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Biomedical subjects

G Cozon

Publications and source records attributed to G Cozon.

At least 19 recordsLinked to original sources
PubMed2007

Impact of spiramycin treatment and gestational age on maturation of Toxoplasma gondii immunoglobulin G avidity in pregnant women.

The objective of the present study was to investigate the maturation of immunoglobulin G (IgG) avidity after Toxoplasma gondii seroconversion during pregnancy and the factors that affect IgG avidity over time. The study used 309 serum samples from 117 women and a multiple linear mixed regression analysis to show the patterns of variation of IgG avidity throughout gestation. The IgG avidity ratios and the patterns of their evolution with time were quite diverse among the women and were statistically heterogeneous (P = 0.011); however, the trend was toward a statistically significant increase (P < 0.0001). On average, a 1.0167-fold increase was observed for each additional gestational week after the putative date of infection. At 12 weeks after putative infection (the expected IgG avidity maturation time), the mean avidity ratio was 16.6% (95% confidence interval, 15.4 to 17.9%). At all times, the avidity ratio remained significantly heterogeneous among the women (P < 0.05); for 95% of them, that ratio ranged from 7.8 to 35.3% at 12 weeks after putative infection. Maternal age at the putative time of infection did not influence the maturation of IgG avidity. However, on average, a 1.009-fold decrease (P = 0.03) in that avidity was observed for each additional week of gestational age before infection and a 1.03-fold increase (P = 0.0003) was observed for each additional week of delay to the onset of spiramycin treatment. The rate of increase in the avidity ratio was lower if infection occurred late in pregnancy and higher if the delay to treatment was long. This information cannot allow accurate determination of the delay since the time of infection. The present results provide support for interpretation of the assay and caution against overinterpretation.

Animals↗
PubMed2006

Pneumococcal surface protein A (PspA) is effective at eliciting T cell-mediated responses during invasive pneumococcal disease in adults.

Humoral immune response is essential for protection against invasive pneumococcal disease and this property is the basis of the polysaccharide-based anti-pneumococcal vaccines. Pneumococcal surface protein A (PspA), a cell-wall-associated surface protein, is a promising component for the next generation of pneumococcal vaccines. This PspA antigen has been shown to stimulate an antibody-based immunity. In the present study, we evaluated the capacity of PspA to stimulate CD4+ T cells which are needed for the correct development of a B cell based immune response in humans. Cellular immunity to PspA was evaluated by whole-blood culture with different pneumococcal antigens, followed by flow cytometric detection of activated CD4+CD25+ T cells. T cell-mediated immune responses to recombinant PspA proteins were assessed in acute-phase and convalescent blood from adults with invasive pneumococcal disease and in blood from healthy subjects. All cases had detectable antibodies against PspA on admission. We found that invasive pneumococcal disease induced transient T cell depletion but adaptive immune responses strengthened markedly during convalescence. The increased production of both interleukin (IL)-10 and interferon (IFN)-gamma during convalescence suggests that these cytokines may be involved in modulating antibody-based immunity to pneumococcal disease. We demonstrated that PspA is efficient at eliciting T cell immune responses and antibodies to PspA. This study broadens the applicability of recombinant PspA as potent pneumococcal antigen for vaccination against S. pneumoniae.

Adult↗
PubMed2001

Depletion of circulating natural type 1 interferon-producing cells in HIV-infected AIDS patients.

Natural interferon-alpha producing cells (IPCs) are a newly characterized blood cell type, which is the major source of type I interferons in antiviral innate immune responses. The relationship between the number of circulating IPCs, HIV disease progression, and the occurrence of HIV-related complications was investigated. The study of 25 healthy donors and 54 HIV-infected subjects demonstrated a direct correlation between blood IPC number, interferon-alpha production, and clinical state of HIV-infected subjects. Asymptomatic long-term survivors had increased IPC number and function relative to uninfected controls and infected individuals with progressive disease. IPC numbers were markedly reduced in AIDS patients developing opportunistic infections and cancer. A negative correlation was found between the IPC number in the blood and the HIV viral load, suggesting that IPCs are important in controlling HIV replication. This study provides the first evidence that IPCs are being affected during the course of HIV infection and suggests that these cells can play a vital role in the protection against opportunistic pathogens and cancer. (Blood. 2001;98:906-912)

AIDS-Related Opportunistic Infections↗
PubMed2001

[Congenital toxoplasmosis. Transitory negative serology].

OBJECTIVES: Toxoplasmosis serology may become temporarily negative in children with congenital toxoplasmosis, leading to a risk of misdiagnosis and inadequate surveillance. The purpose of our work was to better understand the time course of toxoplasmosis serology which has not been studied specifically and to propose practical recommendations. PATIENTS AND METHODS: We conducted a prospective study in 217 children born with congenital toxoplasmosis between January 1988 and December 1997. Clinical, ophthalmological and serology data were collected every three months during their first year of life then every six months until three years of age and every year thereafter for all patients. Negative serology was defined as the absence of IgG at indirect immunofluorescence and ELISA (enzyme linked immunosorbent assay) and by the absence of IgM at ISAGA (immunosorbent agglutination assay). RESULTS: During the mean follow-up of 66 +/- 33 months (range 12-126 months), 33 children (15%) presented a period where the toxoplasmosis serology (ELISA and indirect immunofluorescence) was negative for a transient period reaching a mean 5 months. The dye test was performed in 25 of these children and was negative in 6 (24%). Among the negative conversions observed at routine testing, 73% occurred in children taking pyrimethamine/sulfadoxin therapy and the others occurred a mean 11.7 months after interruption of treatment. There was a positive association between maternal treatment and transient seronegativity in the cases where the maternal contamination had occurred during the first 2 trimesters of pregnancy. The serology became positive again in 30 of the 33 children (91%) and in 22 children there was a rebound. At last follow-up, the 3 other children still had negative serology (mean duration 35 months, range 3-62 months). CONCLUSION: Transient negative toxoplasmosis serology is a frequent phenomenon in children with congenital toxoplasmosis. Although the underlying pathophysiological mechanism remains unknown, it is crucial to avoid questioning the initial diagnosis of congenital toxoplasmosis and to continue regular routine monitoring.

Child↗
PubMed2001

Serological rebound in congenital toxoplasmosis: long-term follow-up of 133 children.

UNLABELLED: Although serological rebound is common in infants with congenital toxoplasmosis, clinical recommendations for management, in particular the need for additional treatment, vary. The goals of our retrospective cohort study in 133 consecutive children with congenital toxoplasmosis were to estimate the incidence and duration of the rebounds, identify predictive factors, assess the long-term risk of eye lesions and the need for treatment. We first estimated the incidence and duration of rebounds and identified predictive factors using an univariate analysis and a Cox model modified to include time-dependent variables. Two cohort studies were then conducted to compare the incidence density of secondary eye lesions in children who had a rebound versus no rebound, and among children who had a rebound after initial therapy, in those who received an additional course of treatment and in those who did not. Of the 133 children, 93 (70%) had at least one rebound during a mean follow-up of 95 months. Of those with one rebound diagnosed after initial treatment, 33 received an additional 3-month course of pyrimethamine/sulphadoxine and 48 were not treated. Intracranial calcification at birth was associated with an increased relative risk (RR) of rebound (RR = 2.601; P = 0.03), and treatment with pyrimethamine/sulphadoxine between 2 and 12 months of age with a decreased risk (RR = 0.3; P = 0.0845), whereas age of pregnancy at maternal infection, type of treatment during pregnancy and sex were not found to be predictive factors. There was no difference in incidence densities of secondary eye lesions in children without rebound (7/3,367 child-months) compared to those with at least one rebound (22/9,609 child-months) (RR = 1.10; 95% CI: 0.47-2.58), and, among the 81 children who had one rebound diagnosed after initial treatment, in those who received an additional course of treatment and in those who did not (RR = 0.72; 95% CI: 0.30-1.72). CONCLUSION: serological rebound is common in children with congenital toxoplasmosis but, due to the risk and constraints, an additional course of treatment and more ophthalmological surveillance than currently practiced do not seem warranted.

Animals↗
PubMed1999

Involvement of enterotoxins G and I in staphylococcal toxic shock syndrome and staphylococcal scarlet fever.

We investigated the involvement of the recently described staphylococcal enterotoxins G and I in toxic shock syndrome. We reexamined Staphylococcus aureus strains isolated from patients with menstrual and nonmenstrual toxic shock syndrome (nine cases) or staphylococcal scarlet fever (three cases). These strains were selected because they produced none of the toxins known to be involved in these syndromes (toxic shock syndrome toxin 1 and enterotoxins A, B, C, and D), enterotoxin E or H, or exfoliative toxin A or B, despite the fact that superantigenic toxins were detected in a CD69-specific flow cytometry assay measuring T-cell activation. Sets of primers specific to the enterotoxin G and I genes (seg and sei, respectively) were designed and used for PCR amplification. All of the strains were positive for seg and sei. Sequence analysis confirmed that the PCR products, corresponded to the target genes. We suggest that staphylococcal enterotoxins G and I may be capable of causing human staphylococcal toxic shock syndrome and staphylococcal scarlet fever.

Enterotoxins↗
PubMed1999

[Evaluation of allergic-type reactions to antibiotics and rapid immunotherapy].

Adverse effects of medications, most notably antimicrobials, are becoming increasingly common and raise difficult challenges in the area of clinical pattern definition (wide variety of symptoms, polypharmacy in many cases), diagnosis, and methodology (need for a rapid diagnosis, frequent obscurity of causative mechanisms, and less than ideal reliability of laboratory techniques). Sixty patients were treated by rush immunotherapy to one or more antimicrobials. The pretreatment evaluation included oriented history taking, skin tests, blood cell counts, IgE assays, and cell activation tests (basophils and lymphocytes). The results of this study confirm the usefulness of skin tests (intradermal, prick, or patch tests), which provided etiological orientation in 54 of the 60 cases. They also provide additional evidence of the lack of reliability of currently available in vitro tests (only 29 of the 60 tests were positive).

Anti-Bacterial Agents↗
PubMed1998

Identification of Encephalitozoon intestinalis in travelers with chronic diarrhea by specific PCR amplification.

With the use of Weber's modified trichrome and Uvitex 2B techniques, spores of microsporidia were detected in the stools of four travelers presenting clinically with chronic diarrhea. The general health of these patients was not impaired, and human immunodeficiency virus screening was negative. Immune evaluation, including the study of lymphocytic subpopulations, assay of serum immunoglobulins, and an intradermal multitest, showed normal results. Molecular identification of microsporidian species was based on the PCR amplification of a small-subunit rRNA sequence followed by HinfI endonuclease restriction. Encephalitozoon intestinalis microsporidiosis was thus shown in two of the four patients examined. In two patients, therapy based on albendazole made stools devoid of microsporidian spores without influence on the intestinal disorders. The pathogenic role of E. intestinalis in immunocompetent individuals remains to be demonstrated.

Animals↗
PubMed1998

Detection of staphylococcal superantigenic toxins by a CD69-specific cytofluorimetric assay measuring T-cell activation.

The presence of staphylococcal superantigenic toxins in the supernatants of liquid cultures was detected by an easy and rapid method assessing the activation of T lymphocytes by cytofluorimetric measurement of CD69 expression. Staphylococcus aureus cells were grown in Eagle's minimum essential medium supplemented with 5% heat-inactivated fetal calf serum. Supernatant fluids from all S. aureus strains producing superantigen-related toxins, including enterotoxins A to E, toxic shock syndrome toxin, and exfoliative toxins A and B, induced CD69 expression in a significantly higher number of T cells than a cutoff of 2%. This CD69 assay might be used for initial detection of superantigens from S. aureus strains isolated in the context of staphylococcal toxemia or related chronic human diseases such as atopic dermatitis or Kawasaki syndrome.

Antigens, CD↗
PubMed1997

[Diagnostic contribution of abnormal delayed-type hypersensitivity to Candida albicans. Characterization test by activation of cells sensitized to successive dilutions of Candida].

By measuring the activation of different cell models (lymphocytes and lymphocytic subsets) in the presence of Candida albicans with flow cytometry reading, it is possible to show that successive dilutions of Candida albicans can lead to lymphocyte activation in abnormally-sensitized subjects. In a first trial, 10 subjects were tested in duplicate. The decrease of activity of the dilutions does not appear to be regular in relation to the progression of the dilutions. The activity of the dilutions wanes relatively rapidly with the first dilutions, then recurs later very distinctly, at the 6th dilution, then ebbs, then reappears in similar manner at the 9th, the 14th, and finally, the 19th dilution. Cell reactivity appears to differ depending on the subject. It can be represented through the calculated slope of the regression line, for each series of data. It therefore appears feasible to determine a threshold of reactivity and a scale of sensitivity, to make it possible to specify the degree of abnormal reactivity existing at a given time for a given subject. The constancy of the activity of the different dilutions tested, on 10 cultures of a single cell suspension, is especially well demonstrated in the second trial, showing unusually small standard deviations. Thus, the question arises as to the exact nature of the observed phenomenon and of its analysis from a physical-chemical point of view, with regard to the pharmacological effect of successive dilutions of Candida albicans.

Adolescent↗
PubMed1996

[Activation of T-lymphocytes in Crohn disease and in ulcerative hemorrhagic rectocolitis. Therapeutic implications].

Inflammatory bowel disease (IBD) encompasses two forms of intestinal inflammation: ulcerative colitis and Crohn's disease. Besides abnormalities of immunoglobulins production and complement activation, T lymphocytes play an important role in pathogeny of these diseases. Although T-cells number is increased in intestinal mucosa of such patients, CD4/CD8 ratio of T lymphocytes subsets is normal in mucosa. Activated T-cells expressing interleukin-2 receptors (CD25) are increased in lamina propria from patients with IBD. Cytokines induce abnormal expression of class II antigens of major histocompatibility complex by epithelial cells which may act as antigen presenting cells to CD4 T-cells. Better understanding of pathogenic mechanisms in IBD might justify new immunosuppressive therapeutics to treat these patients.

Antibodies, Monoclonal↗
PubMed1994

Secretory IgA antibodies to Cryptosporidium parvum in AIDS patients with chronic cryptosporidiosis.

Immune mechanisms that may control Cryptosporidium parvum infection remain unknown. The role of T cell-mediated immunity is suggested by the chronic disease observed in AIDS patients and in athymic or CD4+ T cell-depleted mice. The role of specific antibodies is also unclear. This study sought to determine serum and secretory antibodies to C. parvum in patients infected with human immunodeficiency virus type 1 (HIV-1) with or without chronic cryptosporidiosis. C. parvum-specific antibodies and specific secretory antibodies were determined by ELISA in saliva and sera from 50 HIV-1-infected patients, 27 healthy adults, and 21 healthy children. Despite lower CD4+ lymphocyte counts, patients with chronic cryptosporidiosis had increased levels of C. parvum-specific antibodies in saliva and serum and higher specific secretory antibody levels in saliva than did controls. Persistence of protracted diarrhea despite high levels of both serum and secretory antibodies suggests that specific secretory antibodies are not sufficient to control this protozoan parasite infection of intestinal mucosa.

Acquired Immunodeficiency Syndrome↗
PubMed1994

[Indolent mastocytosis and bronchial hyperreactivity. A case report].

Mastocytosis (MS) may be exclusively cutaneous or, more rarely, systemic. MS may be indolent (benign), aggressive, leukaemic or associated with a myeloproliferative disorder. The clinical expression of MS may be secondary to the direct consequences of the development of mastocytes in tissue or correspond to the paroxysmal features related to the liberation of vasoactive and spasmogenic mediators by activated mastocytes. Dyspnoeic episodes are classical but the physiopathological mechanism is poorly documented. True asthma or bronchopulmonary mastocytosis seems rare. The authors report evidence of non-specific bronchial hyper-reactivity (HRB) to Carbachol in a patient effected with benign cutaneous mastocytosis with secondary elevation of the total serum IGE. Factors determining the HIB are discussed and appear primarily linked to the mastocytosis.

Adult↗
PubMed1994

Lentivirus-induced interstitial lung disease: pulmonary pathology in sheep naturally infected by the visna-maedi virus.

Visna-maedi virus is a lentivirus that causes a chronic disease in sheep affecting, among other organs, the lungs. Interstitial pneumonitis is similar to that in man associated with the infection by the human immunodeficiency virus type-1. We have compared the pathological features of lungs of sheep naturally infected with visna-maedi virus with the results obtained from bronchoalveolar lavage and virus isolation. Semi-quantitative grading of the lesions was performed on 147 sheep lungs obtained from the slaughterhouse. Seventy-seven were macroscopically and histologically normal, 39 had typical lesions of interstitial lung disease (maedi), and 13 had minor lesions of the same type. Eighteen of the affected lungs were heavily infested with parasites. Of these parasite-infected lungs, 9 showed typical maedi lesions and 4 showed minor lesions; parasite infection had no obvious effect on the development of maedi. In keeping with pathological findings, bronchoalveolar lavage disclosed an alveolitis process in the maedi lungs with increased macrophage, lymphocyte and neutrophil numbers. Cytopathic virus was detected from alveolar macrophage coculture with fibroblasts more often from maedi lungs (10/12) than from normal lungs (9/39). Electron microscopy of bronchoalveolar lavage cocultures revealed typical lentiviral particles. Animals with minor lesions may be at an early stage of the disease.

Animals↗