Long-term-care facilities (LTCFs) are reservoirs of resistant bacteria. We undertook a point-prevalence survey and risk factor analysis for specific resistance types among residents and staff of a Bolzano LTCF and among geriatric unit patients in the associated acute-care hospital. Urine samples and rectal, inguinal, oropharyngeal and nasal swabs were plated on chromogenic agar; isolates were typed by pulsed-field gel electrophoresis; resistance genes and links to insertion sequences were sought by PCR; plasmids were analysed by PCR, restriction fragment length polymorphism and incompatibility grouping. Demographic data were collected. Of the LTCF residents, 74.8% were colonized with ≥1 resistant organism, 64% with extended-spectrum β-lactamase (ESBL) producers, 38.7% with methicillin-resistant Staphylococcus aureus (MRSA), 6.3% with metallo-β-lactamase (MBL) producers, and 2.7% with vancomycin-resistant enterococci. Corresponding rates for LTCF staff were 27.5%, 14.5%, 14.5%, 1.5% and 0%, respectively. Colonization frequencies for geriatric unit patients were lower than for those in the LTCF. Both clonal spread and plasmid transfer were implicated in the dissemination of MBL producers that harboured IncN plasmids bearing bla(VIM-1), qnrS, and bla(SHV-12). Most (44/45) ESBL-producing Escherichia coli isolates had bla(CTX-M) genes of group 1; a few had bla(CTX-M) genes of group 9 or bla(SHV-5); those with bla(CTX-M-15) or bla(SHV-5) were clonal. Risk factors for colonization of LTCF residents with resistant bacteria included age ≥86 years, antibiotic treatment in the previous 3 months, indwelling devices, chronic obstructive pulmonary disease, physical disability, and the particular LTCF unit; those for geriatric unit patients were age and dementia. In conclusion, ESBL-producing and MBL-producing Enterobacteriaceae and MRSA were prevalent among the LTCF residents and staff, but less so in the hospital geriatric unit. Education of LTCF employees and better infection control are proposed to minimize the spread of resistant bacteria in the facility.

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Epstein-Barr virus (EBV)-associated smooth muscle tumors following solid organ transplantation are extremely rare, with only 12 cases reported in the literature thus far. The exact pathogenetic role of EBV infection in the oncogenesis of these soft tissue tumors in immunodeficient patients and the biologic behavior of such tumors is still unclear. We report a 26-year-old man in whom multiple smooth muscle tumors developed 36 to 51 months after heart transplantation. All tumors, two synchronous liver nodules, two subsequently occurring paravertebral tumors, and a single tumor in a vein at the left ankle were surgically resected. The tumor tissue was processed for routine histology and immunohistochemical (IHC) stains. Additionally, competitive polymerase-chain-reaction (PCR), reverse-transcriptase PCR (RT-PCR), as well as in situ hybridization (ISH) were used for EBV particle quantification and gene transcription analysis. The histologic features and immunohistochemical profiles were consistent with leiomyosarcoma in all tumor nodules. EBV infection was detected in >95% of tumor cell nuclei by EBER 1/2 ISH. Competitive PCR revealed 3105 EBV particles per milligram of tumor tissue. The EBV gene expression pattern analyzed by RT-PCR and IHC corresponded to the latency type III with specific expression of EBNA1, EBNA2, LMP1, and LMP2A genes. Under continuous antiviral therapy (famcyclovir) the patient currently shows no evidence of disease. Our data indicate that EBV infection plays a causal role in the development of smooth muscle tumors following organ transplantation. A latency type III, identical to EBV-associated posttransplant lymphoproliferative disorders, was identified and suggests a common pathogenetic mechanism in the development of these histogenetically distinct neoplasms. The fact that the patient currently shows no evidence of disease may be the result of the continuous administration of antiviral therapy because the soft tissue recurrences of the leiomyosarcoma occurred while the patient was not receiving antiviral prophylaxis.

We investigated in detail the previously described capacity of pseudohyphae of Candida albicans to bind C3-coated particles. We show that the expression of the C3bi receptor of C. albicans was dependent upon the growth temperature of the fungi. C. albicans grown at 30°C bound strongly to EAC1423bi, whereas those cells grown at 38.5°C were completely devoid of this capacity. The molecule responsible for the attachment of EAC1423bi was heat labile and trypsin sensitive. Several, but not all, monoclonal antibodies to the a-chain of human complement receptor type 3 (CR3) stained C. albicans, and this reactivity was expressed in parallel with the capacity of C. albicans to bind EAC1423bi, i.e., both were dependent on the growth temperature of the fungi and were trypsin sensitive. In contrast to CR3, the binding of EAC1423bi to C. albicans did not require the presence of divalent cations. Rabbit immunoglobulin G antibodies directed against C. albicans inhibited the binding of EAC1423bi to C. albicans but not to human CR3. These inhibiting IgG antibodies recognized antigens expressed on the surface of pseudohyphae but not those of yeast cells. OKM-1, a monoclonal antibody to human CR3 inhibited the attachment of EAC1423bi to CR3 and also to C. albicans. OKM-1 precipitated a 130-kilodalton band from solubilized 12SI-labeled C. albicans. We conclude that the complement receptors on C. albicans and human CR3 were antigenically related but not identical and that they differed in their functional characteristics. Various human cells express, on their surfaces, molecules which are able to bind fragments of complement component 3, like C3b, C3bi, and C3dg. Whereas C3b binds well to complement receptor type 1 (CR1) (1, 8), membrane cofactor protein (3), and decay-accelerating factor (18) and binds weakly to CR3, C3bi can be bound by CR3 (33), CR4 (23a) and, with lower affinity, can be bound by CR1 and CR2. C3dg and C3dboth show a high affinity for CR2 (10, 32), and C3dg binds, although less strongly, to CR3. These C3binding membrane molecules differ in their respective functions. CR1 is important for the binding and clearance of C3-coated immune complexes (20) and seems to contribute to the phagocytosis of some complement-coated microorganisms (34, 35). CR3 and CR4 are the most important receptors for the ingestion of complement-coated particles by phagocytes (31). Decay-accelerating factor seems to protect cells from an attack by homologous complement (21), and CR2 acts as a receptor for growth-promoting signals on B cells (9, 22, 24, 25). C3-binding structures are not specific for human cells or mammalian cells in general but are also found in microorganisms pathogenic for humans. Mammalian cells infected with herpes simplex virus type 1 express, on their surface, glycoprotein C (gC) which is able to bind C3b (12). gC destabilizes in vitro the C3 convertase of the alternative pathway, suggesting that this gC might inhibit complement activation on the cell surface and thus protect the infected cell from complement-mediated lys...

IncN plasmids are broad host-range plasmids that have contributed significantly to the worldwide dissemination of many different resistance genes in Enterobacteriaceae from animal and human sources. This plasmid family is now playing a crucial role in the global spread of diverse carbapenemase genes in Klebsiella spp.