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From September 11 through October 7, 1990, 57 persons (including outpatients, inpatients, and staff) at a community hospital in Puerto Rico had laboratory-confirmed infectious mononucleosis; however, investigation determined that test results may have been misinterpreted. This report describes the investigation of this pseudo-outbreak by the Puerto Rico Department of Health (PRDH) in October 1990.
A total of 121 samples of serum collected from 101 patients was tested to determine the sensitivity and specificity of a commercial latex agglutination test for detecting infectious mononucleosis heterophile antibody, a commercial immunofluorescence test for detecting antibody to Epstein-Barr virus capsid antigen and a rapid enzyme immunoassay for detecting antibody to Epstein-Barr virus nuclear antigen. Although the Epstein-Barr virus capsid antigen IgM indirect immunofluorescence test proved to be the most sensitive, false-positive reactions were seen when samples collected from patients with cytomegalovirus, hepatitis A virus, parvovirus and leptospira infection were tested. False-positive reactions were also seen with samples containing rheumatoid factor.
EBNA-positive lymphoblast cells were detected in 0.1 to 0.9% of the T-cell-depleted lymphocytes obtained from peripheral blood samples of five patients with infectious mononucleosis (IM). The same blood specimens from four of the five patients contained cells that formed EBNA-positive colonies in soft agar containing EBV antibodies. The ratio of the colony formers to EBNA-positive cells was higher in blood samples taken early in the disease than in those obtained in later stages of the disease. The present results strongly suggest that EBV-transformed cells are present in the peripheral circulation of IM patients and that such cells can directly give rise to immortalized cell lines in vitro.
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It has been demonstrated that peripheral blood lymphocytes, particularly the "atypical" ones, are predominantly of the T type in infectious mononucleosis (IM). This is based on membrane marker studies (E rosettes, receptor for complement, receptor for Fc fragment of immunoglobulins (Ig), and membrane Ig) and by anti-T lymphocyte serum. On the other hand, lymphoblastoid cell lines derived from IM patients show the characteristics of B lymphocytes. This permits the suppostion that EBV infects B lymphocytes and stimulates them to proliferate. The cell proliferation is unlimited in vitro and is probably controlled in vivo by T cells. The reduction of cellular immunity in vivo, which contrasts with the high number of T cells in peripheral blood, could be explained by the fact that T cells are engaged in the regulation of B cell proliferation.
The addition of interleukin-2 (IL-2) to lymphocyte cultures from acute infectious mononucleosis (IM) donors dramatically increased the incidence of regression in such cultures and resulted in the emergence of an IL-2 dependent, CD3 Epstein-Barr virus nuclear antigen (EBNA)-negative cell population. Corresponding cultures seeded in the absence of IL-2 rarely regressed and were quickly dominated by IL-2 independent, CD3-negative, EBNA-positive cells. Lymphocyte cultures from Epstein-Barr virus (EBV) seropositive donors showed enhanced regression in the presence of IL-2 but failed to regress after the removal of the E-rosetting population. Cultures from EBV-seronegative donors showed no evidence of regression in the presence or absence of IL-2. E-rosetting cells isolated from cultures from acute IM donors that had been cultured in the presence of IL-2 lysed autologous and allogeneic lymphoblastoid cell lines.
A case of fever of undetermined origin (FUO) demonstrated abnormal intense concentration of Ga-67 citrate in the spleen. Initial workup demonstrated two negative mono spot tests for infectious mononucleosis (IM) but, on hospital day 2, a repeat mono test was positive. The diagnosis was subsequently confirmed by rising heterophilic antibody titers. Six weeks after hospital discharge, repeat Ga-67 citrate imaging demonstrated absence of abnormal splenic activity. To our knowledge, this phenomenon has not been previously described in IM. In the appropriate clinical setting, intense splenic uptake of Ga-67 should alert the clinician to include the possibility of IM in the differential diagnosis.
T- and B-lymphocyte numbers, as well as lymphocyte reactivity to mitogens in vitro, were studied and correlated to other laboratory tests during the acute phase of infectious mononucleosis (30 patients) and up to one year thereafter. During the acute disease an absolute increase in both T- and B-lymphocyte numbers was recorded, the relative increase in B-lymphocytes occurring at the start. B-lymphocyte numbers fell after the second week and T-lymphocyte numbers after the fourth week of disease. Lymphocyte activation was impaired in all patients during the acute phase and was still significantly impaired for some mitogens after 6-9 months. Very few correlates between lymphocyte tests and other laboratory and clinical parameters were found.
We report lethal interstitial pneumonia in an 18-year-old young man with measles infection following recent infectious mononucleosis. We speculate that the documented T cell immune impairment caused by the concurrent Epstein-Barr and measles viral infections (as expressed by a proportionately low CD4+ lymphocyte count) was responsible for the complicated clinical course and unfavorable outcome.
The indirect immunofluorescence (IF) test and the complement-fixation reaction (CFR) were used in examination of over 1500 sera obtained from patients with infectious mononucleosis (IM) and other health disorders. The evidence obtained supports a direct aetiological relationship between Epstein-Barr virus (EBV) and IM and points on a relationship of EBV to some other lymphadenopathies and health disorders. The incidence of the IgG type antibody against virus capsid antigen (EB-VCA) and soluble antigen (CF-SA) obtained from EBV genome-positive cells among different age groups of patients is described along with results of long-term examinations of serum samples from IM patients. The appearance and dynamics of production of both types of EBV antibody and their persistence in the organism varied. Long-lasting oscillations, in particular of the EB-VCA antibody levels were found in sera of patients with prolonged health disorders following IM. The diagnosis value of the IF test and the CFR is discussed.
Fourteen patients admitted to the hospital for heterophil antibody negative infectious mononucleosis (IM) were studied; the causative agent was Epstein-Barr virus, as confirmed by the presence of anti-VCA antibodies (IgG and IgM) and the absence of anti-EBNA antibodies. The patients were from 2 to 69 years old, 7 being less than 10 years old while 4 were more than 45 years old. In all cases, asthenia and adenopathy were found and a deterioration in liver functions was present whenever it was looked for; jaundice occurred in 3 patients. In 6 cases fever persisted for several weeks. Leukocytosis and a high level of mononuclear cells were present in 8 patients and atypical lymphocytes in 10. Anti-EA titers were found to be high in the severe forms of illness. Clinical and laboratory features of these 14 heterophil negative IM patients were compared with a group of 21 heterophil positive IM patients studied under the same conditions; the most striking differences between the two groups were the frequency of patients under 10 and over 45 years old in the heterophil negative group, the frequency of abnormal liver function tests and of persistent fever, and a lower frequency of atypical lymphocytes.
An increased incidence of abnormal values for anti-DNA, anti-deoxyribonucleoprotein (NP) and rheumatoid factor (RF) were found in heterophil antibody-positive infectious mononucleosis (IM). These positive auto-immune reactions were mostly at low levels. Those IM sera which revealed these auto-antibodies in the normal range showed mean values which were significantly higher than the mean values seen in normal sera. No correlation was found between the IM heterophil antibody levels and the concentrations of RF, anti-DNA or anti-NP. In the majority of cases, the anti-DNA and anti-NP responses in IM were predominantly of the IgM class.
The X-linked lymphoproliferative syndrome (XLP) is characterized by a combined variable immunodeficiency with vulnerability to Epstein-Barr virus (EBV)-induced fatal or chronic infectious mononucleosis, acquired agammaglobulinemia, aplastic anemia, or malignant B cell lymphomas. Diagnosis of XLP requires documentation of two or more maternally related males with these phenotypes. Epstein-Barr virus must be demonstrated in circulating blood, lymphoid tissues, or saliva of infected males. Characteristically, the patients have low-titer antibodies to EBV and often lack anti-EB nuclear-associated antibody due to T cell defects. Thymus gland is often depleted and epithelium may be destroyed. Thymic-dependent regions in lymph nodes and spleen are depleted and immunoblastic transformation with plasma cell differentiation is seen. The carrier females exhibit partial immune deficiency and have paradoxically elevated antibodies to EBV. Our registry of XLP provides consultation and comprehensive study of persons and families with the syndrome.
In an examination of excretion patterns of Epstein-Barr virus in 104 throat washings from 20 patients with infectious mononucleosis we found that three persons regularly shed virus from the second week through the third month after onset; 15 demonstrated intermittent excretion over three months, and in two cases, no virus was detected. In oral secretions, the virus appeared to be located extracellularly. Transforming activity was demonstrated in aliquots after centrifugation and filtration, in a sample in which cells were disrupted before filtration, and in specimens after two years' storage. Multiple oropharyngeal sites were examined for presence of the virus. In one patient, virus was regularly demonstrated in throat washings and saliva; swabs from Stensen's duct orifices yielded virus in three of four cases. Demonstration of virus in these oropharyngeal specimens explains increased transmissibility in age groups in which salivary exchange is high.
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