Intoxicação espontânea e experimental por nitrato/nitrito em bovinos alimentados com Avena sativa (aveia) e/ou Lolium spp. (azevém) / Spontaneous and experimental poisoning by nitrate/nitrite in cattle fed Avena sativa (oat) and/or Lolium spp. (ryegrass)

Descrevem-se os dados epidemiológicos, sinais clínicos e lesões da intoxicação espontânea e experimental por nitrato e nitrito em bovinos alimentados com pastagens de Avena sativa (aveia) e/ou Lolium spp (azevém). A enfermidade ocorre em diferentes regiões do Estado de Santa Catarina, quando as pastagens tem crescimento exuberante, após receberem quantidades excessivas de adubo químico e/ou orgânico, principalmente quando ocorrem condições climáticas de seca e posteriormente chuva. Os animais em contato com essas pastagens desenvolvem rapidamente mucosas de coloração marrom, taquipnéia, andar cambaleante, micção frequente, timpanismo, decúbito lateral e morte em poucos minutos, ou recuperação algumas horas após. Na necropsia de quatro animais que adoeceram espontaneamente, as principais alterações encontradas foram a coloração marrom das mucosas, a cor escura do sangue (cor de chocolate) e a coloração vermelho intensa da musculatura esquelética e do miocárdio esquerdo. A reprodução experimental da doença foi realizada em sete bovinos, com pastagens de quatro propriedades onde ocorreu adoença. Aveia e/ou azevém verdes e sob a forma de feno foram administradas aos bovinos. Destes bovinos quatro morreram, dois adoeceram e se recuperam, um naturalmente e outro com a aplicação de azul de metileno a 1%, na dose de 2mg/kg/peso vivo, e um bovino não apresentou alterações. Os sinais clínicos observados e as lesões nos animais que adoeceram e morreram foram idênticos aos casos naturais. Alterações microscópicas não foram observadas nos casos naturais e experimentais. O teste da difenilamina nas amostras de pastagens onde ocorreram os surtos resultou positivo em todas as propriedades. A análise bromatológica realizada em amostras coletadas de várias propriedades em que ocorreram surtos revelou de 0,30 a 3,36% de nitrato na matéria seca. A enfermidade caracterizou-se principalmente por respiração ofegante, sangue de coloração escura, mucosas de coloração marrom e morte rápida dos bovinos e está relacionada á ingestão de pastagens de aveia e/ou azevém super adubados, que acumularam alto teor de nitrato, após um período de chuvas precedido de seca.

Epidemiological data, clinical and pathological findings of the spontaneous andexperimental poisoning by nitrate and nitrite in cattle fed oats (Avena sativa) and/or ryegrass (Lolium spp.), diphenylamine test, and the nitrate content in the samples of the pasture where the outbreaks occurred, are described. The disease occurs in different regions of the State of Santa Catarina, in which pastures have exuberant growth, after receiving excessive amounts of chemical and/or organic fertilizer, mainly when raining occurs after a period of dry wheather. The animals grazing these pastures quickly develop brown mucosa, tachypnea, staggering gait, frequent urination, bloating, lateral recumbency and death in few minutes or hours. At necropsy of four animals that died spontaneously, the main lesions found were brown mucosa, dark color of the blood (chocolate), intense red color of the skeletal muscles and of the left part of the myocardium. The experimental reproduction of the disease was performed in seven cattle, with pastures from four farms where the disease occurred. The animals were fed with fresh oats and ryegrass and/or hay of it. Four animals died, two became ill and recovered, and one was treated with 2mg/kg per body weight of methylene blue 1%, and one cattle did not show changes. Clinical signs and lesions of the diseased animals that died were similar to natural cases. Microscopic changes were not observed in spontaneous and experimental poisoning. The diphenylamine test was positive in all the farms where the outbreaks occurred. The chemical analysis performed on samples of the pastures from several farms, in which outbreaks of the disease occurred, ranged from 0.30to 3.36% of nitrate in the dry matter. The disease is associated with the ingestion of oats and/or ryegrass pastures heavily fertilized, which accumulates high levels of nitrate after a period of rain and is characterized by rapid breathing, dark-colored blood, brown mucous and rapid death.

Biotransformation approaches to alleviate the effects induced by fusarium mycotoxins in swine.

Mycotoxin mitigation is of major interest as ingestion of mycotoxins results in poor animal health, decreased productivity, as well as substantial economic losses. A feed additive (FA) consisting of a combination of bacteria (Eubacterium BBSH797) and enzyme (fumonisin esterase FumD) was tested in pigs for its ability to neutralize the effects of mono- and co-contaminated diets with deoxynivalenol (DON) and fumonisins (FB) on hematology, biochemistry, tissue morphology, and immune response. Forty-eight animals, allocated into eight groups, received one of eight diets for 35 days: a control diet, a diet contaminated with either DON (3 mg/kg) or FB (6 mg/kg), or both toxins, and the same four diets with FA. Inclusion of FA restored the circulating number of neutrophils of piglets fed the FB and DON + FB diets. Similarly, FA counteracted the minor changes observed on plasma concentrations of albumin and creatinine. In lung, the lesions induced by the ingestion of FB in mono- and co-contaminated diets were no longer observed after addition of FA in these diets. Lesions recorded in the liver of pigs fed either of the contaminated diets with FA were partly reduced, and the increased hepatocyte proliferation was totally neutralized when FA was present in the co-contaminated diet. After 35 days of exposure, the development of the vaccinal response was significantly improved in animals fed diets supplemented with FA, as shown by results of lymphocyte proliferation, cytokine expression in spleen, and the production of specific Ig. Similarly, in jejunum of animals fed diets with FA, occurrence of lesions and upregulation of pro-inflammatory cytokines were much less obvious. The ameliorative effects provided by FA suggest that this approach would be suitable in the control of DON and FB that commonly co-occur in feed.

The emerging mycotoxin, enniatin B1, down-modulates the gastrointestinal toxicity of T-2 toxin in vitro on intestinal epithelial cells and ex vivo on intestinal explants.

Enniatins, the most prevalent emerging mycotoxins, represent an emerging food safety issue, because of their common co-occurrence with other fusariotoxins such as trichothecenes co-produced by Fusarium spp on field grains and because of their extensive prevalence in grains. In this study, the intestinal toxicity of enniatin B1 (ENN) alone and mixed with the most toxic trichothecene T-2 toxin (T2) was characterized by using two biological models from pig, the most sensitive species: the intestinal cell line IPEC1 (in vitro exposure) and jejunal explants (ex vivo exposure). Dose-dependent decreases in cell proliferation in IPEC1 and in the histopathological scores of explants were observed for ENN at µM-levels and for T2 at nM-levels, with IC50 values for ENN of 15.8 and 29.7 µM, and for T2 of 9.3 and 15.1 nM in vitro and ex vivo, respectively. Interaction analysis by probabilistic and by determinist approaches showed a less than additive effect both in vitro and ex vivo, at IC50 values, with increasing antagonism with decreasing concentrations of toxins. The results obtained by the determinist median-effect dose analysis and by the nonlinear regression analysis were concordant. All the median-effect doses estimated for IPEC cells were included in the IC50 confidence intervals of the nonlinear regression fitting. Given the occurrence of enniatins, potential synergy following the co-occurrence of enniatins and the major fusariotoxins, especially trichothecene B deoxynivalenol should be investigated.

The food contaminant deoxynivalenol activates the mitogen activated protein kinases in the intestine: interest of ex vivo models as an alternative to in vivo experiments.

Trichothecenes induce changes in the intestinal barrier function through decreased expression of cell junction proteins and apoptosis of enterocytes. The mitogen activated protein kinases (MAPK) play an important role in the signaling pathways of cell turnover and differentiation. Using ex vivo and in vivo approaches, the purpose of this study was to investigate the ability of low doses of DON to induce histological changes in the intestine and to activate the MAPK ERK 1/2, p38 and JNK. Twelve weaning piglets received during four weeks a control diet or a DON-contaminated diet (2.3 mg DON/kg feed). Six weaning piglets were used to prepare jejunal explants (ex vivo model). Explants were exposed during 4 h to vehicle, 5 or 10 µM DON. Intestinal changes were graded using a histological score. Pigs fed a DON-diet and explants exposed to DON showed a significant decrease in the jejunal score. In both models, the toxin significantly enhanced phosphorylation of ERK 1/2 and p38, whereas the increased phosphorylation of JNK was non significant. Taken together these results indicate that in vivo or ex vivo exposure of intestinal tissue to DON lead to similar intestinal lesions and activation of MAPK. These effects could impair the homeostasis of intestinal tissue in the aspects of barrier function and immune protection. The similarity of the in vivo and ex vivo results provides also strong evidence that the jejunal explant model is a good alternative for toxicological studies in intestinal tissue.

Toxicity of deoxynivalenol and its acetylated derivatives on the intestine: differential effects on morphology, barrier function, tight junction proteins, and mitogen-activated protein kinases.

The intestinal epithelium is the first barrier against food contaminants and is highly sensitive to mycotoxins, especially de oxynivalenol (DON). Consumption of DON-contaminated food is associated with outbreaks of gastroenteritis. In cereals and their byproducts, DON is present together with two acetylated derivatives, 3-ADON and 15-ADON. The aim of this study was to compare the intestinal toxicity of DON and A-DONs, using noncytotoxic doses. The toxicity was assessed using in vitro (intestinal epithelial cell line), ex vivo (intestinal explants), and in vivo (animals exposed to mycotoxin-contaminated diets) models. The effects were studied on cell proliferation, barrier function, and intestinal structure. The mechanism of toxicity was investigated by measuring the expression of the tight junction proteins and of phosphorylated ERK1/2, p38, and JNK, which are effectors of signaling pathway involved in cellular programs including embryogenesis, proliferation, differentiation, and apoptosis. On proliferating cells, 3-ADON was less toxic than DON, which was less toxic than 15-ADON. On differentiated cells, 15-ADON impaired the barrier function, whereas DON and 3-ADON did not have a significant effect. Similarly, ex vivo and in vivo, 15-ADON caused more histological lesions than DON or 3-ADON. At the molecular level, the 15-ADON activated the mitogen-activated protein kinases (MAPK) ERK1/2, p38, and JNK in the intestinal cell line, explants, and the jejunum from exposed animals at lower dose than DON and 3-ADON. Our results show that the higher toxicity of 15-DON is due to its ability to activate the MAPK. Given that cereal-based foods are contaminated with DON and acetylated-DON, the higher toxicity of 15-ADON should be taken into account.

Chronic ingestion of deoxynivalenol and fumonisin, alone or in interaction, induces morphological and immunological changes in the intestine of piglets.

Deoxynivalenol (DON) and fumonisins (FB) are mycotoxins produced by Fusarium species, which naturally co-occur in animal diets. The gastrointestinal tract represents the first barrier met by exogenous food/feed compounds. The purpose of the present study was to investigate the effects of DON and FB, alone and in combination, on some intestinal parameters, including morphology, histology, expression of cytokines and junction proteins. A total of twenty-four 5-week-old piglets were randomly assigned to four different groups, receiving separate diets for 5 weeks: a control diet; a diet contaminated with either DON (3 mg/kg) or FB (6 mg/kg); or both toxins. Chronic ingestion of these contaminated diets induced morphological and histological changes, as shown by the atrophy and fusion of villi, the decreased villi height and cell proliferation in the jejunum, and by the reduced number of goblet cells and lymphocytes. At the end of the experiment, the expression levels of several cytokines were measured by RT-PCR and some of them (TNF-α, IL-1ß, IFN-γ, IL-6 and IL-10) were significantly up-regulated in the ileum or the jejunum. In addition, the ingestion of contaminated diets reduced the expression of the adherent junction protein E-cadherin and the tight junction protein occludin in the intestine. When animals were fed with a co-contaminated diet (DON+FB), several types of interactions were observed depending on the parameters and segments assessed: synergistic (immune cells); additive (cytokines and junction protein expression); less than additive (histological lesions and cytokine expression); antagonistic (immune cells and cytokine expression). Taken together, the present data provide strong evidence that chronic ingestion of low doses of mycotoxins alters the intestine, and thus may predispose animals to infections by enteric pathogens.

Individual and combined effects of subclinical doses of deoxynivalenol and fumonisins in piglets.

SCOPE: Deoxynivalenol (DON) and fumonisins (FB) are the most frequently encountered mycotoxins produced by Fusarium species and most commonly co-occur in animal diets. These mycotoxins were studied for their toxicity in piglets on several parameters including plasma biochemistry, organ histopathology and immune response. METHODS AND RESULTS: Twenty-four 5-wk-old animals were randomly assigned to four different groups, receiving separate diets for 5 wk, a control diet, a diet contaminated with either DON (3 mg/kg) or FB (6 mg/kg) or both toxins. At days 4 and 16 of the trial, the animals were subcutaneously immunized with ovalbumin to assess their specific immune response. The different diets did not affect animal performance and had minimal effect on hematological and biochemical blood parameters. By contrast, DON and FB induced histopathological lesions in the liver, the lungs and the kidneys of exposed animals. The liver was significantly more affected when the two mycotoxins were present simultaneously. The contaminated diets also altered the specific immune response upon vaccination as measured by reduced anti-ovalbumin IgG level in the plasma and reduced lymphocyte proliferation upon antigenic stimulation. Because cytokines play a key role in immunity, the expression levels of IL-8, IL-1ß, IL-6 and macrophage inflammatory protein-1ß were measured by RT-PCR at the end of the experiment. The expression of these four cytokines was significantly decreased in the spleen of piglets exposed to multi-contaminated diet. CONCLUSION: Taken together, our data indicate that ingestion of multi-contaminated diet induces greater histopathological lesions and higher immune suppression than ingestion of mono-contaminated diets.

Conidiobolomicose causada por conidiobolus lamprauges em ovinos no estado de Santa Catarina / Conidiobolomycosis caused by conidiobolus lamprauges in sheep in the state of Santa Catarina, Brazil

Descreve-se um surto de conidiobolomicose em ovinos no Estado de Santa Catarina. O surto ocorreu entre os meses de dezembro e março de 2006, no município de Santo Amaro da Imperatriz, região litorânea do Estado. A propriedade possuía 75 ovinos da raça Santa Inês e seis desses animais adoeceram. Clinicamente os animais doentes apresentavam dificuldade respiratória, corrimento nasal seroso a mucossanguinolento e, por vezes exolftalmia. Na necropsia verificou-se uma massa amarelada na região etmoidal e adjacências que, às vezes, atingia os linfonodos regionais, cérebro, globo ocular e pleura. Microscopicamente a massa caracterizava-se por infiltrado inflamatório granulomatoso com áreas necróticas associadas a hifas largas pouco ramificadas. Através de exame molecular detectou-se DNA de Conidiobolus lamprauges. Os aspectos clínicos, epidemiológicos, macroscópicos, microscópicos e moleculares caracterizam a conidiobolomicose causada por Conidiobolus lamprauges em ovinos.

An outbreak of conidiobolomycosis affecting sheep in the State of Santa Catarina, Southern Brazil is reported. The disease occurred in six Santa Inês breed sheep from a flock of 75 during the rainy season. Common clinical signs were noisy respiration and dyspnea, serous to mucosanguineous nasal discharge and exophthalmus. At necropsy there was a dense yellow mass in the nasopharyngeal area affecting the ethmoidal region, turbinate bones and occasionally limph nodes, central nervous system and pleura. Histopathologycally there was multifocal granulomas whith an eosinophilic necrotic reaction containing ribbon type hyphae similar to zygomycetous fungi. At molecular examination Conidiobolus lamprauges DNA was detected. The clinical, epidemiological, macroscopical, microscopical and molecular aspects characterize conidiobolomycosis caused by Conidiobolus lamprauges in sheep.

Intoxicação por Trema micrantha (Ulmaceae) em caprinos no Estado de Santa Catarina / Poisoning by Trema micrantha (Ulmaceae) in goats in the State of Santa Catarina

Vinte e cinco caprinos, criados em piquetes, morreram nos cinco dias subsequentes ao fornecimento de folhas de Trema micrantha (fam.Ulmaceae), uma árvore com nome comum de grandiúva. Quatro caprinos foram necropsiados e amostras de vísceras foram coletadas para exame histológico. As principais alterações clínicas foram: apatia, anorexia, cabeça apoiada contra obstáculos, decúbito e morte. Achados macroscópicos incluíram sufusões no epicárdio e endocárdio; fígado levemente amarelado e com padrão lobular evidente e, em um caso, acompanhado de hemorragias multifocais. Na histologia observou-se necrose hepática, que variava de centrolobular a massiva, compatível com hepatopatia tóxica. No SNC havia satelitose, tumefação neuronal, edema periaxonal, perivascular. O diagnóstico de intoxicação por Trema micrantha foi baseado no quadro clínico e lesional de hepatite tóxica associado ao uso da planta para alimentação de caprinos.

Twenty five goats, maintained in paddocks, had died in five subsequent days after have been offered leaves, mixed in the ration, of Trema micrantha, a tree commonly called grandiúva. Four animals were necropsied and samples were collected for histopathology. Clinical signs included apathy, anorexia, head pressing against obstacles, decubitus and death. Macroscopic findings included suffusions in the epi- and endocardium, a yellowish liver with pronounced lobular pattern, in one goat, the liver presented additionally multiple visible hemorrhages. Histological examination revealed centrilobular to massive hepatic necrosis consistent with acute liver toxicosis. In the brain, satelitosis, neuronal swelling, and perineuronal and perivascular edema was found. The diagnosis of poisoning by Trema micrantha was based in the clinical picture characteristic of toxic hepatitis associated in the feeding of the plant to the goats.

Fatal onion (Allium cepa) toxicosis in water buffalo (Bubalus bubalis).

Toxicosis caused by the ingestion of onion (Allium cepa) by 5 water buffalo (Bubalus bubalis) occurred in the district of Caçador, Santa Catarina, Brazil. The water buffalo died after ingestion of a large quantity of onion that had been left in the pasture. Clinical signs started 8 days postingestion and were characterized by pale mucous membranes, lethargy, and dark urine. At necropsy, pieces of onions were found in the rumen of 1 animal. The carcass smelled strongly of onion, and the kidneys and urine were dark brown. Microscopic renal lesions included tubular degeneration and necrosis with deposits of eosinophilic material in the cytoplasm of renal tubular epithelial cells and tubular lumina. These changes were consistent with hemoglobinuric nephrosis. Centrilobular coagulation necrosis was observed in the liver accompanied by hemorrhage and macrophages containing brown cytoplasmic pigment. A diagnosis of hemolytic anemia caused by onion toxicosis was based on the epidemiological data, clinical signs, macroscopic changes, and histological lesions.

Intoxicação por closantel em ovinos e caprinos no Estado de Santa Catarina: [revisão] / Poisoning by closantel in sheep and goats in the State of Santa Catarina, Brazil: [revisão]

Descrevem-se dois surtos de intoxicação por clo-santel, um em ovinos e outro em caprinos, no Estado de San-ta Catarina. No primeiro surto, de 12 ovinos que adoeceram 5 apresentaram cegueira, desses três morreram (Ovinos 1-3) e dois (Ovinos 4 e 5) foram eutanasiados, 6 meses após ficarem cegos. No segundo surto, de 26 caprinos que adoeceram, seis animais sobreviveram, porém ficaram cegos, e um deles foi eutanasiado. Clinicamente os animais apresentavam depressão, ataxia, incoordenação motora e reflexo pupilar diminuído a ausente. Em alguns animais esse quadro evoluiu para cegueira bilateral com ausência de reflexo de ameaça e midríase bilateral irresponsiva. Ao exame oftálmico verificou-se atrofia dos vasos da retina e hiperreflexia. Pelo exame histológico observou-se edema mielínico levando a status spongiosus no sistema nervoso central e neuropatia compressiva no nervo óptico, acompanhada de degeneração e/ou atrofia da retina. O objetivo deste trabalho é descrever os aspectos epidemiológicos, clínicos e patológicos da intoxicação por closantel em ovinos e caprinos.

Two outbreaks of closantel overdosage in sheep and goat flocks are described. In the first outbreak 12 sheep were affected, 5 of them showed blindness, three sheep died (Sheep 1-3) and two were euthanized 6 months after the onset of clinical manifestation (Sheep 4 and 5). In the second outbreak 26 goats were affected, from which six survived despite blindness and one was euthanized. Clinically the animals showed depression, ataxia, motor incoordination, decreased or absent pupil reflexes. In some animals this clinical picture developed to bilateral blindness, with no reaction to threat and bilateral irresponsive midriasis. In the ophthalmic examination retinal vessel atrophy and hyperreflexia were observed. The histological examination showed myelin edema leading to status spongiosus in the central nervous system and compressive neuropathy of the optic nerve, associated with retinal degeneration and/or atrophy. This report aims to describe the epidemiologic, clinic and pathologic aspects of closantel overdosage in sheep and goats.

Intoxicação experimental por Sida carpinifolia (Malvaceae) em bovinos / Experimental poisoning by Sida carpinifolia (Malvaceae) in cattle

Descrevem-se os achados clínicos e patológicos da intoxicação experimental por Sida carpinifolia em bovinos. Para a reprodução experimental da doença, folhas verdes da planta foram coletadas semanalmente na região do Alto Vale do Itajaí e fornecidas in natura diariamente para cinco bovinos nas doses de 10 e 20g/kg por 120 dias, 40g/kg por 30 dias, e 30 e 40g/kg de peso animal por 150 dias. Um bovino morreu e os outros foram eutanasiados ao final do período de consumo da planta. Os principais sinais clínicos consistiam de andar em marcha, olhar atento e tremores de cabeça e foram de intensidade leve a acentuado conforme a dose de planta e tempo de consumo. A lesão histológica predominante caracterizava-se por vacuolização e tumefação de neurônios (principalmente os de Purkinje), das células acinares pancreáticas e células foliculares da tireóide. Ultra-estruturalmente verificou-se vacúolos, por vezes, contendo material finamente granular em neurônios, células acinares pancreáticas e células foliculares da tireóide. S. carpinifolia causa doença de depósito lisossomal em bovinos quando consumida por período prolongado, mesmo em pequenas doses.

Clinical and pathological findings of experimental poisoning by Sida carpinifolia in cattle are described. A neurologic disease was observed in cattle on farms of the Alto Vale do Itajaí region of the Brazilian state of Santa Catarina. For the experimental reproduction of the disease, fresh green leaves, weekly harvested in the same region where spontaneous case occurred, were force-fed to five cattle at doses of 10 and 20g/kg for 120 days, 40g/kg for 30 days, and 30 and 40g/kg body weight for 150 days. One animal died and the others were euthanatized at the end of the experiment. Clinical signs and lesions varied from mild to severe in the experimentally poisoned cattle and depended on dose and length of the period of consumption. Main histological and ultrastructural lesions consisted of vacuolation and distension of neuronal perikarya (mainly of Purkinje cells), and of the cytoplasm of acinar pancreatic cells and thyroid follicular cells. It is concluded that ingestion of even small amounts S. carpinifolia for prolonged periods of time cause lisosomal storage disease in cattle.

Intoxicação espontânea e experimental por Eupatorium tremulum (Asteraceae) em bovinos / Spontaneous and experimental poisoning by Eupatorium tr tremulum emulum (Asteraceae) in cattle cattle

The spontaneous and experimental poisoning by Eupatorium tremulum in cattle is described. Spontaneous cases were diagnosed in a herd of 19 cattle in the municipality of Lages, Santa Catarina, Brazil. Three of the animals were found dead after having been transferred to a pasture with abundant quantities of E. tremulum. On two of them postmortem examination was performed and several internal organs were sampled for histological examination. Green leaves of E. tremulum were force-fed orally to 5 calves in single doses of 23-32g/kg body weight. Three calves showed clinical signs and two died. The main clinical signs included anorexia, apathy, absence of rumen movements, diarrhea and a flabby abdominal wall. Gross changes were restricted to the fore stomachs and were identical to those observed in the cases of natural poisoning. Rumen and reticulum were slightly reddish from outside; the corneal layer of their internal lining was loosely attached to a markedly red mucosa. The histological examination of rumen and reticulum from spontaneous and experimental cases revealed necrosis and vesicle formation in the epithelium; in some segments of the ruminal mucosa there was detachment of the epithelial covering and infiltration by neuthophils. Poisoning by E. tremulum has clinical course, gross lesions and histopathology very similar to those observed in poisoning caused by ingestion of the plants Baccharidastrum triplinervium, Baccharis coridifolia and Baccharis megapotamica var. weirii. The diagnosis of the spontaneous cases here described was confirmed by epidemiological data and the experimental reproduction of characteristic gross lesions and histopathology.

Descreve-se a intoxicação natural e experimental por Eupatorium tremulum em bovinos. Um surto de intoxicação espontânea por esta planta foi diagnosticado no município de Lages, Santa Catarina. Em um lote de 19 bovinos, três morreram após a transferência para uma invernada aonde havia grande quantidade de E. tremulum. Os animais foram encontrados mortos, e dois foram necropsiados e coletado amostras de vísceras para exame histológico. Experimentalmente, folhas verdes de E. tremulum foram administradas a cinco bovinos, em doses únicas de 23 a 32g/kg de peso animal. Destes, três adoeceram e dois morreram. Os principais sinais clínicos observados foram anorexia, apatia, atonia ruminal, micção freqüente e em pequenos jatos, fezes pastosas e ventre flácido. As lesões macroscópicas restringiram-se aos pré-estômagos e foram idênticas, tanto para intoxicação natural como para a experimental. O rúmen e retículo externamente mostravam tonalidade levemente avermelhada, a camada córnea da mucosa estava frouxamente aderida e a mucosa tinha coloração vermelha acentuada. Ao exame histológico observou-se no rúmen e retículo, tanto na intoxicação espontânea, como experimental, necrose do epitélio da mucosa com formações de pequenas vesículas e em alguns segmentos, desprendimento da camada epitelial e leve infiltrado de neutrófilos. A intoxicação por E. tremulum tem curso clínico, lesões macro e microscópicas muito semelhantes àquelas produzidas pela intoxicação por Baccharidastrum triplinervium, Baccharis coridifolia (mio-mio) e Baccharis megapotamica var. weirii (mio-mio do banhado). O diagnóstico diferencial entre essas quatro intoxicações deve ser feito pela presença da planta e pelos dados epidemiológicos. O diagnóstico dos casos espontâneos foram confirmados pelos dados epidemiológicos e reprodução experimental das lesões macro e microscópicas.

Intoxicação aguda por fluorsilicato de sódio em bovinos no Estado de Santa Catarina / Acute sodium fluorsilicate poisoning in cattle in the state of Santa Catarina

Descreve-se um surto de intoxicação aguda por fluorsilicato de sódio em seis bovinos e a reprodução experimental da intoxicação, através da administração de fluorsilicato de sódio a dois animais. O quadro clínico era caracterizado por tremores musculares em todo o corpo, salivação intensa, gemidos e inquietação, com morte rápida. Na intoxicação experimental foi observado também decúbito lateral, com respiração dificultosa, contração tônica e episódios de pedalagem. As lesões macroscópicas principais foram observadas no rúmen e abomaso, consistindo em mucosa difusamente vermelha, com edema de parede e ulceração. Na histologia havia necrose acentuada de segmentos da mucosa ruminal e abomasal, associada a infiltrado de polimorfonucleares na submucosa e muscular. Além de lesões gástricas os bovinos apresentavam necrose portal hepática, degeneração e necrose tubular renal e necrose de folículos linfóides. O fluorsilicato de sódio produziu sinais clínicos com 300mg/kg e morte com 400mg/kg.

An acute poisoning with sodium fluorsilicate in six cattle is reported, as well as the experimental reproduction by oral administration of the compound to two bovines. Clinical manifestations of the natural poisoning include muscle tremors, hypersalivation, groaning and rapid death. In the experimental poisoning lateral recumbency, dyspnea, tetanic spasms and paddling was also observed. The main necropsy findings were reddening, edema and ulceration of the ruminal and abomasal mucosa. Histopathological findings were necrosis of the epithelium of the forestomachs with polymorphonuclear infiltration of the submucosal and muscular layers. Tubular renal necrosis, liver portal necrosis and necrosis of the lymphoid tissues was also noted. The sodium fluorsilicate caused clinical signs at a dose of 300mg/kg, and death from 400mg/kg on.