Abstract in English:
ABSTRACT.- Peixoto P.V., Nogueira V.A., Gonzaléz A.P., Tokarnia C.H. & França T.N. 2009. Accidental and experimental salinomycin poisoning in rabbits. Pesquisa Veterinária Brasileira 29(9):695-699. Projeto Sanidade Animal Embrapa/UFRRJ, Seropédica, RJ 23890-000, Brazil. E-mail: pfpeixoto@terra.com.br
An outbreak of salinomycin poisoning in rabbits is described. At least 27 out of 2,000 rabbits reared on a farm died after the coccidiostatic drug sulfaquinoxaline was substituted by salinomycin in the feed. An average of 26.9ppm salinomycin was detected in the ration given to the rabbits. Clinical signs included anorexia, apathy and bradykinesia, which progressed to incoordination and recumbency. Gross lesions consisted of pale areas in the skeletal muscles. The histopathological findings showed severe necrotic degenerative myopathy in association with infiltration of neutrophils and macrophages. One rabbit exhibited similar alterations in the myocardium. Mineralization was observed in the affected skeletal muscles in some cases. In order to verify if the poisoning was due to salinomycin, 20 rabbits were divided into five groups and a ration containing the drug at doses of 10, 25, 50, 75 and 100ppm was given. The administration of doses higher than 50ppm resulted in manifestation of the clinical signs seen in the outbreak of poisoning. It was concluded, that probably an error related to the mixture of salinomycin in the feed was the cause of deaths in the spontaneous outbreak of poisoning on the rabbit farm.
Abstract in Portuguese:
RESUMO.- Peixoto P.V., Nogueira V.A., Gonzaléz A.P., Tokarnia C.H. & França T.N. 2009. Accidental and experimental salinomycin poisoning in rabbits. [Intoxicações natural e experimental por salinomicina em coelhos.] Pesquisa Veterinária Brasileira 29(9):695-699. Projeto Sanidade Animal Embrapa/UFRRJ, Seropédica, RJ 23890-000, Brazil. E-mail: pfpeixoto@terra.com.br
Relata-se, pela primeira vez, um surto de intoxicação por salinomicina em coelhos. De 2000 animais, no mínimo 27 morreram após troca do coccidiostático sulfaquinoxalina pela salinomicina. A análise de parte da ração detectou 26,9ppm de salinomicina. Os sinais clínicos observados foram anorexia, apatia e lentidão com evolução para incoordenação dos movimentos e decúbito. As lesões macroscópicas consistiram de áreas pálidas na musculatura esquelética. O exame histopatológico evidenciou miopatia degenerativo-necrótica. Adicionalmente, verificou-se reação inflamatória constituída por neutrófilos e macrófagos. Um coelho apresentou lesões similares no miocárdio. Em alguns casos, mineralização estava presente nos músculos esqueléticos afetados. Vinte coelhos experimentais foram divididos em 5 grupos que receberam 10, 25, 50, 75 e 100ppm de salinomicina por via oral, com a finalidade de reproduzir a intoxicação. Os animais que receberam a partir de 50ppm de salinomicina apresentaram sinais clínicos semelhantes aos observados no surto espontâneo. Nossos resultados indicam que, provavelmente, erro na mistura da substância à ração causou a morte dos coelhos.
Abstract in English:
ABSTRACT.- Macêdo J.T.S.A., Lucena R.B., Tochetto C., Oliveira Filho J.C., Pierezan F., Irigoyen L.F. & Barros C.S.L. 2009. [Primary congenital lymphedema in Red Angus cattle.] Linfedema primário congênito em bovinos Red Angus. Pesquisa Veterinária Brasileira 29(9):713-718. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br
Cases of congenital lymphedema were observed affecting 12 cross Red Angus calves from the central region of the state of Rio Grande do Sul, Brazil. Affected calves presented variable degrees of subcutaneous edema at birth, involving mainly the hind limbs but also other body regions. The injection of methylene blue dye in 5% solution into the interdigital space of the hind limbs of three affected calves and one normal control indicated an interruption of the lymph flow in the affected calves; this suggests a failure of the distal peripheral lymphatics to connect with the central trunks. At necropsy of three affected calves subcutaneous edema was variably observed in the hind limbs, prepuce and ventral abdomen. Edema of body cavities was not observed. In two cases there was hipoplasia of the popliteal lymph nodes associated to dilatation of lymphatic vessels. DNA tests demonstrated that all affected calves were born from cows sired by the same bull suggesting an inherited basis for the disease. Considering the small percentage of affected calves born from cows sired by the suspect bull it is probable that an autosomal recessive mode of inheritance is involved.
Abstract in Portuguese:
RESUMO.- Macêdo J.T.S.A., Lucena R.B., Tochetto C., Oliveira Filho J.C., Pierezan F., Irigoyen L.F. & Barros C.S.L. 2009. [Primary congenital lymphedema in Red Angus cattle.] Linfedema primário congênito em bovinos Red Angus. Pesquisa Veterinária Brasileira 29(9):713-718. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br
Casos de linfedema congênito foram observados acometendo 12 terneiros cruza Red Angus na região Central do Rio Grande do Sul. Os terneiros afetados apresentavam graus variáveis de edema subcutâneo ao nascimento, envolvendo principalmente os membros pélvicos, mas também outras regiões do corpo. A injeção de solução a 5% de azul de metileno no espaço interdigital dos membros pélvicos de três terneiros afetados e um controle, indicaram uma interrupção no fluxo da linfa, sugerindo uma falha dos linfáticos periféricos distais em contactar os troncos centrais. Na necropsia de três terneiros afetados, edema subcutâneo foi observado de modo variável nos membros pélvicos, prepúcio e abdômen ventral. Não foi observado edema nas cavidades orgânicas. Em dois casos, observou-se hipoplasia dos linfonodos poplíteos associadas à dilatação dos vasos linfáticos. Testes de DNA demonstraram que todos os terneiros afetados nasceram de vacas inseminadas pelo mesmo touro, sugerindo uma base genética para a doença. Levando em consideração que uma pequena porcentagem de terneiros nasceram de vacas inseminadas pelo touro suspeito, é provável que um modo autossômico recessivo esteja envolvido na hereditariedade da doença.
Abstract in English:
ABSTRACT.- Sant’Ana F.J.F., Nogueira A.P.A., Souza R.I.C., Cardinal S.G., Lemos R.A.A. & Barros C.S.L. 2009. [Experimentally amprolium-induced polioencephalomalacia in sheep.] Polioencefalomalacia experimental induzida por amprólio em ovinos. Pesquisa Veterinária Brasileira 29(9):747-752. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br
In order to establish an experimental model for the study of the etiology, pathology, and pathogenesis of polioencephalomalacia in ruminants, the condition was induced in five sheep by oral administration of amprolium at daily doses of 500 and 1,000mg per kg of body weight respectively for 28-59 days and for 13-39 days. All sheep died or were euthanized in extremis after illness of 3-7 days. Clinical signs included depression, incoordination, midriasis, grinding of the teeth, blindness, and laying down with opisthotonus and paddling movements. Drooling and a sawhorse stance were observed in one sheep and myoclonus in another one. Main gross lesions were restricted to the central nervous system and included swelling of the brain with flattening of telencephalic gyri, and hemorrhages in the parietal and occipital lobes of the telencephalon, in the submeningeal areas of the spinal cord and in the mesencephalon. Histologically, there was segmental laminar neuronal necrosis (red neurons) associated with edema, swelling of endothelial cells, hemorrhages and infiltration by foamy macrophages (gitter cells). These changes were more marked in the frontal, parietal and occipital telecephalic lobes and there was sharp demarcation between the lesions and the adjacent normal neuropile. Additionally, similar, but less marked lesions were seen in the mesencephalon, thalamus and hippocampus. Considering the consistent reproducible aspects of polioencephalomalacia in sheep using amprolium, this may be an useful model for the study of the disease.
Abstract in Portuguese:
RESUMO.- Sant’Ana F.J.F., Nogueira A.P.A., Souza R.I.C., Cardinal S.G., Lemos R.A.A. & Barros C.S.L. 2009. [Experimentally amprolium-induced polioencephalomalacia in sheep.] Polioencefalomalacia experimental induzida por amprólio em ovinos. Pesquisa Veterinária Brasileira 29(9):747-752. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br
Para estabelecer um modelo experimental para o estudo da etiologia, patologia e patogênese da polioencefalomalacia em ruminantes, a condição foi induzida em cinco ovinos pela administração oral de amprólio nas doses diárias de 500 e 1.000mg/kg de peso animal, respectivamente por 28-59 dias e 13-39 dias. Todos os ovinos morreram ou foram eutanasiados in extremis após um curso clínico de 3-7 dias. Os sinais clínicos incluíam depressão, incoordenação, midríase, bruxismo, cegueira e decúbito com opistótono e movimentos de pedalagem. Salivação excessiva e posição de cavalete foi observada em um ovino e mioclonias em um outro. Os principais achados de necropsia restringiam-se ao sistema nervoso central e incluíam tumefação do encéfalo com achatamento dos giros telencefálicos e hemorragias nos lobos parietal e occipital do telencéfalo; as hemorragias ocorriam também nas áreas submeníngeas da medula espinhal e do mesencéfalo. Histologicamente, havia necrose segmentar laminar de neurônios (neurônios vermelhos) associada a edema, tumefação de células endoteliais, hemorragias e infiltração por macrófagos espumosos (células gitter). Essas alterações eram mais marcadas nos lobos frontal, parietal e occipital do telencéfalo e havia uma demarcação abrupta entre as lesões e o neurópilo normal adjacente. Adicionalmente, lesões semelhantes, mas menos acentuadas, eram observadas no mesencéfalo, tálamo e hipocampo. Levando em consideração a reproducibilidade regular dos aspectos da polioencefalomalacia em ovinos pela administração de amprólio, esse modelo pode ser útil para o estudo da doença.
Abstract in English:
ABSTRACT.- Anjos B.L., Irigoyen L.F., Piazer J.V.M., Brum J.S., Fighera R.A. & Barros C.S.L. 2009. [Experimental acute poisoning by bracken fern (Pteridium aquilinum) in cattle.] Intoxicação experimental aguda por samambaia (Pteridium aquilinum) em bovinos. Pesquisa Veterinária Brasileira 29(9):753-766. Departamento de Patologia, Universidade Federal de Santa Maria, Camobi, Santa Maria, RS 97105-900, Brazil. E-mail: claudioslbarros@uol.com.br
This experiment was design to address the following points in relation to the acute poisoning by bracken fern (Pteridium aquilinum) in cattle: 1) the severity of the thrombocytopenia in different stages of the intoxication and its relationship to possible deficits in the secondary hemostasis, 2) the relationship between neutropenia and the morphological signs of septicemia occasionally found at necropsy, and 3) the mechanism of anemia and its relationship with blood loss, medium life of erythrocytes and the progress of the disease. The fresh green upper parts of P. aquilinum were fed to four mixed breed calves with average age of 18 months and weights ranging from 190 to 215 kg. A calf of similar age and weight was kept together with the other four under the same conditions, except for the ingestion of P. aquilinum. The four fern-fed calves died with typical features of acute bracken fern poisoning after being fed with the plant for 53-58 days daily doses of 8.0, 8.6, 10.2, and 10.6g/kg body weight totaling at the end of the experiment, respectively, 59.3%, 63.3%, 47.4%, and 47.5% of bracken fern in relation to their body weight. The disease was characterized by fever up to 42.5°C and varying degrees of hemorrhages observed clinically, at necropsy and on histological examination. Death occurred 6-7 days after the onset of fever. The hematological changes consisted mainly of marked thrombocytopenia and neutropenia. Two of the four affected calves had mild anemia. The deficits in secondary hemostasis were mild in each case. There were no significant changes thus permitting to rule out the role of secondary hemostasis in the pathogenesis of the hemorrhages in the bracken fern poisoning. The measurement of fibrin degradation products in the serum showed conflicting results and did no allow for a solid conclusion regarding the role of disseminated intravascular coagulation in the pathogenesis of the hemorrhages in fern poisoning. The cytology and the histopathology of bone marrow from the four poisoned calves revealed marked decrease in the numbers of hematopoietic cells from the three marrow lineages, which characterizes marrow failure due to aplasia; it was concluded that the events of the primary hemostasis due to thrombocytopenia are responsible for the hemorrhages. In blood culture from three affected calves there was growth of Klebsiella oxytoca, Staphylococcus hyicus and Staphylococcus aureus, indicating that septicemia, facilitated by neutropenia could have a role in the death of cattle acutely poisoned due to the ingestion of P. aquilinum. Additional points of the interest in the acute experimental poisoning by bracken fern in cattle reported here were the development of hematuria and the so called laryngeal form.
Abstract in Portuguese:
RESUMO.- Anjos B.L., Irigoyen L.F., Piazer J.V.M., Brum J.S., Fighera R.A. & Barros C.S.L. 2009. [Experimental acute poisoning by bracken fern (Pteridium aquilinum) in cattle.] Intoxicação experimental aguda por samambaia (Pteridium aquilinum) em bovinos. Pesquisa Veterinária Brasileira 29(9):753-766. Departamento de Patologia, Universidade Federal de Santa Maria, Camobi, Santa Maria, RS 97105-900, Brazil. E-mail: claudioslbarros@uol.com.br
Este experimento foi delineado para investigar os seguintes pontos em relação à intoxicação aguda por samambaia (Pteridium aquilinum) em bovinos: 1) a intensidade da trombocitopenia em diferentes momentos da intoxicação e sua relação com possíveis déficits na hemostasia secundária, 2) a relação da neutropenia com as manifestações morfológicas de septicemia ocasionalmente observadas na necropsia, e 3) o mecanismo da anemia e sua relação com a perda de sangue, a vida média eritróide e a evolução da doença. As hastes superiores mais verdes de P. aquilinum foram administradas a quatro bovinos sem raça definida, com idade média de 1,5 ano e pesos entre 190-215 kg. Um bovino de idade e peso semelhantes foi usado como controle e, exceto por não ter recebido P. aquilinum, foi mantido nas mesmas condições que os outros quatro. Os quatro bovinos que receberam a planta morreram com quadro característico da intoxicação aguda por samambaia após receberem durante 53-58 dias, doses diárias de 8,0, 8,6, 10,2 e 10,6g/kg de peso corporal, que totalizaram, ao final do experimento, respectivamente, 112,7, 107,6, 85,7, 90,15 kg da planta, o que corresponde, respectivamente, a 59,3%, 63,3%, 47,4%, 47,5% da planta em relação ao peso dos bovinos. A doença caracterizou-se por febre de até 42,5°C e diversos graus de hemorragias observadas clinicamente, na necropsia e na histopatologia. A morte ocorria 6-7 dias após o início do quadro febril. As alterações hematológicas revelaram trombocitopenia e neutropenia acentuadas. Em dois dos quatro bovinos havia anemia leve. Não houve variações significativas nos tempos de coagulação dos bovinos intoxicados, quando avaliados os fatores de coagulação (secundária), excluindo-se assim a possibilidade da participação de distúrbios da hemostasia secundária na patogênese das hemorragias nessa intoxicação. A determinação dos produtos da degradação da fibrina no soro revelou dados conflitantes, não permitindo concluir se a coagulação intravascular disseminada tem participação na patogênese das hemorragias nessa intoxicação. A citopatologia e histopatologia da medula óssea dos quatro bovinos intoxicados revelaram acentuada diminuição no número de células hematopoéticas das três linhagens medulares, caracterizando insuficiência medular por aplasia; conclui-se que apenas eventos da hemostasia primária devidos a trombocitopenia são responsáveis pelas hemorragias. Na hemocultura de três dos bovinos intoxicados houve crescimento de Klebsiella oxytoca, Staphylococcus hyicus e Staphylococcus aureus, indicando que a septicemia, facilitada pela neutropenia, pode ter participação na causa da morte de bovinos na intoxicação aguda pela ingestão de P. aquilinum. Aspectos adicionais de interesse na reprodução da intoxicação aguda por samambaia em bovinos deste relato incluem o desenvolvimento de hematúria na doença aguda e a apresentação da chamada forma laríngea da doença.
Abstract in English:
ABSTRACT.- Camplesi A.C., Sakate M., Simão N.M.B. & Moya C.F. 2009. [Dosing cardiac markers CK-MB and TnIc and electrolytes in experimental toad envenoming in dogs.] Dosagem de marcadores cardíacos CK-MB e TnIc e eletrólitos no envenenamento experimental por veneno de sapo em cães. Pesquisa Veterinária Brasileira 29(8):632-636. Departamento de Clínica Médica Veterinária, Faculdade de Medicina Veterinária e Zootecnia, Universidade Estadual Paulista, Botucatu, SP 18600-000, Brazil. E-mail: annecamplesi@yahoo.com.br
Among the systemic signs of toad venom (bufotoxin) poisoning in dogs, the cardiotoxic effects are one of the most important. Thus, the objective of this experiment was to evaluate potential changes in the cardiac muscle in dogs poisoned experimentally by toad venom and to observe the eletrolyte alterations which may occur in this condition. Twenty dogs divided into control group (n=5) and poisoned group (n=15) were utilized. The toad venom was extracted by manual compression of the paratoidic glands. After general anesthesia, dogs in the control group received placebo and dogs in the poisoned group received the venom by orogastric catheter. Samples for dosage were collected 6 hours and 24 hours after poisoning and 0, 2, 4, 6 and 12 hours after poisoning for electrolytes dosage. The Man-Withney test was used for statistical analysis (P<0.05). The poisoned dogs showed (saline) elevated levels of cardiac markers CK-MB and TnIc, confirming the cardiotoxic effect of the bufotoxin. Hypokalemia and hypocalcemia were also observed.
Abstract in Portuguese:
RESUMO.- Camplesi A.C., Sakate M., Simão N.M.B. & Moya C.F. 2009. [Dosing cardiac markers CK-MB and TnIc and electrolytes in experimental toad envenoming in dogs.] Dosagem de marcadores cardíacos CK-MB e TnIc e eletrólitos no envenenamento experimental por veneno de sapo em cães. Pesquisa Veterinária Brasileira 29(8):632-636. Departamento de Clínica Médica Veterinária, Faculdade de Medicina Veterinária e Zootecnia, Universidade Estadual Paulista, Botucatu, SP 18600-000, Brazil. E-mail: annecamplesi@yahoo.com.br
Dentre os sinais sistêmicos causados pelo envenenamento por veneno de sapo (bufotoxina) em cães, os efeitos cardiotóxicos são um dos mais importantes. O objetivo deste estudo foi avaliar as potenciais alterações no músculo cardíaco de cães envenenados experimentalmente por veneno de sapo e observar as alterações eletrolíticas que podem ocorrer nesse tipo de envenenamento. Utilizaram-se 20 cães divididos em grupo controle (n=5) e grupo envenenado (n=15). O veneno de sapo foi extraído por meio de compressão manual das glândulas paratóides. Após anestesia geral, os cães do grupo controle receberam placebo (solução fisiológica) e os do grupo envenenado uma alíquota do veneno por sonda orogástrica. As colheitas de sangue para dosagem dos marcadores cardíacos foram realizadas seis e 24 horas após o envenenamento. As colheitas de sangue para dosagem dos eletrólitos foram realizadas antes e duas, quatro, seis e 12 horas após o envenenamento. A análise estatística empregada foi o teste não-paramétrico de Mann-Withney (P<0,05). Os cães envenenados por veneno de sapo apresentaram elevação dos níveis dos marcadores cardíacos CK-MB e TnIc, confirmando a cardiotoxicidade do veneno. Hipocalemia e hipocalcemia foram também observadas nos cães envenenados.
Abstract in English:
ABSTRACT.- Oliveira R.R., Mamprim M.J., Rahal S.C. & Bicudo A.L.C. 2009. [Radiography and ultrasonography in the diagnosis of rupture of the cranial cruciate ligament in dogs.] Radiografia e ultrassonografia no diagnóstico da ruptura do ligamento cruzado cranial em cães. Pesquisa Veterinária Brasileira 29(8):661-665. Departamento de Patologia Geral, Universidade Estadual do Paraná, Cx. Postal 261, Bandeirantes, PR 86360-000, Brazil. E-mail: rodrigoreisvet@hotmail.com
Radiography and ultrasonography were evaluated as tools for diagnosis of the rupture of cranial cruciate ligament (CrCL) in dogs. Twenty-five dogs were submitted to radiographic and ultrasonographic examinations and their results were compared with those obtained by artrotomy (gold standard). Radiography detected the rupture in 84% (21/25) of the cases, but 16% (4/25) were false-negative. Ultrasonography identified accurately 76% (19/25) of the cases and gave a probable diagnosis for the remaining 24% (6/25) what means that this technique presented 100% of positive results. It was possible to conclude that radiography and ultrasonography are valuable tools for the diagnosis of CrCL rupture in dogs.
Abstract in Portuguese:
RESUMO.- ABSTRACT.- Oliveira R.R., Mamprim M.J., Rahal S.C. & Bicudo A.L.C. 2009. [Radiography and ultrasonography in the diagnosis of rupture of the cranial cruciate ligament in dogs.] Radiografia e ultrassonografia no diagnóstico da ruptura do ligamento cruzado cranial em cães. Pesquisa Veterinária Brasileira 29(8):661-665. Departamento de Patologia Geral, Universidade Estadual do Paraná, Cx. Postal 261, Bandeirantes, PR 86360-000, Brazil. E-mail: rodrigoreisvet@hotmail.com
Radiografia e ultrassonografia foram avaliadas como técnicas no diagnóstico por imagem na ruptura do ligamento cruzado cranial (LCCr) em cães. Vinte e cinco cães foram submetidos à radiografia e ultrassonografia e seus resultados foram comparados aos obtidos por artrotomia (teste padrão ouro). O exame radiográfico diagnosticou corretamente a lesão em 84% (21/25) dos casos, mas 16% (4/25) apresentaram resultado falso-negativo. O exame ultrassonográfico foi capaz de diagnosticar acertadamente 76% (19/25) dos casos, e sugeriu a ruptura do LCCr nos 24% (6/25) restantes, apresentando 100% de resultados positivos. Concluiu-se que a radiografia e a ultrassonografia são ferramentas valiosas para diagnosticar casos de ruptura do LCCr em cães.
Abstract in English:
ABSTRACT.- Mendes H.M.F., Escobar A., Vasconcelos A.C., Zucoloto S., Alves G.E.S. & Faleiros R.R. 2009. [Morphometrical alterations in myoenteric plexus of experimentally distended equine small colon.] Alterações morfométricas no plexo mioentérico do cólon menor equino distendido experimentalmente. Pesquisa Veterinária Brasileira 29(7):557-562. Escola de Veterinária, Universidade Federal de Minas Gerais, Av. Antônio Carlos 6627, Belo Horizonte, MG 30161-970, Brazil. E-mail: faleiros@ufmg.br
The equine small colon is frequently affected by obstruction, and intestinal motility dysfunction is a common complication after its surgical treatment. This fact may be related to myoenteric plexus lesion caused by distention; however, little is known about the pathophysiology of this condition. The objective of this study was to evaluate the morphological alterations in the myoenteric inervation of segments of small colon of horses subjected to intraluminal distension with reduction of the microvascular perfusion (partial ischemia) of the intestinal wall. Nine horses were used to promote distension of on segment of small colon for 4 hours. Samples of intestinal wall were collected before and at the end of the distension, after 1.5 and 12 hours of reperfusion in the experimental segment and at the end of the procedure in a different distant segment. Samples were processed and histological sections were stained with cresyl violet for the morphometric studies. An image analyzer software was used to measure perimeter, diameter, and area of the neuronal body, nucleus and nucleolus of the neurons and the areas of the cytoplasm and nucleoplasm. Significant reductions (P<0.05) in the areas of the neuronal body and cytoplasm were detected at the end of intestinal distension, returning to the basal values during the reperfusion. In conclusion, intraluminal distension promoted changes in the morphology of the neurons of myoenteric plexus. These morphological modifications may be associated to the motility dysfunction frequently observed in clinical cases.
Abstract in Portuguese:
ABSTRACT.- Mendes H.M.F., Escobar A., Vasconcelos A.C., Zucoloto S., Alves G.E.S. & Faleiros R.R. 2009. [Morphometrical alterations in myoenteric plexus of experimentally distended equine small colon.] Alterações morfométricas no plexo mioentérico do cólon menor equino distendido experimentalmente. Pesquisa Veterinária Brasileira 29(7):557-562. Escola de Veterinária, Universidade Federal de Minas Gerais, Av. Antônio Carlos 6627, Belo Horizonte, MG 30161-970, Brazil. E-mail: faleiros@ufmg.br
The equine small colon is frequently affected by obstruction, and intestinal motility dysfunction is a common complication after its surgical treatment. This fact may be related to myoenteric plexus lesion caused by distention; however, little is known about the pathophysiology of this condition. The objective of this study was to evaluate the morphological alterations in the myoenteric inervation of segments of small colon of horses subjected to intraluminal distension with reduction of the microvascular perfusion (partial ischemia) of the intestinal wall. Nine horses were used to promote distension of on segment of small colon for 4 hours. Samples of intestinal wall were collected before and at the end of the distension, after 1.5 and 12 hours of reperfusion in the experimental segment and at the end of the procedure in a different distant segment. Samples were processed and histological sections were stained with cresyl violet for the morphometric studies. An image analyzer software was used to measure perimeter, diameter, and area of the neuronal body, nucleus and nucleolus of the neurons and the areas of the cytoplasm and nucleoplasm. Significant reductions (P<0.05) in the areas of the neuronal body and cytoplasm were detected at the end of intestinal distension, returning to the basal values during the reperfusion. In conclusion, intraluminal distension promoted changes in the morphology of the neurons of myoenteric plexus. These morphological modifications may be associated to the motility dysfunction frequently observed in clinical cases.
Abstract in English:
ABSTRACT.- Câmara A.C.L., Afonso J.A.B., Costa N.A., Mendonça C.L. & Souza M.I. 2009. [Primary abomasal impaction in 14 cattle from Pernambuco State, northeastern Brazil.] Compactação primária do abomaso em 14 bovinos no Estado de Pernambuco. Pesquisa Veterinária Brasileira 29(5):387-394. Clínica de Bovinos, Campus Garanhuns, Universidade Federal Rural de Pernambuco, Av. Bom Pastor s/n, Cx. Postal 152, Mundaú, Garanhuns, PE 55292-901, Brazil. E-mail: aclcamara@yahoo.com.br
Despite the frequent use of dry and fibrous roughage for feeding cows in many regions, especially during the dry season, impaction of the abomasum has been poorly reported in Brazil, probably because the condition is misdiagnosed by practitioners. The present paper aimed to accomplish a retrospective study on primary abomasal impaction in 14 cattle from Pernambuco State, northeastern Brazil. Eight moderate cases, without severe abdominal distention and with no rumen compaction, were treated conservatively, and four severe cases, with severe abdominal distention and rumen compaction, were treated surgically. One bull was slaughtered and one cow died without treatment. The greater number of abomasal impaction cases was in Holstein cows with six cases (42.9%), followed by crossbred cattle with five cases (35.8%), and the breeds Brown-Swiss, Nelore and Marchigiana, each with one case (21.3%). The food composition was characterized by low quality fibers and varied greatly among cases. Most frequent clinical signs were apathy, dehydration, hypomotility and ruminal bloat, intestinal hypomotility and scanty or absent feces with mucus. The hematological findings revealed leukocytosis with neutrophilia and hyperfibrinogenemia in most cases. Ruminal fluid analysis showed compromised flora and fauna dynamics and increased chlorine ion concentration. Clinical (4/8) and chirurgical (2/4) recovery rate achieved 50%. The clinical and chirurgical methods remain as viable options for the treatment of light and severe impaction, but the prognosis is always reserved especially when associated to late pregnancy.
Abstract in Portuguese:
ABSTRACT.- Câmara A.C.L., Afonso J.A.B., Costa N.A., Mendonça C.L. & Souza M.I. 2009. [Primary abomasal impaction in 14 cattle from Pernambuco State, northeastern Brazil.] Compactação primária do abomaso em 14 bovinos no Estado de Pernambuco. Pesquisa Veterinária Brasileira 29(5):387-394. Clínica de Bovinos, Campus Garanhuns, Universidade Federal Rural de Pernambuco, Av. Bom Pastor s/n, Cx. Postal 152, Mundaú, Garanhuns, PE 55292-901, Brazil. E-mail: aclcamara@yahoo.com.br
Despite the frequent use of dry and fibrous roughage for feeding cows in many regions, especially during the dry season, impaction of the abomasum has been poorly reported in Brazil, probably because the condition is misdiagnosed by practitioners. The present paper aimed to accomplish a retrospective study on primary abomasal impaction in 14 cattle from Pernambuco State, northeastern Brazil. Eight moderate cases, without severe abdominal distention and with no rumen compaction, were treated conservatively, and four severe cases, with severe abdominal distention and rumen compaction, were treated surgically. One bull was slaughtered and one cow died without treatment. The greater number of abomasal impaction cases was in Holstein cows with six cases (42.9%), followed by crossbred cattle with five cases (35.8%), and the breeds Brown-Swiss, Nelore and Marchigiana, each with one case (21.3%). The food composition was characterized by low quality fibers and varied greatly among cases. Most frequent clinical signs were apathy, dehydration, hypomotility and ruminal bloat, intestinal hypomotility and scanty or absent feces with mucus. The hematological findings revealed leukocytosis with neutrophilia and hyperfibrinogenemia in most cases. Ruminal fluid analysis showed compromised flora and fauna dynamics and increased chlorine ion concentration. Clinical (4/8) and chirurgical (2/4) recovery rate achieved 50%. The clinical and chirurgical methods remain as viable options for the treatment of light and severe impaction, but the prognosis is always reserved especially when associated to late pregnancy.
Abstract in English:
Abstract.- Pedroso P.M.O., Bandarra P.M., Bezerra Júnior P.S., Raymundo D.L., Borba M.R., Leal J.S. & Driemeier D. 2009. [Natural and experimental poisoning by Nerium oleander (Apocynaceae) in cattle in Rio Grande do Sul.] Intoxicação natural e experimental por Nerium oleander (Apocynaceae) em bovinos no Rio Grande do Sul. Pesquisa Veterinária Brasileira 29(5):404-408. Setor de Patologia Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@ufrgs.br
This paper describes natural and experimental poisoning of cattle by Nerium oleander in Rio Grande do Sul. Two out of eight cattle died acutely after consumption of leaves of Nerium oleander, branches of which had been cut and placed into a paddock where the animals were kept. An affected cow did not show clinical signs, but a 4-month-old calf presented lateral recumbence, paddling, vocalization and death. Main gross findings in the cow naturally poisoned and in two experimentally intoxicated heifers were observed in the heart and included hemorrhages in the left atrium, clots and hemorrhages in the left ventricular endocardium, and pale areas in the interventricular septum and ventricular myocardium. Histologically, there was coagulation necrosis of individual cardiac fibers or small groups of fibers, characterized by enhanced cytoplasmic eosinophily and picnotic nuclei. These lesions were most severe in the papillary muscle. The diagnosis was based on presence of the trimmed N. oleander in the paddock where the animals stayed, evidence of consumption of the plant, consistent clinical and pathological findings, and experimental reproduction of the disease through oral administration of 0.5 and 1.0g/kg of its green leaves to two cattle.
Abstract in Portuguese:
Abstract.- Pedroso P.M.O., Bandarra P.M., Bezerra Júnior P.S., Raymundo D.L., Borba M.R., Leal J.S. & Driemeier D. 2009. [Natural and experimental poisoning by Nerium oleander (Apocynaceae) in cattle in Rio Grande do Sul.] Intoxicação natural e experimental por Nerium oleander (Apocynaceae) em bovinos no Rio Grande do Sul. Pesquisa Veterinária Brasileira 29(5):404-408. Setor de Patologia Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@ufrgs.br
This paper describes natural and experimental poisoning of cattle by Nerium oleander in Rio Grande do Sul. Two out of eight cattle died acutely after consumption of leaves of Nerium oleander, branches of which had been cut and placed into a paddock where the animals were kept. An affected cow did not show clinical signs, but a 4-month-old calf presented lateral recumbence, paddling, vocalization and death. Main gross findings in the cow naturally poisoned and in two experimentally intoxicated heifers were observed in the heart and included hemorrhages in the left atrium, clots and hemorrhages in the left ventricular endocardium, and pale areas in the interventricular septum and ventricular myocardium. Histologically, there was coagulation necrosis of individual cardiac fibers or small groups of fibers, characterized by enhanced cytoplasmic eosinophily and picnotic nuclei. These lesions were most severe in the papillary muscle. The diagnosis was based on presence of the trimmed N. oleander in the paddock where the animals stayed, evidence of consumption of the plant, consistent clinical and pathological findings, and experimental reproduction of the disease through oral administration of 0.5 and 1.0g/kg of its green leaves to two cattle.
Abstract in English:
ABSTRACT.- Santos-Rodrigues A., Dagli M.L.Z., Avanzo J.L., Moraes H.P., Mackowiak I.I. & Hernandez-Blazquez F.J. 2009. Expression and distribution of connexin 32 in rat liver with experimentally induced fibrosis. Pesquisa Veterinária Brasileira 29(4):353-357. Departamento de Cirurgia, Setor de Anatomia, Faculdade de Medicina Veterinária e Zootecnia, Universidade de São Paulo, Av. Prof. Dr. Orlando Marques de Paiva 87, São Paulo, SP 05508-270, Brazil. E-mail: alexsantos@usp.br
The connexin 32 (Cx32) is a protein that forms the channels that promote the gap junction intercellular communication (GJIC) in the liver, allowing the diffusion of small molecules through cytosol from cell-to-cell. Hepatic fibrosis is characterized by a disruption of normal tissue architeture by cellular lesions, and may alter the GJIC. This work aimed to study the expression and distribution of Cx32 in liver fibrosis induced by the oral administration of dimethylnitrosamine in female Wistar rats. The necropsy of the rats was carried out after five weeks of drug administration. They presented a hepatic fibrosis state. Sections from livers with fibrosis and from control livers were submitted to immunohistochemical, Real Time-PCR and Western-Blot analysis to Cx32. In fibrotic livers the Cxs were diffusely scattered in the cytoplasm, contrasting with the control livers, where the Cx32 formed junction plaques at the cell membrane. Also it was found a decrease in the gene expression of Cx32 without reduction in the protein quantity when compared with controls. These results suggest that there the mechanism of intercellular communication between hepatocytes was reduced by the fibrotic process, which may predispose to the occurrence of a neoplastic process, taken in account that connexins are considered tumor suppressing genes.
Abstract in Portuguese:
ABSTRACT.- Santos-Rodrigues A., Dagli M.L.Z., Avanzo J.L., Moraes H.P., Mackowiak I.I. & Hernandez-Blazquez F.J. 2009. Expression and distribution of connexin 32 in rat liver with experimentally induced fibrosis. Pesquisa Veterinária Brasileira 29(4):353-357. Departamento de Cirurgia, Setor de Anatomia, Faculdade de Medicina Veterinária e Zootecnia, Universidade de São Paulo, Av. Prof. Dr. Orlando Marques de Paiva 87, São Paulo, SP 05508-270, Brazil. E-mail: alexsantos@usp.br
The connexin 32 (Cx32) is a protein that forms the channels that promote the gap junction intercellular communication (GJIC) in the liver, allowing the diffusion of small molecules through cytosol from cell-to-cell. Hepatic fibrosis is characterized by a disruption of normal tissue architeture by cellular lesions, and may alter the GJIC. This work aimed to study the expression and distribution of Cx32 in liver fibrosis induced by the oral administration of dimethylnitrosamine in female Wistar rats. The necropsy of the rats was carried out after five weeks of drug administration. They presented a hepatic fibrosis state. Sections from livers with fibrosis and from control livers were submitted to immunohistochemical, Real Time-PCR and Western-Blot analysis to Cx32. In fibrotic livers the Cxs were diffusely scattered in the cytoplasm, contrasting with the control livers, where the Cx32 formed junction plaques at the cell membrane. Also it was found a decrease in the gene expression of Cx32 without reduction in the protein quantity when compared with controls. These results suggest that there the mechanism of intercellular communication between hepatocytes was reduced by the fibrotic process, which may predispose to the occurrence of a neoplastic process, taken in account that connexins are considered tumor suppressing genes.