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Human herpes virus type 4 (HHV-4), commonly known as Epstein-Barr virus (EBV), and human herpes virus type 8 (HHV-8) are members of Gammaherpesvirinaesubfamily. They both develop latent infections in B lymphocytes. Infection with these viruses in immunocompetent patients is usually mild and self-limiting, but it can have more severe course in immunocompromised individuals. Failure of the immune system often leads to oncogenesis related to gammaherpetic infection. Thus, immunocompromised patients are far more likely to develop proliferative diseases caused by EBV or HHV-8. This problem also applies to HIV-positive individuals coinfected with EBV or HHV-8. Gammaherpesviruses can also be the cause of post-transplantation issues in patients on immunosuppressive drugs and EBV is known to induce severe clinical syndromes in people with specific genetic disorders. Presented article summarizes epidemiology, pathogenesis, clinical syndromes and treatment of EBV and HHV-8 in individuals with immunological disorders.

ABSTRACTAfter the first report in May 2008, the National Reference Center for Susceptibility Testing confirmed 113 cases of infection or colonization by KPC-producing members of the family Enterobacteriaceaein Poland by the end of 2009. The vast majority of patients were found in 18 hospitals; three patients were diagnosed at outpatient clinics. Most of the institutions were in the Warsaw area, including three hospitals with the highest numbers of cases. When available, the data on previous hospitalizations often indicated that these hospitals were the probable acquisition sites; one patient arrived from New York. The group of 119 unique isolates consisted of Klebsiella pneumoniae(n= 114), followed by Klebsiella oxytoca(n= 3), and Escherichia coli(n= 2). The K. pneumoniaeisolates were dominated by the clone sequence type 258 (ST258) (n= 111); others were ST11 and ST23. The ST258 group was heterogeneous, with 28 pulsed-field gel electrophoresis (PFGE) subtypes, ∼25 plasmid profiles, and nine β-lactamase patterns differing by KPC variants (KPC-2 mainly), and SHV-12, CTX-M-3, and TEM-1-like enzymes. Plasmids carrying blaKPCgenes varied in size (∼48 to 250 kb), structure, and conjugation potential. Transferable IncFIIKplasmids of ∼110 to 160 kb, probably pKpQIL or its derivatives, were observed in all K. pneumoniaeclones and in K. oxytoca. Also prevalent were nontypeable pETKp50-like plasmids of ∼50 kb, found in K. pneumoniaeST258 and E. coliisolates (ST93 and ST224). Two K. pneumoniae-E. colipairs from single patients might represent the in vivotransfer of such plasmids. The striking diversity of KPC producers at the early stage of dissemination could result from several introductions of these bacteria into the country, their multidirectional evolution during clonal spread, and transfer of the plasmids.