fibrin and Escherichia-coli-Infections

In experiment on rabbits a comparative analysis of various methods of a biliary peritonitis simulation was conducted. In 6 animals a biliary peritonitis was simulated, using perforation of a gallbladder, local serous-fibrinous peritonitis have occurred in 50% of them. In 7 animals biliary peritonitis was simulated, applying intraabdominal injection of medical sterile bile in a 5-40 ml volume. Diffuse peritonitis with exudates and stratification of fibrin was absent. Most effective method have appeared that, when intraabdominal injection of bile was done together with E. coli culture in the rate of 0.33 microbal bodies McF (1.0 x 10(8) CFU/ml) on 1 kg of the animal body mass. Diffuse biliary peritonitis have occurred in all 23 animals, including serous-fibrinous one--in 17 (76%), and purulent-fibrinous--in 6 (24%).

Topics: Animals; Bile; Colony Count, Microbial; Disease Models, Animal; Escherichia coli; Escherichia coli Infections; Exudates and Transudates; Fibrin; Humans; Peritonitis; Rabbits; Severity of Illness Index

Topics: Animals; Anti-Infective Agents; Cytokines; Disease Models, Animal; Escherichia coli; Escherichia coli Infections; Fibrin; Fibrinolysis; Humans; Mice; Mice, Inbred C57BL; Peritonitis; Protein C; Rats; Time Factors

To assess the effect of a combined antithrombin III and C1-esterase inhibitor treatment on intravascular organ fibrin deposition and cardiorespiratory changes following intravenous Escherichia coli endotoxin (lipopolysaccharide [LPS] 80 microg/kg i.v.) exposure.. Prospective, randomized trial.. Research laboratory of a university medical center.. Anesthetized, instrumented and mechanically ventilated rabbits ([Chbb:CH); n = 40).. Endotoxin was given to 30 animals. Ten animals received no inhibitor (endotoxin control group). The other animals were either treated by high-dose (300 units/kg; n = 10) or low-dose (100 units/kg; n = 10) combined antithrombin III and C1-esterase inhibitor administration. Ten rabbits (time control group) were given placebo (sodium chloride 0.9%). Cardiorespiratory variables were assessed at baseline, 120 mins, and 240 mins after endotoxin or placebo administration. Four hours after endotoxin injection, liver, lung, and kidney tissue samples were examined for intravascular fibrin deposition by light microscopy.. Inhibitor treatment significantly decreased clot formation in lungs and livers without, however, demonstrating a clear dose-dependent effect. Combined antithrombin III/C1-esterase treatment attenuated the decrease of mean arterial pressure and cardiac output observed following endotoxin injection. Blood pressure improvement was significantly dependent on dosage administered.. Combination of antithrombin III and C1-esterase inhibitor treatment during early endotoxin shock decreased organ fibrin deposition and improved cardiovascular stability.

Topics: Animals; Antithrombin III; Antithrombins; Complement C1 Inactivator Proteins; Disseminated Intravascular Coagulation; Dose-Response Relationship, Drug; Drug Combinations; Endotoxins; Escherichia coli Infections; Fibrin; Hemodynamics; Infusions, Intravenous; Injections, Intravenous; Leukocyte Count; Male; Rabbits; Random Allocation; Shock, Septic

E. coli O157:H7 may cause hemorrhagic colitis resembling ischemic colitis. Diagnosis is usually made by finding sorbitol-negative colonies on MacConkey agar that react with O157 and H7 antisera. Most ischemic colitis is idiopathic, but some may be caused by E. coli O157:H7, inasmuch as this organism can produce fibrin thrombi in colon vasculature. The objectives of this study were to determine whether E. coli O157:H7 infection can be diagnosed retrospectively from paraffin blocks of colon sections and whether an association exists between E. coli O157:H7 infection and colonic ischemia.. Paraffin-embedded sections of normal colon (n = 2) and various colitides [ischemic (n = 11), E. coli O157:H7 (n = 2), IBD (n = 8) and pseudomembranous (n = 3)] were used. Sections were deparaffinized, rehydrated, incubated with 3% peroxide in methanol, rinsed, and incubated with peroxidase-labeled antibody isolated from goats immunized with whole E. coli O157:H7. Sections were stained with peroxidase chromagen reagent and counterstained with hematoxylin. Coarse, granular, orange-brown staining was considered positive. To determine the localization of the chromagen deposits, three cases that stained positive, including one of the culture-proved E. coli O157:H7 colitis and two of colonic ischemia, were processed for electron microscopy.. Both cases (100%) of E. coli O157:H7 colitis and three of 11 (27.3%) cases of ischemic colitis stained positive by light microscopy. In one culture-proved case, electron microscopy demonstrated staining of bacillary structures; in two cases of colonic ischemia, extensive deposits of chromagen material were present that were associated neither with inflammatory cells nor with bacterial forms.. Immunoperoxidase staining of archival sections may be used to diagnose E. coli O157:H7 infection. An etiological role for this organism is possible in some cases of colonic ischemia.

Topics: Aged; Antibodies, Bacterial; Chromogenic Compounds; Colitis; Colitis, Ischemic; Colon; Coloring Agents; Enterocolitis, Pseudomembranous; Escherichia coli Infections; Escherichia coli O157; Female; Fibrin; Gastrointestinal Hemorrhage; Hematoxylin; Humans; Immunoenzyme Techniques; Inflammatory Bowel Diseases; Male; Microscopy, Electron; Middle Aged; Paraffin Embedding; Retrospective Studies; Thrombosis

The spectrum of organisms causing native valve endocarditis is changing. Despite an increasing incidence of infections caused by gram-negative organisms, they remain a rare cause of native valve endocarditis. Escherichia coli is especially uncommon. We describe the case of a 47-year-old man with no previous history of cardiac problems, who presented with culture-positive E coli endocarditis of his native aortic valve. His complicated clinical course necessitated emergent valve replacement, emphasizing the virulence of this organism. The high mortality rate and significant morbidity associated with this entity necessitates aggressive medical management and early surgical intervention.

Topics: Aortic Valve; Echocardiography; Endocarditis, Bacterial; Escherichia coli; Escherichia coli Infections; Fibrin; Humans; Male; Middle Aged; Necrosis

Reciprocal interactions between elements of the acute inflammatory response and the coagulation system play important roles in host defense homeostasis during Gram-negative bacterial sepsis. However, derangements in the regulation of the inflammatory-coagulant axis in this setting may result in progressive tissue damage and disseminated intravascular coagulation. In this article, the integrated responses in the baboon model of Escherichia coli sepsis are analyzed as a basis of understanding these response interactions in the critically ill. In particular, three topics will be reviewed. First, the role of tissue factor in mediating the coagulant response to inflammation and the role of tumor necrosis factor (TNF) in initiating and amplifying this coagulant response into a full-blown consumptive coagulopathy are defined. A second and parallel topic concerns the role played by tissue factor pathway inhibitor and other anticoagulant systems in not only regulating this coagulant response, but also in attenuating the initial inflammatory response. The third topic concerns the use of assays of enzyme inhibitor complexes composed of components of these regulatory anticoagulant systems to help define the hypercoagulable state and possibly to make an early, specific diagnosis of sepsis prior to overt failure of the hemostatic system.

Topics: Animals; Blood Coagulation; Blood Coagulation Factors; Disseminated Intravascular Coagulation; Endothelium, Vascular; Escherichia coli Infections; Fibrin; Inflammation; Lipoproteins; Papio; Sepsis; Thromboplastin; Tumor Necrosis Factor-alpha

A fibrin clot model for intra-abdominal abscess formation was used to study the migratory properties of peritoneal cells from rats during the early stages of infection. Peritoneal cells and fibrin clot remnant were harvested 6 h after implantation of a sterile, singly infected (Escherichia coli or Bacteroides fragilis) or mixed infected (E. coli and B. fragilis) fibrin clot. Histological study of fibrin clots, removed 6 h after implantation, showed a deeper infiltration by host cells of B. fragilis infected clots compared to the others. This difference in infiltration by peritoneal cells was not due to differences in fibrinolytic activity of the bacterial strains. Differential cell counts of the peritoneal cells from rats implanted with sterile, singly and mixed infected fibrin clots showed distribution over subpopulations to be independent of the bacterial content of the infected clots used. In vitro migration assays showed no significant differences in migration by peritoneal cells from rats implanted with clots containing a different bacterial composition. Since B. fragilis infected fibrin clots were more deeply infiltrated by host defence cells than the other clots, and only mixed infected clots led to persistent abscesses in this model, we conclude that local conditions within the fibrin matrix rather than intrinsic cellular capacities of the host cells are important for the process of abscess formation.

Topics: Animals; Bacterial Capsules; Bacteroides fragilis; Bacteroides Infections; Cell Movement; Cells, Cultured; Escherichia coli Infections; Fibrin; Fibrinolysis; Humans; Male; Peritoneal Cavity; Rats; Rats, Wistar

Injury severity score and hypothermia can lead to a high level of mortality when combined clinically. In acute trauma, the presence of a coagulopathy is difficult to treat and the aim is prevention. Aliquots of whole blood from healthy human volunteers (n = 9) were added to saline (control) and saline plus endotoxin (activated). The control and activated groups were divided and subjected to 60 minutes of normothermia (24 degrees C) or hypothermia (0 degrees C). The samples were returned to 37 degrees C; then the recalcification times were determined using fibrin formation and the viscous drag as the determining factors. The activated hypothermic group showed a decreased recalcification time of 345 (+/- 48.9) seconds compared to 405 (+/- 60.8) for the activated normothermic group (P less than 0.001). When the normothermic and hypothermic groups were compared without endotoxin added, the differences were not significant. The authors conclude that the effects of endotoxin on clotting time are worsened by hypothermia in vitro and act synergistically to possibly cause the coagulopathy seen in trauma patients.

Topics: Bacteremia; Blood Viscosity; Disseminated Intravascular Coagulation; Endotoxins; Escherichia coli Infections; Evaluation Studies as Topic; Fibrin; Humans; Hypothermia; Injury Severity Score; Multiple Trauma; Whole Blood Coagulation Time

Growth of Bacteroides fragilis and Escherichia coli was monitored during early stages of single (mono-) and mixed intra-abdominal infection in a rat fibrin clot model. When B. fragilis and E. coli were together involved in the infection, B. fragilis numbers increased about 6 h after an initial decline. This increase was not found with B. fragilis mono-infections. The numbers of E. coli increased rapidly in both mono- and mixed infections and stayed high for several days, but only mixed infection resulted in abscesses that persisted for more than 7 days. Macrophages, the main component of the peritoneal cellular defence mechanism, were outnumbered by polymorphonuclear leucocytes during the first 6 h of infection. Further characterisation of the macrophage population by means of monoclonal antibodies showed a shift from resident to exudate macrophages as the result of influx of the latter.

Topics: Abdomen; Animals; Bacteroides fragilis; Bacteroides Infections; Blood Coagulation; Cell Count; Colony Count, Microbial; Disease Models, Animal; Escherichia coli; Escherichia coli Infections; Fibrin; Humans; Male; Peritoneal Cavity; Rats; Rats, Inbred Strains

The synergic relationship between Escherichia coli and Bacteroides fragilis was examined in a model of intra-abdominal abscess formation. The addition of B. fragilis to E. coli in the fibrin clot inoculum increased abscess weight and residual numbers of E. coli in the abscess at 7 days. In a reciprocal fashion, E. coli was capable of enhancing B. fragilis persistence in abscesses. Neither heat-killed E. coli nor heat-killed B. fragilis was able to mimic the synergic effect of its live counterpart. Furthermore, B. fragilis culture filtrate was unable to reproduce the ability of live B. fragilis to act synergically with E. coli. For B. fragilis to act synergically with E. coli, it had to be inoculated locally with E. coli in the peritoneal cavity, indicating that an effect on systemic resistance by B. fragilis was an unlikely mechanism for the production of bacterial synergy. These studies suggest that the synergic relationship between bacteria in polymicrobial infections is a complex one, resulting from intimate interactions between bacteria and the host in the local milieu of the infection.

Topics: Abscess; Animals; Bacteroides fragilis; Bacteroides Infections; Disease Models, Animal; Escherichia coli; Escherichia coli Infections; Fibrin; Male; Peritonitis; Rats; Rats, Inbred Strains

We inoculated 120 rats with 2 X 10(9) Escherichia coli or 2 X 10(9) Bacteroides fragilis suspended in normal saline solution or incorporated into fibrin clots. In the control group, all animals died after inoculation with E coli, but none died after the inoculation with B fragilis; both were suspended in normal saline solution. Escherichia coli entrapped in fibrin did not cause mortality but did result in abscess formation in all animals. Bacteroides fragilis incorporated into fibrin clots resulted in abscess formation in the majority of animals. Treatment with gentamicin sulfate, ampicillin sulfate, and cefoxitin sodium completely abolished the mortality secondary to E coli suspended in normal saline solution but did not influence the rate of abscess formation secondary to E coli incorporated into fibrin clots. Similarly, cefoxitin and clindamycin phosphate did not significantly change abscess formation secondary to B fragilis incorporated into fibrin clots. We conclude that systemic antibiotics are ineffective in the prevention of abscesses secondary to bacteria trapped in fibrin, either because they do not reach bactericidal levels in the fibrin clot, as in the case of gentamicin, ampicillin, and clindamycin, or, as in the case of cefoxitin, because of the inoculum effect caused by the high number of bacteria. Fibrinogen or fibrin itself do not afford any protection of bacteria against the action of antibiotics.

Topics: Abscess; Ampicillin; Animals; Anti-Bacterial Agents; Ascites; Bacteroides fragilis; Bacteroides Infections; Blood Coagulation; Cefoxitin; Clindamycin; Escherichia coli; Escherichia coli Infections; Fibrin; Gentamicins; Male; Rats; Rats, Inbred Strains

The effect of aprotinin on the clinical and pathologic course of experimentally induced peritonitis in the rat was studied. Peritonitis was induced in 40 rats by creating a closed ileal loop 4 cm long 5 cm from the ileocecal valve. The rats were divided into two groups of 20 rats each. Group 1 served as a control group, whereas each animal in Group 2 received a bolus dose of aprotinin (10 ml) intraperitoneally immediately after closing the laparotomy. In the aprotinin-treated group, survival was drastically increased (p less than 0.01) and formation of adhesions and abscesses was considerably reduced. The results of peritoneal cultures showed a decreased incidence of Escherichia coli and Clostridia in the aprotinin-treated group. We conclude that the administration of aprotinin significantly prolongs the survival time of animals with peritonitis and reduces the development of adhesions and abscesses in the peritoneal cavity. This beneficial effect can be attributed to decreased fibrinogen deposits within the peritoneal cavity and the stabilization of the organism after bacterial shock. Thus, bacteria were more susceptible to cellular and noncellular clearing mechanisms.

Topics: Abscess; Animals; Aprotinin; Clostridium Infections; Escherichia coli Infections; Female; Fibrin; Male; Peritonitis; Rats; Rats, Inbred Strains; Surgical Wound Infection; Tissue Adhesions

We measured the rate of lethality and abscess formation in rats that underwent intraperitoneal implantation of fibrin clots contaminated with either Escherichia coli or Bacteroides fragilis alone or in combination, to determine whether the two organisms together would produce a synergistic infection. Ten-day mortality produced by 10(9) colony-forming units (CFU) of E coli was 33.3%. Encapsulated B fragilis led to 3.3% mortality. Escherichia coli (5 X 10(8) CFU) plus B fragilis (5 X 10(8) CFU) led to a sharp increase both in the rate and final ten-day mortality (80.0%). Eighty percent of the rats that received E coli (10(9) CFU within fibrin clots) had abscesses determined on the basis of grossly purulent material. All animals that received B fragilis and survived ten days contained abscesses. Synergy between E coli and B fragilis was noted to occur only when 5 X 10(8) CFU of each organism was present within the fibrin clot. Lower numbers did not produce significant synergy compared with controls that received either E coli or B fragilis. Quantitation of the number of organisms present at 24 hours within contaminated fibrin clots demonstrated a similar amount of growth of both organisms, either when added alone or in combination as copathogens.

Topics: Abscess; Animals; Bacteroides fragilis; Bacteroides Infections; Blood; Blood Coagulation; Disease Models, Animal; Escherichia coli; Escherichia coli Infections; Fibrin; Humans; Peritoneal Cavity; Peritonitis; Rats

Fibrin has classically been considered a defense mechanism of the peritoneal cavity. We have studied the role of purified fibrin in the pathogenesis of intraperitoneal infection. Implantation of 0.5% bovine fibrin clots containing 2 X 10(8) E. coli into the rat peritoneal cavity reduces the 24-hour mortality rate from 100% to 0% compared to bacteria in a similar volume of saline solution. However, the 10-day mortality rate with fibrin is 90%; 100% develop intraperitoneal abscesses. Animals receiving sterile clots lyse than over 1 to 2 weeks without abscess formation. As few as 10(2) E. coli per fibrin clot produce abscesses, but 10(7) or more are required to produce death; without fibrin less than 10(7) E. coli neither kill nor produce intraperitoneal infections. Both late death and abscess size with 2 X 10(8) E. coli are directly proportional to the fibrin clot size but not the concentration of fibrin in the clot. Operative debridement of the fibrin at 4 or 24 hours completely eliminates abscess formation in surviving animals. In vitro growth of E. coli is neither stimulated nor inhibited by fibrin or fibrinogen. Fibrin delays systemic sepsis, but the entrapped bacteria cannot be easily eliminated by normal intraperitoneal bactericidal mechanisms and abscess formation occurs. Thus radical peritoneal debridement or anticoagulation may reduce the septic complications of peritonitis.

Topics: Abscess; Animals; Escherichia coli; Escherichia coli Infections; Fibrin; Fibrinogen; Fibrinolysis; Male; Peritoneal Cavity; Peritonitis; Rats; Time Factors

In this study, an attempt was made to elucidate further the role of intravascular fibrin formation in the pathogenesis of sepsis in the primate. It was found that injected live Escherichia coli caused death in primates within four to 11 hours as a result of microcirculatory failure and acidosis. Pretreatment with Arvin did not prolong the survival rate, probably because of an overloading of the reticuloendothelial system with fibrin degradation products. This study does not support an obligatory role for intravascular coagulation or fibrin formation in primate sepsis and coincides with an earlier report (6) from this laboratory on cats. Vascular damage and malfunction, secondary to mediators released by platelets, leukocytes, red cells or Hageman factor, are not ruled out.

Topics: Ancrod; Animals; Blood; Blood Coagulation; Blood Pressure; Carbon Dioxide; Cardiac Output; Disease Models, Animal; Escherichia coli Infections; Female; Fibrin; Haplorhini; Heart Rate; Hemodynamics; Hydrogen-Ion Concentration; Lactates; Oxygen; Oxygen Consumption; Papio; Shock, Septic

Of 35 newborn infants who died from an infection 19 had postmortem evidence of massive pulmonary hemorrhage. All but 1 of the 19 had evidence of antimortem formation of intravascular fibrin clots in lung tissue. Seventeen infants had low platelet counts. Of the 11 infants in whom coagulation studies were done, 8 had evidence of disseminated intravascular coagulation (DIC) during life. Vasculitis in the lungs, associated with fibrin clots and hemorrhages, was detected in two infants. It is postulated that sepsis is an important cause of hemorrhage in the newborn, probably as a result of the development of DIC.

Topics: Bacterial Infections; Disseminated Intravascular Coagulation; Escherichia coli Infections; Fibrin; Hemoptysis; Humans; Infant, Newborn; Infant, Newborn, Diseases; Infant, Premature, Diseases; Klebsiella Infections; Lung; Male

Ninety-three postoperative patients 1 day to 13 years of age had blood cultures, limulus lysate assay, determination of fibrin degradation products, white blood cell and platelet counts. Seven groups were studied. The limulus lysate assay was often positive (64%) in the presence of gram negative septicemia but there were false positives and negatives. The tests for fibrin degradation products were inconsistent. The white blood cell count was low in babies with gram negative septicemia. One hundred per cent of the infants with gram negative septicemia had a platelet count below 150,000; 71% below 100,000 (average 67,000 septic babies, 257,000 non-septic babies). The drop in platelet count with gram negative septicemia was abrupt---as much as 222,000 in 24 hours. Platelets increased when therapy was effective. Two children with gram negative septicemia had platelet counts of 50,000 and 20,000. The platelet count for patients with gram positive septicemia was 299,000, and above 150,000 in all children with ruptured and non-ruptured appendicitis and major surgery without gram negative septicemia. It was concluded that serial measurements of platelet count in the postoperative infant and child was a rapid and reliable method for early detection of gram negative septicemia and changes in platelet count in response to treatment was an indicator of the effectiveness of therapy.

Topics: Abdominal Muscles; Adolescent; Appendicitis; Bacteria; Bacterial Infections; Blood Cell Count; Blood Platelets; Child; Child, Preschool; Enterocolitis, Pseudomembranous; Escherichia coli Infections; Fibrin; Gangrene; Humans; Infant; Infant, Newborn; Intestinal Obstruction; Klebsiella Infections; Leukocyte Count; Liver Neoplasms; Platelet Aggregation; Postoperative Complications; Pseudomonas Infections; Sepsis; Time Factors

Eight patients with E. coli septicaemia had oliguric renal failure which was associated with haematological evidence of intravascular coagulation. Five of these patients also had the characteristic blood picture of microangiopathic haemolytic anaemia. In an attempt to prevent further deposition of fibrin, intravenous heparin was administered to six patients, three of whom recovered fully and three died. The diagnosis of intravascular coagulation was subsequently confirmed by histological examination of necropsy material and it is suggested that some of the complications of E. coli septicaemia may be attributable to disseminated intravascular coagulation.

Topics: Anemia, Hemolytic; Autopsy; Blood Coagulation Tests; Blood Platelets; Disseminated Intravascular Coagulation; Erythrocyte Count; Escherichia coli Infections; Female; Fibrin; Hemoglobinometry; Heparin; Humans; Infant, Newborn; Injections, Intravenous; Leukocyte Count; Male; Middle Aged; Reticulocytes; Sepsis; Urea

Topics: Animals; Blood Platelets; Blood Protein Electrophoresis; Disseminated Intravascular Coagulation; Dogs; Erythrocytes; Escherichia coli Infections; Fibrin; Fibrinolysis; Lipoproteins; Lung; Microcirculation; Neutrophils; Pulmonary Circulation; Sepsis; Thromboembolism; Time Factors; Triglycerides

Topics: Anuria; Disseminated Intravascular Coagulation; Escherichia coli Infections; Fibrin; Humans; Kidney Failure, Chronic; Sepsis

Topics: Angiography; Animals; Blood Coagulation Disorders; Disseminated Intravascular Coagulation; Embolism, Fat; Escherichia coli Infections; Female; Fibrin; Infarction; Kidney; Kidney Cortex Necrosis; Kidney Diseases; Kidney Glomerulus; Lipids; Rabbits; Shwartzman Phenomenon; Toxemia; Triglycerides

Topics: Animals; Blood Vessels; Cell Membrane; Colitis; Colitis, Ulcerative; Colon; Crohn Disease; Cytoplasm; Disease Models, Animal; Edema; Endotoxins; Epithelium; Escherichia coli Infections; Fibrin; Intestinal Mucosa; Lymphatic System; Macrophages; Microscopy, Electron; Organoids; Phagocytosis; Swine

Topics: Animals; Blood Pressure; Capillaries; Cardiac Output; Dogs; Electrocardiography; Escherichia coli Infections; Fibrin; Heart Rate; Hypotension; Microscopy, Electron; Respiration; Shock, Hemorrhagic; Shock, Septic; Shock, Traumatic

Topics: Adult; Chemical Precipitation; Choroiditis; Diseases in Twins; Endotoxins; Escherichia coli Infections; Extraembryonic Membranes; Female; Fetal Death; Fetal Diseases; Fibrin; Humans; Infant, Newborn; Infant, Premature, Diseases; Obstetric Labor, Premature; Photomicrography; Placenta; Pregnancy; Pregnancy Complications, Infectious; Rupture; Shwartzman Phenomenon

Topics: Animals; Blood Coagulation; Blood Proteins; Dicumarol; Edema; Epilepsy; Epilepsy, Post-Traumatic; Escherichia coli Infections; Fibrin; Heparin; Inflammation; Leukocytes; Pharmacology; Rabbits; Rats; Research; Skin; Sulfur Isotopes