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S Borgmann

Publications and source records attributed to S Borgmann.

At least 19 recordsLinked to original sources
PubMed2007

[Prevention and control of the spread of vancomycin-resistant enterococci: results of a workshop held by the German Society for Hygiene and Microbiology].

The incidence of vancomycin-resistant enterococci (VRE), especially E. faecium, is increasing in several German hospitals and some facilities have experienced VRE outbreaks. The German National Nosocomial Infection Surveillance System has also noticed a sharp increase in the incidence of nosocomial VRE infections per 10,000 patients from 0.5 in 2003 to 11.0 in 2005 accompanied by a rise in VRE-associated mortality. However, the reasons of this increase remain unknown. As VRE may cause severe nosocomial infections, transmission must be restricted. This article provides the guidelines as defined by the workshop of the German Society for Hygiene and Microbiology for the prevention of VRE transmission in both, endemic and epidemic, settings. The following topics are discussed: indication for VRE screening, microbiological diagnostics, general infection control measures (isolation precautions and use of protective clothing) and additional hygiene measures in the nosocomial VRE outbreak setting.

Cross Infection↗
PubMed2006

Fatal multidrug-resistant Acinetobacter baumannii sepsis in a patient with travel history and recent onset of systemic lupus erythematosus: a case report.

Severe infections are a common cause of death in patients suffering from systemic lupus erythematosus (SLE). We here report on a fatal multidrug-resistant Acinetobacter baumannii sepsis in a patient with newly diagnosed SLE, who had to be treated with immunosuppressants due to lupus nephritis. Detailed analysis of the patient's history revealed that colonisation probably had occurred during a recent hospitalisation of the patient in the Mediterranean region. E-test analysis indicated that resistance to carbapenems was mediated by a plasmid-encoded metallo-beta-lactamase. We conclude that travel history including previously visited health care facilities always should be carefully considered for decisions on anti-infective therapy, as travel activities increasingly facilitate spread of antimicrobial resistances.

Acinetobacter Infections↗
PubMed2005

Spread of ampicillin/vancomycin-resistant Enterococcus faecium of the epidemic-virulent clonal complex-17 carrying the genes esp and hyl in German hospitals.

The incidence of vancomycin-resistant Enterococcus faecium isolation was low (<or=5%) in German hospitals before 2003. Within the second half of 2003 and the first half of 2004, however, increasing frequencies of up to 14% were noticed in several hospitals in southwestern Germany. This increase was attributed mainly to the occurrence and spread of epidemic-virulent ampicillin/vancomycin-resistant, vanA- and vanB-positive E. faecium clones, most of which exhibited the virulence factors enterococcal surface protein (esp) and bacteriocin activity and some which exhibited hyaluronidase (hyl). E. faecium possessing hyaluronidase was initially found in U.S. hospitals and recently detected in several European hospitals and, subsequently, in German hospitals as well. Ampicillin/vancomycin-resistant E. faecium clones originating mainly from southwestern German hospitals were characterized by multilocus sequence typing since different sequence types (STs) belonging to the clonal complex-17 are currently disseminated worldwide. Multilocus sequence typing revealed that, in 1998 and 1999, ampicillin/vancomycin-resistant E. faecium clone ST-117 was prevalent in various German hospitals, while in 2003 and 2004, clone ST-203 dominated in several hospitals located in southwestern Germany. Both sequence types display single-locus variants of ST-78, which was frequently recorded in various Italian hospitals between 2000 and 2003, and all of these STs belong to the clonal complex-17. Expression of linezolid resistance was observed in ampicillin/glycopeptide-resistant E. faecium strains (VanA type) from two tertiary hospitals in southwestern Germany due to mutations in domain V of the 23S rDNA (G2576T). While in one hospital the resistance emerged during linezolid therapy, in the other hospital resistance was caused by transfer of an identical linezolid/ampicillin/glycopeptide-resistant E. faecium strain. In conclusion, it is very important to monitor the occurrence of epidemic-virulent clonal complex-17 strains of E. faecium to prevent their spread in hospitals, especially if they are resistant to glycopeptides and linezolid.

Acetamides↗
PubMed2004

Metallo-beta-lactamase expressing multi-resistant Acinetobacter baumannii transmitted in the operation area.

Outbreaks of Acinetobacter baumannii demonstrating multiple antibiotic resistance, including meropenem resistance, have been described as severe therapeutic problems. Here we describe a monoclonal outbreak of infection and colonization with multidrug-resistant A. baumannii over a two-month period. Resistance to meropenem was mediated by expression of a metallo-beta-lactamase enzyme. Four of 14 patients showed clinical signs of infection and two died. Contamination of the environment, water, or instruments were excluded as causes of the outbreak. All patients, except one, underwent surgery in a specific operation theatre where surgery of contamination class IV (infected, dirty) was performed. Although individual surgeon error was eliminated, analyses of the patients' histories suggested that bacterial transmission had occurred during surgery. Five patients showed signs of A. baumannii infection and two of these patients suffered from large abdominal wounds infected with a high density of A. baumannii requiring repeated revisions. Presumably, these revisions favoured the transmission of A. baumannii, which is remarkably resistant to various environmental stresses including soaps, disinfectants and dry conditions. No case of meropenem-resistant A. baumannii had been observed in the hospital before the outbreak. Interestingly, the resistant bacteria appear to have been imported by a patient returning from West Africa. This indicates that, similar to MRSA, multiresistant A. baumannii may be introduced by patients from foreign hospitals. The outbreak was stopped in the following months by reinforcing standard procedures and by taking all necessary precautions such as patient isolation, and finally only one new case was detected.

Acinetobacter Infections↗
PubMed2004

Genetic impact of pathogenesis and prognosis of ANCA-associated vasculitides.

Wegener's granulomatosis (WG), microscopic polyangiitis (MPA) and the Churg-Strauss syndrome (CSS) are small vessel vasculitides associated with anti-neutrophil cytoplasmic antibodies (ANCA). Cytoplasmic (c)-ANCA mainly target proteinase 3 (PR3) and are often observed in WG patients, while perinuclear (p)-ANCA predominantly bind to myeloperoxidase (MPO) and are common in patients with MPA and CSS. It is suspected that a genetic background contributes to disease formation since the diseases are more prevalent in Caucasian populations. This article provides a detailed review of the genetic impact of the pathogenesis and prognosis of ANCA-associated vasculitides. Alpha-1 anti-trypsin is the physiological inhibitor of PR3 and carriage of the defective allele PI*Z was observed as the first genetic risk factor for the development of PR3-ANCA-associated vasculitis. Expression analyses have revealed that PR3 surface expression is genetically determined. Elevated levels of PR3 expression have been observed in WG patients and high levels of PR3 expression corresponded to increased risk of disease relapses. Furthermore, the non-carriage of CTLA-4 allele 86 was associated with WG formation, while homocygotic carriage of the CCR5 allele delta 32 seemed to prevent ANCA-negative WG. MPO-ANCA vasculitides were associated with certain alleles of CD18 polymorphisms. Lack of or only weak allelic associations of ANCA-vasculitides with polymorphic cytokine, HLA, and Fcgamma receptor genes have been shown. Although, in practice, it is sometimes difficult to differentiate between WG and MPA, the diseases appear to be based on different genetic backgrounds.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed2003

Recovery of cell volume and electrolytes of A6 cells after re-establishing isotonicity following hypotonic stress.

Cellular element concentrations and dry weight contents in A6 cells were determined using electron microprobe analysis to establish whether these cells exhibit a regulatory volume increase (post-RVD-RVI) when re-establishing isotonicity following a hypotonically induced regulatory volume decrease (RVD). Hypotonic stress was induced by reducing basolateral [NaCl], and hence, osmolarity fell from 260 to 140 mosmol/l. The alterations in cell volume after re-establishing isotonicity, calculated from the cellular dry weight changes, indicate within the first 2 min cell shrinkage from 120 to 76% of control, compatible with almost ideal osmometric behaviour of A6 cells, and thereafter a post-RVD-RVI to 94%. The cellular uptake of osmolytes necessary to explain the post-RVD-RVI could be accounted for solely by a gain in cellular K and Cl. The involvement of a Na-K-2Cl cotransporter in most of the KCl uptake seems plausible since basolateral bumetanide blocked KCl uptake and post-RVD-RVI. The net uptake of cations (K uptake of 185.2, Na loss of 8.2 mmol/kg dry wt) during the isotonic period exceeded the Cl uptake by 38.2 mmol/kg dry wt, suggesting the uptake of another anion and/or the alteration of cellular buffer capacity. The relatively low Na concentration maintained during the isotonic period (13.3 vs. 20.4 mmol/kg wet wt under control conditions) might favour electrolyte uptake via the Na-K-2Cl cotransporter.

Animals↗
PubMed2002

Contrasting effects of long-term treatment with IFN-gamma in endothelial cells: increase in IL-6 secretion versus decrease in IL-8 secretion, NF-kappa B, and AP-1 activation.

The benefit of neutrophil exclusion from type 1 T helper cell (TH1) inflammatory processes was demonstrated in clinical studies. Increased recruitment of lymphocytes and monocytes to endothelium and impaired recruitment of polymorphonuclear neutrophils (PMNs) following interferon-gamma (IFN-gamma) treatment were described. The present study demonstrates that a 24 h treatment with IFN-gamma increases interleukin (IL)-6 release but reduces IL-8 secretion of both untreated and of tumor necrosis factor-alpha (TNF-alpha)-stimulated endothelial cells (ECs), favoring the attraction of lymphocytes but not of neutrophils. Alteration of cytokine release was accompanied by reduced basal and TNF-alpha-stimulated nuclear factor-kappa B (NF-kappa B) and activator protein-1 (AP-1) activity. However, IFN-gamma application neither altered gene expression of both TNF-alpha receptors (p55 and p75) nor cellular density of TNF-alpha receptor-2 (p75). Therefore, immune-modulatory action of IFN-gamma seems to be mediated by signal transduction molecules.

Antigens, CD↗
PubMed2001

A linkage disequilibrium between genes at the serine protease inhibitor gene cluster on chromosome 14q32.1 is associated with Wegener's granulomatosis.

The frequency of carriers of the alpha1-antitrypsin (alpha1-AT) deficiency allele PI*Z is increased in patients with Wegener's granulomatosis (WG). The polymorphic protease inhibitor (PI) gene is part of a cluster of serine protease inhibitor (serpin) genes (AACT; alpha1-antichymotrypsin, PCI; protein C inhibitor, CBG; corticosteroid binding globulin, PIL; PI-like pseudogene) at chromosome 14q32.1. In this study we investigated whether the serpin gene cluster contributes to the background of Wegener's granulomatosis. Therefore, phenotyping of alpha1-AT was performed and simple tandem repeat polymorphisms (STRP) in the genes for CBG, PI, and PCI as well as two STRP (D14S55 and D14S48) flanking the centromeric and one (D14S51) flanking the telomeric region of the gene cluster were examined in a population of 79 patients with WG and 128 unrelated healthy controls. In WG patients an increased frequency of the PI*Z defective allele is demonstrated as well as a linkage disequilibrium between all members of this gene cluster plus the centromeric and telomeric STRP. These results indicate an involvement of the serpin genes in the pathogenesis of Wegener's granulomatosis and it is possible that other genes located in the vicinity of D14S55 or D14S51 contribute to the genetic background of the disease.

Alleles↗
PubMed2001

Novel SNPs in the CD18 gene validate the association with MPO-ANCA+ vasculitis.

Wegener granulomatosis (WG), microscopic polyangiitis (MP), and Churg-Strauss syndrome (CSS) are characterized by the presence of anti-neutrophil cytoplasmic antibodies (ANCA). Anti-myeloperoxidase (MPO)-ANCA are a typical feature of MP and CSS, while anti-proteinase 3 (PRTN3)-ANCA are highly specific for WG. Several reports indicate that ANCA may directly contribute to pathological processes, ie, through an increase of adhesivity between polymorphonuclear (PMN) and endothelial cells (EC). PMN interact and endothelium interact via the adhesion cascade (AC). CD18 is a key molecule of the AC, as CD18 defects abrogate the adhesion of PMN and cause leukocyte adhesion deficiency, an immunodeficient trait. We have screened the entire coding and regulatory regions of the CD18 gene. Ten single nucleotide polymorphisms (SNP) were identified, four of them showing significant associations with MPO-ANCA(+) vasculitis. One of these SNP's was localized in an alternate transcription initiation site. This polymorphism may influence CD18 gene expression, resulting in dose-dependent increase in adhesion and consecutively facilitated degranulation and respiratory burst. In this manner the pro-adherent genotype may predispose to MPO-ANCA(+) vasculitis.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed2001

Amoeboid leukocyte crawling through extracellular matrix: lessons from the Dictyostelium paradigm of cell movement.

Cell movement within three-dimensional tissues is a cycling multistep process that requires the integration of complex biochemical and biophysical cell functions. Different cells solve this challenge differently, which leads to differences in migration strategies. Migration principles established for leukocytes share many characteristics with those described for ameba of the lower eukaryote Dictyostelium discoideum. The hallmarks of amoeboid movement include a simple polarized shape, dynamic pseudopod protrusion and retraction, flexible oscillatory shape changes, and rapid low-affinity crawling. Amoeboid crawling includes haptokinetic adhesion-dependent as well as biophysical migration mechanisms on or within many structurally and functionally different substrates. We describe central aspects of amoeboid movement in leukocytes and the implications for leukocyte crawling and positioning strategies within interstitial tissues.

Actins↗
PubMed2000

The association of CD18 alleles with anti-myeloperoxidase subtypes of ANCA-associated systemic vasculitides.

Wegener granulomatosis (WG), microscopic polyangiitis (MP), and Churg Strauss syndrome (CSS) are rare systemic autoimmune disorders. Common features are anti-neutrophil cytoplasmic antibodies (ANCA) in patient sera. Whereas WG patients show mainly anti-proteinase 3 ANCA, MP and CSS patients typically present anti-myeloperoxidase (MPO) ANCA. ANCA play an important role in the pathogenesis in the vessel wall by activating polymorphonuclear cells (PMN) and increased adhesivity between PMN and endothelial cells via adhesion molecules. Here we investigated major adhesion molecules as predisposition factors via common polymorphisms in or in the vicinity of the candidate genes ICAM-1, e-selectin, PLAUR, CD11b, and CD18. A restriction fragment-length polymorphism in exon 11 of the CD18 gene was associated with MPO-ANCA(+) systemic vasculitis. Our data indicate that a common variant of the CD18 gene confers increased risk for CSS and MP, supporting that genetic factors are involved in the etiology and pathogenesis of ANCA-associated systemic vasculitides.

Alleles↗
PubMed2000

Antigen presentation in extracellular matrix: interactions of T cells with dendritic cells are dynamic, short lived, and sequential.

Cognate interactions of naive T cells with antigen-presenting dendritic cells require physical cell-cell contacts leading to signal induction and T cell activation. Using a three-dimensional collagen matrix videomicroscopy model for ovalbumin peptide-specific activation of murine and oxidative mitogenesis of human T cells, we show that T cells maintain vigorous migration upon cognate interactions to DC (dendritic cell), continuously crawl across the DC surface, and rapidly detach (median within 6-12 min). These dynamic and short-lived encounters favor sequential contacts with the same or other DC and trigger calcium influx, upregulation of activation markers, T blast formation, and proliferation. We conclude that a tissue environment supports the accumulation of sequential signals, implicating a numeric or "digital" control mechanism for an ongoing primary immune response.

Animals↗
PubMed2000

Proteinase 3 gene polymorphisms and Wegener's granulomatosis.

BACKGROUND: Wegener's granulomatosis (WG) is a rare systemic autoimmune disease characterized by small-vessel vasculitis leading to organ damage and the presence of antineutrophil cytoplasmic autoantibodies (ANCAs). ANCAs were shown to be involved in the pathogenesis of the disease by increasing adhesion of polymorphonuclear cells (PMNs) to endothelial cells and through activation of primed PMN. The main autoantigen of ANCA in WG is proteinase 3 (PR3), a neutrophil- and monocyte-derived neutral serine protease. The association of WG with individuals continuously expressing a high level of PR3 on the surface of PMNs suggests that PR3 variants or altered regulation of PR3 expression might be directly involved in the pathogenesis of the disease. METHODS: We screened the entire coding and promoter sequences of the PR3 gene for polymorphisms by means of polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP). Allelic, genotypic, and haplotype frequencies were compared between 79 WG patients and a cohort of 129 healthy controls. RESULTS: Seven single-nucleotide polymorphisms (SNPs), one amino acid change (Val119Ile), one 84 bp insertion/deletion, and a microsatellite were identified. An association with WG could be demonstrated for the A-564G polymorphism in the PR3 promoter affecting a putative transcription factor-binding site. CONCLUSIONS: This study excludes certain PR3 epitope variants as autoantigenic stimuli in WG, since the Val119Ile polymorphism showed no differences between patients and controls. Overexpression of PR3, however, might predispose the patient to the development of autoimmune ANCA-associated vasculitis.

Alleles↗
PubMed1999

Lack of cortico-striatal projections from the primary auditory cortex in the squirrel monkey.

The projections of the superior temporal gyrus to the caudate nucleus were studied in 10 squirrel monkeys (Saimiri sciureus). It was found that the primary auditory cortex lacks direct connections with the caudate nucleus as well as the putamen. Areas RL and T1 of Burton and Jones, bordering the primary auditory cortex laterally, show a moderate projection to the body and tail of the caudate nucleus; area T2, bordering areas RL and T1, shows an extensive projection into the head, body and tail. A comparison of the temporo-caudate projections of the monkey with those of rodents and carnivores suggests that primary and secondary auditory cortices differ in their connections in primates more than in other mammals, pointing to a greater functional differentiation of these areas in primates.

Animals↗
PubMed1999

A search for chromosome 22q11.2 deletions in a series of 176 consecutively catheterized patients with congenital heart disease: no evidence for deletions in non-syndromic patients.

Microdeletions in chromosome 22q11.2 are associated with DiGeorge syndrome (DGS), velo-cardio-facial syndrome (VCFS), and several other syndromes, collectively referred to as DG/VCF. Non-dysmorphic patients with cardiac defects have also been attributed to deletions in this chromosomal region. In this study 157 consecutively catheterized patients with isolated, non-syndromic cardiac defects, and 25 patients with cardiac defects and additional stigmata (10 of whom were clinically diagnosed as DG/VCF cases prior to chromosome analysis) were analysed by fluorescence in situ hybridization with the DGS-specific probe D0832. Chromosome 22q11.2 deletions were observed only in the ten patients with the clinical diagnosis of DG/VCF. Conclusion In a large unselected cohort of patients with congenital heart disease no association between isolated or non-syndromic heart defects and the 22q11.2 microdeletion was observed. One can conclude that testing for the 22q11.2 microdeletion is clearly indicated in cases when even mild extracardiac abnormalities are present, particularly in very young infants.

Adolescent↗
PubMed1999

Immunogenetic risk factors for anti-neutrophil cytoplasmic antibody (ANCA)-associated systemic vasculitis.

Wegener's granulomatosis (WG) and microscopic polyangiitis are systemic autoimmune diseases characterized by the presence of ANCA in the sera of patients. Little is known about the aetiologic factors and genetic predisposition as well as the pathogenesis of these disease entities. A slightly decreased representation of HLA-DRB1*13 and HLA-DQB1*0603 individuals was observed in our cohort of ANCA-associated systemic vasculitis (AASV) patients compared with controls. In addition, HLA-DRB1*04 individuals were over-represented in a subgroup of patients with WG in end-stage renal disease as a result of renal vasculitis. In order to identify other genes relevant for these diseases, we investigated highly polymorphic markers in the vicinity of several immunorelevant genes, i.e. tumour necrosis factor (TNF)alpha, IL-2, IL-5 receptor alpha (IL-5RA), in a group of 102 patients with AASV and compared the representation with controls. Furthermore, functional polymorphisms were directly analysed in the promotor region of TNFalpha as well as in the coding region of the FcgammaIIRA genes. Polymorphisms of the TNFalpha promotor (TNF-308) as well as in the FcgammaIIRA gene were excluded as risk factors for the disease in our cohort. No major phenotype distribution differences were observed between patients and controls for the IL-2 and IL-5RA microsatellites. Most importantly, several haplotypes on chromosome 6p appeared strongly associated with proteinase 3 (PR3)-ANCA+ AASV. Thus, as in other autoimmune diseases, different predisposing factors play differential aetiopathogenic roles in various groups of AASV patients.

Adolescent↗