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Biomedical subjects

A Ljungh

Publications and source records attributed to A Ljungh.

153 records · Page 9Linked to original sources

Hemagglutination by Escherichia coli in septicemia and urinary tract infections.

The agglutination of erythrocytes from various animal species by Escherichia coli was studied. The 405 strains of E. coli were isolated from urine in patients with urinary tract infections, from blood in septicemic patients, or from feces in persons without intestinal or urinary disorders. In urinary tract infections, d-mannose-resistant agglutination (MRHA) of human erythrocytes was the most common finding (23% of the strains). The highest frequency of mannose-sensitive hemagglutination (MSHA) attributed to type I (common type) pili occurred with guinea pig erythrocytes (11.5%). Of the 78 E. coli strains isolated from blood cultures, 11 (14%) produced MRHA of human erythrocytes and only one gave MSHA. In the stool cultures, only 1 of 170 E. coli strains was MSHA reacting, whereas 28 strains (16.5%) showed MRHA of human erythrocytes. No MRHA strain reacted with antiserum against colonization factor antigen (CFA)/I of pilus nature in enterotoxigenic human E. coli strains (O78:H12). MRHA of bovine erythrocytes, reputedly typical of enterotoxigenic E. coli of serogroups O6 and O8, was shown by only two strains, neither of which agglutinated with CFA/II antiserum. The most common hemagglutinating pattern of E. coli from urine and blood thus was MRHA for human erythrocytes. This agglutination may have been caused by pili or other surface properties of one or more serotypes. These may represent a new class of colonization-promoting antigens (adhesins).

Animals↗

Aeromonas hydrophila in acute diarrheal disease: detection of enterotoxin and biotyping of strains.

Eleven isolates of Aeromonas species from human stool cultures were found to produce enterotoxin activity as determined by assay of culture filtrates in rabbit intestinal loops and rabbit skin and on adrenal Y1 cells. Hemolysin(s) and a cytotoxic protein were found to interfere in all three assay systems but could be inactivated upon heating at 56 degrees C or by specific antihemolysin. Biotyping of each isolate was performed with a conventional test system and with API 50E and APIZYM kit systems (Analytab, Inc.). No single test of the more than 70 biochemical reactions investigated was found to correlate with enterotoxigenicity in the strains of Aeromonas hydrophila examined. All strains were found to belong to ideal phenotypes of A. hydrophila, but each strain possessed its own biochemical profile.

Aeromonas↗

Aeromonas and plesiomonas as possible causes of diarrhoea.

The number of reports on the isolation of Aeromonas from patients with diarrhoeal disease is now large and suggests an etiological role of the bacterium. It is well established that strains of Aeromonas produce an enterotoxin. This enterotoxin is cytotonic, i.e. it does not damage the membrane, and it does not cross-react immunologically with cholera toxin and Escherichia coli heat-labile (LT) toxin. Most enterotoxigenic strains also produce a cytotoxic protein (hemolysin), the role of which is probably limited in diarrhoea but potentially toxic in humans in other kinds of infections. Strains of Plesiomonas shigelloides also seem to be able to cause diarrhoea in some cases. The pathogenesis of Plesiomonas-induced diarrhoea remains to be elucidated, but a heat-stable enterotoxin may be involved.

Aeromonas↗

Helicobacter pylori in endoscopy patients in Zimbabwe: value of enzyme-linked immunosorbent assay and a rapid urease test.

Biopsy and serum specimens were obtained from 95 patients undergoing endoscopy at the University of Zimbabwe Medical School. Common presenting features were epigastric pain, bleeding and dyspepsia. Ulcers were detected in 16 patients (17%), and were more common in men (24%) than in women (7%). Histological examination of biopsies showed that all 95 patients had spiral-shaped organisms that were indistinguishable microscopically from Helicobacter pylori, though the numbers of organisms varied considerably. There was evidence that the degree of inflammation in the mucosa was related to the numbers of H. pylori-like organisms (HPLO) present. Fifty-one biopsy specimens (55%) gave a positive rapid urease test (RUT), with colour change occurring within 4 h. In all but one case, the gastric mucosa from these patients contained moderate to numerous HPLO. We defined the 'gold standard' of H. pylori-associated gastritis as the presence of both moderate to numerous HPLO and moderate to severe inflammation in the gastric mucosa. Using these criteria, RUT had a sensitivity of 67% and a specificity of 68%. Sera from 92 patients were tested for immunoglobulin G antibodies reactive with a glycine-extract antigen of H. pylori, using an enzyme-linked immunosorbent assay (ELISA). Sera giving an indeterminate reaction in the ELISA were also tested by Western blotting. In all, 36 sera (39%) gave a positive ELISA or Western blot reaction. There was poor correlation between serology and RUT results, with only 57% of biopsy specimens from seropositive patients giving a positive RUT, compared with 45% from seronegative patients. Positive serology was found in only 35 patients (61%) with histological evidence of H. pylori-associated gastritis, and the specificity of the test was only 54%. When used in combination with the RUT result, however, 79% of patients with a positive RUT and positive serology had histological evidence of H. pylori-associated gastritis. There was a general trend for increased seroprevalence in patients with mild to moderate atypia. These findings indicate that serology, using an antigen derived from the type strain of H. pylori, is unreliable in detecting H. pylori infection in Zimbabwe. Current studies are aimed at characterizing antigens from organisms isolated from Zimbabwean patients.

Adolescent↗

Binding of vitronectin and clusterin by coagulase-negative staphylococci interfering with complement function.

Coagulase-negative staphylococci (CoNS) are commonly associated with infections of prosthetic devices mediated by adsorbed host factors on biomaterial surfaces. Complement activation is known to occur and induce unspecific inflammation around the biomaterials. Human vitronectin (Vn) and clusterin (Clu), two potent inhibitors of complement, can be bound by CoNS. With a hypothesis whether binding of Vn or Clu influences complement activation, two measurements were determined. For Vn, complement activation was measured with a mouse anti-activated human C9 antibody. In the presence of Vn-binding strain, Staphylococcus hemolyticus SM13I, complement activation on a surface pre-coated with Vn occurred as it did in the absence of Vn pre-coating. For S. epidermidis 3380, which does not express binding of Vn, complement activation on a Vn-presented surface was significantly decreased. For Clu, erythrocytes lysis was measured to reflect the end product of complement activation (membrane attack complex). The complement-induced hemolysis increased when human serum was pre-incubated with Clu-binding strains, S. epidermidis J9P. The enhancement of hemolysis by J9P decreased when serum was supplemented by exogenous Clu. The data imply that interaction between CoNS and Vn or Clu interferes with one of their physiological functions, complement inhibition.

Journal Article↗

Doxorubicin reversibly decreases the antithrombogenicity of heparin immobilized on central venous catheters.

This is an in vitro study of the effects of doxorubicin on heparin immobilized on polyvinyl chloride (PVC) tubing. Doxorubicin contains an amino group that binds up to 16 heparin molecules, forming insoluble complexes if they are added to the same infusion. Three systems were tested: doxorubicin in perfusing blood, cerebrospinal fluid, and 0.9% sodium chloride (NaCl). The antithrombogenicity of immobilized heparin is impaired on exposure to doxorubicin. However, the reaction is reversible provided the PVC tubing system is thoroughly washed. Heparinized tubing perfused for 12 hours in blood with doxorubicin (0.027 mg/mL) decreased the activity of the immobilized heparin to 6.0% compared with 43% of that exposed to blood only. Exposure to doxorubicin (0.27 mg/mL) for 15 minutes in NaCl decreased the activity to 3% compared with that of NaCl only. Continuous washing for 10 minutes (8 mL/min) resulted in regained activity. This indicated a reversible reaction between immobilized heparin and doxorubicin. Cyclophosphamide, netilmicin, and gentamicin did not affect the antithrombogenicity of heparin in any solution.

Biocompatible Materials↗

Role of topical phospholipids in the prophylaxis of silicone elastomer-associated infection in the abdominal cavity.

The present study evaluated the influence of phospholipids (phosphatidyl choline and phosphatidyl inositol) on the prevention of abdominal biomaterial-associated infection. Phospholipid-impregnated silicone elastomer (SE) fragments were either intraperitoneally implanted in rats or immersed in serum for 0, 4, and 14 days, and 3 x 10(9) cfu of 3H-labeled, live Escherichia coli were added in the peritoneal cavity or in vitro incubation medium. Three hours after incubation, the adherence of bacteria significantly decreased to phospholipid-impregnated SE fragments, which had been immersed/implanted for 0 and 4 days. However, the number of adhering bacteria did not differ between the impregnated and unimpregnated SE fragments after 14 days of immersion/implantation. A significantly lower number of adhering bacteria was noted on all unimpregnated SE fragments when phospholipid was supplemented in the peritoneal cavity or in vivo medium, compared with fragments with no supplement. The rate of bacterial DNA synthesis decreased significantly after incubation with phospholipid 2 h or more. Phospholipids did not further influence peritoneal morphology. Thus topical administration of phospholipids by impregnation to the surface of SE fragments or supplement in the incubation medium prevented bacterial adherence onto the SE fragments. This implies that the use of phospholipids might be a mode of preventing biomaterial-associated infections.

Administration, Topical↗