Surto de intoxicação por sal em ovinos no estado do Pará

Abstract

RESUMO.-O presente trabalho relata um surto de intoxicação por sal em ovinos no Brasil, em uma propriedade no estado do Pará. De um total de 545 ovinos, oito animais adoeceram (1,46%) e quatro destes morreram (50%). A avaliação das instalações e do manejo indicaram como fatores predisponentes a ingestão excessiva de mistura mineral e a restrição hídrica. Os principais sinais clínicos foram decúbito, diminuição ou ausência da sensibilidade cutânea, ausência dos reflexos de ameaça, palpebral e auricular, midríase, nistagmo, opistótono, espasticidade de membros, sonolência e estupor. Havia ainda, timpanismo, diarreia, taquipneia, taquicardia, desidratação e poliúria. A evolução do quadro clínico nos animais que morreram variou de duas horas e meia a 48 horas. As médias das concentrações séricas de sódio e de potássio de 31 ovinos do mesmo lote afetado pela intoxicação, em amostras colhidas durante o surto, revelaram hipernatremia (190mEq/l) e hipercalemia (8,2mEq/l). À necropsia, observou-se em um animal, achatamento das circunvoluções cerebrais. Microscopicamente, neste animal, evidenciou-se vacuolização moderada do neurópilo, particularmente nas lâminas intermediárias This paper reports an outbreak of salt poisoning in sheep on a farm in the state of Pará, northern Brazil. Eight (1.46%) animals were affected from a total of 545 sheep and four (50%) of them died. The evaluation of the facilities and the handling indicated as predisposing factors excessive intake of the mineral supplement and water restriction. The main clinical signs were recumbency, decrease or absence of cutaneous sensibility, absence of auricular, palpebral and menace reflex, mydriasis, nystagmus, opisthotonus, spasticity of limbs, somnolence and stupor. Beside these signs bloat, diarrhea, tachypnea, tachycardia, dehydration and polyuria were observed. The course of the disease in animals that died ranged from two hours and a half to 48 hours. The medium of serum concentration of sodium and potassium of 31 sheep from the same group affected on samples collected during the outbreak revealed hypernatremia (190mEq/l) and hyperkalemia (8.2mEq/l). At necropsy, there was flattening of the cerebral gyri in one sheep; in this animal was found vacuolization of the neuropil in the cerebral cortex with moderate intensity in the intermediary and mild on the superficial layers, with increased perineural and perivascular spaces. In these areas there were markedly swollen nucleus of astrocytes with acute neuronal necrosis. The dosage of sodium in the brain of a sheep revealed a high value of 3.513ppm. The diagnosis was made based on the epidemiology, clinical signs, macro and microscopic lesions and in the dosages of sodium in serum and brain.

Adaptability of sheep to three salinity levels in different environments

“…The animals exposed to 32 °C had a higher RR, demonstrating that RR elevation is one of the mechanisms used by sheep to dissipate heat to the environment (Eustáquio Filho et al, 2011;Luz et al, 2014). Duarte et al (2014) reported that sheep under water stress and ingesting excessive minerals had tachypnea, tachycardia, and dehydration, as well as high concentrations of sodium and potassium in the blood. Eustáquio Filho et al (2011) evaluated sheep, andAraújo et al (2017) and Lucena et al (2013) evaluated goats in climatic chambers and found that the ST, RT, RR, and HR increased as air temperature increased.…”

“…These electrolytes are involved in multiple functions, including acid-base balance, maintenance of osmotic pressure, membrane potential, and nerve impulse transmission, and the excess or lack of some macrominerals decreases animal performance (Reece & Dukes, 2006). Sodium concentrations above normal may cause water movement from the intracellular to the extracellular compartment, usually accompanied by excessive salt intake, potentially leading to hypertension, tachypnea, tachycardia, dehydration, severe thirst, weight loss, and death (Duarte et al, 2014).…”

“…), ability to retain water and excrete dry stools and concentrated urine, high tolerance to water stress (Silva, Araújo, Oliveira, Azevedo, & Furtado, 2016), and tolerance to foods with high salt concentrations (Moreno et al, 2015;Castro et al, 2017) and high salinity water (Moura et al, 2016;Yousfi, Marques, Betti, Araus, & Serret, 2016). Potter (1968) reported that the consumption of high salinity water by sheep might increase the osmotic pressure in the rumen, without affecting the ruminal microbiota, and change the heart and respiratory rate of the animals (Duarte et al, 2014).…”

Polioencephalomalacia in ruminants from the semi-arid region of Rio Grande do Norte, Brazil

“…However, nowadays, not all cases of PEM are associated with thiamine deficiency, and several other etiologies are involved in the pathogenesis of this lesion (SANT'ANA et al, 2009b). Among these causes, we may highlight manifestations of excess sulfur intake (LONERAGAN et al, 1998;CUNHA et al, 2010CUNHA et al, , 2011DELFIOL et al, 2013), salt (OSWEILER et al, 1995;DUARTE et al, 2014), lead intoxication (CEBRA; CEBRA, 2004;LEMOS et al, 2004), and thiamine deficiency SANT'ANA et al, 2009b;GRAÇA et al, 2010) or analogues, such as amprolium (SANT'ANA et al, 2009a;NOGUEIRA et al, 2010), besides ingestion of plants rich in thiaminase, and acute poisoning by Phalaris spp. and by bovine herpesvirus type-5 SANT'ANA et al, 2009b).…”

“…In Brazil, PEM is predominant in cattle (NAKAZATO et al, 2000;LEMOS et al, 2004;VIEIRA et al, 2007;CUNHA et al, 2010CUNHA et al, , 2011RIBAS et al, 2013), although there are also reports in sheep (LIMA et al, 2005;VIEIRA et al, 2007;DUARTE et al, 2014), goats (LIMA et al, 2005), and in buffaloes (GUIMARÃES et al, 2008).…”