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D Camus

Publications and source records attributed to D Camus.

143 records · Page 8Linked to original sources
PubMedDate not supplied

[Real-time quantitative PCR for toxoplasmosis diagnosis].

Congenital toxoplasmosis results from foetus contamination by Toxoplasma gondii during pregnancy. It is a frequent and severe condition calling for close monitoring of mothers at risk. During the last decades, numerous advances have been made specially in the antenatal diagnosis. The congenital toxoplasmosis diagnosis relies currently on PCR test of amniotic fluid, with a sensitivity of 80%. More recently, real-time quantitative PCR has been developed to improve toxoplasmosis diagnosis. We therefore compared the diagnosis value of quantitative real-time PCR with our conventional PCR-hybridization for the diagnosis of congenital toxoplasmosis.

Amniotic Fluid↗
PubMedDate not supplied

[Candida albicans meningo-encephalo-myelo-radiculitis at an addict].

Beside immunodepression induced by the human immunodeficiency virus, fungal infections of the central nervous system are extremely rare in heroin-addict patients. We report here a case of meningo-encephalitis with myelo-radicular lesions in a 25-year-old intravenous heroin addict but non-HIV patient, who was admitted for an acute confusion associated with gait disorders. The diagnosis of Candida albicans meningo-encephalo-myelo-radiculitis was established by magnetic resonance imagery and mycological and serological examinations of cerebrospinal fluid. The infection was cured with amphotericin B lipid complex and 5-fluorocytosine. Early diagnosis and antifungal therapy for 6 months resulted in a favorable outcome. The detection of circulating Candida mannan in cerebrospinal fluid with a more sensitive technique combined to MRI were particularly decisive to confirm Candida infection diagnosis, allowing an appropriate antifungal therapy.

Adult↗
PubMedDate not supplied

Introduction of Pneumocystis carinii in a colony of SCID mice.

Pneumocystis carinii-free SCID mice were housed closely exposed to corticosteroid-treated non-SCID mice in a conventional area of our laboratory animal facilities. A one-day exposure was sufficient for P. carinii transmission. The lung infection increased thereafter. Irradiation or splenectomy of SCID mice at the beginning of the exposure resulted in a marked increase of parasite multiplication. Extrapulmonary foci of pneumocystosis were detected in heart and spleen of SCID mice infected by P. carinii via air transmission.

Animals↗
PubMedDate not supplied

Production of a monoclonal antibody using lymphocytes from Pneumocystis infected mice.

A colony of BALB/c mice maintained in a protected area of our laboratory was not infected with Pneumocystis carinii. During corticosteroid treatment, animals became infected by exposure to infected mice. After four months of corticosteroid treatment, BALB/c mice developed severe pneumocystosis. Stopping of treatment was associated with: (i) high mortality of mice, (ii) decreased lung parasite level and (iii) appearance of anti-P. carinii antibodies in survivors. A monoclonal antibody (MAb) 4F2 was obtained by immortalisation of spleen lymphocytes of a female BALB/c mouse 3 months after the cessation of corticosteroid treatment. The MAb 4F2 recognized a 210-220 kDa mouse P. carinii antigen, but did not react with rat-, rabbit- or human-derived P. carinii. This MAb reacted with all stages of mouse P. carinii.

Animals↗
PubMedDate not supplied

Ultrastructural observations on the attachment of Pneumocystis carinii in vitro.

Pneumocystis carinii trophozoites grow in vivo in close contact with host cells. The attachment of Pneumocystis to the lung cells seems to be a critical step in the parasite's development. Up to now, the contact of Pneumocystis with mammalian tissue culture cells was shown using light and scanning electron microscopy. The methods are not sufficient to observed in detail the parasite-feeder cell area of contact. In this work, the attachment of Pneumocystis trophozoites to feeder cells was examined in serial sections using transmission electron microscopy. When the contact of a trophozoite with a feeder cell took place, the development of filopodia penetrating deeply into invaginations of the feeder cell plasma membrane was observed. Then, the apical tips of filopodia become bulged anchoring the parasite to the feeder cell. The behaviour of Pneumocystis in feeder cell cultures is compared to that of the parasite in other in vitro or in vivo experimental models.

Animals↗
PubMedDate not supplied

[Humoral and cellular immunity and sepsis in intensive care (author's transl)].

Different parameters of humoral and cell mediated immunity were studied in 17 patients with sepsis. There is an important decrease of CH 50 (82 p. cent of patients) and variations of serum complement according with activation of alternative pathway in gram negative and gram positive septicemia. The cellular immunity is never normal: the stimulation index of lymphocyte proliferation under the influence of P. H. A. is lower than 3. There is less than 50 p. cent of T lymphocytes forming rosettes. With cure of sepsis a discrimination is observed between patients with transient decreased immunity and those with persistent lower responses.

Adolescent↗
PubMedDate not supplied

Influence of malaria on a pre-existing antibody response to heterologous antigens.

Swiss mice were immunized with various antigens: polyvinylpyrrolidone (PVP), human serum transferrin (HST), bovine serum albumin (BSA) or tetanus toxoid (TT). Fifteen days after the last injection of antigen, the mice were infected with Plasmodium chabaudi AJ. Two weeks after the beginning of malarial infection, parasitaemia became latent and total gammaglobulin levels, as well as IgG and IgM levels, were significantly increased. At that period the antigen-binding capacity (ABC) and the total antigen-binding Sites (Abt) were determined for PVP, HST and BSA. It appeared that the ABC and Abt of anti-HST or anti-BSA antibodies were lower than those of corresponding uninfected controls. With regard to anti-PVP antibodies, only the Abt was modified after infection, but not the ABC. The evolution of anti-TT Ab levels determined by a solid-phase assay with 125I-TT was as above with a marked decrease on and after the 4th week of infection. Injection of low-density lipoproteins (LDL) from day-9-infected mice to TT-immunized mice significantly reduced anti-TT antibody levels. At similar doses, LDL from normal mice did not induce an inhibitory effect. At mouse-equivalent-dose, LDL from infected mice revealed an inhibitory effect compared to LDL from uninfected controls. Our results suggest that LDL from P. chabaudi-infected mice can exert an immunoregulatory role and thus could explain part of the immune impairment observed during the infective process. Moreover, from the present data it might be postulated that the hypergammaglobulinaemia of P. chabaudi infection does not result from a parasite-potentiating effect on a pre-existing antibody response.

Animals↗
PubMedDate not supplied

[Impairment of immune response in parasitic infections].

Parasite escape mechanisms may depend upon factors intrinsic to parasites (host antigen uptake, antigenic variation) and upon partial failure of host's immune mechanisms. Impairment of immune response in parasitic infections, analysed and discussed from literature (138 references), is characterized by a high prevalence of autoantibodies and the common observation of immunosuppression in human parasitic infections as well as in experimental models. The high prevalence of autoantibodies accompanying increased levels of immunoglobulins contrasts with the low prevalence of autoimmune diseases in parasitic endemic areas. Evidence for cell mediated autoimmune process has rarely been reported. This might be related to an impairment of T-helper cell function and to the direct role, on B cells, of mitogens from parasite origin. Immunosuppression has been described in many human parasitic infections and in numerous experimental models. The defect in host's immune response is expressed by an impairment of both humoral and cell mediated immune responses to various heterologous antigens, and increased susceptibility to tumorigenesis, prolonged survival of skin allografts and an increased susceptibility to bacterial or viral infections. Various mechanisms of immunosuppression have been described, including failure of macrophage function or release of soluble immunosuppressive factors by parasites. The authors report some of their recent experiments in experimental schistosomiasis, which have allowed the characterization of such factors. Parasites appear in general to play a role in the regulation of the immune response that they have themselves evoked.

Animals↗
PubMedDate not supplied

[Immunosuppressive factors released by Schistosoma mansoni].

Immunosuppressive factors were evidenced in cell-free supernatant of S. mansoni schistosomes culture and incubation products of the parasite. Both parasitic materials decreased tritiated thymidine and leucine uptake in normal spleen cells from CBA mouse and Fischer rats and in peripheral human blood lymphocytes stimulated either by non specific mitogens (PHA, ConA, or LPS) or by allogeneic cells. The suppressive factor(s) was (were) heat-resistant, dialyzable and of molecular weight 500-1,000. The inhibition of lymphocyte proliferation was not due to cytotoxic or cytostatic activity on lymphoid cells, nor did the parasitic reagents interfere with the binding of fluorescein-labelled ConA. The suppressive activity was also demonstrated in the serum from rats infected for 4 weeks by S. mansoni and in the dialyzable fraction of it. This suggests the release by the parasite in vitro as well as in vivo of inhibitory factor(s) decreasing lymphocyte proliferation and brings therefore a new light on the machanism of immune deficiency in parasitic infections.

Animals↗
PubMedDate not supplied

Induction of antibodies against the Plasmodium falciparum p126 antigen in non-responder H-2b and partial-responder H-2d mice using synthetic peptides.

The p126 Plasmodium falciparum antigen is processed into two fragments, p50 and p73, the latter one containing the subfragments p47 and p18 when the schizonts rupture. An absence of antibody response against the p126 antigen has been reported recently in H-2b mice and limited to the p73 processed fragment in H-2d mice. Synthetic peptides corresponding to various domains of the molecule have been used to immunize mice in order to overcome the absence of an immune response. Synthetic peptides corresponding to the N-terminus of p50 or p18 as well as to the C-terminus of p47 were unable to induce anti-peptide antibodies when injected carrier-free or coupled to ovalbumin. Synthetic peptides corresponding to the C-terminus of p18 or composed of 6 or 9 serines were able to induce anti-peptide antibodies when injected coupled to a carrier protein. However, none of these antibodies was able to recognize the native p126 molecule. Various synthetic peptides corresponding to the 6-octapeptide [Nt47 (6 x 8)] or the 4-octapeptide [Nt47(4 x 8)] repeat sequence localized at the N-terminus of the p47 have also been used to immunize mice. No antibodies were generated using a carrier-free [Nt47(6 x 8)-Cys]2 or [Nt47 (4 x 8)-Cys]2 peptide, an octameric multiple antigen peptide construct [Nt47(6 x 8)]-MAP or the [Nt47(6 x 8)] coupled to one or two palmitic acids. In contrast, [Nt47(6 x 8)]-Cys coupled to either tetanus toxoid (TT) or ovalbumin (OVA) and [Nt47(4 x 8)]-Cys coupled to OVA induced antibodies against the synthetic peptide and the native p126 molecule in both H-2d and H-2b mice. A multiple antigen peptide construct [Nt47(4 x 8)-MSP-3b]-MAP containing 4 [Nt47(4 x 8)] and 4 [MSP-3b] also induced antibodies against the synthetic peptide [Nt47(4 x 8)-Cys]2 and the native p126 molecule in both H-2d and H-2b mice.

Amino Acid Sequence↗