Infectious mononucleosis was first described by Sprunt and Evans in the Bulletin of the Johns Hopkins Hospital in 1920.[1] They described the clinical characteristics of Epstein-Barr virus (EBV) infectious mononucleosis. At the time, their article was entitled "Mononuclear leukocytosis in reaction to acute infection (infectious mononucleosis)," because the causative organism, EBV, had yet to be described.
Since the 1800s, infectious mononucleosis has been recognized as a clinical syndrome consisting of fever, pharyngitis, and adenopathy. The term glandular fever was first used in 1889 by German physicians and was termed Drüsenfieber. The association between infectious mononucleosis and EBV was described in the late 1960s.
EBV is transmitted via intimate contact with body secretions, primarily oropharyngeal secretions. EBV infects the B cells in the oropharyngeal epithelium. The organism may also be shed from the uterine cervix, implicating the role of genital transmission in some cases. On rare occasion, EBV is spread via blood transfusion.
Circulating B cells spread the infection throughout the entire reticular endothelial system (RES), ie, liver, spleen, and peripheral lymph nodes. EBV infection of B lymphocytes results in a humoral and cellular response to the virus. The humoral immune response directed against EBV structural proteins is the basis for the test used to diagnose EBV infectious mononucleosis. However, the T-lymphocyte response is essential in the control of EBV infection; natural killer (NK) cells and predominantly CD8+ cytotoxic T cells control proliferating B lymphocytes infected with EBV.
The T-lymphocyte cellular response is critical in determining the clinical expression of EBV viral infection. A rapid and efficient T-cell response results in control of the primary EBV infection and lifelong suppression of EBV.
Ineffective T-cell response may result in excessive and uncontrolled B-cell proliferation, resulting in B-lymphocyte malignancies (eg, B-cell lymphomas).
The immune response to EBV infection is fever, which occurs because of cytokine release consequent to B-lymphocyte invasion by EBV. Lymphocytosis observed in the RES is caused by a proliferation of EBV-infected B lymphocytes. Pharyngitis observed in EBV infectious mononucleosis is caused by the proliferation of EBV-infected B lymphocytes in the lymphatic tissue of the oropharynx.
EBV infectious mononucleosis is a common cause of viral pharyngitis in patients of all ages, but it is particularly frequent in young adults. In the United States, approximately 50% of the population seroconverts before age 5 years, with much of the rest seroconverting in adolescence or young adulthood. Approximately 12% of susceptible college-aged young adults convert each year, half of whom develop acute infectious mononucleosis.
International
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Mortality/Morbidity
Patients with EBV infection who present clinically with infectious mononucleosis invariably experience accompanying fatigue. Fatigue may be profound initially but usually resolves gradually in 3 months. Some patients experience prolonged fatigue and, after initial recovery, enter a state of prolonged fatigue without the features of infectious mononucleosis.
Mortality and morbidity rates due to uncomplicated primary EBV infectious mononucleosis are low. The rare cases of attributed mortality are usually related to spontaneous splenic rupture. Splenic rupture may be the initial presentation of EBV mononucleosis.
Most cases of EBV infectious mononucleosis are subclinical, and the only manifestation of EBV infection is a serological response to EBV surface proteins discovered with EBV serological tests. Airway obstruction and central nervous system (CNS) mononucleosis are also responsible for increased morbidity in infectious mononucleosis. Selective immunodeficiency to EBV, which occurs in persons with X-linked lymphoproliferative syndrome, may result in severe, prolonged, or even fatal infectious mononucleosis.
Hepatic necrosis caused by extensive EBV proliferation in the RES of the liver is the usual cause of death in affected males. EBV is the main cause of malignant B-cell lymphomas in patients receiving organ transplants.
Most instances of posttransplant lymphoproliferative disorder (PTLD) are associated with EBV. EBV in PTLD is acquired from an EBV-positive donor organ. The likelihood of PTLD is directly proportional to the degree of immunosuppressive drugs administered to the transplant patient.
Depending on the intensity, rapidity, and completeness of the T-lymphocyte response, malignancy may result if EBV-induced B-lymphocyte proliferation is uncontrolled. Hodgkin disease and non-Hodgkin lymphoma (NHL) may result. Other EBV-related malignancies include oral hairy leukoplakia in patients with HIV infection.
Leiomyomas and leiomyosarcomas in immunocompromised children, nasopharyngeal carcinoma, and Burkitt lymphoma are among other neoplasms caused by EBV.
Age
Although primarily a disease of young adults, EBV infectious mononucleosis may occur from childhood to old age.
Most patients with Epstein-Barr virus (EBV) infectious mononucleosis are asymptomatic and, therefore, have few if any symptoms. Most adults (approximately 90%) show serological evidence of previous EBV infection.
The incubation period of EBV infectious mononucleosis is 1-2 months. Many patients cannot recall close contact with individuals with pharyngitis. Virtually all patients with EBV infectious mononucleosis report fatigue and prolonged malaise. A sore throat is second only to fatigue and malaise as a presenting symptom.
Fever is usually present and is low grade, but chills are relatively uncommon. Arthralgias and myalgias occur but are less common than in other viral infectious diseases.
Nausea and anorexia, without vomiting, are common symptoms.
Various other symptoms have been described in patients with EBV infectious mononucleosis, including cough, ocular muscle pain, chest pain, and photophobia.
Importantly, patients without CNS involvement experience no cognitive difficulties. CMV infectious mononucleosis rarely involves the CNS.
Myalgias, which are uncommon, are rarely (if ever) severe.
Physical findings in infectious mononucleosis should be viewed in terms of frequency distribution and time course after clinical presentation.
Early signs include fever, lymphadenopathy, pharyngitis, rash, and/or periorbital edema. Relative bradycardia has been described in some patients with EBV mononucleosis, but it is not a constant finding.
Later physical findings include hepatomegaly, palatal petechiae, jaundice, uvular edema, splenomegaly, and, rarely (1-2%), findings associated with splenic rupture.
CNS findings associated with EBV mononucleosis are rare but usually occur later in the course of the illness.
Splenic tenderness may be present in patients with splenomegaly.
Pulmonary involvement is not a feature of EBV infectious mononucleosis.
The classic presentation of EBV infectious mononucleosis in children and young adults consists of the triad of fever, pharyngitis, and lymphadenopathy.
Older adults and elderly patients with EBV infectious mononucleosis often have few signs and symptoms referable to the oropharynx and have little or no adenopathy. Elderly patients with EBV mononucleosis present clinically as having anicteric viral hepatitis.
Predictably, jaundice develops in less than 10% of young adults with EBV infectious mononucleosis, but jaundice may occur in as many as 30% of affected elderly individuals.
The pharyngitis due to EBV infectious mononucleosis may be exudative or nonexudative.
Exudative pharyngitis is commonly confused with group A streptococcal pharyngitis, which is complicated further by the fact that approximately 30% of patients with EBV infectious mononucleosis have group A streptococcal carriage of the oropharynx. The unwary physician may incorrectly conclude that a throat culture or rapid test positive for group A streptococci in a patient with infectious mononucleosis represents streptococcal pharyngitis.
Nonexudative pharyngitis with or without tonsillar enlargement is common in patients with EBV infectious mononucleosis and resembles viral pharyngitis.
Patients with either exudative or nonexudative EBV infectious mononucleosis are commonly colonized by group A streptococci.
Tonsillar enlargement is common, and massive tonsillar enlargement may be observed. The term kissing tonsils is used to describe extreme enlargement of both tonsils in patients with EBV infectious mononucleosis. Extreme tonsillar enlargement may result in airway obstruction.
Palatal petechiae of the posterior oropharynx distinguish infectious mononucleosis from other causes of viral pharyngitis but do not distinguish it from group A streptococcal pharyngitis, in which palatal petechiae may occur.
Uvular edema is an uncommon finding in infectious mononucleosis, but, if present, it is a helpful sign in distinguishing EBV infectious mononucleosis from other causes of viral pharyngitis or from group A streptococcal pharyngitis.
Early in the course of EBV infectious mononucleosis, patients may present with a maculopapular generalized rash. The rash is faint and evanescent and rapidly disappears. It is nonpruritic. This is a marked contrast to patients mistakenly diagnosed with streptococcal pharyngitis who have been administered ampicillin or amoxicillin and then develop a maculopapular rash as a drug reaction. Drug-induced rash is usually pruritic and is prolonged, in contrast to the viral rash of EBV infectious mononucleosis. Patients with EBV infectious mononucleosis who experience drug reactions to beta-lactams are not allergic to these medications. Administration of beta-lactams after resolution of the infection does not result in drug fevers or rashes.
Splenomegaly is a late finding in EBV infectious mononucleosis. Splenic enlargement returns to normal or near normal usually within 3 weeks after the clinical presentation.
In rare cases, EBV infectious mononucleosis results in various unusual clinical manifestations, including encephalitis, pancreatitis, acalculous cholecystitis, myocarditis, mesenteric adenitis, myositis, and glomerular nephritis.
Neurologic syndromes due to EBV infectious mononucleosis include optic neuritis, transverse myelitis, aseptic meningitis, encephalitis, meningoencephalitis, cranial nerve (CN) palsies (particularly CN VII), and Guillain-Barré syndrome.
Although EBV-induced antibodies to RBC membranes may occur, clinical anemia is uncommon with EBV infectious mononucleosis.
Leukocytosis, rather than leukopenia, is the rule in infectious mononucleosis.
Periorbital edema is an uncommon, and therefore fairly specific, physical finding in infectious diseases.
Bilateral periorbital edema not associated with generalized edema (eg, nephrotic syndrome) suggests trichinosis, Kawasaki disease, allergic reactions, or bilateral periorbital cellulitis.
Unilateral periorbital edema suggests conditions such as thyrotoxicosis, retro-orbital eye tumor, Chagas disease, insect sting, or unilateral conjunctivitis.
EBV infectious mononucleosis is characterized by early and transient bilateral upper-lid edema. In contrast to the disorders mentioned above, which are either unilateral or bilateral and involve the periorbital area, with or without the eyelids, the external eye involvement of EBV infectious mononucleosis is characterized by bilateral upper-lid edema. This finding was first described by Hoagland and is referred to as Hoagland sign. Hoagland noted the association of EBV infectious mononucleosis in young military recruits with EBV infectious mononucleosis. Hoagland sign may be detected when patients look in the mirror early in the course of their illness or when the astute physician notices this early in the clinical presentation. Hoagland sign is present for only the first few days of illness and should not be sought later in the course of the infectious process.
Table 1. Differential Diagnoses of Infectious Mononucleosis
The only predisposing risk factor for EBV infectious mononucleosis is close contact with an individual infected with EBV.
EBV commonly persists in oropharyngeal secretions for months after clinical resolution of EBV infectious mononucleosis.
Patients with congenital immunodeficiencies are predisposed to EBV-induced lymphoproliferative disorders and malignancies.
Acquired immunodeficiencies due to the effects of immunosuppression (eg, PLDT) or infectious disease-induced immunosuppression (ie, HIV) may predispose to oral hairy leukoplakia or non-Hodgkin lymphoma.
Burkitt lymphoma has a distribution (ie, in Africa) that is the same as the distribution of malaria. The geographic location predisposes to Burkitt lymphoma in children.
Epstein-Barr virus (EBV) infection induces specific antibodies to EBV and various unrelated non-EBV heterophile antibodies. These heterophile antibodies react to antigens from animal RBCs.
Sheep RBCs agglutinate in the presence of heterophile antibodies and are the basis for the Paul-Bunnell test.
Agglutination of horse RBCs on exposure to heterophile antibodies is the basis of the Monospot test.
Heterophile test antibodies are sensitive and specific for EBV heterophile antibodies, they are present in peak levels 2-6 weeks after primary EBV infection, and they may remain positive in low levels for up to a year.
The latex agglutination assay, which is the basis of the Monospot test using horse RBCs, is highly specific. Sensitivity is 85%, and specificity is 100%.
The heterophile antibody test (eg, the Monospot test) results may be negative early in the course of EBV infectious mononucleosis. Positivity increases during the first 6 weeks of the illness. Patients who remain heterophile negative after 6 weeks with a mononucleosis illness should be considered as having heterophile-negative infectious mononucleosis.
Patients with heterophile infectious mononucleosis should be tested for EBV-specific antibodies before definitively diagnosing heterophile-negative infectious mononucleosis.
Patients with heterophile- or Monospot-negative infectious mononucleosis should be tested serologically as are patients who present with a mononucleosislike illness who are negative for heterophile antibodies. The heterophile test is less useful in children younger than 2 years, in whom the results are frequently negative.
Although virtual 100% specificity exists with the Monospot test, rarely, other disorders have been reported that may produce a false-positive Monospot test result. These causes of false-positive Monospot test results include toxoplasmosis, rubella, lymphoma, and certain malignancies, particularly leukemias and/or lymphomas.
Testing for EBV-specific antibodies is as follows:
EBV induces a serological response to the various parts of the Epstein-Barr viral particle. IgM and IgG antibodies directed against the VCA of EBV are useful in confirming the diagnosis of EBV and in differentiating acute and/or recent infection from previous infection. EBV IgM VCA titers decrease in most patients after 3-6 months but may persist in low titer for up to 1 year. EBV IgG VCA antibodies rise later than the IgM VCA antibodies but remain elevated with variable titers for life.
False-positive VCA antibody titer results may occur on the basis of cross-reactivity with other herpes viruses, eg, CMV, or with unrelated organisms, eg, Toxoplasma gondii.
Other antigens indicating EBV infection are less useful diagnostically and include early antigen (EA), which is present early in EBV infectious mononucleosis. EBV nuclear antigen (EBNA) appears after 1-2 months and persists throughout life. The presence of elevated EBNA titers has the same significance as elevated IgG VCA titers. The presence of these antibodies suggests previous exposure to the antigen (past infection) and excludes EBV infection acquired in the previous year.
As with heterophile antibody responses, specific EBV antibodies may not be present in children younger than 2 years.
Nonspecific tests are as follows:
Patients with infectious mononucleosis in the differential diagnoses should have a CBC count with differential and an evaluation of the erythrocyte sedimentation rate (ESR). The CBC count is more useful in ruling out other diagnoses that may mimic infectious mononucleosis than in providing any specific diagnostic information. Because leukocytosis is the rule in infectious mononucleosis, the presence of a normal or decreased WBC count should suggest an alternative diagnosis. Lymphocytosis accompanies infectious mononucleosis, increases during the first few weeks of illness, and then gradually returns to normal. The appearance, peak, and disappearance of atypical lymphocytes follow the same time course as lymphocytosis. Patients with fever, pharyngitis, and lymphadenopathy are likely to have EBV infectious mononucleosis if the relative atypical lymphocyte count is equal to or greater than 20%.
Atypical lymphocytes should be differentiated from abnormal lymphocytes. Abnormal lymphocytes are associated with lymphoreticular malignancies, whereas atypical lymphocytes are associated with various viral and noninfectious diseases, as well as drug reactions. Atypical lymphocytes are each different in their morphology as observed on the peripheral smear, whereas abnormal lymphocytes are monotonous in their sameness, which readily permits differentiation on the peripheral smear.
Because anemia is so rare with EBV infectious mononucleosis, patients with anemia should undergo workup for another cause of their anemia.
Thrombocytopenia not uncommonly accompanies EBV infectious mononucleosis, but it may be present in various other viral illnesses, including in patients with heterophile-negative infectious mononucleosis.
An ESR is most useful in differentiating group A streptococcal pharyngitis from EBV infectious mononucleosis. The sedimentation rate is elevated in most patients with EBV infectious mononucleosis, but it is not elevated in group A streptococcal pharyngitis. However, an elevated ESR does not differentiate EBV from the other heterophile-negative causes of infectious mononucleosis, nor does it differentiate infectious mononucleosis from malignancies.
Because the liver is uniformly involved in EBV infectious mononucleosis, mild elevation of the serum transaminases is a constant finding in early EBV infectious mononucleosis. Mild increases in the serum transaminases are also a feature of the infectious agents responsible for heterophile-negative infectious mononucleosis. High elevation of the serum transaminases should suggest viral hepatitis. The serum alkaline phosphatase and gamma-glutamyl transpeptidase (GGTP) levels are not usually elevated in individuals with EBV infectious mononucleosis.
Specific tests are as follows:
Heterophile antibody tests
Patients with infectious mononucleosis should first be tested with a heterophile antibody test. The most commonly used is the latex agglutination assay using horse RBCs, and it is marketed as the Monospot test. Enzyme-linked immunosorbent assay (ELISA) rapid diagnostic tests are also available, which are based on the detection of heterophile antibodies. Physicians should remember that heterophile antibody responses require 1-2 weeks to become positive. In a group of patients with EBV mononucleosis, the number of patients becoming positive increases to a maximum 6 weeks after the onset of the illness.
If results are initially negative, a Monospot test should be ordered weekly for 6 weeks in patients with suspected EBV infectious mononucleosis. If the Monospot test remains persistently negative after 6 weeks of weekly serial testing, then a specific EBV serological test should be ordered. Before patients with an infectious mononucleosis–like syndrome are labeled as having heterophile-negative infectious mononucleosis, specific EBV serological tests should be obtained, and the results should be negative (see below).
The Monospot test has high sensitivity and specificity, eg, 85% and nearly 100%, respectively. Rarely, Monospot test results may be falsely positive, particularly in patients with CMV or rubella but also in patients with SLE and rheumatoid arthritis. Potential false-positive reactions may occur in those with HIV infection or herpes simplex virus (HSV). If a false-positive Monospot test result is suspected, then specific testing using an EBV-based antibodies serological test is indicated. A false-negative Monospot test result may occur if testing is performed too early in the course of the illness or in very young children (< 2 y) and occasionally in elderly patients.
Specific EBV antibody tests
Specific EBV antibody testing is more time-consuming and expensive than the Monospot test. EBV serological tests should be obtained in patients with a mononucleosislike illness and a negative finding on the Monospot test. As with the heterophile test, the EBV antibody response may be falsely negative early in the course of the infection. False negativity may also occur in young children (< 2 y).
The antibody response to specific EBV serological testing consists of measuring the antibody response to surface and core EBV viral proteins. For clinical purposes, the most useful EBV-specific antibodies are the VCAs and the EBNA. Both VCA and EBNA antibodies are usually reported as IgM or IgG antibodies. Acute infection is diagnosed in patients who have an increased EBV IgM VCA titer. Later in the course of infection, the increase in IgM VCA antibodies may be accompanied by an increase in IgG VCA antibodies and an increase in IgG EBNA antibodies. Many laboratories report EBNA titers only, which usually measure the IgG EBNA.
Increased IgG VCA and/or increased IgG EBNA titers indicate past exposure to EBV, which may have been subclinical or clinical. Increased IgG VCA titers are not synonymous with chronic infectious mononucleosis, and these titers are not diagnostic of CFS. Following acute infection, the increase in IgM titers peaks after 4-8 weeks and usually remain positive for as long as 1 year. The Monospot heterophile antibodies follow the same time course as the IgM VCA titers.
Rarely, cross-reactivity occurs between VCA antibodies to EBV and those to CMV or toxoplasmosis. False-positive cross-reactivity to specific EBV antibodies is extremely rare. Such patients have high elevations of IgM CMV or toxoplasmosis titers, which helps to differentiate between the primary infectious agent and the serological cross-reactivity resulting in a false-positive test result.
Patients with heterophile-negative infectious mononucleosis, eg, those with persistently negative Monospot test results for 6 weeks and those with a negative EBV-specific test result, should be tested serologically for the infectious agents that cause heterophile-negative infectious mononucleosis (eg, HIV, HHV-6, toxoplasmosis, CMV, rubella, anicteric viral hepatitis).
Table 2. EBV Serologic Responses in EBV-Associated Diseases
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Other tests are as follows:
Patients with suspected infectious mononucleosis should not have their throats cultured for group A streptococci because the carriage rate is approximately 30% in these patients. The mere recovery of group A streptococci from the oropharynx does not signify the cause of the patient's pharyngitis; it does not differentiate colonization from infection. In such patients, a Gram stain of the oropharynx is used to differentiate patients who have pharyngitis with positive cultures for group A streptococci from those colonized with group A streptococci.
Patients with EBV infectious mononucleosis or other causes of viral pharyngitis and group A streptococcal colonization have little or no white cell response on the Gram stain of the pharynx. Patients with group A streptococcal pharyngitis also have a positive finding on throat culture, but, in contrast to the patients with colonization, they show an intense polymorphonuclear cellular response with cellular debris and fibrous fragments indicating acute infection. The rapid streptococcal test cannot be used to differentiate colonization from infection any more than throat cultures.
Patients with presumed CNS involvement with EBV infectious mononucleosis should undergo serological tests for other causes of viral encephalitis appropriate to the patient's exposure history.
Rarely, if ever, is a bone marrow biopsy or lymph node biopsy needed in patients with EBV infectious mononucleosis. In the diagnosis of EBV infectious mononucleosis, the assessment of lymph node enlargement can be made confidently based on specific EBV antibody testing, and surgery is almost never necessary.
Patients with presumed CNS involvement with EBV infectious mononucleosis should also undergo a lumbar puncture to rule out other causes of encephalitis.
Oropharyngeal epithelium demonstrates an intense lymphoproliferative response in the cells of the oropharynx. The lymph node and spleen show lymphocytic infiltration primarily in the periphery of a lymph node.
Closely monitor patients with extreme tonsillar enlargement for airway obstruction. Steroids are indicated for impending or established airway obstruction in individuals with Epstein-Barr virus (EBV) infectious mononucleosis.
Surgery is necessary for spontaneous splenic rupture, which occurs in rare patients with EBV infectious mononucleosis and may be the initial manifestation of the condition.
Consult an infectious disease specialist in all but the most straightforward cases of EBV infectious mononucleosis.
Consulting a hematologist may be necessary if unusual hematologic manifestations of EBV infectious mononucleosis are present (eg, in anemia to determine the cause of the patient's anemia).
Consulting a neurologist is advised for patients with potential CNS involvement.
Consultation with a cardiologist is advised for the rare patients with EBV infectious mononucleosis who have presumed myocarditis.
Consult a gastroenterologist for patients with EBV-induced acalculous cholecystitis or if anicteric hepatitis is in the differential diagnoses.
No effective antiviral therapy is available for Epstein-Barr virus (EBV) infectious mononucleosis in immunocompetent persons. Acyclovir and ganciclovir may reduce EBV shedding but are ineffective clinically.
Treatment of immunocompromised patients with EBV lymphoproliferative disease is controversial. Acyclovir has not been proven to be beneficial.
Short courses of corticosteroids are indicated for EBV infectious mononucleosis with hemolytic anemia, thrombocytopenia, CNS involvement, or extreme tonsillar enlargement. However, corticosteroids are not indicated for uncomplicated EBV infectious mononucleosis. Corticosteroids should be considered in those with impending airway obstruction.
Patients with EBV infectious mononucleosis who have positive throat cultures for group A streptococci should not be treated because this represents colonization rather than infection (see Workup).
Treatment of group A streptococcal oropharyngeal colonization in patients with EBV infectious mononucleosis may result in a maculopapular rash.
Monitor patients to be sure that the infection is improving over time. Serial CBC counts should document the increase in lymphocytes as well as atypical lymphocytes, and this may be monitored on a weekly basis until these values normalize.
Patients with positive heterophile tests should not be monitored with serial testing because the heterophile test may remain positive for as much as 1 year after infection.
Serial specific Epstein-Barr virus (EBV) antibody testing is usually not necessary in patients with acute infection. Caution patients that increased IgG, VCA, and EBNA levels persist for life. Also, inform patients that titers vary and that IgG titers have no relationship to disease activity or to how the patient feels.
Patients should be advised that fatigue may take some time to resolve, and some patients may develop a state of chronic fatigue that is induced, but not caused by, EBV infectious mononucleosis.
If splenic rupture is recognized and expeditiously treated surgically, the prognosis is good.
Patients with EBV infectious mononucleosis who become asplenic as the result of splenic rupture and/or surgical removal should be treated as other patients with asplenia.
Counsel patients to refrain from strenuous physical activity for the first 3 weeks of illness.
Patients should avoid exposing other people to their body secretions because EBV remains viable in patients with EBV infectious mononucleosis for months after the initial infection.
For excellent patient education resources, visit eMedicineHealth's Bacterial and Viral Infections Center and Back, Ribs, Neck, and Head Center. Also, see eMedicineHealth's patient education articles Mononucleosis and Chronic Fatigue Syndrome.
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specific for Epstein-Barr virus (EBV) infectious mononucleosis (mono)?Which other tests may be indicated in the workup of Epstein-Barr virus (EBV) infectious mononucleosis (mono)?When are imaging studies indicated in the workup of Epstein-Barr virus (EBV) infectious mononucleosis (mono)?When is an EEG indicated in the workup of Epstein-Barr virus (EBV) infectious mononucleosis (mono)?When is a bone marrow or lymph node biopsy indicated in the workup of Epstein-Barr virus (EBV) infectious mononucleosis (mono)?When is a lumbar puncture indicated in the workup of Epstein-Barr virus (EBV) infectious mononucleosis (mono)?What do histologic findings demonstrate in the workup of Epstein-Barr virus (EBV) infectious mononucleosis (mono)?How are patients with Epstein-Barr virus (EBV) infectious mononucleosis (mono) monitored and when are steroids used for treatment?When is surgery indicated in the treatment of Epstein-Barr virus (EBV) infectious mononucleosis (mono)?Which consultations may be necessary in the treatment of Epstein-Barr virus (EBV) infectious mononucleosis (mono)?What type of diet is appropriate in the treatment of Epstein-Barr virus (EBV) infectious mononucleosis (mono)?What level of activity is encouraged in Epstein-Barr virus (EBV) infectious mononucleosis (mono)?Is antiviral therapy available in the treatment of Epstein-Barr virus (EBV) infectious mononucleosis (mono)?Is antiviral therapy available for immunocompromised patients with Epstein-Barr virus (EBV) lymphoproliferative disease?When are corticosteroids indicated in the treatment of Epstein-Barr virus (EBV) infectious mononucleosis (mono)?How is group A streptococcal (GAS) infection treated in patients with Epstein-Barr virus (EBV) infectious mononucleosis (mono)?How are patients with Epstein-Barr virus (EBV) infectious mononucleosis (mono) monitored?What do patients need to know about fatigue and how Epstein-Barr virus (EBV) infectious mononucleosis (mono) titers?What does extreme tonsillar enlargement indicate in Epstein-Barr virus (EBV) infectious mononucleosis (mono)?How can patients avoid contracting Epstein-Barr virus (EBV) infectious mononucleosis (mono)?What are complications associated with infectious mononucleosis (mono)?What is the prognosis of splenic rupture in Epstein-Barr virus (EBV) infectious mononucleosis (mono)?What do patients with Epstein-Barr virus (EBV) infectious mononucleosis (mono) need to know about physical activity restrictions?How can patients with Epstein-Barr virus (EBV) infectious mononucleosis (mono) prevent spreading the disease to others?What patient education resources are available for Epstein-Barr virus (EBV) infectious mononucleosis (mono)?
Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
John W King, MD, Professor of Medicine, Chief, Section of Infectious Diseases, Director, Viral Therapeutics Clinics for Hepatitis, Louisiana State University Health Sciences Center; Consultant in Infectious Diseases, Overton Brooks Veterans Affairs Medical Center
Disclosure: Nothing to disclose.
Chief Editor
Michael Stuart Bronze, MD, David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London
Disclosure: Nothing to disclose.
Additional Contributors
Charles S Levy, MD, Associate Professor, Department of Medicine, Section of Infectious Disease, George Washington University School of Medicine
Disclosure: Nothing to disclose.
References
Sprunt TPV, Evans FA. Mononuclear leukocytosis in reaction to acute infection (infectious mononucleosis). Bulletin of the Johns Hopkins Hospital. Baltimore, 1920. 31:410-417.
Andiman WA, Miller G. Antibody responses to Epstein-Barr virus. Rose NR, Friedman H, eds. Manual of Clinical Immunology. 2nd ed. Washington, DC: American Society for Microbiology; 1980. 628-633.
