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Biomedical subjects

L G Burman

Publications and source records attributed to L G Burman.

At least 127 records · Page 7Linked to original sources
PubMed1978

Time- and media-saving testing and identification of microorganisms by multipoint inoculation on undivided agar plates.

Motility and various biochemical activities of isolates of bacteria and yeasts were tested on undivided agar plates by using a simple, manually operated multipoint inoculation apparatus that allowed the analysis of 25 isolates per 9-cm-diameter petri plate. Fermentation of all 17 carbohydrates tested as well as 13 other biochemical activities commonly used for identification of bacteria were readily demonstrated by the multipoint inoculation plate method, and the results agreed very well with those of conventional tube tests. In addition to speedy inoculation and low cost of materials, the multipoint inoculation plate method offers several other advantages when compared with conventional tube tests or with some of the manufactured test kits currently available for recognizing members of the family Enterobacteriaceae.

Agar↗
PubMed1977

Influence on motility of Escherichia coli and Salmonella typhimurium by a naturally occurring conjugative plasmid.

In a collection of 45 R-plasmids, one was found to be associated with loss of motility of its Escherichia coli K-12 and Salmonella typhimurium host bacteria when tested in conventional motility agar. Genetic experiments, as well as analyses of deoxyribonucleic acid, showed that inhibition of motility was caused by a conjugative plasmid that was separate from the R-plasmid. This second plasmid, named pUM5, was fi- and mediated the same type of sex pilus (F-like) as the accompanying R-plasmid but lacked resistance determinants. Preliminary studies indicated that bacterial cells carrying the motility inhibition plasmid pUM5 were still equipped with flagella. The mechanism by which flagellar action is disturbed by the plasmid is presently not known.

Bacteriophages↗
PubMed1977

Expression of R-plasmid functions during anaerobic growth of an Escherichia coli K-12 host.

The normal habitat of enteric bacteria is largely anaerobic. Expression of the three characteristic properties of R-plasmids, drug resistance, vegetative replication, and fertility, was therefore studied in Escherichia coli K-12 during anaerobiosis. Replication and drug resistance functions were not altered in the 45 R-plasmids studies, whereas the expression of fertility varied considerably among different R-plasmids during anaerobiosis. The R-plasmids could be divided into three groups, one showing a strong, the second a moderate, and the third little or no reduction of fertility by anaerobiosis. Plasmid-determined sensitivity to F-, N-, and I-specific phage, respectively, was well, although not absolutely, correlated with each of three groups mentioned. Anaerobiosis-aerobiosis appears to change the fertility of type F R-plasmids by influencing the degree of repression of their fertility functions such as the formation of sex pili. Although the minimum inhibitory concentrations of ampicillin, chloramphenicol, streptomycin, and tetracycline were unaltered by anaerobiosis, sulfonamide was found to be four- to eightfold less active under this condition in both resistant and sensitive strains. A surprisingly high frequency and uniformity of minimal inhibitory concentrations was observed for R-plasmid-mediated resistance to streptomycin and chloramphenicol.

Ampicillin↗
PubMed1977

R-plasmid transfer and its response to nalidixic acid.

The conjugational transfer efficiency of 41 wild-type R-plasmids was studied in Escherichia coli K-12. Type I R-plasmids were transferred at comparatively high and rather uniform frequencies, whereas type F R-plasmids showed less uniform and, on average, somewhat lower transfer frequencies. R-plasmids not mediating sensitivity to F-, I-, or N-specific phages showed moderate transfer frequencies, and type N R-plasmids showed very low transfer frequencies. Various lines of evidence suggest that a well-expressed, but functionally inefficient, conjugation apparatus is the cause of the poor transfer of type N R-plasmids in liquid medium. Nalidixic acid efficiently inhibited transfer of type I and particularly type F R-plasmids, whereas the transfer of type N plasmids was resistant to the drug. Type F and type I plasmids appear to depend on at least one host function for their transfer, namely, the nalidixic acid-sensitive reaction in vegetative chromosome replication, whereas type N plasmids are independent of this function.

Coliphages↗
PubMed1977

Resistance of Escherichia coli to penicillins: fine-structure mapping and dominance of chromosomal beta-lactamase mutations.

Seven Escherichia coli K-12 mutants with a lowered chromosomal beta-lactamase activity were analyzed genetically. The beta-lactamase-negative mutants isolated from ampA1-carrying strains (resistant to 10 microgram of ampicillin per ml) all carried genetic lesions very close to the ampA1 mutation, which was still present. In an earlier report, two of the mutations mediating a beta-lactamase-negative phenotype (L. G. Burman, T. Park, E. B. Linström, and H. G. Boman, J. Bacteriol. 116:123-130, 1973) were shown to have occurred in the structural gene for beta-lactamase, designated ampC. It is suggested that all beta-lactamase-negative mutants studied here were altered in ampC. The relative order of ampC mutations was (ampC1, ampC8)-ampC9-(ampC12, ampC14)-ampC11, and the gene order was found to be ampC-1mpA-purA. The ampA1 allele was dominant over its wild-type allele but acted only cis and not trans, suggesting that ampA is the promoter or operator region for ampC. A gene dosage effect was found for strains homozygous for ampA+ ampC+ or ampA1 ampC+. Heterozygotes carrying the ampC8 allele on the chromosome showed an apparent derepression of the episomal ampC allele, suggesting a role for beta-lactamase in its own regulation.

Alleles↗
PubMed1976

Autolysis of Neisseria gonorrhoeae.

Autolysis of Neisseria gonorrhoeae was studied under different conditions. It was found that low pH and temperature, as well as the presence of divalent cations, spermine, sucrose, and polyvinylpyrrolidone, stabilized nongrowing gonococci. Ethylenediaminetetraacetic acid alone promoted lysis, whereas lysozyme had only a limited additive effect. The autolytic behavior of gonococci appears to be connected with their prolonged cell division process. The relative dependence on the outer membrane and the peptidoglycan layer for the mechanical stability of gonococci is discussed.

Bacteriolysis↗
PubMed1975

Amplification of sex repressor function of one fi-+ R-factor during anaerobic growth of Escherichia coli.

It has been reported by Mitsuhashi (1965) that transfer of one R-factor was completely inhibited by anaerobic transfer conditions. In contrast, several workers have observed R-factor transfer, although at a reduced rate, in the animal intestines, a largely anaerobic environment. It is shown here that in vitro transfer of the R-factor R1 (F-type pilus, fi-+) in Escherichia coli K-12 is severely depressed, whereas transfer of R64 (I-type pilus, fi-minus) is slightly stimulated by anaerobiosis. Inhibition of R1 fertility is dependent on anaerobic conditions during pregrowth of the donor cells, whereas the oxygen tension during recipient pregrowth, transfer, and plating is of little importance. Anaerobic pregrowth has a less inhibitory effect on the fertility of R1drd19, a mutant of R1 having a defective sex repressor. The fi-+ property of R1 when introduced into F' or Hfr bacteria is amplified during anaerobic growth. These observations strongly indicate that the sex repressor is the mediator of the anaerobic fertility inhibition of the R-factor R1. This hypothesis was supported by studies of the formation of sex pili, the only gene product identified that is controlled by the sex repressor of R1. Using propagation of the F-type pilus-specific phage MS2 as a measure of the degree of sex piliation of a bacterial population, it is shown that in anaerobic cultures sex piliation due to R1 is strongly repressed, whereas piliation due to R1drd19 is repressed to a lesser extent. The possible survival value of the response of R1 towards oxygen tension is discussed.

Anaerobiosis↗
PubMed1973

Resistance of Escherichia coli to penicillins: identification of the structural gene for the chromosomal penicillinase.

A screening procedure was used to isolate a number of mutants of Escherichia coli K-12 with low penicillinase activity. By co-transduction with purA, three of the mutants were found to map near 82 min. Penicillinase was purified from one mutant and from a transductant with a temperature-sensitive enzyme. Comparison with wild-type penicillinase revealed similarities in the Ouchterlony immunodiffusion test but differences in the catalytic properties. It is concluded that the mutations have occurred in the structural gene of the chromosomal penicillinase (designated ampC). Purified enzyme and a temperature-sensitive mutant were used to investigate whether the penicillinase has a physiological function related to biosynthesis or breakdown of murein. No positive evidence for any such function was obtained.

Chromosome Mapping↗
PubMed1972

Murein and the outer penetration barrier of Escherichia coli K-12, Proteus mirabilis, and Pseudomonas aeruginosa.

A penetration barrier operating outside the periplasmic enzyme penicillinase was studied in an ampicillin-resistant mutant of Escherichia coli K-12. Growth in the presence of lysozyme and sublethal concentrations of ampicillin partially opened the barrier. This could be recorded as an increased penetration of penicillin G, sodium cholate, and rifampin to their respective targets. Brief treatments with tris(hydroxymethyl)aminomethane-ethylenediaminetetraacetic acid and sodium cholate effectively impaired the barrier against penicillin and also caused leakage of penicillinase. Wild-type E. coli K-12, Proteus mirabilis, and Pseudomonas aeruginosa also showed an increased sensitivity to cholate after treatment with penicillins. Electron micrographs showed that lysis by cholate was due to a distortion of the cytoplasmic membrane causing a leakage of protein and RNA from the cells to the medium. Physiological data indicated that the increased sensitivity to cholate induced by growth in the presence of ampicillin or lysozyme was due to effects upon the murein. This was supported by measurement of the incorporation of (3)H-diaminopimelic acid. These results indicate that the murein sacculus either is a part of the penetration barrier or is responsible for holding the structure of the outer membrane together.

Ampicillin↗
PubMed1971

Colicin tolerance induced by ampicillin or mutation to ampicillin resistance in a strain of Escherichia coli K-12.

A mutant (G11el) of Escherichia coli selected as being resistant to ampicillin and showing signs of an envelope defect was also found to be tolerant to colicins E2 and E3. The colicin tolerance of G11el could be partially repressed by Mg(2+) ions. Transition from tolerance to sensitivity and vice versa by shifting the concentration of Mg(2+) in the growth medium required several generations. This indicated that synthesis of new envelope material was needed for transition. Previous physiological results have indicated a change in the envelope lipopolysaccharide (LPS) of G11el. However, chemical analyses revealed no differences in carbohydrate composition between LPS from G11el and its parent strain G11al. Genetic experiments showed that the mutation in G11el is located at about 20 min on the E. coli K-12 chromosome. The mutation was dominant over wild type in partial diploids with the mutation located on the episome. Because colicin tolerance was the most striking phenotypic effect as a result of mutation in the actual locus, this gene will be named tolD until the exact gene product is known. Spheroplasts formed from G11al and G11el by ethylenediaminetetraacetate-lysozyme treatment did not adsorb colicin E2; however, penicillin spheroplasts of G11al and G11el were tolerant to colicin E2. Thus, colicin tolerance can be induced biochemically. It is suggested that colicin tolerance often is a secondary consequence of a change in the cell envelope.

Ampicillin↗
PubMed1970

Resistance of Escherichia coli to penicillins. 8. Physiology of a class II ampicillin-resistant mutant.

Class II ampicillin-resistant mutants of Escherichia coli are defined as having a twofold increase in penicillinase-mediated ampicillin resistance when determined by colony formation tests on plates. In this paper, one class II mutant has been compared to its parent strain. In liquid medium, the mutant was less resistant than the parent strain both in the absence and in the presence of R1 and R-factor mediating penicillinase activity. The penicillinase activity was found to be almost completely bound to the cells in the parent strain, whereas it was excreted to a great extent in the class II mutant strain. In liquid medium, resistance was well correlated to the cell-bound penicillinase activity, whereas the excreted penicillinases were also of great importance for survival on ampicillin plates. The mutant also had a changed resistance to a great number of other antibacterial drugs. The mutant was found to be more sensitive than the parent strain to osmotic shock, especially when treated with ethylenediaminetetraacetic acid or washed with sodium ions. However, the osmotic stability was restored by the presence of 1 mm Mg(2+) ions. The class II mutant was more sensitive than the parent strain to sodium cholate, and it adsorbed the phages T4 and T3-1 at a slower rate than did the parent strain. The two strains adsorbed T6 at the same rate. The class II phenotype could be gradually reversed by increasing concentrations of divalent cations. The pleiotropic changes in the phenotype are apparently unrelated to the specific targets for the antibacterial agents tested. They are secondary consequences of a cell envelope mutation. The findings indicate that the class II mutation mediates a structural change in the lipopolysaccharide of the cell envelope.

Ampicillin↗
PubMed1968

Resistance of Escherichia coli to penicillins. V. Physiological comparison of two isogenic strains, one with chromosomally and one with episomally mediated ampicillin resistance.

Two essentially isogenic strains of Escherichia coli K-12 were compared: D31 had chromosomally and D1-R1 episomally mediated resistance to ampicillin. The two strains had the same ability to form colonies on ampicillin plates, but in other tests they were quite different. In serial dilution tests as well as in exponentially growing cultures, D1-R1 was far more resistant to ampicillin than was D31. The inoculum effect with D1-R1 was large and with D31 was rather small. On plates, D31 was more resistant to penicillin G than was D1-R1. The penicillinase activity of buffer suspended cells against dl-ampicillin was 15 times higher for D1-R1 than for D31, but the two strains showed about the same rate of hydrolysis of penicillin G. With dl-ampicillin as substrate, for D1-R1 the apparent K(m) was 1.7 x 10(-4)m, whereas D31 gave a slightly sigmoid curve with a half-saturation concentration of about 5 x 10(-3)m. No induction of penicillinase activity was found. When the growth rate was varied by a factor of four, the amount of penicillinase per cell mass was constant in both D1-R1 and D31, whereas in two wild-type strains the amounts of penicillinase increased with increasing growth rates. With exponentially growing D1-R1, ampicillin disappearance started within 3 min, but at low ampicillin concentrations the rate was less than 10% of the rate of hydrolysis by buffer-suspended cells. Before D31 started hydrolysis, there was a lag period that lasted at least one generation and depended on the concentration of ampicillin. After this lag period, the rate of hydrolysis was 10 times higher than that observed with buffer-suspended cells. These differences between growing and nongrowing cells indicate that both the chromosomally and the episomally mediated penicillinases are controlled by some products present in growing cells.

Ampicillin↗
PubMedDate not supplied

Pathogenesis of Escherichia coli cystitis and pyelonephritis: apparent lack of significance of bacterial motility and chemotaxis towards human urine.

All 45 microscopically motile urinary isolates tested here (37 Escherichia coli, two Enterobacter cloacae, two Citrobacter freundii, three Proteus mirabilis and one Proteus morganii) were strongly attracted to fresh human urine in a capillary chemotaxis assay. This observation suggested that urine taxis of gram-negative bacteria promotes their invasion of the human lower urinary tract and their ascension to the kidney(s). However, the incidence of motile isolates and their activity in urine taxis assays were similar for fecal E. coli isolates, for isolates from patients with recurrent cystitis and from patients with presumed pyelonephritis (E. coli blood isolates with concomitant E. coli bacteriuria). Thus, the present study of E. coli did not support the hypothesis that bacterial motility is a virulence factor in urinary tract infection.

Bacteriuria↗
PubMedDate not supplied

Importance of the environment and the faecal flora of infants, nursing staff and parents as sources of gram-negative bacteria colonizing newborns in three neonatal wards.

Gram-negative bacteria are an important cause of invasive infection among neonates. In this study a novel fingerprinting method was used for the first time to assess the importance of various potential reservoirs of the major gram-negative enterobacteria that colonized 46 consecutive infants in three neonatal special care units during a three to four week period. Such bacteria were isolated from the oropharynx, umbilical cord and faeces in 24%, 33% and 100% of the infants, respectively. Klebsiella/Enterobacter spp. dominated over Escherichia coli and spreading (shared) over sporadic strains. Sixty-one percent of the neonates were colonized with at least one and up to six different strains shown to exist in the ward, mainly in other infants. Environmental reservoirs and the faecal flora of mothers and staff were of minor importance. Vertical transmission occurred in 12% of vaginally delivered infants and in 0% of those delivered by caesarean section.

Age Factors↗
PubMedDate not supplied

Epidemiology and attack index of gram-negative bacteria causing invasive infection in three special-care neonatal units and risk factors for infection.

Of 13 consecutive episodes of gram-negative septicemia (Escherichia coli eight, Klebsiella oxytoca four, Klebsiella pneumoniae one) among 113 infants in three special-care neonatal units studied, five episodes were epidemiologically related according to a novel fingerprinting method for enterobacteria. In ten episodes the invasive phenotype was found in the fecal flora of up to 54% of the fellow infants in the same ward and for periods of up to 70 days. Two units exchanged patients, which further promoted the transmission of invasive strains. The attack index was highest for certain E. coli strains, generally low for K. oxytoca strains, but lowest for other E. coli strains. The infants contracting septicemia had lower birth weight (p = 0.04) or were more often classified as high-risk infants than matched non-infected fecal carriers of the invasive strains (p = 0.04). In summary, gram-negative neonatal septicemia was either due to an apparently high-virulent strain capable of attacking the single full-term infant carrier or a high-colonizing phenotype of lower apparent virulence, which occasionally attacked a high-risk infant among a large number of infants colonized.

Birth Weight↗