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Biomedical subjects

I Gadó

Publications and source records attributed to I Gadó.

34 records · Page 2Linked to original sources

In vitro and in vivo (LD50) effects of human lactoferrin on bacteria.

The in vitro and in vivo effects of human lactoferrin (LF), apoLF, iron saturated LF and of different iron containing compounds (ferric chloride, ferric sodium citrate) were studied on Escherichia coli, Salmonella typhi-murium and Pseudomonas aeruginosa reference and wild-type strains with well-defined virulence markers (i.e. enterochelin, aerobactin production). LF exert in vitro antibacterial effect, and iron-free Vogel-Bonner medium proved to be suitable for its determination. The effect of intraperitoneally administered LF could not be evaluated because of its aspecificity, as any treatment (e.g. saline, Ringer solution) before bacterial challenge activated macrophages. In contrast to the in vitro results, intramuscular challenge failed to inhibit bacterial growth in vivo, as siderophores produced by bacteria were able to acquire lactoferrin-bound iron. LF treatment, like iron addition, enhanced the virulence of bacteria in mice, whereas apoLF - using iron present in the body fluids - turned to LF being unable to acquire siderophore-bound iron from bacteria. These findings do not support the literary view that LF would be useful as an antimicrobial drug.

Animals↗

Association of virulence markers with animal pathogenicity of Escherichia coli in different models.

Employing chicken and several strains of mice, different routes (intraperitoneal, subcutaneous) of infections and isogenic pairs of strains, association of virulence markers with animal pathogenicity was studied in Escherichia coli. Mouse virulence of avian strains was less significant than the lethality for chicks of human strains. LD50 in various animals did not differ significantly. Strains with antigen K1 were more virulent for mice than their K1- derivatives. Loss of haemolysin (Hly), mannose resistant haemagglutinating capacity or antigen K5 less markedly decreased the virulence. As opposed to other virulence factors, increased virulence of K1+ strains could also be demonstrated in mouse sepsis assay based on bacterial counts in the liver. Loss of Hly alone did not influence the persistence in the liver, however, these strains killed less mice. Aerobactin acts together with other factors, it is not per se a virulence factor. In organotropic experiments 19 strains out of 36 belonging to serotypes O7:K1:H-, O18:K1:H-, O78:H- and spontaneously agglutinable K1+ cultures, caused ophthalmitis with purulent discharge, and 4 out of 22 strains that belonged to serotype O78:H- induced uncoordinated movement of mice. Because of its special organotropic affinity to the brain and as it caused two epidemics of meningitis among newborns in Hungary, serotype O78:H- has a special pathogenic property and differs from other O78 strains that were isolated in other countries.

Animals↗

The frequency of aerobactin production and its effect on the pathogenicity of human Escherichia coli strains.

A total of 981 human Escherichia coli strains (including 632 strains isolated between 1979 and 1983 and 349 strains isolated in 1987) was examined for aerobactin production by biological qualitative test. Aerobactin positivity was found in 55.1% and 47.3%, respectively, in the two groups of strains, while enterochelin was produced nearly by 100% of the strains. Aerobactin production was significantly more frequent than the average among blood and CSF strains samples and serogroup O2 and O6 strains. Aerobactin was more frequent among isolates with K1 or K5 antigens and producing haemolysin and mannose-resistant haemagglutination than among the ones lacking these virulence factors. A strict correlation was found between the pathogenicity in mouse following intraperitoneal infection and the frequency of aerobactin production. The distribution of the LD50 values of the aerobactin positive strains was shifted towards the lower values comparing to the aerobactin negative ones, proving statistically the effect of aerobactin in the increase of pathogenicity.

Drug Resistance, Microbial↗

Curing of plasmid pE194 with novobiocin and coumermycin A1 in Bacillus subtilis and Staphylococcus aureus.

Plasmid pE194 determining macrolide-lincosamid-streptogramin B resistance could be eliminated with novobiocin and coumermycin A1 in Bacillus subtilis and Staphylococcus aureus. In both organisms the curing effect depended on the temperature. In the case of Staphylococcus aureus it increased very much at high temperatures, while in the case of Bacillus subtilis only a moderate increase could be observed. The curing activity of coumermycin was substantially weaker than that of novobiocin in both bacteria. This difference decreased at higher temperatures only in Staphylococcus aureus. In Bacillus subtilis the curing with novobiocin could be antagonized with coumermycin in accordance with the growth experiments reported previously.

Aminocoumarins↗

Effect of some aminoglycosides upon a drug dependent Escherichia coli strain.

Escherichia coli Sd-4-73 drug dependent strain was sensitive to kanamycin, gentamicin and neomycin in the absence of drugs stimulating cell multiplication. This senstivity was not considerably influenced by streptomycin, while paromomycin afforded protection against both bacteriostatic and bactericidal effects. The paromomycin concentration optimum for protection was different from its concentration optimum for multiplication.

Aminoglycosides↗