A cluster of four cases of meningococcal disease in a single nuclear family.

A cluster of four confirmed cases of meningococcal disease was seen in the same nuclear family across a 15-week period. The cases were three siblings and a parent and all recovered well. The first case was confirmed by meningococcal PCR only but the subsequent three cases were due to indistinguishable strains of serogroup B (B:NT:P1.19-1,15-11). Contact tracing was initially undertaken and reviewed in detail after each subsequent case. Antibiotic prophylaxis was administered to close family contacts on three separate occasions, including switching of antibiotic agents, with good compliance. Subsequent investigation of the family has not revealed any obvious immunological problem and no further significant infections have been recognised. A cluster of meningococcal disease of this nature and timescale is highly unusual. Details of the cluster, investigation and implications for health protection practice are discussed.

Resistance to beta-lactams and glycopeptides in staphylococci and streptococci.

Molecular mechanisms of the action of beta-lactam and glycopeptide antibiotics, as well as genetic background and phenotypical features of the resistance of staphylococci, streptococci and enterococci to these antibiotics are reviewed. Furthermore, susceptibility patterns concerning beta-lactam and glycopeptide drugs of staphylococcal, streptococcal, as well as enterococcal strains isolated from clinical specimens at the Semmelweis University of Medicine, Budapest, Hungary between January 1997 and December 2000 are also presented.

A pilot study on the antibodies to HHV-6 variants and HHV-7 in CSF of MS patients.

In the possible role for human herpesviruses (HHV) in the pathogenesis of multiple sclerosis (MS) neither clear distinction between the two variants of HHV-6, nor the involvement of HHV-7 have been described. Therefore, we quantitated HHV-6 variant specific and HHV-7 reacting antibodies in the CSF of 13 patients with MS or other neurological disorders by ELISA. Predominance in the positivity of IgG (67%) and IgM (44%) to HHV-6B over that of IgG (44%) with no detectable IgM to HHV-6A, and no antibodies to HHV-7 were found in the CSF of MS patients. None of these antibodies were found in the CSF of controls. This suggests that, intrathecal chronic active or primary HHV-6B infection might contribute to MS progression, while the local effects of HHV-6A and HHV-7 seem to be less important.

[Level of HHV-6A antibodies in symptomless HIV infection as well as in the course of AIDS]. / HHV-6A ellenes antitestek szintje tünetmentes HIV-fertözöttekben az AIDS lefolyása során.

HHV-6A in vitro augments expression of CD4 molecules on the surface of immune cells, facilitates HIV replication and cell death in dual infections. It is hardly known whether these processes take place in vivo; does HHV-6A enhance HIV infection and AIDS progression? To study HHV-6A fresh infections and reactivation, IgM, IgG and low avidity IgG were quantitated in the serum samples of patients with asymptomatic HIV infection, early and terminal AIDS, that of their HIV seronegative homo- or bisexual partners and healthy adults (altogether 65 persons). Indirect immunofluorescent assay on JJHAN cells infected with HHV-6A U1102 was used. It was found that as compared to controls, the mean level of IgM in the sexual partners of HIV infected subjects raised 30-fold, that of IgG increased 10-fold, and 80% of persons had low avidity IgG indicating fresh HHV-6A infection. These suggest that they are frequently infected through sexual intercourse. As compared to healthy adults, mean titre of IgM to HHV-6A remained 10-fold increased in each group of patients with HIV infection. The IgG level was 6-fold increased in asymptomatic HIV infected subjects, 4-fold in early and 5-fold in terminal AIDS patients. More than one quarter of AIDS patients had low avidity IgG to HHV-6A. As compared to slow progressors of AIDS, the IgG level continuously increased in progressor persons. These suggest that HHV-6A maintains a chronic persistent infection in a significant number of HIV infected subjects.

[Serologic study of human herpesviruses 6 and 7 in lymphoma patients]. / Emberi 6-os és 7-es herpeszvírusok szerepének szerológiai vizsgálata lymphomás betegekben.

DNA sequences, antigens and elevated antibodies to HHV-6, and DNA sequences of HHV-7 in patients with Hodgkin's disease and non-Hodgkin's lymphoma have been detected. It is not known whether HHV-6 variants A and B, and HHV-7 contribute to the malignization by different ways, there is any interaction between these viruses, and their primary or recurrent infections occur during the disease progression. Total and high avidity IgG, IgM to HHV-6A, HHV-6B and HHV-7 were quantitated simultaneously in the sera of 12 patients with lymphomas and 12 control persons by indirect immunofluorescent assay and ELISA. It was established that, primary infection by HHV-6B in Hodgkin's disease, its primary or recurrent infections in non-Hodgkin's lymphoma; primary or recurrent infection by HHV-6A in Hodgkin's disease, its recurrent infection in non-Hodgkin's lymphoma; recurrent infection by HHV-7 in Hodgkin's disease may contribute to the deterioration of clinical conditions. Probably, HHV-7 exerts its effects through activating HHV-6B. The simultaneous effects of HHV-7 and HHV-6A, and that of HHV-6B and HHV-6A seem to be independent. Our results supports the recent opinion that, the effect of these herpesviruses on the tumorous cells is exerted indirectly by altered mediators of the immune system.

[Presence of antibodies to human herpesvirus type 6 and 7 in Hungarian children]. / Emberi 6-os és 7-es típusú herpesvírusok elleni antitestek megjelenése magyarországi gyermekekben.

Prevalence of antibodies to variants HHV-6A and B as well as HHV-7, the time of primary infections are not know in Hungarian children. Therefore, antibodies to these viruses were studied in 21 healthy children aged between 6 and 18 months. Lymphoid cultures were infected with standard virus strains for indirect immunofluorescence. IgM, IgG and high avidity IgG after 8M urea treatment were quantified in serial dilutions of sera. It was established that, three of 13 boys had low level (1:20) IgG or IgM antibodies to HHV-6A, but all girls were negative. With exception of one girl and one boy, all had antibodies to HHV-6B in different titres (1:20 to 1:640 by immunofluorescence), in 9 cases only IgM, in further 4 cases only low avidity IgG were detected. Children studied gradually acquired symptom-free HHV-6B infection between age of 8 and 18 months. Antibodies to HHV-7 were found in 3 boys and one girl before their age of 12 months, but the majority were infected after that age. Approximately three quarters of children acquired either HHV-6B or HHV-7 before age of 18 months. More than half of the children were infected with HHV-6B prior to HHV-7. Antibody level to HHV-6B was slightly higher in boys, while that to HHV-7 was higher in girls. In Hungary, childhood infection with HHV-6A seems to be a very rare event. Epidemiology of HHV-6B primary infection is similar to that of industrial countries, while that of HHV-7 resembles data of developing world: onset of antibodies occurs 1 or 2 years earlier than in the industrial nations.

Studies on the antibodies to human herpesvirus type 6 among Hungarian patients with asymptomatic HIV infection.

The occurrence and the possible role in promoting HIV infection by human herpesvirus type 6 (HHV-6) have not yet been revealed in Hungary. In different groups of patients, serum titre of IgM and IgG antibodies, as well as avidity of IgG were quantitated by indirect immunofluorescence and an enzyme-linked immunosorbent assay, using isolate U1102 of HHV-6 variant A as antigen. In 60% of HIV-seronegative adult controls, high avidity IgG antibodies were found in low titre suggesting childhood infection. In HIV-seronegative persons with high risk behaviour for HIV-infection, both IgM and low avidity IgG were frequently found in higher titre, representing either primary or frequent reinfections, or reactivation of latent HHV-6. In asymptomatic HIV-seropositive patients, high titre of high avidity IgG antibodies was predominant, proving virus infection in the near past. These results indicate the contribution of HHV-6 to immunosuppression prior to AIDS, predisposing the organism to HIV infection.