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Biomedical subjects

A Fleer

Publications and source records attributed to A Fleer.

At least 91 records · Page 5Linked to original sources
PubMed1986

Modulation of adherence of coagulase-negative staphylococci to Teflon catheters in vitro.

The mechanism of adherence of Staphylococcus epidermidis to commercially available catheters was studied in vitro in a quantitative assay employing 3H-labelled bacteria. It was found that adherence to Teflon catheters was significantly related to the degree of hydrophobicity of the strains. When hydrophobic groups were removed from Staphylococcus epidermidis by pepsin treatment, adhesion was almost completely abolished. Preincubation of catheters in human serum also caused a 80-90% reduction of adherence. Preincubation of Staphylococcus epidermidis in serum similarly decreased adhesion. This effect of serum was mainly due to albumin, while IgG and fibronectin were less effective. Culture of Staphylococcus epidermidis in subinhibitory concentrations (0.5 MIC) of cephalothin, clindamycin and vancomycin resulted in a 30-80% reduction in adhesion.

Anti-Bacterial Agents↗
PubMed1986

[Typhoid fever in childhood].

Typhoid fever is an uncommon disease in the Netherlands. Acquisition occurs mainly during holidays in an endemic area. The history of three children, admitted in the summer of 1985, will be discussed, in one of them the disease had a complicated course. A short review of the literature is given, especially regarding pathogenesis, diagnosis and treatment. Cultures of blood, faeces and bone-marrow are essential for diagnosis. Bone marrow culture remains the most effective method for recovery of the causative agent, especially in children who previously were treated with antibiotics. Chloramphenicol still is the drug of choice in treatment. Vaccination with the oral typhoid vaccine of children who intend to visit an endemic area is recommended.

Bone Marrow↗
PubMed1985

Opsonic defense to Staphylococcus epidermidis in the premature neonate.

The determinants of opsonic defense to Staphylococcus epidermidis were studied in 47 premature newborns. Opsonic activity for S. epidermidis in serum from premature newborns proved to be proportional to gestational age (r = .664, P less than .001). The level of IgG antibodies to staphylococcal peptidoglycan in neonatal sera was similarly proportional to gestational age (r = .604, P less than .001). However, all opsonic activity of premature neonatal serum proved to be heat labile, i.e., dependent on activation of complement. Thus, no heat-stable, IgG-dependent opsonic activity to S. epidermidis was detected in any of the preterm sera, despite the presence of IgG antibodies to peptidoglycan. Further studies with purified IgG isolated from paired sera from term neonates and their mothers revealed that at similar concentrations the opsonic activity to S. epidermidis of neonatal, transplacentally derived IgG was only 26% of the activity of maternal IgG, a finding that may explain the absence of heat-stable opsonic activity in preterm newborns.

Antibodies, Bacterial↗
PubMed1984

New aspects of staphylococcal infections: emergence of coagulase-negative staphylococci as pathogens.

In contrast to the well-established pathogen Staphylococcus aureus, the coagulase-negative staphylococci, formerly collectively called S. epidermidis, were until recently regarded as harmless commensals. During the last two decades, however, the coagulase-negative staphylococci have clearly emerged as pathogens in patients carrying artificial devices, such as prosthetic heart valves, hip prostheses and cerebrospinal fluid shunts, and in patients with compromised host defenses such as premature neonates and cancer and transplant patients. The present paper reviews current insights on classification, bacteriology, pathogenic potential and virulence factors of coagulase-negative staphylococci. In addition, the role of host defense factors in resistance to staphylococcal infection is summarized as well as the main features of the clinical syndromes in which coagulase-negative staphylococci are involved.

Antibodies, Bacterial↗
PubMed1984

An outbreak of gastroenteritis due to Escherichia coli 0142 H6 in a neonatal department.

An outbreak of gastroenteritis due to Escherichia coli 0142 H6 in a neonatal ward is described. The epidemic affected 16 of 24 infants (infection-rate 66 per cent), of whom one died due to necrotizing enterocolitis. Administration of antibiotics was of limited value in treatment or in eradicating E. coli 0142 H6 from the stools. Termination of the epidemic was only accomplished by isolating the patients, accompanied by strict hygienic measures, including the use of disposable gloves. Gastroenteritis due to this organism occurred only in prematurely born infants during the first 2 weeks of life.

Cross Infection↗
PubMed1983

Staphylococcus epidermidis endocarditis and Staphylococcus epidermidis infection in an intensive care unit.

Staphylococcus epidermidis are the most common agents of prosthetic valve endocarditis (PVE). S. epidermidis isolated from the blood stream of patients with PVE are almost invariably multiple resistant to antibiotics. Antibiotic treatment alone gives unsatisfactory results and carries a mortality rate of 70-80%. That is why early surgical treatment is recommended. S. epidermidis is a less common cause of endocarditis in non-surgical patients, accounting for approximately 5% of the cases, which are mostly patients with pre-existent valvular heart disease. Generally, isolates from the latter patients are sensitive to most antibiotics, and the mortality rate is considerably lower. Recently coagulase-negative staphylococci have emerged as causative agents of septicaemia in patients hospitalized in intensive care units. Especially premature infants of very low-birth weight (less than 1500 g) receiving parenteral nutrition appear to carry a high risk of acquiring this kind of septicaemia. Although the staphylococci isolated from the blood of these patients are the same as in patients with PVE, generally multiple resistant to antibiotics, prognosis is far better than in cases of PVE. In our study carried out in a neonatal intensive care unit, two risk factors for coagulase-negative staphylococcal septicaemia were identified. First, nearly 20% of parenteral nutrition fluids used in the unit were found to be contaminated with coagulase-negative staphylococci, and a significant association was established between septicaemia and the infusion of contaminated fluids. Moreover, opsonization of staphylococci in infant serum proved to be severely deficient. Since host defence to staphylococci is dependent on optimal opsonization of these microorganisms, this defence may be severely compromised in the premature neonate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1981

Male-female differences in the cytotoxic activity of human monocytes in vitro.

The cytotoxic activity of human monocytes towards anti-D-sensitized Rh(D)-positive red cells in vitro was studied in relation to the age and sex of healthy monocyte donors. It was found that cytotoxic activity of monocytes from young females (age range 18-40 years) was significantly less than that of monocytes from age-matched males, irrespective of the use of oral contraceptives. No such difference was found between monocytes from older males and females (age range 43-63 years). The cytotoxic activity of monocytes from the two latter groups of donors was similar to that of young males. In the presence of cytochalasin B, which enhances the cytotoxic activity of monocytes, no male-female difference was detected, indicating that the maximal cytotoxic capacity of monocytes from young females is similar to that of monocytes from young males. We have previously presented evidence that the cytotoxic activity of monocytes is mediated by lysosomal enzymes released by these cells. These present data suggest that the reduction in cytotoxic activity of monocytes from young females might be a result of a reduced lysosomal enzyme release which is possibly related to the in vivo action of female sex hormones. However, we were not able to detect an inhibitory effect of oestrogens and progestagens on cytotoxic activity of monocytes from males in vitro.

Adolescent↗
PubMed1978

The role of adherence to human mononuclear phagocytes in the destruction of red cells sensitized with non-complement binding IgG antibodies.

In patients with IgG incomplete non-complement binding warm autoantibodies, the subclass composition of the antibodies was studied in relation to the occurrence of increased haemolysis in vivo and the adherence of the patients red cells to peripheral blood monocytes (PBM) in vitro. The presence of IgG3 autoantibodies was almost always accompanied by haemolytic anaemia, but the presence of IgG1 autoantibodies only in some patients but not in others. IgG2 and IgG4 autoantibodies were not associated with increased red cell destruction. A relation identical to that between subclass composition and increased haemolysis was found between subclass composition and adherence of the patients erythrocytes to PBM and thus a strong correlation between positive adherence in vitro and increased red cell destruction in vivo. These results support an important role of adherence to mononuclear phagocytic cells in the destruction of red cells sensitized with non-complement binding IgG antibodies. Strong indications were found that IgG1 autoantibodies are of two kinds, only one of which causes adherence to phagocytes and thus increased red cell destruction.

Anemia, Hemolytic↗
PubMed1978

Destruction of IgG-sensitized erythrocytes by human blood monocytes: modulation of inhibition by IgG.

The in vitro interaction between monocytes and erythrocytes sensitized with non-complement binding IgG antibodies (i.e. the Rh antibody anti-D:EAIgG anti-D) is completely inhibited by low concentrations of IgG (E.G. 30--100 microgram/ml). However, the interaction between monocytes and erythrocytes sensitized with IgG anti-A (EAIgG anti-A) is not inhibited by IgG. The findings presented in this paper indicate that this difference is probably due to the difference in the number of IgG antibody molecules per EAIgG. Thus, the higher the number of IgG antibody molecules per EAIgG, the less the interaction between EAIgG and monocytes is inhibited by IgG. A second factor which proved to have a strong influence on inhibition by IgG was the number of EAIgG per monocyte. When the number of EAIgG per monocyte was increased from 1 to 32, the percentage of inhibition by a fixed amount of IgG (50 microgram/ml) decreased significantly. This in vitro effect is only evident when relatively weakly sensitized erythrocytes are used and, in vivo, destruction of these weakly sensitized red cells (e.g. EAIgG anti-D) is confined to the spleen. Since a considerable haemoconcentration occurs in this organ, it is conceivable that a high EAIgG:macrophage ratio is accomplished. The latter data are an indication that this high ratio may allow interaction between weakly sensitized erythrocytes and splenic macrophages despite the presence, in vivo, of a high concentration of IgG, and that, in this way, in the spleen, the inhibitory effect of IgG is overcome.

Cell Adhesion↗
PubMed1978

Monocyte-induced increase in osmotic fragility of human red cells sensitized with anti-D alloantibodies.

The mechanism by which human monocytes increase the osmotic fragility of red cells sensitized with Rhesus alloantibodies anti-D was studied in vitro. Both the increase in osmotic fragility and the lysis of red cells by monocytes were enhanced by cytochalasin B and were inhibited by hydrocortisone. These effects were similar to the effects of these agents on lysosomal enzyme release by monocytes. However, hydrocortisone was completely ineffective when added 1 h after mixing monocytes and sensitized red cells. This indicates that the damage responsible for the fragility increase and lysis is completed within 1 h and suggests that it is due to lysosomal enzymes released by the monocytes. Since for the full expression of the osmotic fragility increase and lysis an incubation time much longer than 1 h is required, it appears that the latter phenomena are the non-specific sequelae of damage inflicted upon the red cell by released lysosomal enzymes.

Cytochalasin B↗
PubMed1978

Destruction of sensitized erythrocytes by human monocytes in vitro: effects of cytochalasin B, hydrocortisone and colchicine.

The purpose of this study was to characterize the destruction of sensitized erythrocytes by human blood monocytes in vitro. The incubation in vitro of human monocytes with 51Cr-labelled human erythrocytes sensitized with IgG rhesus alloantibodies anti-D (EAIgG anti-D) resulted in release of 51Cr from the erythrocytes (lysis) as well as uptake of 51Cr-labelled erythrocytes by the monocytes (phagocytosis). The lysis of EAIgG anti-D by monocytes was not dependent on phagocytosis, because cytochalasin B, which inhibited phagocytosis of EAIgG, enhanced lysis. In contrast, hydrocortisone and colchicine inhibited lysis, but had no effect on phagocytosis. These agents did not affect binding of EAIgG anti-D to monocytes. The effect of these agents on lysis corresponded to their effect on release of lysosomal enzymes by monocytes. The release of lysosomal enzymes, when induced by EAIgG anti-D, was, likewise, enhanced by cytochalasin B and inhibited by hydrocortisone and colchicine. A significant correlation was found between lysosomal enzyme release and lysis. Together, these results strongly suggest that lysosomal enzymes, released by the monocytes when incubated with anti-D-sensitized erythrocytes, are responsible for the cytotoxic activity of these cells towards sensitized erythrocytes. The action of these enzymes only occurs over a short range, probably at the site of attachment of the erythrocyte, because only erythrocytes that were bound to the monocytes were lysed. The finding of other investigators that removal of monocytes from suspensions of human mononuclear leucocytes results in a strong reduction in the cytotoxic activity of these leucocytes towards sensitized erythrocytes in vitro. was confirmed.

Colchicine↗
PubMed1976

[Immunological damage to erythrocytes].

The mechanisms by which red cells are destroyed under the influence of antibodies with different immunochemical and biological characteristics are described. It is shown that the interaction of antibody with the red cell per se does not lead to a disturbance of red cell function. Activation of the whole complement system leads to direct lysis of the erythrocyte (complement hemolysis). The fixation of red cells coated with activated C3:C3 receptors on phagocytic cells is another mechanism which leads to red cell destruction. The hypothesis that adherence to the Fc-receptors of phagocytic cells is essential for the destruction of red cells under the influence of noncomplement-binding antibodies is discussed. Arguments in favour of this theory are correlation between the subclass of IgG red cell autoantibodies and the absence or presence of increased hemolysis in the patient and a correlation between the degree to which red cells of patients with this kind of antibody adhere to monocytes in vitro and the degree of hemolysis in the patient. It is shown by in vitro experiments how this adherence process can take place in vivo in the presence of normal plasma IgG although the latter completely inhibits the adherence phenomenon in vitro.

Antibodies↗
PubMed1976

Correlation of PPD and BCG-induced leukocyte migration inhibition, delayed cutaneous hypersensitivity, lymphocyte transformation in vitro and humoral antibodies to PPD in man.

In a study of healthy human individuals a complete lack of correlation between the results of the agarose leukocyte migration inhibition (LMI) test, using purified protein derivative (of tuberculin) (PPD) and Bacillus Calmette Guérin (BCG) as antigens, and delayed cutaneous hypersensitivity and lymphocyte transformation in vitro to PPD was found. There was a reasonable correlation between PPD- and BCG-induced LMI. Antibodies to PPD proved to have no influence on PPD-induced LMI. Purified polymorphonuclear leukocytes, whether derived from donors sensitive to PPD in the agarose LMI test or from nonsensitive donors, did not show migration inhibition to PPD. It was concluded that polymorphonuclear leukocytes and lymphocytes need to be present simultaneously for migration inhibition of peripheral blood leukocytes by PPD. Furthermore, because a consistent relation with conventional parameters of cell-mediated immunity was lacking, it is doubtful whether the agarose LMI test can be considered as an alternative parameter of this kind of immunity.

Antibodies, Bacterial↗
PubMedDate not supplied

Septicemia due to coagulase-negative staphylococci in a neonatal intensive care unit: clinical and bacteriological features and contaminated parenteral fluids as a source of sepsis.

During the years 1979 to 1981 we experienced an increasing incidence of septicemia due to coagulase-negative staphylococci in the neonatal intensive care unit (NICU). A detailed analysis was performed for the 1981 NICU population. More than 90% of cases occurred in premature infants of low birth weight (less than 2500 g). All septicemic infants were receiving intravenous therapy and total parenteral nutrition (TPN) solutions had been administered to nearly 80% just before or during the septic episode. A case-control study performed for the 1981 NICU population, which included 26 proved cases of coagulase-negative staphylococcal septicemia and 26 matched controls, did not uncover any differences in underlying diseases or modes of treatment between cases and controls. However, the infusion of contaminated TPN fluids was identified as a significant risk factor. Random bacteriological checks of TPN fluids revealed that nearly 20% of these solutions were contaminated, mainly with coagulase-negative staphylococci. The incidence of staphylococcal septicemia in infants who had received contaminated TPN fluids was 10-fold higher than in infants who had received sterile solutions (P less than 0.0005). The majority of coagulase-negative staphylococci isolated from the blood cultures from the NICU were multiply resistant to antibiotics although all isolates were susceptible to cephalothin. Treatment, consisting of removal or replacement of the intravenous devices and the administration of cephalothin and fresh plasma, was universally successful.

Humans↗