PESQUISA VETERINÁRIA BRASILEIRA

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:

Rech R.R., Schild A.L., Driemeier D., Garmatz S.L., Oliveira F.N., Riet-Correa F. & Barros C.S.L. 2005. [Malignant catarrhal fever in cattle in Rio Grande do Sul, Brazil: Epidemiology, clinical signs and pathology.] Febre catarral maligna em bovinos no Rio Grande do Sul: epidemiologia, sinais clínicos e patologia. Pesquisa Veterinária Brasileira 25(2):97-105. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br The epidemiology, clinical signs, necropsy and histopathological findings in cases of malignant catarrhal fever (MCF) occurring in cattle from 15 farms in Rio Grande do Sul, Brazil, from 1973 to 2003, are described. In 9 instances (60%) the disease occurred as sporadic cases affecting 1-3 cattle whereas in six farms (40%) MCF occurred as epizootics involving several cattle in each affected herd. Morbidity rates ranged from 2.4% to 20% and lethality rates were 83.3% and 100%. Cattle of all ages and both sexes were affected. Where the information was available (9 farms) sheep were in contact with affected cattle and cases of MCF occurred more frequently in spring and summer. Clinical courses were acute or subacute and clinical signs included fever, nasal and ocular discharges, conjunctivitis, drooling, hematuria, necrosis and blunting of buccal papillae, enlargement of lymph nodes, diarrhea and neurological disturbances. Necropsy findings included opaque corneas, reddening, erosions and ulcerations in several mucous membranes of the alimentary, respiratory and urogenital tracts, and the conjunctiva; enlargement and haemorrhage of lymph nodes and multiple white foci in the renal cortices and in the hepatic portal triads. Crustous dermatitis was observed in some cases. Main histopathological findings included vasculitis, necrosis of the surface epithelia and accumulation of inflammatory cells in several organs. Vasculitis were associated with fibrinoid necrosis of the medial layer of arteries and inflammatory cells included lymphoblasts, lymphocytes, plasma cells and macrophages.

• Infectious diseases epidemiology viral diseases diseases of cattle pathology.

Abstract in Portuguese:

Rech R.R., Schild A.L., Driemeier D., Garmatz S.L., Oliveira F.N., Riet-Correa F. & Barros C.S.L. 2005. [Malignant catarrhal fever in cattle in Rio Grande do Sul, Brazil: Epidemiology, clinical signs and pathology.] Febre catarral maligna em bovinos no Rio Grande do Sul: epidemiologia, sinais clínicos e patologia. Pesquisa Veterinária Brasileira 25(2):97-105. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br The epidemiology, clinical signs, necropsy and histopathological findings in cases of malignant catarrhal fever (MCF) occurring in cattle from 15 farms in Rio Grande do Sul, Brazil, from 1973 to 2003, are described. In 9 instances (60%) the disease occurred as sporadic cases affecting 1-3 cattle whereas in six farms (40%) MCF occurred as epizootics involving several cattle in each affected herd. Morbidity rates ranged from 2.4% to 20% and lethality rates were 83.3% and 100%. Cattle of all ages and both sexes were affected. Where the information was available (9 farms) sheep were in contact with affected cattle and cases of MCF occurred more frequently in spring and summer. Clinical courses were acute or subacute and clinical signs included fever, nasal and ocular discharges, conjunctivitis, drooling, hematuria, necrosis and blunting of buccal papillae, enlargement of lymph nodes, diarrhea and neurological disturbances. Necropsy findings included opaque corneas, reddening, erosions and ulcerations in several mucous membranes of the alimentary, respiratory and urogenital tracts, and the conjunctiva; enlargement and haemorrhage of lymph nodes and multiple white foci in the renal cortices and in the hepatic portal triads. Crustous dermatitis was observed in some cases. Main histopathological findings included vasculitis, necrosis of the surface epithelia and accumulation of inflammatory cells in several organs. Vasculitis were associated with fibrinoid necrosis of the medial layer of arteries and inflammatory cells included lymphoblasts, lymphocytes, plasma cells and macrophages.

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:

Rech R.R, Fighera R.A., Oliveira F.N. & Barros C.S.L. 2004. [Granulomatous meningoencephalitis in cattle grazing vetch (Vicia spp).] Meningoencefalite granulomatosa em bovinos em pastoreio de ervilhaca (Vicia spp). Pesquisa Veterinária Brasileira 24(3): 169-172. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Granulomatous meningoencephalitis was observed in 7 out of 8 adult dairy cows affected by vetch-associated systemic granulomatous disease, although there was no neurological signs associated with the condition. The cellular inflammatory infiltrates were located in the leptomeninges and as perivascular cuffings within the brain and consisted of epithelioid macrophages, lymphocytes, plasm cells and eosinophils. These inflammatory changes varied from mild to severe from animal to animal and among different brain regions of the same animal. Perivascular cuffings were usually more marked than the leptomeningeal infiltrates. Affected brain regions, in decreasing order of intensity, included diencephalon through the level of massa intermedia, mesencephalon at the level of rostral colliculi, pons and cerebellar peduncles, medulla at the level of obex, frontal lobe at the level of the genu of the corpus callosum, and cerebellum. The character and the distribution of the inflammatory changes are emphasized regarding the differential diagnosis with other diseases and lesions of the bovine central nervous system in the context of the Brazilian surveillance program for bovine spongiform encephalopath.

• Diseases of cattle diseases of the central nervous system meningoencephalitis plant poisoning Vicia spp pathology.

Abstract in Portuguese:

Rech R.R, Fighera R.A., Oliveira F.N. & Barros C.S.L. 2004. [Granulomatous meningoencephalitis in cattle grazing vetch (Vicia spp).] Meningoencefalite granulomatosa em bovinos em pastoreio de ervilhaca (Vicia spp). Pesquisa Veterinária Brasileira 24(3): 169-172. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Granulomatous meningoencephalitis was observed in 7 out of 8 adult dairy cows affected by vetch-associated systemic granulomatous disease, although there was no neurological signs associated with the condition. The cellular inflammatory infiltrates were located in the leptomeninges and as perivascular cuffings within the brain and consisted of epithelioid macrophages, lymphocytes, plasm cells and eosinophils. These inflammatory changes varied from mild to severe from animal to animal and among different brain regions of the same animal. Perivascular cuffings were usually more marked than the leptomeningeal infiltrates. Affected brain regions, in decreasing order of intensity, included diencephalon through the level of massa intermedia, mesencephalon at the level of rostral colliculi, pons and cerebellar peduncles, medulla at the level of obex, frontal lobe at the level of the genu of the corpus callosum, and cerebellum. The character and the distribution of the inflammatory changes are emphasized regarding the differential diagnosis with other diseases and lesions of the bovine central nervous system in the context of the Brazilian surveillance program for bovine spongiform encephalopath.

Abstract in English:

Garmatz S.L., Irigoyen L.F., Rech R.R., Brown C.C., Zhang J. & Barros C.S.L. 2004. [Malignant catarrhal fever in cattle in Rio Grande do Sul, Brazil: Experimental transmission to cattle and characterization of the etiological agent.] Febre catarral maligna em bovinos no Rio Grande do Sul: transmissão experimental para bovinos e caracterização do agente etiológico. Pesquisa Veterinária Brasileira 24(2):93-106. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Two oubreaks of malignant catarrhal fever (MCF) occurring in cattle on two farms (A and B) in the municipality of Santiago, state of Rio Grande do Sul (RS), Brazil, and the transmission of the disease to susceptible calves as well as the detection of ovine herpesvirus-2 (OvHV-2) in tissues of affected cattle are reported. The two epizootics occurred from November 2001 to February 2002 (Farm A) and in January-February 2003 (Farm B). Numbers of cattle at risk, morbidity and letality rates were respectively 170, 10.59% and 83.33% for Farm A and 500, 2.4% and 100% for Farm B. Contact between affected cattle and sheep was detected in both farms, but lambing ewes were present only in farm A. Duration of clinical courses, gross findings and histopathology were the same for the affected cattle in both farms. Most affected cattle died or were euthanatized in extremis after a clinical course of 2-8 days. Clinical signs included fever (40.5 and 41.5°C), nasal and ocular discharge, corneal opacity, conjunctivitis, drooling, erosions and ulcerations of the mucosae, diarrhea, hematuria, and neurological disturbances. Eleven necropsies (9 on Farm A, 2 on Farm B) were performed. Gross lesions included erosions and ulcers affecting the mucosae of nasal turbinates, oral cavity, gastrointestinal and urogenital tracts; hemorrhage and necrosis of the tip of the buccal papillae, lymph node enlargement, multifocal white foci in renal cortex, and hyperemia of leptomeninges. Microscopically, there were arteritis and fibrinoid degeneration in medium and small arteries and arterioles of multiple organs and tissues, necrosis and inflammation in several mucosal surfaces, keratitis, conjunctivitis, uveitis, intersticial nephritis, and encephalitis. Transmission experiments were attempted in five calves (E1-E5) by inocculating each of them intravenously with 500 ml of whole heparinized blood from a MCF affected cow. The transmission was suscessful in at least three (E1-E3) of the experimental calves which became sick after an incubation period of 15-27 days. Four experimental calves either died or were euthanatized in extremis after a clinical course which varied from 3 days to 8 weeks. The remaining experimental calf (E5) recovered from a mild disease and was euthanatized 14 weeks after inocculation. Necropsies were performed in all five calves. Clinical signs, necropsy and histopathological findings of three calves (E1-E3) were characteristic of MCF. OvHV-2 viral DNA was detected by the polimerase chain reaction (PCR) test in paraffin embedded tissues from seven cattle out of the 11 spontaneous MCF cases and from three experimental calves (E1-E3). PCR tests resulted negative in the remaining four of the 11 spontaneous MCF cases tested and in two (E4,E5) of the five experimental calves. Immunohistochemistry performed in sections of lymphoid tissue from calf E4 failed to detect BVD virus antigen. The experimental transmission of MCF and the characterization of the etiological agent as OvHV-2 were successfully attempted in cattle for the first time in Brazil.

• Infectious diseases malignant catarrhal fever viral diseases diseases of cattle pathology polimerase chain reation.

Abstract in Portuguese:

Garmatz S.L., Irigoyen L.F., Rech R.R., Brown C.C., Zhang J. & Barros C.S.L. 2004. [Malignant catarrhal fever in cattle in Rio Grande do Sul, Brazil: Experimental transmission to cattle and characterization of the etiological agent.] Febre catarral maligna em bovinos no Rio Grande do Sul: transmissão experimental para bovinos e caracterização do agente etiológico. Pesquisa Veterinária Brasileira 24(2):93-106. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Two oubreaks of malignant catarrhal fever (MCF) occurring in cattle on two farms (A and B) in the municipality of Santiago, state of Rio Grande do Sul (RS), Brazil, and the transmission of the disease to susceptible calves as well as the detection of ovine herpesvirus-2 (OvHV-2) in tissues of affected cattle are reported. The two epizootics occurred from November 2001 to February 2002 (Farm A) and in January-February 2003 (Farm B). Numbers of cattle at risk, morbidity and letality rates were respectively 170, 10.59% and 83.33% for Farm A and 500, 2.4% and 100% for Farm B. Contact between affected cattle and sheep was detected in both farms, but lambing ewes were present only in farm A. Duration of clinical courses, gross findings and histopathology were the same for the affected cattle in both farms. Most affected cattle died or were euthanatized in extremis after a clinical course of 2-8 days. Clinical signs included fever (40.5 and 41.5°C), nasal and ocular discharge, corneal opacity, conjunctivitis, drooling, erosions and ulcerations of the mucosae, diarrhea, hematuria, and neurological disturbances. Eleven necropsies (9 on Farm A, 2 on Farm B) were performed. Gross lesions included erosions and ulcers affecting the mucosae of nasal turbinates, oral cavity, gastrointestinal and urogenital tracts; hemorrhage and necrosis of the tip of the buccal papillae, lymph node enlargement, multifocal white foci in renal cortex, and hyperemia of leptomeninges. Microscopically, there were arteritis and fibrinoid degeneration in medium and small arteries and arterioles of multiple organs and tissues, necrosis and inflammation in several mucosal surfaces, keratitis, conjunctivitis, uveitis, intersticial nephritis, and encephalitis. Transmission experiments were attempted in five calves (E1-E5) by inocculating each of them intravenously with 500 ml of whole heparinized blood from a MCF affected cow. The transmission was suscessful in at least three (E1-E3) of the experimental calves which became sick after an incubation period of 15-27 days. Four experimental calves either died or were euthanatized in extremis after a clinical course which varied from 3 days to 8 weeks. The remaining experimental calf (E5) recovered from a mild disease and was euthanatized 14 weeks after inocculation. Necropsies were performed in all five calves. Clinical signs, necropsy and histopathological findings of three calves (E1-E3) were characteristic of MCF. OvHV-2 viral DNA was detected by the polimerase chain reaction (PCR) test in paraffin embedded tissues from seven cattle out of the 11 spontaneous MCF cases and from three experimental calves (E1-E3). PCR tests resulted negative in the remaining four of the 11 spontaneous MCF cases tested and in two (E4,E5) of the five experimental calves. Immunohistochemistry performed in sections of lymphoid tissue from calf E4 failed to detect BVD virus antigen. The experimental transmission of MCF and the characterization of the etiological agent as OvHV-2 were successfully attempted in cattle for the first time in Brazil.

Abstract in English:

ABSTRACT.- Fighera R.A., Rozza D.B., Piazer J.V., Copetti M.V., lrigoyen L.F. & Barros C.S.L. 2003. [Interstitial pneumonia in cattle fed moldy sweet potatoes (Ipomoea batatas).] Pneumonia intersticial em bovinos associada à ingestão de batata-doce (lpomoea batatas) mofada. Pesquisa Veterinária Brasileira 23(4):161-166. Depto Patologia, Universidade Federal de Santa Maria, 97105- 900 Santa Maria, RS, Brasil. E-mail: claudioslbarros@uol.com.br Cases of respiratory disease were diagnosed in five out of 23 cattle (21. 7%) after they wete fed moldy damaged sweet potatoes (lpomoea batatas) on a small farm in the county of São Vicente do Sul, state of Rio Grande do Sul, Brazil. Of those five cattle, three died spontaneously and another one was euthanatized for necropsy while showing advanced respiratory clinicai signs. The disease manifested itself approximately 24 hours after the ingestion of the sweet potatoes and lasted from 1 to 4 days. Clinicai signs included dyspnea (labored breathing and abdominal respiration), tachypnea, extended neck with Iow carriage of the head and rhythmical flaring of the nostrils. Two cows were necropsied. Necropsy findings included distended pale and rubbery lungs which failed to collapse when the thorax was open, and marked pulmonar interstitial emphysema and edema. Lymphoid hyperplasia was observed in the hilar nodes and spleen. Histologically, the lesions were those of interstitial pneumonia. Alveolar septa were thickened by fibroblasts and inflammatory cells, and there was hypertrophy and hyperplasia of type li pneumocytes; the interlobular septa were distended by edema and emphysema. The culture of the moldy sweet potatoes yielded Fusarium solani and Fusarium oxysporum.

• Toxic diseases mycotoxicoses respiratory diseases interstitial pneumonia diseases of cattle sweet potatoes lpomoea batatas Intoxicações micotoxicoses doenças respiratórias pneumonia intersticial doenças de bovinos batata-doce.

Abstract in Portuguese:

RESUMO.- Fighera R.A., Rozza D.B., Piazer J.V., Copetti M.V., lrigoyen L.F. & Barros C.S.L. 2003. [Interstitial pneumonia in cattle fed moldy sweet potatoes (Ipomoea batatas).] Pneumonia intersticial em bovinos associada à ingestão de batata-doce (lpomoea batatas) mofada. Pesquisa Veterinária Brasileira 23(4):161-166. Depto Patologia, Universidade Federal de Santa Maria, 97105- 900 Santa Maria, RS, Brasil. E-mail: claudioslbarros@uol.com.br Uma doença respiratória foi diagnosticada em cinco dentre 23 bovinos (21, 7%) após terem sido alimentados com batata-doce (lpomoea batatas) mofada em uma pequena propriedade rural em São Vicente do Sul, Rio Grande do Sul, Brasil. Três dos cinco bovinos afetados morreram espontaneamente, e o quarto foi sacrificado para necropsia quando mostrava sinais clínicos respiratórios avançados. A manifestação clínica iniciara cerca de 24 horas após a ingestão das batatasdoces e a evolução clínica foi de 1 a 4 dias. Os sinais clínicos incluíam dispnéia (respiração laboriosa e abdominal), taquipnéia, pescoço estendido com cabeça baixa e dilatação ritmada das narinas. Dois bovinos foram necropsiados. Os achados de necropsia incluíam pulmões distendidos, pálidos e de consistência borrachenta, que não colapsavam quando o tórax era aberto; enfisema e edema acentuados eram evidentes no pulmão. Os linfonodos e o baço apresentavam alterações características de hiperplasia linfóide. Histologicamente, as lesões eram típicas de pneumonia intersticial. Os septos alveolares estavam espessados por fibroblastos e células inflamatórias, havia hipertrofia e hiperplasia de pneumócitos tipo II; os septos interlobulares estavam distendidos por edema e enfisema. A cultura de amostras das batatas-doces mofadas produziu Fusarium solani e F. oxysporum.

Abstract in English:

ABSTRACT.- Peixoto P.V., França T.N., Barros C.S.L. & Tokarnia C.H. 2003. [Histopathological aspects of Bovine Enzootic Haematuria in Brazil.] Pesquisa Veterinaria Brasileira 23(2):65-81. Depto Nutrição Animal e Pastagem, Instituto de Zootecnia, UFRRJ, Km 47, Seropédica, Rio de Janeiro 23835-000, Brazil. E-mail: peixotop@ufrrj.br The bladder lesions of 59 cattle, from the States of Rio de Janeiro, São Paulo, Minas Gerais, Espírito Santo, Rio Grande do Sul, Santa Catarina, Paraná and Amazon, affected by Bovine Enzootic Haematuria (BEH), were studied histologically. The objective of this study was to describe and redassify neoplastic and non-neoplastic alterations not yet reported, according to the more complete current nomendature used in human medicine. There was an almost complete identity with alterations observed in the bladder of man. Due to the occurrence of two or more neoplasms in the sarne animal, differences in the methodology and in the concept of dassification, a more precise comparison was not possible. Coexistence of different types of epithelial and/or mesenchymal tumour growth was frequently seen. Rare neoplasms or differentiations not previously described were found in the bladder of some animais affected by BEH. These were trabecular carcinoma with Paneth cells differentiation, mesonephroid adenoma, mesonephroid adenocarcinoma, "signet ring" cell carcinoma, plasmocytoid carcinoma, chromophobe cell carcinoma and nested type of transitional cell carcinoma. Haemangiosarcomas originating from haemangiomas were also observed. This study also revealed the occurrence of many tumors with anaplasia and pronounced infiltrative features, but which did not metastasize. The elucidation of the cause of this "barrier against metastases" and its relationship with chemical carcinogenesis induced by the ptaquiloside, the active principie of bracken fern (Pteridium aquilinum), could be of interest to future research on the control of neoplasia in man and animais.

• Histopathology Bovine Enzootic Hematuria bladder tumors Pteridium aquilinum Brazil. Histopatologia Hematúria enzoótica bovina tumores de bexiga Brasil.

Abstract in Portuguese:

RESUMO.- Peixoto P.V., França T.N., Barros C.S.L. & Tokarnia C.H. 2003. [Histopathological aspects of Bovine Enzootic Haematuria in Brazil.] Pesquisa Veterinaria Brasileira 23(2):65-81. [Aspectos histopatológicos da Hematúria Enzoótica Bovina no Brasil.] Depto Nutrição Animal e Pastagem, Instituto de Zootecnia, UFRRJ, Km 47, Seropédica, Rio de Janeiro 23835-000, Brazil. E-mail: peixotop@ufrrj.br Com o objetivo de descrever alterações neoplásicas e não-neoplásicas ainda não relatadas e, paralelamente, reclassificá-las de acordo com nomenclatura mais completa e atual utilizada em medicina humana, foram estudadas, histologicamente, lesões da bexiga de 59 bovinos com Hematúria Enzoótica (HEB), oriundos dos Estados do Rio de Janeiro, São Paulo, Minas Gerais, Espírito Santo, Rio Grande do Sul, Santa Catarina, Paraná e Amazonas. Verificou-se, em termos qualitativos, quase uma perfeita identidade com as lesões de bexiga observadas em seres humanos. Comparações mais exatas com relação à freqüência dessas alterações ficaram prejudicadas, dadas a ocorrência de duas ou mais neoplasias em um mesmo animal e as diferenças da metodologia empregada ou do conceito de classificação. Coexistência entre neoplasias diversas, epiteliais e/ou mesenquimais, foi vista com freqüência. Neoplasias ou diferenciações raras, ainda não descritas na bexiga de bovinos, como carcinoma trabecular com diferenciação em células de Paneth, adenoma e adenocarcinoma mesonefróides, carcino ma "signet ring" (anel de sinete), carcinoma plasmocitóide, carcinoma de células cromófobas e carcinoma transicional tipo ninhado foram observadas na bexiga de alguns animais com HEB. Foram verificados hemangiossarcomas proliferando a partir de hemangiomas. O estudo revelou, ainda, a· ocorrência de. diversos tumores com anaplasia e carácter infiltrativo acentuados, incapazes, porém, de metastizarem. O esclarecimento da(s) causa(s) dessa "barreira à metástase" e suas relações com a carcinogênese química induzida pelo ptaquilosídeo, o princípio ativo de Pteridium aquilinum, talvez possa ser de interesse em futuros estudos que visem combater o câncer no homem e nos animais.

Abstract in English:

ABSTRACT.- Fighera R.A., Souza T.M., Langohr I. & Barros C.S.L. 2002. [Experimental onion Allium cepa (Liliaceae) poisoning in cats.] Intoxicação experimental por cebola, Allium cepa (Liliaceae), em gatos. Pesquisa Veterinária Brasileira 22(2):79-84. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, Rio Grande do Sul, Brazil. Email: anemiaveterinaria@bol.com.br Onion poisoning is reported worlwide in several animal species. The toxic principie (npropyl dissulfide) present in onions causes the transformation of hemoglobin in methemoglobin. In order to study the laboratory, gross and histopathological tindings in onion poisoning in cats, tive 4-month-old cats were fed a single dose of 10g/kg of dried-onion each. Another cat of the sarne age did not receive the onion meal and served as control. AII tive cats developed clinical signs of the toxicosis; one of them died within 24 hours of the ingestion of the onion meal. Clinical signs included apathy, tachycardia, tachypnea, and cyanosis. Laboratory tindings included hemolytic anemia associated with Heinz bodies and methemoglobinemia. Main necropsy tindings were splenomegaly and brown discoloration of blood. Histopathological tindings included splenic and hepatic hemosiderosis and multifocal extramedullary hematopoiesis.

• Poisonous plants Allium cepa onion hemolytic anemia methemoglobinemia Heinz bodies diseases of cats pathology Intoxicação por plantas cebola anemia hemolítica metemoglobinemia corpúsculos de Heinz doenças de gatos patologia.

Abstract in Portuguese:

RESUMO.- Fighera R.A., Souza T.M., Langohr I. & Barros C.S.L. 2002. [Experimental onion Allium cepa (Liliaceae) poisoning in cats.] Intoxicação experimental por cebola, Allium cepa (Liliaceae), em gatos. Pesquisa Veterinária Brasileira 22(2):79-84. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, Rio Grande do Sul, Brazil. Email: anemiaveterinaria@bol.com.br A intoxicação por cebola é relatada em várias espécies animais em muitas partes do mundo. O princípio tóxico (n propil dissulfito) presente na cebola causa a transformação da hemoglobina em metemoglobina. Para estudar os achados laboratoriais, de necropsia e histopatológicos da intoxicação por cebola em gatos, cinco gatos de quatro meses de idade receberam cada um uma dose única de 10g/kg de cebola desidratada por via oral. Um outro gato de mesma idade não recebeu a refeição com cebola e serviu como controle. Todos os cinco gatos desenvolveram sinais clínicos da toxicose; um deles morreu dentro de 24 horas após a ingestão da cebola. Os sinais clínicos incluíram apatia, taquicardia, taquipnéia e cianose. Os achados laboratoriais se caracterizavam por anemia hemolítica associada a corpúsculos de Heinz e metemoglobinemia. Os principais achados de necropsia foram esplenomegalia e sangue de cor marrom. Os achados histopatológicos foram hemossiderose e hematopoese extramedular no baço e fígado.

Abstract in English:

ABSTRACT.- Stigger A.L., Barros C.S.L., Langohr I.M. & Barros S.S. 2001. [Experimental poisoning by Ateleia glazioviana (Leg.Papilibnoideae) in sheep] Intoxicação experimental por Ateleia glazioviarya (Leg.Papilionoideae) em ovinos. Pesquisa Veterinária Brasileira 21(3):98-108. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: cslb@sm.conex.com.br The leaves of Ateleia glazioviana were fed daily to seven sheep. Another sheep was used as côil(rol,. Total amounts (g/kg/body weight) o(;the plant consumed by each animal were 75 during 60 days (Sheep 6), 125 during-25 days (Sheep 4), 13,0 during 13 days (Sheep 7), 150 during 60 days (Sheep 5), 180 during 18 days (Sheep 3), 330 during 33 days (Sheep 2), and 375 during 25 days (Sheep 1 ). Six sheep were fed the green leaves while Sheep 7 was fed dried A. glazioviana leaves. Five sheep (Sheep 1-4 and 7) developed clinical signs 8 to 16, days after the first administration of the plant. The clinical course varied from 6 to 50 days and clinical signs included apathy, loss of appetite, and increased heart and respiratory rates; affected sheep were ·reluctant to move and showed a low carriage of the head, instability of the hind limbs, and staggering gait. Some sheep supported their weight against the wall of the stable. Sheep 1, 3, and 4 died spontaneously; paddling movements preceded death. Sheep 2 and 7 were euthanatized when presenting marked clinical signs of the toxicosis. Sheep 5 and 6 did not get clinically ill and were euthanatized along with the control sheep 103 days after the first administration of the plant. All sheep were necropsied and several of their organs, including heart and brain, were evaluated histologically. Additionally, fragments of the myocardium of Sheep 3 and 4 were evaluated by transmission electron microscopy. To provide more controls for the myocardial changes, the hearts were collected from six animals at an abattoir known to slaughter sheep from regions free of A. glazioviana. These hearts were processed for histology and examined in the same way as the other eight. All seven treated (plant fed) sheep had gross changes at necropsy. There were firm, irregular white or yellow areas in the myocardium of all treated sheep. These pale areas were more evident on the cut surface of the heart. Hydrothorax and/or hydropericardium were observed in five animals (Sheep 1-4 and 7). Nutmeg livers were seen in Sheep 1 and 7. This latter sheep also had ascites. The main histopathological findings in treated sheep were degenerative/necrotic changes in the myocardium. The early changes consisted of acute swollen myocardial fibers associated with bizarre nuclei. Apparently this change progressed until the sarcoplasm disappeared and an empty collapsed sarcolemmal tube remained surrounded by interstitial connective tissue and fibrosis. Overt necrosis (hyaline and floccular) associated with mono nuclear infiltration and phagocytosis of fiber fragments were also observed. Varying degrees of spongy degeneration were seen in the white matter of the brain of Sheep 1, 3, 4 and 7. Mitochondrial swelling and loss of density of the mitochondrial matrix were the earliest ultrastructural changes observed. In advanced lesions cardiac cells had vacuoles in the sarcoplasm, rupture of the sarcolemma and necrosis with intervening macrophages and fibroblasts associated with increased collagen.

• Poisonous plants Ateleia glazioviana diseases of sheep myocardial necrosis myocardial fibrosis toxic cardiomyopathy status spongiosus Plantas tóxicas doenças de ovinos necrose do miocárdio fibrose tio miocárdio cardiomiopatia tóxica.

Abstract in Portuguese:

Stigger A.L., Barros C.S.L., Langohr I.M. & Barros S.S. 2001. [Experimental poisoning by Ateleia glazioviana (Leg.Papilibnoideae) in sheep] Intoxicação experimental por Ateleia glazioviarya (Leg.Papilionoideae) em ovinos. Pesquisa Veterinária Brasileira 21(3):98-108. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: cslb@sm.conex.com.br Sete ovelhas receberam as folhas de Ateleia glazioviana em doses predeterminadas. Um outro ovino serviu de controle. As quantidades totais (g/kg/peso corporal) de planta consumidas pelos ovinos foram 75 por 60 dias (Ovino 6), 125 por 25 dias (Ovino 4), 130 por 13 dias (Ovino 7), 150 por 60 dias (Ovino 5), 180 por 18 dias (Ovino 3), 330 por 33 dias (Ovino 2) e 375 por 25 dias (Ovino 1). Seis ovinos recéberam folhas verdes e o Ovino 7 recebeu folhas dessecadas. Cinco ovinos (Ovinos 1-4 e 7) desenvolveram sinais clínicos. 8 a 16 dias após a primeira administração da planta. A evolução do quadro clínico foi de 6 a 50 dias e os sinais clínicos. incluíram apatia, perda do apetite, taquicardia e taquipnéia. Os ovinos afetados apresentavam relutância em mover-se, cabeça baixa, instabilidade dos membros pélvicos e andar cambaleante. Alguns dos ovinos afetados apoiavam o corpo contra a parede da baia. Os Ovinos 1, 3 e 4 morreram espontaneamente; movimentos de pedalagem precederam a morte. Os Ovinos 2 e 7 foram submetidos à eutanásia com sinais clínicos avançados da toxicose. Os Ovinos 5 e 6 não adoeceram e foram sacrificados junto com o controle 103 dias após a primeira administração da planta. Todos os ovinos foram necropsiados e vários órgãos, incluindo coração e encéfalo, foram avaliados histologicamente. Além disso, fragmentos de miocárdio dos Ovinos 3 e 4 foram avaliados por microscopia eletrônica de transmissão. A fim de se obter mais controles para a avaliação das lesões do miocárdio, coletaram-se os corações de seis ovinos abatidos para consumo em um abatedouro que sabidamente recebe ovinos originários de uma região livre de A. glazioviana. Esses corações foram processados para histologia e examinados da mesma maneira que os outros oito. Todos os ovinos tratados (que receberam a planta) apresentaram lesões macroscópicas. Havia áreas firmes, irregulares, branco-amareladas no miocárdio de todos os ovinos tratados. Essas áreas pálidas eram mais bem vistas na superfície de corte do coração. Hidrotórax e/ou hidropericárdio foram observados em cinco animais (Ovinos 1-4 e 7). O fígado dos Ovinos 1 e 7 tinha aspecto de nozmoscada. O Ovino 7 apresentava ascite. Os principais achados histopatológicos nos ovinos tratados foram alterações degenerativas/necróticas no miocárdio. As alterações iniciais consistiam de tumefação aguda das fibras cardíacas, associada a núcleos com formas bizarras. Essa alteração aparentemente progredia até o desaparecimento do sarcoplasma, resultando num tubo sarcolemal vazio e colapsado envolto por tecido conjuntivo intersticial e fibrose. Necrose franca (hialina e flocular) associada à infiltração mononuclear e fagocitose de fragmentos de fibras foi também observada. Graus variáveis de degeneração esponjosa foram observados na substância branca do encéfalo dos Ovinos 1, 3, 4 e 7. Tumefação de mitocôndrias e perda da densidade da matriz das mitocôndrias foram as alterações ultra-estruturais mais precoces. Em lesões avançadas os cardiomiócitos apresentavam vacúolos no sarcoplasma, ruptura do sarcolema e necrose com aparecimento de macrófagos e fibroblastos associados a aumento de colágeno.

Abstract in English:

ABSTRACT.- Ilha M.R.S., Loretti A.P., Barros S.S., Barros C.S.L. 2001. [Spontaneous poisoning in sheep by Senecio brasiliensis (Asteraceae) in southern Brazil] Intoxicação espontânea por Senecio brasiliensis (Asteraceae) em ovinos no Rio Grande do Sul. Pesquisa Veterinária Brasileira 21(3):123-138. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: ilha76@mailcity.com An outbreak of spontaneous Senecio brasiliensis poisoning in grazing sheep in the county of Mata, Rio Grande do Sul, southern Brazil, is described. The disease occurred on one farm in middlejanuary 1997. Fifty-one (54.25%) out of 94 sheep were affected, and 50 animals (53.2%) died. This flock of sheep had been grazing for approximately 7 months (from June 1996 to January 1997) in paddocks heavily infested with S. brasiliensis. Clinical signs included photodermatitis, progressive emaciation, apathy, weakness, neurological signs such as drownsiness, aimless walking and unsteady gait, jaundice and hemoglobinuria. There was amelioration of the skin lesions in those sheep that developed hepatogenous photosensitization. Main necropsy findings in 9 sheep included small, firm, tan or greenish liver with few to numerous small, yellowish, well-circumscribed nodules measuring up to 3 mm in diameter and randomly scattered throughout the hepatic parenchyma. There was also marked distension of the gallbladder which contained large amounts of inspissated, dark green bile and straw-colored cavitary effusions (hydropericardium and ascitis). Five sheep developed lethal acute hemolytic crisis, secondary to massive release into the blood stream of copper accumulated in the liver (hepatogenous chronic copper poisoning). Apart from the aforementioned liver lesions, other gross findings in those animals included severe and diffuse jaundice, dark brown urine (hemoglobinuria) and swollen, friable, finely stippled or diffusely dark kidneys. The main histopathological findings included hepatomegalocytosis, biliary ductal proliferation (bile duct hyperplasia) and moderate periportal fibrosis. The portal triads were infiltrated with variable numbers of mononuclear cells. There was heavy accumulation of brownish pigment in macrophages identified as ceroid or copper with PAS and rhodanine stainings, respectively. Those ceroid and copper-laden macrophages were scattered on the remnant hepatic parenchyma or formed small aggregates in the portal triads. Main histopathological findings in the kidneys of 5 sheep, that developed fatal hepatogenous chronic copper poisoning, included tubular nephrosis, accumulation of hemoglobin and hemosiderin in epithelial tubular cells and hemoglobin casts (hemoglobinuric nephrosis). Morphological evidence of hepatic encephalopathy included spongy degeneration (status spongiosus) of the cerebral white matter. Ultrastructural changes in the tiver of affected sheep included degenerative hepatocellular changes of varying severity. There was accumulation of numerous lipid droplets in the cytoplasm of the hepatocytes and lysosomes containing substances of high electron-density that corresponded to ceroid-lipofuscin in most of the cases. In addition, there was mild swelling of the rough endoplasmic reticulum and moderate hyperplasia of the smooth endoplasmic reticulum in some areas of the cytoplasm of the hepatocytes. Proximal convoluted tubular epithelial cells showed intracellular edema anda variety of mitochondrial degenerative changes. These included disarrangement and breakup of cristae, finely granular matrix, accumulation of lipid globules and rupture of the membranes in a few cases. Many epithelial tubular cells displayed substances of high electron-densitywithin lysosomes. Chemical analysis of copper in tiver and kidney samples of affected sheep revealed high concentrations varying from 369 ppm to 1248 ppm in the tiver and ranging from 152 ppm to 687 ppm in the kidneys (dry matter). The diagnosis of Senecio brasiliensis poisoning was based on epidemiological data, clinical signs, necropsy findings, histological lesions and laboratory data.

• Senecio brasiliensis Asteraceae diseases of sheep poisonous plants copper toxicosis pathology doenças de ovinos plantas tóxicas intoxicação por cobre patologia

Abstract in Portuguese:

RESUMO.- Ilha M.R.S., Loretti A.P., Barros S.S., Barros C.S.L. 2001. [Spontaneous poisoning in sheep by Senecio brasiliensis (Asteraceae) in southern Brazil] Intoxicação espontânea por Senecio brasiliensis (Asteraceae) em ovinos no Rio Grande do Sul. Pesquisa Veterinária Brasileira21(3):123-138. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: ilha76@mailcity.com Descreve-se a ocorrência de um surto de intoxicação espontânea por Senecio brasiliensis em ovinos em um estabelecimento do município de Mata, Estado do Rio Grande do Sul, em meados de janeiro de 1997. De um total de 94 ovinos, 51 (54,25%) animais adoeceram e 50 (53,2%) morreram. Esse rebanho permaneceu durante aproximadamente 7 meses (de junho de 1996 a janeiro de 1997) em piquetes de pastagem nativa onde havia grande quantidade de S. brasiliensis. O quadro clínico manifestado pelos animais afetados consistia em fotossensibilização, emagrecimento progressivo, apatia, fraqueza, perturbações neurológicas como depressão, andar a esmo e desequilibrado, icterícia e hemoglobinúria. Houve melhora das lesões de pele naqueles ovinos que desenvolveram fotossensibilização hepatógena depois que foram retirados do sol. As principais lesões macroscópicas observadas em 9 dos 10 ovinos necropsiados incluíam fígado diminuído de tamanho, firme, difusamente marrom amarelado ou esverdeado, com quantidades variáveis de nódulos de 1-3 mm de diâmetro, bem circunscritos, salientes na cápsula, amarelados, distribuídos aleatoriamente por todo o parênquima. A vesícula biliar estava repleta e preenchida por bile verde escura e espessa. Havia também derrames cavitários (hidropericárdio e ascite). Crise hemolítica aguda fatal associada à intoxicação crônica hepatógena por cobre foi observada em cinco ovinos. Além das lesões hepáticas macroscópicas já mencionadas, foi observada icterícia generalizada da carcaça, rins tumefeitos, friáveis, difusamente escurecidos ou com fino pontilhado enegrecido; a urina era marrom escura (hemoglobinúria). As principais lesões microscópicas foram observadas no fígado e consistiam em hepatomegalocitose, proliferação de duetos biliares (hiperplasia ductal) e fibrose periportal moderada acompanhada de infiltrado inflamatório mononuclear. Macrófagos carregados de pigmento acastanhado formavam aglomerados nas tríades portais ou estavam dispersos entre os hepatócitos remanescentes. O material armazenado no citoplasma desses macrófagos correspondia a ceróide e cobre, positivo nas técnicas de PAS e rodanina, respectivamente. Nos rins de cinco animais, havia nefrose hemoglobinúrica caracterizada por degeneração e necrose do epitélio tubular, presença de hemoglobina e hemossiderina no citoplasma das células epiteliais dos túbulos contorcidos e cilindros de hemoglobina na luz tubular. Evidência morfológica de encefalopatia hepática incluía degeneração esponjosa (status spongiosus) da substância branca do encéfalo. Achados ultra-estruturais no fígado incluíam graus variáveis de degeneração hepatocelular caracterizada pelo acúmulo de numerosas gotas lipídicas no citoplasma das células hepáticas e presença de lisossomos carregados de material eletrodenso que, na maioria dos casos, correspondia à lipofuscina-ceróide. Adicionalmente, havia discreta dilatação do retículo endoplasmático rugoso e moderada hiperplasia do retículo endoplasmático liso em algumas regiões do citoplasma dos hepatócitos. No epitélio dos túbulos contorcidos proximais do rim foi observado edema intracelular e diversas alterações mitocondriais de caráter degenerativo que incluíam tumefação, desorganização e ruptura das cristas, matriz finamente granular, acúmulo de gotículas de gordura e ruptura das membranas em alguns casos. Lisossomos contendo material fortemente eletrodenso foram observados em muitas células tubulares renais. O exame laboratorial de fragmentos de fígado e rim dos ovinos afetados revelou níveis elevados de cobre que variaram respectivamente de 369 ppm a 1248 ppm e 152 ppm a 687 ppm com base na matéria seca. O diagnóstico de intoxicação por Senecio brasiliensis baseou-se em dados epidemiológicos, clínicos, de necropsia, histopatológicos e laboratoriais.