PESQUISA VETERINÁRIA BRASILEIRA

Abstract in English:

Rissi D.R., Rech R.R., Barros R.R., Kommers G.D., Langohr I.M., Pierezan F. & Barros C.S.L. 2006. [Listeric meningoencephalitis in goats.] Forma nervosa de listeriose em caprinos. Pesquisa Veterinária Brasileira 26(1):14-20. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br A neurologic disease was observed in three young adult goats (indentified as A-C) from a herd of 100 goats during October-December, 2004. Clinical signs included head tilt, torticollis, nystagmus, staggering, falls and eventually recumbency and paddling, with stiff limbs. Treatment of Goat C with antibiotics resulted in a temporary remission of the clinical signs. The clinical courses where 5, 10 and 30 days respectively for Goats A, B and C. Goat A died spontaneously and the other two where euthanatized in extremis. No gross changes were observed. Histologic lesions were predominantly unilateral, with inflammatory and degenerative changes, extending from the medulla oblongata to the thalamus. In all 3 cases there were perivascular cuffings of one or more types of mononuclear cells (lymphocytes, plasma cells, activated macrophages) and occasionally neutrophils associated with areas of malacia where Gitter cells filled spaces of parenchymal loss. Additionally, Goat B had microabscesses in the medulla, pons, and mesencephalon and multifocal neutrophilic and lymphocytic infiltrates within the fascicles of the trigeminal nerve and in the cerebellar leptomeninges. In the brainstem of Goat C, there was multifocal granulomatous inflammation which included epithelioid macrophages and occasional multinucleated giant cells. Listeria sp antigen was detected by imunohistochemistry in routinely processed sections of mesencephalon from Goats A and C and of pons from Goat B.

• Listeria sp Listeria monocytogenes listeriosis encephalitis immunohistochemistry pathology diseases of goats.

Abstract in Portuguese:

Rissi D.R., Rech R.R., Barros R.R., Kommers G.D., Langohr I.M., Pierezan F. & Barros C.S.L. 2006. [Listeric meningoencephalitis in goats.] Forma nervosa de listeriose em caprinos. Pesquisa Veterinária Brasileira 26(1):14-20. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br A neurologic disease was observed in three young adult goats (indentified as A-C) from a herd of 100 goats during October-December, 2004. Clinical signs included head tilt, torticollis, nystagmus, staggering, falls and eventually recumbency and paddling, with stiff limbs. Treatment of Goat C with antibiotics resulted in a temporary remission of the clinical signs. The clinical courses where 5, 10 and 30 days respectively for Goats A, B and C. Goat A died spontaneously and the other two where euthanatized in extremis. No gross changes were observed. Histologic lesions were predominantly unilateral, with inflammatory and degenerative changes, extending from the medulla oblongata to the thalamus. In all 3 cases there were perivascular cuffings of one or more types of mononuclear cells (lymphocytes, plasma cells, activated macrophages) and occasionally neutrophils associated with areas of malacia where Gitter cells filled spaces of parenchymal loss. Additionally, Goat B had microabscesses in the medulla, pons, and mesencephalon and multifocal neutrophilic and lymphocytic infiltrates within the fascicles of the trigeminal nerve and in the cerebellar leptomeninges. In the brainstem of Goat C, there was multifocal granulomatous inflammation which included epithelioid macrophages and occasional multinucleated giant cells. Listeria sp antigen was detected by imunohistochemistry in routinely processed sections of mesencephalon from Goats A and C and of pons from Goat B.

Abstract in English:

Oliveira F.N., Rech R.R., Rissi D.R., Barros R.R. & Barros C.S.L. 2005. [Poisoning in swine from the ingestion of Aeschynomene indica (Leg.Papilionoideae) seeds.] Intoxica-ção em suínos pela ingestão de sementes de Aeschynomene indica (Leg. Papilionoideae). Pesquisa Veterinária Brasileira 25(3):135-142. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br A spontaneous outbreak of a neurological disease in swine caused by the ingestion of Aeschynomene indica seeds and the reproduction of the disease in the same animal species are reported. The natural outbreak occurred in a pig-raising facility in the central region of the state of Rio Grande do Sul, Brazil. On the premises there were 100 pigs (20 breeding sows and 80 young weaned pigs from several categories) that were fed a ration made by mixing 50% of corn bran, 25% of soybean bran, 5% of a commercial mix of vitamins and minerals, and 20% of broken rice contaminated with 40% of A. indica seeds. Although all pigs apparently ingested the same ration, only 45-day-old pigs were affected; morbidity, mortality and lethality rates were respectively 25%-40%, 8.5%-20%; and 25%-66%. Clinical signs appeared 24 hours after the beginning of feeding of A. indica seeds contaminated ration and included variable degrees of incoordinated gait, falls, sternal recumbency with the hind limbs in a wide base stance, lateral recumbency and death. It was not possible to ascertain how many pigs recovered nor the time frame of recovery. One pig was euthanatized and necropsied in the premises. The poisoning was reproduced in 5 young pigs (A-E) which were fed a ration containing 10% (Pig A), 15% (Pig B) and 20% (Pigs C-E) of A. indica seeds, and in one older pig (Pig F) which was fed a ration with 16.5% of A. indica seeds. Pigs A, B and F were euthanatized and Pigs C-E died of an acute disease respectively 16, 21 and 24 hours after the beginning of the experiment. Clinical signs were similar to those observed in pigs of the spontaneous outbreak. Necropsy findings included marked hyperemia of the encephalic leptomeninges of all pigs; there were large amounts of A. indica seeds in the stomach and reddening of the intestinal wall and bloody intestinal content in Pigs C-E. A hematoma was observed in the lungs of Pig C. The histopathological findings in the brain of pigs fed rations with larger concentrations (20%) of A. indica seeds (C-E) included congestion, edema and hemorrhage and swollen vascular endothelia with focal symmetrical distribution in several brain nuclei and in the telencephalic cortex. In Pigs A and B, and in Pig F, the case which received the lower dosage of the seeds of A. indica, and in the pig from the spontaneous outbreak, histopathological changes in the brain consisted of discrete focal symmetrical areas of malacia in which closely packed Gitter cells and astrocytosis, and capillaries with swollen endothelium obliterated the normal neuropil. The symmetrical malacic foci caused by the ingestion of A. indica seeds in swine affected cerebellar and vestibular nuclei, putamen, and the mesencephalic oculomotor and red nuclei. This indicates that the A. indica seeds ingestion was responsible for the neurological condition, that it may be fatal and seems to affect equally young and older swine. The clinical outcome and pathological changes were dose-dependent, and the brain lesions progressed from damaged blood vessels to vasogenic edema, hemorrhage and malacia.

• Poisonous plants plant poisoning Aeschynomene indica Leguminosae Papilionoideae pathology diseases of the central nervous system diseases of swine.

Abstract in Portuguese:

Oliveira F.N., Rech R.R., Rissi D.R., Barros R.R. & Barros C.S.L. 2005. [Poisoning in swine from the ingestion of Aeschynomene indica (Leg.Papilionoideae) seeds.] Intoxica-ção em suínos pela ingestão de sementes de Aeschynomene indica (Leg. Papilionoideae). Pesquisa Veterinária Brasileira 25(3):135-142. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br A spontaneous outbreak of a neurological disease in swine caused by the ingestion of Aeschynomene indica seeds and the reproduction of the disease in the same animal species are reported. The natural outbreak occurred in a pig-raising facility in the central region of the state of Rio Grande do Sul, Brazil. On the premises there were 100 pigs (20 breeding sows and 80 young weaned pigs from several categories) that were fed a ration made by mixing 50% of corn bran, 25% of soybean bran, 5% of a commercial mix of vitamins and minerals, and 20% of broken rice contaminated with 40% of A. indica seeds. Although all pigs apparently ingested the same ration, only 45-day-old pigs were affected; morbidity, mortality and lethality rates were respectively 25%-40%, 8.5%-20%; and 25%-66%. Clinical signs appeared 24 hours after the beginning of feeding of A. indica seeds contaminated ration and included variable degrees of incoordinated gait, falls, sternal recumbency with the hind limbs in a wide base stance, lateral recumbency and death. It was not possible to ascertain how many pigs recovered nor the time frame of recovery. One pig was euthanatized and necropsied in the premises. The poisoning was reproduced in 5 young pigs (A-E) which were fed a ration containing 10% (Pig A), 15% (Pig B) and 20% (Pigs C-E) of A. indica seeds, and in one older pig (Pig F) which was fed a ration with 16.5% of A. indica seeds. Pigs A, B and F were euthanatized and Pigs C-E died of an acute disease respectively 16, 21 and 24 hours after the beginning of the experiment. Clinical signs were similar to those observed in pigs of the spontaneous outbreak. Necropsy findings included marked hyperemia of the encephalic leptomeninges of all pigs; there were large amounts of A. indica seeds in the stomach and reddening of the intestinal wall and bloody intestinal content in Pigs C-E. A hematoma was observed in the lungs of Pig C. The histopathological findings in the brain of pigs fed rations with larger concentrations (20%) of A. indica seeds (C-E) included congestion, edema and hemorrhage and swollen vascular endothelia with focal symmetrical distribution in several brain nuclei and in the telencephalic cortex. In Pigs A and B, and in Pig F, the case which received the lower dosage of the seeds of A. indica, and in the pig from the spontaneous outbreak, histopathological changes in the brain consisted of discrete focal symmetrical areas of malacia in which closely packed Gitter cells and astrocytosis, and capillaries with swollen endothelium obliterated the normal neuropil. The symmetrical malacic foci caused by the ingestion of A. indica seeds in swine affected cerebellar and vestibular nuclei, putamen, and the mesencephalic oculomotor and red nuclei. This indicates that the A. indica seeds ingestion was responsible for the neurological condition, that it may be fatal and seems to affect equally young and older swine. The clinical outcome and pathological changes were dose-dependent, and the brain lesions progressed from damaged blood vessels to vasogenic edema, hemorrhage and malacia.

Abstract in English:

Rissi D.R., Rech R.R., Fighera R.A., Cagnini D.Q., Kommers G.D. & Barros C.S.L. 2005. [Spontaneous Baccharis coridifolia poisoning in cattle.] Intoxicação espontânea por Baccharis coridifolia em bovinos. Pesquisa Veterinária Brasileira 25(2):111-114. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Two outbreaks of Baccharis coridifolia poisoning in cattle in southern Brazil are described. Cases occurred when stressed, hungry and thirsty cattle brought from pastures free of B. coridifolia were placed into pastures heavily infested by this poisonous plant. In the two outbreaks morbidity was 21.73% and 22.51% and lethality was virtually 100%. Clinical signs included mild bloat, instability of hind limbs, muscle tremors, dry muzzle, dry feces or diarrhea, polydipsia and restlessness. Consistent necropsy findings included dehydration, large amounts of ruminal fluid, reddening and erosions of the mucosae of the forestomachs. Degeneration and necrosis of the lining epithelium of the forestomachs and of lymphoid tissue were the main histopathological changes encountered.

• Poisonous plants Baccharis coridifolia Asteraceae diseases of cattle pathology.

Abstract in Portuguese:

Rissi D.R., Rech R.R., Fighera R.A., Cagnini D.Q., Kommers G.D. & Barros C.S.L. 2005. [Spontaneous Baccharis coridifolia poisoning in cattle.] Intoxicação espontânea por Baccharis coridifolia em bovinos. Pesquisa Veterinária Brasileira 25(2):111-114. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Two outbreaks of Baccharis coridifolia poisoning in cattle in southern Brazil are described. Cases occurred when stressed, hungry and thirsty cattle brought from pastures free of B. coridifolia were placed into pastures heavily infested by this poisonous plant. In the two outbreaks morbidity was 21.73% and 22.51% and lethality was virtually 100%. Clinical signs included mild bloat, instability of hind limbs, muscle tremors, dry muzzle, dry feces or diarrhea, polydipsia and restlessness. Consistent necropsy findings included dehydration, large amounts of ruminal fluid, reddening and erosions of the mucosae of the forestomachs. Degeneration and necrosis of the lining epithelium of the forestomachs and of lymphoid tissue were the main histopathological changes encountered.

Abstract in English:

ABSTRACT.- Afonso J.A.B., Ciarlini P.C., Kuchembuck M.R.G., Kohayagawa A., Feltrin L.P.Z., Ciarlini L.D.R.P., Laposy C.B., Mendonça C.L. & Takahira R.K. 2002. [Oxidative metabolism of the neutrophils in sheep treated with sodium monensin and experimentally submitted to ruminal acidosis.] Metabolismo oxidativo dos neutrófilos de ovinos tratados com monensina sódica e experimentalmente submetidos à acidose ruminal. Pesquisa Veterinária Brasileira 22(4):129-134. Clinica de Bovinos, UFRPE, Cx. Postal 152, Garanhuns, PE 55292-901, Brazil. Ruminal acidosis is due to excessive ingestion of carbohydrates of rapid fermentation without previous adaptation of the microorganisms, causing severe metabolic disturbances to the animals. The objective of the present study was to assess the neutrophilic oxidative metabolism in sheep treated with sodium monensin in experimentally induced ruminal lactic acidosis. A total of 18 mate sheep, half-bred (Ideal x Merino), fistulated in the rumen, were used; nine of them received 33 mg/kg of the ionophore diet per day, for 30 days; the others were controls. The acidosis was induced by supplying 15g of sucrose/kg of body weight. The clinical evaluation and the rumen and blood samples were obtained before (Oh) and at 6, 12, 24 and 48 hours post-induction. In both groups, all the animals presented clinical manifestations of ruminal lactic acidosis 6 hours after the induction. From this period on, a significant pH decrease (P<0.05) was observed in the ruminal fluid, which reached levels below 5. There were relevant differences (P<0.05) between the groups 12 hours after the induction, when the sheep treated with monensin had higher values than those of the control group. During this period, the oxidative metabolism of the neutrophils remained inhibited, and the reestablishment of this function only occurred in the sheep which received monensin. Blood pH, plasmatic glucose and the ionizable calcium suffered alterations within its levels. The seric cortisol concentration rose significantly (P<0.05) in both groups, although differences (P<0.05) between them were found at the end of the observation period. The treatment with monensin did not influence the oxidative metabolism of the neutrophils inhibited by the lactic acidosis; however, a faster recovery of this metabolism was verified in the animals treated with the ionophore.

• Ruminal acidosis ionophores sheep Acidose ruminal ionóforos ovinos.

Abstract in Portuguese:

RESUMO.- Afonso J.A.B., Ciarlini P.C., Kuchembuck M.R.G., Kohayagawa A., Feltrin L.P.Z., Ciarlini L.D.R.P., Laposy C.B., Mendonça C.L. & Takahira R.K. 2002. [Oxidative metabolism of the neutrophils in sheep treated with sodium monensin and experimentally submitted to ruminal acidosis.] Metabolismo oxidativo dos neutrófilos de ovinos tratados com monensina sódica e experimentalmente submetidos à acidose ruminal. Pesquisa Veterinária Brasileira 22(4):129-134. Clinica de Bovinos, UFRPE, Cx. Postal 152, Garanhuns, PE 55292-901, Brazil. A acidose láctica ruminal é causada pela ingestão excessiva de carboidratos de fermentação rápida sem uma prévia adaptação dos mocroorganismos, podendo com isso gerar distúrbios metabólicos graves aos ruminantes. Este trabalho tem por objetivo estudar o metabolismo oxidativo dos neutrófilos em ovinos tratados com a monensina sódica na acidose láctica ruminal induzida experimentalmente. Foram empregados 18 ovinos, machos, mestiços (Ideal x Merino), fistulados no rúmen; dos quais nove receberam 33 mg/kg da dieta do ionóforo ao dia, durante 30 dias, os demais ovinos pertenceram ao grupo controle. A acidose foi induzida fornecendo 15g de sacarose/kg de peso corporal. A avaliação clínica e as amostras de rúmen e sangüíneas foram obtidas antes (momento controle) 0h e às 6h, 12h, 24h e 48h pós-indução. Em ambos os grupos os animais apresentaram manifestações clínicas de acidose láctica ruminal 6 horas pós-indução. A partir deste período se observou uma diminuição significativa (p< 0,05) do pH no fluido ruminal, que alcançou valores inferiores a cinco, e diferenças significativas (p< 0,05) entre os grupos a partir das 12h pós-indução foram constatadas, nos quais os ovinos tratados com a monensina apresentaram valores superiores em relação aos do grupo controle. Durante este período ocorreu uma inibição do metabolismo oxidativo dos neutrófilos nos animais estudados, ocorrendo restabelecimento desta função somente nos ovinos que receberam a monensina. O pH sangüíneo, a glicose plasmática e o cálcio ionizável sofreram alterações nos seus índices. A concentração do cortisol sérico elevou-se de forma significativa (p< 0,05) em ambos os grupos, porém diferenças (p< 0,05) entre eles foram constatadas ao final no período de observação. O tratamento com a monensina não influenciou o metabolismo oxidativo dos neutrófilos, inibido pela acidose láctica; porém se verificou uma recuperação mais rápida deste metabolismo nos animais em que receberam o ionóforo.