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

This sample of listerial infection amongst perinates is biased by small numbers and ascertainment. Nevertheless, it includes a broad spectrum of disease, with examples of established intrauterine septicemia, amniotic infection syndrome, intrapartum infection, and postnatal infection. The study shows that amniotic infection may eventuate in gestational loss, with or without invasive bacteremia and septicemia. Noteworthy are the association of perinatal listeriosis with abnormality of the birth canal, the occurrence of mixed primary infection and superinfection, and the frequency of findings suggesting underlying metabolic or humoral abnormalities. Excepting well-established septicemia with characteristic histopathology and distribution of lesions, the morphologic findings are not distinctive and are liable to be dominated by secondary complications, among which are changes reminiscent of disseminated intravascular coagulopathy, endotoxemia, and circulatory compromise.
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PMID:Perinatal listeriosis. 732 25

This report concerns 3 cases of human listeriosis occurred in the area of Trieste between 1974-1979. Two newborns with a listeric early disease were observed in a Neonatal Intensive Care Unit. One child was colonized during the delivery from the infected vaginal mucosa of the mother; no signs of sepsis nor systemic involvement was observed. In the second case a bacteremia was documented with clinical signs of sepsis, and in spite of negative cultures of the mother, an intra-uterine infection was hypothesized. During an investigation carried out in 1977 on prevalence of listeric infection in pregnant women of Trieste, 127 vaginal and rectal swabs were examined and one subject (0.8%) was found harbouring a strain of Listeria monocytogenes in the vaginal secretions. Some bacteriological and epidemiological topics on human listeriosis are discussed.
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PMID:[Human listeriosis in the Trieste area]. 732 95

Infection of endothelial cells by bacteria may be an important component of the bacteria's ability to escape host defenses and cause disease. Listeria monocytogenes cause sepsis and central nervous system infection in domesticated animals and immunocompromised humans, suggesting that this bacterium interacts with endothelial cells in a significant fashion. The experiments presented here tested the hypothesis that L. monocytogenes can invade and replicate within human endothelial cells. We found that L. monocytogenes grows readily in umbilical vein endothelial cells and that its intracellular life cycle involves phagosomal escape, F-actin-based motility, and cell-to-cell spread. We found that L. monocytogenes invaded endothelial cells by cell-to-cell spread from adherent mononuclear phagocytes which were previously infected by this bacterium. Interestingly, L. monocytogenes mutants lacking the invasion protein, internalin, bound less well to endothelial cells than did wild-type bacteria in the absence, but not the presence, of serum, and their invasion of endothelial cells was diminished under both conditions. Thus, endothelial cell infection by L. monocytogenes can occur by two distinct mechanisms: direct bacterial invasion of the endothelial cells in an internalin-mediated fashion or cell-to-cell spread from adherent, infected mononuclear phagocytes. These data support the idea that endothelial cell infection by L. monocytogenes is an important event in the pathogenesis of listeriosis.
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PMID:Listeria monocytogenes infects human endothelial cells by two distinct mechanisms. 759 Oct 57

Listeria monocytogenes is a facultative intracellular pathogen causing mainly meningitis and septicemia in immunocompromised hosts. From July 1988 through December 1989, 16 patients at The Mount Sinai Hospital were diagnosed as having listeriosis shortly after admission, 14 within a one-year period (July 1988-July 1989). Because this incidence was almost double the incidence in previous years (< 8 annually), an epidemiologic and microbiologic investigation was undertaken to determine a potential route of acquisition of L. monocytogenes. On the basis of plasmid profile, bacteriocin (enterocin) susceptibility pattern, and serotype, no single epidemic strain could be identified. Although direct evidence was lacking, we concluded that our patients may have acquired L. monocytogenes through transient contamination of food.
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PMID:Listeria monocytogenes infections: laboratory investigation of an unexpected increase in incidence. 761 77

Infection with Listeria monocytogenes is uncommon in patients receiving cytotoxic chemotherapy, and is even rarer among recipients of bone marrow transplantation. Hemosiderosis, either idiopathic or caused by transfusion, appears to be another risk factor. We report a 3-year-old Chinese girl with transfusion-dependent Diamond-Blackfan syndrome who had L. monocytogenes septicemia when she received an allogeneic bone marrow transplantation. She was treated successfully with intravenous ampicillin. Our case adds to the clinical evidence that patients with iron overload are susceptible to listeriosis, particularly when they are immunocompromised and do not receive iron-chelation treatment.
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PMID:Listeria septicemia complicating bone marrow transplantation for Diamond-Blackfan syndrome. 764 Jan 84

The authors report on a newborn admitted to the Intensive Care Unit of Gaslini Institute for serious respiratory insufficiency who died on the third day of life because of a sepsis due to Listeria monocytogenes. The authors focus on the patient's history and clinical picture and on the histological evaluation of the lesions observed. The importance of infection in pregnancy and the possible severe consequences of listeriosis on the foetus are underlined, stressing the need for early diagnosis and adequate treatment.
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PMID:[Fatal neonatal listeriosis after maternal infection acquired with ingestion of fresh home-made cheese]. 779 87

Immunity to Listeria monocytogenes, an important pathogen in human neonatal sepsis, is mediated by mononuclear phagocytes, which are regulated by the hematopoietic growth factor colony-stimulating factor 1. Neonates with listeriosis had higher circulating colony-stimulating factor 1 levels and subsequent monocyte counts than those of both noninfected newborns and newborns infected with nonlisterial organisms.
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PMID:Colony-stimulating factor 1 in the human response to neonatal listeriosis. 789 Apr 28

We report two cases of sepsis and meningoencephalitis with listeriosis. They died in despite of administering sensitive antibiotics. A 2 day old girl was admitted to our hospital because of fever and cyanosis. Listeria monocytogenes type 4b was cultured from blood, CSF, throat, urine, ear. She was treated with twice exchange transfusion and sensitive antibiotics (ABPC, TOB), but died from DIC. A 48 year old man suddenly experienced an unconscious condition. A CSF culture grew L. monocytogenes type 1/2a. He was treated with sensitive antibiotics (ABPC, CEZ etc), but went bad conditions. Listeria infection of this cases developed as unfortunate infection.
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PMID:[Two cases of Listeria monocytogenes infection in Osaka Municipal Hospital]. 874 12

Listeriosis is primarily a foodborne disease and the pathogenesis of infection is determined by passage of the organism from the gastrointestinal lumen to the reticuloendothelial cells of the liver and spleen. Subsequent invasive events such as sepsis and meningitis develop. The immune response to Listeria is characterized by early macrophage mediated killing followed by the development of a brisk cell mediated immune response. Humoral immunity appears to play no role in infection in the protected response. Organism specific virulence factors such as hemolysin and actin polymerization factor may play important roles in pathogenesis and also illicit specific immune responses. Immunization against listeriosis has been carried in animals but does not appear feasible for this rare infection in human populations.
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PMID:Pathogenesis and immunology of Listeria monocytogenes. 897

IFN-gamma receptor-deficient (IFN-gammaR -/-) mice were used to study the innate immune responses during infection with Listeria monocytogenes. Mutant mice were unable to limit bacterial growth and died of sepsis even with an infection dose of 70 Listeria. At day 2, they showed an exacerbated listeriosis and mice succumbed to infection before the onset of an effective specific immunity, demonstrating a defective innate immunity. Recruitment and extravasation of phagocytic cells to infected organs was present and dominated by neutrophils. However, during the early course of infection, mutant mice responded by an elevated inflammatory type 1 cytokine response, as determined by IL-12, IFN-gamma, TNF-alpha, and IL-1alpha-specific RNA expression. Induction of inducible nitric oxide synthase was present and also increased in mutant mice. Interestingly, IFN-gammaR -/- neutrophils expressed substantial TNF-alpha- and IL-1alpha-specific RNA, suggesting a substantial contribution in the overall inflammatory cytokine response. In contrast, IFN-gammaR -/- macrophages showed reduced MHC class II surface expression levels and impaired TNF-alpha and IL-1alpha but normal IL-6 production after restimulation with heat-killed L. monocytogenes. Moreover, IFN-gammaR -/- macrophages showed defective listericidal activities. In contrast to normal macrophages, Listeria escaped rapidly from the phagosome in IFN-gammaR -/- macrophages to the cytoplasm, where they productively survived. In conclusion, these data suggest that IFN-gammaR signaling activates yet unknown functions in macrophages, preventing Listeria-induced escape from the phagosome and consequent killing of the invader. Together with the impaired cytokine responses, these macrophage defects seem to be responsible for the dramatic susceptibility during innate immunity, whereas predominant neutrophil responses mediate limited protective role in mutant mice.
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PMID:Impaired macrophage listericidal and cytokine activities are responsible for the rapid death of Listeria monocytogenes-infected IFN-gamma receptor-deficient mice. 916 49


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