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Rupture of the spleen in infectious mononucleosis is a rare but potentially fatal complication. Once injured, the "pathologic" spleen may have limited reparative capabilities. In this situation, operative management seems to be the safer therapeutic approach.
PURPOSE: We sought to determine how often acute mononucleosis precipitates chronic illness, and to describe the demographic, clinical, and psychosocial features that characterize patients who report failure to recover. SUBJECTS AND METHODS: We enrolled 150 patients with infectious mononucleosis during the acute illness and asked them to assess their recovery at 2 and 6 months. At baseline, we performed physical and laboratory examinations; obtained measures of psychological and somatic functioning, social support, and life events; and administered a structured psychiatric interview. RESULTS: Self-assessed failure to recover was reported by 38% of patients (55 of 144) at 2 months and by 12% (17 of 142) at 6 months. Those who had not recovered reported a persistent illness characterized by fatigue and poor functional status. No objective measures of disease, including physical examination findings or serologic or laboratory markers, distinguished patients who failed to recover from those who reported recovery. Baseline predictors for failure to recover at 2 months were older age (odds ratio [OR] = 1.4, 95% confidence interval [CI]: 1.1 to 1.8, per 5-year increase), higher temperature (OR = 1.5, 95% CI: 1.1 to 2.2, per 0.5 degrees C increase), and greater role limitation due to physical functioning (OR = 1.5, 95% CI: 1.2 to 1.9, per 20-point decrease in Short Form-36 score). At 6 months, baseline predictors for failure to recover included female sex (OR = 3.3, 95% CI: 1.0 to 12), a greater number of life events more than 6 months before the disease began (OR = 1.7, 95% CI: 1.1 to 2.5, per each additional life event), and greater family support (OR = 1.9, 95% CI: 1.1 to 4.2, per 7-point increase in social support score). CONCLUSIONS: We were not able to identify objective measures that characterized self-reported failure to recover from acute infectious mononucleosis. The baseline factors associated with self-reported failure to recover at 2 months differed from those associated with failure to recover at 6 months. Future studies should assess the generalizability of these findings and determine whether interventions can hasten recovery.
We report a case of acute haemolytic anaemia complicating infectious mononucleosis in a 19-year old male. There was no evidence for an immune haemolysis and red cell studies revealed a previously undiagnosed congenital spherocytosis. We discuss this rare presentation.
Serum beta 2-microglobulin concentrations were assayed in twenty patients with infectious mononucleosis. Pairs of sera taken from each patient in the first week of hospitalisation and two weeks later were tested. There was a significant increase of beta 2-microglobulin levels in these patients compared to the control group. A raised serum beta 2-microglobulin concentration persists during the convalescent period.
The author describes two cases of spontaneous splenic rupture occurring with infectious mononucleosis in young, previously healthy patients. The reports illustrate the variable clinical presentation--from sudden, fatal hemorrhage to bleeding that stops spontaneously. Although conservative nonoperative treatment may be successful in carefully selected cases, laparotomy with splenectomy appears to be the safest therapeutic approach. When a nonoperative approach is selected, the patient should be observed in a critical-care facility with immediate access to an operating room. Normal activity should not be resumed until the spleen has returned to its normal size as demonstrated by computed tomography or ultrasonography.
The results of three tests used for the rapid diagnosis of infectious mononucleosis (IM) were compared with those of Epstein-Barr virus-specific serology. The sensitivities ranged from 15 to 33% in children under 13 years of age and from 59 to 81% in patients over 13 years. The specificities ranged from 86 to 100% in both age groups. These tests have a poor sensitivity for the diagnosis of IM, particularly in children.
The usual leukocyte response in infectious mononucleosis (IM) has been established in adults but not in children. Previously, the diagnosis of IM often was difficult in childhood due to the lack of detectable heterophil antibody response in many patients. Using Epstein-Barr virus-specific serology, we have documented IM in 45 patients between 1 and 15 years of age. the mean and ranges for the total leukocytes, percent lymphocytes, and percent atypical lymphocytes are presented. These do not vary significantly with age and are similar to those reported for adolescents and adults with this illness.
In six patients with Epstein-Barr virus (EBV) induced infectious mononucleosis (IM) and in two patients with IM-like syndrome, peripheral blood lymphocytes in the acute and convalescent phase were tested for human la-like antigens as well as other cell surface markers. The major population of T lymphocytes in the acute phase showed la-like antigens, as detected by indirect immunofluorescence with heteroantisera, and the number of la-like antigen-positive T lymphocytes decreased with convalescence. The crossabsorption study indicated that the amount of la-like antigen on the surface of IM T cells was less than that of Raji cells.
EBV-infected B cells are present in blood during acute infectious mononucleosis (IM) in surprisingly large numbers. These cells share with cells transformed by EBV in vitro the capacity for unlimited proliferation, but this capacity is quite restricted in the normal host. The unusual extent of plasmacytic differentiation seen in infected cells in vivo early in IM and the loss of this differentiation in the late stages of the disease suggest that these cells are subject to the same immunoregulatory mechanisms that affect normal B cells. The host response to virus-altered B cells is quite complex but is perhaps best viewed as an in vivo autologous mixed lymphocyte reaction initiated by the interaction of T cells with virus-activated B cells.
The lymphoid tissues from patients with infectious mononucleosis or, less frequently, with other reactive conditions may contain Reed-Sternberg (RS)-like cells. These tissues also contain cells resembling the lacunar cells or lymphocytic/histiocytic (L/H) variants, which are present in the lymphocyte-predominant type of Hodgkin's disease. The phenotype of these RS- and L/H-like cells was determined with a large panel of antibodies and lectins. The cells expressed sialylated Leu-M1, Con A, LN-2, and, less frequently, interleukin-1, S-100, and peanut agglutinin receptor. They reacted negatively with two markers for RS cells, Ki-1 and HeFi-1. These RS-like cells were consistently negative for T- and B-cell markers, including immunoglobulins. The markers of the RS-like cells are distinctly different from those in B-immunoblasts, but closely resemble those in interdigitating reticulum cells. It is concluded that interdigitating reticulum cells, when stimulated, can be transformed into lacunar-, L/H-, or RS-like cells.
OBJECTIVES: To analyze the patients diagnosed of infectious mononucleosis (IM) in our institution, in order to study the symptoms and clinical evolution. MATERIAL AND METHOD: We retrospectively analyse 37 hospitalized children aged between 3 months and 14 years. Diagnosed of IM by production of immunoglobulin M (IgM) to viral capsid antigen (VCA). RESULT: In our series of 37 children, 14 were less than 4 years old. Among clinical data, lymphadenopathy (86%), fever (81%) and pharyngotonsillitis (70%) were the more striking. We found jaundice only in three of the older children. Upper airways obstruction was common, and specially severe in young children. Three patients developed pneumonia during the disease course. Only ten patients produced heterophile antibodies. Two children showed dual antibody rises to Epstein-Barr virus and cytomegalovirus. Corticotherapy was used in 7 children. The complications are presented in 68% of patients. CONCLUSIONS: Clinical aspects of IM were similar to those in the young adult, and complications occur more frequently. We found lack of heterophile antibodies, more frequent in youngest.
Epstein-Barr virus (EBV) is the etiological agent for acute infectious mononucleosis (AIM). It is also associated with certain malignant disorders in individuals with immunodeficiencies such as B cell lymphoproliferative disorder (BLPD). Our previous study with BLPD patients had demonstrated significantly higher serum IL-4 and IgE levels and significantly decreased IFN-alpha levels. These observations were consistent with the model of regulation of B cell growth by T cell-derived cytokines, in which IL-4 promotes B cell growth and switch to IgE synthesis whereas IFN-alpha and IFN-gamma inhibit these IL-4 mediated effects. Since AIM is also EBV associated, this study was designed to examine IL-4, IFN-alpha, IFN-gamma, IgE, and soluble CD23 (sCD23) serum levels in AIM patients. In this study we report for the first time that in contrast to BLPD patients, AIM patients did not exhibit increased levels of IL-4 and IgE; however AIM patients to exhibit decreased IFN-alpha levels and, additionally, also exhibit significantly higher sCD23 levels. This could result in B cell activation and have implications for the survival of the virus in B cells.
Acute appendicitis is an uncommon complication of infectious mononucleosis (IM) and can readily be misdiagnosed because of the acute abdominal pain with which patients with IM occasionally present. A case report is presented of a patient with IM who developed acute appendicitis during the acute phase of the illness. The appendicitis progressed to the formation of an abscess, which was evacuated at surgery. Histologic examination of the appendix showed absence of lymphoid follicles in the mucosal layer and intense lymphoid infiltration of the mucosa and submucosa by a mixed diffuse proliferation of lymphoid cells with groups of immunoblasts scattered among them. The lymphoid infiltrate was mainly composed of T lymphocytes; the anticomplementary immunofluorescent staining of the appendix for EBNA (Epstein-Barr nuclear antigen) was negative. Three cases of appendicitis complicating IM published in the literature are reviewed. All had clinical and histopathologic features similar to those of our patient and were cured after surgery. Our case report together with the literature review confirms that appendicitis in the acute phase of IM has distinct clinical and histopathologic features and thus has to be considered a true complication of IM rather than merely a simultaneous disease.
We describe a retrospective study of 4 cases of sporadic fatal infectious mononucleosis (IM), 1 case of fatal IM, and 1 case of sporadic severe IM. Patients were 26 months to 17 years old; 3 were male. Five died of complications of IM. All 5 of these patients had the Epstein-Barr virus (EBV) present in examined tissue specimens; EBV was monoclonal in 3 patients and biclonal in 1. EBV clonality studies were not performed in the remaining patient. All 5 patients also had monoclonal gene rearrangements. The sixth patient survived despite a life-threatening clinical course; EBV was oligoclonal, and gene rearrangements were not detected. EBV clonality and gene rearrangement studies may be usefulfor predicting which patients with clinically aggressive IM are at highest risk for fatal outcome. Patients in whom IM has a fatal outcome are more likely to have monoclonal or biclonal EBV and immunoglobulin heavy chain or T-cell receptor gene rearrangements. In contrast, patients with nonfatal IM may lack monoclonal EBV and monoclonal rearrangements of the aforementioned genes. The reasons EBV induces a monoclonal proliferation only in some patients remain to be elucidated.
During the acute phase (1 wk of symptoms or less) of infectious mononucleosis (IM), 70--80% of circulating Epstein-Barr virus nuclear antigen (EBNA)-positive cells have differentiated toward plasma cells. Thus the characteristics of the infected cells in the majority of IM patients during early disease are indistinguishable from EBNA-positive tumor cells of a previously reported child who developed lymphoma during IM. IgA and IgG were the most frequent and IgM the least frequent immunoglobulin isotypes detected in EBNA-positive cells. In acute disease EBNA was present in 5.5--20% of T cell-depleted blood lymphocytes but in the 2nd or 3rd wk of illness the number of EBNA-positive cells sharply decreased to 0.4--1.4%. At the same time the fraction of antigen-positive cells containing cytoplasmic immunoglobulins also diminished, suggesting either that differentiation of infected cells was altered during the disease or that nondifferentiated antigen-positive cells had a survival advantage. Both the high proportion of plasmacytic EBNA-positive cells seen during acute disease and the apparent loss of differentiation by these cells later in disease may be regulated by host immunologic factors. Immunoglobulin-producing EBNA-positive cells may be the source of heterophile antibodies and other seemingly inappropriate antibodies usually found in serum during IM; however, increased numbers of noninfected plasma cells were present in some patients and may also be a potential source of these unusual antibodies.
Primary infection with Epstein-Barr virus (EBV) may arise as infectious mononucleosis (IM) in adolescents and young adults. Morphologically, IM-affected lymphoid tissue is characterized by expanded interfollicular areas with formation of atypical lymphoid blasts. It is assumed that morphology and clinical presentation of IM are related to characteristic patterns of cytokine production by EBV-infected and reactive cells. We studied IM tonsils of eight patients and six normal tonsils with a double in situ hybridization procedure using [35S]-labeled RNA probes specific for various cytokines and digoxigenin-labeled probes for the detection of the nuclear EBV encoded RNA transcripts, EBER 1 and 2. All of the IM cases displayed the same distinct cytokine gene expression pattern. When compared with interfollicular areas of normal tonsils, expression of lymphotoxin (LT), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and IL-1 beta, but not IL-8 or IL-1 alpha was strongly enhanced in interfollicular areas in IM tonsils. LT was expressed predominantly by EBV-infected cells. TNF-alpha transcripts were also present in EBV-infected cells, although in smaller proportions. IL-6 specific signals were only found in few EBV-infected cells. IL-1 alpha-, IL-1 beta-, and IL-8-specific signals were not observed in EBV-infected cells, but were present at high signal intensity in many cells within and around foci of EBV-infected cells (IL-1 beta), next to areas of necrosis (IL-8, IL-1 beta), or in epithelial cells (IL-1 alpha). These data suggest that EBV infection in form of IM results in induction of specific sets of cytokine genes in EBV-infected and in neighboring EBV-negative cells contributing to the characteristic morphology and cellular arrangement of the lesion as well as the clinical presentation.
A study of EB virus antibody was undertaken in a boarding school for boys between 11 and 18 years of age; 35% of boys had EBV antibody when first sampled and a small number acquired antibody each year. Some of these boys had had no recorded illness during the period before the first positive sample and some developed classic infectious mononucleosis which was accompainied by a positive heterophil antibody test and detection of EB virus specific IgM. In a school of 800 boys there were 13 cases of infectious mononucleosis in four years.