Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human infections due to Yersinia enterocolitica have been reported worldwide, predominantly in Europe. However, there have been few reports of Yersinia enterocolitica infection in Taiwan. We report a case of Y. enterocolitica sepsis in a 15-year-old Taiwanese girl with Cooley's anemia and insulin-dependent diabetes mellitus. She presented at admission with fever, shock and consciousness disturbance. She had symptoms of abdominal pain, vomiting and diarrhea for three days before admission. Blood pressure stabilized after intravenous normal saline rescue. Blood culture yielded Y. enterocolitica 2 days later and ceftriaxone was administered according to the results of sensitivity tests. She recovered well after a course of antibiotic treatment. Though Y. enterocolitica sepsis is rare in Taiwan, clinicians should be aware of its tendency to develop in patients with Cooley's anemia, fever and enterocolitis and that its clinical course may include sepsis leading to shock.
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PMID:Yersinia enterocolitica sepsis in an adolescent with Cooley's anemia. 1278 40

Toll-like receptor 4 (TLR4)-mediated recognition of lipopolysaccharide (LPS) is required for efficient recognition of Gram-negative bacterial infections. Two commonly occurring mutations in the human TLR4 gene (Asp299Gly and Thr399Ile) have recently been shown to be associated with blunted physiological responses to inhaled LPS, and with increased risk of Gram-negative bacteraemia in sepsis patients and reduced risk of atherosclerosis in an Italian population. Here we show that monocytes from individuals heterozygous for both mutations in the TLR4 gene exhibit no deficit in recognition of LPS of Escherichia coli, Neisseria meningitidis, Bacteroides fragilis, Yersinia pestis, Chlamydia trachomatis, Porphyromonas gingivalis, or Pseudomonas aeruginosa. We propose that the relatively high frequency of these mutations in the Caucasian population may reflect modified responses of carriers to alternative TLR4 agonists.
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PMID:Monocytes heterozygous for the Asp299Gly and Thr399Ile mutations in the Toll-like receptor 4 gene show no deficit in lipopolysaccharide signalling. 1279 70

Population genetics and comparative genomics analyses of the pathogenic Yersinia species have indicated that arthropodborne transmission is an evolutionarily recent adaptation in Yersinia pestis, the agent of plague. We show that the infectivity of Y. pestis to its most proficient vector, the rat flea Xenopsylla cheopis, and subsequent transmission efficiency are both low. The poor vector competence of fleas likely imposed selective pressure that favored the emergence and continued maintenance of a hypervirulent Y. pestis clone. In particular, the rapidly fatal gram-negative sepsis that typifies plague is a consequence of the high threshold bacteremia level that must be attained to complete the transmission cycle. Epidemiological modeling predicts that, to compensate for a relatively short period of infectivity of the mammalian host for the arthropod vector, plague epizootics require a high flea burden per host, even when the susceptible host population density is high.
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PMID:Poor vector competence of fleas and the evolution of hypervirulence in Yersinia pestis. 1587 Nov 25

In patients with iron overload, opportunistic infections are an underestimated risk. Yersinia enterocolitica is a rare organism to be isolated in this setting. The authors report a case of disseminated Y. enterocolitica sepsis in a 5-year-old boy with sideroblastic anemia. Ultrasound examination revealed massive ascites, a pseudo-appendicitis, and hypoechogenic lesions corresponding to abscess formations in the liver and spleen. The initial antibiotic therapy consisted of cefotaxime, gentamicin, and metronidazole, but only treatment with ciprofloxacin and meropenem led to defervescence and clinical stabilization. The risk of developing uncommon infections in patients with iron overload should be acknowledged by all physicians, and the relevance of ultrasound examination is emphasized. In this case, only a detailed history revealed that several days before the onset of diarrhea, the child was feeding a deer; this is how infection was probably acquired.
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PMID:Multiple spleen and liver abscesses due to Yersinia enterocolitica septicemia in a child with congenital sideroblastic anemia. 1628 98

Yersinia pestis causes bubonic plague, characterized by an enlarged, painful lymph node, termed a bubo, that develops after bacterial dissemination from a fleabite site. In susceptible animals, the bacteria rapidly escape containment in the lymph node, spread systemically through the blood, and produce fatal sepsis. The fulminant progression of disease has been largely ascribed to the ability of Y. pestis to avoid phagocytosis and exposure to antimicrobial effectors of innate immunity. In vivo microarray analysis of Y. pestis gene expression, however, revealed an adaptive response to nitric oxide (NO)-derived reactive nitrogen species and to iron limitation in the extracellular environment of the bubo. Polymorphonuclear neutrophils recruited to the infected lymph node expressed abundant inducible NO synthase, and several Y. pestis homologs of genes involved in the protective response to reactive nitrogen species were up-regulated in the bubo. Mutation of one of these genes, which encodes the Hmp flavohemoglobin that detoxifies NO, attenuated virulence. Thus, the ability of Y. pestis to destroy immune cells and remain extracellular in the bubo appears to limit exposure to some but not all innate immune effectors. High NO levels induced during plague may also influence the developing adaptive immune response and contribute to septic shock.
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PMID:Adaptive response of Yersinia pestis to extracellular effectors of innate immunity during bubonic plague. 1686 91

Some labile cell types whose numbers are normally controlled through programmed cell death are subject to markedly increased destruction during some severe infections. Lymphocytes, in particular, undergo massive and apparently unregulated apoptosis in human patients and laboratory animals with sepsis, potentially playing a major role in the severe immunosuppression that characterizes the terminal phase of fatal illness. Extensive lymphocyte apoptosis has also occurred in humans and animals infected with several exotic agents, including Bacillus anthracis, the cause of anthrax; Yersinia pestis, the cause of plague; and Ebola virus. Prevention of lymphocyte apoptosis, through either genetic modification of the host or treatment with specific inhibitors, markedly improves survival in murine sepsis models. These findings suggest that interventions aimed at reducing the extent of immune cell apoptosis could improve outcomes for a variety of severe human infections, including those caused by emerging pathogens and bioterrorism agents.
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PMID:Prevention of immune cell apoptosis as potential therapeutic strategy for severe infections. 1747 79

The Yersinia genus belongs to the Enterobacteriacae family and comprises strains pathogenic for humans, which causes diseases of the gastrointestinal system. The infection can be transmitted with blood and blood components causing sepsis. The paper presents Yersinia enterocolitica complications after transfusion of blood and blood components as well as the frequency of occurrence and preventive measures.
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PMID:[Infections of the gastrointestinal system--risk of transmission with blood and blood components]. 1767 6

Over last decade problem of infectious diseases in Poland remains stable with trends of decreasing incidence of most reported infectious diseases. In particular there was observed decrease in incidence of tuberculosis and foodborne infections causes by Salmonella sp. On the other hand it was observed increase of reported foodborne infections caused by Campylobacter and Yersinia as well and viral ones caused by noroviruses and rotaviruses. Despite marked increase of diagnosed and reported cases sensitivity of reporting of those infections remains unacceptably low. Reported incidence of HIV infections remains relatively stable over last years. But increased fraction of heterosexually transmitted cases points to the problem of increased incidence out of so called "risk groups" among the general population. It was also noted worrisome increase of incidence of syphilis. The highest incidence was noted regarding influenza and other upper respiratory tract infections. Low level of vaccinations against influenza remains the problem which requires continuous health promotion efforts. The best epidemiological situation was observed among vaccine preventable diseases, which reflects effectiveness of vaccination program. Though widening of our program into several important infections included in vaccination programs of other EU countries would be needed in oncoming years. Infectious diseases caused 0.70% of deaths. Mortality from infectious diseases was 6.8/100,000 and was significantly higher among men (8.8) then among women. (5.0). In urban settings mortality from infectious diseases was higher (7.4/100,000) then in the country (5.8). In particular districts (voivodeships) mortality indices remained in the range of 5.2 (podlaskie) to 9.7 (slaskie). The highest number of deaths was caused by sepsis (41.1%, without neonatal sepsis).
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PMID:[Infectious diseases in Poland in 2006]. 1880 59

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

Antibodies provide a sensitive indicator of proteins displayed by bacteria during sepsis. Because signals produced by infection are naturally amplified during the antibody response, host immunity can be used to identify biomarkers for proteins that are present at levels currently below detectable limits. We developed a microarray comprising approximately 70% of the 4066 proteins contained within the Yersinia pestis proteome to identify antibody biomarkers distinguishing plague from infections caused by other bacterial pathogens that may initially present similar clinical symptoms. We first examined rabbit antibodies produced against proteomes extracted from Y. pestis, Burkholderia mallei, Burkholderia cepecia, Burkholderia pseudomallei, Pseudomonas aeruginosa, Salmonella typhimurium, Shigella flexneri, and Escherichia coli, all pathogenic Gram-negative bacteria. These antibodies enabled detection of shared cross-reactive proteins, fingerprint proteins common for two or more bacteria, and signature proteins specific to each pathogen. Recognition by rabbit and non-human primate antibodies involved less than 100 of the thousands of proteins present within the Y. pestis proteome. Further antigen binding patterns were revealed that could distinguish plague from anthrax, caused by the Gram-positive bacterium Bacillus anthracis, using sera from acutely infected or convalescent primates. Thus, our results demonstrate potential biomarkers that are either specific to one strain or common to several species of pathogenic bacteria.
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PMID:Extensive antibody cross-reactivity among infectious gram-negative bacteria revealed by proteome microarray analysis. 1911 81


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