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At least 1,135 records · Page 63Linked to original sources
PubMed1981

Towards serodiagnosis of Serratia marcescens infections: examination of sera from noninfected patients and from experimentally infected rabbits for anti-H and anti-O antibodies; S. marcescens O-antigen cross-reactions with those of other enterobacteriaceae.

Sera from 100 patients not infected with Serratia marcescens at the time of hospital admission lacked detectable H-immobilizing antibodies against all 20 currently recognized H-antigens of this microorganism. However, various patient sera revealed elevated titers of O-agglutinins against several of the 20 O-antigens of S. marcescens, in a particular O-antigens, O1, O3, O4, O5, O7, O8, O10, O11, O16, O17, O18, O19, and O20. Rabbit anti-Shigella serogroup B immune serum cross-reacted with S. marcescens O-antigens O1 and O10; anti-Shigella serogroup C serum cross-reacted weakly with S. marcescens O-antigen O8. Conversely, rabbit anti-S. marcescens O1 and O10 immune sera cross-reacted with a clinical isolate of Shigella flexneri. None of the anti-S. marcescens O1-O20 rabbit immune sera reacted with commercial febrile antigens of Salmonella serogroups A, B, C1,2, D, E1,2,3,4, Brucella abortus, Francisella tularensis, and Proteus OX19. However, a reference strain of Salmonella typhi (9;d,-) was agglutinated by anti S. marcescens anti-O8 and O10 sera, a reference strain of S. paratyphi B (4,5;-,-) weakly by anti-S. marcescens O8 serum, and a reference strain of S. paratyphi C (6,8;-,-) by anti-S. marcescens anti-O10 and O16 rabbit immune sera. None of the anti-S. marcescens H-antisera cross-reacted with H-antigens of S. typhi (o;d,-), S. paratyphi A (1,2;a,-), S. paratyphi B (4,5;b,0), S. choleraesuis (6,7;-,1,5), typhimurium (4,5;,i,-), and S. enteritidis (9;gm,-). Yersinia enterocolitica reference strain Ye 75 (OI = O3) eas agglutinated weakly by anti-S. marcescens O2 serum, whereas Y. enterocolitica reference strain Ye 373 (OV = O9) cross-reacted with S. marcescens anti-O5 rabbit immune serum. Intravenously and tissue cage-infected rabbits developed anti-H and anti-O-antibodies within 5 to 12 days after infection with representative test strains of S. marcescens. Therefore, it is suggested that the serodiagnosis of human S. marcescens infections consist of serial monitoring of both anti-H and anti-O agglutinins, because determinations of the latter alone might yield false-positive, i.e., potentially misleading results.

Agglutination Tests↗
PubMed1994

Crystallization of monodisperse maltoporin from wild-type and mutant strains of various Enterobacteriaceae.

Maltoporin has been purified by affinity chromatography on starch gel columns. This single-step procedure affords the rapid purification of active protein from wild-type and mutants of E. coli, and from other Gram-negative bacteria. The monodisperse protein was crystallized under various conditions. Several preparations have yielded crystals amendable to X-ray analysis, notably a single cysteine substitution, S57C.

Bacterial Outer Membrane Proteins↗
PubMed2000

Interaction of Xenorhabdus nematophilus (Enterobacteriaceae) with the antimicrobial defenses of the house cricket, Acheta domesticus.

Fifth instar Acheta domesticus nymphs exhibited a decline in total hemocyte counts during the first hour of exposure to dead Xenorhabdus nematophilus; the bacterial level in the hemolymph also declined during this time. Thereafter bacterial numbers in the hemolymph increased as the level of damaged hemocytes increased. The bacteria lowered phenoloxidase activity in vivo by initially reducing the number of hemocytes containing prophenoloxidase and later by inhibiting enzyme activation. Preincubating X. nematophilus in hemolymph with active phenoloxidase in vitro accelerated the removal of the bacteria from the hemolymph in vivo which may be due to modification of the bacterial surface by serine proteases. Lysozyme activity increased in bacteria-injected insects in parallel with an increase in counts of damaged hemocytes; most of the enzyme was located in hemocytes. Lipopolysaccharides of X. nematophilus caused changes in hemocyte counts and phenoloxidase and lysozyme levels comparable to whole bacteria. Lipopolysaccharides also slowed the removal rate of the bacteria from, and accelerated bacterial emergence into, the hemolymph.

Animals↗
PubMed1992

Role of IS1 in the conversion of virulence (Vi) antigen expression in Enterobacteriaceae.

When Escherichia coli HB101 harbors pWR127, a plasmid comprising the viaB gene from Citrobacter freundii WR7004 and the ColE1-derived pACKC1, the strain produces the virulence (Vi) antigen. Vi antigen expression is abolished (Vi- phenotype), however, when an IS1 or IS1-like DNA element inserts into the viaB region. To determine the sites of IS1 insertion, pWR127 DNAs extracted from 95 independently isolated Vi- strains were analyzed by digestion with the restriction endonuclease PstI and agarose gel electrophoresis. Ten insertion sites were found distributed non-randomly in an area of about 1.3 kb. Nine Vi+ strains (two Citrobacter, two E. coli, and five Salmonella strains), four of which contain pWR127, were then tested for the presence of IS1 by DNA-DNA hybridization. Of the nine strains, five were stable Vi+ and did not contain IS1. The other four which generated Vi- strains, contained IS1. When pRR134, a plasmid that contains IS1 was transferred into a stable Vi+ Salmonella typhimurium strain carrying pWR127 (OU5140), Vi- strains were produced from which pWR127 derivatives carrying IS1 inserts could be isolated. It appears, therefore, that the presence of an IS1 or IS1-like element in a strain is required for conversion of the Vi+ expression state to the Vi- expression state.

Antigens, Bacterial↗
PubMedDate not supplied

The in vitro activity and beta-lactamase stability of cefpirome (HR 810), a pyridine cephalosporin agent active against staphylococci, Enterobacteriaceae and Pseudomonas aeruginosa.

The in vitro activity of cefpirome, a new cyclopyridinium cephalosporin, was evaluated against 947 aerobic and anaerobic bacteria. Cefpirome inhibited 90% of Escherichia coli, Klebsiella spp., Citrobacter diversus, Morganella morganii, Proteus vulgaris, Proteus mirabilis, Aeromonas spp., Salmonella spp., Shigella spp. and Haemophilus and Neisseria species at less than or equal to 0.4 mg/l. It had activity comparable to that of cefotaxime, ceftizoxime, ceftazidime, aztreonam, and moxalactam against these species. Only a few Citrobacter freundii, Enterobacter spp. and Serratia marcescens had MICs above 3.1 mg/l. The activity of cefpirome against Pseudomonas aeruginosa, 90% MIC of 12.5 mg/l, was superior to piperacillin, moxalactam, cefotaxime and cefoperazone. The 90% MIC against Staphylococcus aureus was 0.8 mg/l, but methicillin-resistant staphylococci were not inhibited. Cefpirome was not significantly hydrolyzed by most plasmid beta-lactamases (TEM, SHV-1, PSE, OXA) nor by chromosomal enzymes (P99, Branhamella catarrhalis, K1). Cefpirome did not inhibit chromosomal or plasmid beta-lactamases. Mice systemically infected with E. coli, Klebsiella pneumoniae, P. aeruginosa and S. aureus were protected by concentrations of cefpirome ranging from 0.85 mg/kg for K. pneumoniae to 4.467 mg/kg for P. aeruginosa.

Animals↗