Biomedical subjects
Publications and source records attributed to A Ljungh.
Studies in human volunteers as well as animals clearly indicate that Campylobacter pylori is a key component in the development of type B-gastritis as well as in stomach- and duodenal ulcer disease. It seams likely that a better knowledge in how this microbe colonize the stomach mucosa will soon give us new and better possibilities to prevent and treat these diseases and their relapses.
Bone sialoprotein is selectively bound by Staphylococcus aureus cells isolated from patients suffering from infections of bone tissue [Rydén, C., Maxe, I., Franzén, A., Ljungh, A., Heinegård, D. & Rubin, K. (1987) Lancet II, 514]. In the present communication the binding of bone sialoprotein to staphylococcal cells is characterized in more detail. 125I-Labelled bone sialoprotein bound to suspended staphylococcal cells in a time-dependent, saturable and reversible manner. Binding was inhibited by unlabelled bone sialoprotein and by an amino-terminal CNBr fragment of bone sialoprotein that did not contain the eukaryotic cell-binding site. Binding was furthermore inhibited by lysates obtained from Escherichia coli lysogens carrying a lambda gt11 phage-encoding bone sialoprotein. In contrast, binding was not inhibited by a bacterial lysate from an osteopontin lambda gt11 lysogen, nor by N-linked oligosaccharide isolated from bone sialoprotein or by proteoglycan from rat chondrosarcoma containing clustered O-linked oligosaccharides of the same structure as those of bone sialoprotein. These results indicate that the major staphylococcal-binding site resides in the bone sialoprotein core protein and not in the carbohydrate side chains. No inhibition of bone sialoprotein binding could be detected for whole human serum or purified plasma proteins such as fibronectin, fibrinogen and IgG. Likewise, staphylococcal protein A or rat collagen type I did not inhibit the binding of bone sialoprotein. The latter results indicate that the binding site for bone sialoprotein on staphylococcal cells was not any of the hitherto described staphylococcal cell-surface proteins. Binding data indicated an average of 1000 bone-sialoprotein-binding sites/bacterial cell.
Among 250 S. aureus clinical isolates, the incidence of TSST-1 production was 18.0%. S. aureus var. hominis strains were predominant (95.6%), producing high levels of toxin in vitro, within the range of 0.6 to 4.3 micrograms/ml and exhibiting crystal violet binding with C/D pattern. No correlation was found between the level of TSST-1 production in vitro and the clinical course. Two (3.4%) of the var. bovis strains produced toxin in amounts less than 0.6 micrograms/ml and did not bind crystal violet. None of the 24 var. canis isolates produced TSST-1. Fifty five per cent of the isolates of phage group I produced TSST-1 and corresponded to 57.8% of the toxigenic strains. Two of the 250 patients developed toxic shock syndrome.
Full-thickness excision wounds infected with Staphylococcus hyicus, a pig pathogen, or Staphylococcus aureus, a human pathogen, were produced in pigs. The inoculated wounds were kept occluded for 2 days and then exposed and biopsied at intervals for 9 to 12 days. The exposed lesions were edematous and exudative. The S. aureus model was experimentally advantageous because the infection remained localized to the wound without systemic infection or signs of discomfort. The S. hyicus infection caused a rash with skin blisters; thus, its use is discouraged. The concentration of S. hyicus in the wound on day 2 was log 8.6 +/- 0.4 CFU/g (mean +/- standard deviation). On day 4 the mean was log 9.2. For S. aureus the values were log 8.0 +/- 0.9 on day 2 and 6.9 on day 4 (p less than 0.05). Of the 50 individual values in the S. aureus series, 45 were above log 5. The inflammatory reaction was more pronounced after the infection with S. hyicus, whereas with S. aureus the fibroblast response came earlier and was more pronounced. The model parallels typical clinical courses of staphylococcal infection.
Bacteria from full-thickness excision wounds with staphylococcal infection in the pig were cultured quantitatively. The bacterial concentration increased with the size of the inoculum, and after 2 days it had already reached a stable, maximal level of approximately log 8 CFU/g in the tissue. The correlation coefficient was 0.753 in comparing concentrations from superficial and deep biopsy halves and 0.145 from "surface wash" and superficial biopsies. The "within wound" sample distribution was logarithmic. The gain in precision when assessing the mean bacterial concentration from three instead of one biopsy was 45%. The coefficient of variation of between wound and within wound determinations was in the same range (i.e., 7.1-12.5%). Paired observations from a sample population with 7 sites (wounds) were needed to determine a 10% change in the bacterial concentration at a significance level of p less than 0.05, and a similar change could be determined from unpaired observations based on two populations with eleven sites.
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Smooth strains of Shigella dysenteriae type 1, Shigella flexneri, Shigella boydii, and Shigella sonnei which form pigmented colonies (Pcr+) on Congo red agar were virulent in the Sereny test. Smooth variants unable to bind Congo red (Pcr-) were avirulent. Measurements of dye uptake from solution showed that S. dysenteriae type 1 bound the most dye, followed in order of uptake by S. flexneri, S. boydii, and S. sonnei. Using the salt aggregation test (SAT) to determine cell surface hydrophobicity, we found the same order of species. The SAT could not, however, detect differences in surface properties between Pcr+ and Pcr- pairs of isogenic smooth strains. Enteroinvasive Escherichia coli strains used in the study showed SAT and Congo red-binding properties which were similar to those of the S. flexneri strains. A direct correlation was found between pigment-binding ability and the presence of the large 140-megadalton plasmid in S. flexneri, enteroinvasive E. coli, and S. boydii but not in S. dysenteriae type 1 or S. sonnei strains. Congo red interacted with outer membranes and outer membrane proteins of S. dysenteriae type 1 but not with lipopolysaccharides. However, rough mutants of Shigella species deficient in lipopolysaccharides bound Congo red and formed pigmented colonies, showing that dye binding as a virulence assay may be misinterpreted in such cases. There was complete correlation of the Pcr+ phenotype with virulence in the smooth strains in this study, suggesting that Congo red binding can be utilized as a quick and reliable alternative to the Sereny test.
10 Campylobacter pylori strains were screened for the presence of presumptive colonization factors by measuring cell surface hydrophobicity and haemagglutination. All 8 clinical isolates and 2 reference strains caused haemagglutination of rabbit, human and/or sheep erythrocytes in the presence of mannose. None of the strains expressed a hydrophobic cell surface. In preliminary experiments the haemagglutination could be inhibited with monosialogangliosides suggesting that these strains express sialic acid specific haemagglutinin(s) which could be involved in colonization of mucosal surfaces.
A 15-year-old girl with her first relapse of ulcerative colitis was treated with salicylazosulfapyridine, steroids, metronidazole and parenteral nutrition for 4 weeks without significant improvement. Her faecal specimens were negative for established intestinal pathogens, but strains of Escherichia coli producing Shiga-like toxin and expressing binding of fibronectin and collagen were repeatedly isolated. Neutralizing antibodies to Shiga-like toxin were detected in serum samples. Improvement was achieved during treatment with mecillinam to which the E. coli strains were sensitive.
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Sixty-three strains of Group D streptococci and viridans streptococci isolated from blood cultures during a two year period were typed to the species level with conventional biochemical tests and API Strep. Streptococcus faecalis was the most common species isolated followed by S. sanguis, S. mitis and S. constellatus (S. milleri). One of the two isolates of S. faecium was a contamination. The reported increasing frequency of this organism and other Group D and viridans streptococci as well as the association of S. bovis with malignant bowel disease indicate the need for full identification of streptococcal isolates from blood cultures. Pronounced surface hydrophobicity as measured with the salt aggregation test (SAT) was expressed by 59/63 (94%) of the blood culture isolates whereas strains isolated from commercial fermentation products and strains passaged several times were hydrophilic. In the presence of human serum albumin which binds to lipoteichoic acid only one strain decreased in surface hydrophobicity. The surface hydrophobicity of two strains even slightly increased indicating that lipoteichoic acid but marginally contributes to surface hydrophobicity of streptococcal cells from these species.
Two hundred and thirteen Escherichia coli strains originating in 12 countries were included in the study. Of these, 157 were classical enteropathogenic E. coli (EPEC) serotypes, 54 belonged to O138, O139 and O141 serogroups i.e. porcine edema disease strains and two strains were of serogroup O157 associated with haemorrhagic colitis. Surface hydrophobicity was determined by the salt aggregation test (SAT). Haemagglutination was assayed against erythrocytes of six animal species with strains grown under conditions known to promote expression of haemagglutinins. Sixty three EPEC strains were hydrophobic i.e. SAT value less than or equal to 0.1-1.6, and of these 15 did not haemagglutinate. Fimbriae were abundant on non-haemagglutinating strain 2178/58 (O26) when grown in nutrient broth. Fewer fimbriae per cell were present after growth on nutrient agar. Heat- and protease treatment reduces the surface hydrophobicity of EPEC strains. We propose that EPEC strains may carry a number of different surface proteins which determine binding to intestinal cells in a similar way as hydrophobic non-haemagglutinating fimbriae determine binding to rabbit intestinal brush borders, cf rabbit EPEC strain RDEC 1.
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Specific antisera for CFA/I (O78), CFA/II (O6) or enteropathogenic (EPEC) somatic O-antigens (serogroups O26, O86a and O111) were adsorbed to Staphylococcus aureus (strain Cowan I) to produce coagglutination reagents. Conventional agglutination tests with bacterial cells showed that antiserum against strain C922a-1 reacted with strain C91f, whereas anti-C91f did not agglutinate cells of strain C922a-1. Antisera raised against strains 4334f and C91f agglutinated their bacterial cells. Anti-303d did not react with strains C922a-1, 91f, nor with 4334f. Similar results were obtained with tests performed with COA-reagents of the above strains. Homologous antisera diluted 1:1000 gave positive COA reaction, after being adsorbed to Cowan I. Such diluted antisera gave negative agglutination reaction in the conventional agglutination tests. The COA test is at least 100 times more sensitive than the conventional agglutination tests. Hence, preparation of COA reagents implies practically economical use of antisera. Furthermore, the COA technique is much more sensitive and rapid (less than 5 min) than immunodiffusion test which takes greater than or equal to 24 h to read and in which large molecular weight antigens fail to diffuse in to agarose. 30 CFA/I strains (100%) gave COA positive reaction and only 25 CFA/II strains (71,4%) were positive with CFA/II COA reagents. The coagglutination technique was also applicable to identification of enteropathogenic E. coli by using somatic O-antigens (O26, O86a and O111) antisera.(ABSTRACT TRUNCATED AT 250 WORDS)