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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two cases of listeriosis in patients submitted to matched unrelated donor bone marrow transplantation are reported. The patients developed listerial septicemia and listerial septicemia with meningitis and encephalitis 39 and 29 days after transplantation, respectively. Including the present two cases, 19 Listeria monocytogenes infections in related and unrelated donor allogeneic bone marrow transplant recipients have been reported to date. Infection occurred earlier in unrelated donor transplant recipients. Listeriosis is a rare complication in allogeneic bone marrow transplant recipients; however, the widespread practice of performing transplants from a donor-alternative to a human leukocyte antigen-compatible sibling and, in this setting, the need for intensified immunosuppression may predict an increasing and earlier occurrence of listeriosis.
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PMID:Listeriosis in recipients of allogeneic bone marrow transplants from unrelated donors. 1105 7

The interaction of Listeria monocytogenes with endothelial cells represents a crucial step in the pathogenesis of listeriosis. Incubation of human umbilical vein endothelial cells (HUVEC) with wild-type L. monocytogenes (EGD) provoked immediate strong NO synthesis, attributable to listerial presentation of listeriolysin O (LLO), as the NO release was missed upon employment of a deletion mutant for LLO (EGD hly mutant) and was reproduced by purified LLO. Studies of conditions lacking extracellular Ca(2+) suggested LLO-elicited Ca(2+) flux as the underlying mechanism. In addition, HUVEC incubation with EGD turned out to be a potent stimulus for sustained (>12-h) upregulation of proinflammatory cytokine generation (interleukin 6 [IL-6], IL-8, and granulocyte-macrophage colony-stimulating factor). Use of deletion mutants for LLO (EGD hly mutant), listerial phosphatidylinositol-specific phospholipase C (EGD plcA mutant), broad-spectrum phospholipase C (EGD plcB mutant) and internalin B (EGD inlB mutant), as well as purified LLO, identified LLO as largely responsible for the cytokine response. Endothelial cells responded with diacylglycerole and ceramide generation as well as nuclear translocation of NF-kappa B to the stimulation with the LLO-producing strains EGD and Listeria innocua. The endothelial PC-phospholipase C inhibitor tricyclodecan-9-yl-xanthogenate as well as two independent inhibitors of NF-kappa B activation, pyrolidine dithiocarbamate and caffeic acid phenethyl ester, suppressed both the NF-kappa B translocation and the upregulation of cytokine synthesis. We conclude that L. monocytogenes is a potent stimulus of NO release and sustained upregulation of proinflammatory cytokine synthesis in human endothelial cells, both events being largely attributable to LLO presentation. LLO-induced transmembrane Ca(2+) flux as well as a sequence of endothelial phospholipase activation and the appearance of diacylglycerole, ceramide, and NF-kappa B are suggested as underlying host signaling events. These endothelial responses to L. monocytogenes may well contribute to the pathogenic sequelae in severe listerial infection and sepsis.
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PMID:Human endothelial cell activation and mediator release in response to Listeria monocytogenes virulence factors. 1115 83

Syncytial giant cell hepatitis in the neonatal period has been associated with many different etiologic agents and may present initially as cholestasis. Infectious causes are most common and include: (1 ) generalized bacterial sepsis, (2) viral agents, (3) toxoplasmosis, (4) syphilis, (5) listeriosis, and (6) tuberculosis. Viral hepatitis may be due to cytomegalovirus, rubella virus, herpes simplex, HHV-6, varicella, coxsackievirus, echovirus, reovirus 3, parvovirus B19, HIV, enteroviruses, paramyxovirus, and hepatitis A, B, or C (rare). Giant cell hepatitis may result in fulminant liver failure with massive hepatocyte necrosis and severe liver dysfunction leading to death, resolution with severely compromised liver function, or liver transplantation. The authors report a 6-week-old male who had an unremarkable perinatal period, became jaundiced after developing diarrhea, and subsequently developed liver dysfunction with massively increased liver enzymes and a coagulopathy. Open wedge and core liver biopsies were performed to determine if the patient should be listed for liver transplantation. Giant cell hepatitis with a significant mixed lymphocytic and neutrophilic infiltrate was present on both the wedge and core biopsies. The residual 60% of hepatocytes had ballooning degeneration and many possessed pyknotic nuclei. The hepatocytes were arranged in a pseudoacinar pattern. Electron microscopy showed paramyxoviral-like inclusions in the giant cells, characterized as large inclusions with fine filamentous, beaded substructures (18-20 nm). Paramyxoviridae are nonsegmented, negative-sense, single-stranded RNA viruses. This family is divided into the Paramyxovirinae subfamily containing respirovirus (Sendai virus, parainfluenza virus type 3), rubulavirus (mumps, parainfluenza virus type 2), and morbillivirus genera (measles); and Pneumovirinae subfamily (pneumovirus genus [respiratory syncytial virus]). Supportive care to determine if hepatic function resolves following the viral episode, liver transplantation with fulminant liver failure, and ongoing evaluation in those who recover to assess chronic liver disease are necessary. Ultrastructural evaluation may unmask the etiologic agent for hepatitis and direct therapy.
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PMID:Neonatal syncytial giant cell hepatitis with paramyxoviral-like inclusions. 1129 22

P-selectin is a major component in the early interaction between platelets, endothelial cells, and inflammatory cells in the initial phases of the innate immune response. The major ligand for P-selectin is P-selectin glycoprotein ligand-1 (PSGL-1) and this ligand is expressed on the surface of monocyte, lymphocyte, and neutrophil membranes. A truncated form of recombinant human P-selectin glycoprotein ligand-1 has been covalently linked to immunoglobulin G (rPSGL-Ig) and this fusion peptide functions as a competitive inhibitor of PSGL-1. As an inhibitor of neutrophil-endothelial cell adherence, rPSGL-Ig is in early clinical development for the treatment of ischemia reperfusion injury. To determine the potential for deleterious effects from inhibition in P-selectin-mediated neutrophil attachment in the presence of bacterial infection, the effects of therapeutic doses of rPSGL-Ig were tested in three standard laboratory sepsis models. The experimental models included: the murine systemic Listeria monocytogenes infection model, the Pseudomonas aeruginosa bacteremia model in neutropenic rats, and the cecal ligation and puncture (CLP)-induced peritonitis model in rats. Recombinant human PSGL-Ig had no adverse effects on mortality or immune clearance in systemic bacterial infection in any of the three infection models. The PSGL-1 inhibitor did significantly decrease local neutrophil infiltration and bacterial clearance in the peritoneum following CLP, but this did not increase the systemic levels of proinflammatory cytokines, the quantitative levels of bacteremia, or the overall mortality rate following CLP. The results indicate that rPSGL-Ig did not exacerbate infection in these experimental sepsis models.
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PMID:Evaluation of the safety of recombinant P-selectin glycoprotein ligand-immunoglobulin G fusion protein in experimental models of localized and systemic infection. 1130 27

The authors have described the issues surrounding Listeria monocytogenes infection with reference to cases diagnosed and managed during the 5-year period (1995-2000) in the Clinical Department of Neonatal Pathology and Intensive Care of the National Institute of Mother and Child in Warsaw. Four cases of congenital listeriosis have been diagnosed. Some mothers presented with "flu-like" symptoms. All mothers delivered prematurely (29 hbd - 32 hbd). Among the 4 infants the most common clinical features were: perinatal asphyxia, respiratory distress, pathological icterus, haematologic abnormalities. Septicemia occurred in 50% of cases; pneumonia in 100%. Three of them presented skin manifestations; one of the neonates had mucosal abnormalities of the laryngopharynx. Cerebral sonography showed intracranial hemorrhage. One of the infants died within 7 days of birth. The other two neonates developed posthemorrhagic hydrocephalus. Only one infant has normal development. Although listeriosis appears to be not a frequent cause of perinatal infection, clinicians must be aware of Listeria, particularly in gravid patients who present with fever and "flu-like" illness and go into premature labour. Initial therapy implemented in our Department, with ampicillin and aminoglycosides seem to be the most appropriate.
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PMID:[Clinical and laboratory diagnosis of Listeria monocytogenes on the basis of own investigations]. 1132 73

The gram-positive bacterium Listeria monocytogenes is the causative agent of listeriosis, a highly fatal opportunistic foodborne infection. Pregnant women, neonates, the elderly, and debilitated or immunocompromised patients in general are predominantly affected, although the disease can also develop in normal individuals. Clinical manifestations of invasive listeriosis are usually severe and include abortion, sepsis, and meningoencephalitis. Listeriosis can also manifest as a febrile gastroenteritis syndrome. In addition to humans, L. monocytogenes affects many vertebrate species, including birds. Listeria ivanovii, a second pathogenic species of the genus, is specific for ruminants. Our current view of the pathophysiology of listeriosis derives largely from studies with the mouse infection model. Pathogenic listeriae enter the host primarily through the intestine. The liver is thought to be their first target organ after intestinal translocation. In the liver, listeriae actively multiply until the infection is controlled by a cell-mediated immune response. This initial, subclinical step of listeriosis is thought to be common due to the frequent presence of pathogenic L. monocytogenes in food. In normal individuals, the continual exposure to listerial antigens probably contributes to the maintenance of anti-Listeria memory T cells. However, in debilitated and immunocompromised patients, the unrestricted proliferation of listeriae in the liver may result in prolonged low-level bacteremia, leading to invasion of the preferred secondary target organs (the brain and the gravid uterus) and to overt clinical disease. L. monocytogenes and L. ivanovii are facultative intracellular parasites able to survive in macrophages and to invade a variety of normally nonphagocytic cells, such as epithelial cells, hepatocytes, and endothelial cells. In all these cell types, pathogenic listeriae go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. In this way, listeriae disseminate in host tissues sheltered from the humoral arm of the immune system. Over the last 15 years, a number of virulence factors involved in key steps of this intracellular life cycle have been identified. This review describes in detail the molecular determinants of Listeria virulence and their mechanism of action and summarizes the current knowledge on the pathophysiology of listeriosis and the cell biology and host cell responses to Listeria infection. This article provides an updated perspective of the development of our understanding of Listeria pathogenesis from the first molecular genetic analyses of virulence mechanisms reported in 1985 until the start of the genomic era of Listeria research.
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PMID:Listeria pathogenesis and molecular virulence determinants. 1143 15

The intestinal tract is the major portal of entry for Listeria monocytogenes, which becomes ingested via contaminated food. The pathogenic strains penetrate the mucosal tissue either directly, via engulfment by enterocytes, or indirectly, via active penetration of the Peyer's patches. There are now several reports clearly demonstrating that, in some cases, acute enteritis may be the only symptom of Listeria infection or may precede the typical symptoms of listeriosis such as sepsis and meningitis or encephalitis. Therefore, Listeria monocytogenes should be included in the list of foodborne gastrointestinal pathogens. Furthermore, a history of enteritis should prompt the physician to include listeriosis, which is often difficult to diagnose, in the differential diagnosis. Although Listeria monocytogenes is undoubtedly a potential enteric pathogen, it is still debatable whether its detection in a routine bacteriological examination of a stool specimen is of clinical significance.
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PMID:Listeria monocytogenes: a causative agent of gastroenteritis? 1147 34

Listeriosis is a serious disease acquired by ingestion of foods contaminated with Listeria monocytogenes. Special populations at risk are individuals who are immunocompromised to some extent. The most common clinical findings include meningitis, septicemia, encephalitis, and intrauterine/cervical infections. Food related listeriosis is an unusual occurrence but it is now being thought of as a new, and emergent illness. Numerous types of food products have been implicated in listeriosis infections, but of particular concern are ready to eat products such as lunchmeats, hotdogs, ham/chicken salad, sausages, and roast beef. However, to ensure food safety, there are several methods employed to detect L. monocytogenes in food products and the severity of listeriosis warrants stringent guidelines in food processing facilities. Nevertheless, proper food preparation and handling must be emphasized and individuals who are at an increased risk for the disease must be apprised on how to prevent the occurrence of infection.
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PMID:Listeriosis: an emerging food-borne disease. 1151 30

IFN-gamma is a key immunoregulatory cytokine that plays a predominant role in innate immunity. By employing PCR-Select to search for genes differentially expressed in IFN-gamma/TNF-alpha stimulated macrophages, we identified a novel IFN-gamma-induced transcript designated PUMA-G (protein up-regulated in macrophages by IFN-gamma). PUMA-G codes for a protein with seven transmembrane helices, a feature commonly shared with the G protein-coupled receptor superfamily (GPCR). The PUMA-G protein is most similar to the human orphan GPCR HM74 (73 % identity) and GPR31 (30 % identity). PUMA-G mRNA was readily induced in macrophages after stimulation with IFN-gamma, LPS, polyIC and CpG oligonucleotides. In vivo PUMA-G was up-regulated in mice suffering from microbial sepsis or from Listeria monocytogenes infection. Characterization of the genomic locus revealed an intronless PUMA-G open reading frame. Genomic Southern blot analysis indicates that PUMA-G is a single-copy gene. PUMA-G maps to mouse chromosome 5F. Confocal microscopy of transiently transfected 264.7 RAW macrophages and 293T cells with a PUMA-G-EGFP fusion construct showed predominant fluorescence at the cell surface, suggesting a localization at the cell membrane. Taken together, our data indicate that PUMA-G is a new inducible representative of GPCR, with potential importance in macrophage functions.
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PMID:PUMA-G, an IFN-gamma-inducible gene in macrophages is a novel member of the seven transmembrane spanning receptor superfamily. 1174 92

Thirty-one cases of human listeriosis seen from 1971-1999 were reviewed. cases were grouped as follows: Group I composed of 14 patients were studied in the period 1971-1984; and group II composed of 17 cases studied in the period 1985-1999. We tried to assess changes in the incidence, clinical findings and outcome in both periods. The incidence of listeriosis remained constant along the years, 1.2 cases/20,000 discharges. The mean age of the patients significantly increased along the years (55 11 years versus 68 12 years; p 0.002). 77% of cases had one or more underlying diseases predisposing to listeriosis. We observed an increasing number of listeriosis in patients without chronic diseases in recent years. Listeriosis presented as meningitis or primary sepsis. Mortality was 61% and was strictly associated with the severity of the underlying disease. Patients with meningoencephalitis and seizures had a worse prognosis. We did not observe differences in mortality of patients who were treated with beta-lactam monotherapy in comparison with those who were treated with beta-lactam/aminoglucoside combination. Cotrimoxazole was uniformly successful treatment of human listeriosis in this series.
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PMID:[Listeria monocytogenes infections in the adult. Clinical and microbiological issues of a changing disease]. 1174 87


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