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Biomedical subjects

J Verhoef

Publications and source records attributed to J Verhoef.

At least 433 records · Page 24Linked to original sources
PubMed1987

Colonization and infection in surgical intensive care patients--a prospective study.

Nosocomial infections are a major problem in intensive care patients. Thirty-nine patients, requiring intensive care for 5 days or more (mean 15.8 days) were prospectively investigated, to determine the relation between colonisation and nosocomial infection. Thrice weekly, cultures from the oropharynx, respiratory and digestive tract were obtained. Colonization with aerobic gram-negative microorganisms of the oropharynx, respiratory and digestive tract significantly increased during the stay in the Intensive Care Unit. In 29 patients (74%) 78 nosocomial infections were diagnosed. The most frequent nosocomial infections were pneumonia (26 patients, 66.6%), catheter-related bacteraemia (11 patients, 28.2%), and wound infections (7 patients, 17.9%). In 59 instances (75.6%), colonization with the same potential pathogenic microorganism preceded the nosocomial infection. The overall mortality was 25.6% (10 patients), bacteraemia with aerobic gram-negative microorganisms being the cause of death in 7 patients.

Adult↗
PubMed1987

Relationship of bacterial growth phase to killing of Listeria monocytogenes by oxidative agents generated by neutrophils and enzyme systems.

Listeria monocytogenes, a gram-positive motile bacterium which can cause severe bacterial infection in humans, is considered to be pathogenic by virtue of its ability to resist intracellular killing. Since the mechanism of intracellular survival is poorly understood, we assessed the sensitivity of L. monocytogenes to several potent antibacterial products. Phorbol myristate acetate (PMA)-stimulated polymorphonuclear cells (PMNs) produced extracellular antibacterial products which were inhibited completely by catalase, suggesting a role for oxidative agents in this process. L. monocytogenes in logarithmic (log) growth phase resisted PMA-stimulated PMN extracellular products significantly more than L. monocytogenes in stationary (stat) growth phase or Escherichia coli (three strains) in either phase of growth. The role of oxidative agents was studied further by using xanthine oxidase-xanthine, glucose oxidase-glucose, and myeloperoxidase enzyme systems to generate hydroxyl radical (.OH), hydrogen peroxide (H2O2), and hypochlorous acid (OCl-), respectively. L. monocytogenes in log phase resisted the antibacterial products of these enzyme systems under conditions which produced superoxide (O2-) and H2O2 at concentrations similar to those produced extracellularly by PMA-stimulated PMNs, while stat-growth-phase L. monocytogenes and E. coli in either phase of growth were susceptible. Antibacterial activity could be blocked or inhibited by exogenous catalase (for all oxygen radical-generating systems), mannitol, or desferoxamine (for xanthine oxidase-xanthine) and alanine (for myeloperoxidase), suggesting that .OH and OCl- were responsible for this activity. Log-phase L. monocytogenes had 2.5-fold higher bacteria-associated catalase activity, as compared with stat-phase L. monocytogenes. These experiments, therefore, suggest that log-phase L. monocytogenes resists oxidative antibacterial agents by producing sufficient catalase to inactivate these products. This may contribute to the ability of L. monocytogenes to survive intracellularly.

Blood Bactericidal Activity↗
PubMed1987

Injury to endothelial cells by phagocytosing polymorphonuclear leukocytes and modulatory role of lipoxygenase products.

Phagocytosis of microorganisms by polymorphonuclear leukocytes (PMN) is accompanied by inadvertent extracellular release of microbicidal products; this could result in tissue damage. We investigated whether PMN damages endothelial cells when phagocytosis of Staphylococcus aureus occurs on the endothelial surface and how this damage might be modulated. Damage was assayed by the measurement of cell detachment or cell lysis of cultured endothelial cells that were radiolabeled with 51Cr. Uptake of bacteria was accompanied by nonlytic detachment of endothelial cells from the monolayer. This effect was inhibited by alpha-1-antitrypsin but remained unaffected by scavengers of toxic oxygen species. During phagocytosis, PMN adhered to the endothelial cells. Adherence could be prevented by inhibition of the lipoxygenase pathway of arachidonic acid metabolism of the PMN with nordihydroguaiaretic acid. This inhibition also resulted in a marked decrease of the detaching activity of the PMN. The addition of exogenous leukotriene B4 during phagocytosis greatly enhanced the damage to the endothelial monolayer. These results indicate that phagocytosis of staphylococci by PMN is accompanied by injury to endothelial cell monolayers due to released lysosomal proteases and that products of the lipoxygenase pathway of PMN play a modulatory role in this injury.

Arachidonic Acids↗
PubMed1987

Opsonization of Staphylococcus aureus protects endothelial cells from damage by phagocytosing polymorphonuclear leukocytes.

When phagocytosis of Staphylococcus aureus by human polymorphonuclear leukocytes (PMN) takes place on the surface of cultured human endothelial cells, the endothelial monolayers are damaged by lysosomal enzymes that are released by the PMN. Because PMN can phagocytose opsonized as well as unopsonized staphylococci on an endothelial surface, we studied the role of bacterial opsonization in the damage caused to the endothelium. Phagocytosis of unopsonized S. aureus was accompanied by greater damage (expressed as the percentage of the endothelial cells detached from the culture plates) of the monolayers than was phagocytosis of opsonized S. aureus: 52 +/- 10% and 24 +/- 7%, respectively, after 30 min of phagocytosis and 73 +/- 5% and 50 +/- 6%, respectively, after 60 min of phagocytosis. When correlated to the amount of phagocytosis, this difference was even greater (uptake was 35 +/- 4% for unopsonized S. aureus and 56 +/- 5% for opsonized S. aureus after 30 min and 42 +/- 3% and 60 +/- 5%, respectively, after 60 min). Total release of lysozyme and myeloperoxidase and generation of superoxide anion were the same during phagocytosis of opsonized or unopsonized staphylococci. Adherence of PMN to the endothelial cells was greater during phagocytosis of unopsonized S. aureus: 42 +/- 4% verus 27 +/- 3% during phagocytosis of opsonized staphylococci. Possibly, increased adherence of the PMN resulted in a locally higher concentration of enzymes which induced more damage. We conclude that opsonization of bacteria not only improves bacterial uptake, but also protects bystander cells from damage by the phagocytosing PMN.

Cells, Cultured↗
PubMed1987

Bifidobacterium, Bacteroides, and Clostridium spp. in fecal samples from breast-fed and bottle-fed infants with and without iron supplement.

Bifidobacterium, Bacteroides, and Clostridium spp. isolated from the feces of 23 neonates during the first 3 months of life were identified. Of the 23 neonates, 10 were breast fed, 6 received an infant formula with iron supplement (5 mg/liter), and 7 received the formula without iron supplement (iron concentration, less than 0.5 mg/liter). The Bifidobacterium spp. most frequently isolated from the three groups of infants were B. longum, B. breve, B. adolescentis, and B. bifidum. The bacteroides spp. most frequently isolated were B. fragilis and B. vulgatus. The most common Clostridium sp. in the three groups of infants was C. perfringens. The type of milk did not select for species of Bifidobacterium, Bacteroides, or Clostridium, except for Clostridium butyricum, which was isolated significantly more often from bottle-fed infants with iron supplement than from the other groups, and Clostridium tertium, which was more often isolated from breast-fed infants. The species of the three anaerobic genera did not persist for a long period of time in the three groups of infants.

Bacteria, Anaerobic↗
PubMed1987

Carumonam enhances reactivity of Escherichia coli with mono- and polyclonal antisera to rough Escherichia coli J5.

Escherichia coli O111 reacts only slightly with antiserum to its rough mutant E. coli J5 in an enzyme-linked immunosorbent assay. When E. coli O111 was grown in the presence of sub-MICs of the monocyclic beta-lactam antibiotic carumonam, however, the enzyme-linked immunosorbent assay titer increased from 1,280 to 81,920. When the bacteria were grown in the presence of carumonam, the titer that was obtained with antiserum against E. coli O111 was not affected. This reaction was abolished after this antiserum was absorbed with E. coli J5 in the case of the carumonam-treated strain, whereas this absorption did not affect the reaction with E. coli O111. Thus, the O-antigenic side chain of E. coli O111 seems to be affected if this strain is cultured in the presence of carumonam. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed a relative loss of the O polysaccharide in E. coli O111 when this strain was grown in the presence of carumonam. Also, a much stronger reaction of the antibiotic-affected lipopolysaccharide with a monoclonal antibody against E. coli J5 lipopolysaccharide was shown in immunoblots. The results of this study indicate that there is a synergism between certain antibiotics and monoclonal antibodies, something that could have clinical implications.

Anti-Bacterial Agents↗
PubMed1987

Opsonisation and phagocytosis of group B meningococci by polymorphonuclear leucocytes: comparison of sulphonamide sensitive and resistant strains.

A large proportion of disease caused by sulphonamide resistant strains of group B type 15 meningococci affects patients 10-24 years. In contrast, disease caused by sulphonamide sensitive strains conforms to the usual pattern, and most infection occurs in early childhood. In an attempt to explain this phenomenon possible differences in susceptibility of resistant and sensitive strains to phagocytosis by polymorphonuclear leucocytes were investigated, using radioactively labelled bacteria. In initial experiments a group B resistant strain required higher concentrations of normal human serum and longer opsonisation times for phagocytosis than an ungroupable non-pathogenic meningococcus. Comparison of sulphonamide resistant and sensitive group B meningococci showed that with either heat inactivated serum or agammaglobulinaemic serum, phagocytosis did not occur with any of the strains, whereas if these two sera were used together, phagocytosis was restored to the level seen with normal human serum. Thus both antibody and complement are required for phagocytosis. Furthermore, opsonisation depended on an intact classical pathway of complement for each group B strain. In all the experiments there was no significant difference between the phagocytosis of sulphonamide sensitive and resistant group B strains neither with regard to the efficiency of opsonisation by normal human serum nor the exact requirements for antibody and complement.

Adolescent↗
PubMed1987

Comparative in vitro antimicrobial activity of carumonam (Ro 17-2301) and its influence on the activity of other antibiotics.

The antimicrobial activity of carumonam (Ro 17-2301) was compared with that of 20 antibiotics against 338 clinical isolates. Carumonam did not possess activity against gram-positive cocci, MIC90 of carumonam were less than or equal to 0.5 mg/l for Enterobacteriaceae, except for Citrobacter (less than or equal to 8 mg/l) and less than or equal to 32 mg/l for nonfermenters. It was slightly more active than aztreonam against gentamicin-resistant bacilli (MIC90 less than or equal to 64 vs greater than or equal to 256). Combinations of carumonam with antibiotics with activity against gram-positive microorganisms were indifferent.

Anti-Bacterial Agents↗
PubMed1987

Clindamycin at subinhibitory concentrations enhances antibody- and complement-dependent phagocytosis by human polymorphonuclear leukocytes of Staphylococcus aureus.

The influence of subinhibitory concentrations of clindamycin on opsonization and phagocytosis of Staphylococcus aureus was studied. S. aureus was grown overnight in the presence or absence of one half or one quarter of the minimal inhibitory concentration (MIC) of clindamycin. Radioactively labeled S. aureus was opsonized for various periods of time in different concentrations of normal serum, heated antiserum and serum of patients with agammaglobulinaemia or C3 deficiency. Complement- as well as antibody-dependent phagocytosis of the antibiotic treated S. aureus was significantly enhanced, compared to phagocytosis of the untreated control. Killing experiments showed that clindamycin-treated S. aureus was also better killed by the granulocytes than untreated S. aureus. The mechanism of action is likely to be an increased susceptibility of clindamycin-treated bacteria to antibody- and complement-dependent phagocytosis.

Agammaglobulinemia↗
PubMed1987

Antibody and complement-binding activity of viable and nonviable human spermatozoa.

Antibody and complement fixation by viable and nonviable spermatozoa were studied by means of immunofluorescence and a hemolytic assay (CH-50). Spermatozoa were incubated in sera from fertile male and female donors and in peritoneal fluid from fertile women undergoing laparoscopy. Nonviable spermatozoa were able to bind antibody or complement from sera and peritoneal fluid. There was no evidence of antibody or complement fixation by viable spermatozoa. The antibodies present in the serum that bind to spermatozoa belong to the IgG and IgM class; in peritoneal fluid, only IgG could be found. Complement fixation occurred via the classical (antibody-mediated) and alternative pathway. Viable spermatozoa possess antigenic properties different from nonviable spermatozoa. The lack of immunological reaction of women to viable spermatozoa and a possible mechanism for immunological infertility is considered.

Antibodies↗
PubMed1987

Infection prophylaxis in acute leukemia: a comparison of ciprofloxacin with trimethoprim-sulfamethoxazole and colistin.

Fifty-six patients receiving remission induction treatment for acute leukemia were studied in a randomized trial comparing ciprofloxacin with trimethoprim-sulfamethoxazole plus colistin for prevention of infections. Both groups received amphotericin B for antifungal prophylaxis. Six major infections occurred in 28 patients receiving ciprofloxacin, and 11 major infections occurred in 28 patients receiving trimethoprim-sulfamethoxazole plus colistin. No infections caused by gram-negative bacilli were seen in the ciprofloxacin group (p less than 0.02). Ciprofloxacin prevented colonization with resistant gram-negative bacilli, but 12 resistant colonizing strains were isolated from 10 patients receiving trimethoprim-sulfamethoxazole plus colistin (p less than 0.01). Ciprofloxacin was better tolerated: 23 of 28 patients were highly compliant to the drug, compared with 15 of 28 patients in the trimethoprim-sulfamethoxazole group (p less than 0.05). These results suggest that ciprofloxacin is a promising drug for the prevention of infection in patients with granulocytopenia.

Acute Disease↗
PubMed1987

Further evidence against a role for toxic oxygen products as lytic agents in NK cell-mediated cytotoxicity.

Natural killer (NK) cells are implicated in host defense mechanisms against infectious diseases and malignancies, and exert a rapid spontaneous cytolysis of various tumour cells and virus-infected cells without prior sensitization or activation (Herberman & Ortaldo, 1981). Human NK cells are a subpopulation of non-adherent, non-phagocytic lymphocytes defined as large granular lymphocytes (Timonen, Ortaldo & Herberman, 1981). NK cells possess a receptor for the Fc region of IgG (Perussia et al., 1984) that enables them to attack antibody-loaded targets, a process called antibody-dependent cell-mediated cytotoxicity (ADCC). The cytotoxic reaction of NK cells can be described as a 'stimulus-secretion' model, divided into three definable steps: binding, triggering for lysis and a killer cell-independent lytic step (Hiserodt, Britvan & Targan, 1982). The killing reaction involves a Ca2+-dependent activation, cytoskeletal rearrangement, activation of the arachidonic acid cascade, release of lysosomal enzymes and a cytotoxic factor(s) (Henkart, 1985) and, possibly, production of reactive oxygen species (Helfand, Werkmeister & Roder, 1982; Roder et al., 1982). The role and involvement of reactive oxygen species is still controversial. To study a possible participation of toxic oxygen species in NK-cell mediated cytotoxicity, we altered target cell anti-oxidant defence mechanisms and measured spontaneous NK-cell mediated cytotoxicity and ADCC reactions against tumour cells. We showed that alteration of target cell anti-oxidant systems had no effect on target cell susceptibility to NK-cell mediated killing. In contrast, the susceptibility of the anti-oxidant-depleted targets to oxygen-dependent polymorphonuclear leucocyte (PMN)-mediated cytotoxicity was increased.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1986

Coagulase-negative staphylococci as nosocomial pathogens in neonates. The role of host defense, artificial devices, and bacterial hydrophobicity.

In contrast to the well-established pathogen Staphylococcus aureus, the coagulase-negative staphylococci--formerly collectively called Staphylococcus 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 who have artificial devices implanted, such as prosthetic heart valves, hip prostheses, and cerebrospinal fluid shunts, and in those with compromised host defenses such as premature neonates, cancer patients, and transplant recipients. Recently, an increasing incidence of septicemia due to coagulase-negative staphylococci was detected in our neonatal intensive care unit. More than 90 percent of cases occurred in premature infants of low birth weight (less than 2,500 g). All septicemic infants were receiving intravenous therapy, and total parenteral nutrition solutions had been administered to nearly 80 percent just before or during the septic episode. This led us to examine the role of host defense factors in neonates and the possible significance of bacterial surface characteristics in the pathogenesis of catheter-associated infections.

Adhesiveness↗