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Biomedical subjects

V Lindén

Publications and source records attributed to V Lindén.

At least 19 recordsLinked to original sources
PubMed1984

Transient increase of early-onset group B streptococcal septicemia.

Since 1976, all cases of neonatal group B streptococcal (GBS) septicemia/meningitis have been registered at two Swedish University Hospitals. A significant increase in the number of infants contracting early-onset GBS-septicemia was noticed at one clinic in 1981, from 1-3 cases per yr to 8 cases. Six months prior to this increase the number of deliveries increased from about 1500 per yr to nearly 3000 per yr. It is suggested that external factors, e.g., subtle changes in the nursing combined with an extended disadvantage at the ward might influence the development of early-onset GBS septicemia.

Humans↗
PubMed1984

Human IgG antibodies to carbohydrate and protein antigens in mouse protection tests with group B streptococci.

The protective effect of four commercial human gammaglobulin batches (I-IV) in mice was studied using six different strains of group B streptococci (GBS): types Ia; Ib; II, R-protein negative (R-); II, R+; III, R-; and III, R+. Each mouse received 1.0 ml gammaglobulin and 0.5 ml bacteria, 10(6)-10(8) colony forming units (CFU). There was a close correlation between antibody levels measured by the use of radiolabeled protein A and the mouse-protective effect of the gamma-globulins. The mouse-protection tests demonstrated that batch I protected against GBS types Ia and III, R- at low concentration (65 mg/kg mouse weight), against type Ib at medium (260 mg/kg) and against type III, R+ at high concentration. Batch IV protected against types Ia and Ib, although the doses were four times higher than those in batch I, but did not protect against type III, R+. There was no mouse protection by any of the batches against type II. Antibody levels against Ibc and R, protein antigens, were substantially lower in batch IV. Because the results of these mouse-protection studies indicate the importance of such antibodies against protein antigens, batches I-III might be more useful for therapy of neonatal GBS-septicemia.

Animals↗
PubMed1983

The significance of group B streptococci in neonatal pneumonia.

Thirty-eight infants admitted to a neonatal intensive care unit because of pneumonia (14 patients) and pulmonary maladaption syndrome (PMA) (24 patients) were included in the study. Samples of potentially pathogenic, facultatively anaerobic bacteria were taken from the external ear, blood, throat, nasopharynx, umbilicus and gastric aspirates of the children, and from urethra and cervix of the mothers. Group B streptococci (GBS) and Escherichia coli were the only potentially pathogenic bacteria isolated from the infants. Out of 14 infants with pneumonia 11 (79%) harboured one of these bacteria, in contrast to 3 out of 24 (13%) with PMA (P less than 0.001). GBS was found in 8/14 infants with pneumonia and in 1/24 infants with PMA (P less than 0.001). The respective frequencies for Escherichia coli were 3/14 and 2/24 (not significant). The infant and/or the mother in 10/14 pneumonia cases harboured GBS, in contrast to 4/24 pairs in the PMA group (P less than 0.001). The levels of antibodies against GBS in sera of mothers to infants with pneumonia did not differ from the antibody levels in control sera (parturient GBS-carriers giving birth to healthy infants). The results gave evidence for an important manifestation of neonatal GBS-infection: pneumonia without septicemia. The incidence of the disease is estimated to be 1:25 parturient GBS-carriers. Finally, maternal fever, gestational age above 42 weeks, more severe respiratory difficulties and the occurrence of severe changes in fetal heart rate during the first stage of labour were found to be typical characteristics of pneumonia, as compared to PMA.

Escherichia coli↗
PubMed1983

Chlorhexidine for prevention of neonatal colonization with group B streptococci. I. In vitro effect of chlorhexidine on group B streptococci.

Forty-three strains of group B streptococci (GBS) of types Ia, Ib, II and III were tested for susceptibility to chlorhexidine in concentrations ranging from 256 to 0.25 mg/l using the agar and tube dilution methods. The strains showed minimum inhibitory concentration (MIC) values ranging from 0.5 to 1 mg/l. Serum added to the test medium (50%) increased the MIC values to 4-8 mg/l, while amniotic fluid (50%) had almost no effect, increasing the values to 1-2 mg/l. The minimum bactericidal concentration (MBC) ranged from 1 to 5 mg/l. The killing kinetics were related to the concentration of chlorhexidine and the length of exposure. For example, at a concentration of 63 mg/l, 7 h were required for a bactericidal effect in broth, as compared to 1 h at 500 mg/l chlorhexidine. 200 mg/l chlordexidine had no effect on the adherence of two GBS strains to vaginal epithelial cells, and no effect on the phagocytosis of GBS with mouse peritoneal macrophages.

Bacteriolysis↗
PubMed1983

Mouse-protective effect of rabbit anti-R-protein antibodies against group B streptococci type II carrying R-protein. Lack of effect on type III carrying R-protein.

R-proteins was isolated by affinity chromatography from an alkaline extract of group B streptococci, type III. the identity of the protein was demonstrated by pepsin- and trypsin-treatment and in double diffusion-in-gel with antisera from other laboratories. A monospecific rabbit antiserum against the R-protein was studied in mouse-protection tests, using three type II strains with R-protein and three without, and six type III strains, of which four carried R-protein. the serum protected animals from infection by type II strains carrying R-protein, but not against any of the other strains. The capacity of anti-R-protein serum to opsonize type II strains carrying R-protein was also demonstrated in phagocytosis experiments with mouse peritoneal macrophages. Studies with radio-labelled protein A and anti-R-protein antibodies showed that R-protein was localized on the surface of both type II and type III groups B streptococci. Taken together, the results suggest that type II group B streptococci should be divided into two subtypes, II, R+ and II, R-.

Animals↗
PubMed1983

The occurrence of R-protein among isolates of group B streptococci from human sources.

A total of 241 clinical isolates of group B streptococci were tested for presence of R-protein by applying the double diffusion-in-gel technique on streptococcal extracts against monospecific anti-R protein serum, radio-labelled protein A and anti-R protein serum or S. aureus, Cowan I coated with antibodies against group A streptococci, T-type 28. The first two methods proved more sensitive than the latter. R-protein was detected in 51% of 43 type II strains and in 87% of 102 type III strains, whereas none of 79 type Ia and none of 17 type Ib strains contained R-protein. Among 30 isolates from blood and cerebrospinal fluid of infants with neonatal infections, R-protein was detected in 43%, one of two type II strains and 12/14 type III strains. Tests of 37 paired strains from infant/mother pairs showed concordant results with respect to presence or absence of R-protein in the isolates.

Bacterial Proteins↗
PubMed1983

Correlation between low levels of maternal IgG antibodies to R protein and neonatal septicemia with group B streptococci carrying R protein.

A method was designed for quantitation of serum antibodies to R protein in group B streptococci (GBS). Four sera from mothers of infants with neonatal septicemia caused by type II, R+ GBS showed a binding range from 400 to 740 cpm in contrast to a range of 690-1,220 cpm in 5 parturients carrying type II, R+ strains in the urogenital tract giving birth to healthy infants (p less than 0.05). The range of antibodies in sera from 8 mothers to infants infected with GBS type III,R+ was 370-750 cpm, whereas the range in sera from 10 carriers of type III,R+ giving birth to healthy infants varied between 510 and 1,280 cpm (p less than 0.01). These findings indicate that R protein is an important virulence factor in neonatal GBS septicemia/meningitis.

Animals↗
PubMed1983

Deficiency of IgG subclasses in mothers of infants with group B streptococcal septicemia.

Serum IgG subclasses were studied in 19 mothers of infants with serious infections caused by group B streptococci (GBS) and compared with a control group of 20 mothers of healthy infants. 13 of 19 mothers showed decreased subclass levels: 10 of 19 low IgG2, 9 of 19 low IgG1 and 4 of 19 low IgG3. The levels of IgG1, IgG2 and IgG3 were significantly lower among mothers of GBS-infected infants than among the controls. Thus, there is indirect evidence that the infants were immunodeficient at birth.

Adult↗
PubMed1982

Relation between neonatal pneumonia and maternal carriage of group B streptococci.

Obstetrical and neonatal complications were studied among 143 urogenital carriers of group B streptococci (GBS) and their 144 infants and compared with complications occurring in a control group of 157 pregnant non-carriers and their 158 infants. All parturients had experienced uncomplicated pregnancies until week 36. 26 infants, 13 from each group, were transferred to the neonatal intensive care unit for treatment and observation within the first 7 days of life. Among these infants, 11/13 infants of GBS carriers contracted pneumonia and pulmonary adaptation syndrome, in contrast to 3/13 infants of non-carriers (p less than 0.05). The GBS carrier infants transferred to the neonatal intensive care unit had higher birth weights and higher gestational ages. Within the group of infants born to GBS carriers, those with pulmonary diseases evidenced abnormal fetal heart rate changes during labour in a higher rate than in the controls. Puerperal endometritis occurred with a significantly higher frequency among the GBS carriers (7/143) than among the non-carriers (0/157). Maternal carriage of GBS is a high risk factor for both the mother and her newborn, also after an otherwise uncomplicated pregnancy.

Adult↗
PubMed1977

Phenytoin, phenobarbitone and serum cholesterol.

Epileptics receiving phenytoin and/or phenobarbitone medication are observed to have an exceedingly low incidence of myocardial infarction. Serum cholesterol samples from 96 epileptics treated with these anticonvulsant drugs have been measured and found not to deviate from values found in a mass screening carried out in the same geographical area. Since medication with phenytoin/phenobarbitone reduces vitamin D levels in serum and intake of this vitamin is positively correlated to myocardial infarction, we suggest that vitamin D might be a factor to be considered.

Adolescent↗
PubMed1975

Vitamin D and serum cholesterol.

During a mass survey for coronary heart disease in Tromsö, Norway, in 1974, 385 men aged 20 to 50 from one particular electoral district completed an additional questionnaire concering the intake of vitamin D from all sources (natural food, fortified food and vitamin D preparations). The average daily intake of vitamin D during the preceding 12 months was later related to the respective serum cholesterol levels. For the whole material, no association was found. When the men were grouped according to vitamin D intake above and below 2.5 mug and serum cholesterol levels above or below 250 mg %, a significant relationship appeared (using Yates's correction X2=10.3, P=0.0013 and the correlation coefficient 0.011 less than P less than 0.005).

Adult↗
PubMed1974

Vitamin D and myocardial infarction.

A detailed investigation was carried out into the consumption of vitamin D from different sources in patients who had suffered from myocardial infarction, angina pectoris, and degenerative joint diseases. Randomly selected controls of the same ages and sex were drawn from the Central Bureau of Statistics. The consumption was significantly higher in infarction patients. A daily intake of 30 mug may be the critical level. Student's t test for trend showed increasing probability of myocardial infarction with increasing intake of vitamin D, and more infarction patients than controls had a history of kidney stone. Long-term high consumption of vitamin D may be a precipitating cause of myocardial infarction.

Angina Pectoris↗