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Background: In the so-called SPIN UTI study on 176 patients with spina bifida and clean intermittent cathererization (CIC) we have studied the influence of antibiotic prophylaxis (AP) on the number of yearly urinary tract infections (UTIs) and bacterial resistance to commonly used antibiotics. We have proven that stopping AP increased the number of yearly UTIs only slightly and clinically irrelevant patients would have to take AP for two years to prevent one extra non-febrile, non-scarring UTI, We have also shown that bacterial resistance improved over time when AP was stopped. In this article we study the influence of the recommended discontinuation of AP on Health Related Quality of Life (HRQL) in spina bifida. Methods: Participating children aged 4-16 years and their parents were asked to fill out the validated KINDL-R questionnaire, combined with specific spina bifida questions. Scores in study participants were compared with healthy controls. Also, the impact of AP, gender, level of spinal lesion, hydrocephalus, methods of catheterization and defecation, mobility and level of schooling on HRQL was evaluated. Results: One hundred and two of the 133 eligible children (77%) filled out the KINDL-R. Patients and their parents had significantly lower HRQL scores than healthy controls (p

Respiratory syncytial virus (RSV) is a major cause of severe lower respiratory tract infections in children, the elderly, and immune-compromised individuals. CD4 and CD8 T cells play a crucial role in the elimination of RSV from the infected lung, but T cell memory is not sufficient to completely prevent reinfections. The nature of the adaptive immune response depends on innate immune reactions initiated after interaction of invading pathogens with host APCs. For respiratory pathogens myeloid dendritic cell (DC) precursors that are located underneath the epithelial cell layer lining the airways may play a crucial role in primary activation of T cells and regulating their functional potential. In this study, we investigated the role of human monocyte-derived DC in RSV infection. We showed that monocyte-derived DC can be productively infected, which results in maturation of the DC judged by the up-regulation of CD80, CD83, CD86, and HLA class II molecules. However, RSV infection of DC caused impaired CD4 T cell activation characterized by a lower T cell proliferation and ablation of cytokine production in activated T cells. The suppressive effect was caused by an as yet unidentified soluble factor produced by RSV-infected DC.

Background Human red blood cells bind various C3b-coated microorganisms via their C3b/CR1 receptor, a phenomenon referred to as immune adherence. The aim of the present study was to measure pneumococcal adherence to human red blood cells by flow cytometry and to study kinetic aspects of this binding. Materials and methods We quantified pneumococcal adherence to human erythrocytes by FACS analysis and tested the involvement of antibodies and complement activation in this process. Results Pneumococci are able to bind to human red blood cells in the presence of human serum. Coating with C3b/C4b appeared obligatory for pneumococcal adherence to red blood cells. The ligand on erythrocytes was confirmed to be complement receptor 1. Kinetic studies showed that innate (mannose-binding lectin) and specific immune factors (IgG antibodies) contributed to the binding of C3b-coated pneumococci to human erythrocytes. After initial binding, serum-derived factor I was found to induce bacterial detachment from the erythrocyte. Conclusions Pneumococci are able to adhere to red blood cells. Both the classical and lectin complement pathways are important for optimal C3b-coating of pneumococci for immune adherence. Bound pneumococci are detached from red blood cells by factor I. These findings are in line with the hypothesis of immune adherence in which human erythrocytes are able to bind pneumococci and target the bacteria to the reticulo-endothelial system in the spleen.

Early-onset group B streptococcal (GBS) infection can be prevented by intrapartum antibiotic prophylaxis. In the USA the effectiveness of this strategy was demonstrated after the introduction of formal guidelines in 1996. In Europe prevention strategies for early-onset GBS infection have not been implemented universally. In 1998 the Dutch Society of Paediatrics and the Dutch Society of Obstetrics and Gynaecology posted conjoint guidelines for the prevention of early-onset GBS disease based on currently available knowledge and the local situation. These guidelines will be discussed in this overview.

To investigate the role of cell-mediated immunity during respiratory syncytial virus (RSV) infection, interferon (IFN)-gamma and interleukin (IL)-10 levels in nasopharyngeal secretions were measured in infants with lower respiratory tract infection (LRTI) caused by RSV. A novel technique was used to measure in vivo cytokine levels in nasopharyngeal aspirates (NPAs). Cytokine levels in the NPAs of 17 mechanically ventilated infants and 43 nonventilated hospitalized infants were compared. As expected, mechanically ventilated infants were significantly younger than nonventilated infants (7 vs. 14 weeks). IFN-gamma levels were above the limit of detection in the NPAs of 3 (18%) mechanically ventilated infants and in the NPAs of 26 (60%) nonventilated infants. IL-10 levels in the NPAs of mechanically ventilated and nonventilated infants were comparable. It is hypothesized that maturation-related mechanisms have a key role in the development of RSV LRTI that results in mechanical ventilation.

Monocytic cytokine profiles of fifteen children with acute lymphoblastic leukaemia (ALL) were included to determine whether malignancy per se contributes to impaired cytokine profiles in vivo and ex vivo, The ex vivo tumour necrosis factor-alpha (TNF-alpha) and interleukin 1 beta (IL-1 beta) production was positively correlated with the monocyte number and with the number of intracellular TNF-alpha or IL-1 beta positive cells in lipopolysaccharide (LPS)-stimulated MNC cultures. The mean ex vivo TNF-alpha and IL-1 beta production per 1 x 10(4) monocytes in these cultures was not significantly different in children at diagnosis of ALL, at remission or in controls. High IL-10 plasma levels at diagnosis of ALL had no effect on the ex vivo TNF-alpha and IL-1 beta production of monocytes in LPS stimulated MNC cultures. These results show that monocytes of ALL patients have a normal intrinsic capacity to produce cytokines ex vivo. However, the decreased monocyte number is responsible for the lower TNF-alpha and IL-1 beta concentrations ex vivo upon LPS stimulation. (C) 2000 Academic Press.

Although bacterial superinfection in viral respiratory disease is a clinically well documented phenomenon, the pathogenic mechanisms are still poorly understood. Recent studies have revealed some of the mechanisms involved. Physical damage to respiratory cells as a result of viral infection may lead to opportunistic adherence of bacteria. Enhanced bacterial adherence by specific mechanisms has been documented for respiratory cells infected With influenza A virus, respiratory syncytial virus and adenovirus in both in vitro and in vivo models. To date, results of various experimental studies indicate that different mechanisms for increased bacterial adherence induced by viruses are operating for specific viral-bacterial combinations. In the present review, a number of key findings obtained during the past two decades is presented and discussed. (C) 1999 Federation of European Microbiological Societies. Published by Elsevier Science B.V. All rights reserved.