Effective reprocessing of reusable dispensers for surface disinfection tissues – the devil is in the details

Background: It has recently been reported that reusable dispensers for surface disinfection tissues may be contaminated, especially with adapted Achromobacter species 3, when products based on surface-active ingredients are used. Fresh solution may quickly become recontaminated if dispensers are not processed adequately. Methods: We evaluated the abilities of six manual and three automatic processes for processing contaminated dispensers to prevent recolonisation of a freshly-prepared disinfectant solution (Mikrobac forte 0.5%). Dispensers were left at room temperature for 28 days. Samples of the disinfectant solution were taken every 7 days and assessed quantitatively for bacterial contamination. Results: All automatic procedures prevented recolonisation of the disinfectant solution when a temperature of 60–70°C was ensured for at least 5 min, with or without the addition of chemical cleaning agents. Manual procedures prevented recontamination of the disinfectant solution when rinsing with hot water or a thorough cleaning step was performed before treating all surfaces with an alcohol-based disinfectant or an oxygen-releaser. Other cleaning and disinfection procedures, including the use of an alcohol-based disinfectant, did not prevent recolonisation.Conclusions: These results indicate that not all processes are effective for processing reusable dispensers for surface-disinfectant tissues, and that a high temperature during the cleaning step or use of a biofilm-active cleaning agent are essential.     

Advanced-Trauma-Life-Support-Programm (ATLS®)

Trauma und Berufskrankheit - Es ist aus klinischen Untersuchungen bekannt, dass ein standardisiertes, im Team trainiertes Schockraummanagement die Behandlungsergebnisse von Schwerverletzten...     

Matrix metalloproteinases and their tissue inhibitors (TIMPs) in Plasmodium falciparum malaria: serum levels of TIMP-1 are associated with disease severity

BACKGROUND: Molecular mechanisms involved in the pathogenesis of severe malaria caused by Plasmodium falciparum are not fully understood. Matrix metalloproteinases (MMPs) are enzymes that proteolytically degrade both the extracellular matrix and nonmatrix substances with various functions in the modulation of immune response. The key inhibitors of MMPs are the tissue inhibitors of metalloproteinases (TIMPs). METHODS: We studied levels of MMP-8, MMP-9, TIMP-1, and TIMP-2 on admission and after 24 h, using an enzyme-linked immunosorbent assay, in serum specimens from 50 Gabonese children with severe malaria, 43 children with uncomplicated malaria, and 27 healthy control children. RESULTS: Serum MMP-8 and TIMP-1 levels were significantly higher in the severe malaria and uncomplicated malaria groups, compared with those in the control group (P < .001). TIMP-1 levels were significantly higher in patients with severe malaria, compared with those in patients with uncomplicated malaria (P < .001). High TIMP-1 levels were significantly correlated with malaria severity, as determined by the simplified multiorgan dysfunction score (Spearman rank-correlation coefficient, 0.55; P < .001). CONCLUSIONS: TIMP-1 is associated with signs and symptoms of severe malaria. MMP-8 levels are elevated in patients with severe or uncomplicated P. falciparum malaria. MMPs and TIMPs may be relevant in the pathogenesis of severe malaria, either as proteolytic enzymes that degrade the extracellular matrix or as effectors and regulators of the immune response.     

A Hodgkin cell-specific antigen is expressed on a subset of auto- and alloactivated T (helper) lymphoblasts

A Hodgkin cell-specific antigen detected by the monoclonal antibody Ki- 1 was found on T helper lymphocytes after activation by autologous and allogeneic stimulator cells. About 50% of lymphoblasts generated by auto- and alloactivation reacted with the antibody. In contrast, only less than 6% of lymphoblasts stimulated with Con-A, phytohemagglutinin (PHA), or protein A, and none of lymphoblasts activated by oxidative mitogenesis, expressed this antigen. Among several permanent cell lines tested, the K562, MOLT-4, HL-60, and EBV transformed B lymphoblastoid cells reacted with the Ki-1 antibody. The results may indicate possible relationships between the autoreactive subset of T lymphocytes and the pathogenesis of Hodgkin's disease.     

Non-radiotherapy conditioning with stem cell transplantation from alternative donors in children with refractory severe aplastic anemia

Conditioning including total body/lymphoid irradiation is widely used to prevent graft rejection in patients with refractory severe aplastic anemia (SAA) undergoing hemopoietic cell transplantation (HCT) from alternative donors and or after graft manipulation. To reduce regimen-related toxicity we transplanted three children with refractory SAA after conditioning with radiotherapy-free regimens. Conditioning included fludarabine 175-180 mg/m2 in all patients. In addition, patient 1 (failing two previous grafts) received thiotepa 10 mg/kg and Campath-1H 60 mg/m2; patient 2 cyclophosphamide 120 mg/kg, thiotepa 15 mg/kg and OKT-3 0.1 mg/kg/day for 4 weeks; and patient 3 cyclophosphamide 120 and ATG 90 mg/kg. Stem cell source was unmanipulated marrow from the same unrelated donor as for the two previous transplantations in patient 1 and CD34+-purified peripheral blood stem cells from an HLA-matched unrelated donor and from the haploidentical mother in patients 2 and 3. Only patient 1 received graft-versus-host disease (GVHD) prophylaxis with cyclosporine A and mycophenolate mofetil. Follow-up is now 30, 51, and 15 months. None of the patients developed GVHD. All patients have normal counts with complete donor chimerism. Fludarabine-based conditioning is powerfully immunosuppressive and may be used for children with refractory SAA undergoing HCT from alternative donors even after rejection following previous HCT.     

Early immunologic events in mucosal and systemic lymphoid tissues after intrarectal inoculation with simian immunodeficiency virus

The pathogenesis of human immunodeficiency virus transmission via the rectal route remains poorly understood. By use of the simian immunodeficiency virus (SIV)-rhesus macaque model and intrarectal inoculation with pathogenic SIVmac251, a significant increase was found in the percentage of CD11b(+) monocyte lineage cells expressing HLA-DR and/or B7-2 in local and peripheral immune inductive sites, but not in mucosal effector sites, as early as 7 days after inoculation and up to 50 days after inoculation. Moreover, at 21 and 50 days after inoculation, not only the gut but also the lung mucosa were depleted of CD4(+) T cells, which suggests that early loss of CD4(+) T cells may be a common feature of mucosal effector sites. These data suggest that, after intrarectal inoculation with SIV, early activation occurs within the monocyte lineage cell population at immunologic inductive sites, which is followed by a loss of CD4(+) T cells at local and distant mucosal effector sites.     

Transplantation of highly purified CD34+ progenitor cells from alternative donors in children with refractory severe aplastic anaemia

Without transplantation from a human leucocyte antigen-identical family donor, refractory severe aplastic anaemia (SAA) has an unfavourable prognosis. Conventional transplantation from a matched unrelated donor carries a high rate of mortality. We transplanted large numbers of highly purified CD34+ cells from matched unrelated (n = 4), mismatched unrelated (n = 4) and mismatched related (n = 1) donors into nine children with refractory SAA. The grafts consisted of granulocyte colony-stimulating factor-mobilized peripheral positively selected CD34+ cells. A median of 15.1 x 106/kg CD34+ stem cells and 11 x 103/kg CD3+ T-lymphocytes were infused. No additional pharmacological graft versus host disease (GVHD) prophylaxis was given. At a median follow-up of 47 (range 37-72) months, eight patients (89%) were in complete remission with >90% donor chimaerism and no evidence of GVHD. One patient died on day +238 as a consequence of GVHD. The use of highly purified mobilized CD34+ stem cells warrants further clinical exploration in children with refractory SAA.     

Visceral Manifestation of Cat Scratch Disease in Children. A Consequence of Altered Immunological State?

Summary A 12-year-old girl with a 2-month history of fever and abdominal pain was admitted to our hospital. Ultrasound and CT scans of the abdomen showed multiple hypoechoic lesions of liver and spleen. Screening for zoonosis revealed high positive titers to Bartonella henselae. T-cell deficiency was demonstrated and remained almost unchanged during a follow-up of 11 months. A review of the literature shows that disseminated visceral affection is a rare presentation of cat scratch disease (CSD) in childhood and adolescence. Further immunological investigations are needed in more patients with CSD to confirm whether an altered imunological state may be responsible for the atypical visceral manifestation of CSD. Received: May 18, 1999 · Revision accepted: January 19, 2000     

Monocyte/macrophages and their role in HIV neuropathogenesis

Neurological sequelae of human immunodeficiency virus (HIV) infection have been and remain a significant problem. Monocytes and macrophages in humans and monkeys are susceptible to infection by HIV and simian immunodeficiency virus (SIV), and are considered to be a main mechanism by which the central nervous system (CNS) is infected. Within the infected CNS, perivascular macrophages and, in some cases, parenchymal microglia are infected as are multinucleated giant cells when present. While neurons are not themselves directly infected, neuronal damage occurs within the infected CNS. Despite the success of antiretroviral therapy (ART) in limiting virus in plasma to non-detectable levels, neurological deficits persist. This review discusses the continued neurological dysfunctions that persist in the era of ART, focusing on the roles of monocyte and macrophage as targets of continued viral infection and as agents of pathogenesis in what appears to be emergent macrophage-mediated disease resulting from long-term HIV infection of the host. Data discussed include the biology of monocyte/macrophage activation with HIV and SIV infection, traffic of cells into and out of the CNS with infection, macrophage-associated biomarkers of CNS and cardiac disease, the role of antiretroviral therapy on these cells and CNS disease, as well as the need for effective adjunctive therapies targeting monocytes and macrophages.