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Biomedical subjects

B Larsen

Publications and source records attributed to B Larsen.

At least 289 records · Page 16Linked to original sources
PubMed1975

Bacterial growth inhibition by amniotic fluid. III. Demonstration of the variability of bacterial growth inhibition by amniotic fluid with a new plate-count technique.

The ability of 50 human amniotic fluid samples to inhibit the growth of Escherichia coli was measured with a new semimicro plate-count technique. A range from bacterial growth-sustaining fluid to bactericidal fluid was observed. When the inhibitory capacities of the fluid samples were correlated with gestational age, a progressive increase was obtained with maximum inhibitory capacity at 36 to 40 weeks. All fluid samples obtained before 20 weeks' gestation were capable of supporting bacterial growth. Fluid samples of 36 to 40 weeks' gestation were all bactericidal or bacteriostatic. More variability in inhibitory capacity was seen after 40 weeks, with an over-all loss of inhibition observed.

Amniocentesis↗
PubMed1975

Bacterial growth inhibition by amniotic fluid. IV. Studies on the nature of bacterial inhibition with the use of plate-count determinations.

Bacterial growth inhibition in amniotic fluid is associated with a compound or class of compounds which resembles antibacterial cationic peptides. The inhibitor studied in amniotic fluid is sensitive to treatment with monobasic and dibasic potassium phosphate, and the inhibitory activity of amniotic fluid is lost following adsorption onto bentomite. The inhibitory component in amniotic fluid interacts with bacterial cells by adsorption or is internalized by viable cells only. The inhibitory quality of amniotic fluid is not destroyed by heating to 100 degrees C. for 15 minutes, and this heat-stable inhibitory activity is associated with the compound or compounds which are phosphate sensitive. A possible mode of antibacterial action which is consistent with the data presented is discussed.

Adsorption↗
PubMed1975

Host resistance to intraamniotic infection.

In this review the mechanisms whereby amniotic fluid serves to protect the fetus from microbial disease have considered. It appears from the data reviewed that the principal mode of antibacterial action of amniotic fluid is bacteriostasis. Thus, the host is able to cope with a small number of organisms introduced into the amniotic cavity; however when the amniotic fluid is grossly contaminated the host resistance capacity of the amniotic fluid may be overwhelmed. This may be understood best by the quantitative description of disease theroized by Theobald Smith (94). Smith suggested that disease was a function of the number of organisms with which a host is initially infected multiplied by the virulence of the organism. The effects of the number and virulence of the organism in producing disease is lessened by the host's resistance capacity. This concept of disease is summarized by the equation: Disease equals (number) (virulence)/resistance. Although these parameters do not possess numeric values, it is possible to see at least conceptually their interplay with respect to intrauterine infection. For example, the number of organisms reaching the amniotic fluid may be increased by various modes, namely maternal viremia or bacteremia; premature rupture of the fetal membranes, antenatal vaginal examination and possibly intrauterine fetal monitoring. While these circumstances may result in increased rate of infection, some reports conversely indicate that minimal bacterial contamination in the amniotic fluid is not an extraordinary occurrence and may not result in any maternal or fetal complication (73,74). The intrinsic host resistance capacity of the amniotic fluid likewise represents an important part of the Smith equation for disease. We have found that amniotic fluids may vary in antibacterial efficacy from almost no inhibitory activity to profound bactericidal activity (90). Obviously, the likelihood of the production of disease by an equivalent inoculum of a particular organism would be quite different depending upon the intrinsic inhibitory capacity of the amniotic fluid. The measurement of the inhibitory capacity of amniotic fluid holds some promise for enabling a physician to determine which patients may be at special risk of intrauterine infection.

Amnion↗
PubMed1975

Mercaptoethanol-resistant human serum antibodies reacting with endotoxin from Neisseria gonorrhoeae.

Sera from fifty patients with gonorrhoea, thirty with non-specific urethritis, and eighty blood donors were treated with mercaptoethanol (ME) and examined by the indirect haemagglutination test for antibodies against endotoxin from gonococci. Erythrocytes sensitized with determinant a of endotoxin from Strains 8551, V, and VII, or determinant b from Strain V were used. The percentage of sera active in the haemagglutination test was much higher in the gonorrhoea group than in the controls. The geometric mean titre was also significantly higher in the gonorrhoea group. This applied for all four antigens used. Results obtained in an anti-globulin test indicated that the titre of ME-treated serum was determined by IgG antibodies against the endotoxin. Many sera had titres which varied according to the strain origin of the antigen used in the test. The sensitivity of tests for antibodies was increased by using endotoxin from several different strains of gonococci for the examination of each serum. A simplified procedure for determination of antibodies against endotoxin from different strains of gonococci was elaborated.

Animals↗