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To our knowledge this is the first report of a patient with infectious mononucleosis associated with a mononuclear granulomatous mastoiditis and facial paralysis. Pathologic examination of tissue from this patient, removed at the time of radical mastoidectomy, provides a basis for further speculation about the relationship between facial paralysis and infectious mononucleosis.
A method is described for the isolation and purification of infectious mononucleosis receptor (IMR) in high yield from sheep erythrocyte stroma. The procedure involves extraction of the stroma successively with boiling acetone, 100, 75 and 50% ethanol which removes approximately 40% non-infectious mononucleosis-active material. Subsequent phenol/buffered saline extraction of the residue from the organic extraction yields a highly active IMR preparation in the aqueous phases. This material was further purified by ethanol precipitation and gel filtration chromatography. The yield was 0.2% of the stroma. Approximately 0.1 mug/ml of the purified IMR inhibits 4 agglutinating units of infectious mononucleosis (IM) serum. The material is a glycoprotein containing N-acetyl- and N-glycolylneuraminic acids, hexose, hexosamine and approximately 46% protein. It gives one band in immunoelectrophoresis with IM serum and loses IM specificity upon treatment with neuraminidase.
A case of acute viral hepatitis B with features suggestive of infectious mononucleosis in a 20 year girl is described. A differential diagnosis of heterophil negative infectious mononucleosis like syndrome due to varied aetiology based on serology is emphasised.
Sera collected from 372 patients with suspected infectious mononucleosis were examined for heterophile antibodies by the Paul-Bunnell and the Monospot test. Comparison of results showed the latter to be simple, time saving, and of sufficient specificity for routine use in the general laboratory.
The inapparent Epstein-Barr virus (EBV) infection status in healthy Japanese subjects was assessed for their EBV seroepidemiology, oral EBV excretion, and EBV-specific cellular immunity, in comparison with immunosuppressed patients and patients with infectious mononucleosis. The seroepidemiologic data of 1,086 healthy donors indicate that EBV infects the vast majority of young children by 2-3 years of age and the viral persistence follows in nearly all adults throughout life. EBV antibody titers were significantly higher in both early and late ages. When 35 seropositive healthy persons were monthly assessed for their oral EBV excretion during 1 year period, 25% shed the virus consistently, 50% every other time, and the remaining 25% occasionally. EBV was shed more frequently from 17 immunosuppressed patients and all times from 15 cases of infectious mononucleosis, in the acute and convalescent phases and also during 1 year after healing. There was a tendency that high frequency EBV shedders had high titer EBV in the mouth. In infected healthy persons, EBV-specific killer T cells were well functioning throughout life; however, the killer T cell activity were significantly low in immunosuppressed patients. The killer T cell activity first developed in infectious mononucleosis 1 week after the onset and reached the same level as in seropositive healthy persons, by 4 weeks. These findings indicate that EBV-specific cellular immunity plays an important role in the establishment and maintenance of the inapparent EBV infection in humans.
BACKGROUND: Although anti-viral capsid antigen (VCA)-immunoglobin M (IgM) is the most reliable serological marker of primary Epstein-Barr virus (EBV) infection, it could only be detected in limited cases of infectious mononucleosis in children. We analyzed anti-EBV antibodies by an enzyme-linked immunosorbent assay (ELISA), a sensitive method for detecting IgM antibody and compared these results with those obtained by a conventional indirect immunofluorescence (IF) method. METHODS: Anti-Epstein-Barr virus early antigen (EA)-IgM and nuclear antigen 1 (EBNA1)-IgG were examined by an ELISA assay in 180 sera from 70 infants and children with infectious mononucleosis, diagnosed serologically by standard IF methods. RESULTS: Although by IF, VCA-IgM was detected in only 37 of 70 (52.9%) of the sera from the acute phase of the disease, by ELISA, EA-IgM was detected in 65/70 (92.9%) of these sera. Among infants less than 12 months of age. EA-IgM was positive in 11/13 cases (84.6%) while VCA-IgM was detected in only 3/13 cases (23.1%). Anti-Epstein-Barr virus nuclear antigen 1-IgG was not detected by ELISA in the sera from the acute phase of infectious mononucleosis. Anti-EBNA was not detected by IF in about one-third of the sera during 6-8 months after onset of the disease, whereas by ELISA, EBNA1-IgG was detected in 93.0%. Sera that were positive or negative for both EA-IgM and EBNA1-IgG by ELISA were observed in several cases after the patients recovered from the disease. CONCLUSIONS: Although serodiagnosis by the combination of ELISA for EA-IgM and EBNAI-IgG was more sensitive than IF methods, especially in the case of infants and young children, several patients during convalescence and recovery might be judged as seronegative or as being in highly reactivated states.
This report describes the first pediatric case of chronic renal failure as a complication of infectious mononucleosis in a 3 1/2 year old girl. The clinical features were marked at onset by proteinuria and later by nephrotic syndrome. The evolution to chronic renal failure took about two years. In the renal biopsy, lesions characteristic of interstitial nephritis were observed, associated with focal and segmental glomeruloesclerosis and deposits of C3 in granular and discontinued form. Renal participation in infectious mononucleosis is not unusual and fundamentally it is manifested by proteinuria and abnormalities of urinary sediment, with interstitial nephritis as a characteristic lesion in the renal biopsy.
The rapid and simple slide test for infectious mononucleosis designed by Hoff and Bauer (1965) is designed and compared with a modified sheep-cell slide screening test (Maloney and Malzone, 1949) and the differentenial absorption technique (Davidson, 1937). The claim of Hoff and Bauer that their test is more ;specific' is substantiated. Brief clinical histories illustrate the argument.
Thirty-six patients who had had infectious mononucleosis (IM) were followed up a year later and assessed by the Middlesex Hospital Questionnaire and by interview or (in five cases) by postal questionnaire. The results support the view that IM leads to depression in a considerable number of cases, but in this series only women were so affected.
The well-recognised neurological complications of infectious mononucleosis include lymphocytic meningitis, encephalomyelitis with convulsions, cranial and peripheral nerve palsies, Guillain-Barré Syndrome and hemiparesis. Cerebellar involvement is very rare, particularly in females and children. We describe a 14-year-old schoolgirl in whom cerebellar dysfunction proved a dominant feature, and who also gave a previous history of neurological presentation with mumps infection.
Infectious mononucleosis sera gave positive results in enzymoimmunoassay with glutaraldehyde-treated human erythrocytes. This unexpected reaction appeared to be caused by the interaction of Paul-Bunnell (P-B) antibodies with a partial P-B antigen that apparently appears on human red blood cells in a hidden form and becomes exposed by the treatment with glutaraldehyde.
A detailed clinicopathologic analysis of 52 cases of fatal infectious mononucleosis was performed. Fever, rash, generalized lymphadenopathy, hepatosplenomegaly, and blood cytopenias were the characteristic findings. Epstein-Barr virus infection was documented in 44 of the 52 patients. A triphasic process evolved in the blood and bone marrow of 43 patients. Early, the leukocyte count was elevated due to numerous atypical lymphoid cells, and the marrow was hyperplastic. Later, severe pancytopenia developed, and the marrow showed extensive infiltration by lymphoid cells with cellular necrosis and histiocytic hemophagocytosis. Terminally, the marrow showed massive necrosis with severe cellular depletion and marked histiocytic hemophagocytosis. The median survival time of the patients was six weeks. Opportunistic infections and/or acute hemorrhage were the major causes of death. We conclude that bone marrow damage secondary to an Epstein-Barr virus-associated hemophagocytic syndrome plays a major role in the death of patients with infectious mononucleosis.
Jaundice is a less frequent sign in infectious mononucleosis, more often caused by hemolysis, rarely by hepatocytes damage. In subjects with erythrocyte plasmatic membrane defects such as spherocytosis, any infection could increase hemolysis. The authors describe the case of a young spherocytosis patient in whom Epstein-Barr virus caused an intense cholestatic jaundice and they discuss the possible damage mechanisms according to the recent studies on cholestasis pathogenesis.
Spleen rupture has been a rare but feared complication in patients with infectious mononucleosis. There have been many cases reported during the last decade. However, it has rarely been mentioned among the young infant group. Here, we present a case of an infant, two months of age, who suffered from spleen rupture due to infectious mononucleosis, and was latter cured by himself under conservative treatment.
Spontaneous splenic rupture as a complication of infectious mononucleosis was diagnosed in a 19-year-old woman. Sonographic and MRI investigations revealed subcapsular hematoma of the spleen without overt rupture. The patient was managed conservatively. Somatostatin treatment was initiated in order to reduce splanchnic blood flow. Further clinical course of the patient was favourable. Seven days after the diagnosis of splenic rupture the patient was discharged from hospital. Non-operative management should be considered in patients with subcapsular splenic rupture to avoid complications of splenectomy (e.g. post-splenectomy sepsis).
The presentation of Hodgkin's disease and acute infectious mononucleosis (glandular fever) due to Epstein-Barr virus, have similar seasonal features with the peak incidence around March. The extent of seasonal variation is also similar. Seasonality of Hodgkin's disease is most obvious and also significant in adult age groups below the age of 40. Amongst those over 40 years, seasonality was no longer present in the 40-59 but returned over age 60. Seasonal similarity does not prove a relationship. However two speculations are made on possible mechanisms. Firstly glandular fever may accelerate presentation in young adults, destined to present with HD. Secondly the Epstein-Barr virus may have an inherent seasonal behaviour whether causing acute infectious mononucleosis or when latent and playing a role in the aetiology of Hodgkin's disease.
A 14-year-old boy with infectious mononucleosis died unexpectedly in hospital. The most significant finding at autopsy was the presence of marked bilateral tonsillar enlargement with considerable narrowing of the upper airway. There were no other underlying organic diseases that could have caused or contributed to death. Narcotic analgesia had been administered less than 2 h before death and may have contributed to respiratory compromise. The blood morphine level was 0.08 mg/L. Toxicological evaluation of individuals with obstructive lesions of the upper airway may, therefore, be a useful adjunct to the autopsy assessment of such cases as it may reveal factors exacerbating mechanical blockage.
Seven patients with a clinical diagnosis of infectious mononucleosis (IM) and detectable heterophil antibodies were found to have peripheral blood lymphocytes that were cytotoxic for lymphoid cells containing Epstein-Barr virus from a patient with Burkitt's lymphoma. The cytotoxic lymphocytes persisted in the peripheral circulation for up to 45 days. Patients who had had IM 1 to 5 years previously lacked such cytotoxic lymphocytes. Patients who had signs and symptoms of IM but no detectable heterophil antibodies lacked cytotoxic lymphocytes. The lymphocytes of one patient with IM showed progressive diminution of cytotoxic ability after prednisone treatment.