Biomedical subjects
M Huerre
Publications and source records attributed to M Huerre.
Molecular detection and characterization of yellow fever virus in blood and liver specimens of a non-vaccinated fatal human case.
A yellow fever virus of a South American genotype was identified in the liver and blood samples of a non-vaccinated European patient after his return from Brazil. ELISA tests were negative for IgG and positive for IgM against yellow fever. Yellow fever proteins in the formalin-fixed and paraffin-embedded liver biopsy were detected by immunohistochemical procedures. Viral RNA extracted from the liver tissue was also detected using an RT-semi-nested PCR procedure and molecular hybridization. Alignment of the sequence obtained from a gene fragment amplified by RT-semi-nested PCR directly from a blood sample with those of African and South American yellow fever virus strains identified a Brazilian topotype as being responsible for the disease. RT-semi-nested PCR may be used advantageously for clinical specimens for rapid and specific diagnosis, and with archival biopsy material for retrospective studies.
Erythrodermic diffuse cutaneous leishmaniasis with Sézary syndrome.
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Cellular localization of 5-HT1B receptor mRNA in the rat olfactory tubercle: do GABAergic neurons express the 5-HT1B gene?
In situ hybridization with a 5-HT1B receptor probe and immunocytochemistry with gamma-aminobutyric acid (GABA) antibody performed on adjacent sections of rat brains reveal that GABAergic cell bodies, which represent 10-15% of the cellular population, do not express the 5-HT1B gene in rat olfactory tubercle. Most of the cells expressing the 5-HT1B gene were of small to medium size; large neurons expressing RNA transcripts may correspond to cholinergic neurons. It cannot be excluded that the absence of detectable 5-HT1B mRNA in GABAergic neurons was due to limited sensitivity of the in situ hybridization and immunocytochemistry procedures. Our data suggest that GABAergic neurons originating from olfactory tubercle are not directly controlled by serotonin through 5-HT1B receptors.
Murine acariasis: I. Pathological and clinical evidence suggesting cutaneous allergy and wasting syndrome in BALB/c mouse.
We describe here a disease related to mite-associated ulcerative dermatitis in BALB/c mice, a strain previously classified as resistant to this condition. The disease was recognized by pruritic cutaneous pathology and wasting. Pathologic studies showed a marked allergic-type inflammation in the skin. The dominant histologic feature was extensive mast cell infiltration in cutaneous lesions and in lymphoid tissues, associated with a greatly elevated serum IgE concentration. The disease was secondary to infestation with an acarian ectoparasite Myocoptes musculinus, and seemed to represent an allergic reaction to the parasite-derived substances, with an associated wasting syndrome. This condition may be a useful experimental model for allergic diseases.
A case of myospherulosis occurring in the perirenal adipose tissue.
The authors report a case of spontaneous myospherulosis that developed in the right perirenal adipose tissue, presented like an abscess, in an 82-year old man of the A, Rh+ blood group. The patient had a history of chronic lymphocytic leukaemia. Fine needle aspiration and histological examination of the renal cyst allowed the observation of 4- to 7-micron spherules (or endobodies) enclosed in saccular structures (or parent bodies) and accompanied by a foreign body-type response. The walls of the parent bodies were negative for PAS, Gomori's methenamine silver and Giemsa's stain. Immunohistochemical study was positive with anti A antibody specific of A1/A2 blood group and with anti glycophorin A antibody. The authors reviewed the literature concerning this rare lesion: it usually occurs in subcutaneous fat or in the paranasal sinuses, nose and middle ear but, up to now, no previous case has ever been reported in the urinary tract. The only case of visceral myospherulosis previously reported occurred in a cystic teratoma of the ovary. The reported case is also peculiar by the unusual thickness of the parent bodies. The authors also discuss the mechanism of the disease and suggest that, in the present observation, myospherulosis could have been induced by the rupture of a preexisting cyst in the perirenal adipose tissue.
Attenuated virulence of uridine-uracil auxotrophs of Aspergillus fumigatus.
Aspergillus fumigatus mutants that are deficient in the de novo UMP biosynthesis pathway because of a mutation in the pyrG gene encoding orotidine-5'-phosphate decarboxylase (and therefore auxotrophic for uridine or uracil) were evaluated in a murine model of invasive aspergillosis. These mutants were entirely nonpathogenic, and mutant conidia remained ungerminated in alveolar macrophages. Both the germination and virulence defects could be restored by supplementing the drinking water of the animals with uridine. DNA-mediated transformation of one of the pyrG mutants with the Aspergillus niger pyrG gene also restored virulence. These results suggest that uridine and uracil are limiting in the lung environment, thus preventing conidium germination and hence virulence of the pyrG mutants.
Infection of rabbit Peyer's patches by Shigella flexneri: effect of adhesive or invasive bacterial phenotypes on follicle-associated epithelium.
In order to invade the colonic mucosa, the bacterial pathogen Shigella flexneri must find a site of entry. Experiments with the rabbit ligated intestinal loop model described here confirm that M cells of the follicle-associated epithelium (FAE) that covers lymphoid structures of the Peyer's patches represent a major site of entry for invasive microorganisms. In addition, in an isogenic Shigella background, expression of an adhesive phenotype, or of an invasive phenotype, is required for bacteria to efficiently colonize the FAE. A nonadhesive, noninvasive mutant barely interacted with FAE. Adhesive and invasive strains induced dramatic but different alterations on FAE. Invasive strain M90T caused major inflammation-mediated tissue destruction after 8 h of infection. Adhesive strain BS15 caused limited inflammation, but major architectural changes, characterized by an increase in the size of M cells that became stretched over large pockets containing an increased number of mononuclear cells, were observed. M cells progressively occupied large surface areas of the FAE at the expense of enterocytes. This contributed to enterocytes losing contact with the lumen. These experiments demonstrate that various remodeling patterns may occur in Peyer's patches in response to bacterial pathogens, depending on the virulence phenotype expressed by the pathogenic strain.
[Diffuse lepromatous leprosy disclosed by cutaneous vasculitis. The Lucio phenomenon].
INTRODUCTION: Lucio's phenomenon, also called necrotizing erythema, is a rare acute manifestation which sometimes introduces diffuse lepromatous leprosy, almost exclusively in Central American populations. CASE REPORT: A 76-year-old polynesian man of chinese ethnic origin had necrotizing erythema for several months before development of Lucio's leprosy. The patient had necrotizing lesions of the lower limbs with large polygonal scars and poor general health status. Diagnosis was based on the discovery of acid-fast bacilli at the pathology examination of skin biopsies. The necrotizing zones appeared as cutaneous vasculitis with angiogenesis of the superficial dermis and presence of Hansen bacilli within the endothelium. DISCUSSION: This case of diffuse lepromatous leprosy, the first reported in the South Pacific, emphasizes the polymorphism of leprosy and the importance of recognizing rare clinical forms, especially in the tropics. Anti-Hansen drugs are effective.
[Subcutaneous phycomycosis successfully treated with itraconazole].
INTRODUCTION: We report a case of basidiobolomycosis (subcutaneous phycomycosis), an uncommon deep mycosis in the entomophtoromycosis group. CASE REPORT: A 12-year-old girl presented a deep skin infiltration involving the back and buttocks. Histology reported filamentous formations without septa surrounded by Splendore-Hoepple phenomenon, the characteristic aspect of entomophtoromycosis. Outcome was favorable after treatment with itraconazole. DISCUSSION: Basidiobolomycosis is a deep mycosis rarely observed in children. Most reported cases have occurred in the tropics. The clinical presentation can simulate deep scleroderma or a tumoral disease. Treatment is currently based on imidazole derivatives which are particularly effective.
[Diffuse cutaneous leishmaniasis and acquired immunodeficiency syndrome in a Senegalese patient].
Tegumentary leishmaniasis cases associated with HIV infections were rarely reported. We present a case of diffuse cutaneous leishmaniasis in a senegalese patient with HIV 1 infection. The diagnosis was supported by a cutaneous biopsy but no Leishmania strain could be isolated by cultures from cutaneous specimens.
[Anatomopathologic study of five cases of leprosy in HIV seropositive patients].
In an effort to establish whether the human immunodeficiency virus (HIV) modifies the histological image of lepromatous skin lesion, a comparative study was conducted in 1994 at the Marchoux Institute in Bamako, Mali, on persons newly suffering from leprosy who had been tested seropositive and seronegative for the HIV virus. These new leprosy patients had never been treated and could be grouped as follows: 5 HIV-positive (1 TT, 1 BT, 1 BL, 2 LL) and 10 controls testing HIV-negative, selected according to the following criteria: each seropositive leprosy subject was matched with two seronegative controls having the same clinical features, same stage under the Ridley classification system, same age and sex. No discordance between the clinical classifications and the histological features in the subjects testing HIV-positive has been observed. They display features similar to those testing negative, with the presence of histiocytes, in particular epithelioid cells and giant cells in normal proportion depending on the form of leprosy. The only remarkable difference was a greater incidence of oedema in the subjects testing seropositive, compared with patients testing seronegative. In conclusion, HIV infection does not appear to cause major modifications in cellular response to Mycobacterium leprae, and no changes should be made in leprosy control programmes.
Eosinophil recruitment into the respiratory epithelium following antigenic challenge in hyper-IgE mice is accompanied by interleukin 5-dependent bronchial hyperresponsiveness.
A murine model for antigen-induced bronchial hyperreactivity (BHR) and airway eosinophilia, two hallmarks of asthma, was developed using ovalbumin-immunized mice, which produce large amounts of IgE (named BP2, "Bons Producteurs 2," for High Line of Selection 2). A single intranasal ovalbumin challenge failed to modify the bronchial responses, despite the intense eosinophil recruitment into the bronchoalveolar lavage fluid and airways. When mice were challenged twice a day for 2 days or once a day for 10 days, BHR in response to i.v. 5-hydroxytryptamine or to inhaled methacholine was induced in BP2 mice but not in BALB/c mice. Histological examination showed that eosinophils reached the respiratory epithelium after multiple ovalbumin challenges in BP2 mice but remained in the bronchial submucosa in BALB/c mice. Total IgE titers in serum were augmented significantly with immunization in both strains, but much more so in BP2 mice. Interleukin 5 (IL-5) titers in serum and bronchoalveolar lavage fluid of BP2 mice were augmented by the antigenic provocation, and a specific anti-IL5 neutralizing antibody suppressed altogether airway eosinophilia and BHR, indicating a participation of IL-5 in its development. Our results indicate that the recruitment of eosinophils to the airways alone does not induce BHR in mice and that the selective effect on BP2 mice is related to their increased IgE titers associated with antigen-driven eosinophil migration to the epithelium, following formation and secretion of IL-5.
Monoclonal immunoglobulin A antibody directed against serotype-specific epitope of Shigella flexneri lipopolysaccharide protects against murine experimental shigellosis.
To determine the role of humoral mucosal immune response in protection against shigellosis, we have obtained a monoclonal dimeric immunoglobulin A (IgA) antibody specific for Shigella flexneri serotype 5a lipopolysaccharide (mIgA) and used a murine pulmonary infection model that mimics the lesions occurring in natural intestinal infection. Adult BALB/c mice challenged with 10(7) S. flexneri organisms developed a rapid inflammatory response characterized by polymorphonuclear cell infiltration around and within the bronchi and strong systemic interleukin 6 response. Implantation of hybridoma cells in the back of mice, resulting in the development of a myeloma tumor producing mIgA in the serum and subsequently secretory mIgA in local secretions, or direct intranasal administration of these antibodies, protected the animals against subsequent intranasal challenge with S. flexneri serotype 5a. Absence of histopathological lesion and significant decrease in bacterial load of the lungs and of systemic interleukin 6 response were the three major criteria of protection. This protection was shown to be serotype-specific and dependent on local concentration of mIgA. These data demonstrate that mucosal antibodies directed against a single polysaccharidic surface epitope of Shigella can protect against the disease.
The GroES homolog of Helicobacter pylori confers protective immunity against mucosal infection in mice.
Helicobacter pylori is an important etiologic agent of gastroduodenal disease. In common with other organisms, H. pylori bacteria express heat shock proteins that share homologies with the GroES-GroEL class of proteins from Escherichia coli. We have assessed the heat shock proteins of H. pylori as potential protective antigens in a murine model of gastric Helicobacter infection. Orogastric immunization of mice with recombinant H. pylori GroES- and GroEL-like proteins protected 80% (n = 20) and 70% (n = 10) of animals, respectively, from a challenge dose of 10(4) Helicobacter felis bacteria (compared to control mice, P = 0.0042 and P = 0.0904, respectively). All mice (n = 19) that were immunized with a dual antigen preparation, consisting of H. pylori GroES-like protein and the B subunit of H. pylori urease, were protected against infection. This represented a level of protection equivalent to that provided by a sonicated Helicobacter extract (P = 0.955). Antibodies directed against the recombinant H. pylori antigens were predominantly of the IgG1 class, suggesting that a type 2 T-helper cell response was involved in protection. This work reports a protein belonging to the GroES class of heat shock proteins that was shown to induce protective immunity. In conclusion, GroES-like and urease B-subunit proteins have been identified as potential components of a future H. pylori subunit vaccine.
Filariae from a wild gorilla in Gabon with description of a new species of Mansonella.
A search for filariae was performed on a wild male Gorilla g. gorilla from the Lopé Reserve in Gabon, which had died as a result of injuries inflicted by another male gorilla. A female worm of Loa loa and female worms of two species of Mansonella were recovered from the deep tissues of a wounded thigh. In order to analyze these Mansonella, specimens of M. (E.) perstans, M. (E.) vanhoofi and M. (E.) streptocerca from the Collections of the Museum National d'Histoire Naturelle de Paris have been studied and new important discriminative characters characterised, such as the body-swellings in M. (E.) perstans, due to the presence of coelomocytes as in South-american M. (Tetrapetalonema) spp. One of the Mansonella from this gorilla was not identified, but the body-swellings and the microfilarial morphology suggested a possible similarity with M. (Esslingeria) perstans. The other species is new; M. (E.) lopeensis n. sp. is distinguished by its large size, lack of body-swellings, structure of the tegumental sheath, complex vagina, and a tail with a subterminal constriction, a terminal bend and large lappets. Histological sections of organs of this gorilla also showed a microfilaria of M. (E) leopoldi in the blood vessels of the liver, and a male of Mansonella sp., interestingly situated in an afferent lymphatic vessel of an axillary lymph node.(ABSTRACT TRUNCATED AT 250 WORDS)
Brain stem encephalitis due to varicella-zoster virus in a patient with AIDS.
We describe a patient infected with human immunodeficiency virus (HIV) who had localized brain stem encephalitis due to varicella-zoster virus (VZV) and no cutaneous eruption. Diagnosis of the infection was based on the presence of Cowdry type A intranuclear inclusions in neurons, astrocytes, and oligodendrocytes positive for VZV (as shown by immunochemical staining). Although this infection is rare, we demonstrate the need for clinicians to include VZV infection in the differential diagnosis of rapidly progressive multiple cranial nerve palsies in HIV-infected patients, particularly because specific treatment for VZV infection is effective and relatively safe.
Interleukin-10 inhibits antigen-induced cellular recruitment into the airways of sensitized mice.
This report examines the effect of recombinant murine (rm) IL-10 on antigen-induced cellular recruitment into the airways of sensitized Balb/c mice. The intranasal instillation of 10 micrograms ovalbumin induced an early (6-24 h) increase in the number of neutrophils, and a late rise (24-96 h) in that of eosinophils in the bronchoalveolar lavage (BAL) fluid and bronchial tissue. A single intranasal instillation of 0.01-0.1 microgram of rmIL-10, administered concurrently with ovalbumin, but not 1 or 3 h thereafter, dose-dependently inhibited both airway neutrophilia and eosinophilia. This phenomenon was suppressed by treating the sensitized mice with 1 mg/mouse of a neutralizing anti-IL-10 mAb, which increased significantly ovalbumin-induced neutrophil and eosinophil accumulation in the BAL fluid. These results suggest that antigen stimulation may trigger the in vivo generation of IL-10, which, in turn, participates in the leukocyte infiltration into the airways. rmIL-10 also reduced TNF-alpha release in the BAL fluid observed 1 and 3 h after antigen challenge. Furthermore, the intranasal instillation of an anti-TNF-alpha antiserum to sensitized mice markedly reduced ovalbumin-induced neutrophil and eosinophil accumulation in the BAL fluid. These findings indicate that leukocyte infiltration into the airways of antigen-challenged mice is regulated by IL-10. Furthermore, inhibition of TNF-alpha production by rmIL-10 suggests that allergic airway inflammation and TNF-alpha formation are parallel events in this model.