PESQUISA VETERINÁRIA BRASILEIRA

Abstract in English:

ABSTRACT.- Moreira Souto M.A., Kommers G.D., Barros C.S.L., Piazer J.V.M., Rech R.R., Riet-Correa F. & Schild A.L. 2006. [Neoplasms of the upper digestive tract of cattle associated with spontaneous ingestion of bracken fern (Pteridium aquilinum).] Neoplasias do trato alimentar superior de bovinos associadas ao consumo espontâneo de samambaia (Pteridium aquilinum). Pesquisa Veterinária Brasileira 26(2):112-122. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: glaukommers@yahoo.com Thirty bovine with neoplasms of the upper digestive tract (UDT) associated with spontaneous ingestion of bracken fern (Pteridium aquilinum) were studied. They were from 27 farms, located in the municipalities of Jaguari (23) and Nova Esperança do Sul (4), Rio Grande do Sul, Brazil. The total cattle population in those farms was 1,090 and large amounts of bracken fern were found in the pastures. Twenty-six of the affected cattle were cows and four were castrated males, 3-13 years of age; most of them were 7-8 years old (46,6%). Clinical signs observed in the affected animals were progressive weight loss, absence of ruminal movements, cough, dysphagia, regurgitation, halitosis, diarrhea, and bloat. Less frequent signs were selective appetite, dyspnea, and salivation. Two bovine died and 28 were submitted to euthanasia in advanced stage of disease and necropsied. The main gross and microscopic alterations were found in identical areas of the UDT. They consisted of papillomas, transforming papillomas, and squamous cell carcinomas (SCCs). Metastases of SCCs to regional lymph nodes and other organs, such as liver and lungs, were also observed (18/30). Twenty-nine bovine had papillomas of various sizes in several areas of the UDT. The digestive papillomatosis ranged from mild (45%), to moderate (38%), to severe (17%). Three developing phases were observed microscopically in the examined papillomas: an early growing phase, a developing phase, and a regressing phase. In 16 cases, there was malignant transformation of papillomas into SCCs. The SCCs were solitary (12/30) or multiple (18/30) and were histologically well, moderately, or poorly differentiated. Grouping the distribution of SCCs of larger extension in the UDT into cranial region (base of the tongue, pharynx/oropharynx, and epiglottis), medial region (esophagus), and caudal region (cardia and rumen), the distribution was cranial in 39%, middle in 16%, and caudal in 45% of the cases. By the same grouping criteria, but considering the total number of times SCCs of varied extensions were diagnosed in the cranial, middle, and caudal regions, the percentages changed to 34%, 26%, and 40%, respectively. The epidemiological and histomorphological evidences found in this study are in agreement with the observations that point out the co-carcinogenesis between bovine papillomavirus type 4 infection and chemicals of bracken fern in the pathogenesis of the SCCs in the UDT of cattle. However, the presence of pre-neoplastic changes and SCCs in situ or in early stages of development, independently of the presence of papillomas, clearly indicates the possibility of development of SCCs from normal epithelium, probably due to the direct action of the chemical carcinogens contained in bracken fern.

• Poisonous plants Pteridium aquilinum plant poisoning bovine papillomavirus type 4 squamous cell carcinoma diseases of cattle pathology.

Abstract in Portuguese:

ABSTRACT.- Moreira Souto M.A., Kommers G.D., Barros C.S.L., Piazer J.V.M., Rech R.R., Riet-Correa F. & Schild A.L. 2006. [Neoplasms of the upper digestive tract of cattle associated with spontaneous ingestion of bracken fern (Pteridium aquilinum).] Neoplasias do trato alimentar superior de bovinos associadas ao consumo espontâneo de samambaia (Pteridium aquilinum). Pesquisa Veterinária Brasileira 26(2):112-122. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: glaukommers@yahoo.com Thirty bovine with neoplasms of the upper digestive tract (UDT) associated with spontaneous ingestion of bracken fern (Pteridium aquilinum) were studied. They were from 27 farms, located in the municipalities of Jaguari (23) and Nova Esperança do Sul (4), Rio Grande do Sul, Brazil. The total cattle population in those farms was 1,090 and large amounts of bracken fern were found in the pastures. Twenty-six of the affected cattle were cows and four were castrated males, 3-13 years of age; most of them were 7-8 years old (46,6%). Clinical signs observed in the affected animals were progressive weight loss, absence of ruminal movements, cough, dysphagia, regurgitation, halitosis, diarrhea, and bloat. Less frequent signs were selective appetite, dyspnea, and salivation. Two bovine died and 28 were submitted to euthanasia in advanced stage of disease and necropsied. The main gross and microscopic alterations were found in identical areas of the UDT. They consisted of papillomas, transforming papillomas, and squamous cell carcinomas (SCCs). Metastases of SCCs to regional lymph nodes and other organs, such as liver and lungs, were also observed (18/30). Twenty-nine bovine had papillomas of various sizes in several areas of the UDT. The digestive papillomatosis ranged from mild (45%), to moderate (38%), to severe (17%). Three developing phases were observed microscopically in the examined papillomas: an early growing phase, a developing phase, and a regressing phase. In 16 cases, there was malignant transformation of papillomas into SCCs. The SCCs were solitary (12/30) or multiple (18/30) and were histologically well, moderately, or poorly differentiated. Grouping the distribution of SCCs of larger extension in the UDT into cranial region (base of the tongue, pharynx/oropharynx, and epiglottis), medial region (esophagus), and caudal region (cardia and rumen), the distribution was cranial in 39%, middle in 16%, and caudal in 45% of the cases. By the same grouping criteria, but considering the total number of times SCCs of varied extensions were diagnosed in the cranial, middle, and caudal regions, the percentages changed to 34%, 26%, and 40%, respectively. The epidemiological and histomorphological evidences found in this study are in agreement with the observations that point out the co-carcinogenesis between bovine papillomavirus type 4 infection and chemicals of bracken fern in the pathogenesis of the SCCs in the UDT of cattle. However, the presence of pre-neoplastic changes and SCCs in situ or in early stages of development, independently of the presence of papillomas, clearly indicates the possibility of development of SCCs from normal epithelium, probably due to the direct action of the chemical carcinogens contained in bracken fern.

Abstract in English:

ABSTRACT.- Rissi D.R., Oliveira F.N., Rech R.R., Pierezan F., Lemos R.A.A. & Barros C.S.L. 2006. [Epidemiology, clinical signs and distribution of the encephalic lesions in cattle affected by meningoencephalitis caused by bovine herpesvirus-5.] Epidemiologia, sinais clínicos e distribuição das lesões encefálicas em bovinos afetados por meningoencefalite por herpesvírus bovino-5. Pesquisa Veterinária Brasileira 26(2):123-132. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Seven outbreaks and an isolated case of meningoencephalitis caused by bovine herpesvirus-5 (BoHV-5) in cattle in Rio Grande do Sul, Brazil, occurring in 2002-2004, are described. From a total population at risk of 1,359 cattle, 54 1-18-month-old calves from both sexes and several breeds were affected and 50 died spontaneously or were euthanatized while moribund. The highest frequency of cases was in recently weaned calves or calves submitted to other stressing factors. General rates of morbidity, mortality and lethality were respectively 3.97, 3.67 and 92.59%. Clinical courses varied from 3-10 days and included depression, nasal and ocular discharge, grinding of teeth, circling, blindness, fever, nistagmus, trembling, anorexia, dysphagia, drooling, incoordination, head pressing, rough hair coat, tachycardia, tachypnea, abdominal pain, melena, falls, recumbency, opisthotonus, convulsions and paddling. Nineteen calves were necropsied. Necropsy findings were characterized by hyperemia of leptomeninges, swollen rostral portions of the telencephalon, and flattening of frontal lobes gyri; frequently in these frontal areas there were segmental brown-yellow discoloration and softening (malacia) of the cortex. In cases with more protracted clinical courses there were extensive swelling, softening and hemorrhaging of the telencephalic frontal lobes. Microscopically, all affected cattle had a necrotizing non-suppurative meningoencephalitis with variable distribution among the 19 cases and among the various telencephalic regions of the same case. The severity of these changes were more marked, in decreasing order of intensity, in the telencephalic frontal cortex, basal ganglia (nuclei), thalamus, brain stem, parietal telencephalic cortex, occipital telencephalic cortex and cerebellum. Perivascular inflammatory infiltrate consisted predominantly of lymphocytes, plasm cells, and less frequently of neutrophils. Additional microscopic findings included variable degrees of gliosis, edema, neuronal necrosis in the telencephalic cortex characterized by shrinking and eosinophilia of perikaria and nuclear picnosis (red neuron); basophilic intranuclear inclusion bodies in astrocytes and neurons (21.05% of the cases); sattelitosis; and neuronophagia. The areas of softening in the cortical substance consisted of necrosis of the neuroctodermal elements with maintenance of mesenchymal structures (vessels and microglia), infiltrate of Gitter cells, and, in more severe cases, extensive hemorrhages. In chronic cases, only vascular structures and a few Gitter cells remained in the cortical area leaving a cavity between white matter and leptomeninges (residual lesion).

• Bovine herpesvirus-5 BoHV-5 encephalitis diseases of cattle viral diseases neuropathology.

Abstract in Portuguese:

ABSTRACT.- Rissi D.R., Oliveira F.N., Rech R.R., Pierezan F., Lemos R.A.A. & Barros C.S.L. 2006. [Epidemiology, clinical signs and distribution of the encephalic lesions in cattle affected by meningoencephalitis caused by bovine herpesvirus-5.] Epidemiologia, sinais clínicos e distribuição das lesões encefálicas em bovinos afetados por meningoencefalite por herpesvírus bovino-5. Pesquisa Veterinária Brasileira 26(2):123-132. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Seven outbreaks and an isolated case of meningoencephalitis caused by bovine herpesvirus-5 (BoHV-5) in cattle in Rio Grande do Sul, Brazil, occurring in 2002-2004, are described. From a total population at risk of 1,359 cattle, 54 1-18-month-old calves from both sexes and several breeds were affected and 50 died spontaneously or were euthanatized while moribund. The highest frequency of cases was in recently weaned calves or calves submitted to other stressing factors. General rates of morbidity, mortality and lethality were respectively 3.97, 3.67 and 92.59%. Clinical courses varied from 3-10 days and included depression, nasal and ocular discharge, grinding of teeth, circling, blindness, fever, nistagmus, trembling, anorexia, dysphagia, drooling, incoordination, head pressing, rough hair coat, tachycardia, tachypnea, abdominal pain, melena, falls, recumbency, opisthotonus, convulsions and paddling. Nineteen calves were necropsied. Necropsy findings were characterized by hyperemia of leptomeninges, swollen rostral portions of the telencephalon, and flattening of frontal lobes gyri; frequently in these frontal areas there were segmental brown-yellow discoloration and softening (malacia) of the cortex. In cases with more protracted clinical courses there were extensive swelling, softening and hemorrhaging of the telencephalic frontal lobes. Microscopically, all affected cattle had a necrotizing non-suppurative meningoencephalitis with variable distribution among the 19 cases and among the various telencephalic regions of the same case. The severity of these changes were more marked, in decreasing order of intensity, in the telencephalic frontal cortex, basal ganglia (nuclei), thalamus, brain stem, parietal telencephalic cortex, occipital telencephalic cortex and cerebellum. Perivascular inflammatory infiltrate consisted predominantly of lymphocytes, plasm cells, and less frequently of neutrophils. Additional microscopic findings included variable degrees of gliosis, edema, neuronal necrosis in the telencephalic cortex characterized by shrinking and eosinophilia of perikaria and nuclear picnosis (red neuron); basophilic intranuclear inclusion bodies in astrocytes and neurons (21.05% of the cases); sattelitosis; and neuronophagia. The areas of softening in the cortical substance consisted of necrosis of the neuroctodermal elements with maintenance of mesenchymal structures (vessels and microglia), infiltrate of Gitter cells, and, in more severe cases, extensive hemorrhages. In chronic cases, only vascular structures and a few Gitter cells remained in the cortical area leaving a cavity between white matter and leptomeninges (residual lesion).

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:

Rozza D.B., Raymundo D.L., Corrêa A.M.R., Seitz A.L., Driemeier D. & Colodel E.M. 2006. [Spontaneous Baccharis coridifolia (Compositae) poisoning in sheep.] Intoxicação espontânea por Baccharis coridifolia (Compositae) em ovinos. Pesquisa Veterinária Brasileira 26(1):21-25. Departamento de Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Cx. Postal 15094, Porto Alegre, RS 91540-000, Brazil. E-mail: moleta@terra.com.br An outbreak of Baccharis coridifolia (Compositae) poisoning in sheep is reported, which occurred in November 2004 in the county of Caxias do Sul, Rio Grande do Sul (RS), southern Brazil. From a herd of 212 sheep, coming from a Baccharis coridifolia free area, in the county of Jaguarão, RS, 35 sheep died until 5 days after the arrival in the new area where the plant was found with abundance. The clinical signs began 8 hours after introduction of the animals into the new pasture and included apathy, anorexia, abdominal retraction or mild distension, weakness of hind limbs, dry feces, sternal ou lateral decumbency, struggling movements, coma and death. Clinical evolution was from 5 to 48 hours. Other sheep that were already before on the pasture were not affected. Main necropsy findings were in the gastrointestinal tube, with wall and serosal oedema, mainly in the reticulo-ruminal fold and of the abomasum, reddening and detachment of the mucosa of forestomachs, and intense hemorrhage in the submucosa. Histopathological findings were degeneration and necrosis of the epithelium of the forestomachs with polymorphonuclear infiltration associated with bacterial colonies, congestion, hemorrhage and oedema, and lymphoid tissue necrosis.

• Poisonous plants Baccharis coridifolia Compositae plant poisoning diseases of sheep pathology.

Abstract in Portuguese:

Rozza D.B., Raymundo D.L., Corrêa A.M.R., Seitz A.L., Driemeier D. & Colodel E.M. 2006. [Spontaneous Baccharis coridifolia (Compositae) poisoning in sheep.] Intoxicação espontânea por Baccharis coridifolia (Compositae) em ovinos. Pesquisa Veterinária Brasileira 26(1):21-25. Departamento de Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Cx. Postal 15094, Porto Alegre, RS 91540-000, Brazil. E-mail: moleta@terra.com.br An outbreak of Baccharis coridifolia (Compositae) poisoning in sheep is reported, which occurred in November 2004 in the county of Caxias do Sul, Rio Grande do Sul (RS), southern Brazil. From a herd of 212 sheep, coming from a Baccharis coridifolia free area, in the county of Jaguarão, RS, 35 sheep died until 5 days after the arrival in the new area where the plant was found with abundance. The clinical signs began 8 hours after introduction of the animals into the new pasture and included apathy, anorexia, abdominal retraction or mild distension, weakness of hind limbs, dry feces, sternal ou lateral decumbency, struggling movements, coma and death. Clinical evolution was from 5 to 48 hours. Other sheep that were already before on the pasture were not affected. Main necropsy findings were in the gastrointestinal tube, with wall and serosal oedema, mainly in the reticulo-ruminal fold and of the abomasum, reddening and detachment of the mucosa of forestomachs, and intense hemorrhage in the submucosa. Histopathological findings were degeneration and necrosis of the epithelium of the forestomachs with polymorphonuclear infiltration associated with bacterial colonies, congestion, hemorrhage and oedema, and lymphoid tissue necrosis.

Abstract in English:

Medeiros J.M., Tabosa I.M., Simões S.V.D., Nóbrega Jr J. E., Vasconcelos J.S. & Riet-Correa F. 2005. [Perinatal mortality in kids in the semiarid region of Paraíba, Brazil.] Mortalidade perinatal em cabritos no semi-árido da Paraíba. Pesquisa Veterinária Brasileira 25(4):201-206. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Campus de Patos, 58700-970 Patos, PB, Brazil. E-mail: riet@cstr.ufcg.edu.br The causes of perinatal kid mortality were studied from May 2002 to August 2004 in the semiarid region of Paraíba. In 118 necropsied kids the frequency of different causes of death were neonatal infections (50%), distocia (12.71%), hypothermia/starvation (11.86%), malformations (7.62%), floppy kid (6.77%) and abortions (1.69%). Regarding the time of death, 1.69% of the kids died before parturition, 16.94% during the parturition and 81.34 % after birth. The high occurrence of neonatal infections, dystocias, and hypothermia/starvation is probably to due to factors related with error in the sanitary, reproductive and nutritional management. Arthrogryposis of the forelimbs was the main malformation observed. This defect is endemic in goat flocks in the semi-arid of Brazil. Most deaths occurred after birth (25.42%) and from the 4th to the 28th day of life (38.98%) suggesting that care with the kids during their first 28 days of life is important for the improvement of the survival rate.

• Perinatal mortality kids semiarid region Brazil.

Abstract in Portuguese:

Medeiros J.M., Tabosa I.M., Simões S.V.D., Nóbrega Jr J. E., Vasconcelos J.S. & Riet-Correa F. 2005. [Perinatal mortality in kids in the semiarid region of Paraíba, Brazil.] Mortalidade perinatal em cabritos no semi-árido da Paraíba. Pesquisa Veterinária Brasileira 25(4):201-206. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Campus de Patos, 58700-970 Patos, PB, Brazil. E-mail: riet@cstr.ufcg.edu.br The causes of perinatal kid mortality were studied from May 2002 to August 2004 in the semiarid region of Paraíba. In 118 necropsied kids the frequency of different causes of death were neonatal infections (50%), distocia (12.71%), hypothermia/starvation (11.86%), malformations (7.62%), floppy kid (6.77%) and abortions (1.69%). Regarding the time of death, 1.69% of the kids died before parturition, 16.94% during the parturition and 81.34 % after birth. The high occurrence of neonatal infections, dystocias, and hypothermia/starvation is probably to due to factors related with error in the sanitary, reproductive and nutritional management. Arthrogryposis of the forelimbs was the main malformation observed. This defect is endemic in goat flocks in the semi-arid of Brazil. Most deaths occurred after birth (25.42%) and from the 4th to the 28th day of life (38.98%) suggesting that care with the kids during their first 28 days of life is important for the improvement of the survival rate.

Abstract in English:

Langohr I.M., Gava A. & Barros C.S.L. 2005. [Poisoning in cattle by Baccharidastrum triplinervium (Asteraceae).] Intoxicação por Baccharidastrum triplinervium (Asteraceae) em bovinos. Pesquisa Veterinária Brasileira 25(4):235-238. Animal Disease Diagnostic Laboratory, Purdue University, 406 South University, West Lafayette, IN 47907, Estados Unidos. E-mail: ilangohr@purdue.edu An outbreak of poisoning by Baccharidastrum triplinervium in cattle from Paraná, Brazil, is described. The disease occurred during a severe drought in early summer. The onset of clinical signs was two days after 50 cows and 8 heifers had been introduced into a pasture with high density of B. triplinervium that showed signs of having been consumed by the animals. Fifteen animals (9 cows and 6 heifers) got sick. Of these 15, two cows and four heifers died after a clinical course of 12-60 hours. Clinical signs included depression, ruminal atony, moderate bloat, marked dehydration, mild diarrhea and anorexia. The animals were restless, laying down and getting up constantly, remaining progressively longer periods in sternal recumbency. Once in that position, the animals had an extended head or the head turned to one of the sides of the body, and were groaning. Additionally, the cows had an abrupt fall in milk yield. The remaining affected cattle presented milder clinical signs and were partially back to their feed on the day following the onset of the clinical signs. The milk production was back to normal values within one week. The main gross lesions observed in two necropsied cows were in the forestomachs and abomasum, consisting of edema of the ruminal wall, as well as of diffuse reddening of the mucosae of the rumen, reticulum, abomasum and of some of the omasal folds. The main histological lesions included multifocal ballooning degeneration and necrosis of the lining epithelium of the rumen, associated with neutrophilic infiltrate. The diagnosis was based on the epidemiological data and on the experimental reproduction of the disease by force-feeding 3 bovine with the aeral fresh parts (20 and 30g/kg) of B. triplinervium. Chemical analysis of dried material from B. triplinervium harvested at the site of the outbreak was negative for macrocyclic trichothecenes.

• Poisonous plants Baccharidastrum triplinervium Asteraceae plant poisoning diseases of cattle pathology.

Abstract in Portuguese:

Langohr I.M., Gava A. & Barros C.S.L. 2005. [Poisoning in cattle by Baccharidastrum triplinervium (Asteraceae).] Intoxicação por Baccharidastrum triplinervium (Asteraceae) em bovinos. Pesquisa Veterinária Brasileira 25(4):235-238. Animal Disease Diagnostic Laboratory, Purdue University, 406 South University, West Lafayette, IN 47907, Estados Unidos. E-mail: ilangohr@purdue.edu An outbreak of poisoning by Baccharidastrum triplinervium in cattle from Paraná, Brazil, is described. The disease occurred during a severe drought in early summer. The onset of clinical signs was two days after 50 cows and 8 heifers had been introduced into a pasture with high density of B. triplinervium that showed signs of having been consumed by the animals. Fifteen animals (9 cows and 6 heifers) got sick. Of these 15, two cows and four heifers died after a clinical course of 12-60 hours. Clinical signs included depression, ruminal atony, moderate bloat, marked dehydration, mild diarrhea and anorexia. The animals were restless, laying down and getting up constantly, remaining progressively longer periods in sternal recumbency. Once in that position, the animals had an extended head or the head turned to one of the sides of the body, and were groaning. Additionally, the cows had an abrupt fall in milk yield. The remaining affected cattle presented milder clinical signs and were partially back to their feed on the day following the onset of the clinical signs. The milk production was back to normal values within one week. The main gross lesions observed in two necropsied cows were in the forestomachs and abomasum, consisting of edema of the ruminal wall, as well as of diffuse reddening of the mucosae of the rumen, reticulum, abomasum and of some of the omasal folds. The main histological lesions included multifocal ballooning degeneration and necrosis of the lining epithelium of the rumen, associated with neutrophilic infiltrate. The diagnosis was based on the epidemiological data and on the experimental reproduction of the disease by force-feeding 3 bovine with the aeral fresh parts (20 and 30g/kg) of B. triplinervium. Chemical analysis of dried material from B. triplinervium harvested at the site of the outbreak was negative for macrocyclic trichothecenes.

Abstract in English:

Rodrigues A., Fighera R.A., Souza T.M., Schild A.L., Soares M.P., Milano J. & Barros C.S.L. 2005. [Outbreaks of trypanosomiasis in horses by Trypanosoma evansi in the state of Rio Grande do Sul, Brazil: epidemiological, clinical, hematological, and pathological aspects.] Surtos de tripanossomíase por Trypanosoma evansi em eqüinos no Rio Grande do Sul: aspectos epidemiológicos, clínicos, hematológicos e patológicos. Pesquisa Veterinária Brasileira 25(4):239-249. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Cases of trypanosomiasis by Trypanosoma evansi were diagnosed in horses in the state of Rio Grande do Sul, Brazil, between 2003 and 2004. In one stud farm (Farm A) with 125 horses, 52 died. Additionally, around 80 mares were sent to Farm A to be bred. Of those, 66 became ill and 56 died after being returned to their farms of origin. Twenty one horses clinically affected by the disease were observed. Clinical signs included loss of weight (despite voracious appetite), lethargy, incoordination and instability of hindlimbs, atrophy of the large muscles of the hindlimbs, muscle weakness and paleness of mucosae. Specimens of T. evansi were detected in the blood drawn from four affected horses. Normocytic normochromic anemia with PCVs ranging from 15 to 31%, leucocytosis due to lymphocytosis associated to large atypical lymphocytes was observed in several affected horses. High levels of antibodies against T. evansi were detected in the serum of six horses from Farm A. Eight horses presented encephalic neurological signs such as circling, ataxia, blindness, excitation, falls, listlessness, proprioception deficits and head tilt. One horse assumed a “dog-seating position”. Necropsy findings included muscle atrophy, enlargement and lymphoid hyperplasia of the spleen and lymphnodes, edema and softening of the white and grey matter of the brain. Histologically, an overwhelming necrotizing panencephalitis was observed in the seven horses with encephalic signs. This panencephalitis was characterized by marked edema, demyelination and necrosis and perivascular infiltrates of 6-10 layers of lymphocytes and plasm cells affecting both the white and gray matter. Several plasm cells in the inflammatory infiltrate contained numerous eosinophilic globules in their cytoplasm (Mott cells). Similar histological lesions were observed in the spinal cord of the horse with the “dog-seating position”. The brains of five horses with the encephalic signs were submitted to immunohistochemistry stain by the streptavidin-biotin technique. In all of those five brains moderate to abundant specimens of T. evansi in the perivascular spaces and neuropile were marked by the specific antibody. Epidemiological, clinical, hematological, and pathological aspects of equine trypanosomiasis caused by T. evansi are discussed.

• Trypanosomiasis Trypanosoma evansi infectious diseases encephalitis hematology pathology diseases of horses.

Abstract in Portuguese:

Rodrigues A., Fighera R.A., Souza T.M., Schild A.L., Soares M.P., Milano J. & Barros C.S.L. 2005. [Outbreaks of trypanosomiasis in horses by Trypanosoma evansi in the state of Rio Grande do Sul, Brazil: epidemiological, clinical, hematological, and pathological aspects.] Surtos de tripanossomíase por Trypanosoma evansi em eqüinos no Rio Grande do Sul: aspectos epidemiológicos, clínicos, hematológicos e patológicos. Pesquisa Veterinária Brasileira 25(4):239-249. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Cases of trypanosomiasis by Trypanosoma evansi were diagnosed in horses in the state of Rio Grande do Sul, Brazil, between 2003 and 2004. In one stud farm (Farm A) with 125 horses, 52 died. Additionally, around 80 mares were sent to Farm A to be bred. Of those, 66 became ill and 56 died after being returned to their farms of origin. Twenty one horses clinically affected by the disease were observed. Clinical signs included loss of weight (despite voracious appetite), lethargy, incoordination and instability of hindlimbs, atrophy of the large muscles of the hindlimbs, muscle weakness and paleness of mucosae. Specimens of T. evansi were detected in the blood drawn from four affected horses. Normocytic normochromic anemia with PCVs ranging from 15 to 31%, leucocytosis due to lymphocytosis associated to large atypical lymphocytes was observed in several affected horses. High levels of antibodies against T. evansi were detected in the serum of six horses from Farm A. Eight horses presented encephalic neurological signs such as circling, ataxia, blindness, excitation, falls, listlessness, proprioception deficits and head tilt. One horse assumed a “dog-seating position”. Necropsy findings included muscle atrophy, enlargement and lymphoid hyperplasia of the spleen and lymphnodes, edema and softening of the white and grey matter of the brain. Histologically, an overwhelming necrotizing panencephalitis was observed in the seven horses with encephalic signs. This panencephalitis was characterized by marked edema, demyelination and necrosis and perivascular infiltrates of 6-10 layers of lymphocytes and plasm cells affecting both the white and gray matter. Several plasm cells in the inflammatory infiltrate contained numerous eosinophilic globules in their cytoplasm (Mott cells). Similar histological lesions were observed in the spinal cord of the horse with the “dog-seating position”. The brains of five horses with the encephalic signs were submitted to immunohistochemistry stain by the streptavidin-biotin technique. In all of those five brains moderate to abundant specimens of T. evansi in the perivascular spaces and neuropile were marked by the specific antibody. Epidemiological, clinical, hematological, and pathological aspects of equine trypanosomiasis caused by T. evansi are discussed.

Abstract in English:

Lima E.F., Riet-Correa F., Castro R.S., Gomes A.A.B. & Lima F.S. 2005. [Clinical signs, distribution of the lesions in the central nervous system and epidemiology of rabies in northeastern Brazil.] Sinais clínicos, distribuição das lesões no sistema nervoso e epidemiologia da raiva em herbívoros na região Nordeste do Brasil. Pesquisa Veterinária Brasileira 25(4):250-264. Centro de Saúde e Tecnologia Rural, Campus de Patos, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: riet@cstr.ufcg.br Twenty four outbreaks of rabies in cattle, 4 in horses, 2 in sheep, and 2 in goats are reported in northeastern Brazil. All outbreaks occurred in the state of Paraíba, except one in horses that occurred in the state of Rio Grande do Norte. All outbreaks, except one in sheep, were probably transmitted by vampire-bats, but the transmission by foxes (Dusicyon vetulus) is also possible. Clinical signs were characteristic for distribution of the lesions in the central nervous system (CNS). In cattle, signs were mainly of the paralytic form of rabies, caused by lesions on the spinal cord, brain stem and cerebellum; but some animals showed also depression, excitation and other signs due to cerebral lesions. In 3 out of 5 horses, the main clinical signs were due to lesions in the cerebrum, and 2 had the paralytic form. From 4 sheep and 2 goats affected, 4 showed clinical signs of the paralytic form; but in 1 goat and 1 sheep the main clinical signs were caused by cerebral lesions. All affected animals, except 1 goat, had a clinical manifestation period of 2-8 days. The only gross lesions were distention of the urinary bladder in 4 cattle and distention of the rectum in 2 others. Two horses had skin lesions due to traumatic injury. Histologic lesions were diffuse non-suppurative encephalomyelitis and meningitis. In the horses, and in one goat with a clinical manifestation period of 35 days, the lesions were more severe, with neuronal necrosis, neuronophagia, and presence of axonal spheroids. Negri bodies were found in 87% (20/23) of the cattle cases examined histologically. In small ruminants Negri bodies were found in 83% (5/6) of the cases. In sheep, goats and cattle, Negri bodies were more frequent in the cerebellum, but they were found also in brain stem, spinal cord and cerebrum. In horses, Negri bodies were found in small amounts only in the cortex of one animal, and in the cortex and hippocampus of another. Histologic lesions and Negri bodies in the trigeminal ganglia were less frequent than in the CNS. These results show that in rabies of herbivores, clinical signs and distribution of lesions in the CNS are variable, so that for the diagnosis and adequate clinical evaluation and the histologic study of different areas of the CNS are necessary. This also suggests that when the fluorescent antibody test and mouse inoculation test are negative, they should be repeated with samples from different areas of the brain and spinal cord. Frequency data of diseases from 4 diagnostic laboratories were used to estimate cattle deaths due to rabies in 3 Brazilian states. In Paraíba, with a population of 918,262 cattle, the annual death rate is estimated in 8,609 heads. In Mato Grosso do Sul, with a population of 23 millions cattle, deaths caused by rabies are estimated in 149,500 heads, and in Rio Grande do Sul, with a cattle population of 13 millions, cattle deaths due to rabies are estimated in 13,000 to 16,250 heads. If these data are used to estimate cattle losses in Brazil, with a cattle population of 195 millions, it can be estimated that 842,688 deaths are caused annually by rabies.

• Rabies cattle sheep goats horses pathology clinical signs economical impact.

Abstract in Portuguese:

Lima E.F., Riet-Correa F., Castro R.S., Gomes A.A.B. & Lima F.S. 2005. [Clinical signs, distribution of the lesions in the central nervous system and epidemiology of rabies in northeastern Brazil.] Sinais clínicos, distribuição das lesões no sistema nervoso e epidemiologia da raiva em herbívoros na região Nordeste do Brasil. Pesquisa Veterinária Brasileira 25(4):250-264. Centro de Saúde e Tecnologia Rural, Campus de Patos, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: riet@cstr.ufcg.br Twenty four outbreaks of rabies in cattle, 4 in horses, 2 in sheep, and 2 in goats are reported in northeastern Brazil. All outbreaks occurred in the state of Paraíba, except one in horses that occurred in the state of Rio Grande do Norte. All outbreaks, except one in sheep, were probably transmitted by vampire-bats, but the transmission by foxes (Dusicyon vetulus) is also possible. Clinical signs were characteristic for distribution of the lesions in the central nervous system (CNS). In cattle, signs were mainly of the paralytic form of rabies, caused by lesions on the spinal cord, brain stem and cerebellum; but some animals showed also depression, excitation and other signs due to cerebral lesions. In 3 out of 5 horses, the main clinical signs were due to lesions in the cerebrum, and 2 had the paralytic form. From 4 sheep and 2 goats affected, 4 showed clinical signs of the paralytic form; but in 1 goat and 1 sheep the main clinical signs were caused by cerebral lesions. All affected animals, except 1 goat, had a clinical manifestation period of 2-8 days. The only gross lesions were distention of the urinary bladder in 4 cattle and distention of the rectum in 2 others. Two horses had skin lesions due to traumatic injury. Histologic lesions were diffuse non-suppurative encephalomyelitis and meningitis. In the horses, and in one goat with a clinical manifestation period of 35 days, the lesions were more severe, with neuronal necrosis, neuronophagia, and presence of axonal spheroids. Negri bodies were found in 87% (20/23) of the cattle cases examined histologically. In small ruminants Negri bodies were found in 83% (5/6) of the cases. In sheep, goats and cattle, Negri bodies were more frequent in the cerebellum, but they were found also in brain stem, spinal cord and cerebrum. In horses, Negri bodies were found in small amounts only in the cortex of one animal, and in the cortex and hippocampus of another. Histologic lesions and Negri bodies in the trigeminal ganglia were less frequent than in the CNS. These results show that in rabies of herbivores, clinical signs and distribution of lesions in the CNS are variable, so that for the diagnosis and adequate clinical evaluation and the histologic study of different areas of the CNS are necessary. This also suggests that when the fluorescent antibody test and mouse inoculation test are negative, they should be repeated with samples from different areas of the brain and spinal cord. Frequency data of diseases from 4 diagnostic laboratories were used to estimate cattle deaths due to rabies in 3 Brazilian states. In Paraíba, with a population of 918,262 cattle, the annual death rate is estimated in 8,609 heads. In Mato Grosso do Sul, with a population of 23 millions cattle, deaths caused by rabies are estimated in 149,500 heads, and in Rio Grande do Sul, with a cattle population of 13 millions, cattle deaths due to rabies are estimated in 13,000 to 16,250 heads. If these data are used to estimate cattle losses in Brazil, with a cattle population of 195 millions, it can be estimated that 842,688 deaths are caused annually by rabies.

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:

Nóbrega Jr J.E., Riet-Correa F., Nóbrega R.S., Medeiros J.M., Vasconcelos J.S., Simões S.V.D. & Tabosa I.M. 2005. [Perinatal mortality of lambs in the semi-arid region of Paraíba, Brazil.] Mortalidade perinatal de cordeiros no semi-árido da Paraíba. Pesquisa Veterinária Brasileira 25(3):171-178. Centro de Saúde e Tecnologia Rural, UFCG, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: riet@cstr.ufcg.edu.br The causes of perinatal lamb mortality were studied, from March 2002 to October 2004, on 27 farms in the semiarid region of Paraíba, northeastern Brazil. In 90 lambs necropsied the following frequency of different causes of death was found: neonatal infections (41.1%), malformations (23.3%), dystocia (10%), starvation/hypothermia (10%), abortion (4.4%), and predation (2.2%). Regarding the time of death, 4.4% of the lambs died before parturition, 10% during parturition, 30% on the first day after parturition, 20% between the second and the third day, and 35.6% between the 4th and the 28th day after parturition. The assistance during parturition, umbilical disinfection of the neonates, colostrum ingestion between 2 and 6 hours after parturition, and keeping the ewes in healthy environmental conditions during and after parturition could improve lamb surviving. The high frequency of malformations in different breeds suggests that malformations are due to a toxic plant. The main defects were permanent flexure of the front legs, brachygnathia, cleft palate, and other head malformations. In a recent report the authors demonstrated the teratogenic effects of Mimosa tenuiflora, a very common plant in the semiarid region, which is probably the cause of those malformations. Lambs which died due to starvation/hypothermia and had low birth weight (1.37 ± 0.70kg), suggesting that a better nutrition of the ewe during the last trimester of gestation is a way to control this cause of lamb mortality. Considering that in the northeastern region, in most farms, the rams stay with the ewes during the whole year, the adoption of a breeding season would help to control the different causes of perinatal lamb mortality.

• Lamb mortality newborn lambs sheep production perinatal mortality.

Abstract in Portuguese:

Nóbrega Jr J.E., Riet-Correa F., Nóbrega R.S., Medeiros J.M., Vasconcelos J.S., Simões S.V.D. & Tabosa I.M. 2005. [Perinatal mortality of lambs in the semi-arid region of Paraíba, Brazil.] Mortalidade perinatal de cordeiros no semi-árido da Paraíba. Pesquisa Veterinária Brasileira 25(3):171-178. Centro de Saúde e Tecnologia Rural, UFCG, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: riet@cstr.ufcg.edu.br The causes of perinatal lamb mortality were studied, from March 2002 to October 2004, on 27 farms in the semiarid region of Paraíba, northeastern Brazil. In 90 lambs necropsied the following frequency of different causes of death was found: neonatal infections (41.1%), malformations (23.3%), dystocia (10%), starvation/hypothermia (10%), abortion (4.4%), and predation (2.2%). Regarding the time of death, 4.4% of the lambs died before parturition, 10% during parturition, 30% on the first day after parturition, 20% between the second and the third day, and 35.6% between the 4th and the 28th day after parturition. The assistance during parturition, umbilical disinfection of the neonates, colostrum ingestion between 2 and 6 hours after parturition, and keeping the ewes in healthy environmental conditions during and after parturition could improve lamb surviving. The high frequency of malformations in different breeds suggests that malformations are due to a toxic plant. The main defects were permanent flexure of the front legs, brachygnathia, cleft palate, and other head malformations. In a recent report the authors demonstrated the teratogenic effects of Mimosa tenuiflora, a very common plant in the semiarid region, which is probably the cause of those malformations. Lambs which died due to starvation/hypothermia and had low birth weight (1.37 ± 0.70kg), suggesting that a better nutrition of the ewe during the last trimester of gestation is a way to control this cause of lamb mortality. Considering that in the northeastern region, in most farms, the rams stay with the ewes during the whole year, the adoption of a breeding season would help to control the different causes of perinatal lamb mortality.