[Listeria infections following kidney transplantation].
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Adolescent↗
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Results for “LISTERIA INFECTIONS”
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[Neuromeningeal listeria infection in adults, clinical and therapeutic aspects. Retrospective study of 17 cases].
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Female↗
[Placental Listeria infection without fetal involvement].
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Adult↗
A case of hematometra infected by Listeria monocytogenes.
A case of Listeria infection is reported of a 10 year old girl with symptoms of the first menstruation but without the discharge of blood because of the absence of the vaginal duct. The blood retained in the uterus obtained by puncture through the rectum contained Listeria monocytogenes 4b. The infection was possibly acquired from a household pet.
Child↗
Nosocomial infections by Listeria monocytogenes: analysis of a cluster of septicemias in immunocompromised patients.
From December 1994 to November 1995 an unusual accumulation of Listeria infections occurred at the University Hospital Hamburg-Eppendorf, Germany. Eleven immunosuppressed patients from different departments developed septicemia due to Listeria monocytogenes during hospitalization. In a retrospective study, serotyping and pulsed-field gel electrophoresis revealed that six isolates were identical or genetically related. Four of them had been isolated from renal transplant recipients. Listeria monocytogenes was neither detected in food samples of the renal transplantation ward, nor in stool specimens obtained from the ward staff. There had been no close contacts among the infected patients. Before transplantation, the renal transplant recipients had been dialysed in different dialysis centers. Nosocomial foodborne transmission could not be proven but seems likely.
Adult↗
Mice lacking reduced nicotinamide adenine dinucleotide phosphate oxidase activity show increased susceptibility to early infection with Listeria monocytogenes.
Mice lacking the gp91 protein of reduced nicotinamide adenine dinucleotide phosphate oxidase showed heightened susceptibility to Listeria infection. The enhanced susceptibility was noted 2 days after infection, the usual peak time of the neutrophil-dependent lesion in the liver. Infected gp91phox -/- mice had an increase of approximately 30-fold in Listeria in the liver and an increase in the number of microabscesses. The study of the gp91phox mice underscores the early role of the neutrophil and of an oxidative burst in this infection with an intracellular pathogen. These results contrast with others showing that the late macrophage-dependent stage of the infection is dependent on nitric oxide.
Animals↗
Rat cytomegalovirus and Listeria monocytogenes infection enhance chronic rejection after allogenic rat lung transplantation.
The role of infection in the pathomechanism of obliterative bronchiolitis (OB) after human lung transplantation is controversial. In a rat lung transplantation model, we analyzed the effect of viral [rat cytomegalovirus (RCMV)] and bacterial infection [Listeria monocytogenes (LM)] on the development of chronic allograft rejection. Fisher rats underwent single left lung transplantation with allografts from Lewis rats. Postoperatively, animals were infected with either RCMV or LM, or served as noninfected controls. Animals were killed on day 120 and both lungs were evaluated histopathologically for chronic airway and chronic vascular rejection. Infection with RCMV produced a significant increase in the incidence of chronic airway rejection (66.7% vs. 20%), compared with noninfected long-term surviving animals. In rats with bacterial infection (LM) a similar increase of chronic airway changes as in viral infection (50% vs. 20%) was observed. Chronic rejection of allografts infected with either RCMV or LM was associated with significantly enhanced expression of intercellular adhesion molecule-1 (ICAM-1) on the endothelium. More infiltrating leukocytes (CD18, CD11a, CD44) and ED1-positive macrophages were found in allografts of infected animals. In this experimental model of chronic airway rejection in long-term surviving rats, not only viral but also bacterial infection resulted in enhanced development of chronic airway and vascular rejection. These results support our hypothesis that infectious complications have a substantial influence on the development of OB in human lung allografts.
Animals↗
Thalidomide enhances both primary and secondary host resistances to Listeria monocytogenes infection by a neutrophil-related mechanism in female B6C3F1 mice.
Previously, we have reported that thalidomide can modulate the immune responses in female B6C3F1 mice. Furthermore, thalidomide immunomodulation increased primary host resistance to intravenously infected Listeria monocytogenes. The present study was intended to evaluate the mechanisms underlying the enhanced host resistance to L. monocytogenes by focusing on the neutrophils. Female B6C3F1 mice were treated intraperitoneally with thalidomide (100 mg/kg) for 15 days. Exposure to thalidomide increased the numbers of neutrophils in the spleens and livers of L. monocytogenes-infected mice when compared to the L. monocytogenes-infected control mice. Additionally, the percentage of neutrophils was also significantly increased after Thd treatment in L. monocytogenes-infected mice. Further studies using antibodies to deplete corresponding cells indicated that thalidomide-mediated increase in primary host resistance (both the moribundity and colony counts in the liver and spleen) to L. monocytogenes infection was due to its effect on neutrophils but not CD8+ T cells or NK cells. Finally, Thd exposure also increased host resistance to secondary host resistance to L. monocytogenes infection, and depletion of neutrophils abolished the protective effect. In conclusion, thalidomide enhanced host resistance to both primary and secondary L. monocytogenes infections by a neutrophil-related mechanism in female B6C3F1 mice.
Animals↗
Host resistance of CD18 knockout mice against systemic infection with Listeria monocytogenes.
Mice with targeted mutations of CD18, the common beta2 subunit of CD11/CD18 integrins, have leukocytosis, impaired transendothelial neutrophil emigration, and reduced host defense to Streptococcus pneumoniae, a gram-positive extracellular bacterium. Previous studies using blocking monoclonal antibodies suggested roles for CD18 and CD11b in hepatic neutrophil recruitment and host innate response to Listeria monocytogenes, a gram-positive intracellular bacterium. We induced systemic listeriosis in CD18 knockout (CD18-ko) and wild-type (WT) mice by tail vein injection with Listeria. By 14 days postinjection (dpi), 8 of 10 WT mice died, compared with 2 of 10 CD18-ko mice (P < 0.01). Quantitative organ culture showed that numbers of Listeria organisms in livers and spleens were similar in both groups at 20 min postinfection. By 3, 5, and 7 dpi, however, numbers of Listeria organisms were significantly lower in livers and spleens of CD18-ko mice than in WT mice. Histopathology showed that following Listeria infection, CD18-ko mice had milder inflammatory and necrotizing lesions in both spleens and livers than did WT mice. Cytokine assays indicated that baseline interleukin-1beta and granulocyte colony-stimulating factor (G-CSF) levels were higher in CD18-ko mice than in WT mice and that CD18-ko splenocytes produced higher levels of interleukin-1beta and G-CSF than WT splenocytes under the same amount of Listeria stimulation. These findings show that CD18 is not an absolute requirement for antilisterial innate immunity or hepatic neutrophil recruitment. We propose that the absence of CD18 in the mice results in the priming of innate immunity, as evidenced by elevated cytokine expression, and neutrophilic leukocytosis, which augments antilisterial defense.
Animals↗
Perinatal infection with Listeria monocytogenes.
Listeria monocytogenes has been increasingly recognized as a cause of intrauterine sepsis with associated perinatal wastage. The condition is mostly acquired through dietary intake and appropriate advice should be given to all pregnant women. The most common presentations in pregnancy include premature labour, an influenza-like illness and reduced fetal movements. In this report, we present a series of 24 cases of perinatal listeria infection presenting to either our obstetric or neonatal units and confirmed by the microbiology department of the hospital. In particular, we wish to highlight 3 cases in which antenatal diagnosis and aggressive therapy was associated with a successful outcome. Amongst the remaining 21 cases in which an antenatal diagnosis was not made, there were 5 perinatal deaths and 1 mid-trimester loss at 18 weeks. Clinicians must maintain a high index of suspicion for listeria, particularly in gravid patients who present with fever in the setting of a persistent 'flu-like' illness and premature labour. Once suspected, appropriate specimens for listeria culture should include blood, cervical swabs and midstream urine. Empirical antibiotic therapy with amoxicillin should be instituted while waiting for culture results in patients with possible Listeria monocytogenes sepsis.
Adult↗
Role of CD28 for the generation and expansion of antigen-specific CD8(+) T lymphocytes during infection with Listeria monocytogenes.
Infection of mice with the intracellular bacterium Listeria monocytogenes results in a strong CD8(+) T cell response that is critical for efficient control of infection. We used CD28-deficient mice to characterize the function of CD28 during Listeria infection, with a main emphasis on Listeria-specific CD8(+) T cells. Frequencies and effector functions of these T cells were determined using MHC class I tetramers, single cell IFN-gamma production and Listeria-specific cytotoxicity. During primary Listeria infection of CD28(-/-) mice we observed significantly reduced numbers of Listeria-specific CD8(+) T cells and only marginal levels of specific IFN-gamma production and cytotoxicity. Although frequencies were also reduced in CD28(-/-) mice during secondary response, we detected a considerable population of Listeria-specific CD8(+) T cells in these mice. In parallel, IFN-gamma production and cytotoxicity were observed, revealing that Listeria-specific CD8(+) T cells in CD28(-/-) mice expressed normal effector functions. Consistent with their impaired CD8(+) T cell activation, CD28(-/-) mice suffered from exacerbated listeriosis both after primary and secondary infection. These results demonstrate participation of CD28 signaling in the generation and expansion of Ag-specific CD8(+) T cells in listeriosis. However, Ag-specific CD8(+) T cells generated in the absence of CD28 differentiated into normal effector and memory T cells.
Animals↗
The immune response of human neonates to Listeria monocytogenes infection.
Infection with Listeria monocytogenes during pregnancy has a high fetal and neonatal mortality. In rodents, it has been shown that resistance to Listeria infection is dependent upon a T cell-mediated immune response to the bacteria. The immune humoral and cell-mediated response to L. monocytogenes was studied in seven mother infant pairs who had documented evidence of L. monocytogenes sepsis. All studies were carried out 1 year following the initial infection as part of a clinical and immunological follow-up, and compared to an appropriate control group. The microagglutination titre and opsonizing activity of mothers previously infected with Listeria was significantly greater than that of the control mothers or their infected infants. There was no difference between the babies previously infected with L. monocytogenes when compared to control infants. The in vitro lymphoblastogenic response to Listeria, staphylococci, tetanus toxoid, and phytohemagglutinin was assessed. Infected mothers had a significantly greater proliferative response in the presence of Listeria than the control mothers, while the response of the previously infected infants was not different from that of the control infants. The response to the other antigens and PHA was similar in all groups. In conclusion, infants infected with L. monocytogenes during the perinatal period demonstrated neither a specific antibody response nor exhibited a cell-mediated immune response to this bacteria. These data support the idea that perinatally-infected infants have a markedly impaired immune response to L. monocytogenes and may, thus, explain their increased susceptibility to this infection.
Antibodies, Bacterial↗
Listeria monocytogenes causing endovascular infection.
Listeria monocytogenes is an uncommon cause of mycotic aneurysms, endocarditis, and other endovascular infections. When they occur, these infections usually involve patients with relatively normal host defenses, but with abnormal vascular intima or cardiac valves. We have reported a Listeria monocytogenes infection at the site of a posttraumatic aortic aneurysm.
Aged↗
A tumor-associated lactic dehydrogenase virus suppresses the host resistance to infection with Listeria monocytogenes.
Infection of mice with lactic dehydrogenase virus (LDV) causes a lifelong chronic infection which is followed by alterations in immune responses during the acute phase of the infection. LDV was found to impair many functions of the reticuloendothelial system and to suppress macrophage-dependent immune responses. We tested the effect of acute infection with LDV in mice on the macrophage-mediated resistance to infection with a virulent bacterium. We found that LDV reduces the host's capacity to resist infection with Listeria monocytogenes. Many tumor lines which are transferred in mice are infected with LDV, and their growth rate is affected by the presence of the virus. It is therefore important to distinguish between immune alterations in tumor-bearing mice which are caused by the progressive growth of the tumor and those which are secondary to the viral infection. We tested whether LDV and a circulatory factor from tumor-bearing mice with similar suppressive effects on anti-Listeria immunity are two different entities or whether they are similar. We found that the factor is associated with LDV-infected tumor cells and is absent in LDV-free tumor cells. Other biological and physical characteristics supported the assumption that the tumor-associated factor is the LDV.
Animals↗
The development of functional CD8 T cell memory after Listeria monocytogenes infection is not dependent on CD40.
The immunologic requirements for generating long-lived protective CD8 T cell memory remain unclear. Memory CD8 populations generated in the absence of CD4 Th cells reportedly have functional defects, and at least a subset of CD8 T cells transiently express CD40 after activation, suggesting that direct CD4-CD8 T cell interactions through CD40 may influence the magnitude and functional quality of memory CD8 populations. To ascertain the role of CD40 in such direct T cell interactions, we investigated CD8 T cell responses in CD40-/- mice after infection with Listeria monocytogenes, an intracellular bacterium that induces APC activation and thus priming of CD8 T cells independently of CD4 Th cell help through CD40. In this study we show that memory CD8 T cells generated in CD40-deficient mice show in vivo cytotoxicity and cytokine production equivalent to CD8 memory T cells from wild-type mice. Upon secondary Listeria infection, CD40-/- memory CD8 T cells expand to greater numbers than seen in wild-type mice. These results indicate that CD40 ligation on CD8 T cells, although reportedly a part of CD8 T cell memory development in an H-Y-directed response, is not needed for the development of functional memory CD8 T cell populations after Listeria infection.
Animals↗
Non-neonatal infection due to Listeria monocytogenes.
In the period from 1969 through 1983, four cases of non-neonatal Listeria monocytogenes meningitis were encountered in Dallas, representing an incidence rate of 0.3%. Three cases occurring in immunocompetent patients are the subject of this report. A review of the literature since 1945 produced 87 cases of Listeria infections in patients who were from 2 months to 20 years of age. Of these, 54% occurred in immunocompetent persons. The case-fatality rate was 15% in the immunocompetent patients, compared with 42% in immunocompromised patients and with 35% in patients with other underlying illnesses. The diagnosis of listeriosis causes concern about the possibility of an underlying occult malignancy or disorder of T cell function, but on the basis of our review these underlying abnormalities are usually clinically apparent at the time of infection. A rational approach to the child with Listeria infection, who is not known to be a compromised host, would be to examine the history and patient carefully to consider documenting normal numbers of T lymphocytes and assessing delayed hypersensitivity by skin testing.
Adolescent↗
Acquired resistance of BCG-vaccinated red mice to infection with Listeria monocytogenes.
Infection experiments have shown that red mice, belonging to the vole family, could be infected with Listeria monocytogenes and that they were almost as susceptible to intravenous infection as Cf1 mice. Vaccination of red mice with BCG induced a resistance which could be demonstrated by prologation of the survival time of the animals after challenge with Listeria. The resistance was greatest in the second and third week after vaccination and was considerably higher after intravenous injection of BCG vaccine than after intraperitoneal or subcutaneous injection. On the basis of studies concerning the dose of vaccine, the route of vaccination, and the interval between vaccination and challenge, a method by which to evaluate the potency of a strain of BCG has been elaborated. By this method it was found that there was a significant difference between the resistance produced by a strain of BCG which is weakly virulent and one which is strongly virulent for hamsters.
Animals↗
Effects of ozone on the defense to a respiratory Listeria monocytogenes infection in the rat. Suppression of macrophage function and cellular immunity and aggravation of histopathology in lung and liver during infection.
We have investigated the effect of exposure to ozone on defense mechanisms to a respiratory infection with Listeria monocytogenes in the rat. For this purpose rats were continuously exposed to O3 concentrations ranging from 0.25 to 2.0 mg/m3 for a period of 1 week. In this model defense to a respiratory infection with Listeria depends on acquired specific cellular immune responses, as well as on natural nonspecific defense mechanisms. The results confirm earlier findings that show that ozone exposure can suppress the capacity of macrophages to ingest and kill Listeria. Moreover, the results show that ozone can also have a suppressive effect on the development of cellular immune responses to a respiratory Listeria infection, i.e., on T/B ratios in lung draining lymph nodes, delayed-type hypersensitivity responses to Listeria antigen, and lymphoproliferative responses in spleen and lung draining lymph nodes to Listeria antigen. The effects on the specific immune responses are especially overt if exposure to the oxidant gas occurs during an ongoing primary infection. The pathological lesions induced by a pulmonary Listeria monocytogenes infection were characterized by multifocal infiltrates of histiocytic and lymphoid cells. The foci sometimes had a granulomatous appearance. Moreover, the cellularity of the interstitial tissues was increased. In the lung many diffuse alveolar macrophages could be seen in the alveoli. Ozone exposure greatly increased the severity of the lung lesions and also of liver lesions resulting from the pulmonary infection. A prominent finding was the formation of granulomas in ozone-exposed and Listeria-infected rats. This increased severity of the lesions after ozone exposure and subsequent infection with Listeria was presumably not a result of additive ozone and Listeria-induced lesions, but rather an effect of ozone-induced impaired clearance of the bacteria, caused by depressed macrophage activity and cellular immunity. T-cell-dependent immune responses form an important component of defense to respiratory infections with bacteria and viruses, and possibly also to neoplasms. Since our study unequivocally shows an effect on T-cell-dependent immunity, ozone exposure has to be judged potentially hazardous with respect to such challenges of the lung.
Animals↗