Resultado da pesquisa (6)

Termo utilizado na pesquisa Patogênese

#1 - Pathogenesis of Bovine alphaherpesvirus 2 in calves following different routes of inoculation

Abstract in English:

Bovine alphaherpesvirus 2 (BoHV-2) is the agent of herpetic mammilitis (BHM), a cutaneous and self-limiting disease affecting the udder and teats of cows. The pathogenesis of BoHV-2 is pourly understood, hampering the development of therapeutic drugs, vaccines and other control measures. This study investigated the pathogenesis of BoHV-2 in calves after inoculation through different routes. Three- to four-months seronegative calves were inoculated with BoHV-2 (107TCID50.mL-1) intramuscular (IM, n=4), intravenous (IV, n=4) or transdermal (TD) after mild scarification (n=4) and submitted to virological, clinical and serological monitoring. Calves inoculated by the IV route presented as light increase in body temperature between days 6 to 9 post-inoculation (pi). Virus inoculation by the TD route resulted in mild inflammatory lesions at the sites of inoculation, characterized by hyperemia, small vesicles, mild exudation and scab formation, between days 2 and 8pi. Virus or viral DNA was detected by PCR in the crusts/swabs collected from lesions of 3 out of 4 animals inoculated TD from day 2 to 8pi. Viremia was detected in 3/4 animals of the IM group (from day 4 to 8pi); in 2/4 animals of the IV group (days 6 and 8pi) but not in the TD group. Calves from all inoculated groups seroconverted to BoHV-2 in titers from 4 to 64, as indicated by virus-neutralizing (VN) assays performed in sera collected at day 15pi. Administration of dexamethasone (Dex) to the inoculated calves at day 48pi, did not result in virus reactivation as indicated by lack of virus detection in the blood and/or in inoculation sites and no increase in VN antibody titers. These results demonstrated that BoHV-2 was able to replicate efficiently in calves following different routes of exposure, produced viremia after IM and IV inoculation and was not reactivated by Dex treatment.

Abstract in Portuguese:

O alfaherpesvírus bovino 2 (BoHV-2) é um agente etiológico da mamilite herpética (BHM), uma doença cutânea e autolimitante do úbere e tetos de vacas. Pouco se sabe sobre a patogênese do BoHV-2, dificultando o desenvolvimento de medicamentos terapêuticos e vacinas. Este estudo investigou a patogênese do BoHV-2 em bezerros após a inoculação por diferentes vias. Bezerros soronegativos de três a quatro meses foram inoculados com BoHV-2 (107TCID50.mL-1) por via intramuscular (IM, n=4), por via intravenosa (IV, n=4) ou transdérmica (TD, n=4) após escarificação leve e submetidos a monitoramento virológico, clínico e sorológico. Os bezerros inoculados pela via IV apresentaram aumento leve da temperatura corporal entre os dias 6 a 9 pós-inoculação (pi). A inoculação do vírus pela via TD resultou em lesões inflamatórias leves nos locais de inoculação, caracterizadas por hiperemia, pequenas vesículas, exsudação leve e formação de crostas, entre os dias 2 e 8pi. O vírus ou DNA viral foi detectado por PCR nas crostas/swabs coletados de lesões de 3 de 4 animais inoculados TD do dia 2 ao 8pi. Viremia foi detectada em 3/4 dos animais do grupo IM (do dia 4 ao 8pi); em 2/4 animais do grupo IV (dias 6 e 8pi), mas não no grupo TD. Bezerros de todos os grupos inoculados soroconverteram o BoHV-2 em títulos de 4 a 64, conforme indicado por ensaios de vírus-neutralização (VN) realizados em soro coletado no dia 15pi. Administração de dexametasona (Dex) nos bezerros inoculados no dia 48pi, não resultou em reativação do vírus, como indicado pela falta de detecção de vírus no sangue e/ou nos locais de inoculação e pela ausência de aumento nos títulos de anticorpos. Estes resultados demonstraram que o BoHV-2 foi capaz de replicar eficientemente em bezerros seguindo diferentes vias de inoculação, produziu viremia após a inoculação IM e IV e não foi reativado pelo tratamento com Dex.


#2 - Pathogenesis, clinical, hematological, and pathological aspects of Rangelia vitalii infection in 35 dogs (1985-2009), 30(11):974-987

Abstract in English:

ABSTRACT.- Fighera R.A., Souza T.M., Kommers G., Irigoyen L.F. & Barros C.S.L. 2010. [Pathogenesis, clinical, hematological, and pathological aspects of Rangelia vitalii infection in 35 dogs (1985-2009).] Patogênese e achados clínicos, hematológicos e anatomopatológicos da infecção por Rangelia vitalii em 35 cães (1985-2009). Pesquisa Veterinária Brasileira 30(11):974-987. Departamento de Patologia, Universidade Federal de Santa Maria, Campus Universitário, Avenida Roraima 1000, Santa Maria, RS 97105-900, Brazil. E-mail: anemiaveterinaria@yahoo.com.br The pathogenesis, clinical, hematological and pathological features of the natural infection by the protozoan organism Rangelia vitalii (canine rangeliosis) was studied in 35 dogs that died due this condition. The results allow for the following set of conclusions on canine rangeliosis: (1) causes an exclusively extravascular immune mediated hemolysis; (2) is invariably associated with some degree of hemorrhage observed at necropsy, but no always clinically apparent; (3) the clinical signs that are the hallmark of the disease are anemia, icterus and splenomegaly; (4) the main hematological aspect that establishes a clinical suspect is the development of anemia with signs of intense erythroid regeneration; (5) the three main differential diagnosis are leptospirosis, babesiosis and e acute monocytotropic ehrlichiosis; (6) the main observed histopathological lesion is an association of lymphoid hyperplasia with mononuclear inflammatory reaction, predominantly plasmacytic, but occasionally granulomatous; (7) other frequently found lesions are secondary to a marked regenerative anemia; (8) large numbers of the etiologic agent can be easily demonstrate in most tissues, mainly in lymph nodes, spleen, bone marrow, heart, and tonsils.

Abstract in Portuguese:

RESUMO.- Fighera R.A., Souza T.M., Kommers G., Irigoyen L.F. & Barros C.S.L. 2010. [Pathogenesis, clinical, hematological, and pathological aspects of Rangelia vitalii infection in 35 dogs (1985-2009).] Patogênese e achados clínicos, hematológicos e anatomopatológicos da infecção por Rangelia vitalii em 35 cães (1985-2009). Pesquisa Veterinária Brasileira 30(11):974-987. Departamento de Patologia, Universidade Federal de Santa Maria, Campus Universitário, Avenida Roraima 1000, Santa Maria, RS 97105-900, Brazil. E-mail: anemiaveterinaria@yahoo.com.br A patogênese e os achados clínicos, hematológicos e anatomopatológicos da infecção natural pelo protozoário Rangelia vitalii (rangeliose canina) foram estudados em 35 cães que morreram em consequência dessa condição. Os resultados obtidos permitem o seguinte conjunto de conclusões: (1) causa doença hemolítica exclusivamente extravascular e de origem imunomediada; (2) cursa invariavelmente com algum grau de hemorragia à necropsia, mas nem sempre clinicamente perceptível; (3) os principais sinais que devem chamar a atenção para a suspeita clínica são anemia, icterícia e esplenomegalia; (4) o principal achado hematológico e que deve chamar a atenção para a suspeita clínica é a ocorrência de anemia com sinais de intensa regeneração eritroide; (5) os três principais diagnósticos diferenciais são leptospirose, babesiose e erliquiose monocitotrópica aguda; (6) a principal lesão observada é uma associação de hiperplasia linfoide com inflamação mononuclear, predominantemente plasmocitária, mas por vezes granulomatosa; (7) outras lesões frequentes são secundárias à marcada anemia regenerativa; (8) o agente etiológico pode ser facilmente encontrado, pois ocorre em grande quantidade na maioria dos tecidos, principalmente nos linfonodos, no baço, na medula óssea, no coração e nas tonsilas.


#3 - Patogênese das lesões associadas à intoxicação por Ramaria flavo-brunnescens em bovinos, p.533-544

Abstract in English:

ABSTRACT.- Trost M.E., Kommers G.D., Barros C.S.L & Schild A.L. 2009. [Patogenesis of lesions associated with poisoning by Ramaria flavo-brunnescens in cattle.] Patogênese das lesões associadas à intoxicação por Ramaria flavo-brunnescens em bovinos. Pesquisa Veterinária Brasileira 29(7):533-544. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: glaukommers@yahoo.com The pathogenesis of the lesions of Ramaria flavo-brunnescens poisoning in cattle was studied throughout the retrospective evaluation of selected tissues from nine spontaneous and four experimental cases of the disease. The pathogenesis of lesions observed in the tongue, esophagus, hoof, and tail was investigated analyzing microscopic lesions, histochemical and histochemical-ultrastructural changes. Histochemical techniques utilized were Masson’s Trichrome and Selective Oxidation of Keratin (SOK). The histochemical-ultrastructural study was acomplished throughout the Swift method under transmission electron microscopy. Hair shafts of the tip of the tail were analyzed under polarized light. Lesions of varying degrees of severity were observed. All changes observed in the keratinized structures studied, mostly in the hard keratin, showed defective keratinization. The morphologic study and the results obtained with SOK and Swift techniques showed that the defective keratinization results of low amounts of sulphur containing amino acids (cystine) in hard keratin structures. This is probably the main pathogenetic mechanism of the lesions observed in R. flavo brunnescens poisoning in cattle.

Abstract in Portuguese:

ABSTRACT.- Trost M.E., Kommers G.D., Barros C.S.L & Schild A.L. 2009. [Patogenesis of lesions associated with poisoning by Ramaria flavo-brunnescens in cattle.] Patogênese das lesões associadas à intoxicação por Ramaria flavo-brunnescens em bovinos. Pesquisa Veterinária Brasileira 29(7):533-544. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: glaukommers@yahoo.com The pathogenesis of the lesions of Ramaria flavo-brunnescens poisoning in cattle was studied throughout the retrospective evaluation of selected tissues from nine spontaneous and four experimental cases of the disease. The pathogenesis of lesions observed in the tongue, esophagus, hoof, and tail was investigated analyzing microscopic lesions, histochemical and histochemical-ultrastructural changes. Histochemical techniques utilized were Masson’s Trichrome and Selective Oxidation of Keratin (SOK). The histochemical-ultrastructural study was acomplished throughout the Swift method under transmission electron microscopy. Hair shafts of the tip of the tail were analyzed under polarized light. Lesions of varying degrees of severity were observed. All changes observed in the keratinized structures studied, mostly in the hard keratin, showed defective keratinization. The morphologic study and the results obtained with SOK and Swift techniques showed that the defective keratinization results of low amounts of sulphur containing amino acids (cystine) in hard keratin structures. This is probably the main pathogenetic mechanism of the lesions observed in R. flavo brunnescens poisoning in cattle.


#4 - Neuropatogênese experimental da infecção pelo herpesvírus bovino tipo 5 em coelhos, p.1-16

Abstract in English:

ABSTRACT.- Flores E.F., Weiblen R, Vogel F.S.F., Dezengrini R., Almeida S.R., Spilki F.R. & Roehe P.M. 2009. [Experimental neuropathogenesis of bovine herpesvirus 5 infection in rabbits.] Neuropatogênese experimental da infecção pelo herpesvírus bovino tipo 5 em coelhos. Pesquisa Veterinária Brasileira 29(1):1-16. Departamento de Medicina Veterinária Preventiva. Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS. Brazil. E-mail: eduardofurtadoflores@gmail.com Several aspects of the biology of bovine herpesvirus 5 (BoHV-5) have been studied in rabbits, which develop acute infection and neurological disease upon experimental inoculation. The acute infection is followed by the establishment of latent infection, which can be naturally or artificially reactivated. The first experiments in rabbits established a protocol for virus inoculation and monitoring the infection, and characterized the main virological, clinical and pathological aspects of the acute infection. The pathogenesis of acute infection, from the initial viral replication at site of inoculation, pathways and kinetics of viral transport to the brain, distribution and virus replication in the central nervous system (CNS), cellular and tissue tropism, clinical signs and CNS pathology have been extensively studied using this animal model. Subsequently, several biological and molecular aspects of latent BoHV-5 infection have also been elucidated upon inoculation of rabbits. Rabbits have also been used to investigate the phenotype (neuroinvasiveness, neurogrowth) of field isolates and recombinant vaccine candidates, protection by passive immunity, vaccine protection, the efficacy of anti-viral drugs and support therapies for neurological disease. This animal model was also used to investigate the origin and distribution of electric impulses involved in seizures - a hallmark of BoHV-5 induced neurological infection - and also to test the efficacy of anti-convulsivants. In spite of the possible differences between rabbits and cattle - the natural host of the virus - the observations taken from this experimental model have greatly contributed to the knowledge of the biology of BoHV-5 infection. The present article presents a review of the main published and unpublished results and observations by our group, comprising more than a decade of studies on the pathogenesis of BoHV-5 infection in the rabbit model.

Abstract in Portuguese:

ABSTRACT.- Flores E.F., Weiblen R, Vogel F.S.F., Dezengrini R., Almeida S.R., Spilki F.R. & Roehe P.M. 2009. [Experimental neuropathogenesis of bovine herpesvirus 5 infection in rabbits.] Neuropatogênese experimental da infecção pelo herpesvírus bovino tipo 5 em coelhos. Pesquisa Veterinária Brasileira 29(1):1-16. Departamento de Medicina Veterinária Preventiva. Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS. Brazil. E-mail: eduardofurtadoflores@gmail.com Several aspects of the biology of bovine herpesvirus 5 (BoHV-5) have been studied in rabbits, which develop acute infection and neurological disease upon experimental inoculation. The acute infection is followed by the establishment of latent infection, which can be naturally or artificially reactivated. The first experiments in rabbits established a protocol for virus inoculation and monitoring the infection, and characterized the main virological, clinical and pathological aspects of the acute infection. The pathogenesis of acute infection, from the initial viral replication at site of inoculation, pathways and kinetics of viral transport to the brain, distribution and virus replication in the central nervous system (CNS), cellular and tissue tropism, clinical signs and CNS pathology have been extensively studied using this animal model. Subsequently, several biological and molecular aspects of latent BoHV-5 infection have also been elucidated upon inoculation of rabbits. Rabbits have also been used to investigate the phenotype (neuroinvasiveness, neurogrowth) of field isolates and recombinant vaccine candidates, protection by passive immunity, vaccine protection, the efficacy of anti-viral drugs and support therapies for neurological disease. This animal model was also used to investigate the origin and distribution of electric impulses involved in seizures - a hallmark of BoHV-5 induced neurological infection - and also to test the efficacy of anti-convulsivants. In spite of the possible differences between rabbits and cattle - the natural host of the virus - the observations taken from this experimental model have greatly contributed to the knowledge of the biology of BoHV-5 infection. The present article presents a review of the main published and unpublished results and observations by our group, comprising more than a decade of studies on the pathogenesis of BoHV-5 infection in the rabbit model.


#5 - Patogênese, sinais clínicos e patologia das doenças causadas por plantas hepatotóxicas em ruminantes e eqüinos no Brasil, p.1-14

Abstract in English:

ABSTRACT.- Santos J.C.A., Riet-Correa F., Simões S.V.D. & Barros C.S.L. 2008. [Pathogenesis, clinical signs and pathology of diseases caused by hepatotoxic plants in ruminants and horses in Brazil.] Patogênese, sinais clínicos e patologia das doenças causadas por plantas hepatotóxicas em ruminantes e eqüinos no Brasil. Pesquisa Veterinária Brasileira 28(1):1-14. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: franklin.riet@pq.cnpq.br Plants causing hepatic lesions in ruminants and horses constitute one important group of poisonous plants in Brazil. These plants can be placed in three major groups: plants causing acute liver necrosis; plants causing liver fibrosis; and plants causing hepatogenous photosensitization. For some of these plants the toxic principles are known. Cestrum parqui and Xanthium cavanillesi that cause acute liver necrosis contain carboxy-atractylosides. Senecio spp., Crotalaria spp., and Echium plantagineum that cause liver fibrosis contain pyrrolizidine alkaloids. As for the group of plants causing hepatogenous photosensibilization, Myoporum spp. contain furanosesquiterpenes, Lantana spp contain triterpenes, and Brachiaria spp. and Panicum spp. contain steroidal saponins. The clinical and pathologic features of the toxicosis caused by these phytotoxins, general mechanisms of production for the production of the clinical signs and the methods for diagnosis of hepatic failure in farm animals are reviewed.

Abstract in Portuguese:

ABSTRACT.- Santos J.C.A., Riet-Correa F., Simões S.V.D. & Barros C.S.L. 2008. [Pathogenesis, clinical signs and pathology of diseases caused by hepatotoxic plants in ruminants and horses in Brazil.] Patogênese, sinais clínicos e patologia das doenças causadas por plantas hepatotóxicas em ruminantes e eqüinos no Brasil. Pesquisa Veterinária Brasileira 28(1):1-14. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: franklin.riet@pq.cnpq.br Plants causing hepatic lesions in ruminants and horses constitute one important group of poisonous plants in Brazil. These plants can be placed in three major groups: plants causing acute liver necrosis; plants causing liver fibrosis; and plants causing hepatogenous photosensitization. For some of these plants the toxic principles are known. Cestrum parqui and Xanthium cavanillesi that cause acute liver necrosis contain carboxy-atractylosides. Senecio spp., Crotalaria spp., and Echium plantagineum that cause liver fibrosis contain pyrrolizidine alkaloids. As for the group of plants causing hepatogenous photosensibilization, Myoporum spp. contain furanosesquiterpenes, Lantana spp contain triterpenes, and Brachiaria spp. and Panicum spp. contain steroidal saponins. The clinical and pathologic features of the toxicosis caused by these phytotoxins, general mechanisms of production for the production of the clinical signs and the methods for diagnosis of hepatic failure in farm animals are reviewed.


#6 - ARE ALVEOLAR BONE CHANGES A DETERMINANT FACTOR FOR "CARA INCHADA" IN CATTLE ?

Abstract in English:

In order to study possible alterations of the skeleton which might play a role in the pathogenesis of the periodontitis of "cara inchada" in young cattle, ribs from 20 affected calves, 2 to 10 months old, were examined. Electrolytically decalcified longitudinal sections of the costochondral junction and cross sections through the corpus costae, stained with Haematoxylin-Eosin, were studied. In five calves, longitudinal sections of the proximal humerus were examined as well. The status of mineralization was checked by microradiograms. Systemic alteration of the skeleton due to disturbances of mineral metabolism could not be shown in any of the animals. In seven 2 to 4 months old calves, no bone changes were found. The reduced osteogenesis in six 3 to 5 months old calves and the reduced osteogenesis and diminished chondral growth in seven 5 to 10 months old calves are therefore a consequence of the disease. The results show that the development of the alveolar bone was not defective, so this cannot be a determinant factor for the development of the periodontitis of "cara inchada" in cattle.

Abstract in Portuguese:

Para verificar possíveis alterações do esqueleto, que poderiam ter papel importante na patogênese da periodontite da "cara inchada" em bovinos jovens, costelas de 20 bezerros com 2 a 10 meses de idade e afetados pela doença foram estudadas. Examinaram-se cortes longitudinais eletroliticamante descalcificados das junções cartilaginosas e cortes transversais do corpus costae, corados pela hematoxilina-eosina. Em cinco bezerros examinaram-se também cortes longitudinais do úmero proximal. O estado de mineralização óssea foi avaliado através de microrradiogramas. Em nenhum dos animais alterações do esqueleto por distúrbios do metabolismo mineral podiam ser demonstradas. Nos bezerros com 2 a 4 meses de idade nenhuma alteração patológica do esqueleto foi encontrada. Por isso, a osteogênese reduzida observada nos bezerros com 3 a 5 meses de idade, bem como a osteogênese e o crescimento cartilaginoso reduzidos nos bezerros de 5 a 10 meses de idade, devem ser interpretados como consequências da doença. Os resultados desse estudo demonstram que não existe um desenvolvimento deficiente do osso alveolar como fator predisponente para o desenvolvimento da periodontite da "cara inchada" nos bovinos.


Colégio Brasileiro de Patologia Animal SciELO Brasil CAPES CNPQ UNB UFRRJ CFMV