Fatal septic shock with multiple organ failure due to Campylobacter jejuni.
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Biomedical subjects
Publications and source records attributed to G Monneret.
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Enterocytozoon bieneusi is a major cause of chronic diarrhea and malabsorption in patients with AIDS. We report what we believe is the first case of intestinal infection due to E. bieneusi in a heart-lung transplant recipient who was seronegative for human immunodeficiency virus (HIV). The clinical presentation and the evolution of the disease were identical to those usually observed in patients with AIDS and included diarrhea, massive weight loss, and persistent infection despite treatment with albendazole. E. bieneusi was identified in the patient's duodenal mucosa by electron microscopy. No other etiologic agent was detected. We conclude that E. bieneusi may be responsible for serious intestinal infections in patients whose immunosuppression is not related to HIV.
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A large number of clinical studies has described procalcitonin (ProCT) as a marker of bacterial infection and a good predictor of disease severity and antibiotherapy efficacy. Nevertheless, the mechanism of ProCT synthesis remains unclear. The aim of this study was to demonstrate potential ProCT production by peripheral blood mononuclear cells as is the case for cytokines involved in sepsis. In a whole blood model, LPS (10 micrograms/ml) stimulation on blood samples from healthy volunteers (n = 14) was tested. Early (TNF-alpha and IL1-beta) and late (IL-6 and IL-8) cytokines were produced in large amounts in contrast to the absence of ProCT. Additional experiments with nitric oxide or detection of intra-cellular ProCT (cell lysis, flow cytometry) had negative results. It was concluded that ProCT is not produced in this model. Data are still needed to investigate the cellular origin of ProCT in order to better define its clinical usefulness.
High serum concentrations of procalcitonin (PCT) have been found during bacterial and parasitic infections. This is a report of two cases of disseminated aspergillosis with moderate PCT increase in two 14-year-old girls after bone marrow transplantation (BMT) for myelodysplastic syndrome and Fanconi's anemia, respectively. In contrast, the important rise of serum CRP observed in these patients tends to demonstrate that the synthesis of these two proteins is under different control mechanisms.
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One of the strongest known association between human leukocyte antigen (HLA) phenotype and disease is that of ankylosing spondylitis and HLA-B27. Thus, the determination of HLA-B27 status is an useful tool in the diagnosis of ankylosing spondylitis. To date, the 2 reference methods for HLA typing (microlymphocytotoxicity and molecular biology techniques), are costly in terms of both technician time and materials, and require a great deal of experience. In total, these techniques are not well-suited for routine application in clinical immunology laboratories. Use of flow cytometry has recently been applied for HLA-B27 typing. Nevertheless, it requires an extensive validation protocol. We developed a flow cytometry technique as standardized as possible (whole blood, automated lysing system, automated photomultiplier voltage calibration, definition of thresholds stable with time) and validated our results by comparison with microlymphocytotoxicity. In total, 326 samples were analyzed. We found 99% of concordant results between the 2 techniques, and neither false positive results nor false negative results with flow cytometry could be observed. These results illustrate the reliability of the protocol. It should be remembered that reference technique remains necessary to confirm the few results (< 1%) found in "grey zone" by flow cytometry. Standardization of flow cytometry techniques, as described in this work for HLA B27, seems to be a reasonable goal for the next decade in clinical immunology laboratories.
In septic shock, the diminished HLA-DR expression on monocytes has been proposed as a marker of immunoparalysis that correlates with an increased risk for fatal outcome. The present study was designed to determine whether some differences in protocol procedures could lead to discrepant results in HLA-DR measurement. After establishing a reliable protocol, the second objective was to illustrate the immunoparalysis in patients with septic shock. HLA-DR measurement on monocytes was determined by means of flow cytometry in 54 healthy donors and 16 patients with septic shock. We demonstrated that storage temperature, storage duration before staining and red cells lysis constitute crucial steps in HLA-DR measurement. The precision results with coefficients of variation below 5%, were quite convincing for a manual immunoassay. At 48 hours after diagnosis of septic shock, we found severely decreased percentages of monocytes expressing HLA-DR in septic patients (24 +/- 4%, mean +/- SEM) in comparison with healthy donors (90 +/- 1%), p < 0.001). Furthermore, the persistence of a low level of monocytic HLA-DR (less than 50 %) at day 9 after admittance was associated with patients who died. This study illustrates the state of immunoparalysis in patients with septic shock and supports the potential interest in measuring HLA-DR expression on monocytes. However, multicenter studies are now needed to validate this parameter. Based on our analytical results, we conclude that a critical issue in such studies will be the capacity in each center to perform standardized measurement of HLA-DR. It should be remembered that this determination requires the definition of a common analytical procedure between laboratories participating in the trial.