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)

A 37-year-old male, a poorly-controlled insulin-dependent diabetic patient, was admitted to our hospital with complaints of high fever and confusion. Laboratory data showed hyperglycemia, positive inflammatory reaction and liver dysfunction. Blood culture demonstrated Yersinia enterocolitica. Liver CT scan showed multiple low density areas. These data were consistent with a diagnosis of liver abscess secondary to Yersinia enterocolitica. He died of disseminated intravascular coagulation; subsequent autopsy confirmed the clinical diagnosis. Liver abscess secondary to Yersinia enterocolitica with septicemia is rare, but has been reported in compromised hosts. In the mechanism of this disease, the alimentary tract has been suggested to be the port of entry in most cases.
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PMID:Multiple liver abscesses secondary to Yersinia enterocolitica. 142 22

A 47-year old man was operated for a malignant tumour of the bladder. During cystectomia packed red cells had to be transfused. Minutes after the rapid transfusion the oxygen saturation dropped. In the following hours his circulation became unstable and the pulmonary function deteriorated. Signs of disseminated intravascular coagulation occurred, making more transfusions necessary. Inspite of all intensive-care efforts the patient died with a multiorgan failure caused by endotoxin shock 66 hours after having received the first transfusions. In the blood cultures of the patient and in the cultures of the first transfused unit of packed red cells Yersinia enterocolitica was isolated.
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PMID:[Fatal Yersinia infection after intraoperative transfusion]. 908 22

Although bacteremia and sepsis are infrequently reported complications of red blood cell (RBC) transfusion, receipt of transfused blood contaminated with bacterial pathogens may result in sepsis, disseminated intravascular coagulation, and death. Such pathogens have included Yersinia enterocolitica and Pseudomonas fluorescens. From November 1985 through February 1991, a total of 11 cases of sepsis associated with receipt of transfused Y. enterocolitica-contaminated RBCs were reported in the United States. This report describes an additional 10 cases of Y. enterocolitica sepsis reported to CDC during March 1991-November 1996 in patients who received transfusions with contaminated RBCs and describes the development of a study to detect bacteria-associated reactions to transfusion of RBCs and other blood components.
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PMID:Red blood cell transfusions contaminated with Yersinia enterocolitica--United States, 1991-1996, and initiation of a national study to detect bacteria-associated transfusion reactions. 922 23

Although the literature on infections transmitted via transfused blood focuses on viruses, Yersinia enterocolitica can also cause severe infections in patients receiving transfusions. A 13-year-old patient developed severe sepsis after an autologous blood transfusion contaminated with Y. enterocolitica. The patient was an otherwise healthy female undergoing posterior spinal fusion for congenital scoliosis. Prior to surgery, the patient donated blood for perioperative and postoperative use. A few days before the donation, she had complained of abdominal pain and was experiencing mild diarrhea. The patient received four units of packed red blood cells (PRBCs) during the surgery. Intraoperatively, the patient developed fever up to 103.6 degrees F, became hypotensive requiring epinephrine and dopamine, and developed metabolic acidosis with serum bicarbonate concentration dropping to 16 mmol/l. The surgery team believed the patient was experiencing malignant hyperthermia and attempted to cool patient during the procedure. Postoperatively, the patient was transferred to the pediatric intensive care unit and treated for severe shock of unknown etiology. The patient further developed disseminated intravascular coagulation. The patient received supportive care and was started on ampicillin/sulbactam on postoperative day (POD) one which was changed to clindamycin, ciprofloxacin and tobramycin on POD two when blood cultures grew gram-negative bacilli. On POD three, cultures were identified as Y. enterocolitica and antibiotics were changed to tobramycin and cefotaxime based on susceptibility data. Sequelae of the shock included adult respiratory distress syndrome requiring intubation and a tracheostomy and multiple intracranial hemorrhagic infarcts with subsequent seizure disorder. Due to severe lower extremity ischemia, she required a bilateral below the knee amputation. The cultures of the snippets from the bags of blood transfused to the patient also grew Y. enterocolitica. This case illustrates the importance of considering transfusion related bacterial infections in patients receiving PRBCs. All patients in shock following any type of transfusion may require aggressive antibiotic therapy, until the diagnosis and etiology are known.
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PMID:Yersinia septic shock following an autologous transfusion in a pediatric patient. 1262 Feb 65

We report a case of Yersinia pseudotuberculosis (Y. ptbc) infection complicated by disseminated intravascular coagulation (DIC) that presented as Kawasaki disease (KD). A 9-year-old girl had been well until two days before, when she developed a fever, exanthem, and abdominal pain. An erythematous macular rash was observed in the perineum, and she had a strawberry tongue. The patient was admitted to Kawasaki Medical School Hospital because the macular rash spread over her entire body, and edema of her hands and conjunctivitis subsequently developed. Echo cardiography showed dilation of the left coronary artery. Thrombocytopenia and an elevated total fibrin degeneration product level were noted on the third hospital day, and the prothronmbin and partial-thromboplastin times were prolonged. Her clinical presentation was typical of KD and DIC. A stool culture and a blood culture were negative. Serologic tests were positive for antibodies to Y. ptbc. The antibody titer against Y. ptbc-derived mitogen was not elevated after her recovery. Y. ptbc infection should be considered in an older child whose clinical findings fulfill the criteria for KD complicated by DIC.
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PMID:[Yersinia pseudotuberculosis type 4a infection meeting the diagnostic criteria for Kawasaki disease complicated by disseminated intravascular coagulation]. 1636 61

Yersinia pestis, the causative agent of plague, is known to develop strategies to overcome the host immune mechanisms and survive in the host. The molecular changes induced by Y. pestis in the host are not well delineated. Here, we examined the early events triggered after the intracellular infection of Y. pestis in human monocytes and lymphocytes by analyzing the host transcriptional profiles using cDNA arrays. We found that sets of genes that, especially at early time periods, were highly upregulated in monocytes alone when compared with a mixed culture of lymphocytes and monocytes. Gene expression responses revealed genes coding for cytokines, chemokines, transcription factors, inflammatory and apoptosis-related genes. Protein levels were measured, and real-time polymerase chain reaction was used to validate the microarray results. Our data suggest that intracellular infection of human monocytes with Y. pestis results in a strong inflammatory response at early time periods and a downregulation of genes such as thromobomodulin, which may play a role in coagulation, resulting in disseminated intravascular coagulation, a primary cause of death in plague infected hosts. We provide evidence that genomic analysis can provide a solid foundation to mechanistic insights to explain some of the symptoms induced by Y. pestis.
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PMID:Study of proinflammatory responses induced by Yersinia pestis in human monocytes using cDNA arrays. 1742 14

The immune response to infection includes activation of the blood clotting system, leading to extravascular fibrin deposition to limit the spread of invasive microorganisms. Some bacteria have evolved mechanisms to counteract this host response. Pla, a member of the omptin family of Gram-negative bacterial proteases, promotes the invasiveness of the plague bacterium, Yersinia pestis, by activating plasminogen to plasmin to digest fibrin. We now show that the endogenous anticoagulant tissue factor pathway inhibitor (TFPI) is also highly sensitive to proteolysis by Pla and its orthologs OmpT in Escherichia coli and PgtE in Salmonella enterica serovar Typhimurium. Using gene deletions, we demonstrate that bacterial inactivation of TFPI requires omptin expression. TFPI inactivation is mediated by proteolysis since Western blot analysis showed that TFPI cleavage correlated with loss of anticoagulant function in clotting assays. Rates of TFPI inactivation were much higher than rates of plasminogen activation, indicating that TFPI is a better substrate for omptins. We hypothesize that TFPI has evolved sensitivity to proteolytic inactivation by bacterial omptins to potentiate procoagulant responses to bacterial infection. This may contribute to the hemostatic imbalance in disseminated intravascular coagulation and other coagulopathies accompanying severe sepsis.
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PMID:Proteolytic inactivation of tissue factor pathway inhibitor by bacterial omptins. 1898 66