Intoxicação por selênio em suínos no Sul do Brasil

Abstract

RESUMO.-São descritos dois surtos de intoxicação por selênio em suínos na região Sul do Brasil. Foram acometidos leitões em fase de creche, entre 27 e 22 dias, com mortalidade variando de 16% a 15,3% (Surto 1 e 2 respectivamente). Os suínos apresentaram poliomielomalacia simétrica focal e lesões de casco, que inicialmente eram caracterizadas por uma linha avermelhada na borda coronária que evoluía nos suínos sobreviventes para desprendimento do casco. Os sinais clínicos iniciaram após seis dias (Surto 1) e 30 horas (Surto 2) da introdução da ração com alto teor de selênio. O surgimento dos sinais foi abrupto, caracterizado por andar cambaleante, com evolução para paralisia dos membros pélvicos e posteriormente tetraparesia. Macroscopicamente observaram-se focos circulares amarelados com áre-as deprimidas mais escuras, restritas ao corno ventral da substância cinzenta em intumescências cervical e lombar. Microscopicamente essas áreas corresponderam à malacia da substância cinzenta, caracterizada por microcavitações, perda neuronal, cromatólise, neuronofagia, infiltrado de células Gitter, microgliose, astrócitos de Alzheimer tipo II e proliferação de células endoteliais evidenciadas na imunohistoquímica (IHQ) para fator de von Willebrand. Ainda, Two outbreaks of poisoning by selenium in swine in southern Brazil are described. Piglets were affected in the post-weaning period, between 27 and 22 days, with mortality rates ranging from 16% to 15.3% (Outbreak 1 and 2 respectively). The pigs had focal symmetrical poliomielomalacia and hoof lesions, which were initially characterized by a reddish line at the coronary band that evolved in surviving pigs to release of the hooves. Clinical signs were observed after six days (Outbreak 1) and 30h (Outbreak 2) after the introduction of feed with high selenium content. The appearance of the signs was abrupt, characterized by gait and progressing to paralysis of the hind limbs and later to tetraparesis. Macroscopically, in some animals there were yellow circular foci with darker areas restricted to the ventral horn of the gray matter in the cervical and lumbar intumescence. Microscopically, these areas correspond to gray matter malacia, characterized by microcavitation, neuronal loss, chromatolysis, neuronophagia, infiltrating Gitter cells, microgliosis, Alzheimer's type II astrocytes and proliferation of endothelial cells which were labeled by immunohistochemistry (IHC) as von Willebrand factor. Also in the second outbreak, two pigs showed diffuse vacuolation of the cytoplasm of neurons and in one pig gemistocytic astrocytes were observed. In IHC for GFAP astrocytosis and astrogliosis was observed. Besides those spinal changes in two pigs symmetrical polioencephalomalacia in the brainstem was found. In feed samples, 3.38ppm (Outbreak 1) and 154ppm (Outbreak 2) of Se/kg were detected, and in liver samples higher dosages than 3.34ppm (range from 3.34 to 10ppm) were found. In Outbreak 2, 44 days after the withdrawal of the diet, the euthanasia of six pigs was performed to monitor ...

Experimental and iatrogenic poisoning by sodium selenite in pigs

“…The lesions found in the spinal cord of the present experimentally and iatrogenically poisoned pigs were identical to those found in FSPMS reported elsewhere (Harrison et al 1983, Wilson et al 1983, Casteel et al 1985, Mensink et al 1990, Stowe et al 1992, Gomes et al 2014). …”

“…The microscopic spinal cord lesions are similar to those that have been described for FSPMS (Harrison et al 1983, Wilson et al 1983, Casteel et al 1985, Mensink et al 1990, Stowe et al 1992, Gomes et al 2014). There was endothelial degeneration and later activation, variable degrees of neuropil edema, neuronal necrosis, neuronophagia, macrophage infiltration, the occasional presence of eosinophils, mononuclear perivascular cuffing and severe gliosis with "Gitter cells".…”

“…In swine, a distinct condition known as focal symmetrical poliomyelomalacia of swine (FSPMS) has been observed. It is manifested by ataxia of the pelvic limbs that progresses to thoracic limb ataxia, tetraplegia and death (Harrison et al 1983, Wilson et al 1983, Casteel et al 1985, Mensink et al 1990, Stowe et al 1992, Gomes et al 2014. Yellowish--brown bilateral areas of the spinal cord can sometimes be observed macroscopically, especially in the ventral horns of the cervical and lumbar intumescences of the spinal cord (Harrison et al 1983, Wilson et al 1983, Gomes et al 2014.…”

“…It is manifested by ataxia of the pelvic limbs that progresses to thoracic limb ataxia, tetraplegia and death (Harrison et al 1983, Wilson et al 1983, Casteel et al 1985, Mensink et al 1990, Stowe et al 1992, Gomes et al 2014. Yellowish--brown bilateral areas of the spinal cord can sometimes be observed macroscopically, especially in the ventral horns of the cervical and lumbar intumescences of the spinal cord (Harrison et al 1983, Wilson et al 1983, Gomes et al 2014. Microscopically, these lesions appear as focal motor neuron necrosis, microcavitation and myelin vacuolation, in addition to hemorrhage and perivascular cuffing (Penrith & Robinson 1996, Gomes et al 2014.…”

“…Yellowish--brown bilateral areas of the spinal cord can sometimes be observed macroscopically, especially in the ventral horns of the cervical and lumbar intumescences of the spinal cord (Harrison et al 1983, Wilson et al 1983, Gomes et al 2014. Microscopically, these lesions appear as focal motor neuron necrosis, microcavitation and myelin vacuolation, in addition to hemorrhage and perivascular cuffing (Penrith & Robinson 1996, Gomes et al 2014. Hence, the pathogenesis of FSPMS still remains a mystery, and the toxic dynamic of selenium lacks comprehensive explanations.…”