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Clinical course of infectious mononucleosis was analysed in 36 children. Heterophilic antibodies were found in 27.8% of children at the age of six or less, and in 72.2% of older ones, mainly between 5-15 day of disease. Mild, mainly haematological complications occurred in 13.8% of cases.
In the vast majority of cases, diagnosis of infectious mononucleosis is relatively simple and the illness is not serious. Performing tests for specific Epstein-Barr virus (EBV) antibodies in these cases is not necessary. However, when the clinical manifestations are atypical or unusually severe, especially when the heterophil antibody test is negative, specific EBV antibody tests may be needed. The EBV antibodies used in diagnosis are IgG antibodies to viral capsid antigen (VCA), IgM antibodies to VCA, and antibodies to early antigen (anti-D) and Epstein-Barr nuclear antigen (EBNA). The diagnosis of infectious mononucleosis may be made when IgG-VCA, IGM-VCA, and anti-D antibodies are present and EBNA antibodies are absent. EBNA antibodies appear later and, together with IgG-VCA antibodies, persist indefinitely. Still, infectious mononucleosis often cannot be diagnosed with certainty because of the difficulties in interpreting laboratory findings. The diagnosis must be made with caution and possible sources of error considered when test results are interpreted.
Thirty-one cases of infectious mononucleosis treated with Interfon-Alpha were reported. The dose of intramuscular injection was one million units per day for 5-7 days. The recovery course of fever, angina, lymphadenopathy and hepatosplenomegaly was much shorter in the study group than in the control group (27 cases). The results suggested that interfon-Alpha should be efficacious against EBV activity and might shorten the course of this disease.
A young man with an infectious mononucleosis underwent an emergency splenectomy for a spontaneous splenic rupture. This is a rather rare complication of mononucleosis caused on the one hand by a change in the histological structure of the spleen and on the other hand by a splenomegaly. The prognosis is favourable when the diagnosis is made on time and the correct treatment has been started immediately. With the exception of those cases which are haemodynamically stable (the lesion is limited and corresponds to a subcapsular haematoma), splenectomy remains the treatment of choice. Conservatively treated patients must be closely followed and at the first sign of destabilization, surgical intervention is required as soon as possible.
50 cases of infectious mononucleosis by Epstein-Barr virus were studied in patients over and under 4 years age. Clinical evolution did not show any statistical differences between both age groups, except for splenomegalia which was more common in children under 4. Serology was divided into 3 groups: children under 4 year, between 4 and 5 and those over 5 years of age. First group exhibited a positive Davinsonh test in 15.3% of cases; second group in 33.3% and third in 80%. IgG antibodies against virus capsid were positive in 86% of cases with an equal distribution according to age groups. IgM antibodies were positive in 66%, not exhibiting any disparity in age groups.
Tonsils of 50 patients with infectious mononucleosis were examined for the presence of Epstein-Barr virus nuclear antigens (EBNA) and in 11 cases for the presence of Epstein-Barr virus (EBV) nucleic acid sequences. In tonsillar tissue of 42 patients less than 1 to 40 per cent EBNA-positive cells could be demonstrated by anticomplement immunofluorescence. 10 out of 11 tonsils examined by in situ hybridization contained less than 1 to 50 per cent cells with EBV nucleic acid sequences. The histological examination indicated that cells labelled by in situ hybridisation are in the majority proliferating B-lymphocytes and to a small extent cells of tonsillar epithelium.
Sera of 198 patients with infectious mononucleosis (IM), which were obtained during the 3rd or 4th week of the disease, were studied for the presence of antibodies to BS and B antigens of the Paul--Bunnell (P-B) antigenic complex. Six of these IM patients had anti-B antibodies without or with very low-titer anti-BS antibodies and the remaining patients had both types of antibodies at high titers. These 6 IM patients would have been misdiagnosed as seronegative if the traditional P-B tests with sheep erythrocytes had been employed. BS antigen was demonstrated in a large amount in chloroform-methanol extracts of peripheral blood buffy coat and of erythrocytes obtained from 1 of the 6 patients during the 3rd week of the disease and right after recovery.
During the acute stage of infectious mononucleosis (IM), 16 out of 19 patients have reacted to skin tests with ampicillin and/or benzylpenicillin or their derivatives. Two thirds reacted to ampicillin and less than half (10/19) to benzylpenicillin, or their derivatives. No reaction was observed with cloxacillin. The lack of reactivity in 3 of 7 patients and the circumstance that the frequency of reactions with the penicilloylated Escherichia coli proteins makes it likely that the greater reactivity to penicillins and in particular to ampicillin in IM is not due mainly to protein impurities, but chiefly to the antibiotic molecule as such. There was no definite relationship between reactivity and clinical involvement. After the acute stage, disappearance of skin reactivity was noted. Intracutaneous testing with penicillins may be used to monitor the increased cutaneous reactivity during acute IM, and it may be helpful when the acute stage is over to determine when a patient may use these antibiotics without side reactions.
Serial sera from patients with infectious mononucleosis were examined for the emergence of antibodies reactive in antibody-dependent cellular cytotoxicity tests, using Epstein-Barr virus-superinfected Raji cells as targets. For this specific purpose, the antibody-dependent cellular cytotoxicity test proved to be of limited sensitivity because only relatively high serum dilutions can be tested dependably, due to prozone effects at low serum concentrations, and because antibody-dependent cellular cytotoxicity reactions at the 5% level are not always statistically significant. Under the conditions of the test, antibody-dependent cellular cytotoxicity-reactive antibodies were not measurable, or only barely measurable, in early-acute-phase sera, but they became detectable during convalescence and increased thereafter, gradually over many months to the range of titers seen in healthy persons after long-past-primary Epstein-Barr virus infections. The percentages of antibody-dependent cellular cytotoxicity ultimately attained were on the order of 20% in most patients and healthy individuals, but in others did not exceed 10%. The likely identity of the antibodies reactive in the test with antibodies to late Epstein-Barr virus-determined cell membrane antigens has been discussed.
Lymph-node and tonsillar biopsies occasionally are obtained from patients with the infectious mononucleosis syndrome secondary to Epstein-Barr viral infection, particularly if the clinical presentation is atypical and a viral etiology is not suspected. The presence of Reed-Sternberg-like cells in infectious mononucleosis resulting in confusion with Hodgkin's disease is well-known; however, similar difficulty in excluding a non-Hodgkin's lymphoma can be encountered. Eleven cases of reactive lymphoid hyperplasia with the morphologic features of infectious mononucleosis are reported, nine of which had documented Epstein-Barr viral infection. The spectrum of morphologic changes associated with Epstein-Barr viral infection is discussed, with emphasis on the features that permit their distinction from non-Hodgkin's lymphoma. Morphologic features mimicking lymphoma included extensive immunoblastic proliferations in sheets and nodules and marked cytologic atypia. Hodgkin's disease was simulated by the tendency in some cases for the atypical Reed-Sternberg-like cells to cluster about necrotic foci and to show pronounced cytologic atypia. Features permitting the distinction from non-Hodgkin's lymphoma included persistent reactive foci with the classic features of infectious mononucleosis, a polymorphous background of transformed lymphocytes rather than irregular or twisted lymphoid cells as seen in non-Hodgkin's lymphoma, and preservation of underlying reticulin architecture rather than destruction, even in cases with extensive immunoblastic proliferation. Hodgkin's disease was excluded by requiring strict criteria for Reed-Sternberg cells and noting the reactive background as inconsistent with Hodgkin's disease. Immunoperoxidase staining of seven of the cases with anti-Leu-M1 failed to demonstrate immunoreactivity of the Reed-Sternberg-like cells with this monoclonal antibody.
Although upper airway obstruction and superimposed infection are well-known complications of infectious mononucleosis, lingual tonsillitis in this context has not been mentioned in the literature. We describe a case of acute bacterial lingual tonsillitis with airway obstruction complicating infectious mononucleosis. The role of the base of tongue region in the pathophysiology of infectious mononucleosis is discussed.
Two family members developed severe hepatitic dysfunction in association with infectious mononucleosis and acetaminophen administration. Since severe hepatitis is an extremely rare complication of infectious mononucleosis, we postulate that the hepatic dysfunction was induced by acetaminophen.
Tonsillar haemorrhage is a rare complication of infectious mononucleosis. We present a case of life-threatening tonsillar haemorrhage secondary to infectious mononucleosis in a young man whose predominant symptoms at presentation were haematemesis and melaena. The origin of the haemorrhage was not obvious until the patient was examined under anaesthesia. The bleeding was controlled by emergency tonsillectomy.
The quantitative analysis of the cells infected with Epstein-Barr virus was performed on the peripheral blood mononuclear cells from the patients with infectious mononucleosis, by using in situ hybridization with Epstein-Barr virus encoded small nuclear RNA1 (EBER1). An alkaline-phosphatase conjugated oligonucleotide probe complementary to EBER1 was used as an antisense probe, while oligonucleotide DNA probe compatible with the sequence of EBER1 was used as a sense probe, control probe. The EBER1 positive cells on the slide-glass were enumerated microscopically. In situ hybridization revealed that 50,000 peripheral blood mononuclear cells from the patients in the acute phase of infectious mononucleosis contained 35 +/- 36 cells infected with Epstein-Barr virus (n = 11). The cells infected with Epstein-Barr virus apparently decreased in the convalescence of all the patients with infectious mononucleosis and the mean of the cells infected with Epstein-Barr virus was 3 +/- 4 in the convalescence (n = 6) (p < 0.02). On the other hand, no positive cells were detected in healthy individuals with past-infection of Epstein-Barr virus (n = 10) or without any previous Epstein-Barr virus infection (n = 11). The striking increase of the cells with Epstein-Barr virus genome was clearly demonstrated in the peripheral blood mononuclear cells from the patients with infectious mononucleosis.
A polyspecific human monoclonal (auto)antibody, isolated from a patient in the acute phase of infectious mononucleosis, was found to react with all subfractions (H1, H2A, H2B, H3 and H4) of histones. This finding prompted us to study the occurrence of antibodies to histones in sera of patients with infectious mononucleosis. It was found that IgM binding to histones was detectable both in control and patient sera; however, sera from patients showed binding values of IgM antibodies to histones significantly higher than those of healthy controls; moreover, both in control and patient groups anti-histone IgM activity was found to correlate with serum IgM concentration. These findings suggest that anti-histone IgM antibodies belong to the class of antibodies defined as "natural antibodies" and that their increase during infectious mononucleosis is due to Epstein-Barr virus-induced polyclonal B cell activation.
Transient neutrophil aggregation is reported in a case of infectious mononucleosis. The phenomenon was observed on a blood film patient just before splenic infarction and decreased after splenectomy. The aggregation was so important that differential blood count could not be done. A high serum level of circulating immune complexes was found, and fluorescent spots inside of granulocytes, presumably engulfed immune complexes, could be observed. It is suggested that C activation associated with high immune complexes in infectious mononucleosis is a possible pathogenetic mechanism inducing PMNs aggregation and immune tissue damage.
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