Relevant bibliographies by topics / Tropheryma whipplei

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Tropheryma whipplei'

Author: Grafiati
Published: 4 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "Tropheryma whipplei"

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Liang, Zhongxing, Bernard La Scola, and Didier Raoult. "Monoclonal Antibodies to Immunodominant Epitope of Tropheryma whipplei." Clinical and Vaccine Immunology 9, no. 1 (January 2002): 156–59. http://dx.doi.org/10.1128/cdli.9.1.156-159.2002.

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ABSTRACT Recent isolation of Tropheryma whipplei (formerly Trophyrema whippelii), the agent of Whipple’s disease, from the cardiac valve of a patient with Whipple’s disease endocarditis now allows the detection of reactive epitopes that could be used in a serological assay. In order to propose an enzyme-linked immunosorbent assay (ELISA) that uses recombinant T. whipplei antigen, we first determined by Western blotting of human, mouse, and rabbit antisera that the common immunodominant epitope is an 84-kDa protein. We then produced 13 monoclonal antibodies (MAbs) against T. whipplei, 12 of which recognize this immunodominant epitope. These MAbs did not react with phylogenetically closely related bacteria or bacteria previously shown to be cross-reactive with T. whipplei, but they did react with two other strains of T. whipplei isolated, one from an ocular sample and the other from a duodenal biopsy specimen. By confocal microscopy, the MAbs allowed detection of T. whipplei within infected fibroblasts. The identification of the 84-kDa antigen with our MAbs will make it possible to develop a diagnostic antigen for use in a diagnostic ELISA for Whipple’s disease.
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Fenollar, Florence, Jean-Christophe Lagier, and Didier Raoult. "Tropheryma whipplei and Whipple's disease." Journal of Infection 69, no. 2 (August 2014): 103–12. http://dx.doi.org/10.1016/j.jinf.2014.05.008.

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Zhang, Wen Mei, and Ling Xu. "Pulmonary parenchymal involvement caused by Tropheryma whipplei." Open Medicine 16, no. 1 (January 1, 2021): 843–46. http://dx.doi.org/10.1515/med-2021-0297.

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Abstract We report a 26-year-old man with left chest pain for 4 days. His chest CT showed a cavity in the left upper lung. Tuberculosis was suspected first, but metagenomics next generation sequencing (mNGS) in bronchoalveolar lavage fluid only detected Tropheryma whipplei. Tropheryma whipplei is the pathogen of Whipple’s disease. The most frequently involved organs are the eyes, heart, and central nervous system. Pulmonary parenchymal involvement is rare. To our knowledge, this is the first reported case of pulmonary cavity caused by Tropheryma whipplei. Nineteen cases of pulmonary parenchymal involvement were found by literature search. The most common respiratory symptom was cough, followed by dyspnea/breathlessness and chest pain. The most common finding in chest imaging was pulmonary nodules, followed by interstitial changes and patchy infiltration. Our case and literature review highlighted that Tropheryma whipplei infection should be considered in the differential diagnosis of pulmonary cavity, pulmonary nodules, interstitial changes, and patchy infiltration. mNGS is helpful to improve diagnosis rate.
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Genot, Séverine, Andreas Stein, Hubert Lepidi, Melanie Ihrig, Didier Raoult, and Jean-Louis Mege. "Murine Model of Infection by Tropheryma whipplei." Infection and Immunity 74, no. 8 (August 2006): 4915–17. http://dx.doi.org/10.1128/iai.00283-06.

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ABSTRACT We developed an animal model reproducing several aspects of Whipple's disease. Immunocompetent mice were persistently infected with Tropheryma whipplei, its etiological agent, and developed liver granulomas. SCID mice were infected similarly but did not develop tissue lesions. The delayed clearance of T. whipplei suggests a protective role for innate immunity.
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Masselot, F., A. Boulos, M. Maurin, J. M. Rolain, and D. Raoult. "Molecular Evaluation of Antibiotic Susceptibility: Tropheryma whipplei Paradigm." Antimicrobial Agents and Chemotherapy 47, no. 5 (May 2003): 1658–64. http://dx.doi.org/10.1128/aac.47.5.1658-1664.2003.

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ABSTRACT Tropheryma whipplei, the agent of Whipple's disease, grows fastidiously only in cell cultures without plaque production, and only three strains have been passaged. The formation of bacterial clumps in the supernatant precludes enumeration of viable bacteria and MIC determination. We evaluated the bacteriostatic effects of fluoroquinolones against two T. whipplei isolates by measuring the inhibition of the DNA copy number increase by real-time quantitative PCR. The analysis of the T. whipplei genome database allowed the identification not only of the gyrA gene but also the parC gene encoding the alpha subunit of the natural fluoroquinolone targets DNA gyrase (GyrA) and topoisomerase IV (ParC), respectively. The parC gene was detected in actinobacteria for the first time. High ciprofloxacin MICs (4 and 8 μg/ml) were correlated with the presence in T. whipplei GyrA and ParC sequences with an alanine residue at positions 83 and 80 (Escherichia coli numbering), respectively. Alanines at these positions have previously been associated with increased fluoroquinolone resistance in E. coli and mycobacteria. However, the MIC of levofloxacin was low (0.25 μg/ml). The same T. whipplei GyrA and ParC sequences were found in two other cultured strains and in nine uncultured tissue samples from Whipple's disease patients, allowing one to speculate that T. whipplei is naturally relatively resistant to fluoroquinolones.
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Marth, Thomas, Verena Moos, Christian Müller, Federico Biagi, and Thomas Schneider. "Tropheryma whipplei infection and Whipple's disease." Lancet Infectious Diseases 16, no. 3 (March 2016): e13-e22. http://dx.doi.org/10.1016/s1473-3099(15)00537-x.

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Lagier, Jean-Christophe, and Didier Raoult. "Whippleʼs disease and Tropheryma whipplei infections." Current Opinion in Infectious Diseases 31, no. 6 (December 2018): 463–70. http://dx.doi.org/10.1097/qco.0000000000000489.

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Freeman, Hugh James. "Tropheryma whipplei infection." World Journal of Gastroenterology 15, no. 17 (2009): 2078. http://dx.doi.org/10.3748/wjg.15.2078.

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Lagier, Jean-Christophe, Hubert Lepidi, Didier Raoult, and Florence Fenollar. "Systemic Tropheryma whipplei." Medicine 89, no. 5 (September 2010): 337–45. http://dx.doi.org/10.1097/md.0b013e3181f204a8.

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Toma, Tudor P. "Tropheryma whipplei genome." Genome Biology 4 (2003): spotlight—20030225–01. http://dx.doi.org/10.1186/gb-spotlight-20030226-01.

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Dissertations / Theses on the topic "Tropheryma whipplei"

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Fenollar, Florence. "Maladie de Whipple et Tropheryma whipplei." Aix-Marseille 2, 2003. http://www.theses.fr/2003AIX20659.

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Keita, Alpha Kabinet. "Epidémiologie de Tropheryma whipplei." Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM5044.

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Tropheryma whipplei est détectée avec une prévalence variable dans les selles et de salive. Pour déterminer les facteurs épidémiologiques qui peuvent influencer l'histoire naturelle de la bactérie, nous avons réalisé des études sur l'ensemble de la population de 2 villages au Sénégal (Dielmo et Ndiop), chez les personnes sans domicile fixe (SDF) et dans les familles en France. Dans ces différentes populations, la prévalence du portage de T. whipplei dans les selles était respectivement de 31.2% (139/446), 12,9% (21/162) et 37,5% (24/64). En ce qui concerne les résultats des études phylogénétiques, nous avons identifié au Sénégal 22 génotypes, dont 16 étaient nouveaux. Un seul génotype (53) était commun aux deux villages. Parmi les génotypes spécifiques, l'un (n ° 52) était épidémie à Dielmo (15/28, 53,4%, p <10-3) et l'autre (n ° 49) à Ndiop (27,6%, p = 0,002). Deux génotypes, le génotype 3 et le génotype 85, circulent plus fréquemment chez les SDF par rapport à d'autres groupes personnes positives pour T. whipplei. Au Sénégal, la séroprévalence était estimée à 72,8% (291/400). Dans les familles, la séroprévalence était plus élevée chez les membres (23/30, 77%) par rapport à la population générale (143/300, 48%). Nos résultats montrent que T. whipplei est une bactérie fréquente et contagieuse qui est contractée très tôt dans l'enfance. La mise en évidence de génotypes épidémiques associée à l'absence de la bactérie dans des échantillons d'eau, chez les arthropodes vecteurs; la très faible présence (<1%) dans les selles des animaux domestiques et dans les écouvillons de poussière suggèrent une transmission interhumaine du T whipplei
Tropheryma whipplei is detected with variable prevalence in stool and saliva. To investigate the epidemiological factors which influences the natural history of the bacterium; we performed studies in entire population of 2 villages in Senegal (Dielmo and Ndiop) in homeless people and in family in Marseille-France. In these populations, the prevalence of T. whipplei in stool was respectively 31.2% (139/446), 12.9% (21/162) and 37.5% (24/64).Regarding findings from phylogenetic studies we identified in Senegal 22 genotypes, 16 of which were new. Only one genotype (#53) was common to both villages. Among the specific genotypes, one (#52) was epidemic in Dielmo (15/28, 53.4%, p<10-3) and another (#49) in Ndiop (27.6%, p=0.002). Two genotypes, the genotype 3 and the genotype 85, circulate more frequently in the homeless people compared to other people positive for T. whipplei and are epidemic. The same circulating genotype was significantly more common in families compared to other people. In Senegal, the seroprevalence was estimated at 72.8% (291/400). In family study, the seroprevalence was higher in the relatives (23/30, 77%) compared to the general population (143/300, 48%). Our findings show that T. whipplei is a common and contagious bacterium that is contracted early in childhood. Epidemic genotypes associated with absence of the bacterium in water samples, arthropods vector; almost no presence (< 1%) in domestic animals and dust suggest a human transmission of T whipplei
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Ben, Azzouz Eya. "Étude physiopathologique des infections à Tropheryma whipplei." Thesis, Aix-Marseille, 2019. http://www.theses.fr/2019AIXM0243.

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La maladie de Whipple est une maladie systémique rare, causée par l’agent bactérien Tropheryma whipplei.T. whipplei présente un tropisme particulier pour les macrophages. Elle induit un profil d’activation macrophagique atypique, caractérisé par l’expression de molécules anti-inflammatoires, la sécrétion d’IL-16 et l’induction de l’apoptose. Au cours de cette étude, nous nous étions fixé comme objectif d’étudier l’interaction entre T. whipplei et les cellules myéloïdes (macrophages et monocytes). Dans un premier temps, nous nous sommes intéressés à une molécule immuno-régulatrice HLA-G impliquée dans les mécanismes de tolérance. Nous avons montré que HLA-G est fortement exprimée et secrétée in-vivo chez les patients atteints de la maladie de Whipple classique. Par ailleurs, nous avons constaté qu’in-vitro l’infection des monocytes par T. whipplei induisait l’expression de HLA-G accompagnée d’une faible sécrétion de TNF. D’autre part, nous avons montré que le blocage de HLA-G restaure la sécrétion de TNF par les monocytes et inversement, le blocage du TNF favorise la réplication de T. whipplei dans les macrophages.Dans un second temps, nous nous sommes intéressés aux évènements précoces de l’interaction entre T. whipplei et les cellules immunitaires dans le but d’identifier un partenaire cellulaire susceptible d’interagir avec T. whipplei. Nous avons pu montrer que la vimentine, une protéine du cytosquelette appartenant aux filaments intermédiaires est impliquée de manière spécifique dans l’adhésion et l’internalisation de T. whipplei. En définitive, ces travaux ont permis d’apporter des éléments de réponse pour mieux comprendre les infections à T. whipplei
Whipple disease is a rare systemic disease caused by the bacterial agent Tropheryma whipplei. T. whipplei presents a particular tropism for macrophages. It induces an atypical macrophage activation program, characterized by the expression of anti-inflammatory molecules, the secretion of IL-16 and the induction of apoptosis. During this thesis, we analyzed the interaction between T. whipplei and myeloid cells (macrophages and monocytes). First, we focused on an immunomodulatory molecule, HLA-G which has previously been associated with immunotolerance mechanisms. We showed that HLA-G is strongly expressed and secreted in vivo in patients with classical Whipple disease. In addition, we found that in vitro, infection of monocytes by T.whipplei induced HLA-G expression accompanied with low TNF secretion. On the other hand, we have shown that a neutralizing antibody against HLA-G increased TNF secretion by monocytes in response to T whipplei, while a TNF inhibitor promoted bacterial replication. Thus, we were able to highlight the involvement of HLA-G in the persistence of T. whipplei within immune cells, then providing a proper environment for its replication.Second, we looked at the early events of T. whipplei interaction with immune cells in order to identify a cell partner who could interact with T. whipplei. We showed that vimentin, a cytoskeletal protein belonging to the intermediate filaments, is specifically involved in the adhesion and internalization of T. whipplei. In conclusion, this work has provided some answers to a better understanding of T. whipplei infections
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Wetzstein, Nils [Verfasser]. "Genotyping and genomotyping of Tropheryma whipplei – the causative agent of Whipple's Disease / Nils Wetzstein." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1148425187/34.

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Bakkali, Nawal. "Mécanismes moléculaires de résistance au sulfaméthoxazole chez Tropheryma whipplei, l'agent de la maladie de Whipple." Aix-Marseille 2, 2009. http://www.theses.fr/2009AIX20718.

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Les bactéries intracellulaires strictes, de par leur localisation, sont difficiles à neutraliser par les antibiotiques. Dans une première partie nous présentons une revue exhaustive des mécanismes moléculaires associés à la résistance aux antibiotiques et des tentatives de manipulation génétique chez les bactéries intracellulaires. Notre travail de recherche s’est intéressé à l’une d’entre elles: Tropheryma whipplei, l’agent de la maladie de Whipple. Durant le traitement de cette maladie, la combinaison sulfaméthoxazole/triméthoprime est administrée. Un travail récent au laboratoire a démontré l’inefficacité in vitro du triméthoprime du fait de l’absence du gène cible folA dans le génome bactérien. Des cas d’échecs thérapeutiques à ce traitement ainsi que des rechutes ont été également rapportés dans la littérature suggérant la possibilité d’acquisition de résistance au sulfaméthoxazole au cours du traitement. Le 1er objectif de notre travail a été d’étudier le mécanisme moléculaire de la résistance au sulfaméthoxazole chez T. Whipplei. La séquence du gène folP codant pour la cible du sulfaméthoxazole : la dihydropteroate synthase (DHPS) a été obtenue à partir d’isolats cliniques de T. Whipplei et également à partir de prélèvements positifs en PCR d’un patient en échec thérapeutique avant et après le début de son traitement. Les séquences obtenues chez ce patient ont mis en évidence plusieurs mutations par rapport aux séquences obtenues à partir des isolats cliniques de T. Whipplei. L’analyse de ce gène a révélé que chez T. Whipplei folP fait partie d’un gène codant pour une enzyme trifonctionnelle dans laquelle DHPS est combinée avec les 2 enzymes qui la précèdent dans la voie classique de biosynthèse des folates. La complémentation d’une souche d’Escherichia coli knock-out pour le gène folP, par la séquence mutée de folP associée à l’échec thérapeutique a non seulement restauré la fonction de DHPS et par conséquent la voie de biosynthèse des folates mais a aussi induit une résistance au sulfaméthoxazole par rapport à la séquence sauvage. Nous avons ainsi démontré pour la première fois que la séquence mutée de ce gène se traduisant par une séquence protéique différente induisait une résistance in vitro au sulfaméthoxazole et pouvait expliquer les échecs et rechutes observés au cours du traitement de cette maladie. La deuxième partie de cette thèse a porté sur l’évaluation de la sensibilité de T. Whipplei in vitro à un autre sulfamide: la sulfadiazine. Au vu des résultats obtenus et des propriétés pharmacologiques de ce composé, nous proposons son utilisation comme traitement de la maladie de Whipple en alternative à la combinaison de sulfaméthoxazole et de triméthoprime dans les formes neurologiques en association avec la doxycycline et l’hydroxychloroquine
Obligate intracellular bacteria, by their intracellular location, are difficult to neutralize by antibiotics. In a first part, we present a review of molecular mechanisms of resistance to antibiotics and attempts at genetic manipulation of intracellular bacteria. Our work has focused on one of them: Tropheryma whipplei, the agent of Whipple's disease. The recommended empirical treatment for this disease involves the simultaneous administration of sulfamethoxazole and trimethoprim (cotrimoxazole). A recent work in our laboratory has demonstrated the ineffectiveness of trimethoprim in vitro because of the absence of its target gene, folA coding for DHFR in the genome of the bacterium. Cases of treatment failures with this treatment and relapses were also reported in the literature suggesting the possibility of acquiring resistance to sulfamethoxazole during treatment. The 1st objective of this thesis was to study the molecular mechanism of antibiotic resistance of T. Whipplei to sulfamethoxazole. The sequence of folP the encoding gene of sulfamethoxazole’s target: the dihydropteroate synthase (DHPS) was obtained from clinical isolates of T. Whipplei and also from positive samples from a patient with treatment failure before and after starting treatment. The sequences obtained from this patient showed several mutations compared to sequences obtained from other strains of T. Whipplei. Gene analysis showed that folP was identified among genes encoding a unique trifunctional enzyme in which DHPS is combined with the 2 preceding enzymes of the folate biosynthesis pathway. Sequencing showed multiple mutations in folP gene in the patient case. Complementation of an Escherichia coli strain knockout for folP with sequence associated with treatment failure has not only restored the folate biosynthesis pathway but also induced resistance to sulfamethoxazole compared with the wild sequence. We also demonstrated for the first time that the mutated sequence of this gene has led to a different protein sequence and induced resistance in vitro to sulfamethoxazole and could explain the failures and relapses observed during the treatment of this disease. The second part of this thesis has focused on assessing the susceptibility of T. Whipplei in vitro to another sulfonamide: the sulfadiazine. Given the results obtained and the pharmacological properties of this compound, we propose its use as an alternative to the cotrimoxazole in combination with doxycycline and hydroxychloroquine in neurological involvement
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Strauchs, Cornelia Katharina Julie [Verfasser], and Jakob [Akademischer Betreuer] Cramer. "Tropheryma whipplei in Africa study (TWAS) Tropheryma whipplei and coinfections in young infants with diarrhoeal disease in Africa / Cornelia Katharina Julie Strauchs ; Betreuer: Jakob Cramer." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2020. http://d-nb.info/1208002740/34.

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Al, Moussawi Khatoun. "Etude cellulaire et physiopathologique de l'interaction hôte - Tropheryma whippleii." Thesis, Aix-Marseille 2, 2011. http://www.theses.fr/2011AIX20674.

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Tropheryma whipplei a longtemps été uniquement considérée comme l’agent responsable de la maladie de Whipple, une affection rare caractérisée notamment par une perte de poids, des diarrhées chroniques et des douleurs abdominales. Toutefois, au cours de ces dernières années, il est apparu que les infections à T. whipplei peuvent présenter des manifestations cliniques communes telles que des pneumonies, des bactériémies fébriles ou des gastroentérites, ce qui montre que la maladie de Whipple ne constitue pas la seule manifestation de l’infection à T. whipplei. Ma thèse a eu deux objectifs. Le premier a été de caractériser l’interaction entre T. whipplei et la cellule dans laquelle elle se réplique, le macrophage. J’ai montré en utilisant diverses techniques (biologie moléculaire à haut débit, biologie cellulaire et biochimie) que T. whipplei induit une réponse macrophagique inédite caractérisée par une polarisation M2 associée à une réponse interféron de type I. J’ai également montré que ces événements sont associés à l’apoptose des macrophages dont l’induction se fait par voie extrinsèque et que l’IL-16, pour laquelle un rôle au cours de l’infection à T. whipplei était avéré, intervient d’une part dans le blocage de la maturation phagosomale et d’autre part interfère avec l’activation des macrophages. Mon second objectif a été de montrer à travers un modèle animal que la primo-infection par T. whipplei se manifeste par une gastroentérite auto-résolutive. Cet objectif découlait directement de travaux récents qui associent T. whipplei à diverses manifestations cliniques et notamment à des épisodes diarrhéiques chez l’enfant. Mes résultats confortent clairement cette hypothèse et montrent également que des dommages préexistants de la muqueuse intestinale permet l’établissement de l’infection à T. whipplei
Tropheryma whipplei has only been considered as the agent of Whipple‘s disease, a rare disease characterized by weight loss, chronic diarrheas and abdominal pains. It is now believed that infections with T. whipplei result in common clinical manifestations, such as pneumonia, fever, bacteriema or gastroenteritis and, as a consequence, it is likely that the Whipple’s disease is not the only manifestation of T. whipplei infection. During my PhD, I had 2 objectives. The first was to characterize the interaction between T. whipplei and the cell type in which T. whipplei replicates, namely macrophages. I showed using diverse techniques (high throughput molecular biology, cell biology and biochemistry) that T. whipplei induced an unusual macrophage response, characterized by M2 polarization with type I interferon response. I also showed that these events were associated with apoptosis of macrophages induced by the extrinsic pathway and that IL-16, which was already described during T. whipplei infection, was involved in the blockade of the phagosomal maturation and interfered with macrophage activation. The second objective was to show using a murine model that primary infection with T. whipplei results in self-limiting gastroenteritis. This objective directly arose from recent work that associated T. whipplei with various clinical manifestations and, in particular, with diarrheal episodes in children. My results clearly verified this hypothesis and also revealed that pre-existing mucosal damage allowed the establishment of the infection
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EUGENE, JEAN. "Maladie de whipple : a propos d'un cas ; nouvelles acquisitions et revue de la litterature." Nice, 1994. http://www.theses.fr/1994NICE6001.

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Fevereiro, Marta Andrade. "Doença de Whipple : um diagnóstico difícil." Master's thesis, Universidade da Beira Interior, 2013. http://hdl.handle.net/10400.6/1413.

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A doença de Whipple é uma doença bacteriana, multissistémica e rara. O agente etiológico é a bactéria Tropheryma whipplei, um bacilo gram-positivo da família das Actinobacterias e do grupo Actinomycetes. Por ser uma doença sistémica, a doença de Whipple tem manifestações clínicas muito variadas com particular envolvimento do intestino delgado, do sistema nervoso central, das articulações e do coração. A forma mais comum de apresentação inicial é na forma de uma doença gastrointestinal manifestando-se como uma síndrome de má absorção com dor abdominal, diarreia e perda ponderal. A obtenção de biópsias do intestino delgado e de outros órgãos acometidos, com base nos sintomas do paciente, constitui a abordagem primária e mais usada de diagnóstico da doença. O tratamento é à base de antibioterapia prolongada, porém o melhor esquema terapêutico ainda não está completamente definido. Para além disso, mesmo quando detetada e adequadamente tratada, a sua evolução clínica tem de ser monitorizada durante a terapêutica, bem como por vários anos após o término desta, de modo a evitar recidivas tardias. Cerca de um século após a sua primeira descrição, a compreensão da doença de Whipple ainda é limitada. No entanto, nos últimos anos foram feitas várias investigações que resultaram em novas pistas na caracterização desta doença e do seu agente etiológico, bem como na abordagem diagnóstica e terapêutica. Apesar da presença ubiquitária do Tropheryma whipplei, a doença de Whipple é muito rara, com fatores genéticos e imunológicos do hospedeiro a poderem influenciar o curso da doença. Dado que as características clínicas da doença de Whipple clássica são muito inespecíficas, o diagnóstico é frequentemente um desafio. Para além disso, pode manifestar-se de forma localizada ou sob a forma de uma infeção aguda auto-limitada, formas que não se enquadram no conceito clássico da doença. Por estas razões, a doença de Whipple nem sempre é diagnosticada, com significativo prejuízo para a sobrevivência dos doentes, sendo na maioria dos casos descritos identificada tardiamente. Como tal, leva à necessidade de um estabelecimento rápido de um diagnóstico e de uma ampla exploração clínica em cada caso. Desta forma, esta tese de mestrado, baseada na revisão bibliográfica de artigos publicados sobre o tema, tem como objetivo analisar características epidemiológicas, clínicas, diagnósticas e terapêuticas em relação à doença de Whipple. Visa também demonstrar a necessidade da doença estar presente no diagnóstico diferencial dos casos suspeitos e incentivar à realização de mais investigação.
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Liang, Zhongxing. "Rôle des anticorps monoclonaux dans la classification et l'identification des bactéries intracellulaires." Aix-Marseille 2, 2001. http://theses.univ-amu.fr.lama.univ-amu.fr/2001AIX20659.pdf.

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Bartonella, Coxiella and Tropheryma are all intracellular pathogens, which can all lead to endocarditis. In this presentation, we generated and characterized 19 genus-specific monoclonal antibodies, 2 to Bartonella, 3 to Coxiella, and 14 to Tropheryma; 8 species-specific monoclonal antibodies, 7 to B. Quinatana and 1 to B. Henselae; 11 subspecies-specific monoclonal antibodies to B. Henselae sub. Henselae sub. Nov. They were successfully used for identification and classification of these bacteria at genus, species and subspecies levels respectively. Immunoflurorescence, SDS-PAGE and western immunoblotting were used to the differentiation of Bartonella species. Sequencing comparison of 16S rDNA, 35 kDa protein gene and Pap 31 kDa protein gene were also used for the description of two subspecies of B. Henselae, B. Henselae sub. Henselae sub. Nov. And B. Henselae sub. Massiliae sub. Nov
Bartonella, Coxiella, et Tropheryma sont toutes des pathogènes intracellulaires responsables d'endocardites. Dans cette présentation, nous avons produit et caractérisé 19 anticorps monoclonaux spécifiques de genre, 2 contre Bartonella, 3 contre Coxiella et 14 contre Tropheryma; 8 anticorps monoclonaux spécifiques d'espèce, 7 contre B. Quintana et 1 contre B. Henselae; 11 anticorps spécifiques de sous espèces contre des sous espèces B. Henselae. Ils ont été utilisés avec succès pour l'identification et la classification de toutes ces bactéries au niveau du genres, espèces et sous-espèces respectivement. L'immunofluorescence, le SDS-P AGE et le western immunoblot ont été utilisés pour la différentiation des espèces de Bartonella. La comparaison du gène de rARN 16S ribosomique, le gène de la protéine de 35 kDa et le gène de la protéine Pap de 31 kDa ont aussi été utilisés pour la description de 2 sous-espèces de B. Henselae subsp. Henselae et B. Henselae subsp. Massiliae
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Books on the topic "Tropheryma whipplei"

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Venkatesan, Arun. Central Nervous System Whipple Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0169.

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Whipple disease (WD) is a multisystemic infection caused by the bacillus Tropheryma whipplei. Although the organism is ubiquitous in the environment, WD is rare. In affected individuals, the organism resides intracellularly within macrophages and can manipulate host immune responses to avoid clearance. Central nervous system (CNS) involvement can occur as a manifestation of classic WD, in the setting of a relapse of previously treated WD, or rarely as isolated nervous system infection. Diagnosis of CNS WD rests on polymerase chain reaction (PCR) and demonstration of periodic acid-Schiff (PAS) positive macrophages in tissue, and ef
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Book chapters on the topic "Tropheryma whipplei"

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Fenollar, F., and D. Raoult. "Tropheryma whipplei." In Principles and Practice of Clinical Bacteriology, 329–40. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/9780470017968.ch26.

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Geißdörfer, Walter, Annette Moter, and Christian Bogdan. "Tropheryma whipplei." In Manual of Clinical Microbiology, 1159–67. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555817381.ch67.

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Schneider, Thomas, and Verena Moos. "Tropheryma whipplei bedingte Erkrankungen." In SpringerReference Innere Medizin, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54676-1_324-1.

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Altwegg, M. "Tropheryma whippelii and the (Re)emergence of an Old Disease." In Contributions to Microbiology, 137–49. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000060408.

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García-Álvarez, Lara, and José Antonio Oteo. "Tropheryma whipplei Endocarditis." In Advanced Concepts in Endocarditis - 2021. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95378.

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Tropheryma whipplei mainly known as the causative agent of classical Whipple’s disease, also produces acute, sub-acute and chronic localized forms of infection such as endocarditis. The development of molecular tools has allowed increasing the number of cases of endocarditis due to blood culture use to be negative in T. whipplei endocarditis and most of the cases are confirmed post-surgery when molecular analyses of heart valves are performed. Although, T. whipplei endocarditis is an uncommon condition with an atypical presentation it must be considered in the diagnosis of blood culture negative endocarditis and in patients with heart failure in which valve affectation is present. Other clinical features such as long lasting arthralgia can be present in a high percentage of the patients. It is important to know that few cases are diagnosed in the context of the classical Whipple’s disease. The prognosis is very good when an appropriate surgical management and antimicrobial-specific treatment is given. This chapter describes the epidemiological, clinical characteristics, diagnosis and treatments for T. whipplei endocarditis.
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Liu, Dongyou, and Frank W. Austin. "Tropheryma whipplei." In Molecular Medical Microbiology, 1259–66. Elsevier, 2015. http://dx.doi.org/10.1016/b978-0-12-397169-2.00069-x.

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"Tropheryma whipplei." In Color Atlas of Medical Bacteriology, 297–98. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2020. http://dx.doi.org/10.1128/9781683671077.ch37.

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"Tropheryma whipplei." In Encyclopedia of Medical Genomics and Proteomics, 1292–96. CRC Press, 2004. http://dx.doi.org/10.1081/e-emgp-120020921.

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Mahnel, R., T. Marth, F. Fenollar, and D. Raoult. "Tropheryma whipplei." In Encyclopedia of Medical Genomics and Proteomics, 1292–96. Informa Healthcare, 2004. http://dx.doi.org/10.3109/9780203997352.257.

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Hodgson, H. J. F. "Whipple’s disease." In Oxford Textbook of Medicine, 2352–53. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.151006_update_001.

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Whipple’s disease is an uncommon infection caused by the actinomycete Tropheryma whipplei. It is most commonly diagnosed when overt small-intestinal disease leads to malabsorption, but before this there are often several years of nonspecific prodromal manifestations such as fever and arthralgia/arthritis, and the disease can present in many other ways, e.g neurological manifestations (of many forms, including movement disorders, ocular manifestations and meningitis) or endocarditis....
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Conference papers on the topic "Tropheryma whipplei"

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Dulic-Lakovic, Emina, Marianne Hubner, Christian Johannes Muller, Wolfgang Pokieser, Melisa Dulic, Sabine Publig, Meinhard Kneussl, and Michael Gschwantler. "Is The Bacterium Tropheryma Whipplei Cause Of The Disease In A Subgroup Of Patients With Presumed Sarcoidosis?" In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3019.

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DAS, SABYASACHI, SANDIP PAUL, and CHITRA DUTTA. "TRENDS IN CODON AND AMINO ACID USAGE IN HUMAN PATHOGEN TROPHERYMA WHIPPLEI, THE ONLY KNOWN ACTINOBACTERIA WITH REDUCED GENOME." In 4th Asia-Pacific Bioinformatics Conference. PUBLISHED BY IMPERIAL COLLEGE PRESS AND DISTRIBUTED BY WORLD SCIENTIFIC PUBLISHING CO., 2005. http://dx.doi.org/10.1142/9781860947292_0017.

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