[Enterohemorrhagic Escherichia coli. A new contagious disease in Sweden].
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Biomedical subjects
Publications and source records attributed to A Ljungh.
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Four biliary stents inserted for relief of jaundice in patients with biliary obstruction due to carcinoma of pancreatic head were examined for the adsorption of biliary proteins and bacterial colonization. Fibronectin and vitronectin (S-protein) were found to be the two main proteins adsorbed on the inner surface of the stents. Biliary isolates included Escherichia coli, Enterococcus faecalis, and Candida albicans. In vitro studies were performed to clarify the kinetics of biliary protein and bacterial adhesion. Biliary drains of polytetrafluorethylene, polyethylene, polyurethane, and rubber were placed in a flow cell and perfused with human bile at 37% C for 24 hr. The materials were subjected to either detection of adsorbed biliary proteins or perfusion with 3 H-labeled E. coli cells (1 X 10 6 cfu/ml). The results show that the adsorbed biliary proteins were detectable on the surface of biliary stents and able to enhance bacterial adhesion to the surface in the first 24 hrs after the exposure of stent materials to bile, and that both the adsorption of biliary proteins and the adhesion of bacterial cells were material- and strain-dependent. Furthermore, there was a clear correlation between the amount of adsorbed fibronectin and the number of adherent bacteria. The results indicate that, in the clinical situation, biliary proteins may be adsorbed on the surface of inserted stents within a short time after insertion, and some of them may be used by bacterial cells as receptors for adhesion to the surface, and thus involved in the process of bacterial adhesion.
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Staphylococcus aureus, which mediated binding to heparan sulfate, and also strains of coagulase-negative staphylococci (CNS) adhered in high numbers to polymers with end-point attached heparin. A characteristic feature of several cell growth factors is strong affinity for heparin. In the present study, binding of the 125I-labeled heparin-binding growth factors (HBGF), acidic and basic fibroblast growth factor (aFGF, bFGF), and platelet-derived growth factor (PDGF) by S. aureus and CNS strains was examined. Staphylococcal strains used in this study bind bFGF and PDGF, but not aFGF. The binding of bFGF and PDGF was time dependent, influenced by pH and ionic strength for S. aureus Cowan 1. Preincubation of staphylococcal cells with unlabeled bFGF enhanced bFGF binding, but heparin, protamine sulfate, poly-L-lysine, and suramin were potent inhibitors of 125I-bFGF binding to cells of S. aureus Cowan 1. Glycosaminoglycans of comparable size (chondroitin sulfate), other polysulfated polymers (lambda-carrageenan, fucoidan), and some polysulfated polysaccharides (dextran sulfate, pentosan polysulfate) inhibited binding of both GFs to various extents. The partial inhibition of binding of both GFs after protease and periodate treatments indicates that both proteinaceous and other carbohydrate moieties participate in the binding. A lysozyme cell surface extract and bacterial lysates of S. aureus Cowan 1 competitively inhibited binding of 125I-bFGF and 125I-PDGF. These results suggest that staphylococci have the ability to bind two of the HBGFs, bFGF and PDGF, but not aFGF, via more than one cell structure. These binding structures seem to be exposed on the cell surface and deeply anchored in the cytoplasmic membrane as well.
OBJECTIVE: To analyze whether placental inflammation is associated with stillbirth in Zimbabwe. METHOD: Placentas from 66 stillbirths (> 22 weeks' gestation; patients with congenital malformations, diabetes or preeclampsia were excluded) and 66 term live births were studied for the presence and severity of chorioamnionitis. The morphological results were compared with earlier presented microbiological findings in the same material. RESULTS: Chorioamnionitis was present in 79% of stillbirths and 30% of live births (O.R. 8.5, 95% C.I. 4.0-18). Nine percent of stillbirths but no live births presented vasculitis of the chorionic plate, which verified an inflammatory response from the infant (O.R. 14, 95% C.I. 2.8-72). The same types of microorganisms were isolated from stillbirths and liveborns, but Escherichia coli and group B streptococci were more frequent among stillbirths. CONCLUSIONS: Morphological chorioamnionitis occurred 2.6 times more often in women with stillbirths than in women with live births. In 9% of stillbirths the infant showed an inflammatory response. Thus the infant was alive when the infection occurred and it is therefore reasonable to assume that infection was the cause of death.
End-point-attached heparinized polyethylene (H-PE) was implanted for 2 months into the peritoneum of C57B1/6 mice. The proliferation of bone marrow cells (BMCs) from implanted and non-implanted mice was investigated in M-CSF supplemented medium, in the presence or absence of macrophage-specific monoclonal antibodies (mAbs). The mAb HC 7.67.B, recognizing a surface determinant on immature monocytoid cells, inhibited the proliferation of BMCs from H-PE implanted mice without any influence on the proliferation of BMCs from non-implanted animals. The peritoneal macrophages from H-PE implanted mice demonstrated enhanced production of fibronectin (Fn) in comparison to the macrophages from non-implanted animals. Our results suggest changes in the differentiation of murine monocyte-macrophage lineage in the mice bearing H-PE implants for 2 months.
Fractionated mononuclear cells (MNCs) were obtained from peripheral blood of healthy human volunteers, seronegative for H. pylori antibodies. The MNCs were stimulated in culture with whole live or heat-killed H. pylori cells or with bacterial cell surface (SA) or cytoplasmic (CA) antigens. There was a marked proliferative response of T cells in cultures stimulated with 10(5) cells/well of live H. pylori, 5 micrograms/well of CA or 5-20 micrograms/well of SA. However, no proliferation was observed in MNC cultures containing higher "doses" of live H. pylori organisms (10(7)/well) or CA (20 micrograms/well). Moreover, higher "doses" of the bacteria or CA entirely inhibited the response of T cells to PHA.
Heparan sulfate binding proteins (HSBPs) of Helicobacter pylori facilitate bacterial phagocytosis by human polymorphonuclear leukocytes (PMNs). H. pylori 25 strain which demonstrates a strong heparan sulfate binding activity was found to be attached to/ingested by PMNs in greater numbers than H. pylori strain 17874 bacteria which lacked this activity. Moreover, heparin inhibited the uptake of cells of H. pylori strain 25 but not of cells of H. pylori strain 17874 by PMNs.
The heparin-binding properties of six different species of coagulase-negative staphylococci were examined by a particle agglutination assay. Heparin (mol. wt 4000-6000), mildly treated with sodium periodate, was covalently coupled to amino-modified latex beads (0.72 micron diameter). The particle agglutination assay was validated by comparing results with the adhesion (percentage binding of adherent cells) of coagulase-negative staphylococcal strains to heparinised microtitration plates. Of 38 different coagulase-negative staphylococcal strains tested, 30 showed agglutination reactivity with heparin-coated latex beads. Strains of different coagulase-negative staphylococcal species agglutinated heparin-coated latex beads to various extents (e.g., cells of Staphylococcus haemolyticus strains reacted more strongly than cells of S. epidermidis strains). The agglutination reaction was significantly inhibited by fucoidan, suramin, lambda-carrageenan and other sulphated compounds, but not by non-sulphated carbohydrate polymers such as hyaluronic acid. Agglutination of staphylococcal cells with heparin-coated latex beads was completely blocked by a cell-surface extract. These results suggest that structures responsible for heparin binding are exposed on the cell surface.
Staphylococcal infections are a major complication in the usage of biomaterials. Different modifications of polymers have been made to reduce the incidence of such infections. We studied the effects of modifying heparinized polyethylene (H-PE) with mouse recombinant granulocyte-macrophage stimulating factor (rGM-CSF). The elimination of staphylococci (Staphylococcus aureus, S. epidermidis) from the peritoneum of mice implanted with rGM-CSF-coated H-PE was slightly more effective than the elimination of the bacteria from the peritoneum of animals implanted with uncoated H-PE. Most interestingly, the number of staphylococci present in the biofilms covering rGM-CSF-coated implants were significantly lower than the number of bacteria detected on the surface of H-PE not coated with rGM-CSF. In vitro, rGM-CSF restored the anti-bacterial potency of the phagocytes, which had been reduced by surface contact with H-PE. The results suggest that modification of biomaterials with rGM-CSF could be one way of preventing staphylococcal infections; especially in neutropenic disorders, which constitute the highest risk factor for foreign body-associated infections.
Invasive Escherichia coli strains of certain serotypes invade by the same mechanism as the Shigella sp. It has been proposed that invasion of epithelial cells by EPEC strains may also occur; this is a previously overlooked property. In the present study E. coli strains isolated from patients with diarrhoea or ulcerative colitis, lacking the inv plasmid mediating classical invasion, but hybridizing with probes for different adhesins, were analyzed for their ability to invade HeLa and Caco-2 cells. The majority of strains invaded Caco-2 cells to a higher extent than HeLa cells. Adhesion to Caco-2 cells was a prerequisite for subsequent invasion of the cells but EAF, eae, EAgg and other known virulence factors were not sufficient to mediate invasion. In 8/9 E. coli strains invasion was enhanced after growth under iron restriction. Growth during anaerobic conditions did not influence subsequent invasion by E. coli strains whereas 6/9 strains had their invasive ability significantly decreased after growth in the presence of 1% glucose. The invasive process was inhibited by mannose but not by lactose, fucose or galactose. Our data indicate that strains of E. coli may invade Caco-2 cells by novel mechanisms which require adhesion to the cells but which differ from those of Salmonella sp., Yersinia sp., Shigella sp. and classical enteroinvasive E. coli.
OBJECTIVE: To elucidate the role of current syphilis as a risk factor for foetal death. METHODS: Sera were obtained from 57 women with third trimester foetal death (cases) and 58 women with foetus alive (controls) matched for age and parity. All sera reactive in qualitative Rapid Plasma Reagin (RPR) analyses were tested with serial twofold dilutions to determine endpoint flocculation titres and tested with the micro-haemagglutination assay for Treponema pallidum (MHA-TP). Placental biopsies were sectioned and stained by haematoxylin-eosin and Warthin-Starry for light microscopy. SETTING: Central Hospital, in Maputo, Mozambique, from January 1990 to June 1991. RESULTS: The MHA-TP was reactive in 42% of cases and in 12% of controls (OR = 5.3; 95% CI: 1.9-15.4). The RPR card test was reactive at the dilution of 1.32 or greater in 28% of cases and in 7% of controls. All these results were confirmed by MHA-TP (OR = 5.3; 95% CI: 1.5-15.4). In 9/28 (32%) MHA-TP seroreactive women (7 cases and 2 controls) placental morphological changes indicated syphilitic infection. CONCLUSION: MHA-TP seroreactivity and high titre RPR were associated with stillbirth. Morphological changes presumptive of syphilis infection were found in 32% placentas histologically studied. Syphilis is a risk factor for foetal death in Maputo, Mozambique.
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BACKGROUND: Bacterial adherence to the stent surfaces, concomitant colonization, and possible stent blockage are the main complications after the use of biliary stents. The present study was assigned to investigate bacteriologic and morphologic changes in the biliary tract after the implantation of biliary drain materials. METHODS: Rubber and silicone pieces with a surface area of 1 cm2 were implanted into the biliary tract in rats after temporary obstruction of the common bile duct by the use of a mini-occluder. The animals were killed at 4, 8 and 14 weeks, respectively, after implantation, and the implants were retrieved, cultured, and examined by scanning electron microscopy (SEM). Bacterial culture and SEM were also performed on tissue samples obtained from the mucosal surface of the biliary tract. RESULTS: Bacterial colonization and biofilm formation were found on the surfaces of the implanted materials and on the mucosal surface of the biliary tract in animals with implants but not on the biliary tract mucosa in rats without implants. CONCLUSION: Foreign bodies implanted in the biliary tract facilitate bacterial adherence not only to the surface of the implants but also to the mucosal surface in the biliary tract.
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The present study deals with the demonstration of deposited fibronectin (Fn) on the surfaces of implanted biliary drain materials and the role of deposited Fn in promotion of bacterial adherence. Rubber pieces that had been implanted in the biliary tracts of rats for 4 weeks were retrieved and the following approaches employed for further investigations: (1) adherence of [methyl-3H]thymidine-labeled Escherichia coli to implanted and unimplanted rubber pieces; (2) blocking the adherence of radiolabeled bacteria with anti-Fn antibodies; (3) detection of deposited Fn by 125I-labeled anti-Fn IgG; and (4) immunoblotting of the surface eluate from implanted rubber pieces. The results show that in the presence of serum, plasma, or bile, the number of E. coli cells adherent to implanted rubber pieces was 10 times higher than that adherent to the unimplanted pieces (P < 0.001) and that the adherence was reduced by pretreatment of implanted pieces with anti-Fn antibodies. Furthermore, the implanted pieces appeared to have a high affinity for 125I-labeled rabbit anti-Fn IgG rather than the 125I-IgG without anti-Fn fraction. Fn was also found in the surface eluate of implanted pieces by immunoblotting of the eluate. The results in the present study suggest that Fn may be involved in implant-associated infections in the biliary tract.
Aeromonas hydrophila, a ubiquitous inhabitant of aquatic environments, commonly expresses several cell-surface properties that may contribute to virulence. Since many aquatic microorganisms in hostile environments can withstand starvation conditions for long periods, we examined the effect of storage under nutrient-poor conditions on the expression of cell-surface properties of this pathogen. Phenotypes studied were: (1) cell-surface hydrophobicity and charge, and (2) the ability to bind connective-tissue proteins and lactoferrin. Our results suggest that the response of A. hydrophila to nutrient-poor conditions is regimen specific. Generally, A. hydrophila cells became more hydrophobic and significantly increased their ability to bind the iron-binding glycoprotein lactoferrin when the bacterium was stored under nutrient-poor conditions; however, under these conditions, the cells seemed to lose their ability to bind connective-tissue proteins.
OBJECTIVE: To elucidate whether microbial infections are involved in the etiology of intrauterine death. METHODS: One hundred four cases of stillbirth of unknown etiology and 96 age- and parity-matched referents with live births were analyzed with respect to microbial infection by cultures from the placenta, endocervix and internal organs of the fetuses, external sites of the babies and fetuses, and by serology for bacteria, viruses and Toxoplasma gondii. RESULTS: In 17 cases in whom no other infectious agent was diagnosed, Escherichia coli was isolated from the placenta and one or more internal fetal organs. Tests for Treponema pallidum and Toxoplasma gondii were more frequently positive in cases than in referents (O.R. 8.3 and 3.9, respectively). There was no increased risk for intrauterine death in women with human immunodeficiency virus, cytomegalovirus, herpes simplex virus or rubella virus. CONCLUSIONS: Our findings indicate that infections remain an important cause of intrauterine death in Zimbabwe.