Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical features and diagnostic and prognostic values of systemic inflammatory response syndrome (SIRS) were studied in 158 children with rhino-sinusogenic orbital and intracranial complications. Patients, whose condition was more severe, showed more SIRS markers and more often needed surgical removal of the primary infectious process in paranasal sinuses (31%). Increase of the SIRS symptoms led to an increase of organic dysfunction from 3.3% to 53.3%. The main targets for shock are the brain and meninges, with the lungs being often the second target and the hemostasis system being also often involved. Complicated rhinosinusitis should be regarded as septic if in addition to the primary infectious process the child has two or more SIRS symptoms and signs of organic dysfunctions. This approach to the diagnosis and treatment of sepsis results in recovery of 98.5 of children with this condition.
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PMID:[Syndrome of systemic inflammatory response in children with septic pyogenic complications of rhinosinusitis]. 1269 56

Early diagnosis of cranial sepsis is mandatory if morbidity is to be avoided. In the case of structural integrity of the skull, haematogenous spread or extension from adjacent structures, especially the sinuses, are the most common sources of infection. Infections may be limited to compartments by the meninges or spread diffusely. Focal disease includes brain abscess as well as subdural and extradural empyaema. A history or signs of sinus disease should always be sought. Tuberculosis, lyme disease and listeriosis may present specific pathological findings. A series of cases is presented to illustrate the role of imaging in infective disease and to draw attention to diagnostic and management points of which radiologists should be aware.
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PMID:Cranial bacterial infection. 1474 53

Well known complications related to cocaine use are myocardial insufficiency, myocardial infarction, myocarditis, aortic dissection, neurologic damages, ischemic colitis, thrombotic phenomenons, renal infarction and acute liver failure. Cases of splenic infarctions related to cocaine use are extremely rare. A 17-year-old drug addict was found by her boy-friend liveless in her bed. She was well known using cocaine since years. Autopsy revealed multiple splenic infarctions with secondary mixed bacterial infection and abscesses. Petechial bleedings were found and microabscesses in the myocardium, the meninges and the kidneys. The absolutely rare bacterial infection of the cocaine-associated splenic infarction leads to sepsis with lethal course.
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PMID:Cocaine-associated abscesses with lethal sepsis after splenic infarction in an 17-year-old woman. 1501 62

Streptococcus bovis is one of the nonenterococcal species included among the streptococci group D. It is part of the normal bowel flora in humans and animals, but it is also responsible for infectious diseases (10-15% of all cases of bacterial endocarditis). Many cases of bacteremia and metastatic abscesses (spleen, liver, soft tissues, bone, meninges, endocardium) caused by S. bovis were reported as associated with digestive tract diseases, mainly colonic disease, and, in particular colonic neoplasms, or chronic liver diseases. A role in carcinogenesis has been suggested for this microorganism. The authors report two cases of S. bovis sepsis, one associated with colonic neoplasm and the other with liver cirrhosis and gastric carcinoma. Discussion is focused on probable mechanisms that favor gastric colonization and systemic diffusion of S. bovis from the gut in patients with gastrointestinal neoplasms or chronic liver disease and provides clinical recommendations for patients with S. bovis infections.
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PMID:Non-life-threatening sepsis: report of two cases. 1516 50

Advances in neonatal management have led to considerable improvement in newborn survival. However, early (<72 hours) and late (>72 hours) onset systemic infections, both bacterial and fungal, remain a devastating complication and an important cause of morbidity and mortality in these babies. Most neonatal fungal infections are due to Candida species, particularly Candida albicans. The sources of candidiasis in NICU are often endogenous following colonization of the babies with fungi. About 10% of these babies get colonized in first week of life and up to 64% babies get colonized by 4 weeks of hospital stay. Disseminated candidiasis presents like bacterial sepsis and can involve multiple organs such as the kidneys, brain, eye, liver, spleen, bone, joints, meninges and heart. Confirming the diagnosis by laboratory tests is difficult and a high index of suspicion is required. The diagnosis of fungemia can be made definitely only by recovering the organism from blood or other sterile bodily fluid. Amphotericin B continues to be the mainstay of therapy for systemic fungal infections but its use is limited by the risks of nephrotoxicity and hypokalemia. Newer formulations of amphotericin B, namely the liposomal and the lipid complex forms, have recently become available and have been reported to have lesser toxicity. More recently Indian liposomal Amphotericin B derived from neutral lipids (L-Amp-LRC-1) has shown good response with less toxicity. A clinical trial with this preparation has shown to be safe and efficacious in neonatal fungal infections. Compared to other liposomal preparations, L-Amp-LRC-1 is effective at lower dose and is less expensive drug for the treatment of neonatal candidiasis.
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PMID:Systemic fungal infections in neonates. 1651 52

Escherichia coli is the principal gram-negative causative agent of sepsis and meningitis in neonates. The pathogenesis of meningitis due to E. coli K1 involves mucosal colonization, transcytosis of epithelial cells, survival in the blood stream and eventually invasion of the meninges. The latter two aspects have been well characterized at a molecular level in the last decade. Less is known about the early stages of pathogenesis, i.e. adhesion to and invasion of gastrointestinal cells. Here, the characterization of the Hek protein is reported, which is expressed by neonatal meningitic E. coli (NMEC) and is localized to the outer membrane. It is demonstrated that this protein can cause agglutination of red blood cells and can mediate autoaggregation. Escherichia coli expressing this protein can adhere to and invade epithelial cells. So far, this is the first outer membrane protein in NMEC to be directly implicated in epithelial cell invasion.
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PMID:The Hek outer membrane protein of Escherichia coli is an auto-aggregating adhesin and invasin. 1724 Dec 43

In spite of antibiotic treatment, pneumococcal meningitis continues to be associated with significant morbidity and mortality. The complement system is a key component of innate immunity against invading pathogens. However, activation of complement is also involved in tissue damage, and complement inhibition by C1 inhibitor (C1-inh) is beneficial in animal models of endotoxemia and sepsis. In the present study, we demonstrate classical pathway complement activation during pneumococcal meningitis in rats. We also evaluate the effect of C1-inh treatment on clinical illness, bacterial clearance, and inflammatory responses in rats and mice with pneumococcal meningitis. C1-inh treatment was associated with reduced clinical illness, a less-pronounced inflammatory infiltrate around the meninges, and lower brain levels of proinflammatory cytokines and chemokines. C1-inh treatment increased bacterial clearance, possibly through an up-regulation of CR3. Hence, C1-inh may be a useful agent in the treatment of pneumococcal meningitis.
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PMID:C1 inhibitor treatment improves host defense in pneumococcal meningitis in rats and mice. 1753 91

Streptococcus suis, an important swine and human pathogen, causes septic shock and meningitis. The pathogenesis of both systemic and CNS infections caused by S. suis is poorly understood. A hematogenous model of infection in CD1 mice was developed to study the systemic release of cytokines during the septic shock phase and the proinflammatory events in the CNS associated with this pathogen. Using a liquid array system, high levels of systemic TNF-alpha, IL-6, IL-12, IFN-gamma, CCL2, CXCL1, and CCL5 were observed 24 h after infection and might be responsible for the sudden death of 20% of animals. Infected mice that survived the early sepsis later developed clinical signs of meningitis and exhibited lesions in the meninges and in numerous regions of the brain, such as the cortex, hippocampus, thalamus, hypothalamus, and corpus callosum. Bacterial Ags were found in association with microglia residing only in the affected zones. In situ hybridization combined with immunocytochemistry showed transcriptional activation of TLR2 and TLR3 as well as CD14, NF-kappaB, IL-1beta, CCL2, and TNF-alpha, mainly in myeloid cells located in affected cerebral structures. Early transcriptional activation of TLR2, CD14, and inflammatory cytokines in the choroid plexus and cells lining the brain endothelium suggests that these structures are potential entry sites for the bacteria into the CNS. Our data indicate an important role of the inflammatory response in the pathogenesis of S. suis infection in mice. This experimental model may be useful for studying the mechanisms underlying sepsis and meningitis during bacterial infection.
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PMID:Streptococcus suis serotype 2, an important swine and human pathogen, induces strong systemic and cerebral inflammatory responses in a mouse model of infection. 1764 Oct 51

Escherichia coli is the principal gram-negative causative agent of sepsis and meningitis in neonates. The pathogenesis of meningitis due to E. coli K1 involves mucosal colonization, transcytosis of epithelial cells, survival in the bloodstream, and eventually invasion of the meninges. The last two aspects have been well characterized at a molecular level. Less is known about the early stages of pathogenesis, i.e., adhesion to and invasion of epithelial cells. We have previously reported that the Hek protein causes autoaggregation and can mediate adherence to and invasion of epithelial cells. Here, we report that Hek-mediated adherence is dependent on binding to glycosoaminoglycan, in particular, heparin. The ability to hemagglutinate, autoaggregate, adhere, and invade is contingent on a putative 25-amino-acid loop that is exposed to the outside of the bacterial cells.
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PMID:The hek outer membrane protein of Escherichia coli strain RS218 binds to proteoglycan and utilizes a single extracellular loop for adherence, invasion, and autoaggregation. 1816 Apr 75

Neonatal infections and sepsis occur most frequently in calves with failure of passive transfer. If the invading bacteria are not rapidly controlled, they can set up focal infections, such as in growth plates, joints, or meninges, or generalized sepsis may occur. If not successfully treated, sepsis can lead to a systemic inflammatory response, multiple organ dysfunction syndromes, septic shock, and death. Treatments are based on selecting an appropriate antimicrobial drug and dosage, supportive therapy, fluid therapy, nonsteroidal anti-inflammatory drugs, and plasma transfusion. Preventing the failure of passive transfer through good colostrum management is essential.
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PMID:Septicemia and meningitis in the newborn calf. 1917 89


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