Browsing by Author "Oliveira, Luciana Souza de"

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    First report of Ehrlichia ewingii detected by molecular investigation in dogs from Brazil.
    (2009) Oliveira, Luciana Souza de; Oliveira, Karla Andrade de; Pescatore, A. M.; Lamëgo, Márcia Rogéria de Almeida; Conceição, Lissandro Gonçalves; Galvão, Márcio Antônio Moreira; Siqueira, Cláudio Lísias Mafra de
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    Molecular identification of Rickettsia felis in ticks and fleas from an endemic area for Brazilian Spotted Fever.
    (2008) Oliveira, Karla Andrade de; Oliveira, Luciana Souza de; Dias, C. C. A.; Silva Júnior, Abelardo; Lamëgo, Márcia Rogéria de Almeida; Amalda, G.; Bouyer, Donald H.; Galvão, Márcio Antônio Moreira; Siqueira, Cláudio Lísias Mafra de
    Rickettsioses are arthropod-borne diseases caused by parasites from the Order Rickettsiales. The most prevalent rickettsial disease in Brazil is Brazilian Spotted Fever (BSF). This work intends the molecular detection of those agents in ectoparasites from an endemic area of BSF in the state of Espírito Santo. A total of 502 ectoparasites, among them Amblyomma cajennense, Amblyomma dubitatum (A. cooperi), Riphicephalus sanguineus, Anocentor nitens and Ctenocephalides felis, was collected from domestic animals and the environment and separated in 152 lots according to the origin. Rickettsia sp. was detected in pools of all collected species by amplification of 17kDa pro¬tein-encoding gene fragments. The products of PCR amplification of three samples were sequenced, and Rickettsia felis was identified in R. sanguineus and C. felis. These results confirm the presence of Rickettsia felis in areas previ¬ously known as endemic for BSF, disease caused by Rickettsia rickettsii. Moreover, they show the needing of further studies for deeper knowledge of R. felis-spotted fever epidemiology and differentiation of these diseases in Brazil.
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    Neuronal parasitism, early myenteric neurons depopulation and continuous axonal networking damage as underlying mechanisms of the experimental intestinal Chagas' disease.
    (2020) Ricci, Mayra Fernanda; Béla, Samantha Ribeiro; Moraes, Michele Macedo; Bahia, Maria Terezinha; Mazzeti, Ana Lia; Oliveira, Anny Carolline Silva; Oliveira, Luciana Souza de; Radi, Rafael; Piacenza, Lucía; Arantes, Rosa Maria Esteves
    There is a growing consensus that the balance between the persistence of infection and the host immune response is crucial for chronification of Chagas heart disease. Extrapolation for chagasic megacolon is hampered because research in humans and animal models that reproduce intestinal pathology is lacking. The parasite-host relationship and its consequence to the disease are not well-known. Our model describes the temporal changes in the mice intestine wall throughout the infection, parasitism, and the development of megacolon. It also presents the consequence of the infection of primary myenteric neurons in culture with Trypanosoma cruzi (T. cruzi). Oxidative neuronal damage, involving reactive nitrogen species induced by parasite infection and cytokine production, results in the denervation of the myenteric ganglia in the acute phase. The long-term inflammation induced by the parasite’s DNA causes intramuscular axonal damage, smooth muscle hypertrophy, and inconsistent innervation, affecting contractility. Acute phase neuronal loss may be irreversible. However, the dynamics of the damages revealed herein indicate that neuroprotection interventions in acute and chronic phases may help to eradicate the parasite and control the inflammatory-induced increase of the intestinal wall thickness and axonal loss. Our model is a powerful approach to integrate the acute and chronic events triggered by T. cruzi, leading to megacolon.