PESQUISA VETERINÁRIA BRASILEIRA

Abstract in English:

Lima E.F., Riet-Correa F., Tabosa I.M., Dantas A.F.M., Medeiros J.M. & Sucupira Júnior G. 2005. [Polioencephalomalacia in goats and sheep in the semiarid region of northeastern Brazil.] Polioencefalomalacia em caprinos e ovinos na região semi-árida do Nordeste do Brasil. Pesquisa Veterinária Brasileira 25(1):9-14. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: riet@cstr.ufcg.edu.br Seven outbreaks of polioencephalomalacia in goats and 3 in sheep are reported from the semiarid region of northeastern Brazil. Animals of different ages were affected in various seasons of the year. In 5 outbreaks the animals were supplemented with concentrate ration and in 5 others they were only grazing on pastures. In one outbreak sheep were supplemented with an energy-protein-mineral mixture containing 1.3% of sulfur flower. Clinical signs were characterized by blindness, depression, head pressing, circling, grinding of the teeth, incoordination, spastic paralysis, ataxia, depression of the palpebral and pupillary reflexes, lateral strabismus, nystagmus, and dilated pupils. Nine affected animals were treated with thiamine and dexamethasone; 7 of them recovered but 2 died. The diagnosis of the disease was based on the recovered animals after treatment and/or on the histologic lesions. The clinical course varied from 2 to 15 days. On three animals post-mortem examination was made. One had herniation of the cerebellum through the Foramen magnum and softening of the cerebral cortex. The cut surface of the cerebral cortex showed cavitation and yellowish discoloration. Another animal had only cerebellar herniation. In a third animal no gross lesions were observed. Histological changes in the 3 animals were laminar necrosis of the cerebral cortex, and in 2 malacia of the thalamus and the rostral colliculi was also observed. In 9 outbreaks the cause of the disease was not determined, but one was probably due to sulfur toxicosis caused by the high sulfur content of the energy-protein-mineral mixture containing 1.3% of sulfur flower (96% sulfur) and 30% chicken litter (0.39% sulfur).

• Polioencephalomalacia cortical necrosis goats sheep sulfur poisoning thiamine deficiency.

Abstract in Portuguese:

Lima E.F., Riet-Correa F., Tabosa I.M., Dantas A.F.M., Medeiros J.M. & Sucupira Júnior G. 2005. [Polioencephalomalacia in goats and sheep in the semiarid region of northeastern Brazil.] Polioencefalomalacia em caprinos e ovinos na região semi-árida do Nordeste do Brasil. Pesquisa Veterinária Brasileira 25(1):9-14. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: riet@cstr.ufcg.edu.br Seven outbreaks of polioencephalomalacia in goats and 3 in sheep are reported from the semiarid region of northeastern Brazil. Animals of different ages were affected in various seasons of the year. In 5 outbreaks the animals were supplemented with concentrate ration and in 5 others they were only grazing on pastures. In one outbreak sheep were supplemented with an energy-protein-mineral mixture containing 1.3% of sulfur flower. Clinical signs were characterized by blindness, depression, head pressing, circling, grinding of the teeth, incoordination, spastic paralysis, ataxia, depression of the palpebral and pupillary reflexes, lateral strabismus, nystagmus, and dilated pupils. Nine affected animals were treated with thiamine and dexamethasone; 7 of them recovered but 2 died. The diagnosis of the disease was based on the recovered animals after treatment and/or on the histologic lesions. The clinical course varied from 2 to 15 days. On three animals post-mortem examination was made. One had herniation of the cerebellum through the Foramen magnum and softening of the cerebral cortex. The cut surface of the cerebral cortex showed cavitation and yellowish discoloration. Another animal had only cerebellar herniation. In a third animal no gross lesions were observed. Histological changes in the 3 animals were laminar necrosis of the cerebral cortex, and in 2 malacia of the thalamus and the rostral colliculi was also observed. In 9 outbreaks the cause of the disease was not determined, but one was probably due to sulfur toxicosis caused by the high sulfur content of the energy-protein-mineral mixture containing 1.3% of sulfur flower (96% sulfur) and 30% chicken litter (0.39% sulfur).

Abstract in English:

Elias F., Schild A.L. & Riet-Correa F. 2004. [Bovine herpesvirus type-5 meningoencephalitis and malacia: histological lesions distribution in the central nervous system of naturally infected cattle.] Meningoencefalite e encefalomalacia por Herpesvírus bovino-5: distribuição das lesões no sistema nervoso central de bovinos naturalmente infectados. Pesquisa Veterinária Brasileira 24(3):123-131. Laboratório Regional de Diagnóstico, Faculdade de Veterinária, UFPel, Cx. Postal 354, Pelotas, RS 96010-900, Brazil. E-mail: alschild@terra.com.br The distribution of the histological lesions in the central nervous system (CNS) of cattle naturally infected by bovine herpes virus type-5 (BHV-5) was determined in 12 affected calves from 10 outbreaks of the disease diagnosed by the Regional Diagnostic Laboratory (LRD) at Pelotas University, from 1986 to 2003. The epidemiological data, clinical signs and duration of clinical course were obtained from the files of LRD. Transversal sections were performed at different levels in 10% formalin-fixed CNS. The sections were made in the frontal, parietal, temporal e occipital lobes of the telencephalic hemispheres, basal ganglia and internal capsule, thalamus, anterior colliculus, pons, cerebellar peduncles, cerebellum, medulla oblongata and cervical spinal cord. Paraffin embedded tissues were sectioned and stained with hematoxylin and eosin. The severity and distribution of the inflammatory and malacic lesions were evaluated in all sections. These lesions were related with the epidemiological and clinical aspects of the disease. The outbreaks of the disease were observed in different seasons of the year. Affected animals were 2 to 24-month-old, of different breeds and both sexes. Gross lesions characterized by yellow and depressed areas in the cerebral cortex were observed in five calves. In two of them, similar lesions were additionally observed in thalamus, basal nuclei, and internal capsule. Congestion and multifocal hemorrhages were observed in most cases. The histological lesions were characterized by non-suppurative meningoencephalitis in all sections of CNS, but more severe in the frontal cortex. Focal or widespread malacia with infiltration of Gitter cells were observed in all sections of cerebral cortex, basal ganglia, internal capsule, and thalamus. In some cases mild malacia was also observed in the rostral colliculi, pons, medulla, cerebellum and cervical spinal cord. Intranuclear inclusion bodies were seen in all cases studied; they were frequent in regions of the cerebral cortex near mild to moderate inflammatory or malacic lesions. In two cases the inclusion bodies were also seen in the basal ganglia and thalamus. The severity of the histological lesions was not proportional with the clinical course of the disease. The presence of lesions of malacia in different regions of the CNS, an aspect not mentioned in most reports of BHV-5 infections, could be due to variable pathogenicity of different virus isolates. Alternatively, it is possible that BHV-5 encephalitis occurs due to the reactivation of the virus in cattle previously affected by polioencefalomacia; this last sequence of events was already demonstrated experimentally by our research group.

• Bovine herpesvirus type-5 BHV-5 cattle meningoencephalitis polioencephalomalacia.

Abstract in Portuguese:

Elias F., Schild A.L. & Riet-Correa F. 2004. [Bovine herpesvirus type-5 meningoencephalitis and malacia: histological lesions distribution in the central nervous system of naturally infected cattle.] Meningoencefalite e encefalomalacia por Herpesvírus bovino-5: distribuição das lesões no sistema nervoso central de bovinos naturalmente infectados. Pesquisa Veterinária Brasileira 24(3):123-131. Laboratório Regional de Diagnóstico, Faculdade de Veterinária, UFPel, Cx. Postal 354, Pelotas, RS 96010-900, Brazil. E-mail: alschild@terra.com.br The distribution of the histological lesions in the central nervous system (CNS) of cattle naturally infected by bovine herpes virus type-5 (BHV-5) was determined in 12 affected calves from 10 outbreaks of the disease diagnosed by the Regional Diagnostic Laboratory (LRD) at Pelotas University, from 1986 to 2003. The epidemiological data, clinical signs and duration of clinical course were obtained from the files of LRD. Transversal sections were performed at different levels in 10% formalin-fixed CNS. The sections were made in the frontal, parietal, temporal e occipital lobes of the telencephalic hemispheres, basal ganglia and internal capsule, thalamus, anterior colliculus, pons, cerebellar peduncles, cerebellum, medulla oblongata and cervical spinal cord. Paraffin embedded tissues were sectioned and stained with hematoxylin and eosin. The severity and distribution of the inflammatory and malacic lesions were evaluated in all sections. These lesions were related with the epidemiological and clinical aspects of the disease. The outbreaks of the disease were observed in different seasons of the year. Affected animals were 2 to 24-month-old, of different breeds and both sexes. Gross lesions characterized by yellow and depressed areas in the cerebral cortex were observed in five calves. In two of them, similar lesions were additionally observed in thalamus, basal nuclei, and internal capsule. Congestion and multifocal hemorrhages were observed in most cases. The histological lesions were characterized by non-suppurative meningoencephalitis in all sections of CNS, but more severe in the frontal cortex. Focal or widespread malacia with infiltration of Gitter cells were observed in all sections of cerebral cortex, basal ganglia, internal capsule, and thalamus. In some cases mild malacia was also observed in the rostral colliculi, pons, medulla, cerebellum and cervical spinal cord. Intranuclear inclusion bodies were seen in all cases studied; they were frequent in regions of the cerebral cortex near mild to moderate inflammatory or malacic lesions. In two cases the inclusion bodies were also seen in the basal ganglia and thalamus. The severity of the histological lesions was not proportional with the clinical course of the disease. The presence of lesions of malacia in different regions of the CNS, an aspect not mentioned in most reports of BHV-5 infections, could be due to variable pathogenicity of different virus isolates. Alternatively, it is possible that BHV-5 encephalitis occurs due to the reactivation of the virus in cattle previously affected by polioencefalomacia; this last sequence of events was already demonstrated experimentally by our research group.

Abstract in English:

ABSTRACT.- Nakano L., Lemos R.A.A. & Riet-Correa F. 2000. [Polioencephalomalacia in cattle in the states of Mato Grosso do Sul and São Paulo.] Polioencefalomalacia em bovinos nos estados de Mato Grosso do Sul e São Paulo. Pesquisa Veterinária Brasileira 20(3):119-125. Depto Patologia, Fac. Veterinária, Universidade Federal de Pelotas, 96010-900 Pelotas, RS, Brazil. Thirty outbreaks of polioencephalomalacia (PEM) were diagnosed from August 1993 to October 1997. Twenty nine occurred in the state of Mato Grosso do Sul and one in São Paulo. The disease affected cattle from 4 months to 7 years of age. Morbidity rates ranged from 0.02% to 14.28% and case fatalities from 42.5 % to 100%. The disease was not seasonal. All outbreaks occurred in cattle grazing Brachiaria spp, except one affecting feedlot cattle. Only neurologic signs were observed, and the course of the disease varied from 12 hours to 4 days in untreated cattle. Most animals treated with thiamine anel dexamethazone recovered. Moderate cerebral edema was observed at necropsy. Cell changes were characterized by laminar necrosis and gitter cells. In two cases moderate cortical anel submeningeal hemorrhages were observed. Nine cases had perivascular anel submeningeal infiltrations by eosinophils. Sodium ion concentration of the cerebrospinal fluid was elevated in one case. The cause of PEM in the region was not determined, but the results suggest that in some cases sodium chloride intoxication/water deprivation could play a role in the etiology of the disease. PEM represents 4.78% of cattle disease diagnosed at the Pathology Laboratory of the Federal University of Mato Grosso do Sul.

• Polioencephalomalacia cerebrocortical necrosis cattle thiamine salt Polioencefalomalacia necrose cerebrocortícal bovino tiamina sal.

Abstract in Portuguese:

RESUMO.- Nakano L., Lemos R.A.A. & Riet-Correa F. 2000. [Polioencephalomalacia in cattle in the states of Mato Grosso do Sul and São Paulo.] Polioencefalomalacia em bovinos nos estados de Mato Grosso do Sul e São Paulo. Pesquisa Veterinária Brasileira 20(3):119-125. Depto Patologia, Fac. Veterinária, Universidade Federal de Pelotas, 96010-900 Pelotas, RS, Brazil. Trinta focos de polioencefalomalacia (PEM) foram diagnosticados no período de agosto de 1993 a outubro de 1997. Vinte e nove focos ocorreram no estado de Mato Grosso do Sul (MS) e um no estado de São Paulo (SP). Foram afetados bovinos de 4 a 84 meses de idade. A morbidade dos rebanhos afetados variou ele 0,02% a 14,28% e a letalidade de 42,5% a 100%. A doença não apresentou uma sazonalidade e ocorreu em vários municípios do MS. Em todos os focos estudados os animais afetados eram criados em regimes de criação extensiva, com exceção de um foco. Os sinais clínicos observados foram exclusivamente nervosos e a evolução dos casos variou de 12 horas a 4 dias. A maioria dos animais tratados com tiamina e dexametasona recuperou-se. Histologicamente, as lesões consistiam de necrose laminar do córtex cerebral. Adicionalmente em 2 casos observaram-se hemorragias submeningeanas e corticais, e em 9 casos presença ele infiltrado de eosinófilos. A dosagem de sódio no líquor apresentou-se elevada em um caso. A etiologia da PEM não está esclarecida, porém em alguns casos a intoxicação por cloreto de sódio/privação de água pode estar envolvida na etiologia da enfermidade. A PEM representa 4,78% dos casos ele enfermidades de bovinos diagnosticadas no Laboratório de Anatomia Patológica da UFMS. Com bases nos resultados, verifica-se a importância da enfermidade no diagnóstico diferencial de outras doenças com quadro clínico neurológico no MS, principalmente a raiva, a meningoencefalite por herpesvírus bovino tipo 5 (HVB-5) e o botulismo.

Abstract in English:

ABSTRACT.- Lemos K.R. & Alessi A.C. 1999. [Glial fibrillary acidic protein (GFAP) immunoreactive astrocytes in the Central Nervous System of normal horses and horses with leukoencephalomalacia.] Astrócitos imunorreativos à proteína glial fibrilar ácida (GFAP) em sistema nervoso central de equinos normais e de equinos com leucoencefalomalácia. Pesquisa Veterinária Brasileira 19(3/4):104-108. Depto Patologia Veterinária, Faculdade de Ciências Agrárias e Veterinárias, Unesp, Rod. Carlos Tonanni Km 5, Jaboticabal, SP 14870-000, Brazil. The glial fibrillary acidic protein (GFAP), subunit of the intermediary filaments of the cellular cytoskeleton, exists in the cytoplasm of astrocytes. Immunohistochemistry utilizing primary antibodies anti-GFAP is generally chosen to identify astrocytes in the central nervous system (CNS), allowing also to verify their hypertrophy. Several studies show the distribution, morphology and cytoarchitecture of the astrocytes in several areas of the CNS of humans and laboratory animals. However, in domestic animals, especially in horses, little information is available. In the present study the density ánd morphology of GFAP-immunoreactive astrocytes in the white matter of the cerebral cortex of horses with leukoencephalomalacia (LEM) has been compared with such aspects in normal horses. In animals with LEM hypertrophic astrocytes in areas dose to the lesions were observed. There was enlargement of the perikarion, nucleus and the cytoplasmic extension. The astrocytes were reduced in number and the immunoreactivity was increased. In the normal animals constant distribution of immunoreactive cells characteristic of fibrous astrocytes was seen. Vascular changes in the animals with LEM, as for example degeneration of vascular endothelium, were also observed and could be correlated with the astrocytic alterations.

• Astrocytes GFAP horse leukoencephalomalacia Astrócito equino Ieucoencefalomalácia.

Abstract in Portuguese:

RESUMO.- Lemos K.R. & Alessi A.C. 1999. [Glial fibrillary acidic protein (GFAP) immunoreactive astrocytes in the Central Nervous System of normal horses and horses with leukoencephalomalacia.] Astrócitos imunorreativos à proteína glial fibrilar ácida (GFAP) em sistema nervoso central de equinos normais e de equinos com leucoencefalomalácia. Pesquisa Veterinária Brasileira 19(3/4):104-108. Depto Patologia Veterinária, Faculdade de Ciências Agrárias e Veterinárias, Unesp, Rod. Carlos Tonanni Km 5, Jaboticabal, SP 14870-000, Brazil. A proteína glial fibrilar ácida (GFAP), subunidade dos filamentos intermediários do citoesqueleto celular, está presente no citoplasma de astrócitos. Técnicas imunohistoquímicas com anticorpos primários anti-GFAP são geralmente empregadas para identificar astrócitos no sistema nervoso, permitindo verificar também sua hipertrofia. Vários estudos mostram a distribuição, á morfologia e a citoarquitetura de astrócitos em várias regiões do SNC do homem e de animais de laboratório. No entanto, em animais domésticos e, especialmente em equinos, poucas informações estão disponíveis. No presente trabalho, verificou-se a densidade e a morfologia de astrócitos imunorreativos à GFAP na substância branca da córtex cerebral de equinos com leucoencefalomalácia (LEM) comparando-se esses aspectos com o de equinos normais. Animais com LEM apresentaram hipertrofia de astrócitos em áreas próximas às lesões, representada pelo aumento do corpo celular, do núcleo e dos prolongamentos citoplasmáticos. O número de astrócitos apresentou-se reduzido e a imunorreatividade foi mais acentuada. Nos animais normais, verificou-se distribuição constante de astrócitos imunorreagentes com características de fibrosos. Alterações vasculares nos animais com LEM, como por exemplo degeneração de endotélio vascular, também foram observadas, podendo estar associadas às alterações astrocíticas.

Abstract in English:

An outbreak of equine leukoencephalomalacia, associated with moldy corn poisoning occuring during the months of Juné-July in Rio Grande do Sul, is described. Ten horses from 4 different farms in Lavras do Sul county were affected. Clinical signs irtcluded anorexia, circling, head pressing, blindness, ataxia, recumbency and death. All affected horses died within a period of 13-22 hours after the onset of clinical signs. Post-mortem examination was performed in 3 horses. Lesions were restricted to the central nervous system. The most striking gross lesions were focal areas of softening and cavitation of the cerebral white matter. These areas were surroundeci by multiple minute hemorrhagic foci. Histopathological examination revealed these areas of cavitation to consist of hollow spaces surrounded by malacic, hemorrhagic and edematous neuropile. Other microscopic brain lesions included generalized hypertrophic and degenerative changes of the vascular endothelia, perivascular hemorrhages and edema; presence of perivascular eosinophilic globules; edema of the white matter; sludging, margination and pavimentation of leukocytes and mild perivascular cuffings consisting mainly of polimorphonuclear granulocytes, neutrnphils and eosinophils. Fusarium moni/iforme was isolated from the corn used to feed the horses: It is suggested that a primary vascular change is the early event in the pathogenesis of the overt malacic foci.

• Equine leukoencephalomalacia mycotoxicosis moldy corn poisoning equine diseases Fusarium moniliforme

Abstract in Portuguese:

É descrito um surto de ·leucoencefalomalácia associada a ingestão de milho mofado que ocorreu em equinos durante os meses de junho-julho de 1983 no Rio Grande do Sul. Dez cavalos oriundos de 4 diferentes estabelecimentos no município de Lavras do Sul foram afetados. Os sinais clínicos consistiam em anorexia, andar em círculos, pressão da cabeça contra objetos, cegueira, ataxia, decúbito e morte. Todos os eqüinos afetados morreram de 13 a 22 horas após o início dos sintomas. Foram realizadas necropsias em 3 animais. As lesões encontradas restringiam-se ao sistema nervoso central. A lesão macroscópica mais evidente era representada por áreas focais de amolecimento e cavitação da substância branca do cérebro. Essas áreas eram cercadas por vários pequeninos focos hemorrágicos. Ao exame histopatológico, essas áreas consistiam em cavidades vazias cercadas por tecido nervoso necrótico-hemorrágico e edematoso. Outras alterações microscópicas observadas no cérebro foram alterações hipertróficas e degenerativas generalizadas do endotélio vascular, hemorragias e edema perivasculares, presença de glóbulos eosinofílicos no espaço de Virchow-Robin, edema da substância branca, marginação e pavimentação leucocitária e discretos manguitos perivasculares constituídos principalmente de neutrófilos e eosinófilos. O fungo Fusarium moniliforme foi isolado do milho obtido da alimentação dos cavalos. Sugere-se que uma alteração vascular primária seja o evento inicial na patogenia das áreas de malácia.

• Leucoencefalomalácia eqüina micotoxicose intoxicação por milho mofado doença de eqüino Fusarium moniliforme

Abstract in English:

Three cases of spontaneously occurring polioencephalomalacia (cerebrocortical necrosis) of cattle in Rio Grande do Sul, Brazil, are described. The affected animals ranged in. age from 8 to 12 months and were from different areas of the State. Clinical findings included anorexia, salivation, incoordination (ataxia), circling, blindness and opisthotonus. Two of the animals died 4 days after the appearance of clinical signs. Lesions in the central nervous system consisted of depressed, asymetrical, yellow or reddish areas in the cortex of both cerebral hemispheres. Histopathological examination of those areas revealed liquefaction of the gray inatter associated with perivascular infiltration of mononuclear cells. Hemmorrhagic lesions were observed in one case. One of the affected animals recovered after being treated with thiamine.

• Polioencephalomalacia cerebrocortical necrosis liquefactive necrosis cattle pathology

Abstract in Portuguese:

É descrita a ocorrência da polioencefalomalácia (necrose córtico-cerebral) em três bovinos do Rio Grande do Sul, Brasil. Os animais, com idades de 8 e 12 meses, procedentes de diferentes regiões do Estado, mostravam inapetência, salivação, incoordenação de movimentos, andar em círculo, cegueira e·opistótono. A morte de dois animais ocorreu 4 dias apôs o início dos sintomas. As lesões do sistema nervoso central consistiam em áreas deprimidas e assimétricas, de cor amarelada ou avermelhada, atingindo o córtex de ambos os hemisférios cerebrais. Estas lesões correspondiam, microscopicamente, a áreas de necrose de liquefação da substância cinzenta do córtex, associadas a infiltrado inflamatório linfocitário e, em um caso, a hemorragia. Um dos animais doentes recuperou-se apôs o tratamento com tiamina o que encorajou os autores a acreditarem que também na etiologia desses casos, a deficiência desta vitamina esteja envolvida.

• Polioencefalomalácia necrose córticocerebral necrose por liquefação bovinos patologia

Abstract in English:

Three outbreaks of equine leukoencephalomalacia in three counties in Rio Grande do Sul are described. All cases occurred during the wiriter and were associated with the consumption of moldy corn. Fusarium monüiforme was isolated from corn collected during one of the outbreaks. Gross pathological examination showed liquefactive necrosis of the white matter of the cerebral hemispheres. Histopathological changes in the entral nervous system were characterized by myelin and vascular degeneration, hemorraghes, edema, and perivascular cuffing with neutrophils, plasma cells, lymphocytes, macrophages and eosinophilis. The most severe alterations were localized in the white matter of the cer.ebral hemispheres. The vascular lesions and demyelinization found in the grey rnatter of the cerebral cortex, thalamus; colliculi and internal capsule were less severe. Lesions in the cerebellum, pons and medulla were discrete. The meninges were edematous, hemorraghic and infiltrated with inflamrnatory cells.

• Equine leukoencephalomalacia poisoning mycotoxicosis moldy corn Fusarium moniliforme

Abstract in Portuguese:

Descrevem-se três surtos de leucoencefalomalácia em eqüinos no Rio Grande do Sul. Todos os surtos ocorreram durante o inverno e foram associados à ingestão de milho mofado. Em um deles foi realizado o isolamento de Fusarium moniliforme do milho que estava sendo ingerido pelos animais. As lesões macroscópicas estiveram caracterizadas por necrose coliquativa da substância branca dos hemisférios cerebrais. As lesões histológicas do sistema nervoso central caracterizam-se por: desmielinização, edema, hemorragias, degeneração hialina das paredes vasculares e infiltração perivascular por neutrófilos, plasmócitos, linfócitos, macrófagos e eosinófilos. As lesões mais severas estavam localizadas na substância branca dos hemisférios cerebrais. Na substância cinzenta da córtex cerebral, tálamo, tubérculos quadrigêmeos e cápsula interna observaram-se lesões vasculares e desmielinização mais discretas que as da substância branca dos hemisférios cerebrais. No cerebelo, ponte e medula as lesões vasculares eram discretas não se observando lesões de desmielinização. As meninges apresentaram lesões vasculares severas, infiltração por celulas inflamatórias, edemas e hemorragias.

• Eqüinos leucoencefalomalácia intoxicação micotoxicose milho mofado Fusarium moniliforme