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Fattening pigs (n = 751) showed progressive apathy, paralysis, and sudden death after accidental ingestion of excessive concentrations of selenium in mineral feed. Selenium concentrations of 1.09 to 1.32 mg/L in the serum confirmed the diagnosis. Within 3 d all pigs had died spontaneously or were euthanized due to the grave prognosis and on welfare grounds.
Toxicose suraiguë au sélénium suivie de mort soudaine chez des porcs en croissance et des porcs de finition. Des porcs d’engraissement (n = 751) ont manifesté une apathie progressive et de la paralysie, puis sont morts soudainement après l’ingestion accidentelle de concentrations excessives de sélénium dans les aliments minéraux. Des concentrations sériques de sélénium de 1,09 à 1,32 mg/L ont confirmé le diagnostic. En l’espace de trois jours, tous les porcs sont morts spontanément ou ont été euthanasiés en raison d’un pronostic sombre et pour des raisons de bien-être.
(Traduit par Isabelle Vallières)
Selenium is an essential trace element that is involved in several cellular biochemical pathways (1). Since selenium deficiency results in impaired activity of the immune system and in reduced fertility, it has been used as a supplement in the diets of animals. Supplementation also helps to prevent selenium-responsive diseases such as hepatosis dietetica and nutritional myopathy in swine (2–4). However, dietary selenium concentrations > 1 to 5 mg/kg feed are toxic. The European Union (EU) has legislated the concentration of dietary selenium to 0.5 mg/kg with 88% dry matter for several species, including pigs, but has not specified the selenium content in products originating from animal sources.
The effect of accidental overdose of selenium in humans and accidental or experimental overdose in various animals has been widely described in the literature (5–9). Indeed, selenium toxicosis in pigs has been reported, with signs referable to acute or chronic intoxication characterized by high morbidity but low mortality. Clinical signs of a slight increase in selenium concentration in the diet are alopecia, lameness, and lesions of the hoof wall. Less specific symptoms include diarrhea, cardio-respiratory failure, and hyperthermia (10). In severe cases, where the selenium concentration in the feed was nearly 10 mg/kg, paralysis and death of exposed pigs was observed. In these animals, central nervous system lesions involved the cervical and lumbar intumescences of the spinal cord and consisted of a severe, bilateral symmetrical poliomyelomalacia of the ventral horns. The pons and medulla oblongata also exhibited lesions of polioencephalomalacia (11).
Although the course of the disease is dependent on the bioavailability of the selenium (12), this information is usually missing from case reports. This case report describes a peracute form of selenium toxicosis leading to a high mortality in pigs from various age groups, which received a diet that was supplemented with a mineral premix containing an excessive selenium concentration of 2.5 g/kg dry matter.
In a 1-site production system in northern Germany, growing and finishing pigs were reported to be suffering from neurological disorder and sudden death. The breeding stock of 250 sows, and all piglets in the nursery unit were unaffected. Clinical signs were only observed in the growing and fattening groups. All pigs on the farm were fed the same whey-based diet, to which was added varying amounts of home-grown cereals. A commercial mineral supplement was added to the feed. The type and amount of additive varied with the age of the pigs. A total of 751 growing and finishing pigs that were housed in 2 fattening buildings received the same mineral premix, at a concentration of 2.66% in the diet. This unusually wide administration of the same premix to different ages of growing and fattening pigs was due to technical limitations in 1 of the fattening buildings. The farmer reported that the first clinical signs became apparent 24 to 36 h after ingestion of feed to which the last 2 bags from a batch of 40 bags of mineral supplement had been added.
The attending veterinarian performed a clinical examination of pigs from all age groups and production stages. Symptoms were only seen in the exposed group of growing and finishing pigs and were non-specific, characterized by apathy, posterior paralysis (Figure 1), and sudden death. Symptoms were seen in 18% of all growing and finishing pigs. The rate of losses was higher in growing pigs (> 40%) than in finishing pigs (< 10%). None of the pigs that were examined had pyrexia, and there were no signs of infectious disease. Some of the feeders were still full, and those animals still alive and not clinically affected were refusing to eat the food. Serum samples were obtained from 15 randomly assigned pigs and 4 pigs with typical symptoms were submitted to necropsy.
In compliance with the German legislation, notifiable diseases such as classical swine fever and Swine Herpes Virus 1 were ruled out by testing serum samples for antibodies and antigen (State Veterinary Laboratory, Detmold, Germany). In order to confirm the suspected diagnosis of toxicosis, the concentrations of various enzymes (Table 1) in the serum were measured (Veterinary Laboratory, Bakum, Germany). In all samples the aspartate-aminoacid-transferase (AST) was significantly increased (Table 1). Other parameters were shown to be in a physiological range. The mean concentration of selenium in the serum, measured by atomic absorption, varied from 1.09 to 1.32 mg/L (Table 2). Various samples taken from the pre-mixer and the filled feeders on the farm also had high selenium concentrations. If the mineral supplement was used in the whole diet at a proportion of 2.66%, based on dry matter, it was calculated that concentration of selenium in the mixed diet from the trough was 58.6 mg/kg. The concentration of selenium in the mineral supplement was 2506 mg/kg (values based on 88% dry matter). Subsequently, the producer of the mineral feed conceded a cross-contamination due to technical failure and speculated that small amounts of sodium selenate from a former production step might have contaminated the first bag of the batch of mineral feed that had been sold to the farm.
A complete necropsy was performed on 4 pigs after they were euthanized by injection of pentobarbital. Visual inspection of the bodies, the respiratory, alimentary, and reproductive tracts, failed to identify any gross lesions. Samples from brain, thoracic, and lumbar spinal cord, liver, kidney, spleen, oesophagus, and gastric mucosa were submitted for histological examination. Samples of liver, kidney, and muscle were assayed for selenium and found to contain highly elevated concentrations (Table 2). Samples from all 4 animals had varying degrees of a bilaterally symmetrical polioencephalomalacia (Figure 2) and/or poliomyelomalacia (Figure 3). Lesions were confined to the medulla oblongata, pons, and ventral horns of the spinal cord. They were characterized by neuronal eosinophilic degeneration and necrosis, marked spongiosis and microgliosis, multifocal mild hemorrhages and activated endothelial cells. The liver, spleen, and/or kidneys had varying degrees of congestion in all pigs.
On the farm, the number of affected pigs showing clinical signs increased. During the 2nd night after consumption of contaminated feed a further 231 animals died. In addition, 17 pigs had to be culled. Thus, mortality after 48 h was 51%. The course of disease was progressive and spreading, even though the feed with high selenium concentration had immediately been removed. Three days after the accidental contamination all remaining pigs were exhibiting slight to severe signs of neurological disorder. Given the grave prognosis it was decided that all pigs would be culled on welfare grounds. The total loss was 751 pigs.
This case describes a progressive peracute form of selenium toxicosis on a pig farm. Clinical symptoms were partly in accordance with other case reports but, as far as we know, the rapid progression and the severity of the disease has not been reported previously.
When a veterinarian is confronted with an anamnesis characterized by high morbidity, neurological signs, and very high mortality in a group of pigs several differential diagnoses have to be kept in mind. Step by step, each consideration has to be excluded from the differential diagnosis. Infections with certain serotypes of the porcine enterovirus (serotype 1) or the encephalomyocarditis virus can lead to neurological disorders and loss of animals. Several toxic compounds are able to provoke dysfunction of the peripheral and/or central nervous system. For example, high dosages of sodium chloride, high dosage of vitamin D, and the toxin of Clostridium botulinum can cause both high morbidity and high mortality. Finally, an iatrogenic toxicosis by simultaneous administration of ionophors and tiamulin should be considered.
Infections were ruled out because the rectal temperature of the animals was within normal limits and the disease did not spread to other animals but was limited to a group of pigs, which received the same feed. The assumption that selenium and no other toxin was responsible for the symptoms was based on the observation that neurological disorders started with posterior incoordination. In advanced stages, pigs were hypersensitive and incoordinated. Finally, the animals showed paralysis of the extremities and perished. These clinical signs are not consistent with those associated with the other toxins described above.
The clinical effect of any toxicosis usually depends on concentration, duration of exposure, and bioavailability of the agent. The pigs in this case were exposed once to sodium selenate (Na2SeO3) at 58.6 mg pure selenium/kg dry matter. In experimental studies, pigs exposed to different chemical compounds of selenium showed clinical signs of toxicosis after 4 to 5 d and 9 d, dependent upon the bioavailability of the compounded selenium (12). It is noteworthy that the highest serum concentration was observed using seleno-DL-methionine and clinical signs were most obvious when feeding Astragalus bisulcatus. However, pigs receiving sodium selenate have also been affected. Other reports from accidental continual exposure of lower dosages noted that a period of 3 or 6 wk elapsed before clinical signs of toxicosis became apparent. However, neither of these papers specified the source of selenium (7,9).
In contrast to other studies and case reports in the literature, the 1st pigs in this series died within 36 h after ingesting the sodium selenate and within 72 h all exposed pigs had perished or had been culled on welfare grounds. The latter decision was supported by the pathological findings in the cerebrum and spinal cord of animals submitted for necropsy. Polioencephalomalacia and necrosis of neurons, as described in the examined tissue samples, are irreversible and, therefore, preclude a restitutio ad integrum. There is 1 case report (8) in which similar observations of a fatal outcome were made after pigs were fed contaminated mash containing 54.6 mg selenium/kg feed (dry matter). However, in that report, at least 20% of affected pigs recovered sufficiently to be marketed. Mortality was overall significantly lower and again the source and the selenium compound were not specified.
The rapid occurrence of clinical signs in the present case appeared to have been triggered by the enormous concentration of selenium in the wet diet. However, pigs exposed to equal amounts of selenium (10 to 14 mg/kg) in the consumed feed mixture, developed only a moderate form of the disease over several weeks and mortality was only 12% and 15%, respectively, over the whole period (5,11).
Finally, it should be noted that over dosage of the selenium in this case adversely affected the palatability of the diet. It is, perhaps, not surprising that clinically affected pigs might exhibit reduced feed intake. However, it was also observed that unaffected pigs refused the diet, in spite of hunger. To our knowledge, this is the first report of such effects in the case of selenium toxicosis in pigs.
This case report gives an overview of peracute and severe selenium toxicosis in pigs with a fatal outcome for all of the exposed population. In addition to the forensic aspects of this case report and the discussion on reaching the correct diagnosis, it highlights, perhaps for the first time, the welfare issues that arise when the pathological damage is deemed so severe that a recovery cannot be attained. It might also be argued that culling was necessary to prevent animals from entering the human food chain with unacceptably high levels of selenium, although this has never been considered necessary by the various EU authorities. CVJ
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