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)

Relapsing fever caused by Borrelia spirochetes is characterized by episodes of spirochetemia, fever, and DIC. We examined the ability of Borrelia hermsii to induce production of leukocytic pyrogen and thromboplastin from human blood leukocytes in vitro. Organisms were found devoid of endotoxin by the Limulus assay. Human peripheral blood leukocytes were separated into MNC and PMN fractions and were incubated with two to five spirochetes per cell in 10% human serum. Supernatant fluids from MNC-spirochete mixtures produced mean increases in the temperature of rabbits of 0.80 degree to 1.35 degrees C, which were significantly higher than those caused by supernatant fluids of MNC or spirochetes alone (p less than 0.05). MNC-spirochete mixtures possessed seven to 15 times the thromboplastic activity of MNC suspensions alone, assayed with a modified one-stage prothrombin time. Supernatant fluids of PMNs and spirochetes, on the other hand, did not contain leukocytic pyrogen, and PMN suspensions did not produce thromboplastin. Cycloheximide (10 micrograms/ml), and inhibitor of protein synthesis, completely suppressed both pyrogen and thromboplastin production. Although intracellular spirochetes were observed within phagosomes of blood monocytes by electron microscopy, the production of leukocytic pyrogen and thromboplastin was not significantly altered by serum opsonins or by the inhibitors of phagocytosis cytochalasin B (5 micrograms/ml) or phenylbutazone (2 mg/ml). These results showed that Borrelia spirochetes stimulated human MNCs to produce increased amounts of leukocytic pyrogen and thromboplastin and that this stimulation required de novo synthesis of protein, was not mediated by endotoxin, and was not prevented by omitting opsonic proteins or by inhibiting phagocytosis.
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PMID:Interaction of Borrelia spirochetes with human mononuclear leukocytes causes production of leukocytic pyrogen and thromboplastin. 706 69

A small outbreak of louse-borne relapsing fever in Khartoum (May-June 1974) provided material for a clinico-pathological study. The history of the disease in the Sudan is reviewed and the clinical and laboratory findings in 32 patients are presented. Fever, headache, jaundice, epistaxis and hepatosplenomegaly were the commonest clinical findings; thrombocytopenia was detected in 93% of cases. Although elevated levels of fibrin degradation products were found in most patients, disseminated intravascular coagulation could not be diagnosed. Hepatocellular derangement was found in 68% of cases, while 78% had high blood urea. In five autopsied bodies there was bronchopneumonia, interstitial edema with focal myocardial fibrosis, hepatic necrosis, splenic infarcts, increase in size and cellularity of the glomeruli and brain edema and congestion. Intracranial haemorrhage was found in three of the autopsied cases.
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PMID:Louse-borne relapsing fever in the Sudan. A historical review and a clinico-pathological study. 742

Clinical signs and haematological abnormalities of haemophagocytic syndrome of unknown origin are described for a male, nine-year-old rottweiler referred because of weakness, depression, mild weight loss and relapsing fever. Mucous membranes were pale and the spleen was enlarged. Ultrasonography revealed diffuse irregular structures in the enlarged spleen, and cytological examination of multiple fine needle aspirates of the spleen demonstrated extramedullary haematopoiesis. Haematological examination revealed pancytopenia and disseminated intravascular coagulation. A bone marrow smear contained numerous marrow macrophages with a cytologically benign appearance, containing phagocytosed haematopoietic cells. The dog died one week after referral. The differential diagnosis is discussed.
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PMID:Haemophagocytic syndrome with disseminated intravascular coagulation in a dog. 957 64

Thrombocytopenia is common in persons infected with relapsing fever Borreliae. We previously showed that the relapsing fever spirochete Borrelia hermsii binds to and activates human platelets in vitro and that, after platelet activation, high-level spirochete-platelet attachment is mediated by integrin alpha IIb beta 3, a receptor that requires platelet activation for full function. Here we established that B hermsii infection of the mouse results in severe thrombocytopenia and a functional defect in hemostasis caused by accelerated platelet loss. Disseminated intravascular coagulation, immune thrombocytopenic purpura, or splenic sequestration did not play a discernible role in this model. Instead, spirochete-platelet complexes were detected in the blood of infected mice, suggesting that platelet attachment by bacteria might result in platelet clearance. Consistent with this, splenomegaly and thrombocytopenia temporally correlated with spirochetemia, and the severity of thrombocytopenia directly correlated with the degree of spirochetemia. Activation of platelets and integrin alpha IIb beta 3 were apparently not required for bacterium-platelet binding or platelet clearance because the bacterium-bound platelets in the circulation were not activated, and platelet binding and thrombocytopenia during infection of beta 3-deficient and wild-type mice were indistinguishable. These findings suggest that thrombocytopenia of relapsing fever is the result of platelet clearance after beta 3-independent bacterial attachment to circulating platelets.
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PMID:Spirochete-platelet attachment and thrombocytopenia in murine relapsing fever borreliosis. 1285 86