- Volume 39, Issue 3, 1993
Volume 39, Issue 3, 1993
- Articles
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The serotypes of Streptococcus pyogenes present in Britain during 1980—1990 and their association with disease
More LessSummaryA total of 16 909 cultures of Streptococcus pyogenes (Lancefield group A) isolated in Britain during 1980—90 were examined for T- and M-protein antigens. One or other M antigen was detected in 92.6% of the strains. The numbers of isolates of some serotypes, such as M3 and M12, did not show great variation from year-to-year, whereas there were nationwide epidemics, extending over several years, caused by strains of serotypes M1 and M49. Isolates of serotypes M1 and M3 were associated particularly with invasive disease and fatal infections. Representatives of serotypes M80, M81 and the provisional types PT180, PT1658 and PT5757 were isolated most often from cases of pyoderma. Erythromycin resistance was detected in 30 serotypes but one half of all of the resistant isolates belonged to serotype M4.
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Identity of viridans streptococci isolated from cases of infective endocarditis
More LessSummaryThe oral streptococci have undergone considerable taxonomic revision in recent years but there is still little information concerning associations between the newly defined species and disease. This study examined the identities of 47 strains of oral streptococci collected from 42 confirmed cases of infective endocarditis. By means of recently described physiological schemes, the most common species identified were Streptococcus sanguis sensu stricto (31.9%), S. oralis (29.8%) and S. gordonii (12.7%). Other related species including S. mitis and “S. parasanguis” were less common. This indicates that attention should be focused on S. sanguis sensu stricto and S. oralis when considering possible pathogenic mechanisms involved in viridans streptococcal endocarditis.
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Effect of co-aggregation on the pathogenicity of oral bacteria
More LessSummaryThe pathogenicity of oral bacteria was studied by measuring the development of subcutaneous abscesses in mice after infection with Actinomyces viscosus and Streptococcus mitis either singly or as co-aggregated pairs. Heat-treated cells were also tested. The pathogenicity of the co-aggregates was examined in various viable and heat-treated combinations of the two bacterial species. More abscesses were formed by A. viscosus than S. mitis at all the bacterial concentrations tested. Also, abscess formation by co-aggregates of the two strains produced a higher percentage of abscess formation than those caused by infection with pure suspensions of A. viscosus or S. mitis. Co-aggregated cells were more resistant to phagocytosis and killing by neutrophils in vitro and in vivo. Furthermore, A. viscosus in co-aggregates were resistant to killing after engulfment by neutrophils. These results suggest that oral bacteria that are able to co-aggregate may resist phagocytosis, and this ability may be linked with pathogenicity.
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Host response to coagulase-negative staphylococci in abscesses induced within mice
More LessSummaryA model whereby a known number of coagulase-negative staphylococci were packed into capillary tubes and implanted into the peritoneal cavity of mice proved to be a satisfactory method for generating abscesses that could be easily removed free of extraneous host tissue, and that permitted measurement of the survival of the organisms and accumulation of lipid in the lesion. Strains of S. epidermidis, S. schleiferi and S. lugdunensis, differing in their ability to produce fatty acid modifying enzyme (FAME) and lipase, were packed into either glass or plastic capillary tubes and used to generate abscesses. Abscesses produced by S. aureus served as comparators. Lipids accumulated within the abscesses caused by S. aureus in the same manner as previously described for the organism inoculated without tubes.1 Lipids also accumulated within abscesses produced by all the coagulase-negative staphylococci, but the rate of accumulation was slower and the lipid droplets were smaller than seen with S. aureus. The mobilisation of lipid did not differ in response to cocci in plastic or glass tubes. Strains of S. epidermidis and S. schleiferi producing FAME and lipase were better able to survive within abscesses than strains unable to produce these enzymes. However, FAME and lipase production did not appear to be the sole determinants of survival within abscesses. Regardless of whether they produced FAME and lipase, the two S. epidermidis strains were significantly better able to survive within plastic tubes than in glass tubes. No such difference was seen with S. aureus between plastic and glass tubes.
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Chemiluminescence of human polymorphonuclear leucocytes after stimulation with whole cells and cell-wall components of Staphylococcus epidermidis
More LessSummaryThe purpose of this study was to define cell-wall components of Staphylococcus epidermidis responsible for activation of human polymorphonuclear leucocytes (PMNL). Metabolic activation of PMNL was determined by chemiluminescence (CL). Purified peptidoglycan (PG) induced a concentration-dependent metabolic burst in PMNL. The minimal concentration needed for CL induction was 1 μg/ml. Comparison between different S. epidermidis strains showed variation in the capacity to induce CL in PMNL. Purified PG induced a higher CL response in PMNL than its intact parent strain; this effect was found in all S. epidermidis strains. Lipoteichoic acid (LTA), PG stem peptide and muramyldipeptide (MDP) did not induce CL; teichoic acid induced a CL response only at very high concentrations. No differences in CL inducing capacity were found between PG, crude cell walls, and purified cell walls of S. epidermidis. Sonication of PG strongly diminished CL-inducing capacity. PG treatment with mutanolysin immediately resulted in decreased CL-inducing capacity. Treatment of PG with S. aureus lytic enzyme (SALE) 10 μg/ml for up to 15 min enhanced the CL response to PMNL; a similar increase in CL was induced by PG treated with SALE at 1 μg/ml for up to 120 min. Beyond these times, a continuous decrease in PG-induced CL was observed. In conclusion, PG was found to be the major cell-wall component of S. epidermidis involved in CL induction. Moreover, a minimal fragment size or a specific tertiary structure of PG, or both, is required for metabolic activation of PMNL.
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An electronmicroscope study of glycopeptide antibiotic-resistant strains of Staphylococcus epidermidis
More LessSummaryUltra-thin section transmission electronmicroscopy revealed that two of three glycopeptide-resistant strains of Staphylococcus epidermidis had abnormally thick cell walls, a finding consistent with the view that the reduction in susceptibility may result from the overproduction of glycopeptide binding sites within the cell-wall peptidoglycan. The third resistant strain had a slightly thickened cell wall with an irregular, roughened outline; this strain also underwent autolysis on prolonged incubation on blood agar and the resistance may be associated with abnormal cell-wall synthesis. Sub-MIC concentrations of vancomycin and teicoplanin caused surface damage to a proportion of cocci able to grow in the presence of antibiotic. Exposure to teicoplanin was additionally associated with the formation of filamentous forms and variable amounts of extracellular material. Transmission electron-microscopy showed that both antibiotics exerted effects within the bacterial cytoplasm of the resistant strains that were not seen in an NCTC control strain: Intracellular lamellae and structures resembling mesosomes were observed in the former. These effects were more noticeable in cocci exposed to vancomycin. Bacteria exposed to teicoplanin often showed abnormal septation and, in some preparations, a double-layered cell wall.
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Characterisation of Plesiomonas shigelloides strains that share type-specific antigen with Shigella flexneri 6 and common group 1 antigen with Shigella flexneri spp. and Shigella dysenteriae 1
SummaryThree strains of Plesiomonas shigelloides isolated from patients with diarrhoea were agglutinated with Shigella flexneri 6 antiserum in slide and tube tests. All the strains were also agglutinated with a monoclonal antibody to the common group 1 antigen shared between S. flexneri serotypes and S. dysenteriae type 1. Further studies with one strain also showed sharing of antigenicity in an enzyme-linked immunosorbent assay. The results suggest that the strains share type-specific antigen with S. flexneri 6 and the common group 1 antigen with S. flexneri serotypes and S. dysenteriae 1. The sharing of antigens may have implications for cross-protection. One strain adhered to HEp-2 cell monolayers. None of the strains contained high mol. wt plasmids and there was no sequence homology with the invasiveness plasmid of Shigella spp. in DNA probe hybridisation. They were susceptible to the commonly used antibiotics. However, they possessed four other virulence-associated properties of Shigella spp. that included Congo-red biding, hydrophobicity, toxicity to HeLa cells and HEp-2 cell invasiveness (although they gave negative results in the Sereny test for invasiveness). These data suggest that the three unique strains might be considered pathogenic. Studies in animal models and human volunteers would be necessary to establish their pathogenic potential.
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Transferrin-binding ability of invasive and commensal isolates of Haemophilus spp.
More LessSummaryHaemophilus influenzae type b expresses an inducible siderophore-independent iron-acquisition system that depends on a direct interaction between human transferrin and specific iron-regulated transferrin-binding outer-membrane proteins. To evaluate the importance of this iron-acquisition system amongst haemophili, 156 isolates of Haemophilus spp. (78 commensal isolates and 78 isolates from invasive infections) were examined for their ability to bind transferrin. Of the 78 invasive isolates, all of which were H. influenzae type b, 71 (91%) were capable of binding transferrin, with 57 (73%) binding transferrin constitutively (i.e., even when grown in an iron-sufficient medium). In contrast, only 11 (14%) of the commensal isolates bound transferrin constitutively, with a further 16 (21%) binding transferrin only after growth in an iron-deficient medium. Of the 27 commensal strains that were capable of binding transferrin, 12 were H. parainfluenzae biotype III, 14 were non-typable H. influenzae, and one was H. parahaemolyticus. None of the H. influenzae type b invasive or commensal isolates showed evidence of siderophore production, but 50 (66%) of the remaining 76 commensal isolates appeared to produce an iron chelator. Thus, while not a universal characteristic, detectable transferrin-binding was associated strongly with H. influenzae type b isolates from invasive infections, and was also recognised for the first time in isolates of H. parainfluenzae and H. parahaemolyticus.
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The cleavage of immunoglobulin G in vitro and in vivo by a proteinase secreted by the urinary tract pathogen Proteus mirabilis
More LessSummaryEighteen different strains of Proteus mirabilis were all shown to produce an EDTA-sensitive proteinase of c. 50 kDa that cleaved the heavy chain, but not the light chain, of IgG. Digestion of pure IgG with small amounts of pure P. mirabilis proteinase generated Fabc’2 and Fab’2 fragments; greater amounts generated Fab and Fc fragments that were comparable in size to those generated by pepsin and papain, respectively. Incubation of neutrophils with IgG digested with P. mirabilis proteinase or papain resulted in a marked decrease in the respiratory burst activity of the neutrophils that coincided with cleavage of the IgG into Fab and Fc fragments. Analysis of urine from patients with P. mirabilis urinary tract infection revealed in many the presence of Fab and Fc fragments of IgG indistinguishable in size from those generated by P. mirabilis proteinase. These results indicate that, in P. mirabilis urinary tract infections, the proteinase is secreted and cleaves IgG to fragments that have defective immune effector functions, thereby limiting the effectiveness of the immune response.
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Application of the polymerase chain reaction to the diagnosis of candidosis by amplification of an HSP 90 gene fragment
More LessSummaryA 317-base pair (bp) fragment of the Candida albicans heat shock protein 90 (HSP 90) gene was amplified by the polymerase chain reaction (PCR) for detection of C. albicans DNA in clinical specimens. One hundred specimens were examined including swabs (39), urines (36), peritoneal fluid (9), pus (8) and blood or serum (8): 23% gave positive results with routine culture, 31% with extended broth culture and 37% with PCR. The amplified product was identified by hybridisation with a radiolabelled internal probe and their restriction enzyme digest patterns (SspI, HaeIII, EcoRI, RsaI and XhoI), which could be predicted from the known sequence of HSP 90. C. albicans DNA gave the characteristic 317-bp band and specifically hybridised with restriction enzyme-digested candidal DNA. DNA from other sources intermittently gave multiple faint bands especially in the presence of high concentrations of DNA, but these could be readily distinguished. The method was sensitive to 50 pg of DNA (5 pg with radiolabelled probing) and 100 cfu of C. albicans.
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