different ages. Br Med J. Nov 29 1969;4(5682):526-7. [Medline].

  44. Petersen I, Thomas JM, Hamilton WT, White PD. Risk and predictors of fatigue after infectious mononucleosis in a large primary-care cohort. QJM. Jan 2006;99(1):49-55. [Medline].

  45. Porter DD, Wimberly I, Benyesh-Melnick M. Prevalence of antibodies to EB virus and other herpesviruses. JAMA. Jun 2 1969;208(9):1675-9. [Medline].

  46. Resnick L, Herbst JS, Ablashi DV, et al. Regression of oral hairy leukoplakia after orally administered acyclovir therapy. JAMA. Jan 15 1988;259(3):384-8. [Medline].

  47. Rowe M, Lear AL, Croom-Carter D, Davies AH, Rickinson AB. Three pathways of Epstein-Barr virus gene activation from EBNA1-positive latency in B lymphocytes. J Virol. Jan 1992;66(1):122-31. [Medline].

  48. Rowe M, Young LS, Cadwallader K, Petti L, Kieff E, Rickinson AB. Distinction between Epstein-Barr virus type A (EBNA 2A) and type B (EBNA 2B) isolates extends to the EBNA 3 family of nuclear proteins. J Virol. Mar 1989;63(3):1031-9. [Medline].

  49. Schooley RT. Epstein-Barr virus (infectious mononucleosis). In: Mandell. Principles and Practice of Infectious Diseases. 5th ed. 2000:1599-1608.

  50. Schooley RT, Carey RW, Miller G, et al. Chronic Epstein-Barr virus infection associated with fever and interstitial pneumonitis. Clinical and serologic features and response to antiviral chemotherapy. Ann Intern Med. May 1986;104(5):636-43. [Medline].

  51. Straus SE, Cohen JI, Tosato G, Meier J. NIH conference. Epstein-Barr virus infections: biology, pathogenesis, and management. Ann Intern Med. Jan 1 1993;118(1):45-58. [Medline].

  52. Thorley-Lawson DA. Basic virological aspects of Epstein-Barr virus infection. Semin Hematol. Jul 1988;25(3):247-60. [Medline].

  53. Tomkinson BE, Wagner DK, Nelson DL, Sullivan JL. Activated lymphocytes during acute Epstein-Barr virus infection. J Immunol. Dec 1 1987;139(11):3802-7. [Medline].

  54. Tosato G, Taga K, Angiolillo AL, Sgadari C. Epstein-Barr virus as an agent of haematological disease. Baillieres Clin Haematol. Mar 1995;8(1):165-99. [Medline].

  55. Tynell E, Aurelius E, Brandell A, et al. Acyclovir and prednisolone treatment of acute infectious mononucleosis: a multicenter, double-blind, placebo-controlled study. J Infect Dis. Aug 1996;174(2):324-31. [Medline].

  56. Vassallo M, Camilleri M, Caron BL, Low PA. Gastrointestinal motor dysfunction in acquired selective cholinergic dysautonomia associated with infectious mononucleosis. Gastroenterology. Jan 1991;100(1):252-8. [Medline].

  57. Williams ML, Loughran TP Jr, Kidd PG, Starkebaum GA. Polyclonal proliferation of activated suppressor/cytotoxic T cells with transient depression of natural killer cell function in acute infectious mononucleosis. Clin Exp Immunol. Jul 1989;77(1):71-6. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

mononucleosis, Epstein-Barr virus infection, EBV, acute infectious mononucleosis, infectious mononucleosis, mono, human herpesvirus 4, HHV-4, kissing disease, gamma-herpesvirus, human tumor virus, lymphoproliferative disorders, nasopharyngeal carcinoma, Burkitt lymphoma, endemic Burkitt lymphoma, acute glandular fever, non-Hodgkin lymphomas, Hodgkin lymphoma, Duncan syndrome, X-linked lymphoproliferative syndrome, fatal massive hepatitis, disseminated lymphoproliferative disorder, B-cell lymphoma, hypogammaglobulinemia, EBV-associated lymphoproliferative disorders, EBV-associated lymphomas, ataxia-telangiectasia, Chédiak-Higashi syndrome, Wiskott-Aldrich syndrome, posttransplant lymphoproliferative disorder, PTLD, lymphoproliferative syndrome, hairy leukoplakia, leiomyosarcoma, CNS lymphoma, lymphoid interstitial pneumonitis, infectious mononucleosis syndrome, sore throat, splenic rupture, pharyngitis, hepatosplenomegaly, petechiae, tonsillar enlargement, enlarged epitrochlear nodes, hepatomegaly, splenomegaly, maculopapular rash

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Nicholas John Bennett, MB, BCh, PhD, Fellow in Pediatric Infectious Disease, Department of Pediatrics, State University of New York Upstate Medical University
Nicholas John Bennett, MB, BCh, PhD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Pediatrics
Disclosure: Nothing to disclose.

Coauthor(s)

Joseph Domachowske, MD, Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York-Upstate Medical University
Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Medical Editor

Rosemary Johann-Liang, MD, Medical Officer, Infectious Diseases and Pediatrics, Division of Special Pathogens and Immunological Drug Products, Center for Drug Evaluation and Research, Food and Drug Administration
Rosemary Johann-Liang, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Mark R Schleiss, MD, American Legion Chair of Pediatrics, Professor of Pediatrics, Division Director, Division of Infectious Diseases and Immunology, Department of Pediatrics, University of Minnesota Medical School
Mark R Schleiss, MD is a member of the following medical societies: American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; sanofi pasteur Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association
Disclosure: None None None

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.