Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antiserum to the core glycolipid of gram-negative bacteria was prepared by immunization of rabbits with vaccine composed of killed cells of the uridine diphosphate galactose-deficient mutant (J5) of Escherichia coli O:111. Antiserum to J5 not only prevented death of animals from endotoxin but also prevented the local and generalized Shwartzman reactions. Antiserum to endotoxin also prevented renal cortical necrosis and disseminated intravascular coagulation during the evolution of the generalized Shwartzman reaction. Antiserum to be J5 mutant was successful in the treatment of overwhelming bacteremia produced by other gram-negative bacteria; in addition to bacteremia cause by coliform organism, antiserum to J5 was dramatically effective in treatment of bacteremia due to Pseudomonas aeruginosa. One injection of rabbit antiserum to J5 improved the survival rate from 15% in controls to 59% in treated animals (P less than 0.002). Active immunization with J5 vaccine was even more effective against pseudomonas bacteremia: such immunization improved the survival rate from 13% in controls to 92% in vaccinated rabbits. Since an antiserum effective against the J5 mutant of E. coli can be prepared safely in human subjects, such immunotherapy should be considered for patients with gram-negative bacteremia.
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PMID:Antibody to cell wall glycolipid of Gram-negative bacteria: induction of immunity to bacteremia and endotoxemia. 33 Jul 76

Platelets were labelled with 51Cr, fibrinogen with 125I and erythrocytes with 59Fe. Disintegrated Pseudomonas bacteria were injected intravenously and radioactive measurements were made on whole blood; tissue biopsies and clottable fibrinogen. After the infection there was an immediate but transient increase of 51Cr activity in the lung concomitant with a decrease in platelet count and 51Cr activity of blood. In the liver there was a less pronounced increase of 51Cr activity. The fibrinogen concentration decreased slightly, paralleled by the 125I activity of whole blood and of clottable fibrinogen, whereas the 125I activity in the lung and liver remained fairly constant. There was no changes of 51Cr activity or 125I activity in biopsies from muscle, pancreas, small intestine, kidney or spleen. During the experiment (3h) there were no signs of significant disseminated intravascular coagulation other than platelet aggregation. A consumption of fibrinogen related to the formation of fibrin plugs could not be detected. After injection of disintegrated Pseudomonas bacteria reversible platelet aggregates were formed and temporarily trapped in the pulmonary microcirculation. This microembolism might induce tissue damage and could be of importance for the development of septic pulmonary complication.
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PMID:Microembolism in experimental septic shock. Distribution of platelets and fibrinogen after intravenous injection of disintegrated Pseudomonas bacteria to dogs. 84 64

The causes of death were investigated in 315 adults with acute leukemia during a 7-year period (1966-1972). Infection alone or in combination was the most common cause (75%), followed by hemorrhage (24%) and organ failure (9%). Most of the infections were either systemic or pulmonary. Seventy-five percent of the systemic infections and 72% of the pneumonias were caused by bacteria. Klebsiella pneumoniae, Escherichia coli and Pseudomonas aeruginosa were the most frequent organisms isolated. After 1968, there was a sharp decrease in the number of fatal infections caused by Pseudomonas aeruginosa and a marked increase in the incidence of fatal infections caused by Klebsiella spp. and E. coli. Infections caused by Gram-positive cocci occurred in only 3% of the cases. The incidence of systemic fungal infections was 13%; most common fungi causing infection were Candida spp. and Aspergillus spp. Eighty-five percent of 159 patients with a terminal neutrophil count of less than 100/mm3 died of infection, compared to 48% of 62 patients with a terminal neutrophil count of greater than 1000/mm3. Hemorrhage was mostly due to thrombocytopenia (61%) and disseminated intravascular coagulation (12%). This study indicates that infection continues to be the most common cause of death in patients with acute leukemia. Although advances in antibiotic therapy have changed the distribution of causative organisms, ultimate control of infection requires further improvements in supportive care measures which rectify impairments in the patients' host defense mechanisms.
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PMID:Causes of death in adults with acute leukemia. 106 11

We report a retrospective, clinicopathologic study of 139 patients who died during treatment of a severe burn. Fifty-three percent of the patients had central nervous system (CNS) complications-infections, cerebral infarcts and hemorrhages, metabolic encephalopathies, central pontine myelinolysis, and cerebral trauma. Children and adults were equally affected. Sixteen percent of the patients had a CNS infection. Candida species, Staphylococcus aureus and Pseudomonas aeruginosa caused almost 80% of them. S. aureus and candida caused cerebral microabscesses and septic infarcts. P. aeruginosa caused meningitis and infarcts due to meningitis. CNS infections arose as a result of spread from a systemic source. The major risk factors for CNS infection were an extensive burn, S. aureus endocarditis, and a burn wound infection due to candida or P. aeruginosa. Patients with burns of less than 30% of the surface area of their body, those without a systemic infection, and those in the first week after their burn were at low risk. Eighteen percent of the patients had cerebral infarcts. In almost half the patients, the infarcts were caused by septic arterial occlusions or other complications of the burn, viz, disseminated intravascular coagulation (DIC) and septic shock. In only one-third of the patients were infarcts due to atherosclerosis, atrial fibrillation, or other causes prevalent in the general population. Intracranial hemorrhages were only one-fifth as frequent as infarcts and were due to DIC and thrombocytopenia, caused by bacteremia. Diagnosis during life was difficult, because the neurologic picture of focal cerebral lesions and meningitis was indistinguishable from that of metabolic encephalopathies, and because many patients had more than 1 neurologic complication. However, our results suggest that a clinical approach that includes analysis of risk factors for CNS infection, cerebral imaging, examination of cerebrospinal fluid, and tests for DIC can lead to a neurologic and microbiologic diagnosis in most patients.
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PMID:Central nervous system complications of thermal burns. A postmortem study of 139 patients. 152 3

126 cases of sepsis were retrospectively studied in an Internal Medicine Department, giving special attention to the clinical evolution. 67 males and 59 females with a median age of 65 years old were discovered. 92% had one or more diseases, mainly COLD (30%) and diabetes mellitus (28%). The septic sources were urinary (37%) and respiratory (31%). 84% of the germs were gram (-), mainly E. Coli and Proteus sp. A mortality rate of 36% was found, the primary rates being: eighth decade (52%), patients with neoplastic disease (46%), biliary tract diseases (64%), endocarditis (66%), infection by Serratia (60%), Pseudomonas (50%), shock (55%) and DIC (50%). These last two complications were analysed and found to be the more frequent (35% and 6.3% respectively), also being those with higher mortality rate. Finally, the prognostic factors are established based on the results obtained.
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PMID:[Sepsis: clinical course study of 126 patients in an internal medicine department]. 249 19

We experienced 57 episodes of Pseudomonas aeruginosa bacteremia in 55 patients with hematologic disorders in a 16-year period. Ninety-five percent of the patients had hematologic malignancies such as acute leukemia. All but one patient received cytotoxic or immunosuppressive therapy at or prior to the onset of bacteremia. Seventy-seven percent of the episodes occurred during profound granulocytopenia of below 100/mm3. All the patients acquired their infection in the hospital, and 96% had received antibiotic therapy during the preceding two weeks. Periodontal, anorectal, lower respiratory tract, and urogenital infections were the sources of bacteremia in about three-quarters of the episodes. Periodontal infection tended to progress to cellulitis of the face or the floor of the mouth, often resulting in bacteremia of the unimicrobial type, while anorectal infection predisposed to abscess formation, frequently leading to bacteremia of the polymicrobial type. Cellulitis at onset was seen in 35% of the episodes. Most sites of infection did not become apparent until one to three days after the onset of fever, probably because of depressed inflammatory response associated with severe granulocytopenia. The majority of patients complained of gastrointestinal symptoms such as nausea and vomiting, abdominal pain, diarrhea, and abdominal fullness at the onset of bacteremia. Major complications included bacteremic shock (63%), impaired consciousness (25%), ecthyma gangrenosum or hemorrhagic gangrenous cellulitis (18%), and jaundice (12%). Furthermore, there were one case each of endocarditis and disseminated intravascular coagulation. It was thus suggested that the clinical picture of P. aeruginosa bacteremia complicating hematologic disorders is influenced by the predisposing conditions associated with the underlying diseases and their treatment.
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PMID:[Pseudomonas aeruginosa bacteremia associated with hematologic disorders [I]. Predisposing factors and clinical manifestations]. 250 86

In short, bacterial sepsis is associated with a number of peripheral manifestations involving the skin and soft tissues. The pathogenesis of the lesions observed is not fully understood and is almost certainly multifactorial. In ecthyma gangrenosum, the presence of large numbers of gram-negative bacilli in the walls of small blood vessels without a substantial inflammatory response suggests that either the bacteria themselves or bacterial products are responsible for tissue damage. Endotoxin probably plays a prominent role in producing these lesions. That Pseudomonas and Aeromonas species seem to cause ecthyma out of proportion to their prevalence as a cause of bacteremia might suggest that the endotoxin of these organisms has a special predilection for skin and subcutaneous structures. More likely, it indicates that other bacterial substances, such as exotoxins or proteases, are involved. The absence of PMN leukocytes is thought to play a permissive role, allowing unopposed bacterial proliferation. Lesions of symmetric peripheral gangrene characteristically do not have bacteria present. The presence of intravascular fibrin accumulation probably resembles the generalized Shwartzman phenomenon. However, the gangrenous lesions themselves more likely result from systemic hypotension and the resulting hypoperfusion of the tissues than from vessel obstruction. In lesions associated with vigorous inflammatory response, bacterial products may damage tissue either directly or by attracting leukocytes that, in turn, release substances that cause further tissue damage. An etiologic role for endotoxin or the gram-positive bacterial cell wall is likely, since endotoxin is known to produce similar lesions in the localized Shwartzman reaction. Favoring a role for other bacterial substances is the predisposition of V. vulnificus to cause cellulitis or of C. fetus to cause inflammation of the major vessels during sepsis; the mechanisms for these reactions are entirely unknown. It is interesting that in most instances in which peripheral lesions are caused by sepsis, either a large number of bacteria or an intense inflammatory response by PMNs is present, but not both. In both kinds of lesion, the tendency to involve blood vessels by different pathogenetic mechanisms contributes to the evolution of the disease process. In intensely inflamed lesions, veins and arteries can be shown histologically to be occluded. In the absence of inflammation, bacterial invasion of vessel walls or simply the presence of bacterial products adjacent to the vessel may produce spasm. As noted, the pathogenetic significance of thrombosis observed in the lesions of DIC remains unclear.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cutaneous manifestations of bacterial sepsis. 252 95

Pseudomonas putrefaciens is an unusual cause of human disease. Since 1978 only five cases of bacteremia due to this organism have been reported. Within 12 recent months four cases of bacteremia due to P. putrefaciens were seen - two occurred in patients with chronic infections of a lower extremity, one in a patient with neutropenia, and one in a patient with fulminant septicemia and disseminated intravascular coagulation. Two of the patients had prostheses; in neither case did prosthetic infection or prosthetic failure occur. Two syndromes of bacteremic infection with P. putrefaciens are suggested. One syndrome is associated with chronic infection of a lower extremity, is fairly well tolerated, and responds to appropriate antimicrobial agents. The other syndrome is more fulminant and may be associated with severe underlying debility, liver disease, and malignancy. It is not yet known whether this is a meaningful distinction. The significance of the recent increase is the isolation of this organism is not clear at present.
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PMID:Pseudomonas putrefaciens bacteremia. 291

Sputum cultures are not helpful in the immediate management of patients with bacterial pneumonia. Sputum Gram stains may provide a presumptive identification of an etiologic agent; this procedure, however, is insensitive (approximately 50%). Consequently, during the last decade, other more sensitive and specific methods of providing a rapid etiologic diagnosis have been sought. This article discusses data on antigen detection in various body fluids by counterimmunoelectrophoresis and agglutination tests. Results from our own laboratory as well as those reported in the literature are presented. The best estimates of antigen detection rates, by the most sensitive assays, in pneumococcal pneumonia, are as follows: serum, 45%-80%; urine, 50%-64%; and sputum, 75%-100%. There is less information for Haemophilus, Klebsiella, and Pseudomonas pneumonias, but the diagnostic yield is approximately 50%-100%. Data will also be presented on the association between free and complexed antigens and morbidity and mortality in pneumococcal pneumonia. Indicators of morbidity discussed include disseminated intravascular coagulation, duration and severity of illness, and occurrence of nephritis.
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PMID:Antigen detection in the diagnosis and in the prognostic assessment of bacterial pneumonias. 293 73

Platelet-bacterial interactions were examined in vitro by incubating organisms isolated from patients with septicemia with normal platelet-rich plasma. The potency of various species of gram-positive and gram-negative bacteria to induce irreversible platelet aggregation was then determined in an aggregometer. The aggregation curves produced by the bacteria resembled the normal platelet response to collagen and were impeded by the presence of aspirin. Strains of Staphylococcus aureus and Pseudomonas aeruginosa isolated from 25 different patients produced maximum increases in light transmission and irreversible platelet aggregation with relatively rapid mean aggregation times; six of these patients had clinical and laboratory evidence of disseminated intravascular coagulation. In contrast, isolates of alpha streptococcus and Staphylococcus epidermidis induced irreversible platelet aggregation much less commonly and were associated with considerably longer mean aggregation times. None of the latter group of patients had evidence of disseminated intravascular coagulation. Isolates of bacteria from a small number of patients with subacute bacterial endocarditis uniformly induced irreversible platelet aggregation. Addition of paired bacterial isolates to normal platelet-rich plasma demonstrated a synergistic aggregation response. These data suggest that a relative hierarchy exists in bacterial strain potency to induce irreversible platelet aggregation. The rapidity and degree of aggregation in vitro correlated well with the clinical and laboratory evidence for subacute bacterial endocarditis and disseminated intravascular coagulation in vivo. These observations may provide useful adjunctive laboratory information to help establish the diagnosis of subacute bacterial endocarditis, especially in the clinical setting where the classical findings of endocarditis are not obvious during initial presentation.
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PMID:In vitro correlation of platelet aggregation with occurrence of disseminated intravascular coagulation and subacute bacterial endocarditis. 310 30


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